Clinical guidelines for maternity hospitals by Matres Mundi

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CLINICAL GUIDELINES for

MATERNITY HOSPITALS On initiative of:

INTERNATIONAL SCHOOL OF PERINATAL MEDICINE FOR AFRICA With the support of:

MATRES MUNDI (Programme LIFE FOR AFRICA) Thanks to financial support of:

Womenâ&#x20AC;&#x2122;s Health Dexeus And with the collaboration of:

Rotary International

This book will be distributed for Rotary Club Barcelona Condal amongst all the African Maternity Hospitals

General Coordinator José M. Carrera Secretary General of «International School of Perinatal Medicine for Africa» Scientific committee Vicenç Cararach Ernesto Fabre Xavier Carbonell José M. Carrera Jordi Bellart Bernat Serra Dolores Chacón Transalation and linguistic revision Sonia Carrera Ade Rivera José M. Dachs Secretary of Edition M. Ángeles Botija Design, Layaut and Prepress Baber, scp, Barcelona, Spain Secretariat and Coordination of Edition MATRES MUNDI INTERNATIONAL Londres, 6, p8 08029 Barcelona. Spain Tel. 0034/934.190.015 info@matres-mundi.org / jmcarrera@matres-mundi.org www.matres-mundi.org

THE INTERNATIONAL SCHOOL OF PERINATAL MEDICINE FOR AFRICA (ISPEMA) Is an international, independent, solidary, not-profit organisation whose objective is to increase the number and the degree of expertise maternal-infant healthcare professionals (obstetricians, paediatricians, midwives, nurses, reproductive health experts, etc.) in Africa. ISPEMA was founded in the Royal Academy of Medicine of Catalonia, in Barcelona, Spain, on December 10 th, 2012. The Founding Societies are: – Matres Mundi International. – World Association of Perinatal Medicine (WAPM). – International Academy of Perinatal Medicine (IAPM). – European Association of Perinatal Medicine (EAPM). – African Association of Perinatal Medicine (AAPM). – International Society of The Fetus as a Patient. – Ian Donal Inter-university School of Medical Ultrasound. ISPEMA has an International Council integrated by the Presidents of the founding Societies. The president is Prof. Erich Saling, and Secretary General, Prof. José M. Carrera. The Board of Directors, is managed by MATRES MUNDI, through the Life For Africa programme.

MATRES MUNDI Is a specialised Non-Governamental Organization (NGO), whose aim is to promote maternal and infant health in developing countries. Since its foundation in Barcelona in 1996, MATRES MUNDI has conducted more than 250 solidarian sanitary projects all over the world and developed an important number of other social projects (training and educational projects, promotion of social awareness, etc.) MATRES MUNDI roots are the health care professionals (obstetricians, paediatricians, midwives, nurses, etc) working in Maternity Hospitals of developing countries. The founder of MATRES MUNDI was Prof. José M. Carrera, and the current president is Prof. Vicenç Cararach. The programme LIFE FOR AFRICA is developed by MATRES MUNDI, with the support of all the International Societies of Perinatal Medicine.

WOMEN’S HEALTH DEXEUS Founded in 1935 as the first obstetrical private clinic in Spain, today, Women’s Health Dexeus is one of the largest and most specialised centre in Europe when it comes to women’s health care. It is an international reference centre, pioneer in prevention, diagnosis and treatment in women’s health, with its medical protocols that allows to react quickly in case of detecting any disease. The advanced technology used and the constant medical research, conducted by the R & D 1 I department, places Women’s Health Dexeus as one of the most renowned centres for women’s care in Europe Moreover, with more than 75 years of history, the Dexeus School is Spain’s oldest center for training in gynaecology, obstetrics and reproduction. Located in Barcelona, Women’s Health Dexeus treats women at all stages of their lives, infancy, adolescence, youth, maternity, menopause and active ageing —and gives them comprehensive care in its Obstetrics, Gynaecology and Reproductive Medicine departments.

INDEX PROLOGUE by E. Saling PREFACE by A. Ashmaig FOREWORD by J. M. Carrera A. Terminology and classification of the risk . . . . . . . . . . . . . . . . 17 A.1. Terminology in perinatal medicine . . . . . . . . . . . . . . . . . . . . . . . . . . . . 19 A.2. Evaluation and classification of high risk . . . . . . . . . . . . . . . . . . . . . . 23 A.3. Abbreviations . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 27 B. Pregnancy . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 37 B.1. Prenatal attendance . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 39 B.1.1. B.1.2. B.1.3.

Antepartum Care . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 39 Health Education during Pregnancy . . . . . . . . . . . . . . . . . . . . 44 Drugs and Radiations in Perinatal Period . . . . . . . . . . . . . . . . 48

B.2. Proceedings and technology . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 52 B.2.1. B.2.2. B.2.3. B.2.4. B.2.5. B.2.6. B.2.7. B.2.8. B.2.9. B.2.10. B.2.11. B.2.12. B.2.13.

Pregnancy Dating . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 52 Fetal Ubication (Leopoldâ&#x20AC;&#x2122;s Manoeuvres) . . . . . . . . . . . . . . . . . 53 Obstetrical Ultrasonography . . . . . . . . . . . . . . . . . . . . . . . . . . . 53 Amniocentesis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 55 Amnioscopy . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 58 Fetal Lung Maturity . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 59 Cardiotocographic Prenatal Monitoring . . . . . . . . . . . . . . . . . 60 Infectious Disease Screening . . . . . . . . . . . . . . . . . . . . . . . . . . 61 Cerclage Technique . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 62 Clinical pelvimetry . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 64 External Cephalic Version (ECV) . . . . . . . . . . . . . . . . . . . . . . . 65 Amniotic Fluid Index (AFI) . . . . . . . . . . . . . . . . . . . . . . . . . . . . 67 Congenital Deffects: Screening, Diagnosis and Prevention . . 68

B.3. Obstetrical pathology . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 71 B.3.1. B.3.2. B.3.3. B.3.4. B.3.5. B.3.6.

Nausea and Vomiting in Pregnancy . . . . . . . . . . . . . . . . . . . . . 71 Miscarriage . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 72 Ectopic Pregnancy . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 74 Gestational Trophoblastic Disease (GTD) . . . . . . . . . . . . . . . . 75 Molar Pregnancy (Hydatiform Mole) . . . . . . . . . . . . . . . . . . . . 76 Gestational Trophoblastic Neoplasia/Tumour . . . . . . . . . . . . . 78

CLINICAL GUIDELINES FOR MATERNITY HOSPITALS

Index

B.3.7. Multiple Pregnancies . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 81 B.3.8. Cervical Incompetence . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 85 B.3.9. Premature Rupture of Membranes . . . . . . . . . . . . . . . . . . . . . . 86 B.3.10. Preterm Labor (ptl) . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 88 B.3.11. Intraamniotic Infection (IAI) . . . . . . . . . . . . . . . . . . . . . . . . . . 90 B.3.12. Antepartum Haemorrhage (APH) . . . . . . . . . . . . . . . . . . . . . . . 93 B.3.13. Intrauterine Growth Restriction . . . . . . . . . . . . . . . . . . . . . . . . 97 B.3.14. Congenital Defects: Behavior during Pregnancy . . . . . . . . . . . 99 B.3.15. Rh Isoimmunization . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 100 B.3.16. Preeclampsia and Eclampsia . . . . . . . . . . . . . . . . . . . . . . . . . . 102 B.3.17. Postterm Pregnancy . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 112 B.3.18. Oligoamnios (Oligohydramnios) . . . . . . . . . . . . . . . . . . . . . . . 114 B.3.19. Polyhydramnios . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 115 B.3.20. Fetal Demise . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 116

B.4. Medical pathology . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 121 B.4.1. B.4.2. B.4.3. B.4.4. B.4.5. B.4.6. B.4.7. B.4.8. B.4.9. B.4.10. B.4.11. B.4.12. B.4.13. B.4.14. B.4.15. B.4.16. B.4.17. B.4.18. B.4.19. B.4.20. B.4.21.

Anaemia in Pregnancy . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 121 Respiratory Diseases in Pregnancy . . . . . . . . . . . . . . . . . . . . . . 123 Rheumatic heart Disease in Pregnancy . . . . . . . . . . . . . . . . . . 124 Cardiac Disease in Pregnancy . . . . . . . . . . . . . . . . . . . . . . . . . . 127 Gestational Diabetes (gdm) . . . . . . . . . . . . . . . . . . . . . . . . . . . . 129 Diabetes and Pregnancy . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 131 Psychiatric Disorders . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 135 Jaundice . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 136 Thyroid Disorders . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 138 Epilepsy . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 139 Thromboembolism . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 140 Urinary tract Infections . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 142 Infections diseases in Pregnancy . . . . . . . . . . . . . . . . . . . . . . . 144 Listeriosis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 154 Cytomegalovirus . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 155 Toxoplasmosis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 156 Malaria in Pregnancy . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 157 HIV/AIDS in Pregnancy . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 158 Streptococcus Agalactiae . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 163 Chagasâ&#x20AC;&#x2122; Disease . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 164 Injuries during Pregnancy . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 165

C. Labour . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 169 C.1. Labour attendance . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 171 C.1.1. C.1.2. C.1.3. C.1.4.

Management of normal labour . . . . . . . . . . . . . . . . . . . . . . . . . 171 Management of dystocia: practical points . . . . . . . . . . . . . . . . 175 Obstetrician Preparation for Childbirth . . . . . . . . . . . . . . . . . . 178 Traditional Birth Attendant Training (TABS) . . . . . . . . . . . . . . 179

CLINICAL GUIDELINES FOR MATERNITY HOSPITALS

Index

C.2. Proceedings and technology . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 181 C.2.1. Induction of Labour . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 181 C.2.2. Intrapartum Fetal Monitoring . . . . . . . . . . . . . . . . . . . . . . . . . 184 C.2.3. Episiotomy . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 188 C.2.4. Operative Vaginal Delivery: Vacuum, Spatulas and Forceps . 190 C.2.5. Caesarean Section . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 194 C.2.6. Protocol for Postoperative Care . . . . . . . . . . . . . . . . . . . . . . . . 199 C.2.7. Postpartum Revision of the Vaginal Canal . . . . . . . . . . . . . . . . 203 C.2.8. Appropriate Use of Blood and Blood Products . . . . . . . . . . . . 204 C.2.9. Obstetric Anaesthesia and Analgesia . . . . . . . . . . . . . . . . . . . . 207 C.2.10. Spinal Analgesia . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 208 C.2.11. Antibiotic Use in Obstetrics Surgery . . . . . . . . . . . . . . . . . . . . 211

C.3. Obstetrical pathology . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 214 C.3.1. C.3.2. C.3.3. C.3.4. C.3.5. C.3.6. C.3.7. C.3.8. C.3.9. C.3.10. C.3.11. C.3.12. C.3.13. C.3.14. C.3.15. C.3.16. C.3.17. C.3.18.

Perineal Lacerations . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 214 Preterm Delivery: Assistance . . . . . . . . . . . . . . . . . . . . . . . . . . . 215 Macrosomia and Shoulder Dystocia . . . . . . . . . . . . . . . . . . . . 216 Malpresentations . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 218 Breech Presentation . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 221 Uterine Rupture . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 224 Uterine Inversion . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 225 Labour after Genital Mutilation . . . . . . . . . . . . . . . . . . . . . . . . 226 Coagulation Defects . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 228 Amniotic Fluid Embolism . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 229 Cord Prolapse . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 230 Diabetes: Intrapartum Management . . . . . . . . . . . . . . . . . . . . 231 Gestational Diabetes: Intrapartum Management . . . . . . . . . . 233 Cardiac Disease: Intrapartum Management . . . . . . . . . . . . . . 234 Postterm Pregnancy . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 235 Preeclamsia and Eclampsia: Mode of Delivery . . . . . . . . . . . . 236 Twin Gestation: Mode of Delivery . . . . . . . . . . . . . . . . . . . . . . . 237 Mendelsonâ&#x20AC;&#x2122;s Syndrome . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 239

D. Puerperium . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 241 D.1. Puerperium attendance . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 243 D.1.1.

Postpartum Care . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 243

D.2. Proceedings and techniques . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 247 D.2.1. D.2.2. D.2.3. D.2.4. D.2.5.

Inspection of Placenta and Membranes . . . . . . . . . . . . . . . . . . 247 Inhibition of the breast-feeding . . . . . . . . . . . . . . . . . . . . . . . . 248 Puerperal Curettage . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 253 Post-Partum Hysterectomy (Cesarean Hysterectomy) . . . . . . 254 Treatment of Urinary Obstetric Fistulas . . . . . . . . . . . . . . . . . 254

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Index

D.2.6. D.2.7.

Post-Partum Contraception . . . . . . . . . . . . . . . . . . . . . . . . . . . 257 Kangaroo Mother Care . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 261

D.3. Pathology . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 262 D.3.1. D.3.2. D.3.3. D.3.4. D.3.5. D.3.6. D.3.7.

Postpartum Fever . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 262 Postpartum Hemorrhage (PPH) . . . . . . . . . . . . . . . . . . . . . . . . 264 Postpartum Endometritis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 266 Thromboembolism in Puerperium . . . . . . . . . . . . . . . . . . . . . . 267 Mastitis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 268 Puerperal Sepsis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 269 Puerperal Psychosis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 271

E. Neonatology . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 273 E.1. Clinical attendance . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 275 E.1.1. E.1.2. E.1.3. E.1.4. E.1.5.

Neonatal Assistance in Delivery Room . . . . . . . . . . . . . . . . . . . 275 Neonatal Examination . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 276 Breast-Feeding . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 277 Drugs Contraindecated during Breast-Feeding . . . . . . . . . . . . 279 Fetal Necropsy . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 279

E.2. Proceedings and technology . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 283 E.2.1. E.2.2. E.2.3. E.2.4. E.2.5.

Neonatal Resuscitation . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 283 Respiratory Therapy in the Newborn . . . . . . . . . . . . . . . . . . . . 287 Ocular Profilaxis (OP) . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 290 Vitamin K Prophylaxis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 291 Neonatal Transport . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 291

E.3. Neonatal pathology . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 294 E.3.1. E.3.2. E.3.3. E.3.4. E.3.5. E.3.6. E.3.7. E.3.8. E.3.9.

Preterm Infant: Clinical Care . . . . . . . . . . . . . . . . . . . . . . . . . . 294 Neonatal Asphyxia . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 297 Neonatal Sepsis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 298 Neonatal Tetanus . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 299 Neonatal Seizures . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 300 Congenital Syphilis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 301 Congenital Malaria . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 302 Human Immunodeficiency Virus (HIV) in Newborn . . . . . . . 303 Infant Born to a Mother with Hepatitis B virus (HBV) Infection . . . . . . . . . . . . . . . . . . 304 E.3.10. Infant Born to a Mother with Hepatitis C virus (HCV) Infection . . . . . . . . . . . . . . . . . . 305 E.3.11. Screening of Surgical Disease in Neonatal Period . . . . . . . . . 305

SUBJECT INDEX . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 319

PROLOGUE The decision of publishing this book was made in a meeting that took place in Addis Ababa on the occasion of the First African Congress of Perinatal Medicine (2011), given the evidence that some of the African Maternity hospitals were lacking their own guidelines allowing a better organization of their clinical assistance. For this reason, the International School of Perinatal Medicine for Africa (ISPEMA) was founded in Barcelona in 2012. One of the first projects proposed was the production of a Protocol in Perinatal Medicine directed to the Maternity hospitals in Africa. For obvious reason, such pro tocols had to be adapted to the idiosyncrasy and conditions of these centres. The idea was strongly supported by the recently created African Association of Perinatal Medicine. During the last two years, the experts from Matres Mundi (obstetricians, pediatricians, midwives) who, as it is know, are the prime force of ISPEMA, made a review of most of the existing protocols in Europe and EEUU, but mostly in Africa, with the collaboration of some of their African colleagues. In the end, they have produced a publication comprising the main contents of those protocols adapted to the needs and conditions of the Perinatal Medicine in the African countries. As it is also known, ISPEMA and Matres Mundi are developing the program LIFE FOR AFRICA that consists in building, equipping and operating a Maternity Hospital in Addis Ababa as well as an international School of Perinatal medicine that should become a reference point for Sub-Saharan Africa. During the second phase many Schools of Perinatal Medicine will be established in most countries of the area. There many specialists in obstetrics and pediatrics and midwives and specialized nurses will be trained. Courses for general practitioners and specialist will take place as well, with the aim of keepins them updated with the last developments in Perinatal Medicine. Without a doubt, the book the readers are about to enjoy will become helpful in obtaining the objectives of improving the Maternal and infant health in Africa. Finally great appreciation should be expressed to Prof. Jose M. Carrera who is a tireless and an essential sponsor and contributor to «International School of Perinatal Medicine for Africa» (ISPEMA). Prof. Erich Saling President of International School of Perinatal Medicine for Africa

PREFACE It was an honor to be asked to write the preface for this book, the «Clinical Guidelines for Maternity Hospitals». The book covers almost all aspects concerning the practice in Obstetrics as shown clearly in the index of the book. The scope of the book is to improve the obstetric services in Africa to facilitate maternal health and to reduce the maternal and neonatal morbidity and mortality which are considered the highest throughout the globe. Annually 585,000 women die due to pregnancy related complications. 99 % occurs in developing countries, from which 45 % occurs in Africa which constitutes only 12 % of the world’s population. Maternal morbidity is 30 times of the mortality. The International School of Perinatal Medicine for Africa (ISPEMA) took the initiative to make the clinical guidelines book to improve the obstetric and neonatal services which need to be adopted and adapted for each country in Africa under the supervision and help of the African Association of Perinatal Medicine (AAPM). This book is also very useful and constructive to the training of health care providers in the maternity and neonatal services at the community level and the health system, which includes community leaders, social workers, midwives, nurses, specialists and consultants. This will strengthen the capacity of the maternal and neonatal services within the African countries. Thanks and appreciation need to be expressed to Matres Mundi and professor José M. Carrera who has been very much concerned and enthusiastic to help African women and neonates by improving the services provided in their countries and establishing a Maternity hospital in Addis Ababa for training and delivering services within the program «Life for Africa». The appreciation also needs to be extended to all who participated in making this book a reality. Prof. Abdellatif Ashmaig President of African Association of Perinatal Medicine (AAPM)

FOREWORD These protocols are designed specifically to be used in African Maternity Hospitals lacking of their own protocols or guidelines. We have tried to adapt their content to the characteristics and limitations of Perinatal Medicine in this continent. Some readers might get the impression that many of the procedures included in this protocols are not updated. Well, that is not the case. Therefore, we would like to emphazise the importance of keeping in mind the difference, in terms of resources and general conditions, in some African countries if compared with other regions of the world, when approaching the contents of this text. The mission of this book is to provide fast, neat, concise and accurate information on what to do in a given obstetric and neonatological situation, both in the diagnostic and therapeutic aspects. On the other hand, this guide sets out options on how to proceed, of course, without questioning school criteria. Obviously, this work has been specially designed for intra-hospital assistance, where the unification of criteria is very important and where it is rare for doctors on duty to face an unusual condition that requires a prompt decision. As the reader will see, these guidelines refer not only to the various possible disease entities during pregnancy, childbirth and the postpartum period, but also to those relating to the neonate. It is intended that, with this guide, the vision of both the obstetrician and the neonatologist will be as inclusive and perinatal as possible. The technical team that has written this book, the «International School of Peri natal for Africa» (ISPEMA), is made up of experts who are current or former heads of Service of a Maternity Hospital. In order to produce this text, it has been taken into account not only their personal clinical experiences but also various clinical guidelines and protocols from several centres worldwide such as: University Institute Dexeus (Spain), Johns Hopkins University (USA), Radcliffe Hospital of Oxford (UK), Moi Teaching Referal Hospital (Kenya), Standard Treatment Guideline for General Hospitals (Ethiopia and Rwanda) and the «Recommendations and Guidelines for Perinatal Medicine» sponsored by the World Association of Perinatal Medicine (WAPM) and Matres Mundi International (2007). In several cases, the protocols of some of these institutions have been literally transcribed. It has been considered that many of these guidelines resume in a very precise way the opinion of our group and therefore modifications were not required. We are indebted to our colleagues in charge of writing and editing the mentioned protocols. In all cases the recommendations provided have been adapted according to the conditions of the African reality. The desire of all those who have collaborated in the finalization of these protocols is to provide a useful tool for all our dear African colleagues who usually work in unfavourable conditions, daily facing many serious problems in order to provide the best possible care form mothers and children. José M. Carrera Secretary General of the International School of Perinatal Medicine for Africa (ISPEMA)

TERMINOLOGY AND CLASSIFICATION OF THE RISK

A.1.

TERMINOLOGY IN PERINATAL MEDICINE

CONCEPT A precise terminology is required in order to describe all the events associated with perinatal outcome. International comparison of perinatal and neonatal mortality and its components is important. That information allows identifying problems, tracking temporal and geographical trends and disparities and assessing changes in public health policy and practice.

TERMINOLOGY I.

DELIVERY «The complete expulsion or extraction from its mother of the product of conception with a weight of 500 g or more, regardless of the gestational age, whether or not the umbilical cord has been cut or the placenta is attached.» Newborns that weights less than 500 g should not be included in the perinatal statistics. In case of the birth weight be unknown, 500 g of fetal weight is assumed a 22 weeks of gestation if both birth weight and gestational age are unknown, a crown-heel length of 25 cm is equivalent to 500 g.

II.

BIRTH WEIGHT «Birth weight is defined as the first weight of the fetus or newborn obtained after birth. For live births, birth weight should preferably be measured within the first hour of life before significant postnatal weight loss has occurred. While statistical tabulations include 500 grams groupings for birth weight, weights should not be recorded in those groupings. The actual weight should be recorded to the degree of accuracy to which it is measured.» In order to study and predict bad neonatal outcomes, birth weight may be catalogue as: 1. Low birth weight. Birth weight less than 2,500 g (up to and including 2,499 g). 2. Very low birth weight. Birth weight less than 1,500 g (up to and including 1,499 g). 3. Extremely low birth weight. Birth weight less than 1,000 g (up to and including 999 g).

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A. Terminology and classification of the risk

III. GESTATIONAL AGE «The duration of gestation is measured from the first day of the last normal menstrual period. We should express gestational age in completed days or completed weeks.» For the purposes of calculation of gestational age from the date of the first day or the last normal menstrual period and the date of delivery, it should be borne in mind that the first day is day zero and not day one; days 0-6 therefore correspond to «completed week zero»; days 7-13 to «completed week one»; and so on. In order to avoid misunderstanding, tabulations should indicate both weeks and days. If date of the last menstruation is not reliable, it is necessary to apply the ultrasound dating (see page 52). According to the gestational age at delivery, different periods of pregnancy may be defined. 1. Pre-term. Whe delivery occurs before 37 completed weeks (less than 259 days) of gestation. 2. Term. When delivery occurs from 37 completed weeks to less than 42 completed weeks (259 to 293 days) of gestation. 3. Post-term. Whe delivery occurs after 42 completed weeks or more (294 days or more) of gestation. IV. PERINATAL PERIOD «The perinatal period commences at 22 completed weeks (154 days) of gestation. As it has been said before, this is the time when birth weight is normally around 500 grams, and ends seven completed days after birth.» Perinatal period is divided in: PERINATAL PERIOD NEONATAL PERIOD

FETAL PERIOD

22 weeks

EARLY Delivery

LATE 7 days

28 days

Fetal period. The fetal period starts at 22 completed weeks (154 days) of gestation, and ends with birth. Neonatal period. The neonatal period commences at birth and ends 28 completed days after birth. Neonatal period is also divided in: a) Early neonatal period. Early neonatal period commences at birth and ends 7 completed days after birth. b) Late neonatal period. Late neonatal period commences 7 completed days after birth and ends 28 completed days after birth. It is important to remark that late neonatal period is not included in the perinatal period.

CLINICAL GUIDELINES FOR MATERNITY HOSPITALS

Terminology in perinatal medicine A.1.

FETAL AND NEWBORN MORTALITY Live birth: «Live birth is the complete expulsion or extraction from its mother of a product of conception, irrespective of the duration of the pregnancy, which, after such separation breathes or shows any other evidence of life, such as beating of the heart, pulsation of the umbilical cord, or definite movement of voluntary muscles, whether or not the umbilical cord has been cut or the placenta is attached; each product of such a birth is considered liveborn.»

VI. FETAL DEATH Stillbirth: «Fetal death is death prior to the complete expulsion or extraction from its mother of a product of conception, irrespective of the duration of pregnancy; the death is indicated by the fact that after such separation the fetus does not breathe or show any other evidence of life, such as beating of the heart, pulsation of the umbilical cord, or definite movement of voluntary muscles.» Intrauterine death occurs either before onset of labour, antepartum death, or during labour, intrapartum death. Stillbierths represent more than half of perinatal deaths. More than one third of stillbirths take place intrapartum, during delivery, and are largely avoidable. Stillbirth Stillbirth mortality rate 5 ———————— 3 1,000 Total newborns 1. Perinatal mortality. The perinatal mortality covers the deaths occurred during fetal period leading up to birth and the first week of life. Deaths occurring in this period are largely due to obstetric causes. Stillbirth 1 Early neonatal death Perinatal mortality rate 5 ————————————————— 3 1,000 Total newborns 2.

Neonatal mortality. Neonatal mortality relates to the death of live-born infants during the neonatal period, which begins with birth and covers the first four weeks of life. Neonatal mortality may be subdivided into early and late neonatal deaths. Early neonatal mortality. Early neonatal mortality relates to the death of live-born infants during the first week of life, which is also part of the perinatal period. Age at death during the first day of life, day zero, should be recorded in units of completed minutes or hours of life. For the second and following days, age at death should be recorded in days. Early neonatal death Early neonatal mortality rate 5 ——————————— 3 1,000 Live births Late neonatal mortality. Late neonatal mortality relates to the death of live-born infants during the period between the first and fourth weeks of life. Late neonatal mortality is not part of the perinatal period.

Other recommendations. «World Health Organization recommends that, if possible, all fetuses and infants weighing at least 500 g at birth, whether alive or dead, should be included in the

CLINICAL GUIDELINES FOR MATERNITY HOSPITALS

A. Terminology and classification of the risk

statistics. The inclusion in national statistics of fetuses and infants weighing between 500 g and 1,000 fg is recommended both because of its inherent value and because it improves the coverage of reporting at 1,000 grams and over. For international comparison, 1,000 g and/or 28 weeks gestation is recommended». VI. MATERNAL MORTALITY «Maternal death is the death of a woman while pregnant or within 42 days of the end of the pregnancy, irrespective of the duration and the site of the pregnancy, due to any cause related to or aggravated by the pregnancy or its management, but not from accidental or incidental causes.»

Number of mother deaths Maternal mortality rate 5 —————————————— 3 100,000 Live and death births

When time is take into consideration: Late maternal death. Deaths occurring between 43 days and one year after abortion, miscarriage or delivery. They can be due to direct or indirect causes. Identifying late maternal deaths makes it possible to take into consideration deaths in which a woman had problems that began during pregnancy, even if she survived for more than 42 days after its termination. Maternal deaths can be subdivided into further groups: 1. Direct maternal deaths. Those resulting from conditions or complications, or their management, which are unique to pregnancy and occur during the antenatal, intrapartum or postpartum period. 2. Indirect maternal deaths. Those resulting from previously existing disease or disease developing during pregnancy which was not due to direct obstetric causes, but which was aggravated by physiologic effects of pregnancy. Examples of indirect deaths include epilepsy, diabetes, cardiac disease and hormone-dependent malignancies. Other maternal mortality indicators. 1. Lifetime births per woman. The total fertility rate, defined as the number of children a woman would have if current age-specific fertility rates remain constant throughout her childbearing years. 2. Percent of births attended by skilled personnel. Skilled personnel include doctors, nurses, and midwives. 3. Lifetime chance of dying from maternal causes. The probability that a woman will die during her lifetime from causes related to pregnancy and delivery. The measure combines the probability of becoming pregnant and the risk of death from each pregnancy. Reference. Oros D, Rueda S, Fabre E: Terminology in Perinatal Medicine. In: Recommendations and Guidelines for Perinatal Medicine. Matres Mundi /WAPM. Barcelona, 2007: 19-25.

A.2.

EVALUATION AND CLASSIFICATION OF HIGH RISK

CONCEPTS 1. 2

High-Risk pregnancy is defined as one in witch the frequency of adverse events for the mother and for fetus is greater than exists in the general population. In Perinatal Medicine high risk means a higher probability of adverse results in terms of maternal, fetal or postnatal morbidity or death.

CLASSIFICATION OF FETAL RISK 1. Risk 0: Patient with no risk factors identified of all those detailed in the following levels. 2. Medium Risk or risk 1: Pelvic anomaly. Cardiac disease I. Insufficient prenatal control. Age ,16 or .35 years. Uncertain last period date. Twins. Rh incompatibility. Excessive weight gain. Urinary infection. Obesity. Inter pregnancy interval ,12 months. Short height. Social class IV and V. Diabetes A (Gestational diabetes). Previous sterility. Smoker. First trimester hemorrhage. Insufficient weight gain. Maternal infection (VIH, Malaria, Hepatitis, etc.). Multi-parity. Positive VDRL

CLINICAL GUIDELINES FOR MATERNITY HOSPITALS

A. Terminology and classification of the risk

High Risk or risk 2: Threat of Premature Birth. Cardiac diseases II. Prolonged pregnancy. Second and third trimesters hemorrhage. Oligoamnios. Fetal malformation suspicion. Previous uterine surgery. Anomalous presentation. Light hypertension. Anaemia. Drug addiction/Alcohol. Endocrine diseases. Hydramnios. Bad obstetrical background. Uterine malformation. Recurrent perinatal death. IUGR Risk. Very high Risk or risk 3: Cardiac Diseases III and IV. Hypertensive disorders. Linked serious pathology. IUGR Diabetes B or more serious. Isoimmunization. Placenta previa.

The identification of several risk factors means inclusion in the highest group. The risk level should be revised in each prenatal visit and also at delivery. Risk factors could be detected before pregnancy based on the previous obstetric history or the existence of maternal diseases, or during the progress of pregnancy due to the appearance of obstetric pathologies like hypertensive disorders, intrauterine growth restriction, gestational diabetes, etc.

II.

RISK FACTORS FOR MATERNAL MORBIDITY AND DEATH a) The majority of epidemiological studies on mortality related to pregnancy have identified the following risk factors: 1. Socioeconomic and educational status. In all ethnic groups low economical and generally related educational status increases the maternal mortality rate. 2. Marital status. Maternal mortality is three time higher in unmarried patients or patients without couple. This group of patients concentrates near 50 % of all maternal deaths related to abortion or ectopic pregnancy. 3. Ethnic group. Apparent health inequality persists with indigenous mothers continuing to have a higher risk of maternal death in different continents. 4. Age. Until 30 years of age maternal mortality remains stable, but from then on it rises progressively.

CLINICAL GUIDELINES FOR MATERNITY HOSPITALS

Evaluation and classification of high risk A.2.

Parity. The lowest maternal mortality is found in relation with the second and third delivery. With further deliveries the risk increases noticeably, overcoming that of the first delivery. 6. Insufficient prenatal care. The risk of maternal mortality is significantly higher in patients without or with poor prenatal control. 7. Distance to hospital and hospital level. Hospitals with few deliveries have a higher rate or maternal deaths, generally due to the absence of blood banking facilities and the availability of skilled birth attendants. The higher maternal mortality rates found in referral hospitals has to be attributed to the high percentage of high risk pregnancies and deliveries that are attended in these institutions. b) On the other hand there are several medical factors which could have a live threatening impact on the mother. 1. Diabetes. Prior to the discovery of insulin diabetic patients died before reaching the reproductive age, and those who did not, suffered a near 50 % mortality rate during pregnancy. 2. Hypertension and hypertensive disorders of pregnancy. Patients with chronic hypertension have an increased risk of preeclampsia/eclampsia, that by themselves imply a higher mortality risk. 3. Multiple pregnancy. Compared with singleton gestations, women with multiple gestations have a twofold risk of death, preeclampsia, and postpartum hemorrhage and a three fold risk of eclampsia. There is also a significant association between multiple gestation and increased incidence of preterm labor, anaemia, urinary tract infection, puerperal endometritis, and cesarean delivery. 4. Obesity. Compared to women with normal BMI, the following outcomes were significantly more common in obese pregnant women: gestational diabetes mellitus, proteinuric pre-eclampsia, postpartum hemorrhage, genital tract infection, urinary tract infection and wound infection. 5. Stillbirth. Stillbirth and maternal mortality rates are strongly correlated, with about 5 stillbirths for each maternal death. However, the ratio increases from about 2 to 1 in the least developed countries to 50 to 1 in the most developed countries. 6. Previous cesarean section. Compared with mothers who have had primary vaginal births, mothers who have had primary caesarean section and undergo labor in the second birth increased risk of uterine rupture, hysterectomy, postpartum hemorrhage, infection and intensive care unit admission. 7. Previous obstetric complications. In a recent study conducted in Mexico, the history of complications in previous pregnancies was the risk factor for maternal death with the highest odds ratio. Followed by preexisting medical conditions. 8. Preexisting medical conditions. Infectious, hematological, endocrine, renal, hepatic, neurological, cardiac, pulmonary and immunological diseases. Especially in pandemic areas, HIV/AIDS and malaria. 5.

III. RISK FACTORS FOR ADVERSE PERINATAL OUTCOMES All risk factors for adverse maternal outcomes enumerated in the previous section have also a negative impact on the perinatal figures. But on the other hand there

CLINICAL GUIDELINES FOR MATERNITY HOSPITALS

A. Terminology and classification of the risk

are some risk factors that have a specific impact on perinatal outcomes without influencing maternal health. 1. Congenital defects. Malformations constitute one of the important causes of perinatal deaths. Reduction of its contribution to perinatal mortality can only be achieved implementing prenatal diagnosis strategies and referring patients to referral hospitals where affected newborns could be adequately treated. 2. Preterm delivery. Adequate dating of the gestation is of great importance to refer the patients with preterm labor to be delivered in adequate health centers. 3. Intrauterine growth restriction. Infants with intrauterine growth restriction are at risk for increased perinatal mortality, birth adaptation complications, including perinatal acidosis, hypoglycemia, hypothermia, coagulation abnormalities, and selected immunologic deficiencies. IUGR infants also appear to be at great risk for complications of prematurity, including chronic lung disease and necrotizing enterocolitis and an increased risk of neurolo gical disorders, including cerebral palsy and poor neurodevelopmental out come. 4. Intrauterine infections. The failure to apply known effective antiretroviral and antimalarial interventions to infected mothers through antenatal programs continues to contribute substantially to infant deaths globally, especialially in pandemic areas. 5. Birth trauma. Although some are not predictable, antepartum obstetric evaluation of the prognosis of a vaginal delivery, birth assistance by trained health providers, adequate referral protocols and the possibility to perform a caesarean section are some alternatives to lower the impact of birth trauma not only on perinatal but also on maternal outcomes. 6. Rh alloimmunization. The formation of maternal antibodies when any blood group factor inherited from the father is not possessed by the mother, also known as alloimmunization, may lead to various degrees of transplacental passage of these antibodies into the fetal circulation.

Referece. Serra B, Scazzocchio E: Evaluation and classification of high risk. In: Recommendations and Guidelines for Perinatal Medicine. Matres Mundi /WAPM. Barcelona, 2007; 8: 78-82.

A.3.

ABBREVIATIONS

Abbreviations used in this book are recommendad also for the Perinatal Clinical Record. a.c. Before meals. ABC Abacavir. ACA Antiocardiolipin Antibody. ACE Angiotensin conversion enzime. ACLS Advanced Cardiac Life Support. ACOG American College of Obstetricians and Gynecologists. ADH Antidiuretic Hormone. ADR Adverse Drug Reaction. AF Amniotic Fluid. AFI Amniotic Fluid Index. AFP Alpha-fetoprotein. AIDS Acquired immunodeficiency Syndrome. AMS American Medical Association. ANA Antinuclear Antibody. ANC Antenal Care. anti D Anti Rh. anti-HBC Antihepatitis B. anti-HBS Antihepatitis B surface. APGAR Activity, Pulse, Grimace, Appearance and Respiration. APH Antepartum Haemorrhage. ARF Acute renal failure. ARM Artificial Rupture of Membranes (amniotomy). AROM Artificial Rupture of Membranes. ART Anti-Retroviral therapy. ARV Antiretroviral. ASD Atrial septal defect. AST/ALT Aspartato aminotrasferasa/Alanina aminotransferasa. AUB Abnormal uterine Bleeding. AVC Atrioventricular canal. b.i.d. Twice a day. BBT Basal Body Temperature.

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A. Terminology and classification of the risk

BCG Bacillus Calmette-Guérin. BCP Birth Control pill. BD Bis in Die (otwice daily). BG Blood Glucose. b-hCG B-Human Chorionic Gonadotrophin. BID Two times a day. BMI Body Mass index. BP Blood Presure. BPD Biparietal Diameter. BPM Blood Presure measurement. BV Bacterial vaginosis. C/I Contraindication. CA Chorioamnionitis. CBC Complete Blood Cell Count. CCAM Congenital Cystic Adenomatoid Malformation. CDH Congenital Diaphragmatic Hernia. CH Cystic Hygroma. CHO Carbohydrate. CI Cardiac Index. CLD Chronic Long Disease. CLE Congenital Lobar Emphysema. CMV Cytomegalovirus. CNS Central Nervous System. CO Cyclophosphamide/Vincristina. CP Cerebral Palsy. CPAP Continuos Positive Airway Pressure. CPD Cephalo-pelvic disproportion. CPC Choroid Plexus Cyst. CRL Crow-rump Length. CRP C. Reactive Proteins. CS Cesarean Section. CSF Cerebrospinal Fluid. CST Contraction Stress Test. CTG Cardiotocography. CVA Cardiovascular Accident. D&C Dilation and curetage. D&E Dilation and evacuation. d4T Stavudine. ddl Didanosinc. d/c Discharge or discontinue. D/I Drug Interaction. D/S Dextrose in Saline Solution. D/W Dextrose in Water Solution. DACA Drug Administration and Control Authority. DC Dichorionic sets. DCT Direct Coombs´ Test. DDx Diferential Diagnosis.

CLINICAL GUIDELINES FOR MATERNITY HOSPITALS

Abbreviationsâ&#x20AC;&#x201A; A.3.

DI Diabetes Insipidus. DIC Dissemined intravascular coagulation. DKA Diabetes ketoacidosis. DLM Date last menstruation. DNA Deoxyribonucleid Acid. DR Delivery Room. DV Ductus Venosus. DVT Deep Vein Thrombosis. EACA Epsilo-amniocaproic Acid. EBV Epstein Barr Virus. ECMO Extracorporal membrane oxygenation. EDD Estimate date of delivery. EEG Electroencephalography. EFV Efavirenz. EFW Estimated fetal weight. EKG Electrocardiogram. EMA Etoposide/Methotrexate/Actinomicin. EMA-CO Multiagent chemotherapy. ENT Ear, nose and throat. epis Episiotomy. ESR Erytrocyte Sedimentation Rate. ET Tracheal Tubes. ETT Epithelioid Trophoblastic tumour. FA Fetal Assesment. FAS Fetal Alcohol Syndrom. FB Fetal Breathing. FBC Full Blood Count. FBS Fetal Blood Sample. FDA Federal Diseases Agency. FDIU Fetal Death in Utero. Fe Iron. FEV 1 Forced Expiratory volume in 1 second. FFP Fresh Frozen Plasma. FGM Female Genital Mutilation. FH Fundal Heigth. FHM Fetal Heart Monitoring. FHR Fetal Heart Rate. FIO 2 Inspired Oxigen Concentration. FL Femur Lenght. FM Fetal Movements. FMH Fetomaternal Haemorrhage. FPG Fasting Plasma Glucose. FRC Functional Residual Capacity. FT Fetal Tone. FT-4 Free Thyroxine. FTA Fluorescent Treponemal Antigen. FTC Amtricitabine.

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A. Terminology and classification of the risk

FTSVD Full-term spontaneous vaginal delivery. g Gram. GBS Group B Sterptococcus. GC Gonococus. GCT Glucose Challenge Test. GDM Gestational Diabetes Mellitus. Gh Glycosylated Haemoglobin. GIT Gastrointestinal tract. GMH Germinal Matrix Haemorrhage. GnRH Gonadotropin-releasing Hormone. GTD Gestational Trophoblastic Disease. GTN Gestational Trophoblastic Neoplasia. GTT Glucose Tolerance Test. HAV Hepatitis A Virus. Hb Haemoglobin. HBIG Hepatitis B Inmunoglobulin. HBV Hepatitis B Virus. HC Head Circumference. hCG Human Chorionic Gonadotrophin. HCV Hepatitis C Virus. HELLP Hemolysis, Eleved Liver Enzymes. Hgb Aic Glycosylated Haemoglobin. HIV Human Immunoficience Virus. HL Homerus Lenght. HPV Human papillomavirus. HR Heart Rate. Hrs: Hours. HSV Herpes simplex virus. I&D Incision and drainage. I:E Respiratory to expiratory Ratio. IAI Intraamniotic Infection. IAMP International Academy of Perinatal Medicine. IBW Ideal Body Weight. ICT Indirect Coombs´Test. ICU Intensive Care Unit. IDDM Insulin-dependent diabetes Mellitus. IFG Impaired Fasting Glucose. Ig Inmunoglobulin. IM Intramuscular. IMV Intermittent Mandatory Ventilation. IO Intra-ossus route. IPT Intermittent Preventive Treatment. IQ Intellectual Coefficient. ISPEMA International School of Perinatal Medicine for Africa. ITTS Twin-Twin Transfusional Syndrome. IU International Unit.

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Abbreviationsâ&#x20AC;&#x201A; A.3.

IUD Intrauterine Device. IUFD Intrauterine Fetal Demise. IUGR Intrauterine Growth Restriction. IUP Intrauterine Pregnancy. IV Intravenous. IVH Intraventricular Haemorrhage. kg Kilogram. KCI Potasic chloride. KOH Potassium Hydroxyde. KMC Kangaroo Mother-Care. L/ROA Left/Right Occiput anterior. L/ROP Left/Right Occiput posterior. L/ROT Left/Right Occipur Transverse. L/S Lecitin-Sphingomielin Ratio. LAC Lactation amenorrhea. LBW Low birth weight. LDR Labor, delivery, recovery Room. LFD Low-forceps Delivery. LFVD Low-forceps vaginal delivery. LGA Large for gestational age. LH Lutenizing Hormone. LHRH Lutenizing Hormone Releasing Hormone. LMP Last Menstrual Period. LP Lumbar Puncture. LPV/r Lopinavir with a low-dose ritonavir loost. LR Labor Room. MAG3 Mercaptocetyl triglycerine. MAP Mean Arterial Pressure. MAR Anorectal malformations. MAS Meconium Aspiration Syndrome. MC Monochorionic Twins. MCA Middle Cerebral Artery. MCV Mean Corpuscular Volume. MFM Maternal fetal Medicine. MFRP Multifetal Pregnancy Reduction. Mg Miligram. MgGSO4 Magnesium Sulfate. MHAA-TP Microhemaglutination assay for Treponema Pallidum. MICU Medical Intensive Care Unit. Ml Miilliliter. MMR Measles, Mumps, Rubella. MP Multiple Pregnancy. MRSA Methicilin-resistant Staphlococcus aureaus. MSO4 Morphine Sulfate. MSU Midstream urine. MTB Mycobacterium Tuberculosis.

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MTCT Mother to child transmission. MTX Methotrexate. MVA Manual vacuum Aspiration. MZ Monozygotic. NB Nasal Bone. N/S Normal Saline Solution. N/V Nausea/Vomiting. NEC Necrotizing Entercolitis. NF Nuchal Fold. NFU Nelfinavir. NGT Nasogastric tube. NIDDM Non-insuline-dependent Diabetes Mellitus. NND Neonatal Death. NNRTI Non nucleoside reverse transcriptase inhibitor. NRTI Nucleoside analogue reverse transcriptase inhibitor. NS Normal Saline NST Nonstress Test. NT Nuchal Translucency. NTD Neural Tube Defect. NUP Nevirapine. NYHA New York Hearth Association. O&P Ova and parasites. OA Occiput anterior. Oat Aesophageal Atresia. OCP Oral Contraceptive Preparation. OGTT Oral glucose Tolerance Test. Ol Osteogenesis imperfecta. OP Occiput posterior. Opr Ocular Profilaxis. P Parity. P.O. Per os. p.o. by mouth. p.r. by rectum. p.r.n. as needed. p.v. by vagina. P/C Precaution. PaCO2 Presion of CO2. Para Parity. PAS Para-aminosalycilin acid. PCP Pneumocystis Carini Pneumonia. PCR Polymerase Chain Reaction. PCV Packed Cell Volume. PD Prenatal Diagnosis. PDA Patent Ductus Arteriosus. PE Physical Examination. PEEP Positive end-expiratory Pressure.

CLINICAL GUIDELINES FOR MATERNITY HOSPITALS

Abbreviationsâ&#x20AC;&#x201A; A.3.

PFT Pulmonary Function Test. PGA-1 Prostagladin A.1. PI Protease inhibitor. PIH Pregnancy-induced Hypertension. PIP Peak Inspiratory Pressure. PLAP Placental Alkaline Phosphatase. PMN Polymorphonuclear leukocyte. PMPe Previous Menstrual Period. PMR Perinatal Mortality Ratio. PN Parenteral Nutrition. PO2 Presion of Oxygen. POD Postoperative Day. pp Postpartum. PPF Postpartum Fever. PPH Postpartum Hemorrhage. PPPROM Premature, prelabor, prolonged rupture of membanes. PPROM Premature, prelabor, rupture of membranes. PRBC Packed red blood cells. PRL Prolactine. PRN As required. PROM Prelabor (premature)rupture of membranes. PSTT Placental site Trophoblastic Tumour. PT Prothrombin time. PTFE Polytetrafluoroethylene (Teflon). PTL Preterm Labor. PUS Pelvi-ureteric junction. PVHD Posthaemorrhagic Ventricular Dilation. q,o.d, Every other day. q.h.s. Every night. QD Once a Day. QID Four times a Day. RDS Respiratory Distress Syndrome. RDT Rapid Diagnosis Test. reg regular insulin. Rh Rhesus (D). RHD Rheumatic Heart Disease. RNA Ribonucleid acid. ROM Rupture of Membranes. RPP Biophysical Profile. RPR Reactive plasma reaguin. RR Respiratory Rate. FRR Fetal Respiratory Reverse. RSV Respiratory sincityal virus. RU 486 Mifepristine. s.q. subcutaneous. S/D Systolic/diastolic Ratio.

CLINICAL GUIDELINES FOR MATERNITY HOSPITALS

A.â&#x20AC;&#x201A; Terminology and classification of the risk

S/E Side effect. Sd-NPV Single dose nevirapine. SAB Spontaneous Abortion. SAF Stained Amniotic Fluid. SD Shoulder Dystocia. SGA Small for Gestational Age. SIDS Sudden Infant Death Syndome. SMV Spontaneous Mechanical Ventilation. SMX Sulfamethoxacole. sono sonogram. SP Sulfadoxin Pyremethamine. SQV Saquinavir. SROM Spontaneous Rupture of Membranes. ST Screening Test. STD Sexually Transmitted Disease. STG Standard Treatment Guideline. STI Sexually transmited infection. STS Serum Test of Syphilis. t.i.d. Three times a day. T-21 Trisomy 21. T3RU T3Resin Uptake. TAB Therapeutic abortion. TB Tuberculosis. TCF Traquoesofagic Fistula. TDF Tenofovir. TFT Thyroid Function Tests. TGA Transposition of the great arteries. TIBC Total iron -binding capacity. TID Three times a day. TMP-SMX Trimetoptoprim-sulfamethoxazole (Bactrim). TOPS Twin Oligopolyhydramnios Sequence. TPN Total parenteral nutrition. TRAP Arterial Perfusion Sequence. TRH Thyrotropin-releasing Hormone. TSH Thyroid-stimulating Hormone. TSIG Thyroid.stimulating immunoglubulins. TTTS Twin-twin Transfusion syndrome. TVU Transvaginal Ultrasound. tx Treatment. UA Urynalysis. UC Uterine Contraction. US Ultrasounds. UTI Urinary Tract Infection. V/Q Ventilation-perfusion. VD Veneral Disease. VDRL Veneral Disease Research Laboratory.

CLINICAL GUIDELINES FOR MATERNITY HOSPITALS

Abbreviationsâ&#x20AC;&#x201A; A.3.

VRE Vancomycin-resistant enterococcus. VSD Ventricular Septal Defect. vtx vertex. VVFs Vesico-vaginal Fistula. VZIG Varicella-zoster immune globulin. VZV Varicella-zoster virus. WAPM World Association of Perinatal Medicine. WHO World Health Organization. XY/XX Male/Female. ZDV Zidovudine. ZIG Zigote.

PREGNANCY

B.1.

PRENATAL ATTENDANCE

B.1.1.â&#x20AC;&#x201A; ANTEPARTUM CARE CONCEPT AND OBJECTIVES Antenatal care consists in a number of visits, ideally performed before and along the gestation period, in order to minimize the maternal and foetal morbidity and mortality by: 1. Detection of high risk pregnancies. 2. Detection of congenital anomalies. 3. Prevention of obstetric complications. 4. Promotion of sanitary and nutritional education. 5. Preparation to affront labour. 6. Puerperal instructions, recommendations for breastfeeding and new born necessities. The antenatal period offers opportunities for delivering information and services that can significantly enhance the health of women and their infants. Other important sanitary programs such as nutrition, malaria, HIV/AIDS and tuberculosis may be introduced to the mothers through antenatal visits. I.

THE FIRST VISIT Ideally, the first visit should occur in the first trimester, around, or preferably before, week 12 of pregnancy. Written instructions should accompany all verbal advice. Simple written instructions in the local language should be available, even for illiterate women as family members or neighbours can often read. When necessary, materials appropriate for an illiterate audience should be available, such as simple pictures and diagrams describing the advice given at each visit. Information recorded on antenatal card. a) Personal history. 1. Name, age and marital status. 2. Address and telephone number. 3. Tobacco use or use of other harmful substances. 4. Housing: type, size, number of occupants.

CLINICAL GUIDELINES FOR MATERNITY HOSPITALS

B. Pregnancy

5. Sanitary conditions: type of toilet and source of water; electricity. 6. Educational level and economic resources. 7. Type of work and position of patient and husband. b) Medical history (identify specific diseases and conditions). 1. Tuberculosis, heart disease, chronic renal disease, epilepsy, diabetes mellitus, etc. 2. Sexually transmitted diseases. HIV status, if known. 3. Other specific conditions depending on prevalence in study site (for example, hepatitis, malaria, sickle cell trait). 4. Other diseases, past or chronic. 5. Allergies. 6. Operations other than caesarean section. 7. Blood transfusions. Rhesus (D) antibodies. 8. Current use of medicines. 9. Periods of infertility: duration, and causes if known. c) Obstetric history. 1. Number of previous pregnancies. 2. Date and outcome of each event (live birth, preterm birth, stillbirth, abortion, ectopic, hydatidiform mole). 3. Birth weight (if known). 4. Sex of newborns. 5. Periods of exclusive breast-feeding. 6. Special maternal complications and events in previous pregnancies: • Recurrent early abortion. • Induced abortion and any associated complications. • Thrombosis, embolus. • Hypertension, pre-eclampsia or eclampsia. • Placental abruption-Placenta praevia. • Breech or transverse presentation. • Obstructed labour, including dystocia. • Third-degree tears. • Third stage excessive bleeding. • Puerperal sepsis. • Gestational diabetes. 7. Obstetrical operations: • Caesarean section (indication, if known). • Forceps or vacuum extraction. • Manual/instrumental help in vaginal breech delivery. • Manual removal of the placenta. 8. Special perinatal complications and events in previous pregnancies: • Twins or higher order multiples. • Low birth weight (2,500 g). • Intrauterine growth reestriction. • Rhesus-antibody affection (erythroblastosis, hydrops). • Malformed or chromosomally abnormal child. • Macrosomic newborn (.4,500 g). • Resuscitation or other treatment of newborn. • Perinatal, neonatal or infant death. • History of present pregnancy.

CLINICAL GUIDELINES FOR MATERNITY HOSPITALS

Prenatal attendance B.1.

• Date of last menstrual period (LMP). • Habits: tobacco, alcohol, drugs (frequency and quantity). • Any unexpected event (pain, vaginal bleeding...). • History of malaria attacks. Clinical examination. 1. Chest and heart auscultation is convenient for all women as well as checking for sing of severe anaemia. 2. Measure of blood pressure. 3. Maternal weight and height should be measured to assess the mother’s nutritional status. Repeated weighing during pregnancy should be confined to circumstances where clinical management is likely to be influenced. 4. Only one routine vaginal examination during pregnancy is recommended. 5. Identification and treatment of symptomatic sexually transmitted infections should be done concomitantly. 6. Female genital mutilation may be identified at this moment if suspected by ethnicity and it allows planning intrapartum defibulation if needed. 7. The measurement of symphysis-fundal distance must be performed each antenatal appointment since week 20 to detect small or large for gestationalage infants. Analysis. 1. Urine: multiple dipstick test for bacteriuria and test for proteinuria to all women are recommended. 2. Blood: a) Syphilis (rapid test) 1 HiV infection test. b) Blood-group typing (ABO and rhesus). c) Haemoglobin. d) Routine screenig for gestational diabetes mellitos. Interventions and advices. 1. Iron and folate supplements are recommended to for pregnant women: one tablet of 60 mg elemental iron and 250-400 micrograms folate one-two times per day. If Haemoglobin ,70 g/l: dose must be doubled. 2. In malaria endemic areas: sulfadoxine/pyrimethamine, three tablets once in second trimester and repeat in third trimester (check current recommendations for timing and dosage and possibly new drugs). 3. Give advice on safe sex. Emphasize the risk of acquiring or transmitting HIV or other sexual transmitted infections without the use of condoms. 4. Advise women to stop the use of tobacco, alcohol or other harmful substances. 5. Advise women on breast-feeding: When to stop breast-feeding previous child and when to begin breast-feeding the expected child. 6. Give advice on whom to call or where to go in case of bleeding, abdominal pain and any other emergency. Give advice on birth plan, including special transport to delivery institution.

II.

THE SECOND VISIT 1. The second visit should be scheduled close to week 26. 2. The examinations and tests are restricted to measuring blood pressure and uterine height, and performing a multiple dipstick test for bacteriuria, and proteinuria.

CLINICAL GUIDELINES FOR MATERNITY HOSPITALS

B.â&#x20AC;&#x201A; Pregnancy

A blood test should be performed to determine haemoglobin if clinically indicated. Check, compliance with iron intake.

III. THE THIRD VISIT 1. The third visit should take place in or around week 32. 2. If the second visit was missed, the third visit should also include all the activities of the second visit. 3. The examinations and tests are restricted to measuring blood pressure, uterine height, performing a multiple dipstick test to detect bacteriuria glycosuria, proteinuria, and haemoglobin for all women. 4. Special attention should be directed toward discovery of twins during the external abdominal examination and uterine height measurement. 5. Hand-held Doppler or Pinard stethoscope to detect foetal heart sounds is mandatory. 6. Evaluate presence of generalized oedema and other alarming signs of disease: shortness of breath, cough, vaginal bleeding or spotting. 7. Reviewing of the ultrasonography made between weeks 19-22 (see page 54). 8. Some women will go into labour and deliver before the next scheduled visit. Therefore, extra attention must be paid in providing instructions and advice in the event labour starts (e. g. what to do in the event of abdominal pain or leaking of amniotic fluid) and to ensure they have a skilled attendant for the birth. IV. THE FOURTH VISIT 1. The fourth should be the final visit of the basic component and should take place between weeks 36 and 38. 2. At this visit, it is extremely important that women with foetuses in breech presentation should be discovered and referred for obstetric evaluation. An external cephalic version or elective caesarean section should be considered. 3. Physical examination will be similar to third visit and the woman must be inquired for some common symptoms and events that may occur close to delivery like abdominal pain, contractions, bleeding or vaginal discharge. 4. During this visit patients should be again informed of the benefits of lactation and contraception. 5. Request an ultrasonography if the values obtained from the uterine height are not as expected. APENDIX 1.â&#x20AC;&#x201A; New WHO Antenatal Care Model basic component checklist FIRST VISIT for all women at first contact with clinics, regardless of gestational age. If first visit later than recommended, carry out all activities up to that time. DATE: / / Classifying form which indicates eligibility for the basic component of the programme. Clinical examination. Clinically severe anaemia? Hb test.

VISITS 1st ,12 weeks

2nd

3rd

4th

CLINICAL GUIDELINES FOR MATERNITY HOSPITALS

Prenatal attendance B.1.

APENDIX 1. New WHO Antenatal Care Model basic component checklist Continuation Ob exam: gestational age estimation, uterine height. Gyn. Exam (can be postponed until second visit). Blood pressure taken. Maternal weight/height. Rapid syphilis test performed, detection of symptomatic disease. Urine test (multiple dipstick) performed. Blood type and Rh requested. Tetanus toxoid given. Fe/Folic acid supplementation provided. Recommendation for emergencies/hotline for emergencies. Complete antenatal card. SECOND VISIT and SUBSEQUENT VISITS Gestational age-approx. # of weeks DATE: / /26 weeks-32 weeks-38 weeks Clinical examination for anaemia. Ob. Exam: gestational age estimation, uterine height, fetal heart rate. Blood pressure taken. Maternal weight (only women with low weight at first visit). Urine test for protein (only nulliparous women/women with previous pre-eclampsia). Fe/Folic acid supplementation given. Recomemendation for emergencies. Complete antenatal card. THIRD VISIT: add to second visit DATE:

Haemoglobin test requested. Tetanus toxoid (second dose). Instructions for delivery/plan for birth. Recommendations for lactation/contraception. FOURTH VISIT: add to second and third visits. DATE:

Detection of breech presentation and referral for external ce phalic version. Complete ANC card, recommend that it be brought to hospital.

Reference. Tajada M, Ornat L, Carazo B, Fabre E: Antepartum Care. In: Recommendations and Guide lines for Perinatal Medicine. Matres Mundi /WAPM. Barcelona, 2007; 6: 57-65.

CLINICAL GUIDELINES FOR MATERNITY HOSPITALS

B. Pregnancy

B.1.2. HEALTH EDUCATION DURING PREGNANCY CONCEPT Healthcare Education plays a crucial role within the routine prenatal visit. It conveys basic information about lifestyle choices and attitudes to promote both the mother’s and baby’s good health.

HEALTH CARE DURING PREGNANCY I.

THE PRE-CONCEPTION VISIT The pre-conception visit allows the healthcare provider to obtain information about several physical, mental and social aspects as well as other everyday life issues which could impact the future pregnancy and fetal development. Its main objectives are: 1. To diagnose the patient’s individual risks and/or those associated with her environment. 2. To provide general health information to the future parents. 3. To give counsel regarding lifestyle changes. 4. To warn about the possibility of having to progressively reduce the amount of physical activity (work). 5. To prescribe folic acid to prevent neural tube defects (NTD).

II.

PRENATAL CARE This is the time for healthcare providers to answer all the questions and queries that the parents may have which may prevent them from fully enjoying pregnancy. A. Nutrition. This is a very important aspect of Healthcare Education. Nutrition excesses or deficits can have serious consequences during gestation. An adequate nutrition plan should ensure the normal growth and development of the fetus. Overall weight gain should not exceed 10 to 12 kilograms and should be more pronounced during the last months of pregnancy, when the fetus grows in volume. a) Calories. 1. Do not increase calorie intake during the first trimester of pregnancy. 2. Increase 300 calories dayly during the second and last trimesters of pregnancy. 3. Emphasize that diets of less than 1,600-1,700 calories should not be followed due to the possible production of ketonic bodies which produce psychomotor damage in the fetus. 4. The recommended percentages of macro nutrients in the Total Caloric Value are: • Carbohydrates: 55 % (increase intake of complex carbohydrates, grains, fruits and vegetables). • Proteins: 15 % (recommended daily intake: 60 grams per day).

CLINICAL GUIDELINES FOR MATERNITY HOSPITALS

Prenatal attendance B.1.

• Fat: 30 % (increase intake of omega 3 and 6 fatty acids). b) Water. Water intake is necessary due to the increment of blood and fluids during pregnancy. A daily intake of 2 liters of water promotes proper renal function and prevents infections. The water requirement should be higher in patients engaging in strenuous physical activity. c) Fiber. An adequate intake of fiber maintains the healthy peristaltic activity of the colon. A diet that incorporates 25 to 35 grams of fiber daily prevents constipation, a condition that is very common during pregnancy. d) Vitamins. Vitamins are essential for tissue metabolism, especially during growth. Therefore, the requirement of vitamins increases during pregnancy. B. Lifestyle. Prenatal exposure to alcohol, nicotine, and illegal drugs has been associated with adverse perinatal outcomes. 1. Caffeine. It is recommended to limit the consumption of caffeine during pregnancy. Caffeine is known to cross the placenta; therefore, its intake should not exceed 400 milligrams a day (2-3 coups of cofee), at least until definitive answers about its toxicity for the fetuses are found. 2. Alcohol. Alcohol consumption during pregnancy can cause birth defects, ranging from those with little significance to lasting disabilities. The term «Fetal Alcohol Spectrum Disorders» describes all disorders associated with fetal exposure to alcohol before birth. The most serious one is the Fetal Alcohol Syndrome (FAS), which presents with a combination of physical and mental birth defects. FAS in one of the leading causes of mental retardation and the only one that is completely preventable. Consumption of alcohol during pregnancy increases the chances of spontaneous miscarriage, low weight births (less than 2,500 grams) and stillbirths. Its consumption should be forbiden during pregnancy. 3. Tobacco. Tobacco consumption is linked to spontaneous abortion (genetically normal embryos), intrauterine growth restriction, birth defects, and sudden infant death. Consequently, patients should be warned of the risks associated with smoking during pregnancy. 4. Illegal Drugs. The consumption of illegal drugs by pregnant women is unequivocally associated with a clear increase in birth defects, such as cardiac and musculoskeletal defects, and absence of limbs. In many cases it triggers miscarriages and stillbirths, or is allied to malnourished newborns. The patients should be counselled about the risks that the consumption of illegal drugs pose for the mother-to-be and the fetus. C. Exercise. Several studies suggest that regular exercise during pregnancy may carry many important benefits not only for the mother, but for the fetus as well. The American College of Obstetricians and Gynecologists (ACOG) drew up guidelines on recommended exercise during pregnancy: • Given its beneficial cardiovascular, metabolic and biomechanical effects, regular exercise is recommended to healthy women with low risk pregnancies.

CLINICAL GUIDELINES FOR MATERNITY HOSPITALS

B. Pregnancy

•

Exercise should be done regularly, three or more times per week, with a moderate intensity that should not cause fatigue. If the patient exercised regularly before becoming pregnant, she can follow a more intensive exercise regime. • Exercise sessions must be of limited duration and intensity, and should be carried out in an optimal environment with respect to hydration and nutrition. • Each exercise session should be preceded by a warm-up period and followed by a subsequent cool-down time. • The type of exercise should minimize fetal risk and maternal injury. Stationary bicycles and swimming are strongly recommended. • Pregnancy complications or chronic diseases are relative or absolute contraindications of physical activity. D. Work. Pregnant women are faced with the challenge of balancing a career and domestic duties, such as caring for children and household chores, which are oftentimes more demanding than their own jobs. The medical recommendations concerning work during pregnancy can be grouped into three different categories: 1. Healthy women who have no complications during their pregnancy, whose jobs do not pose more risks than those of every day life, and who can work without interruptions up to their labor day, and can return to work a few weeks after delivery without any complications This is the scenary of the majority of the cases. 2. Pregnant women who can continue to work but only after adjustments in their work environment or modifications of their activities are carried out in order to eliminate all risks to their pregnancies. 3. Pregnant women who should not work by medical prescription, whose health care providers consider their jobs a risk to their health or to that of their developing fetus. Recommendations should not only specify the adjustments that need to be made at work, but also a time frame for them to be completed at the date of the next prenatal visit. The American Medical Association produced the following recommendations for working pregnant women. 1. Take breaks every two hours. 2. Take a longer break and eat every four hours. 3. Drink plenty of fluids during the work day. 4. Change positions frequently while at work: sitting to standing and walking. 5. Lifting heavy objects and bending down should be kept to a minimum. E. Accident prevention. 1. The most serious injuries suffered by pregnant women are usually caused by automobile accidents. It is vital to advise patients to drive carefully and always buckle up. 2. The vertical band of the seat belt should be positioned between the breasts and the horizontal band adjusted across the lap, avoiding any pressure on the abdomen. 3. Air bags should not be deactivated; it has been proven that air bags save

CLINICAL GUIDELINES FOR MATERNITY HOSPITALS

Prenatal attendance B.1.

lives. It is not the impact against the air bags that causes injuries to the fetus, but the impact of the car crash itself. If the pregnant woman is involved in an car accident, she should never underestimate it, as many fetal injuries may present with no clear symptoms, and especially if the accident occurs after the sixth month of gestation. F. Promotion of breastfeeding. 1. World Health Organization (WHO) recommends breastfeeding exclusively for the first six months, and continuing breastfeeding with a complementary diet up to two years of age. 2. There are several factors that influence a mother’s decision to breastfeed, such as socio-economic status (family structure, income, family support and healthcare nets), cultural issues, and, in the case of working women, plans to return to work after maternity leave, and working conditions (longer work days and conditions at work which favour breastfeeding). 3. It is imperative to offer patients the appropriate counselling about breast-feeding. Moreover, during the patient’s prenatal visits, the obstetrician must conduct a breast examination (proven to positively influence nursing) so the mother understands the importance of breastfeeding on demand, counsel on adequate hydration and nutrition, show the different nursing positions, promote the active participation of the father in the nursing process and encourage his collaboration at home, and offer information about how to face the mother’s return to work without compromising breastfeeding. G. Training and support for parents-to-be. This is a series of workshops aimed to prepare the mother-to-be, physically and mentally. They begin at week 26th of gestation (sixth month) and are structured around as group work. Topics to be explored include: 1. Human reproduction mechanisms. 2. Pregnancy stages and their normal signs. 3. Risk factors and warning signs during the different stages of the reproductive process. 4. Importance of early, regular and complete prenatal care. 5. Physical activities to improve posture, muscle strengthening and stretching, and relaxation and breathing techniques. 6. Sexuality during pregnancy. 7. Characteristics and functioning of Labor and Delivery rooms and hospital stay after delivery, ideally with guided tours. 8. Tips on care during normal pregnancy and puerperium. 9. Mother-newborn-father relationship. 10. Typical fears during pregnancy. 11. Care, nursing and special characteristics of the newborn. 12. Birth control during puerperium and nursing.

Reference. Voto L, Mattioli J: Health Education during pregnancy. In: Recommendations and Guidelines for Perinatal Medicine. Matres Mundi /WAPM. Barcelona, 2007; 3: 32-39.

CLINICAL GUIDELINES FOR MATERNITY HOSPITALS

B.â&#x20AC;&#x201A; Pregnancy

B.1.3.â&#x20AC;&#x201A; DRUGS AND RADIATIONS IN PERINATAL PERIOD A. CLASSIFICATION OF DRUGS. CONCEPT Drugs have been classified by US FDA in five categories depending on its teratogenicity (A, B, C, D, X) as follows:

US FDA RISK CLASSIFICATION IN PREGNANCY CATEGORY

EXPLANATION

Controlled studies in women fail to demonstrate a risk to the fetus in the first trimester; possibility of foetal harm appears remote.

Either animal studies do not indicate a risk to fetus and there are no controlled studies in women or animal studies have shown an adverse effect, but controlled studies in women failed to demonstrate the risk.

Either animal studies indicate a fetal risk and there are no controlled studies in women, or studies in women and animals are not available.

There is positive evidence of fetal risk, but benefits may be acceptable despite de risk.

There is definitive fetal risk based on studies in animals or Humans or based on human experience, and the risk clearly outweighs any possible benefit.

In turn, the category of a given drug can vary depending on the trimester of pregnancy at which it is administered to the woman or if it is used during lactation. Therefore not only the drug, but also the chronology of pregnancy has to be taken into account when treating pregnant women. If the drug to which the patient has been exposed during pregnancy is associated with an increased risk of congenital malformations that could be prenatally diagnosed, the woman has to be advised and available prenatal diagnosis techniques capable to diagnose the related malformations should be recommended to the patient. The nex table provides information about the teratogenic of currently used drugs: DRUGS

CATEGORY

EFFECTS ON FETUS

B/C and D

1st trimestrer. Several studies do not indicated any increased risk of malformations.

Prochlorperazine

Most evidence indicates that the risk of births defects is low, however there is some controversy.

Progesterone

Promethazine

Prednisone

Sulfamethoxazole

Most evidences indicate that fenotiatines and antiemetics risk is low, however there are controversies. Interferes with folic-acid activity on the mo ther.

Sulfamethoxazole/ trimethoprim

Most evidence does not indicate an increased risk of malformation; however some malformations have been reported.

Terbutaline

Malformations have not been, reported.

Terconazole Triamcinolone, topical

Topical vaginal. C/D

1rd trimester.

B. RADIATIONS AND NUCLEAR MEDICINE 1. On human tissues the X and gamma rays could cause biological and genetic effects in a dose-dependent way. During the peri-implantation (0-14 days) and immediate post implantation (14-21 days) periods, radiation has an all or none effect. Exposure in this phase is likely to cause miscarriage, although in those embryos that do survive, there is no risk increase of congenital malformations or growth restriction. 2. Exposure to radiation during organogenesis (3 to 9 weeks), could cause a wide range of congenital malformations and severe growth restrictions. 3. Exposure during the fetal stage (9-40 weeks) could cause growth restriction. As the Central Nervous System (CNS) specially develops from week 8 to 25, exposure during this period of pregnancy could cause disturbances in the posterior neurobehavioral development of the fetus or newborn. 4. Again it should be taken in account that the baseline risk of suffering a spontaneous abortion is 15 % and of having a fetus with a major malformation or a restricted fetal growth of 3-4 % each. 5. The mean radiation doses to which the fetus is exposed during diagnostic radiological examinations vary between less than 0.01 mGy for a chest explo ration and 7.5 mGy for several projections of the lumbar spine. A colecistography implies a 0.6 mGy exposure, that rises to 6.1 mGy if a barium enema is done. Fetal exposure varies between 3.6 mGy for a liver exploration and 89 mGy for a pelvic one.

CLINICAL GUIDELINES FOR MATERNITY HOSPITALS

Prenatal attendance B.1.

THE MOST COMMON POSSIBLE EFFECTS OF DIAGNOSTIC RADIATION ARE: 1. Risk of malformations and mental retardation. The risk of malformations after exposure to radiological imaging doesn’t increase significantly, although decline in intellectual coefficient (IQ) has been estimated to be about 30 IQ points per Grey during the most sensitive period, that is between 8 and 15 weeks post conception. 2. Risk of cancer. The National Radiological Protection Board (USA) has estimated an excess absolute risk (EAR) coefficient for cancer incidence under 15 years of age following low dose intrauterine irradiation of 0.006 % per mGy compared to 0.0018 % per mGy for a exposition just after birth. Different studies have failed to prove any significant risk increase of suffering a malignancy in childhood, including leukaemia, central nervous system tumours or other malignancies, after the intrauterine exposition to diagnostic X-rays. 3. Risk in hereditary disseases. Irradiation of males may produce possible genetic injuries. Therefore it is recommended to delay conception after radiotherapy at least 6 months. In those settings where it is possible, advise regarding the frozen storage of semen obtained prior to the irradiation should be given.

II.

RADIOTHERAPY DURING CONCEPTION AND THE TWO FIRST TRIMESTERS OF GESTATION Radiotherapy is contraindicated during pregnancy, although in certain clinical situations it may be administrated. The incidence of cancer during pregnancy is quite frequent: cervical cancer (0.5 ‰ to 0.08 ‰), Hodgkin lymphomas (1 ‰ 6 ‰), breast cancer (0.3 ‰ to 0.1 ‰) and melanoma (0.2 ‰). In turn, radiotherapy plays a major role in the multidisciplinary treatment of most of them. With an appropriate abdominal shielding, the estimated fetal exposure can be reduced by more than 50 % in most cases. Modern imaging and irradiation techniques allow calculating the irradiation doses to which the fetus is going to be exposed.

III. NUCLEAR MEDICINE 1. Radionucleotides used in medicine like technetium-99 have short disintegration times and do not cross the placenta. Its use therefore doesn’t cause a great exposure of the fetus to radiation, as this latter proceeds from the surrounding tissues of the mother. 2. The use of radioisotopes is contraindicated during pregnancy. Therapeutic abortion may be considered when the fetus is supposed to have been exposed to radiation doses exceeding 150 mGy between the second and the 15th week of conception. If the exposure ranges between 50 and 150 mGy pregnancy termination should only be considered in case of added compromising circumstances. The fetal exposure to less than 50 mGy only implies a minimal risk and doesn’t justify a therapeutic abortion. Reference. Mallafré J, Serra V.: Medicines, drugs and radiations in Perinatal period. In: Recommendations and Guidelines for Perinatal Medicine. Matres Mundi /WAPM. Barcelona, 2007; 5: 48-53.

B.2.

PROCEEDINGS AND TECHNOLOGY

B.2.1. PREGNANCY DATING I.

CLINICAL DATING a) The average duration of human pregnancy is 280 days from the first day of the last menstrual period (LMP) until delivery. The 40-week gestational period is based on menstrual weeks, with an assumption of ovulation and conception on the fourteenth day of a 28-day cycle. b) The most reliable clinical indicator of gestational age is an accurate LMP. Using Nägele’s rule, the estimated date of delivery is calculated by subtracting 3 months from the first day of the LMP, then adding 1 week. c) A Dopler device allows detection of fetal heart tones by 11 to 12 weeks’ gestation. d) Quickening is noted at about 19 weeks in the first pregnancy; in subsequent pregnancies, quickening usually is noted about 2 weeks earlier. e) The uterus reaches the umbilicus at 20 weeks.

II.

ULTRASOUND DATING Ultrasound dating is most accurate in the first 12 weeks of pregnancy. If LMP dating is consistent with ultrasound dating within the established range of accuracy for ultrasound (Table), the estimated date of delivery (EDD) is based on LMP. Before 20 weeks’ gestation, if LMP dating is outside of the range of accuracy, then ultrasound dating is used. TABLE. Range of accuracy of pregnancy dating by ultrasound according to gestational age

GESTATIONAL AGE

ULTRASOUND MEASUREMENTS

RANGE OF ACCURACY

,8 wk 8-12 wk 12-15 wk 15-20 wk 20-28 wk .28 wk

Sac size CRL CRL of BPD BPD/HC/FL/AC BPD/HC/FL/AC BPD/HC/FL/AC

6 10 days 6 7 days 6 14 days 6 10 days 6 2 wkp 6 3 wkp

AC, abdominal circumference; BPD, biparietal diameter, CRL, crown-rump length; FL, femur length; HC, head circumference Reference. Russell JB, Wood E, Schwartz D: Preconception counseling and prenatal care. In: The John’s Hopkings manual of Gynecology and Obstetrics. Edit. by KJ Kurt, MW Evik, JL Bienstock et al. Lippincott Williams and Wilkins. Philadelphia, 2011: 66-67.

CLINICAL GUIDELINES FOR MATERNITY HOSPITALS

Proceedings and technology B.2.

B.2.2. FETAL UBICATION (LEOPOLD’S MANOEUVRES) CONCEPT Leopold’s Manoeuvres consist of a series of four abdominal palpations of the gravid uterus to ascer tain fetal location and presentation.

MANEUVERS 1.

First, the fundus is palpated to ascertain the presence or abscence of a fetal pole (vertical vs. transverse lie) and the nature of the fetal pole (cranium vs. breech). Second, the lateral walls of the uterus are examined using one hand to palpate and the other to fix the fetus. In vertical lies, the sides are usually occupied by the fetal spine (long, firm and linear) and small parts of extremities. Third, by palpating above the symphysis pubis, the nature of the presenting part is determined. In addtion, determining the degree of descent of the presenting part below the pubic bone indicates the station of the presenting part. Fourth, The cephalic prominence is palpated. In cephalic presentations, provided that the head is not too deep in the pelvis, the chin will be prominent if the head is neither flexed nor extended, as in a military presentation. If the head is not flexed, as in face presentation, the occiput will be felt below the spine. If the head is well flexed, neither chin nor occiput will be prominent.

Limitations. Although Leopold´s maneuvers are limited by several factors: 1. Maternal obesity. 2. Polyhidramnios. 3. Multiple gestations. On the other hand, the procedure is a valuable adjunct to vaginal examination.

References. Robinson E, Bienstock J: Fetal Assesment, normal Labor and Delivery. In: the John Hopkins Manual of Gynecology and Obstetrics Lippincott Williams and Wilkins; Baltimore, 1999: 24. | Aguirre F, Chour B: Normal Labour in the John Hopkins Manual of Gynecology and Obstetrics. Edit by KJ Hurt, MW Guile, JL Bienstock. Williams and Wilkins. Phyladelphia, 2011: 75.

B.2.3. OBSTETRICAL ULTRASONOGRAPHY GENERAL CONCEPTS a) Obstetric ultrasound allows visualization and monitoring of the ovular structures, from the fifth week of gestation until the delivery. b) The most suitable equipment in obstetrics are the ones on real time. (RT). c) As there is no evidence of fetal risks with the use of ultrasound, it is possible to use it routinely in all pregnancies. d) There are, however, specific instructions for its use.

CLINICAL GUIDELINES FOR MATERNITY HOSPITALS

B.â&#x20AC;&#x201A; Pregnancy

ROUTINE MONITORING OF GESTATION In this case it is advisable to perform, if possible, three standard ultrasound examinations: a) First trimester (8-14 weeks). Currently possible to identify: 1. Gestational age (very accurately). 2. Twin pregnancy (early diagnosis). 3. Egg Pathology (abortion, ectopic and mole). 4. Associated gynecological pathology (ovarian cysts, fibroids, etc.). 5. Some malformations (anencephaly, etc.). b) Second trimester (19-22 weeks). In this case it is particularly also useful to diagnose: 1. Placental location. 2. IUGR type I. 3. Malformations (almost all the ones that can be diagnosed by ultrasound). c) Third trimester (32-36 weeks). At this late stage it can be assessed: 1. Maturity and fetal nutrition. 2. IUGR type II and III. 3. Chronic fetal distress. If Doppler Ultrasound is available, the information obtained will be more reliable. 4. Gender of the fetus. 5. Placental or funicular pathologies.

ULTRASOUND BY INDICATION Ultrasound is specifically indicated for: a) Doubts about the gestational age. b) Danger of abortion. c) Clinically suspected mole. d) Confirmation of a twin pregnancy. e) Gestation and IUD. f) Possible associated gynecological pathology. g) Clinical suspicion of stunted fetal growth. h) Confirmation of stillbirth. i) Bleeding in the last trimester of pregnancy. j) Suspicion of placenta previa. k) Suspected fetal malformation. l) Confirming a breech presentation.

SPECIAL ULTRASOUND TECHNIQUES In some circumstances specific ultrasound techniques are required: a) Anatomical ecobiometrics in controlling fetal growth and investigating some malformations: 1. Biparietal diameter (DBP). 2. Cephalic circumference (CA). 3. Abdominal circumference (AC). 4. Length of the femur. b) Functional eco-biometrics, when there is suspicion of placental insufficiency: 1. Fetal somatic kinetics. 2. Fetal breathing movements. 3. Urinary hourly rate.

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Proceedings and technology B.2.

4. Functional biometric indexes. 5. Study of placental structure. 6. Study of vascular flow (ultrasound flowmetry) in cardiac malformations and high-risk pregnancies with possibility of chronic or sub-acute fetal distress (retarded growth, etc.). Specially: Doppler in umbilical and cerebral arteries. 7. Biophysical Profile. Reference. Carrera JM, Mallafré J, Serra B: Protocolos de Obstetricia y Medicina Perinatal del Instituto Universitario Dexeus. 4th Edition, Elsevier. Barcelona, 2005: 78-80.

B.2.4. AMNIOCENTESIS CONCEPT Amniocentesis is the most common invasive prenatal diagnostic procedure undertaken. Most amniocenteses are performed to obtain amniotic fluid for karyotyping in the second trimester or later in the third-trimester for others indications. I.

GENETIC AMNIOCENTESIS a) Timing. The ideal time for genetic amniocentesis is 15–20 weeks of gestation. Doing the procedure before 18–20 weeks usually leaves enough time to complete cell cultures and evaluate laboratory tests before it is too late to consider pregnancy termination should an abnormality be detected. Technically, the procedure can be performed before 15 weeks. However, early amniocentesis, performed between 11 weeks and 14 weeks 6 days, has been associated with a higher pregnancy loss rate than the traditional procedure, as well as an increased incidence of positional foot deformities. b) Technique. 1. A full bladder is not necessary for genetic amniocentesis. 2. A scan is performed to confirm fetal viability and gestational age, and to determine the placental location and amniotic fluid volume. 3. The area of the abdomen just above the chosen site should then be prepared with a povidone-iodine solution. 4. A sterile sleeve (or a sterile glove) is placed over the ultrasound transducer. 5. Sterile ultrasound gel or povidone-iodine solution is applied on the abdomen. 6. Needle insertion during amniocentesis should be carried out under simultaneous ultrasound visualisation by the practitioner performing the ultrasound guidance. 7. Transplacental passage of the amniocentesis needle should be avoided unless it provides the only safe access to an adequate pool of liquid. 8. Maximum outer needle gauge size of 0.9 mm (20-gauge) should be used to perform amniocentesis, but a 22 gauge needle is ideal for all amniocentesis procedures. 9. The stylet is removed, a syringe is attached to the needle, and gentle suction applied to draw amniotic fluid into the syringe.

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10. If no fluid appears, the needle should be rotated 90° (to clear any membrane from the beveled edge) and suction applied again. 11. Occasionally, the needle pushes the membranes ahead of it (tenting of the membranes), which should be visible by sonography —in this setting, the stylet should be reinserted and the needle briskly advanced a short distance to achieve membrane puncture. 12. The first 3 to 4 mL of fluid should be aspirated into a 5 mL syringe. Because this fluid could be contaminated with maternal cells, it should not be used for genetic studies. 13. A larger (10 or 20 mL) syringe is then attached to the needle, and approximately 20 mL of amniotic fluid is aspirated. 14. If the procedure is being done on a multiple gestation and it is not obvious which sac has been sampled, 2 mL of indigo carmine diluted in 8 mL of sterile saline can be injected into the sac after the fluid specimen has been collected but before the needle has been removed, as a marker. 15. When sufficient fluid has been collected withdraw the needle rapidly; it is not necessary to reinsert the stylet. 16. If the patient is Rh-negative and unsensitized, 300 mg of Rh-immune globulin is administered. 17. The amniotic fluid can be kept at room temperature and transported to the laboratory as soon as possible (within 24 hours). c) Complications and risks of amniocentesis. The safety of amniocentesis is directly related to the gestational age at which they are performed and the experience and skill of the operator. 1. Spotting or leaking of fluid also occurs after 2-3 % of amniocenteses; usually fluid leaking is self limited. 2. True rupture of the membranes occurs rarely, increasing the risk of chorioamnionitis, complete anhydramnios and pregnancy loss. 3. Pregnancy loss: The rate of pregnancy loss after second trimester amniocentesis is 1 in 400 to 1 in 1,600 based on recent data. II.

THIRD-TRIMESTER AMNIOCENTESIS The techniques for aspiration of amniotic fluid via abdominal needle placement in the third trimester of pregnancy do not differ substantially from the techniques used in the second trimester. The indications and risk–benefit profiles for third trimester amniocentesis are different than those for second trimester procedures. a) Indications. Third trimester amniocentesis should be performed only when the results would provide clinically useful information to the patient and her care provider that might alter treatment strategies. The primary reasons in the third trimester are: 1. Pulmonary maturity testing prior to planned delivery. 2. Evaluation for infection and pulmonary maturity in patients with preterm labor, premature rupture of the membranes or growth restriction. 3. Bilirubin testing in amniotic fluid of isoimmunized pregnancies. 4. Karyotype analysis or DNA testing after third trimester identification of fetal structural abnormalities, amniotic fluid volume abnormalities, and growth restriction.

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b) Risks. Discussions with the patient should include an evaluation of the following risks. 1. Failure to obtain a sample: the risks of failure to obtain amniotic fluid were 0.5-1.5â&#x20AC;&#x2030;%. 2. Rupture of the membranes: The risk is inferior to 0.5â&#x20AC;&#x2030;%. 3. Need for urgent delivery: Women should be informed that third-trimester amniocentesis does not appear to be associated with a significant risk of emergency delivery. 4. Direct fetal or cord injury: No direct fetal or cord injuries have been informed 5. Infection: While infection is the likely etiology of many of the pregnancy losses following second trimester amniocentesis, there is little data to make that assertion in third trimester procedures. 6. Fetal-maternal hemorrhage: If possible the placenta should be avoided due to the increased risk of fetal-to-maternal hemorrhage with transplacental amniocentesis. If avoidance is not possible, choose a relatively thin portion of the placenta for needle placement. Rh-negative women at risk for isoimmunization should receive RhIg at the time of amniocentesis. 7. Laboratory failure: The risks of failure were increased if there was bloodstained fluid. The presence of meconium can impair biochemical analysis for pulmonary maturity testing. c) Procedure. 1. After discussing the possible risks of the procedure and the relative importance of the information to be gained, the patient should affirm her consent by signing a document. 2. Ask the patient to empty her bladder. 3. An ultrasound can be performed to confirm fetal head position, localize the placenta, and identify available pockets of amniotic fluid. 4. Wash the abdomen, typically with an iodine and/or alcohol-containing fluid. 5. Use ultrasound guidance for all procedures. The transducer should be covered with sonic gel and then encased in a sterile sleeve, such as a sterile glove. 6. Place sterile sonic gel on the maternal abdomen or on the sterile covered ultrasound transducer. 7. Localize the pocket of fluid, trying first to avoid pockets near the fetal face and other relatively immobile body parts, and secondarily try to avoid the placenta. 8. Using a 20 or 22 gauge sterile needle clearly long enough to reach the selected fluid pocket, insert the needle through the skin using ultrasound guidance. 9. Once the needle is placed in the amniotic cavity, remove the stylet from the needle and withdraw the necessary amount of fluid required for the tests to be done. 10. If a karyotype analysis is to be done, confirm that the appropriate syringes and tubes that are non-toxic to fibroblasts are available. 11. If bilirubin testing is to be done, confirm that dark tubes are available to avoid light exposure of the fluid.

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12. If the fluid begins to flow and then stops, rotate the needle to reposition the bevel. 13. If the flow does not restart, re-image the needle tip to confirm appropriate placement of the needle. 14. After completing the withdrawal of the fluid, remove the needle with one smooth move. d) Follow-up. 1. After completing a third trimester amniocentesis, fetal monitoring for 20–30 minutes is appropriate. 2. Antibiotic prophylaxis is not necessary. 3. If reassuring, the patient can be discharged from the testing unit. 4. The patient should be alerted to the fact that it is common to feel some uterine contractions following an amniocentesis. 5. The patient should be informed to report the loss of a large volume of fluid, the onset of fevers or chills, or uterine contractions that do not subside. Reference. Carrera JM, Mallafré J, Serra B: Protocolos de Obstetricia y Medicina Perinatal del Instituto Universitario Dexeus. 4th Edition, Elsevier. Barcelona, 2005: 47-50.

B.2.5. AMNIOSCOPY CONCEPT Amnioscopy that was proposed by Saling in 1962, had been used as a first line intervention for detection of meconium passage. Amnioscopy is a form of obstetric endoscopy employed to visualize the forebag of the amnionic sac and to determine the characteristics of amniotic fluid such as color, consistency, presence of meconium, etc. Although it is still applied in some of the obstetric units, there is controversy surrounding this method. Serial amnioscopy can be used to monitor the fetus in the last weeks of pregnancy. a) Technique. 1. The patient is placed in the lithotomy position. According to the state of the cervix, the largest suitable amnioscope is selected. The external diameters of the amnioscope tubes available being 12, 20 and 25 mm. 2. The suitable speculum applied, then, the selected tube is guided into the cervical canal. 3. The obturator is removed and a light source is inserted so that the amnion sac could be inspected through the intact forewaters. Patients were classified as amniotic fluid characteristics as follows: 1. Clear. 2. Emulsification of vernix (indicate prematurity). 3. Green or yellow, scanty that are signs of threatened danger to the fetus. b) Complications. 1. Accidental rupture of the membranes (1.4 %). 2. Serious infections with chorioamnionites (rarely).

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c) Conclusions. We agree with those authors who advise its use only when adequate management through CTG and ultrasound is not possible, and in anyway only in pregnancies at term. Reference. Carrera JM, Mallafré J, Serra B: Protocolos de Obstetricia y Medicina Perinatal del Instituto Universitario Dexeus. 4th Edition, Elsevier. Barcelona, 2005: 51-53.

B.2.6. FETAL LUNG MATURITY 1.

In cases when knowledge of lung maturity is vital antenatally, it is best assessed by measuring the lecithin/sphingomyelin (L/S) ratio of amniotic fluid obtained by amniocentesis. An L/S ratio $2:1 suggests that the lungs are mature. The «shake-test», a simple, rapid method for looking at pulmonary surfactant levels, is both easy to perform and compares favourably with the L/S ratio. It is based on the action of phospholipids, lecithin and sphingomyelin in particular, in keeping a ring of bubbles on the surface of increasing dilutions of amniotic fluid.

«Shake test» technique (Clement’s Test) At least 3 ml of amniotic fluid are required, obtained either: 1. By amniocentesis. 2. By vaginal collection, either at ARM. Five test tubes (10 ml) are labelled 1-5, and then amniotic fluid and normal saline are added in the following pro portions: 1

Amniotic fluid (ml)

TEST TUBE

1.00

0.75

0.5

0.25

0.2

Normal saline (ml)

nil

0.25

0.5

0.75

0.8

1 ml of 95 per cent ethyl alcohol is added to each tube, and they are then shaken vigorously for 15 seconds. The results are read after the tubes have been left undisturbed for 15 minutes. Only a clear full ring of bubbles is regarded as positive. Interpretation of the «shake-test» FINDING

INTERPRETATION

Positive result in 3 or more tubes

lungs mature

Positive result in tubes 1 and 2

acceptable lung maturity

Positive result in tube 1

borderline lung maturity

No tubes positive

lungs immature

References. Carrera JM, Mallafré J, Serra B: Protocolos de Obstetricia y Medicina Perinatal del Instituto Universitario Dexeus. 4th Edition, Elsevier. Barcelona, 2005: 60-61. | Stirrat GM, Fetal lung maturity: Obstetrics (Pocket Consultant). Grant McIntyre. London, 1981: 148.

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B.2.7.â&#x20AC;&#x201A; CARDIOTOCOGRAPHIC PRENATAL MONITORING CONCEPT a) It consists of the simultaneous recording of fetal heart activity and uterine activity (including fetal movements), using electronics cardiotocography (CTG). b) Monitoring cardiotocography aims to determine the so called fetal respiratory reserve (FRR). 1. The FRR is conditioned therefore placental transport capacity oxygen as resilience to hypoxia by the fetus. 2. The antenatal evaluation of this parameter is important not only to identify fetuses that are in a dangerous situation during pregnancy, but also those who may succumb at the start of delivery. 3. The time interval between records will depend on the clinical situation in particular.

NON-STRESS TEST (NST) I.

TECHNICAL PROCEDURE 1. Registration CTG without overload, for at least 30 min. The fetal movements can be noticed in topographic mapping. Important considerations to be taken: a) Do the test after a meal (or at least that the mother is not on an empty stomach). b) That patients adopt a semi-Fowler position, avoiding interference with the venous return. c) If the fetus does not move, try to wake with external manipulation or sonic stimulation.

II.

INTERPRETATION Five parameters are measured. 1. Baseline FHR. 2. Fluctuation baseline. 3. Fetal Kinetics. 4. Reactivity of FHR to fetal movement. 5. Reactivity of FHR to spontaneous contractions. The evaluation is done according to the Dexeus test (table) so that each of these parameters scored from 0 to 2.

III. EVALUATION OF THE MONITORING RESULTS 1. The FRR is considered normal when the CTG gets a score between 9 and 10 in the Dexeus test. In this case there is no fetal DISTRESS. 2. The result is considered pre-pathologic when the Dexeus test scores 7 or 8. 3. If the test Dexeus is less than 7, the result is considered pathological are diagnosed a decreased FRR, with decompensated chronic fetal distress. VI. OBSTETRICAL CONDUCT It depends on the deterioration of the FRR and gestational age. 1. In the case of a test 7-8, the clinician should choose the time of delivery and its route, depending on the maturity of the product and other factors (parity,

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neck status, history, etc.), and correlate monitoring data provided by cardiocotographics with other indices of fetal well-being. If a low route is decided, birth registration should be monitored by continuous CTG and adequate biochemical control. A score under 7 in a pregnant more than 32 weeks, a cesarean section should be indicated. Labor could exacerbate chronic fetal distress and cause fetal death or irreparable brain damage. DEXEUS TEST ANALYZED PARAMETER

PUNCTUATION

FHR

Less than 100 or more than 180

100 -120 or 160-180

120-160

Fluctuation baseline

Less than 5

5-10 or less than 25

10 -25

Fetal Kinetics

No movements Or M/l less than 0.2

Less than 20/h or M/l: 0.2-1

Less than 20/h or Ml less than 1

Reactivity of FHR to fetal movement

No changes

Reaction Lambda or elliptic type

Reaction Omega or periodic

Reactivity of FHR to spontaneous contractions

Late decelerations

Nonreactive tracing or early decelerations

Acelerations

Punctuation: 9-10: Normal, 7-8; pre pathologic Less than 7: pathologic Total

Reference. Carrera JM, Mallafré J, Serra B: Protocolos de Obstetricia y Medicina Perinatal del Instituto Universitario Dexeus. 4th Edition, Elsevier. Barcelona, 2005: 107.

B.2.8. INFECTIOUS DISEASE SCREENING 1.

Patients at risk for congenital rubella syndrome can be identified by preconception screening and prevented by vaccination. Providers sometimes hesitate to vaccinate women if they are not confident that the women will use effective contraceptives, as recommended, for three months after the vaccination. However, no case of congenital rubella syndrome has ever been reported after immunization within 3 months before or after conception. Hepatitis B virus (HBV). Women with social or occupational risks for exposure to HBV should be counselled and offered vaccination. If they are not immunized appropriately, infants of HBV-infected women have a high probability of becoming chronic HBV carriers, and 25 % of these children eventually die of related disease.

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3. Patients at risk for tuberculosis should be tested if their histories of bacillus Calmette-Guérin vaccination do not meet the guidelines for screening or preventive therapy. 4. Cytomegalovirus (CMV) screening should be offered to women who work in neonatal intensive care untis, child care facilities, or dialysis units. Unlike rubella and other viral infections, past exposure to CMV, indicated by IgG antibodies in serum, does not confer complete immunity to pregnant women. Because no therapy or vaccine is effective against CMV and fetal risk is low, screening either before or during pregnancy is not cost-effective and is generally not recommended for the general population. 5. Toxoplasmosis. Routine toxoplasmosis screening to determine antibody status before conception mainly provides reassurance to those who are already immune; a more prompt and definitive diagnosis can be made if seroconversion occurs during pregnancy. Counseling focuses on good hygiene. Someone other than the woman should dispose of cat litter daily. Women should wear gloves when gardening in a yard to which cats have access, avoid eating raw or undercooked meat, and wash their hands after handling such meat. 6. Screening for varicela antibody should be performad if a positive history cannot be obtained. The varicella zoster virus vaccine is now available and recommended for all nonimmune adults. 7. Human immunodeficiency virus (HIV) counselling and testing should be offered to all women. 8. Toxicologic examination is a useful tool to encourage abstinence in women with a history of substance abuse. Standard informed consent and confidentiality restraints should be in effect. 9. Neisseria gonorrhea, Chlamydia trachomatis, or Treponema pallidum testing should be performed if is possible. Reference. Stohl H, Satin AJ: Perinatal Infections. In: The Johns Hopkins Manual of Gynecology and Obstetrics. Edit by Hurt KJ, Guile MW, Bienstock JL et al. 4th Edition, Lippincott Williams and Wilkins. Baltimore, 2011; 11: 137-153.

B.2.9. CERCLAGE TECHNIQUE CONCEPT The procedure aims to close the internal cervical os by placing sutures around it.

INDICATION The only absolute indication in proven cervical incompetence. To see protocol B-3-8.

CONDITIONS The procedure should only by carried out under the following circunstances: 1. There is no rupture of membranes. 2. The area is free from infections.

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3. 4. 5.

There is abscence of uterine hemorrhage. It is non-irritable uterus. Thee is absence of cervical dilatation.

CONTRAINDICATIONS It is considered to be contraindicated when there is: 1. Dilatation greater than 4 cm. 2. Preterm premature rupture of membranes. 3. Cervicovaginal infection. 4. Malformation or fetal chromosomal alteration.

TECHNIQUE There are several techniques: 1. Shirodkar operation. A transverse, anterior an posterior cervical incision is made and the suture material is passed from one cut to the other using a Deschamps or aneurysm needle. The material used in the original technique (fascia lata) was subsequently replaced by mersilene or nylon tape. The cerclage is fixed by means of silk stitches at both incisions and closed with 00 sutures. 2. MacDonald operation. Six loops are placed around the cervix. Neither anterior o posterior colpotomy is performed and part of the suture (mersile tape or perlon of lafil numbers 3 or 4) remains outside the mucosa in an alternating fashion. 3. Palmer operation. Six stitches are placed around the cervix (every 1.5 cm) passing the needle through the exit hole for the previous loop. The original technique included a small anterior colpotomy in order to move the blader aside. The suture material used is the same as in MacDonald operation. 4. Szendi operation. This involves closing the cervix by means of three stitches (lafil, mersilene, nylon, etc.) which join the anterior and posterior labia. 5. Combined cerclage of Carrera. This technique avoids the main causes of failure. The technique is relatively straightforwards. Its fundamental aspects are as follows: a) The bladder is moved aside wich a valve (without colpotomy). b) A Palmer-type suture (Submucose) is used, aiming to ensure that there are no fragments of thread outside the mucose. A monofilament thread is used, such as lafil, tefdek or perlon, number 3 or 4. The needle is atraumatic, curved, belleved and narrow (so that it can be easily hundled). c) The cerclage thread is anchored to the cardinal ligaments, therefore avoiding their dissection. d) The cervical circulation is protected (loops below the cervical artery). e) The external cervical os is occluded by means of three Szandi stitches, using the same sutura material as in the cerclage. f) No instruments (or the finger) are introduced into the endocervical canal.

CAUSES OF CONVENTIONAL CERCLAGE FAILURE Provided that conventional cerclages is properly indicated and performed, its failure should be attributed to one or more of the following causes:

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1. Excessive trauma, This occur in those cerclages involving colopotomy, whether anterior or posterior (Shirodkar, Palmer, etc.). 2. Cerclaje slipping. This is more common in those operations where the suturing in not anchored (Palmer, MacDonald, Shirokdar, etc.). 3. Lesion of cervical vascularization. Such lesions promote necrosis and infection. 4. Cervical infection with chorioamnionitis. It is usually the result of the infection in the cervicovaginal area due to external suturing (Palmer, etc.) traumatic operation. Scheduling and postoperative period 1. Time of cerclage: Cerclage should be performed between 12 and 15 weks. 2. Removal of cerclage: the cerclage can be removed prophylactically at 38 weeks of gestation o when birth is triggered spontaneously. The cerclage should also be removed, regardless of the period of gestation, if there are signs of infection, uterine contractions, and the membranes rupture prematurely.

Reference. Carrera JM: Cervical incompetence and its treatment. In: Controversies in Perinatal Medicine, Edit. By Carrera JM, Chervenak FA and Kurjak A. Parthenon Publishing. New York, 2003; 24: 267-278.

B.2.10. CLINICAL PELVIMETRY CLINICAL EXAMINATION 1. A vaginal examination is performed in the routine manner (37 weeks). 2. An attempt is made to reach the sacral promontory with the middle finger. If the pelvis is normal the sacral promontory will not usually be felt. 3. The sacrum itself is palpated to note any angulation, straightening, irregularities or false promontories. 4. Convergence of the pelvic side walls is then checked for. 5. The prominence of the ischial spines and the middle of the sacrosciatic notches are assessed. 6. To assess the outlet the hand is partially removed and the fingers placed in the sub-pubic arch to assess its shape and angulation. 7. Finally, the hand is removed and the knuckles of the clenched fist are placed between the ischial tuberosities.

TYPES OF PELVISES Based on the general bony architecture pelvises may by classified into four basic types. 1. Gynecoid and anthropoid pelvises are amenable to fetus. 2. Android and platypelloid pelvises, which, because of a smaller amount of space in the posterior pelvis. For this reason it is important the measurement of the posterior sagital diameter.

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TYPE

Gynecoid Anthropoid Android Platypelloid

SHAPE

POSTERIOR SAGITAL DIAMETER

PROGNOSIS

Round

Average

Good

Long, oval

Long

Good

Heart shaped

Short

Poor

Flat, oval

Short

Poor

IDEAL PELVIS The brim is round and the sacral promontory is not prominent. The angle of inclination is about 55º to the horizontal. The cavity is shallow with straight, non-converging walls. The sacrum is smoonthly curved. In the outlet the sacro-sciatic notches are wide and shallow. The sacrum does not project forward. The ischial spines are not prominent. The pubic arch is wide and domed (like a Norman arch rather than a Gothic arch). The sub-pubic angle is a virtual right angle. The intertuberous diameter is wide, accommodating four knuckles of an average-sized hand with ease.

CEPHALO-PELVIC DISPROPORTION (CPD) Antenatal suspicion of cephalo-pelvic disproportion can be tested by pressing the head into the pelvic brim, as follows: 1. The patient lies on a couch with knees separated and partially raise. 2. The examiner places the third, fourth and filth fingers of both hands on her abdomen over the fetal sinciput and occiput. 3. The index fingers are placed on top of the symphysis pubis. 4. The thumbs press backwards on the parietal eminence. 5. An assistant is asked to steer the fetus towards the pelvis by pressure on the breech. If the biparietal diameter passes the pelvic brim, there is no CPD at the inlet. If the parietal eminence overlaps the symphysis pubis, the suspicion of CPD is increased. References. Sirrat GM: Obstetrics. Pocket consultant, Grant MCIntyre. Oxford, 1981: 11-9. | Carrera JM, Mallafré J, Serra B: Protocolos de Obstetricia y Medicina Perinatal del Instituto Universitario Dexeus. 4th Edition, Elsevier. Barcelona, 2005: 110-111.

B.2.11. EXTERNAL CEPHALIC VERSION (ECV) CONCEPT The ECV is to turn the fetus by external maneuvers on the womb. I.

PATIENT SELECTION a) All women with a singleton pregnancy with the fetus in the breech position in an ultrasound performed between 30 and 35 weeks. The possibility of a VCE will be discussed at 36 weeks.

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b) Absolute contraindications for ECV: 1. Premature rupture of membranes. 2. Placenta previa. 3. Suspicion of abruption. 4. Multiple gestation. 5. Intrauterine growth restricted with hemodynamic impairment. 6. AFI ,5. 7. Rh sensitization. 8. Nonreactive pattern. 9. Uterine abnormalities (polymiomatous uterus, uterus bicornis). 10. Coagulation disorders. 11. Hypertensive disorders. 12. Indication of cesarean section for other reasons. 13. Labor started. II.

METHODOLOGY a) The patient should attend the obstetric area early in the morning, without breakfast. Then, the breech presentation will be checked by ultrasound, a CTG recording will be held for 30 min. Before starting the version, the availability of the operating room should be confirmed. If the all the previous requirements have been taken: 1. The treatment starts by administrating Prepar 60 ml/h 30 min before starting the ECV (20 mgs 5 2 ampoules in 500 ml of glucosalin serum). The heart rate of the patient will be monitored all the time, as well as the fetal CTG registration. In those patients in whom Prepar is contraindicated (heart disease, thyroid disease, diabetes insulinizadas…), a bolus of Atosiban will be administrated 30 min before the ECV with a posterior perfusion at 24 ml/h. 2. Five minutes before the ECV, the anesthesia service should start a perfusion of remifentanil 0.1 ml. During the ECV, boluses of remifentanil 30 mg should be administered depending on the tolerance of the patient. The anesthetist must be present during all the ECV. Oxygen should be administered to the patient by mask. However, usually anesthesia is not necessary. 3. The patient should be placed in Trendelenburg. The ECV must be performed by two obstetricians, located on both sides of the mother. One of them remove the podalic pole outside the pelvis, while the other will accompany the cephalic pole in the opposite direction of the fetal back. A maximum of three attempts will be made and between each of them it should be checked, by ultrasound, the FHR and where the cephalic pole is located. The midwife should present in the delivery room during the VCE. 4. Regardless the success or failure of the ECV, a CTG recording must be ob tained during the following 2 h. Initially, the CTG recording is usually very reactive. 5. After 24 h a monitoring with CTG record must be performed. 6. A dose of anti-D globulin should be administered to pregnant women with negative Rh. b) Positive prognostic factors: 1. Multiparity. 2. Posterior Placenta.

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III. COMPLICATIONS 1. Retroamniotic bruising (frequently), especially if the placenta is above, at the level of the bottom tab. They are easily identified by ultrasound. They are usually self-limiting. 2. Poor self-limiting metrorrhagia. 3. Premature rupture of membranes / onset of labor. 4. The transient fetal bradycardia is relatively common, but self-limiting when maneuvers are completed.

Reference. Serra B, Mallafré J: Protocolos de Obstetricia y Medicina Perinatal del Instituto Universitario Dexeus. 5th Edition, Elsevier. Barcelona, 2014: 133-134.

B.2.12. AMNIOTIC FLUID INDEX (AFI) CONCEPT a) The semi-quantitative value of the amniotic liquid volume is an important element for the prognosis or the fetus condition. b) From all the echography procedures described, the system of the four quadrants is probably de most efficient. That is the procedure to calculate the amniotic fluid index. (AFI).

METHODOLOGY a) The mother’s abdomen is mentally divided in four quadrants, using the bellybutton and the «brownish medial line» as reference points. b) With the transducer of the ultrasound equipment located perpendicularly in relation with the mother´s spine, it is possible to calculate the maximum density of the amniotic liquid in each quadrant. c) The sum, in centimeters, of those four values constitutes the AFI.

INTERPRETATION a) In a normal gestation the AFI should be between 8 and 25 cm. If the AFI doesn’t reach the 5 cm it is considered pathologic. (oligoamnios). b) If its value is inferior from 8 it is suggested to perform de following procedures of fetal evaluation. c) A value higher then 25 is considered as moderate hydramnios. Once it reaches the 32 cm it is considered severe.

Reference. Serra B, Carrera JM, Mallafré J: Protocolos de Obstetricia y Medicina Perinatal del Instituto Universitario Dexeus. 4th Edition, Elsevier. Barcelona, 2005: 104-105.

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B.â&#x20AC;&#x201A; Pregnancy

B.2.13.â&#x20AC;&#x201A; CONGENITAL DEFFECTS: SCREENING,

DIAGNOSIS AND PREVENTION

PREVENTION OF CONGENITAL DEFFECTS There are three types of prevention of congenital defects. 1. The primary prevention tries to avoid the production of the defect. This is the case of the prophylactic administration of folic acid to reduce the appearance of neural tube defects. 2. The aim of the secondary prevention is the early prenatal detection of defect, making possible the early termination of pregnancy. However, the decision depends on the local legal system and the religious beliefs of the parents. Naturally it is there in that kind of prevention, where the ultrasonography has a fundamental role. 3. Finally in the tertiary prevention, the objective is only the treatment and social adaptation of the malformed child.

TYPES OF SECUNDARY PREVENTION In the case of secondary prevention it is important to distinguish between. 1. Screening test, whose main objective is the identification of pregnancies at risk, through first level test or detection test. 2. The diagnostic methods that achieve prenatal diagmosis of the congenital defects using second level tests. 3. In the case of congenital defects for chromosomopathies, the first level will be the blochemical and sonographic test, meaning diagnostic test will be the amniocentesis o villus sampling. 4. But in the case of malformations, the ultrasonography is at the same time the detection test and the diagnostic test. The level of the exploration is the only thing that differentiates both tests.

ULTRASONIC SCREENING AND DIAGNOSIS Ultrasonography allows for a detalled morphological functional, behavioral and developmental analysis of the fetus. If possible, it is advisable to make three sonographic examinations during pregnancy. 1. At 10-14 weeks (for detection of gross malformations and markers of aneuploidies. 2. At 20-22 weeks (for detailed study of fetal anatomy, and detection of the majority or malformations), and 3. Al 34-37 weeks (for study of fetal growth).

GENERAL CONSIDERATIONS ABOUT THE USE OF ULTRASONOGRAPHY 1. If the Health Center disposes of ultrasonogrphy all pregnant women schould be examined by means of this procedure at least to 20-22 weeks. 2. The experience and training of the sonographer is very important. The result obtained depends also of the quality of the equipment used and the working conditions.

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Proceedings and technologyâ&#x20AC;&#x201A; B.2.

3. The sonographer must know quite well the embriology, dismorphology and the pathology of development. 4. Sonographers should not remain satisfied with merely having detected a malformation. It is necessary look for other anomalies and carry out complementary test (cytogenetic, immunological or biochemical studies). 5. If is possible the ultrasound scan at week 20, should be performed at level 2. The level system is the best way to get the highest standards of quality. 6. Sonographers should always bear in mind the feelings and the psychological state of the parents as well as the ethical an legal aspects of each case. 7. No decisions should be made without having first clearly defined the disorder of the fetus. 8. A detailed postmortem examination should be carried out. The purpose is to provide appropiate counselling and quality control.

ULTRASOUND TECHNIQUE As most of the fetuses with chromosomal abnormalities have structural malformations, the so called genetic ultrasound is used for first and second trimester scanning for special markers, which are used in calculation alone or with maternal biochemical screening, for detection of chromosomal abnormalities. When the risk is higher, karyotyping is recommended.

GENERAL CONSIDERATIONS 1. Severe fetal structural malformations are found to be closely related to fetal chromosomal abnormalities. 2. Structural malformations that strongly suggest fetal chromosomal abnormalities are: nuchal edema, cystic hygroma, ventriculomegaly, hydrocephalus, Dandy-Walker complex, holoprosencephaly, fetal hydrops, duodenal atresia, some cardiac anomalies, some urinary tract abnormalities, etc. 3. Structural malformations suggesting low risk for fetal chromosomal anomalies: isolated cleft lip and clef palate, gastrochisis, jejunal atresia, large bowel obstruction, unilateral polycystic, renal hypoplasia, mesenteric cyst, ovarian cyst, isolated cross-foot, etc. 4. Each type of chomosomal abnormality has its own variety of structural malformation. 5. More fetal structural malformations suggest higher risk for fetal chromosomal abnormalties.

US MARKERS I.

NUCHAL TRANSLUCENCY a) Nuchal translucency (NT) is subcutaneous accumulation of fluid in the fetal neck. This echolucent zone is observed by ultrasound during first trimester (nuchal translucency) and second trimester (nuchal fold) of pregnancy. b) Both, nuchal translucency and nuchal fold are suggestive of chromosomal defects, whereas cystic hygroma is considered a congenital malformation of variable expression in terms of both morphology and chronology. From a pathophysiological pont of view, nuchal fluid comes from the paracervial lymphatic system, which drains into the internal jugular vein. Enlarged NT occurs due to the cardiac failure in association with cardiac abnorma-

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B. Pregnancy

lities, venous congestion, abnormal development of the lymphatic system, failure of lymphatic drainage, fetal anaemia or hypoproteinemia or congenital infection. Spontaneous resolution of the nuchal fluid is more likely to occur in euploid fetuses, although it has also been described in aneuploid ones. c) Value of NT $ 3 mm in the first trimester implies a detection rate between 28 to 100 % of T21, with a specificity of 48-99 %. d) Measurement should be performed between 11 weeks and 13 weeks and 6 days, when CRL is about 45 to 84 mm. It can be measured both transvaginally and transabdominally. e) Strong association between NT and congenital heart defects has been found; therefore NT is accepted as a marker for CHD. II.

NUCHAL FOLD a) Nuchal fold (NF) is measured between 16 and 22 weeks of gestation, at the transverse plane of fetal cerebellum. b) NF $ 5 mm is considered to be abnormal. c) It is used for trisomy 21 screening.

III. CYSTIC HYGROMA a) Fetal cystic hygroma (CH) is a congenital malformation characterized by distended fluid-filled spaces in the region of the fetal neck. b) It results from misconnection of jugular lumph sacs to the jugular vein, which is causing accumulation of lymph fluid at the back of the neck instead of appropriate drainage into the venous system. c) Cystic hygroma can be diagnosed early or late in the pregnancy. d) In the first trimester cystic hygroma is associated with chromosomal defects in 50 % of cases, particularly autosomal trisomies, but with low incidence of adverse perinatal outcome or dysmorphological sequels. e) When diagnosed in the second trimester of pregnancy, about 80 % of the cases are associated with aneuploidy: in particular with monosomy X and trisomy 21 or other structural malformations. Prenatal diagnosis always requires very careful assessment meaning kayotyping and ultrasound. IV. NASAL BONE a) Hypoplasia or absence of the nasal bone when scanning one should obtain mid-sagital view of the fetal profile and only echogenic skin could be seen in nasal area. b) Perform scanning between 11 weeks and 13 weeks of gestation. c) The nasal bone is absent in 65 to 70 % of trisomy 21 fetuses, in more than 50 % of trisomy 18, and 30 % of trisomy 13 fetuses. V.

SHORT FEMUR AND HUMERUS a) Length of femur (FL) and humerus (HL) has also been proposed as a marker in screening for aneuploidies in the second trimester of pregnancy. b) Short FL is associated with trisomy 21. c) Use combination of FL and HL, higher specificity.

Reference. Kurjak A, Marton I, B Miskovic: Congenital deffects: screening and diagnosis. In: Recommendations and Guidelines for Perinatal Medicine. Matres Mundi/WAPM. Barcelona, 2007; 17: 160-169.

B.3.

OBSTETRICAL PATHOLOGY

B.3.1. NAUSEA AND VOMITING IN PREGNANCY CONCEPT 1. Nausea and vomiting are common complaints in the first trimester of pregnancy affecting about 50 % of pregnant mothers, and is considered by many as diagnosis of pregnancy. 2. The symptoms are severe in multiple gestations and gestational trophoblastic neoplasm. 3. Protracted vomiting associated with dehydration, starvation, weight loss, electrolyte disturbances, acidosis and ketonuria is known as hyperemesis gravidarum. The cause is not exactly known. 4. In most cases it is very slight, so treatment is not necessary. It usually goes away between weeks 12-14. If that is not the case, treatment with Doxylamina and Vit. B6 (10 mg of each every 8-12 hours) should be applied.

DIAGNOSIS a) Clinical. Excessive vomiting, signs of dehydration, deranged vital signs, etc. Rule out medical causes like hyperthyroidism, food poisoning, diabetes, etc. b) Laboratory. Ketonuria, Elevated AST and SGOT.

TREATMENT a) Objectives of treatment. 1. Adequate fluid, electrolyte and calorie replacement. 2. Arrest the vomiting with anti-emetics. 3. Identify obstetrics conditions that are associated with hyperemesis gravidarium. 4. Rule out other medical or surgical causes. b) Non-drug treatment. 1. For uncomplicated nausea and vomiting at pregnancy, give reassurance. 2. Advice on small, high calorie frequent feeding. 3. Emotional support. 4. Remove a stressful home environment. 5. Advice, temporary withdrawal of oral nutrition and fluid.

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B. Pregnancy

c) Drug tratment. Hyperemesis gravidarum requires admission for in-patient care. 1. Re-hydrate with N/S, Ringers lactate, D/W, D/S eight hourly. 2. Calorie replacement: Add 40 % Glucose 2 vials (40 ml) in each bag. 3. Add Vit. B complex 2 ampoules in each bag. d) Control vomiting. • Chlorpromazine; 12.5-25 mg I.M. BID until vomiting is controlled and the P.O. • S/Es: bone marrow suppression, drowsiness, apathy, alteration in liver function, cutaneous reactions, occasionally tardive dyskinesia. • C/Is: bone marrow depression, coma caused by CNS depressants. • Dosage forms: Tablet, 25 mg, 50 mg, 100 mg; Drop, 25 mg/ml in 10 ml bottle, 40 mg/ml in 10 ml and 30 ml bottles; syrup, 25 mg/5 ml; Injection, 25 mg/ml in 1 ml and 2 ml ampoules, 50 mg/ml in 2 ml ampoule. e) Alternatives. 1. Promethazine, 25 mg IM/IV BID, followed by 25 mg P.O BID. • S/ES: drowsiness, sedation, headache, blurring of vision Gl disturbance. • PC: Close monitoring of the patient is required during the first few days of therapy. • Dosage forms: Elixir, 5 mg/5 ml; injection, 25 mg/ml 1 ml and 2 ml ampoules; suppository, 25 mg, 50 mg; tablet, 10 mg, 25 mf, Tablet, 10 mg, 25 mg. 2. Metoclopromide, 10 mg IM BID. • S/Es: drowsiness, fatigue, dizziness, weakness. • C/Is: epilepsy, pheochromocytoma, and mechanical bowel obstruction, concomitant administration of atropine like drugs. • S/P: concomitant administration of phenothiazines. • Dosage forms: tablet, 10 mg; syrup, 5 mg/5 ml; injection, 5 mg/ml in 2 ml ampoule; drop, 0.2 mg/drop. 3. Pyridoxine hydrochloride, 20 mg/day orally. • S/Es: Rare. • Dosage forms: Injection, 50 mg/ml in 2 ml ampoule. 150 mg/ml; Tablet, 5 mg, 10 mg, 100 mg, 300 mg.

Reference. Drug Administration and Control Anthority of Ethiopia Contens. Standard Treatment Guideline for General Hospitals. Addis Abeba, 2010; VIII: 339-341.

B.3.2. MISCARRIAGE CONCEPT Miscarriage or spontaneous abortion is the natural or spontaneous end of a pregnancy at a stage where the embryo or the foetus is incapable of surviving, generally defined at a gestation of prior to 20 weeks. Miscarriages are the most common complication of pregnancy.

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Obstetrical pathology B.3.

CAUSES 1. Miscarriages can occur due to many reasons, not all of which can be identified. 2. Most miscarriages (more than three-quarters) occur during the first trimester. Chromosomal abnormalities are found in more than half of embryos mis carried in the first 13 weeks. Another cause of early miscarriage may be progesterone deficiency. 3. Up to 15 % of pregnancy losses in the second trimester may be due to uterine malformation, grow of fibroids within the uterus or cervical problems. These conditions may also contribute to premature birth. 4. Other causes are: pregestational diabetes, high blood pressure, tobacco, hypo thyroidism, autoimmune diseases…

DIAGNOSE a) Clinical Diagnosis. 1. The most common symptom of a miscarriage is bleeding. 2. Moderate or mild pelvic pain. 3. Cervix can be dilated and uterus can be enlarged in an extent appropriate or minor for gestational age of the pregnancy. A pregnancy test will be positive. b) Ultrasonographic diagnosis. 1. Pelvic ultrasound is used to visualize foetal heartbeat and to determine whether a pregnancy is still viable. 2. The measure of the embryo length determines its gestational age. 3. We have to differentiate if it is a threatened miscarriage (uterine bleeding with embryo alive), complete miscarriage (products of conception have expelled out of the uterus) or incomplete miscarriage (products of conception persist in the uterus). c) Analitic diagnosis. Blood levels of serial human chorionic gonadotrophin (hCG) may help to determine the viability of a pregnancy if the ultrasound examination is inconclusive.

TYPES OF MISCARRIAGE 1. 2.

5. 6.

Threatened miscarriage. Uterine bleeding at early pregnancy that may be accompanied by cramping or lower backache. The cervix remains closed. Inevitable or incomplete miscarriage. Miscarriage is inevitable when there is a dilation or effacement of the cervix and/or rupture of the membranes. Bleeding and cramps may persist if the miscarriage is not complete. Complete miscarriage. The embryo or products of conception have emptied out of the uterus. Bleeding should subside quickly, as should any pain or cramping. Missed miscarriage. Embryonic death has occurred but there is not any expulsion of the uterus. Signs of this would be a loss of pregnancy symptoms and the absence of fetal heart tones found with ultrasound. Recurrent miscarriage. Defined as three or more consecutive miscarriages. Blighted ovum. Also called anembryonic pregnancy. A fertilized egg implants into the uterine wall, but foetal development never begins.

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B. Pregnancy

TREATMENT 1. No treatment is necessary for a diagnosis of complete abortion (as long as ectopic pregnancy is ruled out). 2. In cases of an incomplete abortion, empty sac, or missed abortion, there are three treatment options. a) With no treatment, most of these cases (65-80 %) will pass naturally within two to six weeks. This path avoids the side effects and possible complications due to medications and surgery. b) Medical management usually consists of using oral or vaginal prostaglandins (misoprostol) to encourage completion of the miscarriage. About 95 % of cases treated with misoprostol will complete within a few days. c) Surgical treatment, most commonly dilation and curettage (D&C) is the fastest way to complete the miscarriage. It also shortens the duration and heaviness of bleeding, and is the best treatment for physical pain associated with the miscarriage. If women’s blood group is Rh negative, they will also need the Rhogam shot within 72 hours of the abortion. Reference. Bescos E, Ibáñez P, Tajada M, Fabre E: Haemorrhage in the first term of the pregnancy. In: Recommendations and Guidelines for Perinatal Medicine. Matres Mundi/WAPM. Barcelona, 2007; 9: 83-85.

B.3.3. ECTOPIC PREGNANCY CONCEPT In an ectopic pregnancy, a fertilized egg has been implanted outside the corps uterus. The egg settles in the fallopian tubes more than 95 % of the time. This is why ectopic pregnancies are commonly called «tubal pregnancies». The egg can also implant in the ovary, abdomen or the cervix.

DIAGNOSE 1. An ectopic pregnancy is to be suspected in any woman with lower abdominal pain and/or unusual bleeding who is or might be sexually active and whose pregnancy test is positive. 2. Early symptoms in ectopic pregnancy are either absent or subtle. Clinical presentation of ectopic pregnancy occurs at a mean of 7.2 weeks after the last normal menstrual period, with a range of 5 to 8 weeks. 3. Patients with a late ectopic pregnancy typically have pain and bleeding. This bleeding will be both vaginal and internal and has two discrete pathophysiologic mechanisms: a) External bleeding due to the falling progesterone levels. b) Internal bleeding due to haemorrhage from the affected tube. 4. The vaginal bleeding can be indistinguishable from an early miscarriage or the implantation bleed’ of a normal early pregnancy. 5. The pain and discomfort are usually mild. A corpus luteum on the ovary in a normal pregnancy may give very similar symptoms.

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Obstetrical pathology B.3.

6. A urine test for pregnancy will nearly always be positive but it might be only weakly positive. In cases of doubt, a blood pregnancy test may be performed, which is always positive in ectopic pregnancy.

COMPLEMENTARY TESTS Transvaginal ultrasound is a valuable diagnostic tool. The presence or absence of an intrauterine sac must be documented. 2. A B-hCG . 2,400 mulU/ml with no intrauterine sac present is diagnostic of an abnormal pregnancy and highly suggestive of an ectopic pregnancy. The hCG discriminatory concentration is dependent on the hCG standard utilized in any given laboratory. In addition, ultrasonic detection of adnexal cardiac activity is useful in determining the appropriate therapy for ectopic pregnancy. 3. A laparoscopy or laparotomy can also be performed to visually confirm an ectopic pregnancy. 1.

TREATMENT 1. The advent of methotrexate (MTX) treatment for ectopic pregnancy has reduced the need for surgery. 2. MTX, long used in treatment of gestational trophoblastic neoplasia, is also effective in treating ectopic pregnancy. It is particularly effective as primary treatment when the diagnosis can be made without surgery. MTX may be administered intramuscularly in either single (0.4 -1 mg/day, 3-5 days) or alternate day doses (1 mg/kg, days 1, 3, 5, 7). However, the optimal dose and time of MTX has yet to be determined. 3. Surgical intervention is still required in cases where the Fallopian tube has ruptured or is in danger of doing so. 4. If intraperitoneal haemorrhaging has already occurred, surgical intervention may be necessary if there is evidence of ongoing blood loss. The option to go to surgery is thus often a difficult decision to make in an obviously stable patient with minimal evidence of blood clot on ultrasound. 5. Surgeons use laparoscopy or laparotomy to gain access to the pelvis and can either incise the affected Fallopian and remove only the pregnancy (salpingectomy). 6. If women’s blood group is Rh negative, they will also need the Rhogam shot. Reference. Bescos E, Ibáñez P, Tajada M, Fabre E: Haemorrhage in the first term of the pregnancy. In: Recommendations and Guidelines for Perinatal Medicine. Matres Mundi/WAPM. Barcelona, 2007; 9: 85-87.

B.3.4. GESTATIONAL TROPHOBLASTIC DISEASE (GTD) DEFINITION GTD refers to a spectrum of interrelated diseases resulting from the abnormal proliferation of the trophoblastic epithelium of the placenta.

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B. Pregnancy

TYPES OF GTD a) Hydatidiform moles (80 % of GTD) cases: result from aberrant fertilization. Characterized by swelling of placental villi, proliferation of trophoblast, absence of normal fetus. 1. Complete: 46,XX (most common, all paternal chromosomes); 46,XY (less common). • Absent fetus, diffuse swelling of villi, diffuse trophoblastic hyperplasia, b-hCG . 100,000. • Elevated hCG levels lead to theca lutein cysts, hyperemesis, early preeclampia, and subclinical hyperthyroidism. 2. Partial: Triploid (69,XXX or 69,XXY). • Fetus present but abnormal, focal swelling of villi, focal trophoblastic hyperplasia, b-hCG , 100,000. Smaller chance of malignant transformation. b) Gestational trophoblastic neoplasia/tumour: 1. Persistent/invasive mole: 20 % of complete moles, 0.5 % of partial xmoles. 2. Choriocarcinoma: as a result of mole, abortion, term, ectopic pregnancies. 3. Placental Site Trophoblastic Tumour (PSTT-origin non-villous trophoblast). 4. Epithelioid Trophoblastic Tumour (ETT. Origin intermediate trophoblast).

Reference. Moi Teaching and Referrnal Hospital (MRTH). Protocol of Dept. Of Reproductive Health. Kenya, 2012.

B.3.5. MOLAR PREGNANCY (Hydatiform mole) CONCEPT A molar pregnancy is an abnormality of the placenta, caused by a problem when the egg and sperm join together at fertilization. Molar pregnancies are also called hydatidiform mole or simply referred as a «mole».

CLASIFICATION 1. The complete mole, this occurs when the nucleus of an egg is either lost or inactivated. The sperm then duplicates itself because the egg was lacking genetic information. Usually there is no foetus, no placenta, no fluid and no amniotic membranes. The uterus is rather filled with the mole that resembles a bunch of grapes. The fluid filled vesicles grow rapidly, which can make the uterus seem larger than it should be for gestational age. 2. The partial mole, this most frequently occurs when two sperm fertilize the same egg. There may be partial placentas, membranes or even a foetus present in a partial mole. However, there are usually genetic problems with the baby.

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Obstetrical pathology B.3.

3. The gestational trophoblastic diseases (GTD) include complete and incomplete molar pregnancy. The term gestational trophoblastic neoplasia (GTN) replaces the terms chorioadenoma destruens, metastasizing mole and choriocarcinoma. These were pathologic diagnoses.

DIAGNOSE 1.

The main symptoms of a molar pregnancy are increased nausea and vomiting, and vaginal bleeding. 2. Increased hCG levels. 3. A rapidly growing uterus; but no foetal movement or heart tone is detected. 4. It is frequent to find pregnancy induced hypertension prior to 24 weeks and hyperthyroidism. 5. Ultrasound can also help to determine a molar pregnancy. The typical «snow storm effect» may be seen on the screen.

TREATMENT 1. 2.

3. 4. 5.

If the pregnancy has not ended on its own, suction is usually used to evacuate the mole from the uterus. Ongoing treatment includes b-HCG levels to be taken two times a week, then weekly, until they are «normal» for three weeks. Afterwards it will be tested monthly for six months, and every two months until a total of one year has passed. Pelvic exams should be done too. A rising level of b -HCG and an enlarging uterus could indicate the presence of a choriocarcinoma. If women’s blood group is Rh negative thew will also need the RhoGam shot. Pregnancy should be avoided during the period of one year. Any method of birth control, with the exception of an intrauterine device, is acceptable. Differential diagnosis of haemorrhages of the first term of the pregnancy

THREATENED MISCARRIAGE

ECTOPIC PREGNANCY

MOLAR PREGNANCY

Genital bleeding.

Pelvic pain.

Uterus bigger than gestational age.

Embryo with/without beating.

Uterus is emply and there is a tubal increase.

«snow storm effect» with/without embryo.

B-HCG according or lower to gestational age.

Lower increase of b-HCG.

b-HCG very increased.

Reference. Bescos E, Ibáñez P, Tajada M, Fabre E: Haemorrhage in the first term of the pregnancy. In: Recommendations and Guidelines for Perinatal Medicine. Matres Mundi/WAPM. Barcelona 2007, 9: 87-88.

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B. Pregnancy

B.3.6. GESTATIONAL TROPHOBLASTIC NEOPLASIA/TUMOUR Diagnostic criteria for persistent/invasive mole/choriocarcinoma 1. Rising (rise of . 20 % in level between any two measurements) or plateau levels of serum b-HCG (,10 % fall in hCG with 4 measurements over 3 weeks). 2. Serum b-HCG elevated 6 months post-evacuation. 3. Histological evidence of choriocarcinoma at any site. 4. Non-pulmonary metastases. 5. Persistent bleeding despite repeat evacuation.

STAGINC FOR GTN Stage I Disease confined to the uterus. Stage II GTN extends outside of the uterus, but is limited to the genital structures (adnexae, vagina, broad ligament). Stage III GTN extends to the lungs, with or without known genital tract involvement. Stage IV All other metastatic sites. Score: The total score for a patient is obtained by adding the individual scores for each prognostic factor. Total scaore 0-6 5 low risk; $7 5 high risk. PROGNOSTIC FACTORS

Age (years)

,40

$40

Previous pregnancy

Mole

Abortion

Term

Months since last pregnancy

4-6

7-12

.12

Pretreatment b-HCG (IU/L)

,1,000

1,000-10,000

10,000-100,000

.100,000

Largest tumour size including uterus (cm)

3-5

Site of metastases

Lung

Spleen/kidney

Brain/liver

Number of metastases

1-4

5-8

1 drug

$2 drugs

Previous failed chemotherapy

INVESTIGATIONS 1. Serum b-HCG levels, FHG, UECs, LFTs, HIV, blood group, GXM. Consider TSH, VDRL. 2. CXR, Ultrasound of abdomen and pelvis. 3. IF CXR of CT Chest positive do CT Brain.

MANAGEMENT The treatment of this malignancy depends on the availability of serum b-HCG assays. The management decisions depend on whether the patient is low risk (0-6) or high risk (7 or greater) acording to the modified WHO/FIGO scoring system. a) Low Risk Patients: Single agent chemotherapy i.e. Methotrexate or Actinomycin D.

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Obstetrical pathology B.3.

b) High risk Patients: 1. Multi-agent chemotherapy: EMA-CO (See under chemotherapy). OR 2. Surgery: Hysterectomy (with the option of concurrent chemotherapy) is indicated when: • Drug resistance to chemotherapy AND disease confined to uterus. • Emergency procedure where there is uncontrollable haemorrhage. • Completed childbearing. • Local resection of easily accessible or chemo-resistant solitary metastases. Follow up after treatment b-HCG weekly until normal for 3 consecutive weeks then monthly for 12 months. Ensure reliable hormonal contraception for one year. Managing placental trophoblastic tumour (PSTT) Epithelioid Trophoblastic Tumour (ETT). 1. Individualise treatment. 2. Surgery is the cornerstone of treatment. 3. Chemo and radiotherapy are occasionally indicated. Points to remember. 1. Do not forget to look for vaginal metastases. 2. DO NOT biopsy any metastases in patients with GTN. 3. Histology is not required for the diagnosis of choriocarcinoma. 4. Single agent prophylactic chemotherapy (1/2 hysterectomy) post-evacuation may be considered in hydatidiform mole, when loss to follow-up is a high possibility. 5. If evidence of resistance to chemotherapy, refer to special considerations below. 6. Women with GTD should use the same lab in the measurement of b-HCG in follow-up. 7. Women should be advised to seek early prenatal care at the time of the next pregnancy for ultrasound evaluation and placental pathology evaluation at time of delivery.

CHEMOTHERAPY PROTOCOLS (Fixed dosing using body surface area of 1.5 is recommended to reduce errors and is indicated in bold and in brackets.) 1. Low risk (FIGO score 0-6) (Single agent chemotherapy). a) Actinomycin D 1.2 mg/m2 (1.5 mg) IV every second week. OR b) Methotrexate 50 mg/m2 (75 mg) IM weekly. • Continue cytotoxics until b-HCG negative and administer at least 2. additional cycles after b-HCG level is negative. • If serum b-HCG level «plateaus» or rises, change to multiple agent chemotherapy. • Note: Chest x-ray signs may take 6 months to return to normal. 2. High-risk (FIGO score .7) (EMA-CO Multiple agent chemotherapy). It consists of 2 parts: a) EMA (Etoposide, Methotrexate & Actinomycin D) is given on days 1 and 2.

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B. Pregnancy

b) CO (Cyclophosphamide, Vincristine) is given on day 8. EMA requires overnight admission, CO does not. • Next EMA-co cycle starts on day 15. • Patients should have bloodwork evaluation prior to the start of each cycle. • Repeat cycles until serum b-HCG level is negative and administer 2 additional cycles. CHEMOTHERAPY

EMA

Day 1

Day 2

Day 15

Day 8

DOSE

Etoposide

100 mg/m2 (150 mg) IV infusion in 200 ml NS over 30 min.

Actinomycin D

0.5 mg IV stat.

Methotrexate

300 mg/m2 (450 mg) in 1l NS over 12 hrs.

Etoposide

100 mg/m2 N (150 mg) IV infusion in 200 ml NS over 30 min.

Actinomycin D

0.5 mg IV stat.

Leucovorin

15 mg IM OR, 15 mg PO BD for 4 doses beginning 24 hours after starting methotrexate.

Cyclophosphamide

600 mg/m2 N (900 mg) IV in NS.

Vincristine

1 mg/m2 (max 2 mg) (1.5 mg) IV stat.

Draw blood for b-HCG level, FHG, EUDs, LFTs. Repeat 8 day cycle of EMA-CO.

Especial considerations: 1. Failure to respond to EMA-CO: Modify regime as follows: a) Omit Actinomucin D and Etoposide on day 2 of EMA. b) Replace CO with Cisplatinum 75 mg/m2 (112.5 mg) IV and Etoposide 120 mg/m2 (180 mg) IV alternating weekly with EMA. Consider alternative chemotherapy in case of ongoing failure. CHEMOTHERAPY

Day 15

Day 8

EMA

Day 1

DOSE

Etoposide

100 mg/m2 (150 mg) IV infusion in 200 ml NS over 30 min.

Actinomycin D

0.5 mg IV stat.

Methotrexate

300 mg/m2 (450 mg) in 1l NS over 12 hrs.

Leucovorin

15 mg IM OR, 15 mg PO BD for 4 doses beginning 24 hours after starting methotrexate.

Cisplatin

75 mg/m2 (112.5 mg) IV.

Etoposide

120 mg/m2 (180 mg) IV in 200 ml NS over 30 min.

Draw blood for b-HCG level, FHG, EUDs, LFTs. Repeat 8 day cycle of EMA-CO.

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Obstetrical pathology B.3.

CNS metastases: Methotrexate is the drug of critical importance. Modify as follows: a) Methotrexate dosage in the EMMA-CO regimen is increased to 1 g/m2 (1.5 g) to reach an effective drug concentration in the CSF. Leucovorin dosage is indreased to 30 mg PO/IM TDS 3 4/7, starting 24 hour after starting methotrexate. Intrathecal methotrexate 12.5 mg is given with each dose of CO (see table below). b) Consider radiotherapy, surgery or alternative chemotherapy if indicated. CHEMOTHERAPY

EMA

Day 1

Day 2

Day 15

COM

Day 8

DOSE

Etoposide

100 mg/m2 (150 mg) IV infusion in 200 ml NS over 30 min.

Actinomycin D

0.5 mg IV stat.

Methotrexate

300 mg/m2 (450 mg) in 1l NS over 12 hrs.

Etoposide

100 mg/m2 N (150 mg) IV infusion in 200 ml NS over 30 min.

Actinomycin D

0.5 mg IV stat.

Leucovorin

15 mg IM OR, 15 mg PO BD for 4 doses beginning 24 hours after starting methotrexate.

Vincristine

1 mg/m2 (max 2 mg) (1.5 mg) IV stat.

Cyclophosphamide

600 mg/m2 N (900 mg) IV in NS.

Intrathecal Methotrexate

12.5 mg IT.

Draw blood for b-HCG level, FHG, EUDs, LFTs. Repeat 8 day cycle of EMA-CO.

Reference. Moi Teaching and Referral Hospital (MRTH). Protocol of Dept. of Reproductive Health. Kenya, 2012.

B.3.7. MULTIPLE PREGNANCIES GENERAL CONCEPTS 1. Only 1 in 80 pregnancies are twins, and the incidence of higher multiples is very much smaller. 2. The artificial induction of ovulation has increared the incidence of high multiple pregnancin. 3. In general, the most important clinical problems are preterm birth and low birth weight. Not only are these problems the greatest contributors to perinatal morbidity and mortality, but their importance is also related to the fact that current management has no effective remedies to avoid them. 4. In terms of prenatal diagnosis, the most important variable is chorionicity because monochorionic (MC) twins are by far more disadvantaged compared

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to dichorionic (DC) sets. In addition, MC twinning is associated with extremely complex situations which definitely deserve the attention of experienced tertiary centers.

DIAGNOSIS 1.

Ideally, all pregnancies should be screened at the first trimester to exclude the presence of multiple pregnancy (MP). 2. Once a MP is found, the first trimester scan is the best means to establish the number of gestational sacs, the number of embryos, and chorionicity. 3. Dichorionic (DC) placentarion is certain if the «twin peak» (Lambda sign) is seen. 4. If a DC placenta is excluded, third level ultrasound is indicated to establish the diagnosis of MC twins and to assess amnionicity (bi-vs. monoamniotic twins). 5. MC twins occur also in triplets or in higher-order sets.

FIRST TRIMESTER COUNSELING 1. The patient should receive information related to the potential risks of her MP, as derived from plurality and chorionicity. 2. Zygosity is certain in unlike-sexed twins (dizygotic) or in MC twins (monozygotic). Zygosity cannot be established in the remaining sets (about 45 %, i.e., in like sexed twins with a DC placenta). 3. Weight gain should be encouraged. Overall, a minimal 14 kg weight gain by 24 weeks was associated with improved outcomes in terms of fetal weight. 4. Each fetus in a MP has a similar risk of chromosomal aberrations as singletons. However, it is believed that the probability of the maternal-age related risk of having at least one affected child is almost doubled in dizygotic twins. 5. If multifetal pregnancy reduction (MFPR) is contemplated, the risks and benefits should be explained and tailored to the maternal phenotype as well as to her wishes. MFPR should be scheduled at 11-13 weeks’ gestation. 6. If invasive cytogenetic studies are not considered, an estimated risk of aneuploidy by nuchal translucency (NT) measurements should be performed. NT is also advisable in all MC twins to assess the risk of early onset twin-twin transfusion syndrome (ITTS). 7. A late first trimester scan can establish the diagnosis of embryonic death («vanishing» twin syndrome). 8. All MC twins should be evaluated to exclude the presence of unique, but rare, MZ-related complications such as monoamnionicity, twin reversed arterial perfusion (TRAP) sequence, and conjoined twins. If found, expert consultation should be offered.

SECOND TRIMESTER FOLLOW UP 1. Standard of care should be at least as extensive as it is for singletons. Thus, routine follow up as performed in singletons should be performed in MP as well. 2. Iron and folate supplementation should be given, as anaemia of pregnancy is likely in MP.

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Early (15-16) anatomical scan should be routine in all MC twins. This is derived from the increased (3 2-3) risk of structural malformations in MZ twins. Since zygosity cannot be established in a significant proportion of MPs, early anatomical scan is advisable in DC sets as well. 4. Selective reduction of a twin with structural malformations in DC sets is performed by intracardiac injection of Potasic clorur (KCI). In MC sets, selective umbilical cord occlusion should be performed. 5. If amniocentesis is indicated, it should be performed after careful «mapping» of the fetuses, without installation of dye, and with careful designation of the sampled gestational sac. 6. Growth assessment should be performed at a 2-4 weeks intervals in order diagnose early discordant growth. Cases with severe 2nd trimester growth discordance should be referred to experienced centers.

SECOND TRIMESTER MANAGEMENT OF MC TWINS 1. Since TTTS may occur anytime during the 2nd trimester, one should look for the first (simple) sing of Twin Oligopolyhydramnios Sequence (TOPS). 2. Early growth discordance can be seen by comparing crown-rump lengths. 3. Both TOPS and early discordance should be defined as complicated MC twinning, and these cases should be referred to experienced centers. 4. Severe early growth discordance in MC twins increases the risk of fetal death and subsequent damage to the survivor. Doppler studies of umbilical artery blood flow should be performed to assess this risk. Such cases should be referred to experienced centers, and in cases with impending single fetal demise, preventive umbilical cord occlusion should be considered.

MANAGEMENT OF SINGLE FETAL DEATH 1. The risk of maternal DIC is extremely rare. There is no need to test the mother’s coagulation system. 2. Single fetal death in DC twins has no consequence to the survivor and no intervention is required. 3. Single fetal death in MC twins may cause death of the co-twin and if not, there is a 30 % risk of end-organ damage. Careful targeted sonography (in particular of the brain and kidneys) should be performed. 4. Most authorities hold that immediate (preterm) delivery is not indicated if single demise is seen in MC twins.

PREVENTION OF PRETERM BIRTH 1. 2.

There are no proven prophylactic measures that reduce preterm birth in MP. Some authorities suggest that early weight gain, sedentary life style, and progestatives, may increase gestational age. There is no indication for prophylactic cerclage as well as for prophylactic hospitalization. 3. Biweekly measurement of cervical length (24 to 32 weeks) is advisable in order to screen for silent impending preterm birth. 4. No tocolytic agent is superior in MP. However, the side effect profile of several agents (i.e., betamimetics) is increased among MP. 5. The current standard is to administer corticosterioids as in singletons,

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although data indicate that the dose might be insufficient to significantly reduce the risk or respiratory distress syndrome. 6. Management of preterm rupture of membranes in MP is not different from that in singletons.

THIRD TRIMESTER FOLLOW UP 1. Growth assessment should be performed bi-weekly as growth aberrations usually begin around 28 weeks. 2. Severe (.25 %) discordance in estimated fetal weight should be assessed with Doppler studies to exclude genuine growth restriction 3. Most of the morbidity and mortality related to severe growth discordance is seen in the smaller twin, but mainly if this twin is also small-for-gestational age (SGA). Differentiation between relative (discordant) and genuine growth restriction should be done by using MP-specific growth charts. 4. Severe discordance has no significant implication if the smaller twin is not SGA. 5. Signs of maternal hypertensive disorders should be looked for. This is because pre-eclampsia is more frequent, occurs earlier, and manifest in a more severe form. 6. Prophylactic preterm birth for uncomplicated MC twins is not indicated.

PERIPARTUM CONSIDERATIONS 1. 2.

5. 6. 7.

Most twins and certainly all higher-order multiples will be born before 38 weeks. However, some mother will continue their pregnancy beyond 37 weeks. There is much circumstantial evidence that «term» occurs earlier in twins –at 38 weeks. Consequently, twin gestations carried beyond this date should be managed as post-term pregnancies. Vaginal delivery is probably safe in the vertex-vertex combination, and is also permissible in vertex-nonvertex sets. However, many cases, in particularly those considered as «premium» pregnancies, those with small fetuses, those following a complicated gestational course, and where manual dexterity is not available, should be offered an elective caesarean section. Because of the a priori increased risk to twin B, combined vaginal and caesarean births should not be an option when counselling patients about the mode of delivery. Labor induction and augmentation appears to be safe when vaginal births is desirable. It is imperative that fetal heart rate monitoring should be performed during labor. Care should be given to trace each twin separately. Labor and delivery of twins should be carried out in a facility with an operating theatre and blood banking. Anesthesia and bedside ultrasound may help in complex deliveries. The presence of a neonatolgist is mandatory. The placenta should be examined postpartum to establish chorionicity and amnionicity. This should be recorded in the patient’s chart.

Reference. Blickstein L: Multiple pregnancies. In: Recommendations and Guidelines for Perinatal Medicine. Matres Mundi/ WAPM. Barcelona, 2007; 13: 115-133.

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B.3.8. CERVICAL INCOMPETENCE CONCEPT Cervical incompetence or insufficiency, as the loss of structural o functional integrity in the sphincter mechanism of the internal cervical so, resulting in the effacement and dilatation of the uterine cervix and the subsequent interruption of the gestation at between 14 and 28 weeks without uterine contractions.

CLASSIFICATION There are 4 types: 1. Congenital cervical incompetence. Include cervical incompetence thought to be related to «in utero» exposure to chemical product, as a diethylstilbrestrol (DES). 2. Acquired cervical incompetence, secondary to sphincter trauma: a) Obstetric trauma (cervical lacerations). b) Forced dilatation of the cervix during an abortion. c) Cervical surgery. 3. Dysfunctional cervix by: a) Hyper-relaxinemia. b) Family history of elastin deficiency. 4. Anatomical cervical incompetence due to malformations (such as a double or bicornuate uterus, etc.).

PREGESTATIONAL DIAGNOSIS 1.

Suspected diagnosis by: a) Two o more spontaneous abortions in the second trimester showing the characteristics typically associated with this condition: rapid, with protrusion of the amniotic sac and the expulsion of a living fetus. Confirmation of diagnosis. a) Excessive permeability of the internal cervix os confirmed by the easy passage of either a number 6 Hegar dilator (15-19 in the case of Pratt dilators) or a number 16 Foley catheter (6 mm diameter with 1 ml of water). b) Hysterography, performed in the second stage of the cycle (if possible with progesterone treatment) and using a cervical suction cannula. An internal cervical os greater than 6 mm and the morphology typical of the cervical canal (finger-shaped) usually confirm the existence of cervical incompetence. c) Transvaginal ultrasound examination of the cervix showing that the width of the internal cervical os is greater than 10 mm.

GESTATIONAL DIAGNOSIS During pregnancy the cervical incompetence should be suspected when, regardless of the patient´s history, clinical examination reveals:

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1. Short and/or dilated cervix (prior to 28 weeks). 2. Visualization of membranes, with or without protrusion of the amniochorionic sac. This findings is practically pathognomonic. Diagnostic confirmation during pregnancy may be attemted by means ultrasound (isthmic saculation, isthmic-cervical saculation, cervical opening . Currently a diagnostic of cervical incompetence is considered appropiate when the internal cervical os has a diameter of 23-25 mm or more, it being ruled out with lesser diameter.

TREATMENT See protocol (B-2-9).

Reference. Carrera JM: Cervical incompetence and its treatment. In: Controversies in Perinatal Medicine. Edit by Carrera JM, Chervenak FA and Kurjak A. Parthenon Publishing. New York, 2003; 14: 267-278.

B.3.9. PREMATURE RUPTURE OF MEMBRANES CONCEPT Premature Rupture of Membranes (PROM) consists in the rupture of fetal membranas before the onset of labor. If PROM occurs before term (37 weeks of gestation) then is called Pre-Term PROM and if occurs at term Term-PROM.

DIAGNOSIS 1.

The diagnosis is obvious in more than 90 % of cases by the clinical symptoms (leakage of transparent and inodorous liquid). 2. Observation of the watery liquid in the sterile speculum introduced in the vagina. 3. A sterile swab of fluid should be obtained from the posterior fornix of the vagina and placed on a clean glass slide, and on a piece of nitrazine paper. If the pH is higher the 6.5 it is quite probable that the liquid was AF as its pH level usually is higher than 7, and the vaginal pH without AF is lower than 5 except in cases of presence of urine, semen, bacterial vaginosis or Trichomonas infections, or in cases with plenty of blood. 4. With the observation of the glass slide at the microscope at low magnification after waiting 10 minutes, in case of AF (PROM) it is possible to see images of arborisation («ferning»). 5. Also the observation by ultrasound (US) of oligohydramnios not existing previously, accompanied by the antecedent of leakage of liquid is very suggestive of PROM.

MANAGEMENT The management of PROM is clearly depending of the gestational age, as are the main risks: prematurity, infection, fetal distress, and fetal lung hypoplasia. Due to these reasons it is very important to be sure about the following:

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In all cases. a) In any moment if signs of Chorioamnionitis (CA) proceed to deliver. b) At admission: • Confirmation of PROM. • To exclude CA signs. • Confirmation of gestational age (better by US before 20 weeks). • To perform blood analysis (Hemograma, PCR, and coagulation). • To take samples for vagina/rectum exclusion of carrying S. agalactiae, to cervical culture and Gram stain of vaginal extension. c) To programme: • Periodic blood analysis. • Periodic NST. • Weekly US. d) To avoid digital vaginal exploration. According to gestational age. a) ,24 weeks: • Patient counselling to decide expectant management or induction. • In both cases antibiotic treatment. b) 24-31 weeks: • Expectant management (level A of recommendation). • Antibiotic treatment (level A of recommendation). • Corticosteroid therapy (level A of recommendation). • Tocolytic therapy if uterine contractions (no agreement). c) 32-34 weeks: • Expectant management unless fetal lung maturity. • Antibiotic treatment (level A of recommendation). • Corticosteroid therapy if no documented lung maturity (level B of recommendation). • Tocolytic therapy if uterine contractions (no agreement). d) 34-36 weeks: • Antibiotic treatment (level A of recommendation if S. agalactiae carrier or not documented, level B in other cases). • Induce the labour if documented lung maturity. • Not to use tocolytic therapy if uterine contractions. e) .37 weeks of gestation: • Antibiotic treatment (level A of recommendation if S. agalactiae carrier or not documented, level B in other cases). • Proceed to inducing labour (level A of recommendation) within the 6 hours of admission unless labour was spontaneously started: −− With perfusion of Oxitocine if Bishop Index .6. −− With local prostaglandin if Bishop Index ,6.

Reference. Cararach V, Palacios M, Botet F: Premature rupture of the membranes. In: Recommendations and Guidelines for Perinatal Medicine, Matres Mundi/WAPM. Barcelona, 2007; 18: 170-176.

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B.3.10. PRETERM LABOR (PTL) CONCEPT AND DEFINITIONS World Health Organization (WHO) defined «preterm born» as the outcome of a pregnancy under 37 weeks, considering gestational age from the very last menstruation date to birth.

CLINICAL DIAGNOSIS Preterm labor (PTL) is defined as six to eight contractions per hour, or four in 20 minutes, that are associated with cervical change at less than 37 weeks’ gestation. PTL also may be defined as cervical effacement greater than 80 %, or dilation over 2 cm, at less than 37 weeks’ gestation.

EVALUATION The evaluation of suspected PTL should include a thorough history, physical examination, laboratory studies, ultrasound, and evaluation of the continuous fetal heart rate tracing. 1. The history should elicit previous occurrences of preterm labor, preterm delivery, or both; infections during the present pregnancy or symptoms of current infection, including urinary infection. 2. The physical examination should focus on vital signs (fever, maternal tachycardia, and fetal tachycardia), any potential source of infection, uterine tenderness, and contractions. a) Sterile speculum examination should include Nitrazine and fern test to rule out membrane rupture and procurement of specimens for cervical cultures. b) If no evidence of membrane rupture is found, proceed with a bimanual examination. Repeat the examination at appropriate intervals to determine whether cervical change has occurred. If rupture has occurred, initiate treatment for PROM. I.

MANAGEMENT 1. Intravenous hydration with 500 mL of isotonic crystalloid solution is a common initial approach to treatment, although hydration is not a proven benefit for patients who are not dehydrated. Maintenance fluid should be Ringer’s lactated solution or 0.9 N saline, with or without dextrose to minimize the risk of pulmonary edema. 2. Patients should remain on strict bed rest, initially with continuous fetal monitoring. 3. Antibiotic therapy should be initiated for prophylaxis against GBS infection until all cervical and urine cultures return negative findings. Penicillin or ampicillin is recommended unless the patient is allergic to penicillin, in which case clindamycin is recommended. All specific infections implicated by positive culture findings should be treated appropriately. 4. Corticosteroids (12 mg i.m. of betamethasone, with a repeat dose in 24 hours) should be administered to induce fetal lung maturity between 24 and 34 weeks’ gestation if no obvious signs of infection are present. Opti-

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II.

mal benefit is achieved 24 hours after the second dose and last for 7 days. Prophylactic penicillin should be administered until negative results of cervical and urine cultures are returned (if positive findings appear, the specific infection should be treated). Penicillin should be administered during labor for patients with gestations of less than 37 weeks or with a history of a positive finding for GBS on cervical or urine culture.

TOCOLYTIC THERAPY In assessing whether a patient is a candidate for tocolysis, gestational age should be confirmed and fetal anomalies ruled out. 1. General contraindications to tocolysis for PTL include acute fetal distress, chorioamnionitis, eclampsia or severe preeclampsia, fetal demise (singleton), fetal maturity, and maternal hemodynamic instability. 2. Goals of tocolysis are similar regardless of which agent is chosen, and include decreasing uterine contractions and arresting cervical dilatation using the lowest effective dose, decreasing or stopping the drug if significant side effects develop, and stopping the drug or switching to an oral agent after intravenous or subcutaneous therapy has produced sustained clinical improvement for 12 to 48 hours. 3. Betamimetic drugs. Ritodrine and terbutaline are the most common drugs used for prevention of preterm delivery. Ritodrine is administrated intravenously, in continuous perfusion, starting with 50 ug/min, and increasing 50 ug/min every 15 minutes until uterine contractions stop. Maximum dose recommended is 360 ug/min or when mother heart rate exceeds 120 bytes per minute. As betamimemetic drugs are powerful agents with adverse effects that are related to the dose administered, this would seem to be undesirable. It has, therefore, been proposed to lower the infusion rate as soon as uterine inhibition is achieved to a level that is sufficient to maintain uterine inhibition. Terbutaline can be administrated orally (2.5 mg/4-6 h), subcutaneously (0.25 mg/20 min) or intravenously. a) Relative contraindications include antepartum hemorrhage, vascular disease, hyperthyroidism, and uncontrolled diabetes (even patients with well-controlled diabetes may require a concomitant insulin drip). b) Maternal side effects consist of tachycardia, tremor, palpitations, axiety, shortness of breath, pulmonary edema, substernal pain, and mild hyperglycemia. c) Fetal side effects include tachycardia (variability should be maintained) and hyperglycemia. d) Due to the fact that in pregnancy there is a fluids plethora, the joint administration of the betamimetic drugs and corticoids, can unchain a acute pulmonary edema with risk of the motherâ&#x20AC;&#x2122;s death. Therefore, it is necessary not to associate them and, in any case, make an estrict liquids balance and a continued survillance of the first symptoms of pulmonary edema. 4. Nifedipine blocks contraction of smooth muscle by inhibiting intracellular calcium entry. The recommended dose is 10 to 20 mg every 6 hours p.o. Nifedipine has been administered in a loading dose of 10 mg sublingually every 20 minutes up to three doses. a) Contraindications include congestive heart failure, aortic stenosis, and

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concomitant use of magnesium sulphate, which can precipitate severe hypotension. b) Side effects consist of hypotension, flushing, nasal congestion, tachycardia, dizziness, nausea, nervousness, bowel changes, and, in one case report, skeletal muscle blockade. Indomethacin interferes with the synthesis of prostaglandins. The usual course begins with a loading dose of 100 mg p.r., and therapeutic levels are maintained with doses of 25 mg p.o. or 50 mg p.r. every 4 to 6 hour for a maximum of 48 hours. a) Because indomethacin affects fetal kidneys, amniotic fluid volume may decrease. An AFI should be established before beginning therapy and should be checked after 48 hours. The effect of indomethacin on the fetal kidney is reversible. b) Contraindications include peptic ulcer disease, estimated gestational age of greater than 32 weeks, renal disease, coagulopathy, and oligohydramnios. c) Headache, dizziness, gastrointestinal discomfort, fluid retention, nausea and vomiting, and pruritus are the primary maternal side effects. d) Oligohydramnios and potential ductal closure are the two most worrisome fetal side effects.

References. Morrill K, Hanna G: Preterm labor. In: The Johns Hopkins Manual of Gynecology and Obstetrics. Lippincott Williams and Wilkins. Edit by Lambroo NC, Morse AN, Wallads EE. Baltimore, 1999. | Ministry of Health of Rwanda: Preterm labor. In: Gynecology and Obstetrics. Clinical Protocols and Treatment Guidelines. Kigali, 2012: 87-90.

B.3.11. INTRAAMNIOTIC INFECTION (IAI) CONCEPT 1.

It refers to infection of amniotic cavity, which can affect only membranes and fluid or extend to the mother and/or the fetus. 2. Differential diagnosis includes: a) Intraamniotic infection: Presence of microbes in amniotic fluid, with or without clinical signs. b) Chorioamnionitis: Clinical syndrome associated to intraamniotic infection. The key clinical findings are fever, uterine tenderness, maternal tachycardia (.100/min), fetal tachycardia (.160/min) and leucorrea. c) Hystological chorioamnionitis: infiltration of the chorioamnion and umbilical cord by polimorfonuclear leukocites (20 % of pregnancies). It often doesn’t produce maternal or fetal effects. 3. Incidence: 0.5-2 % of the deliveries. In preterm deliveries it rises to 30 %. It can also be found related to 30-40 % of premature ruptures of membranes.

PATHOGENESIS 1.

Intraamniotic infection (IAI) has different gateways: a) Migration of cervicovaginal flora through the cervical canal to infect the

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fetal membranes, placenta, amniotic fluid and fetus. Rupture of membranes facilitates this process. The activity of bacterial enzymes in the amniotic fluid may increase the synthesis of prostaglandins, which leads to contractions and cervical dilatation, increase of the intramniotic pressure and higher risk of preterm rupture of membranes (PROM) and preterm labor. b) Hematogenous spread: due to maternal bacteriemia (Listeria monocitogenes, group A Streptococcus, Campylobacter, etc.). c) Uncommonly, the amniotic fluid/placenta is inoculated with bacteria during an invasive procedure (eg, amniocentesis —1/1,000—, chorionic villus sampling, fetal surgery, etc.). The fetal consequences differ according to the gateway of infection: a) If it is ascending, it contaminates the amniotic fluid, being able to cause a congenital pneumonia and a preterm delivery. b) If it is hematogenous, it contaminates the intervellosum space, leading to a fetal/maternal hematogenous infection which can cause a widespread infection.

RISK FACTORS Several obstetric factors have been associated with intraamniotic infection (IAI): 1. Prolonged labor, specially if preceeded by an insidious pre-labor. The contractive activity may contribute to the infection progression through the decidua. 2. Prolonged membrane rupture. Specially when the latency until the beginning of labor lasts more than 48 hours. 3. Internal fetal or uterine monitoring. 4. Multiple vaginal examinations (especially with ruptured membranes and low level of asepsia). 5. Host-related factors: very young age, nulliparity, malnutrition, chronic diseases, history of prematurity, presence of genital tract pathogens (eg, sexually transmitted infections, group B streptococcus [GBS], bacterial vaginosis).

ETIOLOGY a) Polymicrobial: In 80 % of the cases both aerobes and anaerobes are found. b) Genital mycoplasmas (Ureaplasma and mycoplasma species) are the most common. Anaerobes (including Gardnerella vaginalis), enteric gram-negative bacilli and group B streptococcus (GBS) are other frequent pathogens.

CLINICAL DIAGNOSIS a) According to the clinical criteria: 1. Maternal: The essential criterion for clinical diagnosis of intraamniotic infection (IAI) is maternal fever (85-100 %), which is a manifestation of systemic inflammation; Maternal tachycardia (greater than 100 beats/ minute) (20-80 %); Maternal leukocytosis (greater than 15,000 cells/mm3); Uterine tenderness. 2. Fetal: Fetal tachycardia (greater than 160 beats/minute) (30-80 %); absence of respiratory movements; decrease of variability. 3. Amniotic Fluid criterion: Foul odour of the amniotic fluid (5-25 %), detection of organisms in gram stain or culture, glucose .10 mg/dl, .50 leukocytes/field.

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b) Special considerations: 1. The clinical signs may be absent at the beginning, especially in those cases with intact membranes. 2. The negativity of the amniotic fluid culture doesn’t exclude the infection, due to the bactericide capacity of the amniotic fluid. 3. The amniotic fluid samples must be obtained through aseptic techniques, avoiding cervical and vaginal flora and skin flora. Intrauterine pressure catheters or sterile amniocentesis must be used. 4. Amniocentesis may be a complicated technique in those cases with rupture of membranes. 5. In front of a threat of preterm labor or persistency of uterine contractions despite tocolysis, the suspicion of a chorioamnionitis must be con sidered.

PREVENTIVE MEASURES 1. Avoid traumatic and multiple digital vaginal examinations at the end of the pregnancy. 2. Induce labor as soon as possible after a preterm rupture of membranes according to the fetal maturity. In term pregnancies the induction must be started before 12 hours. 3. If the labor has to be delayed due to fetal immaturity, extreme hygienic measures must be taken, specially after micturition and defecation. 4. Avoid prolonged labor. 5. Early detection and treatment of the genitourinary tract infections. 6. Early detection of premature rupture of membranes and threats of preterm labor.

TREATMENT Pregnancy must be finalized. The route of delivery will depend on the urgency of the situation and the obstetric conditions. If the estimated time to delivery is shorter than 6 hours, and there are no signs of fetal/maternal compromise, vaginal delivery can be attempted, always under adequate antibiotic therapy. Cesarean must be done in the rest of cases. Antibiotic treatment. Antibiotics are administered to control intrauterine infection, but intraamniotic infection (IAI) can only be considered cured once the in fected products of conception have been delivered. Ideally, it has to be a lapse of 2 hours between the administration and the delivery of the foetus, to reach therapeutical levels at the moment of the delivery. a) The antibiotic regimen options, in case of unknown miroorganism are: Ampicilin load 2 g (intravenously) and, followed by 1 g every 4 hours 1 1 Gentamicin 80 mg every 8 hours. b) In severe cases: Piperacilin-tazobactam 2-4 g every 4-6 hours (intravenously). c) Alternative antibiotic regimens for allergic patients: 1. Eritromicin 500 mg every 6 hours (intravenously). 2. Clindamicin 900 mg every 8 hours (intravenously).

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The treatment should be adapted according to the microbiological results. After the delivery, the treatment has to be continued at least for 24 hours after the relapse of signs or symptoms.

Reference. Serra B, Mallafré. J: Protocols de Obstetricia y Medicina Perinatal del Instituto Universitario Dexeus. Masson. Barcelona, 2014: 180 -182.

B.3.12. ANTEPARTUM HAEMORRHAGE (APH) CONCEPT Ante partum haemorrhage (APH) is any vaginal bleeding from 28 weeks gestation.

INCIDENCE APH occurs in 2 % to 5 % of all pregnancies. The primary causes of APH include: 1. Abruptio placenta 40 %. 2. Placenta previa 20 %. 3. Unclassified 35 %. 4. Lower genital tract lesion 5 %. I.

ABRUPTIO PLACENTA a) Definition. Abruptio placenta: premature separation of the placenta. Bleeding into the deciduas basalis leads to placental separation, and may compromise fetal blood supply. b) Incidence. Placenta abruptio occurs in 1 % to 2 % of all pregnancies. c) Predisposing factors. Most abruptions are idiopathic, other most common factors: 1. Maternal hypertension. 2. Prior abruption. 3. Abdominal trauma. 4. Rapid uterine decompression (i.e. premature rupture of membranes (PROM), ROM in polyhydramnios or after delivery of the first twin). d) Diagnosis (see pag. 92). e) Treatment: The management of placenta abruption depends on the severity of the abruption and on fetal well being: 1. Women with small abruption who are stable and have premature fetus in a good condition should be treated conservatively. 2. If premature delivery is expected, the fetus should be treated by administration of steroid, to enhance fetal lung maturity. 3. Vaginal delivery is appropriate when an active rapid labor progress and satisfactory fetal heart monitoring exist. 4. Low segment cesarean section is required for obstetric indications, e.g. transverse lie, etc., fetal distress, failure of labor progression o when hemorrahge is uncontrollable.

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5. Most of women with placental abruption and dead fetus will develop coagulopathy in contrast to women with live fetus. After fetus delivery fresh frozen plasma and platelet transfusion should be administrated. II.

PLACENTA PREVIA a) Definition. Placenta previa: implantation of the placenta in the lower segment of the uterus so that it comes close to/completely covers the internal cervical os. b) Incidence. Incidence of placenta previa is 0.3 % to 0.4 % of all term pregnancies. c) Predisposing factors. 1. Previous Cesarean delivery or uterine surgery. 2. Multiparity and/ or advanced maternal age. 3. Prior placenta previa. d) Classification. 1. Marginal placenta previa → edge lies , 2 cm from the os. 2. Partial placenta previa → internal os is partially covered. 3. Total placenta previa → covers os. Not pictured: (low lying → 2-3.5 cm).

Wherever possible, diagnosis of placenta previa is made by ultrasound. e) Clinical differences between abruptio placenta and placenta previa. CLINICAL SIGNS ABRUPTIO

CLINICAL SIGNS PREVIA

Associated with hypertensive disorders/uterine overdistension/abdominal trauma.

Associated with previous uterine surgery.

Presenting part may not be engaged. Normal presentation/stable lie.

Head or presenting part is high, or the lie is unstable.

Abdominal pain and/or backache.

Painless (unless in labour contractions).

Uterine tenderness/increased tone/ irritability (or contractions).

Uterus not tender/soft/no uterine irritability.

Fetal heart abnormal/absent.

Fetal heart usually normal.

Shock and anaemia seems out of proportion to apparent blood loss, may be concealed.

Shock and anaemia correspond to apparent blood loss.

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CLINICAL SIGNS ABRUPTIO

CLINICAL SIGNS PREVIA

Coagulopathy. Abruptio may be seen on US, but a negative ultrasound does not rule out.

US is the definitive diagnostic test for placenta previa.

e) Treatment: 1. Maternal hospital admission must be individualized according to symptomatic placenta previa, gestational age, number and severity of bleeding episodes and other factors, such as patient reliability and distance from the hospital. 2. Tocolytic therapy is only indicated when the fetal prematurity is significant, but the pregnant should be hospitalized in a tertiary care unit. 3. Vaginal delivery is not indicated because of the risk of massive hemorrhage, dystocia and premature placental separation. 4. Indications for operative delivery with available blood is recommended when life threatening bleeding occurs o when bleeding persist or when the fetus is distressed. III. PLACENTA ACCRETA a) Definition. Placenta accreta is the abnormal adherence of the placenta with villus attachment to the myometrium. Placenta accreta can progress into placenta percreta → vascular processes of the chorion may invade the full thickness of the myometrium (may grow through the myometrium and the outside covering of the uterus —serosa— can lead to complete rupture of the uterus). b) Incidence. 0.2 % of all deliveries → 78 % accreta, 17 % increta, 5 % percreta. With a placenta previa in place, risk rises with each Cesarean delivery NUMBER OF CESAREAN DELIVERIES

RISK OF PLACENTA ACCRETA

Normal (Decidua) Stratum basalis of endometrium

Increta (17 %)

Myometrium Accreta (75-78 %)

Percreta (5 %)

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c) Clinical management: 1. It is ideal to diagnose placenta accreta during the antenatal period. Strong clinical suspicion is required in the presence of risk factors. 2. In most cases, the placenta accreta will be encountered unexpectedly. 3. If the placenta cannot be delivered at the time of cesarean section or following vaginal delivery, one management option is to leave the placenta in situ, without further attempts at delivery if the woman is not actively bleeding. Important considerations related to placenta accreta: 1. The incidence of placenta accreta has increased significantly, due to increased cesarean section surgery rates. 2. Accreta should be suspected in the case of placenta previa, especially if there is a history of prior uterine surgery. d) Treatment: 1. It has been established that once the clinical diagnosis of placenta accreta is made, the best results are obtained when a hysterectomy is performed. 2. The mortality rate in patients treated conservatively is four times a great. IV. VASA PREVIA a) Definition. Vasa previa is when fetal blood vessels in the membranes run across the cervix in front of the presenting part. b) Incidence. Vasa previa occurs 1 in 5,000 pregnancies. Higher in twin preg nancy’s. c) Morbidity and mortality. Fetal mortality is estimated to be as high as 50 % to 70 %. d) Diagnosis. 1. Prenatal diagnosis is unlikely, but may be made by observing fetal vessels crossing the internal os on transvaginal sonography. 2. The clinical diagnosis should be considered when rupture of the membranes is associated with acute painless vaginal bleeding and an abrupt change in the fetal heart rate. e) Clinical management. When vasa previa is suspected, the baby needs to be delivered very quickly and is likely to be compromised. Emergent cesarean section should be performed when the fetus is alive. V.

GENERAL MEASURES IN APH a) Unstable woman. 1. Administer oxygen to all women who are hypotensive (oxygen consumption is increased 20 % in pregnancy and the fetus is sensitive to hypoxia). 2. Monitor maternal oxygen saturation, where possible. 3. Active fluid resuscitation and/or blood transfusion using two large bore (16-gauge) intravenous lines. Rapidly infuse intravenous fluids. –– Aim to replace 2–3 times the estimated fluid loss. 4. Ongoing assessment of maternal vital signs, including urine output. 5. A cesarean section is required unless vaginal delivery is imminent. If the cervix is dilated, operative vaginal delivery may be an option in cases of placenta abruption/marginal placenta previa. Disseminated intravascular coagulopathy (DIC) should be considered. The «bedside clot test» may be helpful.

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b) Stable woman. 1. Continue maternal and fetal surveillance for 12 to 24 hours. 2. All women with an APH are at risk for recurrent bleeding. References. Moi Teaching and Referral Hospital (MRTH). Protocols of Dept. Of Reproductive Health. Kenya, 2012. | Ministry of Health of Rwanda: Bleeding in Late Pregnancy. In: Gynecology and Obstetrics. Clinical Protocols and Treatment Guidelines. Kigali, 2012: 17-24.

B.3.13. INTRAUTERINE GROWTH RESTRICTION CONCEPT a) Intrauterine growth restriction (IUGR) is defined as any process capable of blocking (during the intrauterine stage) the intrinsic potential growth of the fetus, becoming a heterogeneous entity with multiple etiologies. b) A newborn is considered as Small for Gestational Age (SGA) when its weight is below the 10th percentile for its gestational age.

ETIOPATHOLOGY AND CLASSIFICATION The restricted intrauterine growth can be genetically conditioned or be a consequence of a noxa attacking the mother, the fetus or the placenta. According to the specific stage when the noxa attacks we might be facing: a) IUGR type I, symmetric or on an early stage. There is a proportional decrease of the abdominal and cephalic circumference. b) IUGR type II, asymmetric or late. It is distinguished by a greater reduction of the abdominal and cephalic circumference. The noxa tends to have a late effect. The most common cause is the utero-placental insufficiency. c) IUGR type III or mixed. Caused by a mixed mechanism that attacks in a relatively early gestation stage and tend to be secondary to infectious or toxic embryopahties.

DIAGNOSIS a) Identification of the patient at risk. There should a be closer monitoring of the fetal growth and well-being in patients with an increased risk of IUGR. 1. Low weight increase during pregnancy. 2. Background of IUGR. 3. Toxic habits (snuff, alcohol, drugs). 4. Maternal Associated disease: hypertension, antiphospholipid syndrome, lupus, diabetes, kidney disease, cardiovascular disease, etc. 5. Obstetrical pathology: preeclampsia, multiple gestation, etc. 6. Extremes of age (adolescents or older women). 7. Low socioeconomic status. b) Clinical suspicion: fundal height. For its simplicity and relative effectiveness, it remains as a useful procedure to detect cases of IUGR.

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c) Ultrasound diagnosis. 1. Confirm gestational age. The correct assignment of the gestational age should be made during the first ultrasound scan. Preferably, it will be held by measuring the crown-rump length (CRL) before week 12 by transvaginal probe, with an error of 64 days. In the second quarter, gestational age is obtained from the biparietal diameter and femur length with an accuracy of 614 days. 2. Fetal biometric study. It includes measuring the CRL, in the first quarter, and the biparietal diameter (BPD), cephalic circumference (CC), abdominal circumference (AC) and femur length (LF) in the second and third quarters. The presence of IUGR is suspected, when there is a biometry less than the 10th percentile. The biometrics that best reflects the fetal growth is the abdominal circumference. 3. Fetal growth is a dynamic concept; therefore, to assess growth it is recommended to use ultrasound examinations at minimum intervals of 2 weeks in order to assess the evolution of the measured parameters. 4. After viability, than each Center needs to be decided (in weeks and estimated fetal weight) is necessary to monitoring not only the fetal growth but the possible hypoxia (monitoring FHR register, and study Doppler of the fetal adaptation to hypoxia by ratio between resistance of cerebral artery and resistance fo umbilical artery). d) Diagnosis of fetal condition: 1. IUGR Type I. • Ultrasound study. −− Suggestive structural chromosomal abnormalities. −− Signs of nonspecific fetal infection. −− Limb and facies abnormalities, in order to discard genetic syndromes. −− Echocardiography. • Invasive techniques. −− Amniocentesis: karyotyping, isolation of the pathogen agent by PCR or culture. −− Cordocentesis: karyotype, serology, biological profile (blood count, hepatic function), in exceptional cases. 2. IUGR Type II. • Nonstress test (NST). There is a good correlation between computer analysis of NST and blood gas status. The decreased variability in the short term is the variable that best correlates with acidosis and severe hypoxia. The decrease of short term variability appears only days or hours before fetal decompensation. • Functional biophysical profile. Includes sonographic evaluation of fetal movements, fetal tone, breathing movements and amniotic fluid, and fetal heart monitoring (NST). • Although the two previous explorations are useful for detecting the imminent fetal death, the biophysical profile than the FHR monitoring alone, is even clearly better because let us to follow the fetal adaptation to a hypoxia, the use of the ratio between the middle cerebral artery resistance and the umbilical artery resistance.

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OBSTETRIC BEHAVIOR a) General measures. 1. Remove the hypothesized cause: stress, work, drugs, etc. 2. Maintain a proper diet. 3. Relative rest at home. 4. Between 24 and 34 weeks: lung maturation with corticosteroids to reduce the risk of respiratory distress in the event of requiring the termination of the pregnancy. b) Termination of pregnancy. Although it is the best therapeutic measure, in cases of prematurity risks are to be assessed. A rigid protocol on the completion of pregnancy can not be established. References. Serra B, Mallafré J: Protocolos de Obstetricia y Medicina Perinatal del Instituto Universitario Dexeus. 5th Edition, Elsevier. Barcelona, 2014: 143-147.

B.3.14. CONGENITAL DEFECTS:

BEHAVIOR DURING PREGNANCY

GENERAL CONCEPTS a) Currently, 80 % of congenital defects with some anatomical expression, can be diagnosed during pregnancy. b) Almost all chromosomal abnormalities can be detected by amniocentesis early in high risk pregnancies. c) Parents should be informed not only about the current possibilities of early diagnosis, but also on the possible existence of fetal birth defect. d) The behaviour to follow depends on: 1. The importance of the defect found (if it is compatible or not with life, if there is a mental outlook, etc.). 2. Period of gestation when the diagnosis is being done. 3. Possibility of neonatal treatment. 4. Possibility of intrauterine treatment. 5. Ethical, legal, religious and social circumstances.

MANAGEMENT After reviewing the current diagnostic and therapeutic possibilities, there have been identified five types of defects, implying five different reactions: a) Defects susceptible to selective abortion (anencephaly, renal agenesis). b) Defects requiring preterm induction (progressive defects). c) Defects requiring elective caesarean (Siamese fetuses, etc.). d) Defects requiring immediate surgical correction after childbirth. e) Defects susceptible to intrauterine treatment.

Reference. Carrera JM: Protocolos de Obstetricia y Medicina Perinatal del Instituto Universitario Dexeus. 4th Edition, Elsevier. Barcelona, 2006: 140-146.

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B.3.15. RH ISOIMMUNIZATION DEFINITION / BACKGROUND 1.

Rhesus blood group system is most important blood group system after ABO. Rh blood group system consist of 50 defined blood group antigens among which the 5 antigens D,C,c,E and e are most important. 2. The major antigen in this group is D or Rh factor. «Rh positive» denotes the presence of the D antigen and ‘Rh negative’ denotes the absence of D antigen. 3. A woman who is lacking the Rh factor may carry an Rh positive fetus. 4. In Rh negative mothers carrying an Rh positive fetus who do not receive AntiD, the overall risk of isoimmunization is about 16 % (1.5-2 % antepartum, 7 % within 6 months of delivery and 7 % early in second pregnancy). 5. In Rh negative mothers carrying an Rh positive fetus who do receive Anti-D, the risk of isoimmunization is reduced to 0.2 %.

CONCERNS / RISKS a) General considerations: 1. Isoimmunization usually occurs as a result of fetomaternal haemorrhage (FMH) in a rhesus D (RhD)-negative woman with an RhD-positive fetus but may also occur following incompatible blood transfusion. Fetomaternal hemorrhage most often occurs during pregnancy and at time of delivery. 2. Anti-D Ig (Rh-IgG) does not protect against the development of other antibodies which can cause haemolytic disease of the newborn. 3. With no apparent predisposing factors, fetal red cells have been detected in maternal blood in: • 6.7 % of women during first trimester. • 15.9 % during the second trimester. • 28.9 % during third trimester. 4. As little as 0.1 mL of Rh positive cells can cause sensitization. Importantly, about 30 % of Rh negative persons never become sensitized when given Rh positive blood. b) Risks of fetal maternal hemorrhage (sensitizing events) include: 1. Amniocentesis. 2. Chorionic villus sampling. 3. Abdominal trauma. 4. Manual removal of placenta. 5. Cesarean section. 6. Placenta previa. 7. Abruption placentae. 8. Fetal death. 9. Multiple pregnancy. c) Clinical manifestations of the hemolytic disease of fetus and neonate are: 1. Hydrops fetalis. 2. Icterus gravis neonatorum. 3. Congenital anaemia of newborn.

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DIAGNOSIS All women should be screened for ABO and Rh blood groups early in pregnancy.

MANAGEMENT a) Preconception Care. 1. Indirect Coombs Test (ICT) is performed to screen for the presence of maternal Rh antibodies if high index of suspicion of previous isoimmunization. 2. Previous stillbirths or child with clinical manifestations of hemolytic disease of the fetus/neonate. 3. Previous blood transfusion. b) First prenatal visit. ABO/Rh screening. c) Prenatal Visit at 28 weeks. 1. ICT is performed to screen for the presence of Rh antibodies 2. If negative, give Anti-D Ig 300 ug IM. 3. If positive, manage patient as Rh-sensitized. 4. Women first presenting for Prenatal Care after 28 weeks should still have Antibody screening done at that time and if negative, offered Anti-D Ig at that time d) Prenatal Visit at 35 weeks. ICT Antibody screening is repeated. 1. If negative, patient is observed. 2. If positive, patient managed as Rh-sensitized. d) Intrapartum. For Rh negative patients, cord blood should be obtained for fetal ABO/RhD blood group typing, Direct Coombs Test (DCT), HB and Bilirubin. f) Postpartum. If the infant is Rh positive, 300 ug of Anti-D Ig is given to an Rh negative mo ther if her antibody screen is negative. Anti-D Ig should be given as soon as possible after delivery but always within 72 hours. It has been shown to be effective if given up to 28 days after delivery. If the pregnancy is non-viable and no sample can be obtained from the ba by, Anti-D Ig should be administered to a non-sensitised RhD-negative woman.

SPECIAL CONSIDERATIONS a) Abortion / Threatened Abortion / Termination of pregnancy. 1. Anti-D Ig should be given to all non-sensitised RhD-negative women. 2. RhD-negative women who have a spontaneous complete or incomplete miscarriage or threatened abortion at or after 1210 weeks of gestation. In women in whom bleeding continues intermittently after 1210 weeks of gestation, Anti-D Ig should be given at 6-weekly intervals. 3. Anti-D Ig is not required for spontaneous miscarriage before 1210 weeks of gestation, provided there is no instrumentation of the uterus. 4. Anti-D Ig should be given to non-sensitised RhD-negative women under-

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b) c) d) e) f) g)

going surgical and medical evacuation of the uterus, regardless of gestation. 5. Anti-D Ig should be considered in non-sensitised RhD-negative women if there is heavy or repeated bleeding or associated abdominal pain as gestation approaches 1210 weeks. 6. Anti-D Ig should be given to all non-sensitised RhD-negative women having a therapeutic termination of pregnancy, whether by surgical or medical methods, regardless of gestational age. Amniocentesis. Anti-D Ig is recommended. Antepartum Hemorrhage (placenta previa, abruption placenta). Anti-D Ig administration is recommended if pregnancy has been carried more than 12 weeks from the time of the previous Anti-D Ig dose. External Cephalic Version. FMH occurs in 2-6 % of patients who undergo external cephalic version whether failed or successful. Patients should receive Anti-D Ig. Ectopic Pregnancy. Anti-D Ig should be given to all non-sensitised RhD-negative women who have an ectopic pregnancy, regardless of management. Transfusion of RhD-positive blood components. In the event of inadvertent transfusion of RhD-positive platelets, prophylaxis against Rh alloimmunisation should be given. Sensitising events before delivery. A minimum dose of 250 IU (50 ug) is recommended for prophylaxis following sensitizing events up to 1916 weeks of gestation. For all events at or after 2010 weeks of gestation, a minimum dose of 500 iu (100 ug) Anti-D Ig should be given and a test to identify FMH greater than 4 ml red cells performed; additional Anti-D Ig should be given as required (an extra 125 ug for every ml). In the event of recurrent vaginal bleeding after 2010 weeks of gestation, anti-D Ig should be given at a minimum of 6-weekly intervals. Below is schematic diagram summarizing management of RhD-negative non-sensitised and sensitized pregnant women.

References. Moi Teaching and Referral Hospital (MRTH) Protocols of Dept. of Reproductive Health. Kenya, 2012. | Ministry of Health of Rwanda: Rhesus Isoimmunization. In: Gynecology and Obstetrics. Clinical Protocols and Treatment Guidelines. Kigali, 2012: 81-82.

B.3.16. PREECLAMPSIA AND ECLAMPSIA CONCEPTS AND DEFINITIONS a) Chronic hypertension in pregnancy. High blood pressure with systolic BP equal or more than 140 mmHg and/or diastolic BP equal or more than 90 mmHg with or without proteinuria before pregnancy or prior to 20 weeks gestation.

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b) Gestational hypertension. New onset hypertension with systolic BP equal or more than 140 mmHg and/ or diastolic BP equal or more than 90 mmHg after 20 weeks gestation without proteinuria. c) Preeclampsia. New onset hypertension with systolic BP equal or more than 140 mmHg or diastolic BP equal or more than 90 mmHg after 20 weeks gestation with at least 2 1 proteinuria or urine protein to creatinine ratio greater than 0.6. Signs and symptoms of severe preeclampsia: 1. Systolic blood pressure above 160 and/or diastolic blood pressure above 110 mmHg. 2. The presence of headache, visual changes, right upper quadrant pain or epigastric pain. 3. Intra-uterine growth restriction. 4. Maternal end organ damage (elevated creatinine, oliguria, anuria, elevated AST/ALT at least three times normal, eclamptic seizure, stroke). 5. HELLP syndrome. d) HELLP syndrome. Evidence of hemolysis, elevated liver enzymes, and low platelets with or without elevated blood pressure. e) Chronic hypertension with superimposed preeclampsia. A rise in systolic BP by 30 mmHg above non pregnant level and/or a rise in the diastolic BP rise by 15 mmHg above non pregnant level accompanied by proteinuria beyond 20 weeks gestation. f) Eclampsia. A diagnosis of preeclampsia based on new onset hypertension with systolic BP equal or more than 140 mmHg or diastolic BP equal or more than 90 mmHg after 20 weeks gestation with at least 2 1 proteinuria or urine protein to creatinine ratio greater than 0.6 accompanied by unexplained convulsions or coma.

MANAGEMENT OF PREECLAMPSIA The goals of the management of preeclampsia are to achieve optimal maternal and fetal outcome. Therefore management can vary depending on gestational age. In general the aims of treatment are: 1. To stabilize the patients blood pressure. 2. To control or prevent eclamptic seizures. 3. To monitor maternal well being, to prevent maternal complications such as pulmonary edema, liver failure, renal failure, and eye damage and stroke. 4. To monitor fetal well being. 5. To decide on appropriate timing of delivery. 6. To choose of mode of delivery. The only definitive treatment for preeclampsia is putting end to the gestational process. The antihypertensive drug treatment aims to mantain the BP between 140/155 and 90/105. The BP should not decrease below 140/90 in order to avoid fetal hypoperfusion. Any of the antihypertensive drugs described below can be used. However, givenits high effectivity, few side effects and the fact that it can be taken orally

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or intravenous, it is recommended to start with labetolol. Before exceeding 300 mg/6 hours it is recommended to associate it to hydralazine. In most cases, oral treatment can be applied unless the systolic BP is .180 or dyastolic BP .110, in such case intravenous treatment should be used from the beginning. The main side effect produced by labetolol is the risk of bradycardia for both, mother and fetus, when consumed in high dose. For this reason, it combines well with hydrazine which produce tachycardia. I.

STABILIZE BLOOD PRESSURE The goal is to stabilize the patient’s BP between 120-140/70-90 using antihypertensives and non pharmacologic therapy. For hypertensive emergencies (diastolic $110 mmHg)/ (systolic $160 mmHg). Give antihypertensives: 1. Labetalol 20 mg IV bolus, 10 minutes later can give 40 mg, 10 min later can give 80 mg. To a maximum dose of 220 mg, OR 2. 5 mg Hidralazine slow IV push over 2 minutes. If BP still elevated about 160/110 give: 10 mg Hydralizine slow IV push over 2 minutes. If BP still elevated above 160/110 give: 15 mg Hidralazine slow IV push over 2 minutes, OR 3. 40 mg Hydralazine in 500 ml of Normal Saline at 20 drops per minute titrated against diastolic BP by 65 drops till diastolic BP is 90 -100 mmHg then maintain the number of drops per minute. Monitor BP every 10-30 minutes and start concomitant oral therapy with one of the following. Only add a second oral agent if one agent is at maximum dose and is unable to stabilize the BP. 1. Nifedipine 20 g Retard BD (maximum dose: 90 mg /day). 2. Methyldopa 500 g TDS (maximum dose: 3 g/day). In case of a very high BP and resistance to treatment (which is rare) Nitroglycerin 5 mcg/min can be used, doubling the dose every 5 min, up to 100 mcg/min. It is a good option if associated with pulmonary edema, but not in cases of hypertensive encephalopathy. Non pharmacological therapy, such as bed rest and a quiet room can be used to lower BP and prevent worsening of disease.

II.

PREVENTION AND TREATMENT OF ECLAMPTIC SEIZURES Magnesium Sulfate is the drug of choice for both prevention and treatment of eclamptic seizures. It has been shown to be superior to other anti epileptics and anxiolytic medications. Midwives and medical officers can administer this drug when necessary for an eclamptic seizure or for severe preeclampsia in labour. a) For seizure prophylaxis. Give 4 gm Magnesium Sulfate infusion over 10-15 minutes as loading dose followed with a maintenance dose of 1 gm/hour IV, continue until 24 hours postpartum. b) For seizure treatment. 1. Give 10 gm Magnesium Sulfate IM (5 gm in each buttock) then obtain IV access and start a maintenance dose of 1 gm/hour IV, continue until 24 hours postpartum,

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OR Give 4 gm Magnesium Sulfate IV over 15 minutes and then continue a maintenance dose of 1 gm/hour IV, continue until 24 hours postpartum. 2. For repeat seizures while on magnesium treat with 2 gms IV stat dose and maintain as 2 gm/hour until 24 hours postpartum. 3. Turn patient on lateral side to protect airway from aspiration. 4. Provide one-on one nursing and a guarded bed. 5. If Magnesium Sulfate is out of stock then use another anxiolytic such as Diazapam or Phenytoin. c) Monitoring. While on Magnesium Sulfate, monitor the following: 1. Respiratory rate (goal: $12/min). 2. Pulmonary exam (goal: clear breath sounds). 3. Urine output (goal: $30 ml/hr). 4. Patellar reflexes (goal: must be present). In order to prevent a cardiac arrest and the consequent risk of maternal death, strict monitoring and availability of antidote (calcium gluconate) is necessary following these controls. It is not necessary to measure serum levels if patella reflexes and respiratory rate are normal. Serum level measurement is only necessary in patients with oliguria because renal clearance will be impaired. If patient is noted to have loss of DTRs, pulmonary edema, or respiratory depression then treat for Magnesium toxicity: • Give IV Calcium Gluconate, 1-2 gm (10-20 ml of 10 % solution given slowly) until the respiratory rate improves. • Check and EKG to rule out cardiac toxicity.

III. MONITOR MATERNAL WELL BEING a) Mild preeclampsia. The following bedside and lab monitoring is required for all mild preeclamptic patients admitted to MBH. 1. Blood pressure measurement every ½ hr - 4 hrs. 2. Input/output chart (bladder catheterization may be necessary). 3. Urinalysis for protein at admission and daily to monitor for worsening disease. 4. Urea/Electrolytes/Creatinine at least weekly. 5. Liver function tests at least weekly. 6. Complete blood count (including platelet in) at least weekly. b) Severe preeclampsia. The following bedside and lab monitoring is required for all severe preeclamptic patients: 1. Blood pressure measurement every ½ hr - 4 hrs. 2. Input/output chart (bladder catheterization may be necessary). 3. Urinalysis for protein at admission and daily to monitor for worsening disease. 4. Urea/electrolytes/creatinine at least twice weekly. 5. Liver function tests at least twice weekly.

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6. 7. 8.

Complete blood count (including platelet in) at least twice weekly. Coagulation panel on admission and daily if abnormal. Peripheral blood smear on admission.

IV. MONITOR FETAL WELL BEING The following bedside and ultrasonographic monitoring is required of all preeclamptic patients. 1. Fetal heart rate monitoring with every BP measurement. 2. Fundal height monitoring at least weekly. 3. Daily fetal kick chart. 4. Ultrasound biophysical profile with umbilical and cerebral Doppler studies at least weekly. 5. Full obstetrical US for fetal growth once every 3-4 weeks. V.

TIMING OF DELIVERY a) Mild preeclampsia. Mild preeclamptic patients should be delivered at 38 weeks gestation. b) Severe preeclampsia. Ideally severe preeclamptic patients should be delivered at 34 completed weeks unless if the patients status worsens. The patient should be delivered earlier if: 1. The patients blood pressure is unable to be controlled on the maximum doses of two antihypertensive agents. 2. The patient is experiencing persistent headache, visual changes or epigastric pain. 3. There is evidence of severe IUGR, BPP ,4/8, absent end diastolic flow on umbilical Doppler. 4. If the patient has been diagnosed with HELLP she should be delivered immediately. c) Eclampsia. If the patient has had an eclamptic seizure she should be started on IV blood pressure medication (goal DBP: below 100), stop the seizure, and evaluate labs and plan for delivery immediately. If the patient will need to be delivered prior to term gestation then maternal corticosteroids should be administered. Give either: 1. Betamethasone 12 mg every 24 hours for 2 doses. 2. Dexamethasone 6 mg every 12 hours for 4 doses.

VI. MODE OF DELIVERY Patients with mild preeclampsia, severe preeclampsia, HELLP and eclampsia may undergo induction of labour. Cesarean Section should only be performed for obstetrical or fetal indications such as arrest of dilatation, arrest of descent or fetal distress. Eclamptic patients with a Bishops score greater than 5 can be induced. The goal is for delivery with in 12 hours. a) Special considerations during induction of labour for preeclamptic and eclamptic patients. • The MO on duty must review all eclamptic patients. • Vital signs must be taken every 30 minutes.

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• • • •

•

Fetal heart rate must be monitored every 15-30 minutes and after every contraction in the second stage. Complete blood count, EUC, liver function tests and coagulation studies must be monitored at least daily during the induction of labour. Urine Foley’s catheter must be placed and strict intake and output must be recorded for all severe preeclamptic and eclamptic patients. All severe preeclamptic and eclamptic patients should be placed on Magnesium Sulfate during induction of labour and continued until 24 hours postpartum. Thus patients must be monitored for Magnesium toxicity during induction of labour. For patients on Magnesium Sulfate, the nursing and medical staff should be prepared for postpartum hemorrhage as per the RMBH protocol on PPH however Ergometrine is CONTRAINDICATED in hypertensive patients.

VII. IMMEDIATE POST PARTUM MANAGEMENT Monitor blood pressure half-hourly for the first 2 hours post partum then 4 hourly for the next 24-48 hours then taper off drugs as per maternal improvement. Continue therapy with: • Magnesium Sulfate for at least 24 hours postpartum. • Monitor strict intake and output for at least 24 hours postpartum with a Foley’s catheter in place. In case of end organ damage, refer for management in the specialized care units (Intensive Care Unit, the Renal Unit, Ophthalmology Unit.). VIII. DISCHARGING ANTENATAL PATIENTS PREECLAMPSIA Patients with mild preeclampsia with no other co-morbidities or risk factors may be candidates for outpatient management. Patients should first be assessed for the severity of disease, once the patient’s blood pressure has been stabilized and there is no evidence of severe preeclampsia, the patient may be discharged home with weekly follow up in High Risk OB clinic. Prior to discharge the patient must be educated to return to clinic for any of the following: • Danger signs of preeclampsia. • Performance of Fetal kick chart fore 10 movements in 12 hours and return for decreased movement. • Danger signs of labour. • Home bed rest.

Reference. Moi Teaching and Referral Hospital (MRTH). Protocols of Dept. of Reproductive Health. Kenya, 2012.

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ALGORITHM FOR CHRONIC HYPERTENSION IN PREGNANCY Aims: 1. 2. 3. 4. 5. 6.

To stabilize the diastolic blood pressure to 90-100 mmHg. To monitor for superimposed pre-eclampsia or eclampsia. To monitor maternal well being. To monitor fetal well being. Accomplish delivery at optimal time in maternal and fetal interests. To monitor urine protein weekly. CHRONIC HYPERTENSION IN PREGNANCY High BP before 20 wks gestation

MILD (,160/110 mmHg)

SEVERE ($160/110 mmHg)

Outpatient management – Advice on rest.

Inpatient managment

– Low salt diet. – TCA: 2 wks (gestation before 28 wks). – TCA: 1 wk (gestation after 28 wks).

No superimposed preeclampsia.

With superimposed preeclampsia.

Treat BP

Follow algorithm for severe preeclampsia.

– UA with every visit. – Monitor parameters as below. – Monitor fetal and maternal wellbeing. – Deliver at 39 weeks.

Monitor maternal and fetal wellbeing.

Good BP Control. No end organ failure.

Deliver at 39 weeks.

MONITORING

1. 2. 3. 4.

U/E/Cs weekly. CBC weekly. Urine proteins daily. LFTs weekly.

Poor BP Control or end organ failure.

Follow algorithm for sereve preeclampsia.

5. Uric acid weekly. 6. Fetal kick chart. 7. Monitor Symptoms: headache, epigastric pain, oliguria, blurred vision.

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ALGORITHM FOR MILD PREECLAMPSIA MILD PREECLAMPSIA BP , 160/110 mmHg No symptoms No maternal or Fetal Complications

MATERNAL ASSESSMENT AT DIAGNOSIS – Blood pressure measurement every ½ hr → 4-6 hrs. – Input/output chart (Bladder catheterization may be necessary). – Urinalysis for protein at admission and daily to monitor for worsening disease. – Urea/Electrolytes/creatinine at least weekly. – Liver function tests at least weekly. – Complete blood count (including platelet in) at least weekly.

FETAL ASSESSMENT AT DIAGNOSIS – Fetal heart rate monitoring with every BP measurement. – Fundal hight monitoring at least weekly. – Daily fetal kick chart. – Ultrasoound biophysical profile with umbilical doppler studies at least weekly. – Full Obstetrical US for fetal growth once every 3-4 weeks.

If maternal and fetal status are stable discharge home with percautions.

Plan delivery at 38 weeks.

If maternal or fetal status worsens manage as severe preeclampsia algorithm.

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ALGORITHM FOR MANAGEMENT OF SEVERE PREECLAMPSIA SEVERE PREECLAMPSIA BP . 160/110 mmHg - Symptoms - Lab Abnormalities

Stabilize BP Draw Labs Start magnesium

Fetus alive

Fetus dead

Induce labour

,24 weeks

24-28 weeks

28-34 weeks

.34 weeks

Consel family

Assess fetal wellbeing

Terminate pregancy for maternal safety

,1,000 gms

.1,000 gms

Consel family

Administer corticosteroids

Expectant managment until 34 weeks or worsening disease

Delivery

Terminate pregnancy for maternal safety

Delivery

INDICATIONS FOR DELIVERY FOR SEVERE PREECLAMPSIA MATERNAL

FETAL

34 completed weeks

IUGR

Uncontrolled BP on 2 agents at maximum doses

BPP 4/8

Platelets ,100,000

Oligohydramnios/Anhydramios

Liver enzymes 3 times abnormal

Dopplers with absent end diastolic flow

Deterioration in renal function (elevated creatinine, oliguria, anuria) Persistant severe headache or visual changes Persistant severe epigastric pain or nausea and vomiting Suspected abruption

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MANAGEMENT OF ECLAMPSIA AIRWAY / BREATHING / CIRCULATION

BRIEF MATERNAL FETAL ASSESMENT

START MAGNESIUM SULFATE 4 gms IV loading dose then 1 gm per hour

STABILIZE BP Use IV hydralazine or Labetolol

DRAW LABS CBC, EUC, LFTS, COAGS, UA

Evaluate for induction of labor

Bishops score .5

Bishops score ,5

Induction of labor per protocols

Plan for CS after BP is stabilized

Deliver within 12 hours

Obtain anestetist review

Consider postpartum ICU

DOSING GUIDE FOR IV MAGNESIUM SULFATE SEIZURE PROPHYLAXIS

SEIZURE TREATMENT

4 gm

1 gm hourly

2 gm hourly

Loading Maintenance

Monitoring on magnesium • • • •

Respiratory rate (goal: $16/min). Pulmonary exam (goal: clear breath sounds). Foley’s catheter to monitor urine output (goal: $30 ml/hr). Patellar reflexes (goal: must be present).

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Magnesium toxicity

SYMPTOM/SIGN

MAGNESIUM LEVEL

EKG changes

5-10 mEq / litre

Loss if DTRS

10 mEq / litre

Respiratory suppression

15 mEq / litre

Cardiovascular collapse

.25 mEq / litre

If a patient is noted to have loss of deep tendon reflexes, pulmonary edema, or respiratory depression treat for Magnesium toxicity: • Give IV Calcium Gluconate, 1 gm IV(10-20 ml of 10 % solution given slowly) until the respiratory rate improves. • Check and EKG to rule out cardiac toxicity.

B.3.17. POSTTERM PREGNANCY CONCEPT 1. 2.

Postterm pregnancy is a pregnancy that lasts 42 weeks from LMP. Should be distinguished from the term «postmature», which refers to an infant with recognizable features indicating a pathologically prolonged pregnancy. 3. Many providers refer incorrectly to postterm pregnancy as «post dates» or «postdatism». 4. Postterm pregnancy occurs in approximately 5-10 % of women. This frequency decreases if the dating of pregnancy is confirmed by US in the first trimester.

RISK FACTORS AND ETIOLOGIES OF POSTTERM PREGNANCY INCLUDE 1. Incorrect dating. 2. Primiparity. 3. Previous or family history of postterm pregnancy. 4. Fetal anomalies e.g. anencephaly.

POSTTERM PREGNANCY CONCERNS Postterm pregnancies carry risks for the pregnant woman and foetus/neonate. Perinatal mortality (neonatal and stillbirth) it is 2-3/1,000 up to 40 weeks, doubles at 42 completed weeks, 4-6 3 higher . 44 weeks. Risks Associated with Postterm Pregnancy MATERNAL RISKS

FOETAL / NEONATAL RISKS

Cephalopelvic disproportion.

Perinatal death.

Dystocia.

Macrosomia/LGA.

Perineal trauma.

Dysmaturity syndrome.

Operative vaginal delivery.

Cord compression.

Emergency cesarean delivery.

Meconium Aspiration Syndrome and Neonatal complications: seizures, hypogycemia.

DIAGNOSIS OF POSTTERM PREGNANCY 1. Accurate pregnancy dating is critical. All efforts should be made to be as accurate as possible in the assessment of fetal age based on a sure normal LMP,

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quickening, positive pregnancy test, and specially by ultrasound in the first trimester. 2. Using ultrasound in the 1st trimester of pregnancy to determine gestational age affords the most accurate method of dating and can reduce rates of induction of labour for postterm pregnancy. When using ultrasound for estimation, the following margins of error must be considered. 1st trimester: 60.4 week. 2nd trimester: 62 weeks. 3rd trimester: 63 weeks. 3. When gestational age by ultrasound is greater than gestational age by LMP by 1 week or 2 weeks in the first and early second trimester, the estimated due date should be changed to the due date by ultrasound. Caution should be exercised in redating pregnancies in the third trimester.

MANAGEMENT OF POSTTERM PREGNANCY a) Antenatal clinic. 1. At first antenatal visit. • Try to ascertain whether the patient has a sure normal LMP, appropriate fetal growth and ascertain whether the dating is correct. • If she is unsure of her LMP, periods are irregular or fundal height does not match gestation by dates then obtain an US as early in pregnancy as possible. 2. At 39 weeks. • Offer sweeping of membranes after 39 weeks to reduce risk of postterm pregnancies. 3. At 41 weeks. • Confirm the dating of the pregnancy. Review LMP, timing of quickening, fundal height, and previous ultrasounds. • Start the discussion of possible induction of labour if she reaches 41 weeks with no signs of labour. Induction can be offered as of 41 weeks. • Give the patient and admission date for no later than 42 weeks. • Sensitize mothers on importance of being keen on fetal movements and educated patients to return to hospital if there is a perception of reduction of movements. A patient should not wait until there are no fetal movements perceived. 4. At 42 weeks. • Admit to labour ward for induction of labour. b) Antepartum Fetal Surveillance. There is no consensus on the specific regimen between 40-42 wks. There is lack of evidence to suggest that monitoring improves perinatal outcomes; however, it is reasonable to assess fetal wellbeing using the Non Stress Test (NST): considered reactive is $2 accelerations in fetal heart rate (15 beats/ min for 15 sec) in a 20 minute period. A non-reactive NST can only be de termined when there is not #2 accelerations after a 40 minute period. Reference. Moi Teaching and Referral Hospital (MRTH). Protocols of Dept. of Reproductive Health. Nairobi (Kenya), 2012.

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B.3.18. OLIGOAMNIOS (OLIGOHYDRAMNIOS) DEFINITION Oligohydramnios is defined as the presence of an AFI less than 8. Less than or equal to 5 is considered as severe oligohydramnios/anhydramnios.

CAUSES a) Membrane/Placental. Up to 50 % of oligohydramnios are secondary to PROM. b) Placental/fetal causes. Three groups: 1. Intrauterine growth restriction (IUGR) with or without preeclampsia: it is the second most common cause of oligohydramnios in the 2nd - 3rd trimester, chronologically prolonged gestation, and recent fetal death. 2. Fetal malformations third leading cause of oligohydramnios. • Kidney malformations: renal agenesis (4/10,000 newborns), bilateral multicystic dysplasia, urinary tract obstruction (posterior urethral valve, bilateral ureteral obstruction). • Pulmonary malformations: pulmonary hypoplasia. • Neural tube defects. 3. CMV Infection. c) Maternal causes. Maternal medication (inhibitors of prostaglandin synthesis, inhibitors of the enzyme of angiotensin conversion [ACE]).

STUDY PROTOCOL 1. Discard PROM: Performing a maternal history won´t be enough, as there may be up to 20 % of uncertain diagnosis, either by intermittent fluid loss or contamination of the sample. A test with high sensitivity and high negative predictive value as the Prom Test or Amniosure must be performed. If not available, Nitrazine test or Fern test, could help, but are less specific. 2. Discard IUGR: estimated fetal weight assessment and Doppler study. 3. Discard fetal malformations: Perform a detailed anatomical study, focusing on the nephro-urologic system and the central nervous system. If necessary, Amnioinfusion could be used to improve the visualization of the structures. 4. Discard CMV infection: Perform maternal serological tests and ultrasound markers of fetal infection. 5. Discard drugs intake.

CLINICAL MANAGEMENT It will be conditioned primarily by its origin and gestational age at diagnosis. a) In those that are diagnosed with a PROM or IUGR, the specific protocol of each pathology should be applied. The management or termination of the pregnancy should be indicated according to each case. b) In the case of fetal malformation, the patient must be informed of the diagnosis and the risk of pulmonary hypoplasia especially if it happens before the 24 weeks and is manteined for more than 2 weeks. Then parents can then decide whether to adopt. If parents decide to continue the pregnancy, the study can be completed by requesting a fetal karyotype and an analysis of renal function (b microglobulin). c) Any drug intake should be interrupted immediately and, in case of the use of

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Obstetrical pathology B.3.

inhibitors for prostaglandin synthesis, an assessment of ductus arteriosus should be performed. d) In the case of oligohydramnios by idiopathic causes: 1. Antepartum Management: Implementing Doppler study weekly until week 36.6. Estimation of fetal weight assessed every 2 weeks. Amnioinfusion has not shown to improve the results. 2. Finalization: assessing the end of the of gestation after 37 weeks. There is no contraindication to the use of prostaglandins. 3. Intrapartum management: perform continuous monitoring. Perform amnioinfusion with physiological serum at 35-36 °C in those patients with alterations in CTG recording and/or meconium in AF as it has shown to improve perinatal outcomes. Reference. Carrera JM, Mallafré J, Serra B: Protocolos de Obstetricia y Medicina Perinatal del Instituto Universitario Dexeus. Elsevier. Barcelona, 2006: 182-183.

B.3.19. POLYHYDRAMNIOS DEFINITION a) AFI: 18 to 25: normal high limit. b) AFI: 25-32: moderate polyhydramnios. c) AFI: .32: Severe polyhydramnios.

CAUSES a) Idiopathic (60 %). b) Fetal causes: 1. Congenital malformations: • Central nervous system: anencephaly, spina bifida, encephalocele. • Gastrointestinal atresia of the esophagus, duodenum, jejunum and ileum. Gastroschisis. • Skeletal: achondroplasia, thanatophoric dysplasia. • Renal: ureteropelvic obstruction, multicystic dysplasia. Usually unilateral. Tubulopathies (fetal diabetes insipidus, tubular hipernatriuria). • Structural Heart Disease: arrhythmias, truncus, coarctation of aorta. • Thoracic/mediastinal disorders: MAQ, pulmonary sequestration, HDC, chylothorax. • Neuromuscular disorders: myotonic dystrophy, arthrogryposis. • Metabolic abnormalities: Gangliosidosis, Gaucher disease. • Chromosomal abnormalities: T18, T21, Turner syndrome. • Fetal tumors causing high cardiac output (sacrococcygeal teratoma). 2. Fetal Anaemia: secondary to Isoimmunization or congenital infection. 3. Fetofetal transfusion syndrome: in the context of a monochorionic twin pregnancy. c) Maternal causes (20 %). 1. Diabetes mellitus. 2. Toxic habits (drugs). d) Placental causes. Some placental abnormalities together with an increase in the amount of AF (chorioangioma).

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STUDY PROTOCOL a) Maternal tests: 1. Dismiss diabetes: OGTT. Often, but not always, polyhydramnios is associated with suspected fetal macrosomia. 2. Discard Isoimmunization: Coombs and irregular Ac. Assess fetal anaemia. 3. Dismiss infectious disease: TORCH, parvovirus B19, VEB, syphilis. In case of suggestive clinical maternal of nonspecific febrile illness, evaluate the analisys of adenovirus, enterovirus. b) Morphological fetal ultrasound: detailed anatomic study, with special focus on the movements and fetal attitude. Estimation of fetal weight.

CONDUCT a) Control of Polyhydramnios. 1. AFI: 18 to 25: control in 2 weeks. 2. AFI: 25-32: assess cervical length, weekly control. 3. AFI: .32: assess cervical length, income for the study and consider amniodraining. Measure the cervical length to all patients with uterine dynamics, regardless of its severity and consider the amnioreduction (amniodraining) in those patients with moderate maternal polyhydramnios but great discomfort or risk of preterm delivery. b) Treatment: 1. Etiological: If the cause is known. 2. Symptomatic: when the cause is untreatable inside the uterus or un known. Aimed at reducing maternal symptoms and preterm labor, so it should not be performed beyond the week 34-35. • Amnioreduction: of choice. Potential complications but very rare: amniorrhexis, chorioamnionitis, abruptio placenta. In order to limit the risk of the latter, it is advisable not to remove more than 2,000 ml. • Treatment with antiprostaglandin (oral indomethacin 50 mg/8-12 h pathway). It aims to reduce the fetal glomerular filter, secondarily decreasing the urinary output, pulmonary resorption and promotes the course through the membranes. Reference. Carrera JM, Mallafré J, Serra B: Protocolos de Obstetricia y Medicina Perinatal del Instituto Universitario Dexeus. 4th Edition, Elsevier. Barcelona, 2006: 185-186.

B.3.20. FETAL DEMISE CONCEPT In its narrower sense, intrauterine fetal demise (IUFD) is the death of the fetus in the second or third trimester of pregnancy before the onset of labor. Synonyms include (antepartum/antenatal) intrauterine fetal death and stillbirth. In a broader

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sense, deaths occurring during labor (intrapartum deaths) are also regarded as intrauterine demise.

ETIOLOGY Causes of fetal death can be categorized as fetal, placental, or maternal, although a sharp distinction between these groups is usually impossible a) Fetal causes include: 1. Congenital anomalies. 2. Malnutrition. 3. Anti-D-isoimmunization. 4. Non-immune hydrops. 5. Infections. 6. Congenital syphilis. 7. Parvovirus B19. 8. Cytomegalovirus. 9. Rubella. 10. Varicella. 11. Listeriosis can also cause lethal infections of the fetus. b) Among placental causes: 1. Placental abruption is the most common single cause of fetal death. 2. Malaria and tuberculosis may affect the placenta without signs of fetal infection. 3. Extensive and centrally located placental infarcts, which are frequently associated with hypertensive disorders, especially preeclampsia, can be fatal by causing placental insufficiency or, if followed by hemorrhage, by leading to placental abruption. 4. Fetal-maternal hemorrhage usually occurs after severe maternal trauma. 5. Twin-to-twin transfusion is a major cause of stillbirth in monochorionic multifetal gestations. 6. Stillbirth in the third trimester is most frequently caused by umbilical cord accidents. 7. Insertion abnormalities such as marginal and velamentous insertion can also lead to stillbirth since these vessels are susceptible to folding, torsion rupture and inflammation, especially if they are located at or near the level of the internal cervical os. c) Maternal causes: 1. Hypertensive disorders and diabetes are the most common maternal causes of fetal death. 2. Maternal obesity is also an important risk factor of fetal demise, partly through the increased rate of hypertension among affected women. 3. Pregnancies of women with lupus anticoagulant and anticardiolipin antibodies. 4. Certain types of hereditary thrombophilia (especially factor V Leiden mutation, protein C and S deficiency, prothrombin G20210A mutation, and hyperhomocysteinemia) also increase the risk of fetal death. As a rule of thumb, we can state that the major causes of pregnancy losses are genetic in the first, infections in the second, and cord accidents in the third trimester.

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FETAL (25-40 %)

–– Chomosomal anomalies. –– Nonchromosomal birth defects. –– Nonimmune hydrops. –– Infections-viruses, bacteria, protozoa.

PLACENTAL (25-35 %)

–– Abruption. –– Fetal-maternal hemorrhage. –– Cord accident. –– Placental insufficiency. –– Intrapartum asphyxia. –– Placenta previa, vasa previa. –– Twin-to-twin transfusion. –– Chorioamnionitis.

MATERNAL (5-10 %)

UNEXPLAINED (25-35 %)

–– Antiphospholipid antibodies.

–– Diabetes. –– Hypertensive disorders. –– Trauma. –– Abnormal labor. –– Sepsis. –– Acidosis. –– Hypoxia. –– Uterine rupture. –– Postterm pregnancy. –– Drugs.

DIAGNOSIS a) Signs and symptoms. 1. Clinically, the first sign of fetal death is usually the absence of fetal movements, which may be preceded by a short period of hyperactive mo vements of the agonizing fetus. 2. Later on, the patient may complain that her abdomen has become smaller or that her womb has «descended». 3. After 1 or 2 weeks, she may feel some unpleasant metallic taste in her mouth. b) Special proceedings. 1. Fetal heart tones cannot be detected using a Doppler device. 2. Ultrasonography confirms the absence of fetal movements and cardiac activity. 3. X-ray examination of the stillborn fetus may reveal overlapping of cranial bones (Spalding’s sign), extreme bending of the spine (Kehrer’s sign), bubbles in the heart, aorta and umbilical cord (due to intravasal gas formation) as well as the classical Buddha position and the glory-like rim around the fetal head. These signs can also be detected by ultrasound examination, which is the method of choice for confirmation of fetal demise.

POTENTIAL COMPLICATIONS 1. 2.

Fetal death does not generally pose a health risk to the mother within 2 to 3 weeks unless it is caused by placental abruption. Carrying a dead fetus for a longer time, however, increases the risk of coagulation disorders.

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The condition, known as dead fetus syndrome, is a special form of disseminated intravascular coagulation (DIC), which occurs after 4 or more weeks of fetal death. It is probably caused by the release of thrombogenic substances from placental tissue that enter the maternal circulation, leading to severe bleeding disorders during delivery.

MANAGEMENT 1. 2.

Spontaneous onset of labor occurs within 2 to 3 weeks in about 80 % of cases. Watchful expectancy is not always an acceptable approach because of the emotional burden of carrying a dead fetus, the possibility of chorioamnionitis and the risk of DIC. 3. Induction of labor is advisable if spontaneous contractions do not begin within a few days after intrauterine death. 4. Cervical ripening with the use of prostaglandin E2 vaginal gel or suppositories, followed by amniotomy and oxytocin infusion is the method of choice. 5. The use of epidural analgesia is preferred for pain relief, which also has an advantageous effect on cervical dilatation. Prevention of DIC 1. Fibronogen levels should be monitored closely along with repeated hematocrit and platelet counts as well as measurements of prothrombin and partial thromboplastin times. 2. Mildly decreased fibrinogen levels associated with slightly elevated prothrombin and thromboplastin times in the absence of bleeding do not usually necessitate transfusion therapy. 3. If the coagulation defect is more severe or if bleeding is observed, fresh frozen plasma or specific coagulation components should be given before any obstetrical intervention. 4. Episiotomy is usually avoided during vaginal delivery. 5. Perforation of the fetal head, decapitation, cleidotomy or evisceration of the fetus might be necessary in very rare cases. 6. Internal podalic version followed by breech extraction may be performed if the fetus is in transverse lie. 7. Cesarean section should be done if maternal indications (e.g. placental abruption, heart disease etc.) are present.

EVALUATION OF THE STILLBORN I.

CONCEPT In addition to emotional support, determining the cause of fetal death can also help in finding the necessary therapy or intervention to prevent a similar outcome. The fetus, placenta, and membranes should be examined thoroughly at delivery. Photographs and a full radiograph of the fetus are particularly important if the parents decline a full autopsy (See Fetal Necropry). Protocol for examination of stillborn infants a) Infant description. 1. Malformations. 4. 2. Skin staining. 5. 3. Degree of maceration.

Color —pale, plethoric. Cytogenetic studes.

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b) Umbilical cord. 1. Prolapse. 2. Entanglement —neck, arms, legs. 3. Hematomas or strictures. 4. Number of vessels. 5. Length. 6. Wharton’s jelly —normal, absent. c) Amniotic fluid. 1. Color —meconium, blood. 2. Consistency. 3. Volume. d) Placenta. 1. Weight. 2. Staining —meconium. 3. Adherent clots. 4. Structural abnormalities —circumvallate, accessory lobes, velamentous insertion. 5. Edema —hydropic changes. e) Membranes. 1. Meconium —stained or cloudy. 2. Thickening. Compared with all other analyses, a complete autopsy usually yields much more information on the cause of fetal demise, which is why parents should be encouraged to allow full autopsy of the fetus. II.

PSYCHOLOGICAL ASPECTS Emotional support has a very important role in the follow-up of cases with fetal demise. The patient should be isolated from breastfeeding women and abractation should be started as soon as possible after delivery.

PREVENTION OF RECURRENT STILLBIRTH 1.

Hereditary disorders as well as some maternal conditions, such as diabetes, chronic hypertension, and hereditary thrombophilias increase the risk of repeated stillbirth. In general, earlier losses are associated with a higher risk of recurrence. 2. Strict glycemic control starting from the pre-conceptional period to decrease the malformations linked to hyperglycemia during the periconceptional period, and the fetal death during the rest of pregnancy especially in the last weeks for patients with disorders of carbohydrate metabolism. 3. Prophylactic doses of low-molecular-weight heparin, administered to patients with known thrombophilic conditions throughout their subsequent gestation, can prevent recurrent pregnancy loss. 4. Low-dose aspirin therapy may decrease the incidence of IUGR and severe preeclampsia. 5. As a general rule, antepartum surveillance should begin earlier in women with a history of stillbirth, including regular non-stress tests (NST). Reference. Papp Z: Fetal Demise. In: Recommendations and Guidelines for Perinatal Medicine. Matres Mundi/WAPM. Barcelona, 2007; 22: 203-207.

B.4.

MEDICAL PATHOLOGY

B.4.1. ANAEMIA IN PREGNANCY DEFINITION Anaemia in pregnancy is defined as when the Hemoglobin (Hgb) level is below 11 g/dl in the first and thrid trimesers, and below 10.5 g/dl in the second trimester of gestation. Severe anaemia is defined as when the Hgb level is less than 8.5 mg/dl. The fall in Hgb level seen in healthy normal pregnancies (physiological or dilutional anaemia of pregnancy) is caused by a relatively greater expansion of plasma volume (50 %) compared with the increase in red cell volume (25 %).

CLASIFICATION 1. Anaemia can be classified based on mean corpuscular volume (MCV). If the MCV is less than 80 fL, the anaemia is microcytic; the two most common causes are the ion deficiency and thalassemia. 2. If the MCV is 80 to 100 fL, the anaemia is normocytic, The most common causeis sickle cell disease. 3. If the MCV es greater than 100 fL, the anaemia is considered macrocytic, the most common causes are B-12 and folate deficiencies.

CONSEQUENCES 1. According to the World Health Organization, severe anaemia contributes to 40 % of maternal deaths in underdeveloped countries. 2. Anaemia has been associated with increased risk of preterm birth, premature rupture of membranes, infections and fetal growth restriction. 3. The symptoms of mild anaemia are often indistinguishable from those related to pregnancy, and include fatigue, breathlessness, palpitations, difficulty in concentration, and low intellectual and productive capacity.

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4. Physical examination may reveal significant pallor of the conjunctiva and other parts of the body.

MICROCYTIC ANAEMIA Because most cases of microcytic anaemia in pregnancy are due to iron deficiency and because serum ferritin is an excellent indicator of body iron stores, the initial step should be assessment of serum ferritin levels. Serum ferritin is the most sensitive screening test for iron deficiency, with a level ,16 ng/mL indicating depleted iron stores.

NORMOCYTIC ANAEMIA A reticulocyte count enables distinguishing of cases of recent blood loss due to hemolysis (e.g., drug induced, or immune based, as witnessed by a positive direct Coombs test) or hemorrhage from early stage of iron deficiency. Low reticulocyte count with normal or high serum ferritin levels can be seen in the presence of hypothyroidism or chronic disorders, such as inflammatory bowel disease, systemic lupus erythematosus, granulomatous infections, malignant neoplasms and rheumatoid arthritis.

MACROCYTIC ANAEMIA 1. Vitamin B12 deficiency is rare, as most healthy individuals have 2-3 yearsâ&#x20AC;&#x2122; storage available in the liver. However, vitamin B12 deficiency can be encountered in individuals with pernicious anaemia (an extremely uncommon autoimmune disease in women of reproductive age which is diagnosed by the presence of serum intrinsic factor antibodies), and in those with malabsorption (e.g., Crohn disease or ileal resection). 2. Folate deficiency is less common nowadays given the supplementation of foods with folate. In addition to macrocytic anaemia, folate deficiency often also causes thrombocytopenia. Recommended folate requirements are 400 mg/day for pregnant women. However, higher requirements are recommended in the presence of multiple gestations, hemolytic disorders such as sickle cell anaemia or thalassemia, and in patients taking antiepileptic therapies or sulfa drugs (e.g., sulfasalazine). If a diagnosis of folate deficiency is made or the woman previously had infants with neural tube defects, the recommended dose of folic acid is 4 mg/day. By 4 to 7 days after beginning treatment, the reticulocyte count is increased. 3. In the case of macrocytic anaemia with normal folate and vitamin B12 levels, a consultation with a hematologist is indicated for bone marrow biopsy.

PROPHYLAXIS OF IRON DEFICIENCY 1. In a typical singleton gestation, maternal iron requirements average 1 g over the course of pregnancy. 2. Supplementation with elemental iron (30 mg/day) is recommended for all pregnant non-anemic women. The prophylaxis should be continued until 3 months postpartum in areas with high prevalence of anaemia.

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TREATMENT OF IRON DEFICIENCY ANAEMIA a) Oral therapy. Higher doses of iron are required for therapy of anaemia than for prophylaxis (up to 120-150 mg/day). Enteric coated forms should be avoided because they are poorly absorbed; absorption is increased by intake of iron on an empty stomach and with vitamin C or orange juice. A relationship is present between dose of oral iron and gastrointestinal side effects. Occurrence of such side effects leads to discontinuation of the therapy in 50 % of women. To ensure patients’ compliance it is thus important to minimize the side effects: 1. Prescribe ferric iron, which seems to have fewer side effects than ferrous fumarate or ferrous sulfate. 2. Increase the doses of iron gradually. 3. Stool softeners may be needed to prevent constipation. The rate of increase of hematocrit is typically slow, and it increases about 1 % per week. To replenish iron stores, oral therapy should be continued for 3 months after the anaemia has been corrected. b) Intravenous iron is more effective than oral therapy at improving hematological indices, with higher maternal Hb levels at 4 weeks of therapy and lower rates of gastrointestinal side effects. But, it is only indicated in cases of severe anaemia with intolerance to oral therapy or malabsorption. c) Blood transfusion is indicated only for anaemia associated with hypovolemia from blood loss or in preparation for a cesarean delivery in the presence of severe anaemia.

Reference. Standard Treatment Guideline for General Hospitals. Edit. By Drug Administration and Control Anothority of Ethiopia Contents, 2010: 353-364.

B.4.2. RESPIRATORY DISEASES

IN PREGNANCY

BRONCHIAL ASTHMA Pregnancy has no consistent effect on asthma and cases should be managed medically in the normal manner. 1. Sympathomimetic bronchodilators (e.g. salbutamol or orciprenaline) do not affect pregnancy adversely, and disodium cromoglycate can be used safely in pregnancy. 2. Management of status asthmaticus. a) Steroids in high doses. b) Bronchodilators. c) Artificial ventilation, if necessary, in medical intensive care.

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PULMONARY TUBERCULOSIS Treatment of pulmonary tuberculosis (TB) in pregnancy is done with: 1. Streptomycin 1.0 g daily, with isoniazid 300 mg daily, and either para-aminosalicylic acid (PAS) 150 mg/kg/day or ethambutol 15 mg/kg/day. 2. This regimen can be reduced to two drugs only, when the sensitivities of the tubercle bacilli are known. 3. Rifampicin can be used after the first trimester and isoniazid should be continued. 4. Treatment needs to continue for 1-2 years (9 months if rifampicin can be used). If a patien has open tuberculosis and inhalational anaesthesia is used, the anaesthetic machine must be sterilised carefully afterwards. Management of infants of mothers with tuberculosis. BCG vaccination is necessary. Give isoniazid 20 mg/kg/day until the Mantoux test is positive. It is necessary to separate the infant from the mother only if the mother has open TB, and only until Mantoux conversion occurs. Breastfeeding is contraindicated only if the patient has sputum-positive TB.

PNEUMONIA 1.

Bacterial preumonia causes a high fever and systemic toxicity, which may lead to pre-term labour or intrauterine death of the fetus. Treatment is with penicillin G 1 megaunit 6-hourly. The fever can be lessened by tepid sponging and paracetamol. Viral pneumonia carries a high maternal mortality and there is no specific treatment. Superadded bacterial infections (often staphylococcal) must be treated vigorously with penicillin and cloxacillin. Intensive supportive care (e.g. tracheostomy, renal dialysis) may be necessary in severe cases.

References. Sirrat GM. Despiratory Diseases. In: Obstetric. Pocket Consultant. London, 1981; 7-6: 102103. | Birsner M, Graham EM: Respiratory disorders of Pregnancy. In: The Johns Hopkins Manual of Gynecology and Obstetrics. 4th Edition. Edit by Hurt J, Guile MV, Bienstock J. et al. Lippincott Williams and Wilkins. Baltimore, 2011; 15: 205-207.

B.4.3. RHEUMATIC HEART DISEASE IN PREGNANCY GENERAL CONCEPTS • •

Rheumatic heart disease (RHD) is a preventable cause of maternal mortality worldwide. The most common valvular lesion associated with RHD is mitral stenosis.

NORMAL CARDIOVASCULAR CHANGES IN PREGNANCY •

Changes begin as early as 5-8 weeks in pregnancy.

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•

Blood volume and cardiac output peak at 24-28 weeks. INCREASE

Blood volume.

REDUCTION

Systemic vascular resistance.

Cardiac output (30-50 %). Heart Rate (15-20 bpm).

Blood pressure.

Stroke volume.

DURING LABOUR

Cardiac output and blood pressure increase.

IMMEDIATE POST-DELIVERY

Increase in preload (cardiac filling pressure) and plasma volume from autotransfusion from placenta.

WITHIN SIX WEEKS POST-PARTUM

Cardiovascular changes regress.

IMPLICATIONS FOR WOMEN WITH VALVULAR HEART DISEASE a) Normal cardiovascular changes place women with valvular heart disease at high risk of complications due to their inability to adequately adapt. These include: PREGNANT WOMAN

FOETUS

Congestive heart failure.

Foetal demise.

Arrhythmia.

Intrauterine growth restriction.

Stroke.

Low birthweight.

Cardiac arrest.

Preterm delivery.

Death.

b) Critical times in pregnancy when symptoms may worsen are: • 24-28 weeks gestation. • Intrapartum when cardiac output can rise up to 80 %. • Immediately postpartum.

ASSESSING THE SEVERITY OF VALVULAR HEART DISEASE In order to measure the severity of valvular heart disease, four main methods of assessment are used and should be clearly documented in every patient’s chart: 1. Clinical symptoms. 2. Physical signs. 3. Echocardiogram findings. 4. High risk features.

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CLINICAL SYMPTOMS New York Heart Association Functional Classification of Heart Failure (NYHA) classifies a patient according to the severity of the symptoms caused by her heart disease. NEW YORK HEART ASSOCIATION (NYHA) Functional Classification of Heart Failure

CLASS

No limitation of physical activity. Ordinary physical activity does not cause undue fatigue, palpitations, or dyspnea (shortness of breath).

Slight limitation of physical activity. Comfortable at rest, but ordinary physical activity results in fatigue, palpitations, or dyspnea.

Marked limitation of physical activity. Comfortable at rest, but less than ordinary activity causes fatigue, palpitations, or dyspnea.

III

Unable to carry out any physical activity without discomfort. Symptoms of cardiac insufficiency at rest. If any physical activity is undertaken, discomfort is increased.

To assess the functional class of the patient at baseline, ask questions like: In the last few weeks, 1. Have you been able to clean the house? Dress yourself? Take a bath? Go to the bathroom? 2. How many times do you have to stop between the hospital gate and arrival at mother baby hospital? 3. When you walk up the hill, how often do you have to stop and rest? When assessing the functional class of the patient at baseline, if you are uncertain about how to categorise the functional status of a patient, it is best to mark the patient’s symptoms, UP. II.

PHYSICAL SIGNS The following should be assessed and recorded: 1. Heart rate, rhythm and presence of murmurs. 2. Blood pressure. 3. Distended neck veins. 4. Respiratory rate, lung sounds, presence of wheeze or crackles. 5. Use of accessory muscles for breathing. 6. Peripheral oedema. 7. Evidence of cyanosis.

III. ECHOCARDIOGRAM Echocardiogram is used to determine the severity of the valvular lesion. A patient’s valvular disease can then be classified as «Mild», «Moderate», or «Severe». Valvu-

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lar severity is determined in the Cardiac Centre and will be found on the report (i.e., echocardiogram report or catheterization report). Impairment of cardiac function is reported according to ejection fraction: mild (,50-55 %), moderate (35 %), severe (,20-25 %). To book an echocardiogram, fill out a request form and the test should be completed within 48 hours. Echocardiogram evaluations are available on an emergency basis on the weekend and on public holidays. IV. HIGH RISK FEATURES IN PATIENTS WITH RHD Can be used to predict cardiac complications in pregnancy: CARDIOVASCULAR PREGNANCY RISK INDEX IN PATIENTS WITH RHD

POINTS

Prior Cardiac Event (Heart Failure, Transient Ischemic Attack, Stroke before pregnancy) or Sustained Arrhythmia requiring treatment.

Baseline NYHA Class III or IV or Cyanosis.

Left Heart Obstruction (mitral valve area ,2 cm2, aortic valve area ,1.5 cm2, or peak left ventricular outflow tract gradient .30 mmHg by echocardiography).

Reduced Systemic Ventricular Systolic Function (ejection fraction ,40 %).

1. 2. 3.

Assign 1 point for any high risk feature. Use the sum of all points to estimate the risk of a cardiac event in pregnancy. Counsel the patient. If 0, 1, and .1 points, the risk of a cardiac event in pregnancy is 5 %, 27 %, and 75 %, respectively. Cardiac events include: pulmonary oedema, sustained tachyarrhythmia or bradyarrhythmia requiring treatment, stroke, cardiac arrest, or cardiac death. Document any high-risk features in the patient’s file.

Reference. Moi Teaching and Referral Hospital (MTRH). Protocols of the Dept. of Reproductive Health. Nairobi (Kenya), 2012.

B.4.4. CARDIAC DISEASE IN PREGNANCY ROUTINE ANTENATAL MANAGEMENT 1. 2. 3. 4. 5. 6.

Arrange regular antenatal visits to obstetrician and cardiologist. Ensure adequate rest. Ban smoking. Prevent anaemia. Treat respiratory infection promptly. Cover dental work with antibiotics.

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7. Be watchful for incipient pulmonary congestion and arrhythmias. Termination of pregnancy is not medically indicated, except perhaps for Eisen menger’s syndrome or primary pulmonary hypertension.

MANAGEMENT OF LABOUR When a patient starts labour with good cardiac reserve, the risk of heart failure is low. 1. Aim for vaginal delivery at term. 2. Cover labour with antibiotics, e.g. crystalline penicillin or ampicillin and gentamicin. 3. Provide adequate analgesia —epidural anaesthesia is safe. 4. Experienced hands as long as hypotension is avoided. 5. Shorten the second stage by use of «lift-out» forceps or vacuum extractor (without raising legs into lithotomy position if possible). 6. Avoided Ergometrine. 7. Do not attempt caesarean section in the presence of heart failure. 8. Have oxygen and relevant drugs immediately available.

CARDIAC FAILURE This can occur in young, previously asymptomatic women at any stage of pregnancy. The risk increases as pregnancy advances, and the early postpartum period is the most hazardous. The clinical features of cardiac failure are as follows: 1. Pulmonary congestion. 2. Frank pulmonary oedema. 3. Right heart failure. Pulmonary congestion signs 1. Dyspnoea. 2. Persistent moist sounds at lung bases. 3. Haemoptysis (serious). 4. Vascular congestion on X-ray management. Management 1. Bed rest in hospital. 2. Digitalise (guided by degree of tachycardia). 3. Diuretics 1 potassium supplements. 4. Salt restriction. 5. Vigorous treatment of any intercurrent infection. Acute pulmonary oedema and right heart failure There are MEDICAL EMERGENCIES, which are particularly liable to occur a few minutes or hours after delivery. The management is as follows: 1. Nurse in semi-recumbent position. 2. Give oxygen. 3. Keep airways clear. 4. Morphine 10-20 mg s.c. or i.v. 5. Aminophylline 250 mg i.v. 6. Frusemide 40 mg i.v. 7. Digoxin (if not previously digitalised).

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8. If there is no improvement, proceed to endotracheal intubation and assisted respiration. 9. If the patient is in labour, the fetus must take second place until the situation is under control.

INFECTIVE ENDOCARDITIS This is mostly due to Streptococcus viridans. Treat energetically on suspicion in women with mitral incompetence, without awaiting results of blood culture. Antibiotic prophylaxis is required for dental work (3 days) and labour (7 days), as follows: Either 1. Crystaline penicillin 0.5 megaunits i.m., then penicillin V 250 mg orally twice daily. Or 2. Erythromycin 300 mg i.m., then 250 mg orally 6-hourly (use if patient allergic to penicillin). Or 3. Cephaloridine 2 g i.m., then cephalexin 250 mg 6-hourly. Or 4. Ampicillin 250 mg i.m. 8-hourly, gentamicin 40 mg i.m. 6-hourly for 24 hours to cover labour.

MANAGEMENT OF ARRHYTHMIAS a) Atrial fibrillation. This is a MEDICAL EMERGENCY and should be managed as follows: 1. Bed rest in hospital. 2. Digitalise. 3. Anticoagulate (possibly). 4. If the ventricular rate does not fall, consider use of beta-adrenergic blocking agents. 5. Consider electroconversion to re-establish sinus rhythm. b) Atrial tachycardia. This can precipitate heart failure rapidly. Try carotid sinus pressure, and if that fails. DC shock therapy. References. Sirrat GM: Cardiac Disease. Ins: Obstetrics. Pocket Consultant Grant McIntyre. London, 1981; 7: 95-100. | Birsner M, Graham EM: Cardiac Disorders of Pregnancy. In: The Johns Hopkins Manual of Gynecology and Obstetrics. 4th Edition. Edit by Hurt KJ, Guile MV, Bienstock J. et al. Lippincott Williams and Wilkins. Baltimore, 2011; 15: 195-205.

B.4.5. GESTATIONAL DIABETES (GDM) CONCEPTS 1.

Gestational diabetes is defined as carbohydrate intolerance of variable severity with onset or first recognition during the current pregnancy.

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2. Timely detection and treatment can reduce the risks of potential complications, including macrosomia, birth trauma, intrauterine demise, and neonatal hypoglycaemia and hyperbilirubinemia. 3. Women with GDM usually can be managed on an outpatient basis without hospitalization for dietary instruction and glycemic management.

MANAGEMENT 1.

Dietary therapy. Dietary therapy is the mainstay of management of GDM. The daily caloric intake requirement for women whose weight is less than 80 % of their ideal body weight (IBW) is 35 to 40 kcal/KG. This requirement decreases to 30 kcal/kg/day for women whose weight is 80 % to 120 % of their IBW and further decreases to 24 and 12 to 15 kcal/kg/day for women whose weights are 120 % to 150 % and greater than 150 % of IBW, respectively. Insulin therapy. Even with strict adherence to dietary therapy and close monitoring. The institution of insulin therapy is recommended when dietary management is insufficient to maintain fasting glucose levels of less than 105 mg/dL or 2-hour postprandial glucose levels of 120 mg/dL. Evidence suggests that prophylactic insulin therapy of women with GDM according to postprandial, rather than preprandial, glucose levels improves glycemic control and decreases the risk of neonatal hipoglycemia, macrosomia, and caesarean de livery. Glucose monitoring. Fasting and postprandial glucose levels in women with GDM are recommended once a week. Daily self-monitoring should be mandatory for patients who require insulin therapy for glycemic control. Fetal control. Patients who achieve good control are at low risk for intrauterine fetal death. Patients who require insulin therapy should undergo fetal surveillance similar to that recommended for patients with pregestational diabetes. Timing of delivery. In patients with well-controlled GDM, delivery may be delayed until the spontaneous onset of labor or a term gestation. In patients with poorly controlled GDM, however, induction of labor as soon as pulmonary maturity is documented is recommended. Method of delivery. If the estimated fetal weight (EFW) is between 4,000 and 4,500 g, the patient’s management should be based on the adequacy of the maternal pelvis and the previous obstetric history. A caesarean section should be considered if the EFW is greater than 4,500 g. Labor and delivery. Maintenance of maternal euglycemia si important during labor. Glucose levels should be monitored at 1-to 2-hour intervals in women with GDM who require insulin. Postpartum followup. Because patients with GDM are at increased risk for developing overt DM, follow-up testing using fasting glucose values or a 2-hour, 75-g oral GTT is recommended 12 weeks or later postpartum and yearly thereafter.

Reference. Abularach S, Callan N.: Diabetes Mellitus. In: the Johns Hopkins. Manual of Gynecology and Obstetric. Lippencot Williams and Wilkins. London, 1999; 7: 80.

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B.4.6. DIABETES AND PREGNANCY CONCEPT Chronic Metabolic disease, due to deficit of circulating pancreatic insulin. This fact produce an hiperglucemy with increment of catabolism of proteins and lipids.

CLASIFICATION Diabetes can be classified into the following four categories: 1. Clinical (symptomatic) diabetes, with symptoms (e.g. thirst, polyuria) and/or signs (e.g. retinopathy, neuropathy, nephropathy). 2. Chemical (asymptomatic) diabetes, with an abnormal GTT only. 3. Gestational diabetes, in which the abnormal GTT occurs only in pregnancy and reverts to normal after delivery (B.4.6). 4. Potential diabetes, in which risk factors associated with a higher incidence of diabetes are present.

DIAGNOSIS I.

SYMPTOMATIC PATIENTS OR CLINICAL DIABETES It is not adequate to make a glucosa tolerance test (GTT).

II.

ASYMTOMATIC PATIENTS, WITHOUT RISK FACTORS In this care the diagnosis control will consist only in a basal glucemy, but if the glycemia is up to 130, the patient is probably diabetic. Glycemias between 120-130 need GTT.

III. ASYNTOMATIC PATIENTS, WITH RISK FACTORS Its necessary to make a GTT. Glucose tolerance test (GTT) Despite being unphysiological, the GTT will reveal impaired carbohydrate homeostasis better than any other available test. It should be carried out under the following standard conditions: 1. 12 hours of fasting and 30 minutes sitting quietly beforehand. 2. Patient remains seated and does not smoke during the test. 3. After obtaining the blood sample 50 g of glucose in 200-250 ml of water is administred. 4. Zero time is the beginning of the drink and samples are withdrawn at 30 minute intervals for 2 hours. The criteria of normality for a GTT depend on the type of blood sample taken and the method for estimating the blood glucose. Plasma glucose is about 10 per cent higher than whole blood, and capillary levels are different from venous. In addition enzymatic methods (e.g. the glucose oxidase method) give lower levels than chemical estimations. Using the glucose oxidase method on venous plasma, the criteria for normality after a 50 g glucose load should roughly be as follows: • Fasting plasma glucose: #5.5 mmol/l (100 mg/100 ml).

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• 1 hour level: #10.0 mmol/l (180 mg/100 ml). • 2 hour level: #6.7 mmol/l /120 mg/100 ml). The indications for a GTT in pregnancy are as follows: 1. Plasma glucose $7.7 mmnl/l/140 mg/100 ml) 1 hour after a 50 g glucose load (this can be used as a screening test for all pregnant women). 2. Significant glycosuria on two or more occasions antenatally or in a single fasting urine sample. 3. Mother, father or siblings with diabetes. 4. Previous babies .4.5 kg. 5. Previous gestational or chemical diabetes (see below). 6. Previous unexplained perinatal death. 7. Acute hydramnios. 8. Maternal obesity (.20 per cent above ideal weight). If a GTT is abnormal, admission should be arranged to carry out a blood sugar series on normal diet, checking plasma glucose concentrations before breakfast, before lunch, before supper and at 9 p.m. The mean level should be ,5.0 mmol/l. Risks of diabetes in pregnancy 1. Nephropathy (class F). 2. Proliferative retinopathy (class R). 3. Neuropathy. 4. Obstetric risks. a) Polyhydramnios. b) Preterm labour. c) Macrosomia. d) Pre-eclampsia. e) Urinary tract infection. f) Monilial vaginitis. 5. Congenital malformations. 6. Perinatal morbi-mortality.

MANAGEMENT 1.

Pre-conception counselling and care. Optimal glycemic control should be achieved before conception. Glycosylated haemoglobin (Hgb A1C) levels can be monitored as a reflection of the patient’s degree of glycemic control durings the preceding 4 to 8 weeks. Normal levels are associated with an incidence of congenital malformations similar to that seen in nondiabetic women, and, although normal values vary among different laboratories, Hgb A1C levels greater than 10 % indicate the most significant risk of malformation development. In addition to glycemic control, the patient’s general medical status, including the presence or absence of retinopathy, nephropathy, hypertension, and ischemic heart disease must be assessed. Dietary therapy. The average caloric intake for diabetic patients of average height and normal weight should range between 2,200 and 2,400 kcal/day. Protein should constitute 12 % to 20 % of the total energy intake, with car bohydrates accounting for 50 % to 60 %, and fat constituting the remainder. Approximately 25 % of daily calories should be consumed at breakfast, 30 % at lunch, 30 % at dinner, and 15 % as a bedtime snack.

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Insulin therapy. a) Insulin preparations • The American diabetes Association recommends the use of human insulin. • Insulin is available in three different forms, which may be mixed in one syringe or injected separately. Short-acting insulins (regular and Semilente) have peak action at 2 to 4 hours postinjection. In termediate-acting insulins (Lente and NPH) have peak action at 5 to 12 hours. Long-acting insulins (protamine zinc and Ultralente) have peak action of 12 to 24 hours. b) Insulin requirements increase throughout gestation, from approximately 0.7 U/kg body weight per day during weeks 6 to 18, to 0.8 U/kg during weeks 18 to 26, to 0.9 U/kg during weeks 26 to 36, to 1.0 U/kg during weeks 36 to 41. c) Regimens. Recommended regimens should be considered starting points and must be adjusted to each patient’s specific needs. Generally, for a patient who is familiar with her diabetes, it is best to maintain the form of administration that she used before pregnancy, if possible. • Two-injection regimen. Two-thirds of the total daily dose in given in the morning (2:1 ratio of NPH to regular insulin) and one-third in the evening (1:1 ratio of NPH to regular). • Three-injection regimen. Administration of NPH or Lente insulin at bedtime, rather than with dinner, has been found to prevent nocturnal hypoglycaemia and result in improved control of fasting morning glucose levels. • Four-injection regimen. Fifty percent to 60 % of the total daily insulin requirement is given as Ultralente, together with regular insulin at premeal times. • Continuous subcutaneous insulin infusion. A pump system, which is usually attached to the patient’s abdominal wall, delivers regular insulin continuously to maintain basal blood glucose levels, with additional boluses administered at mealtimes. The pump has not been shown to be superior to multiple injection regimens as a means of glycemic control. Monitoring blood glucose levels. Most insulin regimens require glucose level monitoring at least four times a day: fasting (i.e., in the morning before breakfast) and either before or after each meal (either 1 or 2 hours postprandial). Postprandial monitoring is preferred to preprandial for tight glucose control in pregnant diabetics. a) Recommended levels. The following glucose levels are recommended as therapeutic objectives for pregnant women: fasting levels between 60 and 90 mg/dL; before lunch, dinner, or bedtime snack levels between 60 and 105 mg/kl; after meals, 1-hour levels no higher than 130 to 140 mg/dL and 2-hour levels no higher than 120 mg/dL; and from 2 to 6 a.m., levels of 60 to 90 mg/dL. Monitoring during the night should be instituted if nocturnal hypoglycaemia is suspected. b) Supervision. Frequent visits and phone calls, is essential to ensure optimal glucose control. Hospitalization is recommended for patients whose glycemic control is poor, such as those whose blood sugar levels consis-

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tently exceed 200 mg/dL or those who experience significant hypoglycaemic episodes. Antepartum assessment. a) Maternal assessment. Because approximately 25 % of diabetic patients develop preeclampsia, it is imperative to monitor blood pressure, proteinuria, and the development of nondependent edema closely. Ophthalmologic, cardiac, and renal function should be assessed at the initial visit and reassessed during gestation as indicated. A urine specimen should be submitted for culture every trimester so that asymptomatic bacteriuria can be treated in a timely fashion. b) Fetal assessment. • A sonogram should be done at 18 to 20 weeks’ gestation to rule out fetal anomalies. • A fetal echocardiogram also should be performed at 20 to 22 weeks’ gestation for patients with greater diabetes. • Because infants of diabetic mothers are at risk for both macrosomia and intrauterine growth restriction (IUGR), serial sonograms should be performed as clinically indicated. • The fetal timing and frequency of testing depend on the degree of risk present; nonstress tests, biophysical profiles, and contraction stress test are the modalities most commonly employed. • Doppler ultrasound is being used at some institutions as a means of detecting changes in vascular resistance that may precede fetal compromise.

Factors determining timing of delivery 1. Degree of control of maternal diabetes. 2. Maturity and size of baby (including pulmonary maturity). 3. Presence and severity of pre-eclampsia. 4. Previous obstetric history. 5. Adverse features on monitoring (e.g. abnormal fetal heart trace). 6. Other clinical factors (e.g. polyhydramnios). Clinical indications for delivery Time of delivery clinical indications. ,36 weeks

Only for very strong reasons and is available good neonatal intensive care. If the latter is not available, transfer of the patient to the nearest centre is advisable before delivery.

36-37 weeks

For strong reasons and when test of Clements 1

37-38 weeks

The majority of patients are delivered at this time because the risk of IUD is now becoming greater than that of RDS.

38-40 weeks

Very good control and careful monitoring allow some patients to continue towards, but never later than, term.

Postpartum glycemic management Insulin requirements decrease after delivery, leading to a «honeymoon period» during which insulin doses significantly lower than those required during the third trimester of pregnancy for reasonable glycemic control. Because strict glucose control is no longer mandatory after delivery, blood glucose levels of 200 mg/dL or less

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are acceptable. Breast-feeding should not be discouraged for diabetic women; patients should be instructed to increase caloric intake just before nursing (e.g., by drinking a glass of milk), because hypoglycaemia may occur after breast-feeding. References. Van Asche FA: Diabetes and Pregnancy. In Recommendations and Guidelines for Perinatal Medicine. Matres Mundi/WAPM. Barcelona, 2007; 11: 97-103 | Stirrat GM: Diabetes Mellitus. In: Obstetrics Pocket Consultant Grant McIntyre. London, 1981; 703: 91-96.

B.4.7. PSYCHIATRIC DISORDERS DURING PREGNANCY 1.

Emotional disorders may present as severe anxiety, depression or hypomania. Occasionally delusions and hallucinations may point to a schizophrenic illness. 2. Psychological and practical support may be all that is needed in milder cases. 3. In severe cases a psychiatrist should be consulted so that the potential benefits and risks of medication be known.

AFTER DELIVERY A psychiatric illness is said to be puerperal if it occurs within 12 months of delivery. The three main types of disturbance are: a) Postpartum blues. 1. This is a transient mild disturbance characterised by weeping, irritability, variation in mood, a feeling of helplessness, sensitivity to criticism and poor sleep. 2. It tends to develop around the third postpartum day and may last for a few hours or days. 3. It can be recognised in at least half of all women delivered. 4. Treatment should be by psychological support and reassurance rather than medication. b) Depressive illness. 1. This may start at any time after delivery and can last for a few weeks to several months. The peak incidence is about 3 months postpartum with a lesser peak at 12 months. 2. Tiredness, lethargy, irritability and anxiety may be more prominent than depressive mood change. 3. The condition is often brought on by psychological and social stress, and there may be a previous psychiatric history. 4. Treatment is by psychological and practical support, combined where necessary with tricyclic antidepressant drugs. c) Puerperal psychosis. 1. This can take the form of an affective disorder with depression or hypomania, or schizophrenia with delusions and hallucinations. It usually begins 2-4 days after delivery. 2. There is a risk of suicide, and harm to, or neglect of, the child. 3. A psychiatrist should be consulted because treatment usually entails admission of the mother and her baby to a mental hospital.

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4. The depressive form may require treatment with antidepressants and ECT: hypomania should respond to chlorpromazine or haloperidol.

PSYCHOTROPIC DRUGS IN PREGNANCY 1. Monoamine oxidase inhibitors are contraindicated in pregnancy, but withdrawal must be gradual. 2. Chlorpromazine 25 mg 6-hourly. 3. Promethazine hydrochloride 25 mg 6-hourly should be used, both during and after withdrawal. 4. If anaesthetic intervention is necessary within 2 weeks of withdrawal the anaesthetist must be informed.

DRUG ABUSE AND PREGNANCY Drug abusers are, almost by definition, poor antenatal clinic attenders, and may present for the first time in labour. Arms should be examined for scars, tattoo marks and thrombophlebitis. Chlormethiazole will control withdrawal symptoms in the mother. a) Opiates. 1. Intravenous abuse of heroin or methadone with dirty syringes carries among its risks hepatitis, septicaemia, syphilis and rhesus sensitization. 2. Unbooked «mainliners» should be given pethidine or methadone during labour. 3. Sudden withdrawal can cause fetal death, so gradual weaning is necessary. 4. The infant must not be given opiate antagonists (e.g. nalorphine). Signs of withdrawal in the infant are: irritability; shrill cry; sneezing; diarrhoea; muscle tremors; and convulsions. These signs may not develop until several weeks after delivery 5. Treatment with chlorpromazine 2 mg/kg is often needed. b) Barbitures. It is very difficult to wean patients from these drugs and the outlook for the infant, both socially and physically, is poor. c) Alcohol. The impairment of fetal brain growth (fetal alcohol syndrome) seen in association with a heavy alcohol consumption is not common, despite a high incidence of alcohol abuse by society. References. Stirrat GM: Psychiatric Disoders. In: Obstetries. Pocket Consultant Grant McIntgre. London, 1981; 7.10: 106-108. | Serra B, Mallafré J: Trastornos Psiquiátricos. In: Protocolos de Obstetricia y Medicina Perinatal del Instituto Universitario Dexeus. Elsevier-Masson. Barcelona, 2014: 460-461.

B.4.8. JAUNDICE CLASSIFICATION It can be considered under the following headings: Jaundice caused by pregnancy and intercurrent jaundice in pregnancy.

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Medical pathology B.4.

JAUNDICE CAUSED BY PREGNANCY a) Intrahepatic cholestasis. • Clinical diagnosis. The patient typically complains of generalised pru ritus in the second half of pregnancy. Some patients never become jaundiced. • Laboratory. The bilirubin is raised but is usually .100 mmol/l (6 mg/ 100 ml). The transaminases are mildly elevated (usually ,250 iu/l). • Consequences. There is an increased risk of pre-term labour fetal distress and perinatal death. • Treatment. 1. Cholestyramine will reduce itching, but is very unpleasant to take. 2. Ursodexicolic acid (10 -15 mgs/kg/day). 3. Parenteral vitamin K is required if jaundice causes prolongation of the prothrombin time. b) Jaundice complicating pre-eclampsia is a rare but very serious compli cation, usually associated with disseminated intravascular coagulation and severe systemic upset. The only treatment is delivery, after which it resolves rapidly. c) Acute fatty degeneration of the liver. The incidence is increased in association with poor maternal nutrition and needs intravenous tetracycline therapy. • Clinical diagnosis. It presents with: 1. Abdominal pain. 2. Vomiting. 3. Headache, usually after 36 weeks gestation. 4. Rapid progression may occur through severe jaundice, uraemia, and haematemesis, to coma and death. Both maternal and fetal mortality are high. • Laboratory and treatment. The frequent profound hypoglycaemia should be treated energetically and delivery must be expedited.

II.

INTERCURRENT JAUNDICE IN PREGNANCY Viral hepatitis, is due either to hepatitis B (long incubation, serum hepatitis), or hepatitis A (short incubation, infective hepatitis). Hepatitis B is associated with Australia antigen, now know as HBs Ag. In these cases the infants may be protected by gamma-globulin rich in antibodies to HBs Ag. But its effectiveness is by no means certain. • Diagnosis. Ultrasound or transhepatic cholangiography may be useful in confirming the diagnosis. • Treatment. 1. All viral hepatitis can be managed conservatively. Cholelithiasis constitutes 6 percent of all cases. 2. Cholecystectomy can be carried out in pregnancy, preferably in the second trimester rather than the first or last. Drug toxicity and haemolysis are other causes of intercurrent jaundice in pregnancy.

III. PRE-EXISTING LIVER DISEASE Pregnancy is uncommon in the presence of cirrhosis due, for example, to active chronic hepatitis, or primary biliary cirrhosis. The prognosis is good for mother

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and baby in familial non-haemolytic jaundice, e.g. Gilbert’s and the DubinJohnson syndromes. Pregnancy may increase jaundice in the latter. References. Stirrat GM: Jaundice. In: Obstetrics (Pocket Consultant) Gran Mc Intyre. Oxford, 1981: 104105. | Carrera JM, Mallafré J, Serra B: Colestasis intrahepática gestacional. In: Protocolos de Obstetricia y Medicina Perinatal del Instituto Universitario Dexeus. 4th Editon, Elsevier-Masson, 2006: 232-235.

B.4.9. THYROID DISORDERS HYPERTHYROIDISM Diagnosis a) Clinical features. 1. Goitre. 2. Weight loss. 3. Raised sleeping pulse rate. 4. Exophthalmos. 5. Lid retraction. 6. Periorbital swelling. b) Laboratory. 1. Investigations show a raised T4 and Free T4 Index (FT4I). In addition, the T3 resin uptake (T3RU) is low for pregnancy. 2. When control is achieved, which can take 4-6 weeks, the antithyroid drugs can be gradually reduced to carbimazole #20 mg daily. PTU # 200 mg daily. 3. Propranolol 20 mg 8 hourly may be used if necessary to control the serious peripheral effect of thyrotoxicosis. 4. Control is assessed on clinical grounds and by serial FT4l, serum T3 and TSH levels. 5. Combined treatment should be continued throughout the puerperium, but breastfeeding is contraindicated if mother is on antithyroid drugs.

SUBTOTAL THYROIDECTOMY This may be indicated in the following situations: 1. Large goitre is causing obstruction. 2. Failure to control symptoms with reasonable doses of drugs. 3. Toxic reactions to drugs. Babies born to thyrotoxic mothers should be screened for hyperthyroidism.

HYPOTHYROIDISM The commonest causes are autoimmune thyroiditis and partial thyroidectomy. a) The clinical features are as follows: 1. Excess weight gain. 2. Dry skin.

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Medical pathology B.4.

3. Undue fatigue. 4. Cold intolerance. 5. Slow pulse. b) Laboratory. Investigations show a raised TSH ($10 mU/ml), with a low T3 and FT4l. c) Treatment. 1. Treatment is with thyroxine 2 mg/kg body weight. The T4, T3RU, FT4l and TSH levels should be measure every 1 or 2 months. 2. The dose can be reduced after delivery, and breastfeeding is not contraindicated. 3. If the mother has previously had thyrotoxicosis, check for neonatal thyrotoxicosis, and if she has had autoimmune thyroiditis, check the baby for hypothyroidism. Reference. Stirrat GM: Thyroid Disorders. In: Obstetrics (Pocket Consultant) Grant McIntyre. London, 1981: 100-101. | Buckley de Meritens A, Hurt KJ, Milio LA: Thyroid Disorders. In: The Johns Hopkins Manual of Gynecology and Obstetrics. 4th Edition. Edit by Hurt KJ, Guile MV, Bienstock JL. et al. Lippincott Williams and Wilkins. Baltimore, 2011; 13: 175-182.

B.4.10. EPILEPSY CONCEPT The risk of an epileptic mother having an epileptic child is about 1 in 40. Pregnancy does not provoke epilepsy in mothers, but the frequency of seizures may increase because anticonvulsants are cleared more quickly.

TERATOGENICITY OF ANTICONVULSANTS The incidence of congenital malformations is increased two-to threefold in infants of women on anticonvulsants. No one drug can be said to be free of problems. Among the problems are: 1. Cleft lip and/or palate (increased tenfold). 2. Congenital heart defect (increased fourfold). 3. Hypoplasia of terminal phalanges of fingers. 4. Characteristic facial appearance of wide-spaced eyes: low posterior hair line; short neck: prominent brow; trigoncephaly. 5. Retarded growth, delayed development and, occasionally, mental retardation. These problems may be associated with drug-induced folic acid deficiency.

ROUTINE MANAGEMENT OF EPILEPSY IN PREGNANCY 1. Continue anticonvulsants in adequate dosage (the risks from seizures is greater than that of congenital anomalies). 2. Folic acid should be fiven 5 mg orally 8-hourly throughout pregnancy. 3. Vitamin K 10 mg orally daily from 32 weeks gestation. Vitamin K should also be fiven 1 mg i.m. to all neonates of treated mothers. 4. Note that breastfeeding is not contraindicated.

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MANAGEMENT OF STATUS EPILEPTICUS 1. 2.

Maintain airway and give oxygen. Treat mother with diazepam 10 mg i.v. as a bolus injection, then 40 mg in 500 ml dextrose/saline at 100 ml/hour reducing the dose as seizures come under control.

References. Stirrat GM. Epilepsy. In Obstetric (Pocket Consultant) Grant McIntyre. London, 1981; 7-5: 100-102. | Carrera JM, Mallafré J. Serra B: Epilepsia. In: Protocolos de Obstetricia y Medicina Perinatal del Instituto Universitario Dexeus. Elveiser-Masson. Barcelona, 2005: 255-257.

B.4.11. THROMBOEMBOLISM SUPERFICIAL THROMBOPHLEBITIS 1. Superficial thrombophlebitis does not carry a significant risk of thromboembolism (unles it extends to the deep veins). 2. An area of localised inflammation over the vein is acutely tender. 3. Symptomatic relief can be achieved with traditional remedies such as kaolin or glycerine and ichthyol bandages.

DEEP VEIN THROMBOSIS (DVT) a) Clinical diagnosis. The classical signs are oedema, local tenderness, a positive Homan’s sign and an increase in the diameter of the affected leg. Most cases are less clear-cut, and some are silent. Because clinical signs are unreliable, and treatment is not without risk, it is important to positively confirm the diagnosis before treatment, if at all possible. b) Diagnosis. 1. Doppler is the method of choice during pregnancy. 2. Detection of lack of patency of leg veins using ultrasounds is not accurate enough. 3. The main risk from DVT is of pulmonary embolism, but also if the trombosis is extensive enough chronic vascular insufficiency of the leg may persist.

PULMONARY EMBOLISM This is still the second most common cause of maternal death. a) Among the factors which are associated with an increased incidence of pulmonary embolism are: 1. Increasing age and parity. 2. Obesity. 3. Confinement to bed. 4. Supression of lactation with oestrogen. 5. Caesarean section (particularly in pre-eclamptic women).

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6. Blood groups other than O. 7. Sickle-cell disease. b) Diagnosis. 1. The symptoms and signs of pulmonary embolism can be missed all too esasily. 2. Typically, there is a pleuritic pain, haemoptysis, dyspnoea, and varying degrees of hypotension. 3. The diagnosis must also be considered in the presence of a dry cough, a fever of unknown origin, unexplained tachycardia, or bronchospasm without a past history of asthma. 4. The clinical picture is frequently confused with that of an acute pulmonary infection, and there may be no evidence of a preceding DVT. c) Investigation of suspected pulmonary embolus. 1. Ches X-ray may be helpful, but can be totally normal. 2. The ECG is usually normal except when the embolus is large and has produced acute cor pulmonale. Even these changes may be obscured by the usual ECG changes which occur in pregnancy.

TREATMENT Nowadays the most adequate treatment is the use of Low-Molecular-Weight-Heparin (LMWH). a) Prophylactic treatment. LMWH at the following dosage: • Daltarinez 5.000 UI/day Or • Enoxaparine: 40 mgs/day b) Treatment in the acute stage: • Daltarine: 5.000 UI/12 h. Or • Enoxaparine: 40 mgs/12 h. c) Dose adjusted to weight: • Daltarine: 100 UI/kg/12 h. • Enoxaparine: 1 mg/kg/12 h. d) Treatment during post-delivery. In post-delivery and puerperium the use of Warfarin continues being recommended. It is carried out during 4 to 6 weeks with initial superposition with LMWH. • Warfarin sodium 30 mg is given orally as a loading dose (day 0). No more is administered until the evening of day 2 when the correct dose is determined by the one-stage prothrombin time in a blood sample taken that morning. This should be kept at 2-2 1/2 times the control value. The average dose required is 5 mg 12 hourly. Fresh frozen plasma and K vitamin should be given to the mother. • The baby’s prothrombin times must be monitored carefully.

LABORATORY The control of the treatment with LMWH is done measuring its concentration in plasma. The anti Xa activity is measured at 4 h from the start of its administration. Recommended ranges are 0.5 to 1.2 U/ml. Neutralization is done using protamine sulphate.

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PROPHYLAXIS 1. As a general guide, if the patient had a confirmed pulmonary embolism in a past pregnancy, subcutaneous heparin should be given commencing at 16-20 weeks gestation. 2. Anticoagulation is also necessary postnatally 3. For a DVT alone it may be best to confine anticoagulation to the puerperium. 4. If the history of thromboembolism is equivocal or dubious it may be justifiable not to use anticoagulants at all. References. Stirrat GM: Thromboembolis. In: Obstetrics (Pocket Consultant) Grant McIntyre. London, 1981; 10 -1: 141-144. | Ibrahim SA, Saymanski LM: Tromboembolic Disease. In: The Johns Hopkins Manual of Gynecology and Obstetrics. 4th Edition. Edit by Hurt J, Guile MV, Bienstock JL. Lippincott Williams and Wilkins. Baltimore, 2011; 17: 230-237.

B.4.12. URINARY TRACT INFECTIONS CONCEPT There are different types of urinary tract problems that need special attention during pregnancy. These include: 1. Asymptomatic bacteriuria. 2. Symtomatic bacteriuria. 3. Cystitis. 4. Pyelonephritis. E. coli is the most common cause of urinary tract infection in pregnancy. Urinary tract infection is common in women with diabetes.

ASYMPTOMATIC BACTERIURIA Half of the women with asymptomatic bacteriuria become symptomatic later in pregnancy, for this reason treatment should be instituted. a) Diagnosis. Laboratory: 1. Urine analysis. 2. Urine culture: Growth of bacteria 105 organisms/ml of urine. b) Treatment. Drug treatment. The treatment would be rational if the choice of antibiotics is based on culture and sensitivity result. −− Amoxicillin, 500 mg P.O. TID for three days. Alternatives −− Nitrofurantoin, 100 mg P.O. QID for three days. OR −− Trimetoprim suphamethoxazole 480 mg BID for three days.

SYMTOMATIC BACTERIURIA 1.

Bacteriuria is significant when there are .100,000 organisms/ml of cultured urine.

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2. Routine culture of a midstream urine (MSU) sample is necessary at booking for each pregnant woman. 3. Escherichia coli is the infecting organism in 90 per cert of cases 4. Appropriate treatment is guided by the senstivities of the organism but co trimoxazole is best avoided in pregnancy and definitely in the first trimester. 5. Repeat the MSU culture after 5 days of antibacterial treatment. Consequences The detection os symptomatic bacteriuria in pregnancy is important, because of its association with the delivery of low birthweight infants and the increased risk of pyelonephritis.

CYSTITIS AND URETHRITIS The symptoms are often difficult to distinguish from those due the pregnancy itself. Features that may indicate true infection include hematuria, dysuria, urethral discharge and suprapubic discomfort. Treatment Treatment is the same as asymptomatic bacteruria but for 7 days.

ACUTE PYELONEPHRITIS a) Clinical picture. 1. Patient flushed and ill. 2. Rigors. 3. Vomiting. 4. Frequency of micturition and dysuria. 5. Abdominal pain. 6. High pyrexia. 7. Renal angle tenderness. 8. Pyuria. Acute pyelonephritis needs to be differentiated from other causes of an acute abdomen, e.g. appendicitis. b) Management of acute pyelonephritis. 1. Maintain adequate fluid intake, if necessary intravenously. 2. Send MSU for culture immediately. 3. Check blood culture if fever high. 4. Tepid sponging for high pyrexia and also Paracetamol. c) Treatment. Treatment of acute pyelonephritis (while awaiting culture and sensitivity results): 1. Severe cases: pivmecillinam (Selexid) 200-400 mg 6-8 hourly for 5 days is very effective against most gram-negative organisms, particularly E.coli. It is not effective against Pseudomonas pyocyaneus, and it cannot be used if the patients is allergic to penicillin. 2. Mild I moderate cases: sulphadimidine 2 g start, then 1 g 6-hourly for 5 days. Other antibiotics which can be used are: • Ampicillin 500 mg 6-hourly. • Cephalexin 500 mg 6-hourly.

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• Nalidixic acid 1 g 6-hourly. • Nitrofurantoin 100 mg 6-hourly. 3. Treatment of P. pyocyaneus infections requires gentamicin 40 mg 8-hour ly, and blood levels should be checked daily. Tratment is for 5 days in the first instance. Check another MSU on the third day (mentioning the antibiotic therapy in the request card). MSU samples need to be cultured at regular intervals thereafter. d) Recurrence of acute pyelonephritis. If the pyelonephritis recurs, treat again and consider maintaining antibacterial therapy for the remainder of the pregnancy with, for example, sulphadimidine 1 g b.d. nitrofurantoin 100 mg b.d., or nalidixic acid 1 g b.d. Reference. Standard Treatment Guideline for General Hospitals. Drug Admistration and Control Anthority of Ethiopia Contents. 2010.

B.4.13. INFECTIONS DISEASES IN PREGNANCY CONCEPT A pregnant woman can be affected by an important number of infections, from the moment of conception itself to delivery. These infections not only can deteriorate her health, to a greater or lesser degree, they can also affect the foetus negatively. Effectively, the infectious agent (virus, bacteria, etc.) can reach the embryo or foetus by different paths: by the transplacenta form, by swallowing contaminated amniotic liquid, through membranes, and so on.

SEXUALLY TRANSMITTED INFECTIONS I.

SYPHILIS a) Concept. Infection produced by a spirochete called Treponema pullidum, which is impossible to culture. It is transmitted to the foetus via vertical and horizontal pathways. It evolves in three stages: 1. Primary, characterized by the appearance of the first clinical manifes tation, from 3 weeks to 3 months following contagion, in the form of a chancre, located at the site of infection, painless, which disappears in 3 to 5 weeks. 2. Secondary, which manifests as a cutaneous eruption. 3. Tertiary, which —after a period of clinical silence— manifests in the form of late lesions in the skin, bones and cardiovascular and central nervous systems. b) Diagnosis. 1. Clinical diagnosis is based on the detection of the chancre and on laboratory tests. 2. Serology must be performed on all pregnant women in the first trimester or in the first prenatal visit in areas of high incidence.

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Treatment. 1. In primary syphilis: • Benzathine penicillin G (2.4 million units), in a single dose. • If there is allergy. −− Ceftriaxone 125 mg/day intramuscularly for 10 days. −− Erythromycin 500 mg orally every 6 hours for 15 days. 2. In cases of secondary syphilis or when neurological affectation is suspected: • Procaine penicillin G (2.4 million IU) every 2 days, up to a total of 10 injectios. • In children born to allergic mothers treated with erythromycin, neonatal treatment with penicillin is recommended. c) Consequences. Congenital syphilis is considered a fetopathy. Up to the 9th week of gestation, a small quantity of treponema can cross the placenta, without causing infection. From the 9th to the 18th week, there is a possibility of infection, especially if there are circulatory problems or alterations in placenta filtering. After the 18th week, the risk of contagion increases progressively until birth: the more recent and more evolved the maternal syphilis is, the greater the foetal risk. 1. In the case of symptomatic early syphilis, foetal mortality is 50 %. Among the survivors, generally premature infants, 50 % develop asymptomatic congenital syphilis. 2. In the case of early latent syphilis, the rates of mortality, premature birth and congenital syphilis are 20 %, 20 % and 40 %, respectively. 3. In the case of late syphilis, the incidences of premature birth and of syphilis are both 10 %. It maternal syphilis of more than 8 years’ evolution, the risk is minimal. c)

II.

GONORRHOEA a) General concepts. 1. Infection produced by Neisseria gonorrhoeae. It is most frequently located in: cervix, urethra, para-urethral glands, Bartholin glands, anorectal channel and pharynge. 2. It runs its course asymptomatically in most women (80 %). 3. Transmission is mainly through sexual contact and asymptomatic carriers are the main source of contagion. 4. The incubation period is 3-5 days. 5. It is frequently associated other sexually-transmittted diseases (Chlamydia in 50 % of the cases). b) Clinical picture. 1. It consists of infections of the Bartholin and Skeene glands. 2. Purulent cervicitis. 3. Greenish yellow leucorrhoea and dysuria, generally mild. c) Complications. 1. Pelvic inflammatory disease (15 %) and 2. Disseminated gonorrhoea (2 %). Complications are rarely produced after the first trimester.

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Diagnosis. This is based on detection of Neisseria. 1. Gram tincture in endocervical and/or urethral swabs. 2. Endocervical and or urethral culture: This is the most sensitive and specific test. 3. Antigenic detection of Neisseria. d) Treatment. 1. Treatment of localised infection (urogenital, anorectal, pharyngeal). The treatment of election is cephalosporins. • Ceftriaxone: 125 mg intramuscularly, a single dose. • Cefixime: 400 mg orally, a single dose. • If intolerance or allergy to cephalosporins exists: Spectinomycin, 2 g intramuscularly, a single dose. • The couple must be treated. Other options are added to the previous ones. • Concomitant treatment is recommended in the case of Chlamydia, given its high association (unless its presence has been eliminated through the appropriate tests). 2. Treatment of disseminated infection. • Ceftriaxone 1 g. intramuscularly or intravenously every 24 hours. • Cefotaxime/ceftizoxime 1 g/8 hours intravenously. • If Allergy or intolerance to cephalosporins exists: Espectinomycin 2 g/12 hours intramuscularly. Treatment must be maintained until 24-48 hours after improvement begins: after that, it can be substituted by: cefoxim 400 mg/12 h orally, for one week of antimicrobial treatment. 3. Prevention of ophthalmia neonatorum. Any of the following measures must be applied after delivery, whether vaginal or caesarean. • Opthalmic preparation of erythromycin at 0.5 % (a single application). • Opthalmic preparation of tetracycline at 1 % (a single application). • Aqueous solution of silver nitrate at 1 % (a single application). d)

III. CHLAMYDIA a) General Concepts. 1. Infection caused by Chlamydia trachomatis. This is one of the most frequent causes of sexually-transmitted diseases (STD). 2. Infections through Neisseria gonorrhoeae are associated in up to 50 % of Chlamydia cases. 3. The most frequent site in women is the cervix. 4. The role of Chlamydia in the increase of premature births, restricted intrauterine growth and/or postpartum endometritis is under discussion. b) Clinical Picture. 1. Cases can be asymptomatic, but up to 30-50 % of cervicitis cases from Chlamydia present symptoms (vaginal discharge, abdominal discomfort, bleeding following sexual relations and dysuria). 2. The risk factors for infection during pregnancy are: Multiple partners, age ,20, presence of other concomitant STDs, non-gonococcic urethritis

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in the couple, presence of mucopurulent endocervicitis, sterile pyuria (acute urethral syndrome), low socioeconomic status and late or nonexistent obstetric follow-up. 3. Chlamydia should be suspected in all cases of urethritis or genital infection in which no other specific agent (gonococcus, etc.) can be diagnosed. c) Treatment. Treatment alternatives. 1. Amoxicillin 500 mg/8 h for 7 days. 2. Base erythromycin 500 mg/6 h for 7 days (tolerated worse by the patient). The use of doxycycline, ofloxacin and erythromycin estolate is contraindicated during pregnancy. IV. HERPES SIMPLEX a) General Concepts. 1. This is one of the most frequent sexually-transmitted diseases. 2. It is produced by the group of the herpesvirus (DNA virus). It is characterised by being neurotropic viruses. 3. They can be grouped into two serological groups: Type I (HSV-1) and Type II (HSV-2). 4. Both the primary infection and recurrences are more frequent during pregnancy (triple the frequency). 5. The risk of a herpes outbreak in the moment of birth is 36 % if the primary herpes infection is produced during pregnancy. b) Transmission pathways. The majority are intra-delivery, but 5 % can be intrauterine. Postnatal transmission (through mouth and hand lesions, from the parents and health staff) also exists. c) Clinical manifestations. 1. HSV-1 • Primary infection: gingivostomatitis. This also produces up to 30 % of the genital primary infections, although with less frequent relapses than in Type II. • Recurring infection: labial herpes and buccal blisters. 2. HSV-2. Primary infection and genital recurrence: pruriginous erythemna followed by the appearance of papules, vesicles, ulcerations and scabs. Similar lesions can appear in nearby dermatome (sacral area, gluteus, etc.). The presence of antibodies against HSV-1 can make primary infection through HSV-2 asymptomatic. In both serological types, primary infection can give rise to a disseminated infection and even mortality: fever, anicteric hepatitis and ulcerative pharyngitis. The incubation period is 2-7 days. Neonatal affectation is more serious and more frequent in cases of primary maternal infection than in those of recurrent infection (40-50 % against 5 %). d) Diagnostic methods. 1. Clinical suspicion in the case of orolabial or genital manifestation during pregnancy. 2. Seroconversion of specific antibodies.

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e) Prevention. 1. Consider high-risk patients to be all those with a history of genital herpes during pregnancy or during the previous 6 months. Included in this group are also those whose sexual partner has this infection. 2. Advise sexual abstinence during the pregnancy if the couple present active oral or genital herpes. 3. Periodic clinical vigilance, above all during the third trimester. Oral treatment with acyclovir (200 mg/6 h or 300 mg/8 h) from the 36 th week until the moment of birth lessens the rate of hepes outbreaks at delivery by 50 % (especially in cases of primary infection during pregnancy). Such treatment also lowers the rate of asymptomatic excretion of the virus. 4. Cesarean section does not prevent the possible appearance of neonatal herpes, given that up to 20-30 % of newborns with herpes infection were born through caesareans. At any rate, this is still the method of choice when faced with active lesions at the moment of birth. 5. Postnatal care, Isolation the newborn from the mother is not necessary, but the neonate must be isolated from the other newborns. f) Treatment. Topical and oral acyclovir (200 mg/6 h for 7-10 days).

HUMAN PAPILLOMAVIRUS a) Concept. Infection by the virus of human papilloma (HPV) is a very frequent sexuallytransmitted disease. b) Clinical types. 1. The majority of the infections are sub-clinical and can often go unde tected. 2. The most frequent clinical manifestations are condylomata acuminate (genital warts), generally caused by the low risk types 6 and 11. 3. Although there is a possibility of spontaneous regression, the tendency is to treat clinical lesions (condylomata acuminate) in order to control the disease. c) Treatment. The choice of treatment type depends on a series of factors, such as the number, size and anatomical distribution of the lesions. 1. Some of the treatments normally used are contraindicated in pregnant women (5-fluorouracyl, interferon, podophyllin, podophyllotoxin). 2. Treatment can be carried out by: Trichloroacetic acid, diathermic loop, cryotherapy, laser or surgical removal. The advantages of vaporisation with CO2 laser make this the technique of choice. It presents a cure rate of nearly 95 %. 3. The existence of HPV infection during pregnancy does not constitute an indication for caesarean section, except in cases of bulky condylomatosis that obstruct the birth canal or represent a serious risk of haemorrhage. The risk of laryngeal condylomatosis in the newborn is very low; therefore, it is not a reason for doing caesareans.

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VI. VAGINITIS a) Concept. During gestation, not only physiological vaginal secretions increase, the pathological ones do, as well. The incidence of inflammatory processes of microbial origin of the vagina doubles. b) Diagnosis. Any excessive vaginal secretion, especially if accompanied by inflammatory symptoms (itching, burning, bad odour, etc.), must be etiologically investi gated. In practice, it is particularly important to ascertain if it is a mycosis, trichomoniasis or bacterial vaginosis. 1. On many occasions, anamnesis can give an orientation as to the causal agent. Leucorrhoea usually produces burning if a mycosis is involved, or pruritis if it is a trichomoniasis. 2. Leucorrhoea type is also very orientative: a cheesy type, in the case of mycoses; a foamy yellow colour, if it is a trichomoniasis; yellowish-white colour, in the case of vaginosis. 3. Confirmation must be microscopic, with the help of double fresh examination (potassium hydroxide drop and physiological serum). In the case of mycoses, the hyphas are observed; mobile protozoa are seen in the case of trichomoniasis. c) Treatment. 1. Mycotic infection by Candida. Only topical therapies should be used; 7 days of treatment are advised. Oral therapy and ketoconazole are contraindicated throughout pregnancy. • Nystatin: 2 applications of cream a day for 7 days, or clotrimazole vaginal tablets (100 mg) for 7 nights (before the 16th week of gestation). • Clotrimazole: 1 vaginal tablet (100 mg) for 7 nights. The couple can also be treated together, preferably with fluconazole. 2. Trichomoniasis infection. It is recommended not to treat this during the first trimester and to do so after that with a single dose of oral metronidazole (2 g), in asymptomatic patients. The couple must be treated with tinidazole, 2 tablets every 12 h, for a day. 3. Chlamydia infection. Erythromycin, oral pill of 500 mg every 6 h for 7 days. VII. VIRAL INFECTION a) Concept. The repercussions of virosis, especially in the foetus, are varied, depending on the virus itself and on the moment of gestation: from malformations (German measles, chickenpox, cytomegalovirus, etc.), premature birth from maternal hypoxia (influenza), growth restrictions (poliomyelitis), typical exanthematic cutaneous lesions (measles), etc. Risk of viral contagion during pregnancy Exposure of a pregnant woman to a viral infection by direct, person-to-person contagion makes specific prophylactic measures advisable, in certain cases.

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Norms according to virosis INFECTIOUS AGENT

POTENTIAL FOETUS EFFECTS

LEVEL OF PERINATAL TRANSMISSION

Herpes simplex: Primary or recurrent infections

Primary: –– Foetal loss. –– Congenital syndrome. Primary and recurrent: –– Mucocutaneous lesions. –– Disseminated disease. –– Encephalitis.

–– Birth transmission in 90-96 % of the cases. –– Primary form in 41 %; recurrent in 4 %. –– Neonatal infection rate: 1/5,000 births.

Human Immunodeficiency Virus (HIV)

Progression during infancy (practically eradicated with triple antiretroviral therapy).

–– With zydovudine, 8 % transmission; with triple antiretroviral therapy, ,1 %. –– Most infected in the 1st trimester or when breast-feeding.

B19 Parvovirus (5th disease)

–– Foetal loss. –– Hydropexia. –– Anaemia. –– Congestive heart failure.

–– 17-33 %. –– Maternal infection: if ,20 weeks of gestation, 17 % foetal loss; if .20 weeks, 6 % foetal loss.

Cytomegalovirus (CMV): Primary or recurrent

Congenital syndrome: –– Deafness. –– Hepatosplenomegaly. –– Jaundice. –– Microcephaly.

–– Primary maternal infection: 15 % transmission. –– Recurrences: 5 %. –– About 2,3 % of newborns affected if intrauterine infection. –– 10-20 % if HBeAg (1).

Hepatitis B

–– Hepatitis. –– Cirrhosis and/or hepatic cancer.

–– Normally transmitted at delivery.

Hepatitis C

–– Hepatitis. –– Cirrhosis and/or hepatic cancer.

–– Transmission 10-20 % if DNA-VHC, but ,1 % if DNA-VHC (-).

German Measles (Rubella)

–– Foetal loss. Congenital syndrome: –– Chorrioretinitis. –– Hydrocephaly. –– Intracerebral calcifications.

–– 67-85 % in the 1st trimester, associated with serious infection. –– 25-35 % in the 2nd and 3rd trimesters.

Varicella-Zoster (VZ)

–– Primary. Congenital syndrome: –– Limbic hypoplasia. –– Ocular abnormalities. –– CNS alterations. –– Eruption limited to dermatome. Perinatal period: –– Chickenpox. –– Encephalitis.

–– 5-7 % of pregnancies complicated by VZ. –– 2 % risk of congenital VZ if the mother develops VZ in the first 20 weeks. –– 20-40 % neonatal VZ if the mother gets infected around the delivery period.

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MATERNAL FILTERING

PREVENTION

–– Determine virus (RCP) if primary infection suspected. –– Lesion inspection at delivery (remains can be emitted without lesions).

–– If herpes lesions exist at delivery: Caesarean. –– Acyclovir in third-trimester infections.

–– CA Anti-HV as a rule in the 1st trimester. –– Repeat in the 3rd trimester if risk factors exist.

–– Avoid high-risk behaviours. –– If HIV (1), prenatal and perinatal antiretrovirals. –– Avoid maternal breast-feeding.

–– Not routinely requested. –– If maternal exposure or suspicion of infection, determine IgG and IgM against Parvovirus.

–– Avoid contacts. –– If serologies (1), series echographs. –– If hydropexia foetal in echo: cordocentesis, correction of foetal anaemia and Parvovirus determination.

–– Not recommended as routine.

–– Hand-washing (especially when changing nappies). –– At-risk staff, teachers, nursery personnel.

–– Routine HBsAg in the 1st trimester. If (1), determine HBeAg and anti-HBeAg.

–– At birth, immunoglobulin and vaccine for newborn –– In non-immune and exposed pregnant women, vaccine and immunoglobulin.

–– Routine HCV CA in the 1st trimester. –– If positive, determine qualitative DNA-HCV (quantitative has litte validity, from discordant values).

Avoid risk behaviours: –– Greater control in IVDA and transfusions prior to 1992. –– No prophylaxis available.

–– Routine serology in the 1st trimester and preconception determination.

–– Vaccine before or after the pregnancy (never during). –– Avoid contact.

–– Not recommended as routine. –– If the pregnant woman was exposed, determine IgG. –– If primary infection is suspected, lesion study and serological analyses (IgG and IgM).

–– Non-immunised women: vaccine before or after pregnancy. –– Exposed non-immunised pregnant woman: vaccine within 96 hours. –– If the newborn is exposed, vaccine.

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Prognosis and treatment according to causal agent a) Cytomegalovirus (CMV). 1. Up to 40 % of pregnant women lack immunity against CMV. 2. Primary infections presents in 1.2 % of them, with a risk of vertical transmission of 40 % before 20 weeks. Vertical transmission rate drops to 0.5-1 % in cases of recurrence. 3. Primary infection cases develop asymptomatically in adults in 90 % of the cases, the most frequent long-term sequela being unilateral or bilateral deafness (5-10 %). 4. There is no prophylaxis or specific therapy for CMV infection b) FLU (influenza). 1. The influenza virus belongs to the group Myxovirus. 2. Symptoms consist of an upper-chest respiratory symptoms, fever, myalgia and cephalea. 3. It has a short incubation period (1-4 days) and it lasts approximately 3 days. 4. Special attention should be given to pneumonic risk and bacterial overinfections, which generally require hospital admittance and broad spectrum antibiotic treatment. 5. Maternal treatment is symptomatic. c) Hepatitis. 1. The complications are the same as those in cases outside gestation. It increases the risk of abortion and premature birth. 2. There is no formal contraindication against breast feeding in hepatitis cases. 3. If it occurs near the time of delivery, the possible haemorrhagic repercussions from hepatic dysfunction must be taken into consideration. d) Parotiditis. No greater incidence of malformations has been associated to this, but mis carriages are more frequent. Maternal treatment is symptomatic. e) Parvovirus B19 (infectious erythema or 5th disease). 1. This is a DNA virus of the family Parvoviridae. 2. Transmission pathway: respiratory. 3. Incubation: 4-14 days. 4. Viremia: at 7-8 days of initial infection, lasting 4 days. 5. After that, a rash appears and the patient stops being contagious and acquires permanent immunity. Clinical picture • Maculopapular rash at 17-21 days following contagion (initially on the cheeks and then spreading to the trunk and extremities). It can be preceded by a non-specific respiratory symptoms. • Symmetrical polyarthralgia. • The appearance of pure red cell aplasia or pancytopenia is less frequent (resolution in 2-3 weeks). • Up to 25 % of the cases run asymptomatically, but such lack of symptoms is not associated with a better foetal prognosis when infected. • If infection occurs during the first half of the pregnancy, anaemia,

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along with myocarditis and affectation of the endothelium, can cause an abortion. If infection occurs later than this, it can set off a nonimmune hydrops caused by cardiac insufficiency secondary to foetal anaemia. • The infection is confirmed through specific antibodies (IgG and IgM). Treatment • Treatment can be conservative, especially in the case of mild hy dropexias in which a progressive improvement of the echographic signs is seen, or when a foetal haemoglobin $8 g/dl can be observed. • Foetal transfusion: This can be considered with haemoglobin values #8 g/dl. f) Poliomyelitis. 1. This can provoke some paralysis in the foetus, as well as intrauterine growth restriction. 2. Isolation measures should be instituted, both for the mother and for the newborn, to avoid dissemination through excreta. g) Rubella (german measles). 1. The risk of congenital German measles is 81 % if the rash is produced between the 12th day and the 12th week with respect to the date of the last menstruation (DLM). If the rash appears before the aforementioned 12th day, there is no risk to consider. 2. Systematic filtering before gestational desire is recommended. 3. Maternal German measles treatment is symptomatic. g) Varicela (chickenpox) 1. Risk of congenital chickenpox. • 0.4 % before week 13. • 2 % between week 13 and week 20. • Minimal risk during the second trimester. • Moderate rate of foetal affectation when the maternal rash is pro duced between 3 weeks and 7-5 days before delivery. • 10-20 % when the maternal rash is produced between 5-10 days before or after delivery. 2. Symptomatic maternal treatment and isolation during the contagious period. Attention to chickenpox pneumonia that, although it is not the most frequent, it is the most serious result and generally requires hospital admission. The use of hyper-immune immunoglobulins systematically is not recommended, unless the patient is immuno-depressed.

Reference. Carrera JM, Mallafré J. Serra B: Infections Disease in Pregnancy. In: Recommendations and guidelines for Perinatal Medicine. Matres Mundi/WAPM. Barcelona, 2007; 14: 120-133.

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B.4.14.â&#x20AC;&#x201A; LISTERIOSIS CONCEPT 1.

Listeria Monocytogenes is a gram-positive aerobic bacteria. It is found particularly in soft cheese, milk, vegetables and seafood. 2. Asymptomatic carriers exist in the digestive tract and vagina. 3. The disease is generally benign in the mother, but the foetus can be seriously affected (abortion, intrauterine death) Infection during pregnancy is often asymptomatic. Some patients can present a pseudo-flu symptomatology, characterised by chills, fever and lumbar pain; this occasionally mimics a pyelonephritis. It can begin as a threat of preterm birth, or as the work of preterm birth founded on brownish liquid that can be confused with meconium. Foetal infection can be produced by: a) Transplacental infection. Foetal haematogenic dissemination (foetal septicaemia) is produced from the placenta. b) Amniotic infection. Infection produced by swallowing or breathing liquid contaminated with foetal urine. c) Ascending infection. From the cervix, where the listerias are lodged, and through the ovular membranes. d) Transcervical infection. At the moment of delivery, when the foetus passes through a contaminated cervical canal.

DIAGNOSIS a) Listeriosis must be suspected in the following circumstances: 1. Antecedents of abortions, stillborn foetuses or neonatal sepsis. 2. Febrile outbreaks of uncertain etiology (pseudo-flu syndromes, pseudopyelitics, etc.). 3. Women in contact with rodents or birds (rural or professional settings), or who consume unpasteurized milk or raw meat. b) During pregnancy. Listeriosis is clinically difficult or impossible to identify. Laboratory tests (serological) must therefore be used.

TREATMENT Ampicillin 1 g/6 h and gentamicin 2 mg/kg/8 h for 7-14 days, intravenously. Antibiotic prophylaxis during pregnancy is not recommended.

SANITARY-DIETETIC RECOMMENDATIONS TO PREVENT LISTERIOSIS FROM CONTAMINATED FOOD a) b) c) d)

Cook raw meat from calves, pigs and colts thoroughly. Wash raw vegetables carefully before eating them. Keep raw meat separate from vegetables and precooked or cooked foods. Avoid consumption of non-pasteurised milk or dishes prepared with raw milk. e) Wash your hands, the knives and the cutting boards after having worked with raw foods.

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Avoid soft cheeses (brie, camembert, etc.) and choose cured cheeses, cream cheese, cottage cheese or yoghurt instead. g) Precooked food must be reheated. Reference. Carrera JM, Mallafré J, Serra B: Infection Disease in Pregnancy. In: Recommendations and Guidelines for Perinatal Medicine Matres Mundi/WAPM. Barcelona, 2007; 14: 120-133.

B.4.15. CYTOMEGALOVIRUS CONCEPT It is a viral infection caused by cytomegalovirus (CMV), which belongs to the herpes virus group. The majority of patients with CMV infections are asymptomatic o present a febrile syndrome or more rarely a mononucleosis syndrome in patients with normal immune system.

DIAGNOSIS IN THE PREGNANT WOMAN 1. 2.

Systematic study of all pregnant women is not recommended. CMV infection should be excluded in the presence of suggestive clinical features or any cause of immunodeficiency (HIV infection) 3. It is particularly important to exclude CMV infection when early intrauterine growth retardation is diagnosed especially in association with enlarged organs, as well as in the presence of microcephaly, hydrops fetalis or polyhydramnios. 4. Very high serological titers of lgG-and IGM-specific CMV antibodies are found. The diagnosis of fetal CMV infection should be confirmed by CMV DNA identification by PCR in the amniotic fluid.

DIAGNOSIS IN THE NEWBORN The diagnosis of CMV infection may be suspected in the presence of intrauterine growth retardation, microcephaly, and petequiae.

TREATMENT 1.

There is no approved treatment for the management of congenital CMV infection. In infants with high viral load, infection of the nervous system, or severe thrombocytopenia, attempts have been made with i.v. gamma globulin and gamnciclovir (6 mg/kg/dose i.v. every 12 h during 6 weeks), with frequent haematological controls due to the risk of neutropenia. Breastfeeding is not forbidden. Freezing breast milk and pasteurization re duces virus transmission, and should be considered in premature infants born to CMV carrier mothers.

Reference. Carrera JM, Mallafré J, Serra B: Infection Disease in Pregnancy. In: Recommendations and Guidelines for Perinatal Medicine Matres Mundi/WAPM. Barcelona, 2007; 14: 120-133.

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B.4.16. TOXOPLASMOSIS CONCEPT 1. This is an anthropozoonosis disease caused by Toxoplasma gondii. Foetal infection takes place through the placenta, as a consequence of primary maternal infection during gestation. 2. The risk of foetal transmission increases with gestational age; however, at the same time, the severity of the affectation decreases. 3. Occasionally, it causes a non-specific picture, with fever, general feeling of illness, lymphadenopathies, photofobia and/or painful cervical adenopathies. 4. The most frequent congenital foetal pathology is chorrioretinitis, although up to 87 % of congenital toxoplasmosis cases are asymptomatic at birth or present non-specific symptoms.

PREVENTION a) Measures of primary prevention are vital, as they avoid contact with the invasive form of the toxoplasma (cyst or trophozoite): 1. Avoid contact with the transmitting agent of the disease (especially cats) or materials that might be contaminated by their faecal matter. 2. Always cook meat at temperatures above 66 ºC, to achieve cyst inactivation. 3. Wash fruit and vegetables properly. b) Secondary prevention consists in serological determination of the maternal immunological state against the toxoplasma, thus establishing the diagnosis of the disease. Diagnosis of seroconversion can be simple, but establishing the chronology of the infection is difficult when the prior immunological situation of the mother is unknown (see Diagnosis).

DIAGNOSIS A toxoplasmosis must be suspected when faced with the following circumstances: 1. A pregnant woman with lymphadenopathy, fever and fatigue. The clinical picture sometimes simulates infectious mononucleosis. Any adenopathy during gestation must make the doctor suspect a toxoplasmosis. 2. A pregnant woman who consumes meat that is not well-cooked or who is in contact with animals chronically infested (cats, dogs, pigeons, chicken). Diagnosis of maternal infection during pregnancy is established by: Maternal seroconversion through determination of specific antibodies against the toxoplasma.

TREATMENT 1.

When a maternal infection is diagnosed and while waiting for confirmation of foetal infection, spiramycin 4 g/8 h should be administered for 3 weeks. Following this, the cycle is repeated every 2 weeks or the treatment is continued uninterrupted until delivery. 2. When foetal infection is diagnosed (through detection of toxoplasma DNA or the parasite itself in amniotic fluid):

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a) First trimester: spiramycin, 1 g/h continuously. b) Second and third trimester: pyrimethamine (Daraprim®), 25 mg/day, and sulphadiazine (Flammazine®), 4 g/day in 3-week cycles, alternating with 3 weeks of spiramycin. Supplement with folinic acid, 10 mg/12 h. Reference. Carrera JM, Mallafré J, Serra B: Infection Disease in Pregnancy. In: Recommendations and Guidelines for Perinatal Medicine, Matres Mundi/WAPM; Barcelona, 2007; 14: 120-133.

B.4.17. MALARIA IN PREGNANCY CONCEPT Malaria is caused by infection with one or more of four species of Plasmodium (p. falciparum, P. vivax. P. ovale, and P. malariae) and is a devastating health problem. It is transmitted by the bite of an infective female Anopheles sp. Mosquito although it can be also transmitted through transfusion of infected blood and from the mother to the fetus.

PUBLIC HEALTH PROBLEM 1. As a result malaria is becoming one of the major indirect causes of maternal death along with HIV/AIDS. Pregnant women, particularly in the second and third trimesters are more likely to develop severe malaria than other adults, often complicated by pulmonary edema and hypoglycemia. Maternal mortality is 50 % higher than in the non-pregnant period. 2. The commonest complications are: maternal anaemia, spontaneous abortion, still birth, premature labour, and low birth weight.

DIAGNOSIS 1. 2.

Clinical: Fever, chillness, rigor, anaemia, headache, joint pain etc. Laboratory: Blood film (thin and thick), Rapid Diagnostic test (RDT).

PREVENTION OF MALARIA IN HIGH TRANSMISSION AREAS Intermittent preventive treatment (IPT): In high transmission area, despite the adverse effects on fetal growth, malaria is usually asymptomatic in pregnant women and hence IPT minimizes the effect of malaria in pregnancy.

TREATMENT Sulfadoxin pyrimethamine (SP), 500 1 25 mg, three doses to be given after quickening (first fetal movement) at least one month apart. Pregnant women with the following condition would benefit from this IPT regimen: 1. Pregnant women in their first and second trimester. 2. HIV positive. 3. Aged 10 to 24 years.

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4. Have unexplained anaemia during pregnancy. 5. Live in low malaria transmission area. 6. Migrated from low malaria transmission areas. SP should not be given to pregnant women whose gestational age is less than 16 weeks (4 months). Dosage forms: sulfadoxine (500 mg)-pyrimethamine (25 mg) 3 tablets orally as a single dose. References. Standard Treatmen Guidelines for General Hospital. Drug Administration and Control Anthority of Ethiopia Contents, 2010. | Cabero L. Calle A: Tropical Disease and Pregnancy. In: Recomentadions and Guidelines for Perinatal Medicine. Matres Mundi/WAPM. Barcelona, 2007; 15: 134-150.

B.4.18. HIV/AIDS IN PREGNANCY CONCEPT The infection is caused by the «Human Immunodeficiency Virus» (HIV) that produce a longstanding immunodeficiency syndrome.

IMPORTANCE 1. In the last 20-25 years HIV/AIDs has become the major indirect killer of mothers in pregnancy and delivery. 2. The majority of HIV/AIDS women (77 %) live in Sub-Saharan Africa, being 57 % of the adult HIV positive population. 3. Child transmission (MTCT) during pregnancy (5-10 %) and in labour and delivery (10-15 %). 4. Quite significant numbers could be infected through breast feeding (5-20 %). 5. Pregnancy by itself does not affect the course of the disease, but HIV may increase the risk of premature deliveries, small for gestational age and the rate of still births. 6. Factors that influence MTCT include: maternal viral load, nutritional status of the mother, presence of concomitant parasitic infection like malaria, severe immunodeficiency, advanced HIV/AIDS stage, presence of PROM and injury to the fetus and birth canal during labour and delivery.

DIAGNOSIS a) Clinical. 1. Symptoms suggestive of opportunistic infections/malignancies or direct effects of HIV. 2. History of seropostivity, history of HAART anf other HIV/AIDS related illnesses, duration of illness, status of partner, WHO staging, any medication given for HIV-related illnesses since the beginning of pregnancy. b) Laboratory. 1. Serological test for HIV after conseling… If she is HIV positive CD4 count, viral load, baseline tests such as CBC, RFT, LFT tests.

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2. 3.

Test for syphilis (VDRL), Hgb. Test for opportunistic infections like TB.

PREVENTION a) HIV women who intend to get pregnant: The following general health measeure should be taken: 1. Adequate nutrition that includes: high calories and food rich in iron, micronutrient supplementation such as iron, zinc and folic acid at least for three months prior to getting pregnant. 2. Prevention of malaria infection. 3. Prevention and treatment of STIs. 4. Prophylaxis and treatment of opportunistic infections. 5. Avoid pregnancy for at least six months following recovery from TB and other opportunistic infections. 6. Administer ART for eligible women, if not already on treatment and ARVs for PMTCT for those who are not eligible for ART. b) During antenatal care (ANC): Advocate the benefits of VCT and persuade all pregnant women to be tested. If the any pregnant woman turns out to be positive apply the primary preventive measures that include; early and appropriate treatment of STI, education about safer sex practice during pregnancy and lactation. c) Intrapartum care: Labour and delivery: These include, avoiding invasive procedures, application of infection prevention and performing elective C/S on selected patients. d) Post partum care: Avoidance of breast feeding or exclusive breast feeding.

PMTCT CLINICAL SCENARIOS AND ARV REGIMENS: a) Scenario 1. Women who become pregnant while on ARV treatment: 1. Women on EFV. • Consider possible teratogenicity in 1st trimester. • Stop EFV and start NVP if in the 1st trimester. • Continue EFV if already in 2nd or 3rd trimester. • Discuss with ARV trained physician. • If co-infected with TB, consider other options (e.g. triple NRTI) but not PI based as first line. 2. Women on d4T/3CT/NVP OR AZT/3TC/ NVP. • Continue treatment. • ALT monthly when indicated. 3. Women on AZT/DDI/LPV/r. • Continue treatment. • Full blood count monthly. • Monitor sugar levels as appropriate. • In the presence of severe Anaemia (Hgb , 7 mg/dl) → switch to D4T from AZT. b) Scenario 2. Pregnant women eligible for ART. WHO Guidelines-screen for ART Eligibility.

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WHO CLINICAL STAGING

CD4 NOT AVAILABLE

CD4 AVAILABLE

Do not treat.

Treat if CD4 , 200

Treat.

Treat if CD4 , 350

Treat.

Treat at any CD4

Pregnant women who present with CD4 , 350/mm3, with WHO stage III, IV disease or CD4 , 200/mm3 and stage I,II disease. Start first-line treatment: • AZT 300 mg every 12 hours. • 3TC 150 mg every 12 hours. • NVP 200 mg daily for 2 weeks, then 200 mg every 12 hours. 2. Pregnant women with early stage HIV, or not requiring ARV therapy according to protocol: Follow national protocol mentioned above. c) Scenario 3. Pregnant women not eligible for ART but require prophylaxis. 1. Women presenting in pregnancy where ART is available. Mother: AZT 300 mg BID starting at 28 weeks of pregnancy or as soon as thereafter, NVP 1 AZT/3TC during labour (NVP 200 mg single dose, AZT 600 mg at onset of labor and 3TC 150 mgg every 12 hours until delivery) and AZT/3TC (AZT 300 mg BID and 3TC 150 mg BID) for 7 days in the postpartum period. Infant: NVP (single dose 2 mg/kg) 1 AZT (4 mg/kg/day) for 7 days. If mother has less than 4 weeks on AZT before labour, then AZT should be extended to 4 weeks. 2. Women presenting during pregnancy in facilities without ART services. Mother: NVP 200 mg at the onset of labour. Infant: NVP 2 mg/kg within 72 hours. d) Scenario 4. Pregnant women presenting in labor. 1. Women presenting in labor who have not received antenatal prophylaxis; where ART is available. Mother: Intrapartum: NVP 1 AZT/3TC, in the postpartum period AZT/3TC for 7 days. Infant: NVP and AZT for 4 weeks. 2. Women presenting in labor who have not received antenatal prophylaxis; where ART not available. Mother: NVP 200 mg at the onset of labour. Infant: NVP 2 mg/kg within 72 hours. e) Scenario 5. Woman and child presenting post-partum. Women who present after giving birth without previous ART: Mother: Before contemplating to give drug evaluate for ART eligibility. Infant: NVP 2 mg/kg within 72 hours. (For S/Es, C/Is and dosage forms of different ARVs, see under HIV/AIDS). 1.

References. Standard Treatment Guideline for General Hospitals. Drug Administration and Control Authority of Ehiopia Contents, 2010. | Coll O., Hernández S, Pascual J: Acquired immunodeficiency Syndrome (AIDS) in Pregnancy. In: Recommendations and Guidelines for Perinatal Medicine. Matres-Mundi/ WAPM. Barcelona, 2007; 16: 151-159.

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Clinical Staging of HIV Disease. World Health Organization Classification System Clinical Stage 1 1. Asymptomatic infection. 2. Persistent generalized Lymphadenopathy. 3. Acute Retroviral (HIV) Syndrome. Performance Status 1: asymptomatic, normal activity. Clinical Stage 2 1. Unintentional weight loss ,10 % body weight. 2. Minor mucocutaneous manifestations (e.g., PPE seborrheic dermatitis, prurigo, fungal nail infections, cheilitis). 3. Herpes zoster within previous 5 years. 4. Recurrent upper respiratory tract infections. Performance Status 2: symptoms, but nearly fully ambulatory. Clinical Stage 3 1. Unintentional weight loss .10 % body weight. 2. Chronic diarrhea .1 month. 3. Prolonged fever .1 month (constant or intermittent). 4. Oral candidiasis. 5. Oral hairy leukoplakia. 6. Pulmonary tuberculosis within the previous 2 years. 7. Severe bacterial infections. 8. Vulvovaginal candidiasis. 9. Unexplained Anaemia, Neutropenia or chronic thrombocytopenia. Performance Status 3: in bed more than normal but ,50 % of normal daytime during the previous month. Clinical Stage 4 1. HIV wasting syndrome. 2. Pneumocystis carinii pneumonia. 3. Toxoplasmosis of the brain. 4. Crytosporidiosis with diarrhea .1 month. 5. Isosporiasis with diarrhea .1 month. 6. Cryptococcosis, extrapulmonary. 7. Cytomegalovirus disease of an organ other than liver, spleen or lymph node. 8. Herpes simplex virus infection, mucocutaneous. 9. Progressive multifocal leukoencephalopathy. 10. Any disseminated endemic mycosis (e.g., histoplasmosis). 11. Candidiasis of the esophagus, trachea, bronchi, or lung. 12. Atypical mucobacteriosis, disseminated. 13. Non-typhoid Salmonella septicemia. 14. Extrapulmonary tuberculosis. 15. Lymphoma. 16. Kaposi’s sarcoma. 17. HIV encenphalopathy. 18. Visceral Leishmaniasis. 19. HIV-associated cardiomyopathy. 20. HIV-associated nephropathy. Performance Status 4: in bed .50 % of normal daytime during previous month.

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Drug information on Antiretrovial drugs DRUG

MAJOR S/E

C/I

DOSAGE FORMS

NRTIs Zidovudine

Anaemia, nausea, hyperpigmentation.

Severe nemia

Didanosine

Pancratitis, neuropathy.

Tablet, 25 mg, 150 mg; chewable/ dispensable, 100 mg.

Lamivudine

Gl disturbances.

Tablet 150 mg; Oral solution, 100 mg/ml.

Stavudine

Pancratitis, neuropathy, liver damage.

Capsule, 15 mg, 20 mg, 30 mg, 40 mg; Oral solution, 100 mg/ml.

Abacavir

Hypersensitivity.

Emitricitabine

Headache, diarrhea, nausea, rash.

Tenofovir

Gl disturbances.

Hypersensitive to it

Tablet, 150 mh, 300 mg; Capsule, 100 mg, 250 mg; Syrup, 50 mg/ml; I.V. infusion, 10 mg/ml.

Tablet, 300 mg. Tablet 100 mg. Tablet 300 mg.

NNRTIs Efavirenz

Skin rashes.

Capsule 50 mg, 100 mg, 200 mg.

Nevirapine

Hepatitis, rash, fever, arthralgia, myalgia.

Tabler, 200 mg; Oral suspension, 50 mg/5 ml. Pis

Indevanir

Nephrolithiasis, thrombocytopenia, GL disturbances.

Nelfinavir

Capsule, 200 mg, 400 mg.

Tablet, 250 mg; Oral solution, 50 mg/ml

Ritonavir

Paresthesia, altered taste, Gl disturbances, hyperlipemia, liver damage.

Capsule, 100 mg; Oral solution, 80 mg/ml

Saquinavir

Gl disturbances.

Capsule, 200 mg; Tablet, 500 mg; Oral solution, 80 mg/vial.

Atazanivir

Headache, nausea, Know vomiting, diarrhea, hypersensitivity rash, itching, swelling.

Tablet, 100 mg, 150 mg, 200 mg.

Emitricitabine 1 1 T enovofir

The combination of individual S/ls.

Fixed Combinations Tablet, 200 mg 1 300 mg.

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Drug information on Antiretrovial drugs (continuation) DRUG

MAJOR S/E

C/I

DOSAGE FORMS

Lamivudine1 1 Stavudine

The combination of individual S/ls.

Tablet, 150 mg 1 30/40 mg.

Lopinavir 1 1 Ritonavir

The combination of individual S/ls.

Capsule, 133.33 mg 1 33.33 mg; Tablet, 200 mg150 mg; oral Suspension, 80 mg 1 20 mg/5 ml.

Efavirenz1 1 Emiticitabine 1 1 Tenofovir

The combination of individual S/ls.

Tablet, 600 mg 1 200 mg 1 1 300 mg.

Lamivudine 1 1 Nevirapine 1 1 Stavudine

The combination of individual S/Is.

Tablet, 50 mg 1 200 mg 1 1 39/40 mg.

Lamivudine 1 1 Zidovudine 1 1 Nevirapine

The combination of individual S/ls.

Tablet, 150 mg 1 300 mg 1 1 200 mg.

B.4.19. STREPTOCOCCUS AGALACTIAE GENERAL CONCEPTS 1.

Streptococcus agalactiae or Group B streptococcus (Group B strep or GBS) is a gram-positive coccus that fundamentally causes infections in newborns, pregnant women and adults having other diseases. 2. GBS is at present, in the absence of prevention measures, the most frequent cause of vertically-transmited perinatal bacterial infection. 3. The gastrointestinal tract is the reservoir of GBS. Vaginal colonisation is intermittent, and the colonisation rate in pregnant women ranges from 11 % to 18 %. 4. CGS transmission from the mother to the newborn mainly occurs at the beginning of delivery, or following rupture of the membranes. The frequency of colonisation of newborns from colonised mothers is around 50 %, and 1-2 % of colonised newborns develop infection.

DETECTION OF CARRIERS 1. If possible, a vaginal and rectal culture should be performed on all pregnant women between the 35th and 37th week of gestation. 2. If the pregnant female has had bacteriuria from GBS during the gestation, or if antecedents of a child with GBS neonatal infection exist, it is not necessary to do the culture and prophylaxis should always be administered. 3. The culture must be repeated if after 5 weeks take place between the woman remain undelivered.

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Samples are obtained from the external third of the vagina (a speculum is not required) and from introducing a swab in the rectum. Cervical cultures are not acceptable. In a programmed caesarean, even though the culture is positive for GBS, prophylaxis is not given, as long as the delivery has not begun and the membranes are intact.

ANTIBIOTIC RECOMMENDATIONS •

•

Drug of choice. Intravenous penicillin G, 5 million units as an initial dose at the beginning of labour; repeat 2.5 million units every 4 hours until the baby is born. Antibiotic of second choice. Intravenous ampicillin, 2 g when the labour begins; repeat 1 g every 4 hours until the baby is born. If the woman is allergic against Penililin an antibiogram should be requested.

Reference. Carrera JM, Mallafré J, Serra B: Infections disease in Pregnancy. In: Recommendations and Guidelines for Perinatal Medicine, Matres Mundi/WAPM. Barcelona, 2007: 132-133.

B.4.20. CHAGAS’ DISEASE GENERAL CONCEPTS 1.

It is an infection caused by Tripanosoma cruzi transmitted to humans by bugs of the genera Triatome, Panstrongylos and Rhodanius. 2. The infection is transmitted by reduviid bugs in endemic areas and blood transfusion or transplantations in non-endemic areas. The disease is occasionally transmitted via the placenta to the newborn infants. 3. There is no evidence of passage of infection through the breast milk, so that breastfeeding in positive mothers is allowed.

DIAGNOSIS Demonstration of T. cruzi in a concentrate leukocyte culture (parasitological diagnosis), or positive serological serum antibody by ELISA, Western blot (serological diagnosis).

TREATMENT 1. Treatment is only indicated if parasitological and immunological tests are positive. 2. Benzonidazol orally 5-7 mg/kg/day during 60 days. 3. In infants weighing ,3,000 g treatment should be initiated with 2-3 mg/kg/ day, assessing haematological tolerance, and increasing the dose along one week until the standard dose. Reference. Cabero L, Calle A: Tropical Diseases and Pregnancy. In: Recommendations and Guidelines for Perinatal Medicine, Matres Mundi/WAPM. Barcelona, 2007: 138-142.

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B.4.21. INJURIES DURING PREGNANCY CONCEPT a) The injuries of diverse origin and traffic accidents are, in some geographical areas, the leading cause of non-obstetric maternal death. b) The correct treatment of this condition requires prompt attention of the mother and proper coordination between the various specialists involved.

INITIAL EMERGENCY MEASURES When there is a pregnant woman in critical condition, the following measures shall be implemented successively: a) Resuscitation measures. 1. Rapid assessment of the constants. Call for the necessary specialists. 2. Maintenance of the airway. Intubation, if necessary. 3. CPR, heart massage, etc. 4. Treatment of shock. b) Diagnostic measures. 1. Interrogation of the patient or their family about the circumstances of traumatism. 2. Meticulous physical examination, while starting the treatment of severe head, thorax and abdomen injuries. Stabilization of possible fractures with splints. 3. General Analytical blood count. 4. Radiologic studies, according to specific circumstances and using abdominal protection. 5. Exhaustive examination of the abdomen. • Bladder catheterization. • External examination of the abdomen (fetal size, uterine contracture, pain, fetal auscultation, etc.). • Vaginal examination (fetal presentation, cervical conditions, vaginal bleeding, amniorrhexis, etc.). c) Evaluation of the fetal state. 1. Cardiotocographic Monitoring. 2. Ultrasound (fetal vitality, potential fetal trauma, placental abruption, etc.). d) Prophylaxis against tetanus. 1. If you know that she was vaccinated: 0.5 ml of tetanus toxoid. 2. Unvaccinated patients: 250-500 u intramuscular immune serum globulin and 0.5 ml of tetanus toxoid. 3. If there is significant tissue necrosis: increase serum immunoglobulin 400 U, and take prophylaxis with antibiotics.

BLUNT ABDOMINAL TRAUMA Its origin can be a fall, more often, at present, an automobile accident. The most immediate obstetric complications that may occur after this type of injury are premature detachment of membranes, preterm labor, uterine rupture and premature rupture of membranes.

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a) Diagnostic measures. 1. Women who have suffered minor trauma: • Cardiotocographic examination for 30 min (if pregnancy over the 25 weeks). • Ultrasound examination, trying to determine fetal status and possible premature discharge of the placenta. 2. Women who have suffered major trauma: • Evaluation of possible hemoperitoneum (liver, splenic or vascular trauma). • Evaluation of fetal conditions. −− Detailed sonographic examination. −− Laparoscopy / laparotomy, in case of doubt about a possible hemoperitoneum. b) Therapeutic measures. 1. In case of a non-significant blunt trauma, it is advisable the observation with proper maternal and fetal assessment only for a few hours. 2. If the trauma is important, decisions depend on the intrauterine situation and the possibility of hemoperitoneum that directs towards visceral or vascular lesion. • Apparent normality (good fetal vitality, with no signs of hemoperitoneum, etc.): careful observation for 48 h, with repeated CTG, ultrasound and analytical tests (fibrinogen, Kleihauer). The abruption may occur up to 5 days after the trauma. • Clinical evidence of placental abruption with a live fetus requires performing a cesarean section. • Confirmation of a hemoperitoneum requires an immediate laparotomy (Medium and large incision) by a trained, multidisciplinary surgical team. The objective is to evaluate the lesions, control the bleeding and repair the affected organs. −− If the fetus is well and immature: not to do a Caesarean. −− If the fetus is mature, it is dead or the presence of gravid uterus hinders the adequate exposure of the injured organs: Caesarean section is to be performed. −− If there is an extensive uterine rupture: a cesarean-hysterectomy must be performed.

PENETRATING ABDOMINAL TRAUMA a) Basics concepts. 1. Most times produced by gunshot or stab. Less often, wounds are originated by a different kinds of accident. 2. In all cases, the large gravid uterus protects the remaining intra-abdominal organs and for this reason the maternal prognosis is good. By contrast, the prognosis for the fetus is 40-80 % mortality. b) Behaviour. 1. Measures to stabilize the patient. 2. Ballistic trauma.

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•

Diagnosis: −− Locate bullet (radiology). −− Fetal condition (ultrasound). • Treatment: −− Bullet in the utero, with a living fetus: assess whether to perform an immediate caesarean section (possible fetal injury, amnionitis, etc.) or whether to do it after fetal maturation. −− Bullet in utero with a dead fetus: consider a conservative attitude, practicing laparotomy only if there are signs of peritonitis. −− Extrauterine bullet: laparotomy (possible visceral lesions). Cesarean section will be performed only if the fetus is mature or dead, and if the mother’s condition is very unstable. Stab wound. • Diagnosis: −− Peritoneal penetration (physical examination, Fistulography, etc.). −− Fetal condition (ultrasound). • Treatment: −− There is no peritoneal penetration: observation. −− Peritoneal penetration in the upper abdomen: immediate surgical exploration. −− Peritoneal penetration in the lower abdomen (possible uterine injury, but not visceral): A. Stable, with immature fetus patient: strict observation. B. Unstable patient: immediate surgical exploration. Fetal extraction given the circumstances.

PELVIC FRACTURES a) When suspecting a pelvic fracture in a traumatized pregnant woman, it is urgent to assess whether it is a complicated fracture (retroperitoneal hematoma, urinary trauma, etc.). b) Procedure. 1. Uncomplicated fracture: symptomatic treatment. 2. Complicated fracture: • Injury repair (urinary, etc.). • Hemostasis. The hemostasis of the gluteal artery superior can be especially difficult, in some cases requiring the ligation of the internal iliac artery (fetal compromise). c) Type of birth. It will depend on the distortion of the pelvic canal and the presence of urinary injuries that required surgical repair.

BURNS a) The fetal prognosis depends on the mother. The percentage of body surface and its depth is directly correlated with the maternal prognosis. When the burned body surface is 40 %, maternal mortality is 2-4 % and fetal of around 20 %. If the extension reaches 50 %, maternal mortality raises to 25 %, and fetal up to 50 %.

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b) Procedure: 1. Burn Treatment according to the usual rules (prevent hypovolemia, sepsis, acidosis, etc.). 2. The most common obstetric complication is preterm birth. It is triggered by dehydration and hypoxemia. The treatment of APP should be individualized. The use of betamimetics is contraindicated. 3. Obstetrically, if the extension of the affected body surface is greater than 50 %, the fetal extraction is indicated during the first few hours, provided that the fetus is considered viable.

PERIMORTEM CAESAREAN a) It is rarely necessary, but is performed in patients alive with viable fetus, which has not been successful with maternal resuscitation for a period of 4 min. 1. To be considered when the mother has died or her chances of survival are minimal. 2. The best chances of neonatal survival occur when the pregnancy has exceeded 28 weeks, the fetus weighs more than 1,000 g and the interval between the maternal and fetal death extraction is less than 10 min. 3. If maternal brain death occurs, but the cardiovascular function is maintained and stable, could be maternal life artificially, prolonged in cases where the fetus is immature, reaching its viability. b) Technique. The caesarean section should be immediate and quick «stabbing» by performing a vertical incision from the xiphoid to the pubis, without identification of parietal planes and accessing the fetus through a wide body longitudinal uterine incision. Reference. Carrera JM, Mallafré J, Serra B: Protocolos de Obstetricia y Medicina Perinatal del Instituto Universitario Dexeus. 4th Edition, Elsevier. Barcelona, 2005: 337-339.

LABOUR

C.1.

LABOUR ATTENDANCE

C.1.1. MANAGEMENT OF NORMAL LABOUR ADMISSION It refers exclusively to systematic measures applied from the time of admission of the patient a) Previously, the patient should be warned of symptoms that should advise her admission. 1. Uterine more or less rhythmic contractions. 2. Rupture of membranes with amniotic fluid ejection. 3. Blood loss. b) At the time of admission, one should not omit the following measures: 1. Immediate consultation of perinatal history, with the aim of knowing the case (obstetric or associated pathology, risk pregnancy, serology, state if streptococcus agalactiae carrier, etc.). 2. In the meantime, the staff should perform an analytical control of urine (Proteinuria, glucose, pH, etc.). 3. Interrogation of the patient, to determine the circumstances in which childbirth started (ruptured membranes, contractions, etc.). 4. External Abdominal examination, between contractions, to pinpoint the fetal location and fetal heartbeat. 5. Aseptic vaginal examination to define: • Type of presentation. • Degree of encasement. • Cervical dilation and characteristics of the cervix. • Features of the pelvis. • Existence of intact membranes. • Possible pathology: prolapses, meconium, etc. This exploration should be skipped in amniorrhexis in preterm gestation and it should be substituted by a sterile speculoscopy. 6. A brief general exploration should also be made. It should include:

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• Constants: TA, blood pressure, pulse and temperature. • Identification of edema, conjunctival staining, etc. c) If there are doubts about the actual onset of labor: 1. Registration CTG with a minimum duration of 30 min to evaluate the uterine dynamics. 2. It is necessary to repeat the cervical exploration after 60 min from the previous one to see if there have been modifications in the cervical range. d) If there are doubts about the amniorrhexis, try to clarify the diagnosis by: 1. Checking the pH of the vaginal content (blue-green reaction with nitrate paper). 2. Cytology. 3. Bracken form of vaginal fluid by placing it on a slide and drying it.

DILATATION PERIOD a) General assistance. When there is no doubt that labor has begun, the following measures are to be taken: 1. Perineal cleaning of external genitals with an aseptic solution. 2. Shower, if considered necessary. 3. The patient should stay in bed if the membranes are broken and the presentation is not engaged. In the remaining cases walking around could be allowed, since it generally has a positive influence in on the duration and tolerance of childbirth. The mother should be allowed to take the position in which she is most comfortable. 4. Adequate psychological support of pregnant women should be provided. The presence of the couple or a family memeber in the delivery room should be promoted. b) Obstetric care. 1. Control of the progress of labor. • External abdominal exploration. • Periodic and sterile vaginal exploration evaluating cervical dilation and descent and rotation of the presentation (attitude, position, etc.). Although there are no rules on the frequency of these examinations, it is considered that, with a well-established labor, they must be performed at least every 2 h. c) Fetal Control. 1. Ideally, continuous and permanent monitoring but in «low risk» can to be intermittent. Perform external monitoring of both the FHR and uterine dynamic. This might not be feasible to perform in two circumstances: • Lack of this resource. • Intact membranes, not allowing internal register. 2. If one does not have electronic monitoring, it is possible to perform: • Fetal auscultation by stethoscope, every 15-30 minutes during the first phase of the delivery process. • Fetal auscultation using a Doppler apparatus. It is better to auscultate at the end of the contractions (in order to detect a late decele ration).

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•

Periodical determination of the fetal pH if anomalies of the FHR are found. 3. If the membranes remain intact: • Perform external monitoring of both the FHR and the uterine dynamics, continuously and permanently (this may be uncomfortable for the patient). • Perform periodical monitoring for 20 minutes every 60-80 minutes, allowing the patient to walk during the intervals if there are no contraindications. 4. In all cases, if anomalies of the FHR where the fetus is suffering are registered, it is necessary to perform: • An artificial amniorrhexis (if the membranes are still intact). • Determination of the fetal acid-base balance. d) Control of the mother in labor. 1. Control of vital signs: blood pressure, pulse, breathing and temperature. These controls are carried out every 15 min if epidural anesthesia has been applied. 2. Perform uterine dynamics control, either by electronic CTG or by timing contractions at regular intervals. 3. Control diuresis (it must exceed 30 ml/h). 4. Urine analysis (proteins, glucose and acetone) every six hours. 5. Attention to the emotional state of the patient. e) Therapeutic Conduct. 1. Sedation and pain relief with analgesics or antispasmodics (eg., Dolantine). It is not advisable too sedate the patient in the last stages of labor. 2. Stimulation with oxytocin if a persistent hypodynamy occurs. 3. Epidural analgoanesthesia. Only if necessary and under the following conditions: • 3-4 cm in a nullipara. • Dilatation and cervix softening and thinning in a multiparous woman. 4. Proper hydration by intravenous infusion.

EXPULSION PERIOD a) Preparation. 1. Placing the patient in dorsal lithotomy position on an appropriate delivery table. There are some alternatives: • Sitting position (in an obstetrical table with backup or designed specifically for this position). • Squat, if not on a permanent basis, sometimes (it presents some difficulties for conventional medical care). 2. Catheterization with disposable probe. 3. Cleaning and antisepsis of the external genitalia, perineum, mons, proximal part thighs and anal region by chlorhexidine solution. 4. Placement of sterile drapes. 5. Preparation of the table with precise instruments. • Small and medium gauze.

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• • • • •

Urinary catheter. Surgical scissors. Kocher forceps (minimum 3). Needle carrier. Suture material (synthetic polyglycolic acid suture fast reabsorption 00 and 0). • Sterile sizes. • Postpartum kit: two Doyen cusps, two clamps foster type, dissection forceps. b) Assistance to the expulsion. 1. Vaginal exam to confirm that the patient is in complete dilatation and with the presentation in 3rd - 4th plane. 2. Allow the patient to start pushing (avoid forced pushing). 3. When the fetal head bulges: Medial-lateral episiotomy. Decide if you can avoid it, especially in multiparous. 4. Adequate protection of the perineum. In some cases, it may be indicated to perform the maneuver of Ritgen. Avoid using the maneuver of Kristeller. 5. External rotation of the head. Discrete expression of Mucus. Release or impingement and separation of the circulars of the cord, if there are any. 6. Drive down the fetal head, in order to lower the anterior shoulder. 7. Lift the direction of traction, releasing the posterior shoulder. An adequate protection of the perineum at this moment is necessary. 8. Once the shoulders have been unattached, hold the infant with the right hand while the left hand remains at the vulvar introitus, wait for the fetal feet, and then hold them with the thumb, index and middle fingers. 9. The infant should remain in a declined position in relation with the mother. Shortly after the cord between the two of them should be cut with Kocher forceps once it has stopped beating. 10. If the expulsion process takes more than 60 minutes for a multipara and more than an 2 hours for a primipara, an instrumental intervention should be considered. Choose the proper instrument (forceps, spatula or uacuum) according to the conditions of the patient. 11. Bladder catheterization. c) Control and treatment of the expulsive. 1. Permanent venoclisis containing oxytocin in case of hypodynamy. Systematic administration during the fetal expulsion. 2. Permanent control of FHR and uterine dynamics through continuous CTG. If not possible, then perform fetal auscultations after each con traction. 3. Frequent monitoring of vital signs: in particular blood pressure and pulse. This control should be stricter if the patient is under the effect of the epidural.

DELIVERY OF THE PLACENTA (Third stage of labour) a) Established assistance. 1. Assessment of signs of placental separation, especially: • Sign of Küstner: move the uterus up. If the cord also ascends, it means the placenta has not yet detached.

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•

Sign of Ahlfeld: With the detachment progress the tweezers should descend. In order to accelerate the process, the maneuver of Wagner (refuse blood to the placenta by putting the tweezers in a higher position) can be applied. This is contraindicated if the patient is a negative Rh. In such case it is recommended to «bleed» the placenta. 2. Placental expulsion, making a gentle massage at the bottom of the uterus and a firm but careful cord traction. 3. If the placenta is not expelled after 20 -30 minutes and the patient has been anesthetized (epidural), it can be manually removed to reduce blood loss. If the patient is a negative Rh, it is recommended to allow a spontaneous birth, if possible. 4. Review of the placenta and cord. 5. Systematic uterine review (In some cases it is compulsory only in surgical delivery). 6. Revision of the channel. 7. Suture the injuries. b) Therapeutic measures. 1. Directed delivery, increasing the speed of the drip of oxytocin when the anterior shoulder of the infant has been detached (alternative: administration of methylergobasine). 2. The drip closes once the fetus expelled, and reopens with the placental expulsion. 3. Take cord blood for analytical: Rh, acid-base balance, Coombs test, etc. Reference. Carrera JM, Mallafré J, Serra B: Protocolos de Obstetricia y Medicina Perinatal del Instituto Universitario Dexeus. 4th Edition, Elsevier. Barcelona, 2006: 355-359.

C.1.2. MANAGEMENT OF DYSTOCIA: PRACTICAL POINTS CONCEPT AND TYPES Management of dystocia depends on the underlying factors. When dystocia is the result of inadequate uterine contractions, oxytocin is used. Dystocia resulting from abnormal fetal position can be corrected and managed by forceps or caesarean delivery.

UNSATISFACTORY PROGRESS OF LABOUR I.

PROBLEMS 1. The latent phase is longer than 8 hours. 2. Cervical dilatation is to the right of the alert line on the partograph. 3. The woman has been experiencing labour pains for 12 hours or more without delivery (prolonged labour).

II.

GENERAL MANAGEMENT 1. Make a rapid evaluation of the condition of the woman and fetus and provide supportive care.

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2. 3.

Test urine for ketones and treat with IV fluids if ketocic. Review partograph.

III. DIAGNOSIS Diagnosis of unsatisfactory progress of labour. FINDINGS

DIAGNOSIS

Cervix not dilated. No palpable contractions/infrequent contractions.

False labour.

Cervix not dilated beyond 4 cm after 8 hours of regular contractions.

Prolonged latent phase.

Cervical dilatation to the right of the alert line on the partograph: –– Secondary arrest of cervical dilatation and descent of presenting part in presence of good contractions. –– Secondary arrest of cervical dilatation and descent of presenting part with large caput, third degree moulding, cervix poorly applied to presenting part, oedematous cervix, ballooning of lower uterine segment, formation of retraction band, maternal and fetal distress. –– Less than three contractions in 10 minutes, each lasting less than 40 seconds. –– Presentation other than vertex with occiput anterior.

Prolonged active phase: –– Cephalopelvic disproportion. –– Obstruction. –– Inadequate uterine activity. –– Malpresentation or malposition.

Cervix fully dilated and woman has urge to push, but there is no descent.

Prolonged expulsive phase.

IV. MANAGEMENT a) False labour. Examine for urinary tract or other infection or ruptured membranes and treat accordingly. If none of these are present, discharge the woman and encourage her to return if signs of labour recur. b) Prolonged latent phase. The diagnosis of prolonged latent phase is made retrospectively. When contractions cease, the woman is said to have had false labour. When contractions become regular and dilatation progresses beyond 4 cm, the woman is said to have been in the latent phase. Misdiagnosing false labour or prolonged latent phase leads to unnecessary induction or augmentation, which may fail. This may lead to unne cessary caesarean section and amnionitis. If a woman has been in the latent phase for more than 8 hours and there is little sign of progress, reassess the situation by assessing the cervix. 1. If there has been no change in cervical effacement or dilatation and there is no fetal distress, review the diagnosis. The woman may not be in labour. 2. If there has been a change in cervical effacement or dilatation, rupture the membranes with an amniotic hook or a Kocher clamp and induce labour using oxytocin or prostaglandins: • Reassess every 4 hours.

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If the woman has not entered the active phase after 8 hours of oxytocin infusion, deliver by caesarean section. 3. If there are signs of infection (fever, foul-smelling vaginal discharge): • Step up labour immediately with oxytocin. • Give a combination of antibiotic until delivery: −− Ampicillin 2 g IV every 6 hours. −− Plus gentamicin 5 mg/kg body weight IV every 24 hours. • If the woman delivers vaginally, discontinue antibiotics post partum. • If the woman has a caesarean section, continue antibiotics PLUS give metronidazole 500 mg IV every 8 hours until the woman is feber-free for 48 hours. c) Prolonged active phase. 1. If there are no signs of cephalopelvic disproportion or obstruction and the membranes are intact, rupture the membranes with an amniotixc hook or a Kocher clamp. 2. Assess uterine contractions: • If contractions are inefficient (less than three contractions in 10 mi nutes, each lasting less than 40 seconds), suspect inadequate uterine activity. • If contractions are efficient (three contractions in 10 minutes, each lasting more than 40 seconds) suspect cephalopelvic disproportion, obstruction, malposition or malpresentation/see below). 3. General methods of labour support may improve contractions and accelerate progress. d) Cephalopelvic disproportion. Cephalopelvic disproportion occurs because the fetus is too large or the maternal pelvis is too small. If labour persists with cephalopelvic disproportion, it may become arrested or obstructed. The best test to determine if a pelvis is adequate is a trial of labour. Clinical pelvimetry is of limited value. 1. If cephalopelvic disproportion is confirmed, deliver by caesarean section. 2. If the fetus is dead. • Deliver by caesarean section. e) Inadequate uterine activity. If contractions are inefficient and cephalopelvic disproportion and obstruction have been excluded, the most probable cause of prolonged labour is inadequate uterine activity. Inefficient contractions are less common in a multigravida than in a primigravida. Hence, every effort should be made to rule out disproportion in a multigravida before augmenting with oxytocin. 1. Rupture the membranes with an amniotic hook or a Kocher clamp and step up labour using oxytocin. 2. Reassess progress by vaginal examination 2 hours after a good contraction pattern with strong contractions has been established: • If there is no progress between examinations, deliver by caesarean section. • If progress continues, continue oxytocin infusion and re-examine after 2 hours. Continue to follow progress carefully. •

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Prolonged expulsive phase. Maternal expulsive efforts increase fetal risk by reducing the delivery of oxy gen to the placenta. Allow spontaneous maternal «pushing», but do not encourage prolonged effort and holding the breath. 1. If malpresentation and obvious obstruction have been excluded, augment labour with oxytocin. 2. If there is no descent after augmentation: • If the head is not more than 1/5 above the symphysis pubis or the leading bony edge of the fetal head is at 0 station, deliver by vacuum extraction or forceps. • If the head is between 1/5 and 3/5 above the symphysis pubis or the leading bony edge of the fetal head is between 0 station and 22 station: −− Deliver by vacuum extraction and symphysiotomy. −− If the operator is not proficient in symphysiotomy, deliver by caesarean section. −− If the head is more than 3/5 above the symphysis pubis or the leading bony edge of the fetal head is above 22 station, deliver by caesarean section.

References. Ministry of Health of Rwanda: Labor Dystocia. In: Gynecology and Obstetrics. Clinical Protocols and Treatment Guidelines. Kigali, 2012: 91-92. | Gyllogley KM: Abnormal labor and Delivery. In: Manual of Obstetrics. 5th Edition. Ed. by Niswander KR and Evans AT. A Little Brown. Boston, 1995; 27:415-429.

C.1.3. OBSTETRICIAN PREPARATION FOR CHILDBIRTH GENERAL CONCEPTS 1. The preparation of the obstetrician in charge of the delivery differs from the requirements for a caesarean operation or a laparotomy. 2. The obstetricians outfit should be the usual (trousers, jacket, cap and mask).

METHODOLOGY a) Vaginal delivery. 1. Wear the mask (covering nose and mouth) and the cap properly. 2. Remove bracelets and rings. 3. Wear a plastic apron over your suit. 4. Cover your hands and forearms with soap for at least two minutes. Then, remove with warm water. 5. Clean your nails, fingers and palms using a brush an antiseptic solution for at least one minute. 6. Repeat the action with the forearms. 7. Dip both hands in an antiseptic solution for half a minute. 8. Wear a sterile gown. Your hands should not touch the external surface. (Alternative: wear a sterile apron).

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9. Wear sterile gloves making sure that your hands do not touch the external surface. b) Abdominal delivery. 1. Follow the same rules mentioned above but changing the timing: • Hands brushing: 4-5 minutes. • Forearms brushing: 2 minutes. 2. Always wear surgical gown. Reference. Carrera JM, Mallafré J, Serra B: Protocolos de Obstetricia y Medicina Perinatal del Instituto Universitario Dexeus. 4th Edition, Elsevier. Barcelona, 2005: 362-363.

C.1.4. TRADITIONAL BIRTH ATTENDANT TRAINING (TABs) It is ideal that delivery takes place in a Medical Center, assisted by trained professionals, However, there are circumstances that make it difficult in certain developing countries. In rural areas, located far from hospitals and without proper transport systems, amongst other limitations, women are still giving birth through the traditional procedures, assisted by empirical midwives. In such circumstances, the Na tional Health Systems and some NGOs, provide the midwives a delivery kit with the aim of minimizing infections and further obstetric complications.

CONCEPTS 1. In many developing countries, the majority of the deliveries are not performed by health professionals. 2. Traditional birth attendant are an important source of social and cultural support to women, and the role of TBAs providing support during childbirth is potentially important. 3. TBAs are quite heterogeneous and play a central role in many societies that ignoring them does not seem realistic. 4. The goal of TBA training is to improve each individual’s skills and to strengthen links within the healthcare system. 5. Training programs put emphasis kits kitson infection prevention and include such approaches as the promotion of the «Three Cleants» and the provision of clean delivery kits (CDKs).

THREE CLEANS AND CLEAN DELIVERY KITS a) Three cleans: 1. Clean hands. 2. Clean delivery surface. 3. Clean cord cutting. b) Clean delivery kit: 1. Soap. 2. Plastic sheet. 3. New razor blade. 4. Clean cord ties.

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CLEAN DELIVERY KIT COMPONENTS Step 1: Measuring string for cord ties. Step 2: Cutting string. Step 3: Wrapping cord ties and razor blade into paper packet. Step 4: Cutting soap pieces. Step 5: Cutting sheets of papers into squares. Step 6: Placing wrapped components into kit plastic bag. Step 7: Placing the pictorial instruction sheet into kit plastic bag. Step 8: Sealing kit plastic bag with candle flame. Step 9: Placing delivery kits in large plastic bags for storage.

LIMITATIONS OF THE TBAs 1. A key element of TBAs is be the identification of obstetric complications and their referral. 2. Postpartum haemorrhage is a major cause of maternal mortality, and, unfortunately, timely referrals are not always feasible, as transportation is difficult to obtain and essential obstetric care facilities are often unavailable. This is the major limitation in the role of TBAs. 3. One alternative currently is the postpartum use of Misoprostol.

Reference. Buekens P: Traditional birth Attendant Training. In: Textbook of Perinatal Medicine. 3th Edition. Edit. Asim Kurjak and Frank A Chervenak. Jayppe, New Delhi; 198: 1838-1839.

C.2.

PROCEEDINGS AND TECHNOLOGY

C.2.1.â&#x20AC;&#x201A; INDUCTION OF LABOUR CONCEPT Induction of labour is defined as the initiation of labour by medical or surgical methods before the spontaneous onset of labour leading to birth of the baby. This includes both women with spontaneous rupture of the membranes and with intact membranes that are not in labour.

INDICATIONS Indication for labour is when it is felt that the benefits of finishing pregnancy outweights potential maternal and fetal risks of continuing with gestation when there are not contraindications for induction and the best conditions for labour and delivery can be provided. These are the most common therapeutic indications: 1. Medical and pregnancy complications. 2. Prelabour rupture of membranes at term. 3. Some maternal diseases (diabetes, hypertension...). 4. Chorioamnionitis. 5. Evidence of fetal compromise. 6. Intrauterus fetal death. 7. Prolonged pregnancy. 8. Logistic factors (e.g. long distance from hospital, history of rapid labour...).

RISKS Labour induction is an active procedure with potential risks for the mother and foetus. Some of the possible risks are. 1. Increased rate of operative vaginal delivery, caesarean birth. 2. Excessive uterine activity. 3. Abnormal fetal heart rate (FHR) pattern. 4. Uterine rupture. 5. Maternal water intoxication (rare). 6. Delivery of preterm infant due to incorrect estimation of dates. 7. Cord prolapse with artificial rupture of membranes.

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CONTRAINDICATIONS 1. 2.

Previous classical caesarean section, inverted-T or unknown uterine incision. Previous uterine surgery involving entry to uterine cavity (except the segmentary caesarean surgery). 3. Previous uterine rupture. 4. Active genital herpes. 5. Presence of placenta previa. 6. Transverse lie or any other labour contraindication. 7. Invasive carcinoma of the cervix. 8. Absence of fetal wellbeing.

INDUCTION PREREQUISITES 1.

Before induction begins, the indication and the method of induction for every patient must be clearly established. 2. Precise gestational age and the Bishop score of the cervix must be established. Different reports about labour induction show that the ripeness of cervix is the most important predictor of success. A Bishop score of $6 is considered favourable and is likely to result in successful labour induction (table). Modified bishop’s score SCORE

Dilatation

1-2

2-4

Cervical length

2-4

1-2

Station

21/10

11/12

Firm

Average

Soft

Posterior

Mid/Anterior

PARAMETER

Consistency Position

3. Wherever induction of labour happens, facilities should be available for continuous foetal heart rate and uterine monitoring. 4. Foetal wellbeing and uterine monitoring should be established prior to induction of labour. 5. The process of induction of labour should only be considered when vaginal delivery is felt to be the appropriate route of delivery.

METHODS ON INDUCTION OF LABOUR I.

NON PHARMACOLOGICAL a) Breast stimulation. Breast massage and nipple stimulation have been shown to facilitate the release of oxytocin from posterior pituitary gland. b) Mechanical modalities. • Hygroscopic dilator, that absorb endocervical and local tissue fluids, causing the device to expand within the endocervix and providing con trolled mechanical pressure. • Folley catheter (26 Fr), or specifically designed balloon devices can be used.

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These methods are effective for cervical ripening in women with an unfavourable cervix. c) Surgical methods. • Membrane sweeping. Membrane sweeping means that the doctor or the midwife insert the finger through the internal cervical ostium and move it in a circular direction to detach the inferior pole of membranes from the lower uterine segment. • Amniotomy. Risks associated with this procedure include umbilical cord prolapse or compression, maternal or neonatal infection (vertical transmission of HIV could be increased after the amniotomy), fetal heart rate deceleration, bleeding from low-lying placenta and possible fetal injury. II.

PHARMACOLOGICAL a) Prostaglandins. To be used in preference to the use of oxytocin when induction of labour is undertaken in unfavourable cervix (Bishop ,6). In this case, the use of prostaglandins analogs markedly enhances the success of induction. 1. Misoprostol. It is a synthetic prostaglandin E, (PGE) analogue that has been found to be a safe and unexpensive agent for cervical ripening, although it is not labelled in many countries for such purpose. The primary advantage of misoprostol is low cost and convenience. The optimal regimen is 50 mcg applied in the posterior vaginal fornix every 4 hours, using a maximum of six doses. It is an effective dosage for labour induction and has less adverse effects and complications than 100 mcg vaginally dose. In a closely supervised hospital setting with adequate monitoring, 100 mcg oral misoprostol has the potential to induce labour as safely and effectively as its 50 mcg vaginal analogue. As oral use of the drug is easier for both, the patient and doctor, oral misoprostol probably be is preferable to the vaginal route. Con tinuous fetal monitoring is currently recommended for at lest 3 hours after misoprostol application. When oxitocin augmentation is necessary, a minimal interval of three hours is recommended after the last dose. 2. Dinoprostone (PGE2). Administered intravaginally or intracervical it is the pharmacologic agent most widely used for ripening the cervix. Dinoprostone should be administered with the patient in or near labour and delivery suite. The patient should be monitored for a further 30 to 120 minutes. Currently, two PG analog are available for the purpose of cervical ripening: the gel containing 0.5 mcg of dinoprostone with optimal interval of administering second dose at six hours. The manu facturer recommends that no more than three doses be administrated per 24 hours, PGE2 vaginal insert containing 10 mcg of dinoprostone that provides a lower constant release of medication (0.3 mcg per hour) than gel. Its efficacy is similar, and it is inserted and removed more easly if uterine hyperstimulation occurs. The vaginal insert placement appears to be safe for both mother and newborn.

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b) Oxytocin. Once the cervix is riped, oxytocin is still the favoured pharmacologic agent for induction of labour. It should not be started before a lapse of 6 hours after administration of vaginal prostaglandins. In women with intact membranes amniotomy should be performed where never feasible prior to initiate oxytocin induction. When induction of labour is undertaken with it, the recommended regimen is a starting dose of 1-2 milliunits per minute, increased at interval of 30 minutes or more. The minimum dose possible should be used. Adequate contractions may be established at 12 milliunits per minute. The maximum dose is 20 milliunits per minute. To be delivered through a syring drive or via an infusion pump with a non return valve. To reduce error, a standard dilution shoul always be used. Suggested standardised dilutions and dose regimens include 30 UL oxytocin in 500 ml of normal saline, hence 1 ml/h 5 1 milliunit oxytocin per minute, and, 10 Ul oxytocin in 500 ml of normal saline (hence 3 ml/h 5 1 milliunit oxytocin per minute). Uterine hyperstimulation and uterus rupture may also occur. It is for these circumstances the importance of continuous FHR monitoring. When the labour induction fails or there exists a change in the maternal or foetal status it is necessary to do a caesarean section; it may be the end of this procedure. Reference. Tajada M, Carazo B, Ornat L, Fabre. E.: Induction of labor. In: Recommendations and Guidelines for Perinatal Medicine Matres Mundi/WAPM. Barcelona, 2007; 25: 223-229.

C.2.2. INTRAPARTUM FETAL MONITORING CONCEPT The purpose of intrapartum monitoring is to detect fetal hypoxia. The effect of hypoxia on the fetus depends on its reserves of glycogen. Thus, a growth-retarded fetus will be affected earlier and to a greater degree than the well-nourished fetus. I.

METHODS OF INTRAPARTUM MONITORING 1. Intermittent recording of FHR using a fetal stethoscope. It should only be applied to low risk patients with no obstetric abnormalities. 2. Continuous recording of the FHR. Continuous recording of the FHR is a screening technique which facilitates the detection of fetal hypoxic stress. It is at its most useful when combined with measurement of fetal scalp pH. FHR AND SCALP pH ARE COMPLEMENTARY TO ONE ANOTHER.

II.

INDICATIONS FOR INTENSIVE MONITORING a) Antepartum problems. 1. Primigravidae over 35 years of age. 2. Great multiparity. 3. Multigravidae aged 40 or more. 4. Suspected IUGR.

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5. Pre-eclampsia. 6. History of APH during this pregnancy. 7. Bad obstetric history. 8. Diabetes. 9. Hypertension. 10. Twins. 11. Rh iso-immunisation. 12. Oligohydramnios. 13. Reduced fetal movements. 14. Abnormal antenatal FHR tracing. b) Intrapartum abnormalities. 1. FHR . 160 or , 120 b.p.m. 2. Meconium-stained liquor. 3. Prolonged labour. 4. Epidural anaesthesia. 5. Augmentation of labour. 6. Pre-term labour. 7. Supine hypotension. 8. Breech presentation. III. INTERPRETATION OF FETAL HEART RATE (FHR) TRACINGS IN THE FIRST STAGE OF LABOUR a) General measures. 1. The whole clinical situation must be considered. 2. Tracings should be marked with the patient’s name, date and time of starting. 3. Significant events, e.g. vaginal examination, insertion of an epidural block or FBS, should also be marked. 4. It is useful for each unit to make its own collection of normal and abnormal tracings and display them on a board in the labour ward. b) Normal pattern. 1. A FHR between 120 and 160 b.p.m. 2. No significant change in rate during uterine contractions. 3. Baseline irregularity (previously called beat-to-beat variability) of 5 or more b.p.m. Tracings obtained using an ultrasound transducer may show less baseline irregularity than those from a scalp clip. Traces obtained by ultrasound are therefore more difficult to interpret. This suggests that the fetus is in good health. Nothing further is indicated. c) Loss of baseline irregularity. The FHR has a variability of less than 5 b.p.m. Loss of irregularity is the feature most commonly associated with fetal hypoxia. The fetal pH should be determined if the pattern persists or if other adverse features administration (e. g. pethidine) can affect baseline irregularity. d) Baseline bradycardia. A FHR of less than 120 b.p.m. This is an adverse feature only if it is accompanied by loss of baseline irregularity and/or decelerations (complicated bradycardia) Turn the patient on her side, give oxygen and determine the fetal pH.

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e) Baseline tachycardia. A FHR of 160 b.p.m. or more. The fetal pH should be determined if the tachycardia is persistent or accompanied by decelerations or loss of baseline irregularity. f) Acceleration pattern. An increase in FHR at the start of a contraction, returning to baseline during or at the end of the contraction. g) Early deceleration (Type 1 dip). 1. The deceleration begins with the onset of the contraction. 2. It returns to the baseline rate by the end of the contraction. 3. It is usually, but not necessarily, of low amplitude (,40 b.p.m.). This pattern may be due to head compression or it may be an early sign of cord compression or hypoxia due to placental insufficiency, if the pattern deteriorates into variable or late decelerations, the fetal pH should be determined. h) Variable deceleration. 1. The deceleration appears at a variable time during the contraction. 2. Its shape is irregular with an amplitude of more than 50 b.p.m. If it appears consistently with each contraction, it is likely that fetal hypoxia is developing. The fetal pH should therefore be measured, especially if it is accompanied by other adverse features or if the pattern persists after turning the patient on her side. i) Late deceleration (Type 2 dip). A deceleration whose lowest point is past the peak of the contraction, i.e. there is a lag time. The greater the lag time the more serious its significance: the most ominous pattern is of shallow late decelerations acoompanied by loss of baseline irregularity and tachycardia. A fetal pH measurement is mandatory. IV. NORMAL UTERINE CONTRACTIONS (AS DISPLAYED BY THE CTG) 1. 3-4 contractions every 10 minutes. 2. A duration of up to 75 seconds. 3. Baseline tone of 5-12 mmHg. 4. Peak pressure between 30 and 60 mmHg. 5. Measurement by intrauterine catheter. V.

FETAL BLOOD SAMPLING The equipment required is shown below: 1. pH meter. 2. Cold light source (for the amnioscope). 3. Ethyl chloride spray. 4. Antiseptic lotions and cream. 5. Silicone pelly. 6. Small magnet with iron «fleas» to stir the sample. 7. Sterile pre-packed tray, containing a range of amnioscopes: long forceps to hold swabs; a long-handled blade holder: a 2 mm guarded disposable blade (Rocket) to fit the holder: 2 pre-heparinised glass capillary tubes: 2 rubber mouthpieces to fit the tubes: cottonwool balls and dental swabs. Samples are obtained from the fetal scalp (or buttocks in a breech presentation).

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The procedure is not difficult, but practice is necessary for the consistent collection of good samples. a) Technique. 1. Explain to the patient what is happening and why. 2. The operator should wear sterile gown and gloves. 3. Place the patient in the left lateral position and wash and drape her routinely. (If the lithotomy position is used, the patient should be tilted 10-15ª to one side to prevent caval obstruction by the uterus). 4. Assess cervical dilatation and the level of the presenting part in the pelvis. A FBS should be obtainable if the cervical dilatation is $3 cm. 5. Use the shortest, widest amnioscope which will pass through the cervix. Take care to totally exclude the cervix from view. Fit the light source to the amnioscope. 6. The fetal scalp (or buttock) is cleaned and dried and a smear of silicone jelly applied. 7. An assistant sprays the area on view with ethyl chloride for 10 seconds. The resultant hyperaemia facilitates collection of the sample. 8. Stab the presenting part once with the guarded 2 mm blade. 9. Collect a 15 cm column of blood by capillary action into one tube. If necessary facilitate collection by gentle suction using the mouthpiece. It is important to exclude air bubbles from the sample because they affect the validity of the readings obtained. Fill a second capillary tube similarly if possible. 10. Insert the iron «fleas» into the samples and mix the heparin with the blood by moving them up and down the tube with the magnet. 11. An assistant takes the samples immediately to the previously prepared pH meter. 12. Ensure that the fetal scalp has stopped bleeding before removing the amnioscope. Pressure with a dental swab for 2-3 minutes is usually effective. b) Interpretation of fetal blood samples in the first stage of labour. pH

7.3-7.4

INTERPRETATION

Normal.

ACTION

None indicated.

7.25-7.29

Borderline normal.

Repeat pH in 45 minutes.

7.20-7.24

Abnormal.

Caesarean section must be considered depending on clinical circumstances. If labour is in active phase and progressing rapidly it may be justifiable to await vaginal delivery. The patient should be nursed on her side.

,7.20

Highly abnormal.

Immediate delivery.

c) Maternal effects on fetal pH. A significant maternal acidosis will contribute to a low fetal pH. Therefore if, such a situation is suspected, a full acid-base analysis of the fetal sample and maternal capillary blood can be carried out, as long as someone experienced in blood gas analysis is available. If there is a base excess difference of

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8 mEg/l or more between mother and fetus, the latter has a significant independent metabolic acidosis due to hypoxia. This technique is not often used in practice. d) FBS in the second stage of labour. An FBS is indicated in the second stage if there is evidence of «fetal distress» but the presenting part has not yet descended far enough to make an instrumental delivery acceptably safe. The fetus normally becomes acidotic in the second stage of labour and it may be justifiable to accept pH 7.15 as the absolute lower limit of normal at this time.

Reference. Van Geijn HP: Intrapartum Fetal Surveillance and management of fetal distress. In: Recommendations and Guidelines for Perinatal Medicine. Matres Mundi/WAPM. Barcelona, 2007; 24:216-222.

C.2.3. EPISIOTOMY CONCEPT An episiotomy is an incision performed between the vagina and the anus (excluding the rectum and its muscles) when the bay’s head is exposed to a diameter of 3 to 4 centimeters to increase the opening of the vagina to assist in delivery of a baby.

TYPERS According to the direction of the cut there are two different types of episiotomy. 1. Mediolateral, angled down away from the vagina and into the muscle. 2. Midline, straight down between vagina and anus.

INDICATIONS Episiotomy is performed to increase the size of the outlet and to reduce maternal and fetal injury: • To prevent a tear (episiotomy is easier to repair). • To relieve obstruction of the unyielding perineum. • Controversy over whether it is preferable to make a cut, or let the perineum tear as needed: current evidence suggests letting perineum tear and then repair as needed.

BENEFITS 1. Shorter second stage of labor. 2. A clean straight incision to repair (rather than more irregular lacerations). 3. Reduced damage to the pelvic floor (although it has never been proven that episiotomy prevents pelvic relaxation. Mediolateral episiotomies may help avoid damage to the rectal sphincter. This type of episiotomy might benefit a patient with a history of inflammatory bowell disease or previous rectal surgery.

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RISKS AND COMPLICATIONS • • • • • •

Bleeding. Infection with suture disunion. Hematoma. Extension into anal musculature or rectal mucosa causing fecal incontinence. Fistula formation. Dyspareunia.

Manegement • Repair as in perineal tear (2nd Degree). • Post episiotomy hygiene education. Mediolateral episiotomies are more difficult to repair and more uncomfortable to the patient during recovery than median episiotomies.

TECHNIQUE 1. An incision is made vertically in the perineal body, taking care to avoid the fetal presenting part. The incision should be approximately half the length of the perineal body. 2. Mediolateral incisions should be made at a 45- degree angle to the midline of the perineum. The incision should extend into the vagina approximately 2 to 3 cm. The episiotomy should be performed when approximately 3 cm of the fetal presenting part is visible between the labia. Excessive blood loss can result from per forming the episiotomy too early. The episiotomy can be performed either before or after the application of forceps or a vacuum.

REPAIR Most commonly, chromic suture is used for repair. First, the vaginal incision is closed with a running or running locking stitch until the hymenal ring is reached. The hymenal ring is then reapproximated. The suture may be cut and tied at this point, or carried down to the perineum. A few interrupted deep sutures may be placed in the fascia and muscles of the perineum. Next, a running suture is carried down to the apex of the incision, closing the superficial fascia. Finally, the perineal skin is closed with a running subcuticular stich. 1. Third-degree episiotomy. The transected muscles of the external anal sphincter are isolated and the fascia on all four sides of the sphincter is reapproximated using interrupted sutures. 2. Fourth-degree episiotomy. The rectal mucosa is reapproximated by placing interrupted sutures through the submucosa approximately 0.5 cm apart. The suture line then may be reinforced with a layer of continuous stitches. The patient should be given stool softeners for at least 1 week after repair. The typical healing time for an episiotomy is about 4-6 weeks, depending on the size of the incision and the type of suture material used to close the episiotomy. Normal activities can be resumed shortly after birth. The stitches are absorbed by the body and do not need to be removed. References. Aguirre F, Chou B: Episiotomy. In: The Johns Hopkins Manual of Gynecology and Obstetric Lippincott Williams and Wilkins. Philadelphia, 2011: 82-83. | Ministery of Health of Ruanda: Clinical Protocols and Treatment Guidelines in Gynecologycant Obstetrics. Kigali, 2012; 1: 105-106.

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C.2.4. OPERATIVE VAGINAL DELIVERY:

VACUUM, SPATULAS AND FORCEPS

CONCEPTS 1.

Operative vaginal delivery refers to the use of a vacuum, spatulas or forceps in vaginal deliveries. 2. This methods are safe and reliable for assisting childbirth, if appropriate attention is paid to the indications and contraindications for the proce dures. 3. The benefits and risks to both the woman and her fetus of using either instrument or the risks associated with proceeding to the alternative of cesarean section delivery must be considered in every case. 4. Operative vaginal delivery should be avoided in women who are HIV positive to reduce mother-to-child transmission.

ASSESSING THE DESCENT OF THE FETUS Prior to performing an operative delivery, it is essential to determine that the vertex is fully engaged. Descent of the baby may be assessed abdominally or vaginally. When there is a significant degree of caput (swelling) or moulding (overlapping of the fetal skull bones), assessment by abdominal palpation using —fifths of head palpable, is more useful than assessment by vaginal examination. I.

VACUUM ASSISTED DELIVERY 1. The vacuum should not be regarded as an easier alternative to forceps. Use of vacuum equipment requires different but not less skill. The vacuum is designed to produce traction upon the fetal scalp in order to assist maternal expulsive efforts. It cannot be used to apply rotational forces. 2. Trying to complete a rotation can cause a skull fracture or a hemorrhage resulting in serious harm to the baby. 3. The vacuum will less likely succeed in absence of maternal expulsive effort. 4. Vacuum may be used judiciously to correct attitude (deflexion), if it is properly applied and appropriate traction used. a) Indications. • Fetal. –– Evidence of fetal compromise that requires immediate delivery. • Maternal. –– Failure to deliver spontaneously following the appropriate management of the second stage of labour. –– Conditions which require a shortened second stage or in which pushing is contraindicated (e.g. some maternal medical conditions). –– Maternal exhaustion. b) Contraindications. Contraindications can be divided into absolute and relative. As with any re lative contraindication to a procedure, the applicability of the criteria will depend on the clinical circumstances and the skill of the health care provider.

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Absolute. –– Non-vertex presentation. –– Face or brow presentation. –– Unengaged vertex. –– Incompletely dilated cervix. –– Clinical evidence of cephalopelvic disproportion (CPD). –– Obstructed labour. • Relative. –– Preterm less than 34 weeks. –– Mid-pelvic station. –– Unfavourable attitude of the fetal head. c) Prerequisites. 1. Vertex presentation. 2. Engaged vertex. 3. Term fetus. 4. Fully dilated cervix. 5. Ruptured membranes. 6. Adequate maternal pelvis by clinical assessment. 7. Empty maternal bladder. 8. Appropriate local analgesia, if available. 9. Adequate facilities and backup available (theatre for CS and neonatal resuscitation). 10. Health care provider knowledgeable about the instrument, its use and the complications that may arise from its use. 11. Ongoing fetal and maternal assessment. d) Technique. The vacuum should be applied with rigorous adherence to the mnemonic provided. Provide emotional support and encouragement: 1. Analgesia is not essential. 2. The bladder should be empty. If the woman is not able to void, consider catheterization. 3. Final confirmation of full dilatation and fetal position should be made. 4. The proper function of the vacuum equipment should be determined before the cup is applied. 5. The cup is applied by compressing it in an anteroposterior diameter and then introducing it into the posterior fourchette while protecting the maternal tissues and making space with the opposite hand. 6. It is important to apply the vacuum cup to the flexion point for the best result. Once in the vagina, the cup is moved approximately 3 cm from the anterior fontanelle toward the posterior fontanelle over the sagittal suture. 7. When the vacuum extractor cup is centered over the flexion point, flexion and asynclitism are promoted. Placing the cup off to the side of the sagittal suture or closer to the anterior fontanelle promotes asynclitism, deflexion and cup disengagement. 8. Take care to ensure that no maternal tissue is between the fetal head and the vacuum cup. This should be reconfirmed before each pull on the vacuum and following any re-application or suggestion of loss of contact during traction. •

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9. No rotational force is applied; the fetal head may rotate on its own with descent. 10. Traction should always be in the direction of the pelvic curve-initially downward and finally upward. A common error is to attempt to extend the head prematurely, thereby increasing the diameter that must pass over the perineum and increasing the likelihood of perineal trauma. 11. Apply traction with contractions and with maternal expulsive efforts. 12. After every vacuum delivery, the newborn should be observed to ensure that the expected swelling on the head does not enlarge significantly and that there is no evidence of developing hypovolemia, which might occur with a subgaleal hemorrhage. When to halt-beware 1. 3 pulls over 3 contractions, no progress → abandon procedure. 2. 3 pop-offs: after 1, reassess carefully before reapplying. 3. After 20 minutes of application with no progress → reassess. e) Potential complications. Complications usually result from not observing the conditions of application or from continuing efforts beyond the guidelines described above. Fetal complications 1. Localized scalp oedema (artificial caput or chignon) under the vacuum cup is harmless and usually disappears within a few hours. 2. Cephalohematoma requires observation. It will usually resolve in 34 weeks. 3. Scalp abrasions (common and harmless) and lacerations may occur. Clean and examine lacerations to determine if sutures are necessary. Necrosis is extremely rare. 4. Intracranial bleeding is extremely rare. It requires immediate intensive neonatal care. Maternal complications 1. Tears of the genital tract may occur. Examine the woman carefully and repair any tears to the cervix or vagina, or repair the episiotomy. II.

FORCEPS a) Conditions. 1. Maternal: • Fully dilated cervix. • Known and sufficient pelvis. • Ruptured membranes. 2. Fetal: • Engaged fetal head. • Known cephalic variety and suitable for the instrument. 3. Healthcare: • Appropriate surgical environment (assistants, etc.). • Adequate anesthesia. • Forceps suitable type. b) Indications. 1. Maternal: • Shortening of the expulsive period in cardiac patients, pulmonary disease or other medical conditions.

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• Shortening of the expulsive period in previous cesarean. • Maternal fatigue (prolonged labor, etc.). • Inhibition of straining by the epidural anesthesia. • Relative pelvic disproportion. 2. Fetal: • Risk of loss of fetal well-being in the expulsion. • Anomalies of position or presentation. • Head retained in breech delivery. c) Classification. 1. According to the application plane. • High forceps. Biparietal diameter is in the superior strait, and the leading point is located above the ischial spine. Not recommended. • Medial Forceps. The biparietal diameter is below the superior strait and the leading point is located at the level of the ischial spines. Must be done by experienced obstetricians in exceptional situations. • Low Forceps. The fetal head is deeply embedded in the lower starit, and the biparietal diameter is below the sciatic spines. 2. According to its mechanics. • Classic. Parallel or crossed branches (e.g. Naegele forceps). • With axial tension. Similar to the mentioned above, but with a tension member. In rare occasions Tarnier or Demelin are used. • Specials. Designed for special applications. Kjelland and Piper are commonly used. d) Choosing forceps according to its application. 1. Low forceps in the lower narrow: short Naegele (alternative: Simpson). 2. Mid forceps in the excavation. • Anterior varieties: Long Naegele. (Alternatives: Salinas, Tarnier, Lev ret, etc.). • Posterior varieties: Kjelland (alternative: Simpson). 3. High forceps, at the superior strait: Kjelland. (Alternatives: Barton). 4. Forceps in face presentation: Anterior chin: Long Naegle. (Alternatives: Long Simpson, Tarnier). 5. Forceps in last head: Pipper. (Alternatives: Kjelland). 6. Forceps in cesarean section: short Naegele. (Alternatives: Short Simpson, short Hale). e) Contraindications. 1. Evident pelvifetal disproportion. 2. Incomplete cervical dilatation. 3. Presentation not engaged. 4. No indication. III. SPATULAS a) Conditions. 1. Maternal: • Complete cervical dilation. • Pelvis recognized an sufficient. • Ruptured membranes. • Soft parts not excessively rigid.

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Fetal: • Engaged fetal head. • Variety of presentation known and proper. • Alive fetus (relative condition). b) Indications. 1. Maternal: • Need of shortening of the expulsive stage. • Insufficient contractile activity. • Protection of the uterine wall (previous cesarean). • Prolonged expulsion. 2. Fetal: • Risk of loss of fetal well-being in the expulsion. • Prematurity. c) Contraindications. The same as for the forceps. d) Recommendations. 1. It is usually desirable to practice a prophylactic episiotomy (possibility of tearing). 2. Do not use them in all the cases where the need for maneuvers requiring large rotations or strong traction is expected. 3. The only correct dam is the transverse; oblique and antero-posterior shots are not permissible. 4. The loss of parallelism of the spoons can be dangerous and it is also an indication of a faulty application or a difficulty in the fetal progression. It is better to remove them. 2.

References. Carrera JM, Mallafré J, Serra B: Protocolos de Obstetricia y Medicina Perinatal del Instituto Universitario Dexeus. 4th Edition, Elsevier. Barcelona, 2006: 359-363. | Moi Teaching and Referal Hospital (MTRH). Protocols of the Dept. of Reproductive Health. (Kenya), 2012.

C.2.5. CAESAREAN SECTION DEFINITION Caeserean section is defined as the birth of a foetus through incision in the abdominal wall (laparotomy) and the uterine wall (hysterotomy).

CLASSIFICATION 1.

Indication’s Type. a) Elective: Indicated before starting delivery. b) Intrapartum: Indicated during labour or delivery. Urgency’s Type. a) Urgent: Need to act very quickly (with increased mortality and risk for the child and the mother, for example in some haemorrhage ante partum, abruption placenta) b) Semi urgent: For example dystocia during the delivery.

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In function of uterine incison. a) Low transverse segment. Transverse incision in the uterus segment, It’s most frequently used, because less risk of bleeding and uterine ruptures. b) Corporal. Incision inside the uterus body. It may be longitudinal (classical) or transverse.

INDICATIONS We summarize the more frequent indications, divided in to those indicated before the delivery and the ones decided during the course of delivery. I.

ANTEPARTUM In the Prenatal Consultation we can identify some potential/risk situations which tell us of the contraindication to have a home delivery or in health centres, and it advise us, to carry out the delivery in a Hospital because the increased risk in maternal and foetal morbimortality. 1. High risk delivery. Several illnesses that do not make possible a delivery: like pelvic malformation which causes contracted pelvis, etc. or genital maternal infection as herpes genital active, very extensive condilomatose. 2. Uterine scars. For previous CS it is the main indication. A new CS must be done when two previous CS had been performed. If it is a corporal caesarean, normally not frequent, we must do a CS before the labour of delivery. In reference to other not obstetrical uterine scars, as a myomectomy, we can try the vaginal trial, with much caution and close monitoring. 3. Malpresentations. Definition: all presentations, that are not cephalic presentations. a) Refer to the hospital from antenatal care (ANC) in case of breech pre sentation. b) Transverse or oblique lie. c) Twin pregnancies of primipara especially if the foetuses presents a breech (non vertex) 1st twin, possibly not vertex for 2nd twin.

II.

INTRAPARTUM A. Emergency. Caesarean section to be avoided at all times unless no other possible alternative. 1. Ruptured uterus. 2. Placental abruption when not in labour. 3. Failed internal rotation. Transverse presentation. 4. Failed vacuum and forceps. 5. Obstructed labour when all other options have failed. B. Semiemergency. Labour dystocia. Dilatation period or expulsion much prolonged. It could be a Cephalo-pelvic disproportion (dystocia), malpresentations or deflected presentations, fetal distress or not enough contractions (dyscinesie) as failure to progress. Diagnosis. 1. Time limits of work for dilating the cervix 2-3 cm; dilatation of 1 cm per hour with good contractions. 2. Theoretical limits for expulsion time: 1 hour from start correct push and childbirth delivery for multiparas and 2 hours for primigravidas.

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a) Clinical signs of cephalo-pelvic disproportion. 1. No descent of presenting part. 2. No cervical dilatation/progress. 3. Internal Rotation. 4. Formation of caput. 5. Excessive moulding. 6. Thick fresh meconium. b) Malpresentations or deflected presentations. There are presentations of face, brow and bregma. 1. FACE. When we practise the vaginal exploration, the nose is in the centre of the presentation, the mouth; the chin (mentum) in one side and in the other side the occiput is in contact with the foetal back. Management: We have good progression of labour if the chin is in menton anterior try vaginal delivery. If limited pelvis, stationary dilatation or posterior chin considerer eventual CS. 2. BROW. We note in vaginal exploration the front at centre of presentation, the big fontanel in one side and the nose in the other side. We don’t feel the mouth not the chin. 3. BREGMA. It’s the presentation of the big fontanel that who does the vaginal exploration feels in the centre of the presentation. Management: Vaginal delivery possible if we have good pelvis or premature, so far expulsion with vacuum extractor often needed. 4. BREECH. A completely independent topic 5. OTHER PRESENTATIONS. The oblique presentations or 1st shoul der are always indications to referral for C-section, vaginal delivery not possible. The table shows the «guides points» and possible findings in a vaginal examination and also its possible repercussion in the progression of de livery. PRESENTATION

VAGINAL EXPLORATION

PROGRESSION LABOUR

Face

–– No suture or fontanelle. –– Prominence delimitate one triangle with the mouth. –– Easy palpation eyes and nose. –– Possible palpation ears.

–– All depends on the position the mentun; mentum posterior: caesarean. –– Mentum anterior: possible vaginal delivery with episiotomy.

Browm

–– Palpation nose, orbits, sometimes the eyes. –– No touch of chin or posterior fontanelle.

–– Cesarean except if it is very small foetus.

Deflexed (bregma)

–– Bregma of big fontanelle in the center of pelvis. –– Not fontanelle posterior (occipitum) nor nose.

–– To perform one episiotomy if head descends normaly. –– If head can’t engage: cesarean.

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PRESENTATION

VAGINAL EXPLORATION

PROGRESSION LABOUR

Breech

–– Soft mass separated in two. –– One or two legs felt in case of complete breech. –– More down mass in the pelvis with incomplete breech.

–– Incomplet breech: normal delivery possible. –– Complet breach: caesarean except for the very small foetus.

Shoulder

–– Feel back if broken membranes. –– Sometimes hand or arm fall in to vagina.

–– Impossible vaginal delivery. –– Cesarean.

c) Foetal distress. It may originate during pregnancy (chronic pathology of more or less prolonged duration that origins FGR). 1. Foetal Distress during labour. During the labour there are some situations that can cause foetal distress: Cord prolaps, abruption placenta or total occlusive placenta previa. The indications for foetal distress that mandate a CS are: • Cord prolapse not for a long time. • Abruption placenta that compromises life of mother. • And total occlusive placenta before and/or during labour. • Also eclampsia or grave preeclampsia can cause foetal distress. Do a CS on after 1 hour with convulsing patients and no observation of good progress of delivery labour.

TECHNIQUE I.

GENERAL CONCEPTS 1. Nowadays, the most recommended technique is to act through the low segment of the uterus. The access is transperitoneal and the abdominal incision may be a medium infra-umbilical laparotomy or transverse suprapubic (Phannenstiel incision). 2. The second one has some advantages: less postoperative pain and best aesthetical results. However the Phannestiel incision needs more time to enter into the uterus, so it needs more ability from the surgeon. 3. The high incision is indicated when: a) An inaccessible lower segment due to dense adhesions from previous caesarean sections. b) Transverse lie (with baby’s back down) for which a lower uterine segment incision cannot be safely performed. c) Foetal malformations (e.g. conjoined twins). d) Large fibroids over the lower segment. e) A highly vascular lower segment due to placenta previa. f) Carcinoma of the cervix. g) Emergency caesarean. 4. Follow the pre/intra and postoperative cares described for all kinds of surgery. 5. Empty the bladder of the patient, through an urine catheter before, doing the operation.

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6. In all cases and especially in isolates places, and when we donâ&#x20AC;&#x2122;t know with certaint which are the aseptical conditions. 7. Administer intravenous antibiotic before opening the cavity (example with: Ampicilline 2 gr or Cefazolin 1 gr) and continuous 24-48 h i.v. then change to oral until to complete 5-7 days treatment. II.

PROTOCOL INTRA/POSTSURGERY a) Antibiotics. All women undergoing CS get a prophylactic dose of antibiotics in the operating theatre. Next women should recive antibiotics after CS following: 1. Prolonged labour .24 hours. 2. Attempted home delivery. 3. Ruptured membranes for more than 12 houres. 4. Fever during labour. 5. Fever during more than 24 hours Post-operative (if Para check negative). b) Urine catheter. Early catheter removal reduces the risk of infection and encourages the woman to walk. Wait 48 hours after surgery before removing the catheter if there was: 1. Uterine rupture. 2. Severe obstructed labour. 3. Massive perineal or vulvar oedema. 4. Puerperal sepsis with pelvic peritonitis. Leave the catheter in place for 7 days or more if the bladder was injured. d) Ambulation. Ambulation enhances circulation and deep breathing and stimulates returm of normal gastro-intestinal function. Encourage foot and leg exercises and mobilize as soon as possible, usually within 24 hours. d) Analgesia. Adequate postoperative pain control is important. A woman who is in severe pain does not recover well.

III. SURGERY TECHNIQUE 1. Asepsis for abdomen, perineum and vagina with iodine povidone and to put sterilised surgical lines. 2. Skin incision and underlying tissues. 3. Incision and detach the vesicouterine peritoneum at the level of inferior segment and descend downwards. 4. Segmentary Hysterotomie (small transverse incision continued with stretching with the fingers). 5. Broken Membranes. 6. Foetal Extraction as quick as possible. 7. Wash (stimulation) and aspiration of foetal respiratory tract. 8. Cut umbilical cord and give the newborn to the person who looks after care and the reanimation (paediatrician or midwife). 9. Artificial extraction of placenta (check if it is complete and do if it is necessary a review of the cavity). 10. Administration of 10 Ul of Oxytocine I.V. 11. Take the edge of the uterine incision with the Duval clothes.

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12. Hysterorrafie: Suture (separate or cross) of the uterus in ½ plane with reabsorbable yam 1/0. 13. Clothe the visceral peritoneum with reabsorbable suture 2/0. 14. Clothe the planes of abdominal wall in separates planes. 15. Apply a sterile bandage. 16. Do a vaginal washing to take out the sewage coagulum. Some big problems with the surgery: 1. Primary Hemorrhagie with uterus atonie and possible hypovolemic shock. 2. Septicaemia with postoperative peritonitis. 3. Secondary Hemorraghie. 4. Formation of Retrovesical Haematoma. 5. Pulmonary Embolism. 6. Wound infection. 7. Thrombophlebitis. 8. Vesico-vaginal Fistulae. Reference. Foradada C, Costa L: Caesarean Section. In: Recomendations and Guidelines for Perinatal Medicine. Matres Mundi/ WAPM. Barcelona, 2007; 32: 272-282.

C.2.6. PROTOCOL FOR POSTOPERATIVE CARE CONCEPT Patients undergoing obstetrical surgery require specialized care. Early mobilization, timely feeding, attentive care to wound healing and continuous support are important in reducing surgical morbidity and mortality.

MANAGEMENT Please note that the day of surgery is considered here at post-operative day zero. All patients must have a postoperative check 6-8 hours after surgery and each subsequent day the following should be assessed and documented in the patient’s file: 1. Ask the patient:

–– Chest Pain? –– Shortness of breath? –– Calf pain? –– Walking?

2. Examine patient:

–– Vitals (heart rate, blood pressure, respiratory rate, temperature, urine output). –– Lungs for breath sounds. –– Heart for murmurs. –– Abdomen: Distended? Soft? Tender? Acute? –– Vaginal bleeding? –– Incision: clean? dry? intact?

3. Assessment:

An assessment of the patient’s post-operative day, procedure, indications for the procedure, omplications and current status should be documented.

–– Voiding? –– Eating? –– Passing flatus?

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Standard post-op medication orders on the T-sheet should include the following: –– IV fluids 3 litres over 24 hours 3 1/7. –– Pethidine: 100 mg IM every 4 hours OR Morphine: 4 mg IV every 6 hours 3 2/7 OR Morphine: 30 mg IM TDS. –– Diclofenac: 50 mg po TDS OR Brufen: 400-800 mg PO QID starting on POD#2. –– Bisacodyl: 10 mg po starting on POD #2. –– Heparin 5000 IU sc TDS for patients with malignancy or immobilized for more than 48 hours. Note that post-op antibiotics should not routinely be prescribed

a) Postoperative day #0. Care in the First 24 hours: 1. Diet: start oral sips 6 hours after completion of surgery. 2. Activity: ambulate 12 hours after completion of surgery. 3. Vitals: Every 4 hours measure and document heart rate, respiratory rate, blood pressure, and urine output. • If heart rate . 120 notify Medical Officer and prepare for possible need for additional intravenous normal saline. • If urine output is ,30 cc/hour over 4 hours notify Medical Officer and prepare for possible need for additional intravenous normal saline. • If blood pressure , 90/60 notify Medical Officer. • If temperature $ 38.5 °C orally or $38 °C axillary, notify Medical Officer. 4. IV fluids: 3 liters in 24 hours. 5. Drugs: see T-sheet standard orders. b) Postoperative day #1. 1. Diet: Advance diet to clear fluids (clear tea/water), unless otherwise in dicated. 2. Activity: ambulate. 3. Vitals: Every 8 hours, measure and document heart rate, respiratory rate, blood pressure, and urine output. • If heart rate . 120 notify Medical Officer and prepare for possible need for additional intravenous normal saline. • If urine output is ,30 cc/hour over 8 hours notify Medical Officer and prepare for possible need for additional intravenous normal saline. • If blood pressure , 90/60 notify Medical Officer. • If temperature $38.5 °C orally or $38 °C axillary, notify Medical Officer. 4. IV fluids: If patient is tolerating clear fluids, stop IV fluids. Otherwise, continue 3 liters in 24 hours. 5. Drugs: see T-sheet standard orders. 6. Dressing: Abdominal dressing should be removed and patient instructed to let water run over incision and keep dry. Vaginal packs should be removed. 7. Drains: Remove Foley catheter on AM rounds if urine output has been 30 cc/hr or 0.5 cc/kg/hr. c) Postoperative day #2. 1. Diet: Advance to full diet as tolerated, unless otherwise indicated. 2. Activity: ambulate. 3. Vitals: Every 8 hours, measure and document heart rate, respiratory rate, blood pressure, and urine output.

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If heart rate . 120 notify Medical Officer and prepare for possible need for additional intravenous normal saline. • If urine output is ,30 cc/hour over 8 hours notify Medical Officer and prepare for possible need for additional intravenous normal saline. • If blood pressure ,90/60 notify Medical Officer. • If temperature $ 38.5 °C orally or $38 °C axillary, notify Medical Officer. 4. IV fluids: IV fluids should be stopped. 5. Investigations: Check Hb on AM rounds. • If Hb # 6 g/dl, then transfuse. • If Hb . 6 but ,8 g/dl, then transfuse only if symptomatic. 6. Drugs: see T-sheet standard orders. d) Postoperative day #3. Discharge home with follow-up if patient is tolerating regular diet, urinating without difficulty and ambulating. e) Pain Control. Adequate pain control is crucial for patient comfort and to encourage ambulation which decreases the incidence of many surgical complications such as ileus and deep venous thrombosis. Administration of pain medication should be given around the clock and not as needed. Postoperative pain generally responds well to NSAIDs. Choose 1 narcotic for post-operative day #0 Pethidine: 100 mg IM every 4 hours Morphine: 4 mg IV/IM every 6 hours AND Choose 1 NSAID from post-operative day #0 until discharge Diclofenac: 75 mg IM BD Diclofenac: 50 mg po TDS Brufen 400-800 mg PO QID. Maximum 3,200 mg per day NSAIDS should be avoided if patient is receiving concurrent treatment for deep venous thrombosis or pulmonary embolus Add Paracetemol 500 mg PO QID as needed for fever, HA or pain, Maximum 4,000 mg per day

All these medications work in different ways and can be taken together. Ideal pain control comes from regular use of an NSAID with Pethidine or Mor phine. Special considerations: Management of patients following Caesarean delivery. 1. Early mobilization, removal of Foley catheter and dressing should be strictly implemented on such patients on post-operative day #1. 2. Family planning should be discussed daily. Patients should be started on a method at time of discharge. 3. Patients with two Caesarean deliveries should be advised that all subsequent deliveries must be via Caesarean delivery.

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HOW TO MANAGE COMMON POST-OPERATIVE COMPLICATIONS a) Wound Infection. Wound infections can be greatly reduced by pre-op antibiotics (ceftriaxone 1 g IV # 60 minutes prior to incision). Signs of wound infection: 1. Pain. 2. Redness. 3. Warmth. 4. Purulent Discharge. 5. Fever. 6. Leukocytosis. If you are uncertain about an area of redness, draw a line around the margins. If the redness increases, it is likely an infection. b) Superficial Skin Infections. Cloxacillin 500 mg po QID OR Amoxicillin/Clavulanate 500 mg po BD. c) Abscess/Seroma. Incision must be opened and the abscess drained and irrigated at the bedside. Pack the defect with saline soaked gauze and cover with a dressing. This must be changed twice daily while the wound heals by secondary intention. d) Fascial dehiscence. Fascial dehiscence most frequently presents as copious watery discharge. This is a surgical emergency and the patient must be taken back to theater for repair. e) Fever. A fever is .38.0 axilllary and .38.5 orally. Consider the following sources in your assessment: • Wind (atelectasis or pneumonia). • Water (urinary tract infection). • Wound (wound infection, abscess, line infection, endometritis). • Walking (DVT). • Wonder drug (drug reaction/allergy/transfusion reaction). f)

Nausea/Vomiting. Post-op nausea and vomiting are common and should be managed with antiemetics. If symptoms are associated with abdominal distension/no flatus, post-op ileus should be suspected. Patients should be placed NPO, given antiemetics and have their electrolytes checked and corrected. If symptoms do not resolve, bowel obstruction should be considered. An abdominal X-ray should be ordered and the consultant informed if evidence is found of obstruction.

g) Oliguria/Anuria. Adequate urine output is $30 cc/hr or 0.5 cc/kg/hr. Consider pre-renal, intrarenal and post-renal causes. Post-op Discharge Instructions: 1. If anemic, start oral hemaetinics. 2. All patients should follow-up 2 weeks following C/S; discuss coitus restrictions.

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3. Start a family planning method in all post- cesarean patients. 4. Discharge with pain medication and bowel regimen in case of consti pation.

Reference. Boi Teaching and Referral Hospital (MRTH) Protocols of Dept. of Reproductive Health. Nairobi (Kenya), 2012.

C.2.7. POSTPARTUM REVISION OF THE VAGINAL CANAL CONCEPTS Manual and instrumental examination (shells and pincers) of the vaginal canal, once completed the delivery and uterine proven integrity.

INDICATIONS 1. 2. 3. 4. 5.

Operative delivery. Suspicion of injury channel. Hemorrhage after delivery. Maneuvers on the cervix. Blood loss during the dilation or expulsion.

METHODOLOGY a) The revision of the canal must be: 1. Early. 2. Complete. 3. Efficient. b) Technique. 1. After the uterine revision check with your hand if there is any of continuity solution in the vaginal fornices and cervix. 2. Make the cervix visible with oval leaflets and tweezers. The entire circumference of the cervix can be recognized by successive changes of the clamps. 3. If there are tears they should be sutured. 4. Examination of the vagina, through the «gauze maneuver». • A medium-sized gauze is inserted into the vagina and pressed against the cervix. • Then cervix and gauze rejected with the anterior leaflet moving up and to the right. • The posterior leaflet, inserted deep into the vagina, is withdrawn slowly, visualizing the anterior vaginal wall. • Identical maneuver, with the anterior and posterior leaflet rejecting the gauze and cervix upwards to display the posterior fornix. When removing the posterior leaflet, posterior and lateral vaginal walls are visible.

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Repeat the maneuver with the anterior leaflet rejecting the gauze and the cervix, this time up and to the left. When removing the posterior leaflet it should be possible to visualize the right and posterior vaginal walls. 5. Suture vaginal lacerations that have been found, adopting a suitable technique for each type of lesion: • Interrupted sutures (small bleeding tears). • Points in «X» or «Z» (short lesions, but bleeding). • continuous suture (prolonged and bleeding lesions). • It is important to identify and suture correctly the upper corner of the tear. 6. Inspection of the vulva and perineum, recognizing orderly and successively: • Anterior commissure. • Posterior commissure. • Perineal region. • Anoperineal region. 7. Suture the anterior commissure lesions: • Proper exposure. • Atraumatic singel points. 8. Suture perineal tears. Reference. Carrera JM, Mallafré J, Serra B: Protocolos de Obstetricia y Medicina Perinatal del Instituto Universitario Dexeus. 4th Edition, Elsevier. Barcelona, 2006: 435-436.

C.2.8. APPROPRIATE USE OF BLOOD

AND BLOOD PRODUCTS

a) Acute and Peri-operative Blood loss. 1. Evaluate patient for ischemia risk. 2. Estimate blood loss: • If .30-40 % of rapid blood loss: transfuse RBC’s and use volume expanders. • If ,30-40 % of rapid blood loss: RBC’s not usually needed in a healthy person. 3. Monitor vital signs: • Tachycardia and hypotension not corrected with plasma expanders: RBC’s needed. 4. Measure Hb: • If Hb .10 g/dl: RBC’s rarely needed. • If Hb ,5 g/dl: RBC’s usually needed. • If HB 5-10 g/dl: RBC’s may be needed, determined by additional clinical conditions. b) Chronic anaemia. 1. Transfuse only to decrease symptoms and minimize risk (generally at Hb , 5 g/dl) do not transfuse .5 g/dl unless patient is symptomatic.

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2. Treat nutrional and mild blood loss anaemia with specific therapeutic agents as indicated (iron, folic acid B12). 3. Use specific strategies for sickle cell disease and ß-thalaessemia (see section below).

BLOOD TRANSFUSION IN PREGNANCY 1. In pregnancy, maternal plasma volume increases by 40 %, and red blood cell mass by 25 %. Blood loss is usually well tolerated during pregnancy. The mean blood loss during vaginal delivery is 500 ml while 1,000 ml is lost during caesarean section. Indications for transfusion in the pregnant and post partum patient are similar to those for the non-pregnant patient. 2. In addition to the clinical assessment of pallor, all women should have their hemoglobin measured at the first antenatal visit, and subsequently once during every trimester. Clinical evaluation of mucous membranes (conjunc tivae and tongue) or palmar pallor may not detect mild or moderate anaemia that may lead to adverse effect later in pregnancy or at the time of deli very. 3. All women should have ABO blood grouping and Rhesus factor typing performed at the first ante natal visit. Where facilities exist, a screen for unexpected antibodies should be done. All Rh-negative women, with no evidence of immunization, delivering and Rh-positive foetus (or who have an abortion) should be given Rh immune Globulin (RhoGAM) in a dose of 300 mg IM within 72 hours of the delivery or abortion. 4. Nutritional education must be an integral part of routine antenatal care, including recommendations for protein and green leafy vegetables in the diet. 5. All women should receive the following prophylactic regimens during pregnancy: • Folic acid 5 mg daily through the period of pregnancy. • Ferrous sulphate 400 mg daily through the period of pregnancy. • Treatment for helminth infections (in endemic areas, after first trimester). 6. Women with an Hb , 10 g/dl should receive Ferrous sulphate 200 mg (60 mg elemental iron) three times a day throughout pregnancy. Clinically stable pregnant women with severe anaemia (,7g/dl) should be evaluated for the cause of their anaemia and treated appropriately. These women should be monitored every 2-4 weeks, including measurement of the Hb level. It may be necessary to admit or refer women with an Hb level persistently ,7 g/dl for closer clinical monitoring and treatment. 7. Blood transfusion should be considered for pregnant women with an Hb level ,5 g/dl who become symptomatic with dyspnoea, shock, or orthostatic hypotension. 8. Blood should be ordered and made available in the delivery room for immediate transfusion in case of hemorrhage at the time of delivery for pregnant women with an Hb level , 7 g/dl. 9. Blood transfusion is not indicated in anaemic women who are clinically stable after delivery. 10. In the case of postpartum hemorrhage, the source of bleeding must be identified and corrected. The first therapy of acute blood loss is volume replacement.

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CLINICAL TRANSFUSION PROCEDURES Procedures 1. Assess the patient’s need for blood transfusion. 2. Record the indications for transfusion in the patient’s notes. 3. Complete a request form accurately and legible. Include: a) Patients identification. b) Reason for transfusion. c) Component and amount required. d) Date required: urgency. 4. Collect and correctly label blood samples (5 ml in a plain tube) for grouping and compatibility testing. 5. Send blood request form and sample to the laboratory. 6. Collect or receive blood or bloodproducts from the laboratory. 7. Check the identity of patient and the blood product, by checking: a) Patient’s name(from the patient record and ask the patient). b) Hospital number. c) Label on the blood bag. 8. Confirm blood or plasma is compatible by checking the blood group on: a) Patient’s notes. b) Label on the blood bag. 9. Check expiry date of blood or plasma. 10. Check blood for: a) Clots. b) Haemolysis. 11. Check for leakage of blood bag. 12. Start transfusion of whole blood and red cells within 30 minutes of removal from refrigerator. 13. Return unused blood or blood products to the laboratory within 30 minutes of removal from the refrigerator. 14. Complete infusion of whole blood and red cells within 4 hours, and platelets and plasma within 30 minutes. 15. Monitor patient before, during and after transfusion of blood product: a) Before starting the transfusion. b) As soon the transfusion is started. c) 15 minutes after starting the transfusion. d) At least every half hour during the transfusion. e) On completion of the transfusion. f) 4 hours after completion of the transfusion. 16. Record the following: a) Patient’s appearance. b) Pulse. c) Temperature. d) Blood pressure. e) Respiratory rate. f) Fluid balance: input/output. 17. In the patient’s notes record: a) Date of transfusion. b) Time transfusion started and ended.

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c) Volume and type of blood/blood products given. d) Blood or plasma unit numbers. e) Any adverse effects. 18. Sign the patient’s notes. 19. Report any adverse reactions immediately to the laboratory. 20. Return used/partially used blood bags to the laboratory.

Reference. Boi Teaching and Referral Hospital (MTRH). Protocols of the Dept. of Reproductive Health. Nairobi (Kenya), 2012.

C.2.9. OBSTETRIC ANAESTHESIA AND ANALGESIA CONCEPT By anaesthesia we assume the lack of sensations, mainly painful ones, associated to lack of conscience, and this can be achieved with general anaesthetics drugs. Analgesia is the lack of pain sensation, and this has no effect on conscientious; this is what is desirable in obstetrics and what is achieved with loco-regional analgesia.

NON PHARMACOLOGICAL METHODS 1. 2.

4. 5.

Labor support. Labour support must be considered effective in labour pain relief. Sterile water blocks. Intradermal injection of 0.05-0.1 ml of sterile water in 4 sites over the sacrum (2-3 cm below and 1-2 cm medial to the posterior superior iliac spine, after 30 seconds with itching and/or local pain, induces low back pain relief that lasts 60-90 min. This can be applied by a doctor or a nurse and can be repeated in an hour. Immersion in water. It is recommended the immersion in 37 ºC water and only to the level of superior abdomen, once cervical dilatation is more than 4-5 cm, and for a maximum of 1-2 hours. Psichoprophilaxis. Classes for women labour pretend a good psychological preparation and generally teach breathing and relaxing techniques, designated to diminish pain. Hypnosis. Women taught self-hypnosis have decreased requirements for pharmacological analgesia. The effectiveness of this method is limited in a small group of patients, and it should only be used in previously selected women as it can produce severe psychiatric alterations. Acupuncture. Although some studies have appointed the benefit of acupuncture on pain relief, and some have quoted an efficacy about 60 % or a reduction in the need of analgesia.

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FARMACOLOGIAL METHODS 1. 2.

Inhalatory analgesia: nitrous oxide. Nitrous oxide relieves pain of many labouring woman and it is secure for both mother and foetus. Parenteral analgesia (intramuscular or intravenous): opioids. The most popular opioid in obstetric is meperidine, that has a quick action and is very cheap. Secondary effects include sedation, respiratory depression, nausea and vomit in the mother; for this reason it is usually used in combination with drugs, like fenotiacide or metoclopramide, that have the opposite effect. Paracervical block. Local anaesthetic punction in cervical perimeter is useful for pain relief during the first phase of labour, although its efficacy is reduced in the second one. Pudendal block. Blockade of internal pudendal nerves with their three branches reduces pain over the second phase of labour, in which pain is generated by pelvic distension. To reach these nerves we can use a perineal or transvaginal approach, being the latest easier and, quicker, and so we need to puncture less tissue and use less anesthetic. If we position women as for normal vaginal labour, we can introduce the needle, guided by the second and third finger of our hand in the vagina, with a lateral and slight medial direction with respect to the sciatic spine, over the supraspinous ligament. This high efficacy technique for second phase of labour has the advantage of easiness, has no need of vigilance and decreases the rate of vaginal tear. Local analgesia. To repair tears and episiotomy several mucous or cutaneous analgesics can be used over the vagina or perineum. The best are those with quick action, like lidocaine, that has action over 20-40 min. To ensure no vascular injection, a soft aspiration is advised, and this way most severe complications are avoided. General analgesia. Only it has to be realized under general anaesthesia when the mother specifically demands it or if a contraindication exists for the spinal blockade.

Reference. Melchor JC, Miño M, Cordón J: Obstetric anaesthesia and analgesia. In: Recommendations and guidelines for Perinatal Medicine. Matres Mundi/WAPM. Barcelona, 2007; 34: 290-298.

C.2.10. SPINAL ANALGESIA CONCEPT Spinal anesthesia is the supresión of pain in labour by injection of an analgesia drugs o local anesthethic into the space around the spinal cord.

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EFFICACY Spinal analgesia provides pain relief for the three phases of labour superior to that of any other method and it is of greatest security. For this reason, this is the method of election and should be abailable for all women in labour.

INDICATIONS Simply, the request of a labouring woman (in absence of contraindications) should be enough to guarantee the most secure and efficient analgesia, the spinal one. In addition, in some circumstances it provides benefits not contributed by other analgesic methods, and so it is medically indicated. These are. a) Obstetrical indications: 1. Dynamic dystocia. 2. Preterm labour. 3. Instrumental vaginal delivery. 4. Multiple gestations. 5. Previous caesarean section. b) Medical indications: 1. Preeclampsia. 2. Heart disease. 3. Severe respiratory disease. 4. Cronical neural diseases. 5. Epilepsy. 6. Contraindication for maternal effort: detachment of the retina, cerebral vascular pathology. 7. Contraindication of general anaesthesia.

CONTRAINDICATIONS a) Absolute: 1. Severe hypotension resistant to treatment, severe bleeding, shock. 2. Intracranial hypertension due to a lesion. Eclampsia. 3. Local (on punction site) or general infection. 4. Coagulopathy: although reassuring, it is not considered necessary a platelet recount in a previous sane woman, and women with platelets between 50,000 and 100,000/mL are candidates after an individual evaluation. 5. Anticoagulant: women with therapeutical doses of heparin are candidates if they have a normal partial time of activated tromboplastine (TTPa), and those with prophylactic doses of heparin or with low dose aspirin present no contraindication. Low weight heparins has longer mean life, and its anticoagulant effect does not affect the TTPa. Moreover, regional analgesia in women under this anticoagulant has been associated with spinal or epidural haematoma. So a woman with a single dose of low weight heparin can only receive regional analgesia after 12 hour from last dose, and she is not to receive any other until 12 hours after catheter with drawal. There are not enough studies about women with two doses of low weight heparin a day. For women under the effect of any anticoagulant therapy, intradural analgesia is preferred.

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b) Relative: 1. Woman refusal, not understanding or no acceptance of the method, no signature of written consent. 2. Lack of professional staff, or material to initiate, continue or treat the complications derived from the technique. 3. Opioids or local anestesic allergy. 4. Severe cardiopathy (New York Heart Association classe III-IV). 5. Spine deformity. 6. Bening endocraneal hypertension. 7. Not reassuring fetal cardiotocogram. 8. Tattoo in puncture site.

REQUIREMENTS 1. 2. 3. 4. 5. 6. 7.

Indication, rule out contraindications. Adequate information, before labour as preferred. Technique comprehension and acceptance. Obtain informed consent. Qualified anaesthesiologist. Suitable material. Anamnesis and occasionally physical exam and/or blood analysis. Previous fetal cardiotocography. Maternal blood pressure and temperature.

TYPES/TECHNIQUE Spinal analgesia can be epidural, intradural (subarachnoid) or combined. 1. Epidural analgesia allows inserting a catheter though which continuous infusion can be administered. 2. Intradural analgesia does not allow the insertion of a catheter so the analgesic effect derived from a single bolus. 3. Combined analgesia (epidural-intradural or walking epidural) shows a reduced time from first injection to effective maternal analgesia.

CONSEQUENCES OF EPIDURAL ANALGESIA Epidural analgesia is associated, not always as a cause, with: 1. Longer second phase of labour (14 minutes approximately). 2. More alterations with fetal rotation during second phase of labour. 3. More operatory vaginal deliveries (15 % with epidural vs 9 % with parenteral opioids; number needed to treat: 15). 4. More need of oxitocine administration (45 % with epidural vs 32 % with parenteral opioids, number needed to treat: 7.9). 5. More maternal fever (23 % with epidural vs 5 % with parenteral opioids, number needed to treat: 5.6) The mechanism is unknown, but it does not seem to be infectious. It is necessary to accept these effects because there are mechanisms to diminish its consequences.

COMPLICATIONS OF EPIDURAL ANALGESIA Complications are many, but more frequent are:

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Maternal hypotension. Blood pressure descends 20-30 % with respect to basal and affects close to 10 % of women. 2. Headache after dural puncture: accidental dural punction affect 3 % of women and after severe headache develops in 70 % of them. 3. Itching: beside hypotension it is the most frequent complication and it is related to opioids administration. 4. Fetal cardiotocographic alterations: epidural analgesia increases cardiac fetal decelerations (RR 5 3.7; CI 95 %: 2.2-6.2). 5. Failed technique: 10 % women.

SURVEILLANCE/CONTROL DURING EPIDURAL ANALGESIA 1. 2. 3. 4.

Maternal blood pressure control. Maternal temperature. Fetal cardiac and uterine activity continuous surveillance. Bladder emptying.

Reference. Melchor JC, Miño M, Cordón J: Obstetric anesthesia and analgesia. In: Recommendation and Guidelines for Perinatal Medicine. Matres Mundi/WAPM. Barcelona, 2007: 293-297.

C.2.11. ANTIBIOTIC USE IN OBSTETRICS SURGERY INTRODUCTION 1. The goal of antimicrobial prophylaxis is to eradicate or retard the growth of endogenous microorganisms that may cause surgical site infection. 2. The antibiotic chosen for prophylaxis should be effective against bacteria found in most infections, but not an agent used routinely for treatment of serious infectious complications. In addition, the antibiotic should be of low toxicity and able to achieve appropriate tissue levels in the surgical field.

ANTIBIOTIC PROPHYLAXIS FOR ELECTIVE CESAREAN SECTION AND CESAREAN SECTION WITHOUT RUPTURE OF MEMBRANES All patients should receive intravenous prophylactic antibiotics prior to skin incision. 1. First Choice: 1 gram ceftriaxone IV. If the patient weighs more than 80 kg she should receive 2 grams of ceftria xone. 2. Second Choice: 1.5 grams cefuroxime IV. If the patient weighs more than 80 kg she should receive 2 grams of cefturo xime. 3. Third Choice: 1 gm amoxicillin/clavulanate acid plus 1 gram metronidazole IV. Second and Third choice antibiotics should only be used if the first choice is unavailable if there is a medical contraindication to using a cephalosporin. No postoperative antibiotics are necessary if prophylactic antibiotics are administered.

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ANTIBIOTICS FOR CESAREAN SECTION IN LABOUR I.

CESAREAN SECTION IN A PATIENT WITH CHORIOAMNIONITIS Diagnostic criteria for chorioamnionitis. Patients with an axillary temperature in labor greater than 37.5 degrees Celsius and one of the following: 1. Elevated white blood count. 2. Fundal tenderness. 3. Fetal tachycardia All patients who undergo cesarean section with a diagnosis of chorioamnionitis should be started pre-operatively on one of the following antibiotic regimens and maintained until 48 hours afebrile post operative. There is no need for additional oral antibiotics after the patient has been 48 hours afebrile on IV antibiotics. Listed in order of preference: 1. First Choice: 2 gram Ceftriaxone IV every 24 hours alone. 2. Second Choice: 1.5 mg/kg Gentamycin IV every 8 hours AND 900 mg Clindamycin IV every 8 hours. 3. Third Choice: 2 grams Ampicillin IV every 6 hours AND 1.5 mg/kg Gentamycin IV every 8 hours AND 900 mg Clindamycin IV every 8 hours. Second choice therapy should only be used if patient remains febrile for greater than 24 hours on first choice of antibiotics. Third choice therapy should only be used if the patient remains febrile on second choice of antibiotics for more than 24 hours.

II.

ANTIBIOTIC PROPHYLAXIS FOR PATIENTS WITH OUT EVIDENCE OF CHORIOAMNIONITIS AT THE TIME OF CESAREAN All patients should receive intravenous prophylactic antibiotics prior to skin in cision. 1. First Choice: 1 gram ceftriaxone IV. If the patient weighs more than 80 kg she should receive 2 grams of ceftria xone. 2. Second Choice: 1.5 gram cefuroxime IV. If the patient weighs more than 80 kg she should receive 2 grams of cefturo xime. 3. Third Choice: 1 gm amoxicillin/clavulonic acid plus 1 gm metronidazole IV. Second and Third choice antibiotics should only be used if the first choice is unavailable or there is a medical contraindication to use a cephalosporin. Daily temperatures should be taken postoperatively. If there is an axillary temperature greater than 37.5 degrees Celsius in the postoperative period then initiate IV antibiotics. Listed in order of preference: 1. First Choice: 2 gram Ceftriaxone IV every 24 hours alone. 2. Second Choice: 1.5 mg/kg Gentamycin IV every 8 hours AND 900 mg Clindamycin IV every 8 hours. 3. Third Choice: 2 grams Ampicillin IV every 6 hours AND 1.5 mg/kg Gentamycin IV every 8 hours AND 900 mg Clindamycin IV every 8 hours. Second choice therapy should only be used if patient remains febrile for greater

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than 24 hours on first choice of antibiotics. Third choice therapy should only be used if the patient remains febrile on second choice of antibiotics for more than 24 hours. IV treatment should be continued until the patient has been afebrile for 48 hours. There is no need for additional oral antibiotics after the patient has been 48 hours afebrile on IV antibiotics.

Reference.â&#x20AC;&#x201A; Moi Teaching and Referral Hospital (MTRH). Protocols of the Dept. of Reproductive Health. Nairobi (Kenya), 2012.

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OBSTETRICAL PATHOLOGY

C.3.1.â&#x20AC;&#x201A; PERINEAL LACERATIONS DEFINITION They are tears of the perineal tissue between the vagina and rectum.

GRADES 1. 1st degree injury to perineal skin. 2. 2nd degree injury to perineum involving perennial muscles but not the anal sphincter. 3. 3rd degree involvement is of the anal sphincter. 4. 4th degree involvement of the anal sphincter and anal mucosa.

CAUSES/RISK FACTORS 1. Routine episiotomy. 2. Assisted delivery. 3. Prolonged secong stage of labor. 4. Lack of experience of service provider. 5. Nulliparity. 6. Macrosomia. 7. Patient age ,21 years. 8. Occiput posterior position.

MATERNAL COMPLICATIONS 1. PPH. 2. Anesthesia risk. 3. Injury to bladder, uterus, bone, pelvic nerve damage. 4. Anal incontinence. 5. Infections. 6. Dyspareunia.

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MANAGEMENT 1. Surgical repair of the tear. 2. Repair of the external anal sphincter end to end and internal inner sphincter should be repaired by interrupted sutures. 3. Repair of the 3rd and 4th perineal tear should be done in theatre under general or regional anesthesia. 4. Its recommended to repair perineal tears with vicryl 2-0 which causes less irritation and discomfort. 5. Check the anal canal if it is not closed during the repair. 6. Antibiotics and laxatives are recommended to be used after anal sphincter repair. 7. Women with history of anal sphincter injury in previous pregnancy who are symptomatic should be advised about elective cesarean section.

Reference. Ministry of Health of Ruanda: Clinical Protocols and Treatment Guidelines in Gynecology and Obstetrics. Kigali, 2012; 1: 103-104.

C.3.2. PRETERM DELIVERY: ASSISTANCE GENERAL CONSIDERATIONS Every preterm delivery should be considered a high-risk birth. That implies: 1. Biophysical continuous fetal monitoring since the dilation begins, and biochemical monitoring when necessary. 2. Permanent presence of appropriate staff (doctor or midwife) near the mother in labor. 3. The neonatologist on duty should be warned.

SPECIFIC MEASURES The following should considered as specific measures: 1. Avoid untimely oxytocin stimulation. 2. Do not administer analgesics. 3. Delay the breakdown of amniocorial bag as long as possible. 4. Administer oxygen intermittently. 5. Use local or regional anesthesia. 6. Episiotomy if is necessary. 7. Give vitamin K to the newborn. 8. Emphasize the aseptic measures in the management of the newborn. 9. The possibility of a transfer should be foressen (see: Neonatal transport).

Reference. Carrera JM: Protocolos de Obstetricia y Medicina Perinatal del Instituto Universitario Dexeus. 4th Edition, Elsevier. Barcelona, 2006: 407-408.

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C.3.3. MACROSOMIA AND SHOULDER DYSTOCIA CONCEPT A newborn presenting a BW of 4,500 grams or more is defined as macrosomic accor ding to the ACOG and the internacional Classification of Diseases (ICD 9:766.0).

GENERAL CONCEPTS 1. As far as the fetus is concerned macrosomia can only be «suspected» on the basis of clinical examination, fundal height (FH) measurement or ultrasonic fetal biometry. 2. The observation of a weight superior to the 90th percentile cannot be con sidered as synonymous of macrosomia. In fact it is unlikely that a fetus or a newborn presenting a weight over the 90th percentile at 30 weeks will reach 4,500 grams. 3. The threshold of 4,500 grams better reflects the risk of complications.

DIAGNOSIS Before birth the fetal weight can only be estimated in order to make a prevision of the macrosomia. Different methods have been proposed. 1. Leopold’s maneuvers. 2. Fundal height meassurement. This method is poorly predictive of macrosomia 3. Ultrasonic fetal biometry. The observation of a weight superior to the 90th percentile will be a suspect of macrosomia. In the majority of modern equipments a software for the automatic calculation of the weight is available.

COMPLICATIONS According to the severity the complications can be indicated: 1. Cephalo-pelvic disproportion. 2. Shoulder dystocia. 3. Brachial plexus injury. 4. Hypoxic-ischaemic encephalopathy. I.

CEPHALO-PELVIC DISPROPORTION 1. The most common complication in case of macrosomia is represented by labor anomalies. First and second stage can be prolonged and arrest of progression can occur. 2. Arrest of the dilatation is defined when there is no cervical modification for 2 hours. 3. Arrest of the progression is the absence of descent of the head for 1 hour. 4. The possibility of prevision of cephalo-pelvic disproportion is poor. In fact it depends not only on the fetal size but also on the characteristics of the maternal pelvis. 5. In case of labor arrest for cephalo-pelvic disproportion the only management is represented by caesarean delivery. In some circumstances tocolysis can be performed in order to avoid fetal hypoxaemia while waiting for the operative delivery.

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II.

SHOULDER DYSTOCIA (SD) 1. This condition is characterized by the impact of the anterior shoulder on the pubis or of the posterior on the sacrum. It has been defined as «an un frequent, unexpected, unpredictable nightmare for the obstetrician» SD is the major complication of labor in case of macrosomia. 2. The so called «turtle sign» is characteristic. At any contraction the fetal head pushes against the perineum and then recede. 3. In this situation it is necessary to extract the fetus as quickly as possible in order to avoid the catastrophic hypoxic-ischaemic encephalopathy. Management Many maneuvers have been proposed for treating the shoulder dystocia. 1. The maternal thighs must be flexed (45 degrees) against the abdomen and abducted. In this way pelvic diameters can be modified and the shoulders can be engaged and enter into the pelvis. 2. Pression should be applied posterior to the anterior fetal shoulder in order to facilitate rotation and reduction of bisacromial diameter. In must be stressed that for any maneuver neonatal trauma are observed in about 20 % of cases.

III. BRACHIAL PLEXUS INJURY The most relevant neonatal complication after shoulder dystocia (but not only) is the brachial plexus injury. According to the level of the lesion it is possible to distinguish between: 1. The Erb’s Palsy when it is at C5-C6 or Klumpke’s Palsy when at C7-T1. 2. Clavicola or humeral fractures usually do not have functional consequences. IV. HYPOXIC-ISCHAMIC ENCEPHALOPATHY In case of shoulder dystocia the fetal extraction should be performed as quickly as possible (six to ten minutes). Acute fetal hypoxaemia can lead to permanent damage of the CNS or death.

MATERNAL COMPLICATIONS The frequency of maternal complications is proportional to the BW particularly if it exceeds 4,500 grams. These complications are mainly represented by: 1. Risk of CS. 2. Postpartum hemorrhage. 3. Uterine rupture. 4. Infections 5. III and IV degree perineal lesions and pelvic floor disfunction. a) Risk of CS. In case of macrosomia there is a 2 to 3 fold increased risk of CS. The risk is even greater for BW exceeding 5,000 grams. b) Postpartum hemorrhage. The risk of postpartum hemorrhage is doubled in case of macrosomia without regard to the modality of the delivery. c) Uterine rupture. The relationship between macrosomia and uterine rupture is controversial also in case of previous CS.

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d) Infections. The rate of infections (chorioamnionitis and endometritis) is significantly increased in case of CS after trial of labor as compared to vaginal delivery or elective CS. e) Perineal lesions. It has been observed that when the BW is between 4,500 and 4,999 grams there is a 4 fold increase in the risk of IV degree lacerations and 7 fold for BW exceeding 5,000 grams.

PREVENTION OF COMPLICATIONS The possible strategies for their prevention are: 1. Induction of labor in case of suspected macrosomia. 2. Elective CS for suspected macrosomia. a) Elective induction From the analysis of the available studies it is possible to conclude that a policy of elective induction for suspected macrosomia does not improve the clinical outcome but increases the caesarean section rates. b) Elective cesarean section. The target of a policy of elective CS in case of suspected macrosomia is the prevention of shoulder dystocia and brachial plexus injury. All the considered studies conclude that the number of CS necessary to avoid one single case of shoulder dystocia or brachial plexus injury is so large that a trial of labor is suggested also for estimated weight between 4,500 and 5,000 grams in absence of maternal diabetes. The ACOG suggests elective CS for estimated weight superior to 5,000 grams. c) Previous CS. Macrosomia per se is not a contraindication for a trial of labor in case of previous CS. It is recommended that in this case emergency CS facilities must be available. d) Diabetes. The characteristics of the somatic fetal growth in case of maternal diabetes increases the risk of shoulder dystocia. In this condition a threshold of 4,500 estimated fetal weight can be considered as an indication for effective CS. Reference. Mandruzzato CP: Macrosomia and Shoulder Dystocia. In: Recommendations and Guidelines for Perinatal Medicine. Matres Mundi/WAPM. Barcelona, 2007; 30: 257-266.

C.3.4. MALPRESENTATIONS A. ROTATION DYSTOCIA CONCEPT Rotation dystocia is defined as a lack of progression of a vertex in transverse position (right or left) or occiput posterior position, generally in a II-III Hodge plane, generally with completed cervical dilation.

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MANAGEMENT The management depends on the cause of the disorder: Hypocontractile uterine activity, cephalopelvic disproportion, android o platipeloid pelvis. In front of this obstetric situation, it is essential to reevaluate the birth canal. a) If the woman’s pelvis seems normal, and the cause seems to be related to hypodinamic uterine activity, an oxytocic perfusion should be started. Nevertheless, once the uterine activity is adequate and the presentation does not progress in 2 h, an operative delivery or caesarean section should be done. b) If the patient has normal contractions woman’s pelvis is narrow but apparently sufficient, vaginal delivery should be attempted through: 1. Occiput transverse position. Manual rotation should be attempted before instrumental rotation. Vaccuum extraction or forceps delivery may be considered. A low rotation should be done on the first place, followed by a soft traction. 2. Occiput posterior position: • Scanzoni’s Maneuver. Scanzoni maneuver, the Kjelland forceps are applied as though the head is OA and then the head is rotated 180º to the OA position. It may be helpful to dislodge the head to a higher station before rotation to facilitate the procedure. After the rotation the head is slightly pulled down to fix the head in the anterior po sition. The forceps, that is now upside down after the rotation, is removed and reapplied allowing the forceps-assisted delivery of the head in the anterior position. • If the fetus is not very big and the tissue of the vaginal canal is lax, instrumental fetal extraction in OP position may be considered. • If trial of labour is not successful: caesarean- section. 3. If there is a pelvic stenosis: Caesarean-section.

B. FACE PRESENTATION CONCEPT Face presentation refers to a fetal presentation in which the fetal face from fo rehead to chin is the leading fetal body part descending into the birth canal. The fetal neck is sharply deflexed and the occiput may touch the back. It is the most deflexed cephalic presentation. Normally, is the spontaneous evolution of an inicial brow presentation.

DIAGNOSIS a) The external exploration of the abdominal wall sometimes shows a deep depression between the head and the back. b) The diagnosis of face presentation is made by vaginal examination at the end of the first stage of labor or during the second stage. Palpation of the orbital ridge and orbits, saddle of the nose, mouth, and chin is diagnostic of face presentation. At diagnosis, nearly 60 percent of face presentations are mentum anterior, 26 percent are mentum posterior, and 15 percent are mentum transverse, and may be designated as left or right.

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Face presentation may be misdiagnosed as a frank breech presentation on digital examination since the latter is more commonly encountered (and therefore expected). Both presentations are characterized by soft tissues with an orifice; however, careful palpation will identify the bony facial structures and lead to the correct diagnosis. c) Sonography of a face presentation will show a hyperextended fetal neck. Although imaging studies can be performed to confirm the diagnosis if it is uncertain or internal examination cannot be done, imaging is not mandatory and results do not have prognostic value for predicting the outcome of labor.

MANAGEMENT a) An evaluation of the maternal pelvis must be performed, using radiologic pelvimetry and even a MRI. b) In a mentum anterior face presentation, the fetal neck extends even further backward after the fetus is engaged and the occiput may touch the back. Internal rotation occurs between the level of the ischial spines and ischial tuberosities, making the chin the presenting part of the face. If the face descends to the perineum and the fetal chin passes under the maternal symphysis, slight flexion of the neck occurs, and delivery is possible. No special maneuvers need to be perfomed, only close monitoring. C-section indication must be done by the same criteria as flexed presentations. c) In the mentum posterior face presentation, the head, neck, and shoulders attempt to enter the pelvis simultaneously, but the pelvis is usually not large enough to accommodate the fetus in this position. The fetal neck must extend the length of the maternal sacrum (average 12 cm) in order to reach the perineum, but the fetal neck is too short to accomplish this task. Lastly, an open fetal mouth may act as a fulcrum against the sacrum preventing further descent. Therefore, the mentum posterior face presentation will not deliver vaginally unless spontaneous rotation occurs or the fetus is very small. Cesarean section must be performed.

C. BROW PRESENTATION CONCEPT Brow presentation refers to a intermediate presentation between complete flexed an complete extended (face) presentation. Fetal surface presenting in the birth canal extends from the anterior fontanelle to the brow (orbital ridge), but does not include the mouth and chin.

DIAGNOSIS a) The diagnosis of brow presentation is made by vaginal examination in the second stage of labor. Palpation of the forehead, orbital ridge, orbits, and saddle of the nose, but not the mouth and chin is diagnostic of brow presentation. The brow may be anterior or posterior. b) If the diagnosis is uncertain on physical examination, ultrasound may be helpful.

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MANAGEMENT a) After entering the pelvis, brow presentation spontaneously converts to face presentation in about 30 percent of cases and to vertex presentation in about 20 percent of cases. So an spontaneous evolution is accepted for the firsts stages of labour if the pelvis seems adequate. In women with a narrow or contracted pelvis, cesarean delivery early in labor is a reasonable option because conversion to a more favorable presentation is unlikely. If there is no progress, manual maneuvers can be tried (e.g. Thorn). b) Labor should be monitored closely, and if conversion to vertex or face presentation is not spontaneous or manually achieved, cesarean section should be performed. If progress is protracted or arrested, c- section should be done.

Reference. Serra B, Mallafré J: Protocolos de Obstetricia y Medicina Perinatal del Instituto Universitario Dexeus. Masson. Barcelona, 2014.

C.3.5. BREECH PRESENTATION CLASIFICATION There are different types of breech presentation. a) Frank breech (45-50 %): hips flexed over anterior body. Knees extended. b) Complete breech or full breech (10-15 %): Hips flexed, knees flexed. c) Footling breech or incomplete breech (35-45 %): one or both hips and knees extended. One or both feet presenting.

FETAL RISK FACTORS The risk factors for breech presentation are: 1. Prematurity. 2. Multiple prior pregnancies. 3. Polydydramnios or olygohydramnios. 4. Fetal abnormalities (Down syndrome, hydrocephalus). 5. Macrosomia. 6. Breech presentation in prior pregnancy and absolute cephalopelvic disproportion. Before labour, there is a higher risk of premature rupture of membranes and cord prolapse.

DIAGNOSIS The signs of breech presentation are: 1. Leopolds’ maneuvers: longitudinal fetal lie, being the head palpated in the uterine fundus, although it may be obscured by maternal ribs. 2. Fetal heart tone auscultation. Breech fetal heart is best heard above the um bilicus. 3. Vaginal examination.

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MANAGEMENT The management of the breech presentation requires an evaluation for the possible causes of the situation. In frank or complete breech, an external version may be attempted. In case of failure, according to the operatorâ&#x20AC;&#x2122;s experience, a vaginal delivery or a caesarean section should be performed. In footling or incomplete breech, a caesarean section should be indicated. The indications for caesarean section should be liberal. Indications for caesarean section The indications for caesarean section should be liberal: 1. Pelvis contraction or nongynecoid pelvis. 2. Previous caesarean section. 3. Bad obstetric history. 4. Maternal stature less than 150 cm. 5. Elderly primigravida. 6. Excessive maternal obesity. 7. Hypertension/Preeclampsia. 8. Diabetes. 9. Dysfunctional labor. 10. Uterine myomata. 11. Prolonged rupture of membranes. 12. Premature rupture of membranes. 13. Bicornuate uterus. 14. Placenta previa. 15. Abruptio placenta. 16. Oligohydramnios. 17. Cord prolapse. 18. Large fetus (more than 4,000 g). 19. Footling brech. 20. Hyperextension on the fetal head. 21. Prematurity. 22. Fetal distress or suspected fetal compromise. 23. Hemolysis disease. 24. IUGR. 25. Fetal hydrocephalia. 26. Uncooperative patient.

EXTERNAL CEPHALIC VERSION 1. The main indication is the breech presentation at 34-36 weeks of gestation. It may also be performed in transverse or oblique presentations. 2. The contraindications are: pregnancy induced hypertension, prior uterine surgery (e.g. caesarean section), multiple gestation with first twin breech (might be attempted if first vertex and second breech), non-reassuring fetal heart tracing, utero-placental insufficiency and placenta previa.

Technique 1. A preparation is required. Two attendants must be present. One examiner performs manual version and the other monitors the fetus. An immediate

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caesarean section must be available if needed. Ritodrine 15 min before should be considered. Administer RhoGAM if the patients is negative. The patient needs to have an empty bladder and an intravenous access. 2. The technique needs a thorough fetal assessment. Before starting, a non-stress test or a biophysical profile should be made. During the procedure, ultrasonographic assessment of the fetus is recommended. The position of the mother is supine, Trendellenburg and with the knees slightly bent; in order to help breech fetus to rise above the pelvic brim. 3. The first examiner elevates the breech by pushing the buttock up suprapubically. The second examiner flexes the head and rotates the fetus into oblique lie. 2/3 of the pressure is applied to the breech and 1/3 to the head. A massaging motion should be used to rotate the baby, without an excessive force. Once the fetus has rotated past the transverse lie, the examiner hands push the fetus into vertex position. 4. The procedure should be stopped if the mother feels sharp pain, there is no success after 20 minutes or a fetal bradicardia appears. If such bradicardia persists, one should return the fetus to its original breech position. If it still persists, a caesarean section should be pursued.

Failures and complications The most frequent reasons for a failed procedure are fetal macrosomia, olygoamnios, fully extended position of the fetus, fetal malformations, short umbilical cord, anterior placenta, nulliparity, obesity, or gestational age of 37 weeks or more. The most common complication is the fetal bradicardia or fetal heart rate decelerations. They spontaneously resolve in 40â&#x20AC;&#x2030;% of the cases. Some rare, serious complications are partial placental abruption, uterine rupture, umbilical cord accident, or amniotic fluid embolism.

BREECH DELIVERY 1. The indications of a planned vaginal breech delivery are a complete or full breech presentation, an estimated fetal weight of 2 to 4 kg and the presence of an expert birth attendant. 2. The contraindications are unfavourable pelvis (e.g. android or platypelloyd, small), fetal macrosomia, utero-placental insufficiency, intrauterine growth restriction, footling breech, fetal hydrocephalia, inexperienced attendant, hyperextension of the fetal head, (assessed by ultrasound) and severe prematurity.

Technique The breech delivery requires experience and patience. In most cases, nothing should be done until the inferior angle of the scapulas appear. The complete spontaneous delivery is uncommon in nulliparous women and might take too long, jeopardizing the fetus wellbeing. Therefore, some active maneuvers should be performed. A large episiotomy is desirable.

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There are several proceedings Bracht. Delivery of a fetus in breech position by extending the legs and trunk of the fetus over the pubic symphysis and abdomen of the mother, which leads to the spontaneous delivery of the fetal head 2. Deventer-Müller. If the shoulders cannot be exteriorized, the DeventerMüller maneuver should be performed. The fetus needs to be rotated until its biacromial plane is parallel to the mother’s sagital plane. Then it is stretched downwards until the anterior shoulder appears and the arm is exteriorized. The posterior shoulder is then converted to anterior and the second arm is liberated. 3. Mauriceau-Veit-Smellie. A method of delivering the head in an assisted breech delivery in which the infant’s body is supported by the right forearm while traction is made upon the shoulders by the left hand. The operator’s index is introduced in the fetus’ mouth to ensure the maximum flexion of the head. 4. Use of the Forceps for the extraction of the head, once all the maneuvers result unsuccessful. 1.

Complications The most frequent maternal complications are placental abruption and fourth degree tear. The described fetal complications are intracranial hemorrhage (ruptured tentorium cerebelli, ruptured falx cerebri), neck trauma due to traction (dislocation of the neck, Erb-Duchenne paralysis, torticollis from sternocleidomastoid muscle trauma), ruptured viscera secondary to abdominal grasp (kidney or liver), genital edema due to caput formation, shoulder and arm trauma on delivery of the arms (shoulder dislocation, humerus or clavicle fracture), cord pro lapse (more common in footling breech), hip and leg trauma from traction/hip dislocation, femur fracture, knee joint dislocation). Reference. Barri P: Abnomal fetal presentations. In: Recommendations and Guidelines for Perinatal Medicine. Matres Mundi/WAPM. Barcelona, 2007; 29: 250-256.

C.3.6. UTERINE RUPTURE CONCEPT The commonest antenatal cause is a previous caesarean section scar often classical. The inappropriate use of oxytocin to augment labour (e.g. in multiparous women) and previous cervical surgery, are two of several other causative factors.

SIGNS AND SYMPTOMS a) Evident signs. 1. Severe bursting pain. 2. Unexplained tachycardia. 3. Variable amount of vaginal bleeding.

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4. Fainting and ensuing shock. 5. Cessation of contractions. 6. Disappearance of the presenting part from the pelvis. 7. Fetal distress. b) Unrecognised rupture. 1. Bleeding continues after delivery despite a well-retracted uterus. 2. A cervical laceration has been noted and sutured, but haemorrhage persists and the patient is becoming shocked. 3. There is unexplained shock. All of these are more relevant if she has had an instrumental delivery or previous caesarean section.

MANAGEMENT 1. 2. 3. 4. 5.

Crossmatch 6 units of blood and begin transfusion with Group O Rh negative, screened blood. Arrange immediate laparotomy. Carry out the least extensive surgery compatible with the patient’s immediate health and future welfare. Take great care to identify the ureters and exclude them from any sutures. Prescribe broad-spectrum antibiotics.

FUTURE PREGNANCIES Sterilisation should be discussed with the patient. If she decides against it, close observation is required during any future pregnancy and delivery should be by elective caesarean section at 38 weeks. Reference. Holcroft C, Pressman E: Complications of Labor and Delivery. In: The Johns Hopkins. Manual of Gynecology and Obstetrics. Ed. by Lambrou NC, Morse AN, Wallach EE. Lippincott Willams and Wilkins. Philadelphia, 1999; 4: 47.

C.3.7. UTERINE INVERSION CONCEPT Uterine inversion is diagnosed by partial delivery of the placenta that is followed by massive blood loss and hypotension. Inversion occurs most commonly with fundal placentas and is classified as incomplete if the corpus travels partially through the cervix, complete if the corpus travels entirely through the cervix, and prolapsed if the corpus travels through the vaginal introitus.

TREATMENT Treatment of uterine inversion consists of manually replacing the uterus. 1. If the uterus can be replaced easily without removing the placenta, less blood will be lost; if the bulk of the placenta prevents replacement of the uterus, however, the placenta should be removed to facilitate uterine replacement.

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2. If the cervix has contracted around the corpus of the uterus, uterine relaxant agents may be necessary to effect replacement. Several uterine relaxant agents are available including nitroglycerin, betamimetics such as terbutaline or ritodrine, magnesium, and halogenated general anesthetics such as halothane or isoflurane. If the patient is normotensive and has been given adequate analgesia, then nitroglycerin is the preferred agent because it has a rapid onset of 30 to 60 seconds and wears off within 5 minutes, which enables the uterus to contract again after it has been replaced, minimizing further blood loss. If nitroglycerin, betamimetics, or magnesium, alone or in combination, is unsuccessful in freeing the uterus, general anesthesia should be employed. 3. After the uterus is replaced, uterine contractile agents should be used. 4. If the obstetrician is unable to replace the uterus manually, it may be necessary to perform laparotomy. Traction can then be placed on the round ligaments, adding to vaginal pressure. If traction is unsuccessful, a vertical incision can be made on the posterior lower uterine segment to enable replacement of the uterus. 5. The following hydrostatic method for reduction is also usually effective: a) Attach 1 or 2 litres of warm saline to cystoscopy tubing, such as the Uromatic Y-type TVR administration set (Trevenol). b) The inverted uterus is held within the vagina, using the right hand which is also holding the free end of the tubing. c) An assistant occludes the vagina, using the labia to encircle the operator’s hand. d) Two litres of warm saline are infused rapidly and the even hydrostatic pressure exerted usually reduces the inverted uterus. Reference. Holcroft C, Pressman E: Complications of Labor and Delivery. In: The Johns Hopkins. Manual of Gynecology and Obstetrics. Ed. by Lambrou NC, Morse AN, Wallach EE. Lippincott Willams and Wilkins. Philadelphia, 1999; 4: 47.

C.3.8. LABOUR AFTER GENITAL MUTILATION DEFINITION AND TERMINOLOGY The World Health Organization defines Female Genital Mutilation (FGM) as «all procedures involving partial or total removal of the female external genitalia or other injury to the female genital organs whether for cultural or other non-therapeutic reasons». There are other accepted forms of description for FGM such as traditional female surgery or cutting or female circumcision. Terms that women may use include circumcision, cutting, traditional female cutting or surgery, or sunna.

CLASSIFICATION The World Health Organization (WHO) classifies the different types of FGM by the extent of the surgery: 1. Type I. Excision of the prepuce, with or without excision of part or the entire clitoris.

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2. 3. 4.

Type II. Excision of the clitoris with part or total excision of the labia minora. Type III. Excision of part or all of the external genitalia and stitching/narrowing of the vaginal opening (infundibulation). Type IV. Unclassified, but includes: pricking, piercing or incising the clitoris and/or labia, stretching of the clitoris and/or labia, cauterization by burning of the clitoris and surrounding tissue, scraping of the tissue surrounding the vaginal orifice or cutting of the vagina, the introduction of corrosive substances or herbs intro the vagina to initiate tightening, bleeding or narrowing of the vagina, as well as any other procedure which falls under the WHO definition of FGM.

HEALTH CONSEQUENCES OF FGM Many health problems may be associated with FGM but not every author accepts all of them. The most frequents cited in literacy are the following. a) Short term health consequences. 1. Severe pain during and after the procedure. 2. Local infection. 3. Damage to adjacent tissues. 4. Urinary retention. 5. Haemorrhage, shock and, some times, death of the girl. b) Long term health consequences. 1. Recurrent urinary tract infections. 2. Dysuria, dysmenorrhoea. 3. Perineal lesions: Implantation cysts, neuromas, keloidal scars... 4. Vaginal infections and sexual transmission diseases that may lead to pelvic inflammations disease and infertility. 5. Higher prevalence of bacterial vaginosis and herpes simplex virus 2. It suggests that cut women may be at increased risk of HIV infection. 6. Sexual problems: dyspareunia, frigidity, necessity of surgical reversal of scar tissue in order to achieve intercourse. 7. Psychologial problems: Anxiety, humiliation, terror nightmares... c) Reproductive consequences. 1. Higher perinatal morbidity because of labour complications. 2. The mechanism by which FGM might cause adverse obstetric outcomes is unclear. Although practices vary from country to country, FGM is generally done in girls younger than 10 years and leads to varying amounts of scar formation. The presence of this scar tissue, which is less elastic than the perineal and vaginal tissue would normally be, might cause differing degrees of obstruction and tears or episiotomy. 3. A long second stage of labour, along with direct effects on the perineum, could underlie the findings of an increased risk of perineal injury, post partum haemorrhage, resuscitation of the infant, and fresh stillbirth associated with FMG2.

CARE OF FGM DURING LABOUR 1.

If the woman presents a FGM type I or II with a well healed scar and no complications, no special measures or treatment is necessary during the labour.

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It is sufficient to reassure the patient that she and her baby are under no special risk. If FGM is type III (infibulation), defibulation is needed to remove the obstruction in front of the vaginal opening. Under no circumstance should a woman be subjected to caesarean section solely to avoid defibulation, regardiess of whether she requests it or the provider suggests it. For some authors the optimum time for a defibulation is the second trimester under local or spinal anaesthesia.

Technique of intrapartum defibulation. 1. Before the procedure, the woman is placed in the lithotomy position. 2. The vulva and perineum are cleaned with chlorhexidine and the bladder is emptied using a catheter. 3. The defibulation involves infiltrating the anterior scar tissue with 1 % or 2 % lidocaine solution and inserting the index and middle fingers of the left hand between the crowning head and the scar tissue, and then cutting the scar in the middle between the two fingers during uterine contractions. Care must be taken not to injure intact parts of the clitoris that may be buried under the anterior part of the hood. 4. Midline or mediolateral episiotomy may or may not be necessary. 5. After delivery, sutures are inserted for haemostasis if required. The edges of the skin are stitched apart with a running absorbable, non reactive suture. Any extension of the anterior incision above the urethra may be repaired at this time. A routine repair of the episiotomy or perineal tear is also frequently required post labour. 6. Foley catheter may be kept in situ for 24 hours and local care for the vulval area may be necessary for two-four weeks. Sexual intercourse abstinence is also advisable for six weeks. Reference. Tajada M, Ornat L, Carazo B, Fabre E: Labor after Genital Mutilations. In: Recommendations and Guidelines for Perinatal Medicine. Matres Mundi/WAPM. Barcelona, 2007; 33: 283-289.

C.3.9. COAGULATION DEFECTS GENERAL CONCEPTS a) The main causes of coagulation defects in pregnancy are: 1. Placental abruption. 2. Retention of a dead fetus. 3. Amniotic fluid embolism. 4. Endotoxic shock. b) The principles of management of hypovolaemic or endotoxic shock should be familiar to all medical practitioners.

CLINICAL DIAGNOSIS 1. 2.

The patient may be bleeding heavily and the blood fails to clot properly. These crises may occur suddenly and at inopportune moments.

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3. Complex clotting investigations are therefore hardly ever of practical value, even if they are abailable. 4. A haematologist should, however, be consulted whenever possible.

LABORATORY 1.

Clot observation test. Take a 5 ml sample of blood into a round-bottom 10 ml glass tube. Note the time and keep the blood sample in a pocket. Observe each minute for clot formation. It should clot within 5-6 minutes and remain stable for a further 30 minutes. Failure to clot strongly suggests a significant coagulation defect. Platelet count. This will be markedly reduced.

MANAGEMENT 1. The coagulation defect is usually self-limiting if the stimulus producing it is removed. 2. Therefore in placental abruption THE UTERUS SHOULD BE EMPTIED AS EXPEDITIOUSLY AS POSSIBLE. 3. The transfusion of fresh blood is ideal. If this is not available, transfuse as fresh blood as possible, alternating with fresh frozen plasma (FFP) and, if possible, platelets; 1 litre of whole blood or FFP contains 3 g of fibrinogen. 4. For every 5 units of citrated bank blood transfused, 10 ml of calcium gluconate should be given, to counteract the anticoagulant effect of the citrate. 5. Heparin should only be given in these circumstances after specific instructions from and guidance of a haematologist. 6. Excessive fibrinolysis is virtually never the main problem, and drugs such as epsilon-aminocaproic acid (EACA) or Trasylol are not necessary (except when specifically indicated and under expert guidance, as above). 7. Avoid plasma expanders, e.g. dextran, which reduce platelet aggregation and dilute remaining clotting factors. This plan has been simplified greatly, but contains principles which may be life saving in what can be a frightening and complex clinical situation.

Reference. Stirrat GM: Coagulation Defect. In: Obstetrics (Pocket Consultant). Gran McIntyre. London, 1981; 12,5: 209-210.

C.3.10. AMNIOTIC FLUID EMBOLISM ETIOLOGY 1. 2. 3.

Precipitate labour. Hypertonic uterine action. Oxytocin injudiciously.

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CLINICAL DIAGNOSIS This produces profound shock, cyanosis, dyspnoea and a severe coagulation defect.

MANAGEMENT The first objective is to prevent immediate death from pulmonary vascular obstruction: 1. Oxygen must be fiven, initially by mask. 2. Endotracheal intubation and ventilation may be necessary, so call an anaes thetist urgently. 3. Inject hydrocortisone 1,000 mg i.v. 1-2 hourly. 4. Give heparin 5,000 units i.v. to reduce intravascular coagulation in the pulmonary vessels. Reference. Sciarra GM: Obstetrics (Pocket Consultant). Gran McIntyre. London, 1999; 12. 6: 210.

C.3.11. CORD PROLAPSE CONCEPT Cord presentation discovered before rupture of membranes is an indication for immediate caesarean section. The risk is that the prolapsing cord will become compressed and occluded.

EMERGENCY MEASURES Emergency measures attempt to keep the presenting part from occluding the prolapsed cord. Depending on the circumstances the following can be tried (all together if needs be): 1. Displace the presenting part with the examining hand. 2. If possible, drop the head end of the bed or stretcher. 3. Fill the bladder with 500-750 ml of normal saline, using a size 16 Foley catheter which is clamped and kept in place. 4. If all but the first are impossible (e.g. if she is at home), get the patient info the knee-elbow position. 5. Try to keep the cord within the vagina. 6. If the cervix is fully dilated, delivery should be effected by forceps (cephalic presentation) or breech extraction (breech presentation), providing that the presenting part is low enough in the pelvis. Otherwise caesarean section is indicated. 7. If the cervix is not fully dilated and the baby is still alive, carry out an immediate caesarean section: in a well-organised unit it should be possible to deliver the baby within 15 minutes of the prolapse being noted. Reference. Stirrat GM: Cord Prolapse. In: Obstetrics (Pocket Consultant). Gran McIntyre. London, 1981; 12: 205.

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C.3.12. DIABETES: INTRAPARTUM MANAGEMENT DIABETES a) Goal. To avoid maternal hyperglycemia and/or hypoglycaemia during labor in order to minimize the risk of neonatal hypoglycemia. b) General principles. 1. The rapid changes in glucose and insulin requirements during labor mandate frequent monitoring of blood glucose (BG) concentration every four hours during the latent phase and hourly during the active phase. 2. In general, all home antihyperglycemic medications should be stopped in pregnant patients and insulin should be started to maintain appropriate blood glucose levels during labour. 3. Do not administer any oral antihyperglycemic dose prior to elective surgery as these patients will be fasting. d) Blood glucose goals. Blood glucose in labour should be maintained between 3.9 to 6.1 mmol/L (70 to 110 mg/dL). d) Glucose monitoring. 1. The patient will be provided with a glucometer and test strips during her admission. 2. Blood glucose should be monitored every four hours during latent phase of labor. 3. Blood glucose should be monitored every one-hour during active phase of labor. 4. Nursing staff will need to document blood glucose levels on the Intrapartum Blood Glucose Monitoring Forms and the Cardex. 5. Insulin and Fluid adjustments should be made as per the intrapartum glycemic management algorithm below. 6. If patient is hypoglycemic, treat as per the following: • If BG . 2.75 mmol/L (50 mg/dL) , 3.85 mmol/L (70 mg/dL) 1 1 SYMPTOMS (SX): −− Give 250 mL milk. Recheck BG in 15 minutes. −− Repeat milk if still , 3.85 mmol/L (70 mg/dL) 1 Symtoms Follow-up with bread with margarin or peanut butter. −− Repeat BG check every 15 minutes until BG . 3.85 mmol/L (70 mg/dL) 3 2. • If BG , 2.75 mmol/L (50 mg/dL) 1 Syntoms: −− Give 1 cup juice or sweet tea. −− Recheck BG in 15 minutes. If . 2.75 mmol/L (50 mg/dL) 1 1 symptoms, give 250 mL milk. −− Repeat BG check every 15 minutes until BG . 3.85 mmol/L (70 mg/dL) 3 2. −− If blood glucose level is still low and/or patient is exhibiting signs and symptoms, administer D50 or D5W. Recheck blood glucose every 15 minutes until blood glucose is within normal range. • If found unconscious: −− Give 50 mL Dextrose 50 (D50). Start D5W (IV) or 42 drops/min (rate and solution concentration depends on clinical response).

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GLYCEMIC MANAGEMENT FOR PATIENTS UNDERGOING ELECTIVE CESAREAN DELIVERY When possible, plan for the procedure for early morning to prevent maternal hypoglycemia due to prolonged fasting. Insulin: 1. Morning surgery (,9:00): the patient should plan on taking her usual nighttime dose of intermediate-acting insulin or oral anti hyperglycemic. 2. If surgery 12:00-17:00: Allow to eat or defer surgery: Administer one-third of the morning intermediate insulin dose with a 5 % dextrose infusion. 3. If surgery lasts .1 hour, anaesthesia should use sliding scale and check hourly. 4. Surgery for emergency obstetric indications should not be delayed to obtain euglycemia.

POSTPARTUM MANAGEMENT Patients may have a drastic decrease in their insulin requirements after delivery; therefore close monitoring is required. STOP previous insulin orders and place patients on one-half previous home insulin requirement.

MONITORING 1. 2. 3.

4. 5.

Chronic diabetes: involve the clinical pharmacist, home glucose monitoring program staff and adjust insulin. Gestational diabetes: stop insulin/anti-hyperglycemics for the first 24 hours. For all patients s/p Cesarean delivery: clinical team should involve clinical diabetologist and home glucose monitoring staff to strictly maintain euglycemia to promote wound healing. For all postpartum patients, early breastfeeding should be strongly encouraged. When possible, patients should reinitiate self-monitoring of glucose. Blood glucoses should be obtained four times daily, fasting and three one-hour post prandial blood glucose levels. Patients will adhere to goals set forth for non-pregnant patients. a) Preprandial plasma glucose (or FPG): 3.9–7.2 mmol/l (70–130 mg/dl). b) Postprandial plasma glucose: ,10.0 mmol/l (,180 mg/dl). c) Postprandial glucose measurements should be made 1–2 h after the beginning of the meal, generally peak levels in patients with diabetes. Postpartum patients who give birth to a child who weighs .4,000 g should have a fasting blood sugar or random blood sugar ordered for detection of hyperglycemia.

DISCHARGE 1. Patients should be discharged with follow-up through the post-natal clinic in order to rule out chronic diabetes. On an outpatient basis, a 2-hour OGTT will take place after 6 weeks to check for chronic diabetes. 2. Preconception care should be advised for subsequent pregnancy. 3. Contraception advice should be initiated antepartum and provided before discharge.

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4. It is the responsibility of the medical team to counsel the patient on the importance of follow-up. The medical team will explain to the patient that they may have gestational diabetes or overt diabetes and will need further testing in the post-natal clinic. The medical team will ensure that the patient has a 6-week follow-up appointment with an overnight fast and 75 g OGTT (oral glucose tolerance test) scheduled. Reference. Moi Teaching and Referral Hospital (MTRH). Protocols of the Dept. Of Reproductive Health. Kenya, 2012.

C.3.13. GESTATIONAL DIABETES:

INTRAPARTUM MANAGEMENT

MANAGEMENT UPON DELIVERY: 1. Upon delivery, blood glucose levels should return to normal and medication (oral hypoglycemics and insulin) should no longer be necessary. 2. To ensure blood glucose levels have returned to normal, the patient’s blood sugars should be assessed prior to discharge. Once blood glucose levels have returned to normal, medication can be discontinued. 3. Approximately 50 % of women with gestational diabetes will develop DM2 within 5-10 years following their pregnancy. Because of these statistics, the patient will be advised to return to clinic for follow-up testing 6-12 weeks after delivery. 4. Testing may be completed by either a FBS or a 75 g OGTT test to assess for impaired fasting glucose or impaired glucose tolerance

LIFESTILE 1.

Lifestyle modifications should be placed in effect to help decrease the woman’s chances of developing DM2. 2. Patients with GDM should be counseled on the importance of incorporating these modifications into her daily routine to reduce the risk of developing DM2. 3. She should be encouraged to continue the low glycemic diet from pregnancy as well as continue to achieve 150 minutes of moderate exercise per week. 4. Breastfeeding is encouraged in patients with gestational diabetes to help the patient achieve her pre-pregnancy weight. 5. For patients whose preconception BMI was .25, a target of 5-7 % weight loss should be achieved, if possible. 6. Family planning/contraceptives should be addressed as well. Depo-Provera and progestin-only oral contraceptives are less preferred in patients who have had gestational diabetes, as they can accelerate the development of type 2 diabetes. In patients with pre-existing diabetes, Depo-Provera may worsen glycemic control. 7. The intrauterine device (IUD) is preferred in monogamous partnerships because it is a metabolically neutral and highly effective form of contraception.

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8. In addition to incorporating lifestyle modifications to reduce the risks of developing DM2, it is recommended patients with GDM follow up 6-8 weeks post-partum with the following specialists if able: ophthalmology, dietary, and endocrinology. FBG and 75 g OGTT test results at 6 weeks postpartum FBS

Normal Impaired Fasting Glucose/Glucose Tolerance Diabetes

2-HOUR OGTT

,5.5 mmol/l

,7.7 mmol/l

5.5-6.9 mmol/l

7.7-11.0 mmol/l

.7.0 mmol/l

.11.0 mmol/l

Reference. Moi Teaching and Referral Hospital (MTRH). Protocols of the Dept. Of Reproductive Health. Kenya, 2012.

C.3.14. CARDIAC DISEASE: INTRAPARTUM MANAGEMENT BASIC CONCEPTS OF INTRAPARTUM CARE 1. Inform the Consultant-on-call of all cardiac patients in labour. 2. Aim for short vaginal delivery. Pushing in labour is a form of valsalva, which causes increased heart rate and decreased blood pressure and, therefore, causes increased cardiovascular stress for a woman with valvular heart disease. Prepare for assisted vaginal delivery to shorten 2nd stage of labour. 3. Aim for excellent anaesthesia: give IV/IM pain medication (if Morphine unavailable, then Pethidine 25-50 mg IM every 4 hours). 4. Treat according to obstetric indications: a) Most patients who are able to progress past 28 weeks gestation with only mild cardiac symptoms (ie. NYHA Class I and II) also tolerate labour well. Therefore, assisted/operative delivery should be done according to obstetric indications for these patients. b) Induction and Caesarean section should be done for obstetric indications. c) If augmentation is necessary, use Protocol on Augmentation of Labour. d) Anaesthesia and surgery are usually more harmful to the patient with valvular heart disease than assisted delivery. e) Active management of third stage of labour is important. Avoid use of Ergometrine in the case of PPH. 5. Maintain left lateral decubitus position as much as possible during labour. 6. Continuously monitor and evaluate cardiac function. In addition to routine obstetric monitoring, check: a) Stage 1. Vital signs and listen to heart and lungs every 2 hrs. b) Stage 2. Vital signs every 1 h, listen to heart and lungs every 30 min. 7. Treat pulmonary oedema if it develops during labour. Give higher dose of furosemide 80 mg IV once and repeat as necessary after 30 mins if no urine output. Maximum daily dose is 240 mg IV. Do not use prophylactic furosemide during labour to prevent pulmonary oedema.

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POSTNATAL 1. Prevent pulmonary oedema: Give furosemide 40 mg IV once immediately after delivery. If pulmonary oedema is already present-treat with furosemide 80 mg IV. 2. Monitor urine output. 3. Take vital signs immediately after delivery. Repeat every 15 mins for 1 hr, then every 30 mins for 1 hour, then every 4 hr thereafter for 24 hours. 4. Respiratory exam: every 30 mins for 2 hours, then every 4 h for 24 hours. 5. Continue antenatal medications. 6. Avoid aggressive fluid replacement. Give IV fluids according to usual postnatal care. Encourage oral intake of fluids. 7. Give antibiotics if indications arise; however, prophylactic antibiotics are not routinely indicated for valvular heart disease patients.

DISCHARGE CRITERIA 1. Patients with NYHA Class III/IV or any high risk features, should be kept in the labour room for the first 24 hours to ensure close monitoring, then can be transferred to the postnatal ward at the discretion of the consultant-on-call. 2. All patients should be counseled on family planning options. The following should be advised not to become pregnant again and should be offered bilateral tubal ligation or other long-term methods of contraception prior to discharge from the hospital: a) Diagnosis of any cyanotic heart disease. b) Eisenmenger’s syndrome. c) Severe pulmonary hypertension. d) Severe or symptomatic aortic stenosis. e) Left ventricular dysfunction (ejection fraction , 40 %). f) Aortic root disease (Marfan’s syndrome, severe aortic insufficiency). g) Severe or symptomatic mitral stenosis. 3. Patients should remain in the hospital for at least one week post-delivery and may only be discharged with approval from the consultant-on-call. All patients should be advised to follow-up with cardiology and OB/GYN consultant clinic within 2 weeks. Reference. Moi Teaching and Referral Hospital (MTRH). Protocols of the Dept. of Reproductive Health. Kenya, 2012.

C.3.15. POSTTERM PREGNANCY INDUCTION OF LABOUR 1.

According to the WHO and ACOG recommendations, induction of labour can be offered to women who are known with certainty to have reached 41 weeds. Such a policy is associated with fewer fetal/neonatal deaths and there does not seem to be any increased risk of assisted vaginal or cesarean delivery:

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a) Prior to induction of labour counsel the patient on the process an duration of induction of labour (up to 3 days). b) Prior to induction of labour for postterm all admitted patients should receive a NST in labour ward. 2. If there is concern for foetal intolerance of labour, a CST can be undertaken prior to attempting induction of labour. To conduct a CST-give IV oxytocin 5 units in 500 ml on NS at 5 drops per minute increasing every 30 minutes until the patient is aware of 3 contractions within 10 minutes. If positive CST, a Cesarean delivery should be offered. If negative or indeterminate CST, induction can proceed. 3. Induction with misoprostol should be reserved to patients with reactive NST or negative CST. In the event of a patient non-reactive NST, or indeterminate CST, induction should proceed with oxytocin and/or Foley catheter. 4. Women undergoing induction of labour postterm should be carefully monitored intrapartum for foetal distress.

Reference. Moi Teaching and Referral Hospital (MTRH). Protocols of the Dept. Of Reproductive Health. Kenya, 2012.

C.3.16. PREECLAMSIA AND ECLAMPSIA: MODE OF DELIVERY GENERAL MANAGEMENT 1. 2. 3.

Patients with mild preeclampsia, severe preeclampsia, HELLP and eclampsia may undergo induction of labour. Cesarean Section should only be performed for obstetrical or fetal indications such as arrest of dilatation, arrest of descent or fetal distress. Eclamptic patient with a Bishop score greater than 5 can be induced. The goal is for delivery within 12 hours.

Special considerations during induction of labour for preeclamptic and eclamptic patients. 1. Vital signs must be taken every 30 minutes. 2. Fetal heart rate must be monitored every 15-30 minutes and after every contraction in the second stage. 3. Complete blood count, liver function test and coagulation studies must be monitored at least daily during the induction of labour. 4. Urine Foley’s catheter must be placed and strict intake and output must be recorded for all severe preeclamptic and eclamptic patients. 5. All severe preeclamptic and eclamptic patients should be placed on Mag nesium Sulfate during induction of labour and continued until 24 hours postpartum. Thus patients must be monitored for Magnesium toxicity during induction of labour. 6. For patients on Magnesium sulfate, the nursing and medical staff should be prepared for postpartum hemorrhage as per the RMBH protocol on PPH, however Ergometrine is CONTRAINDICATED in hypertensive patients.

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Immediate post partum management. Monitor blood pressure half-hourly for the first 2 hours post partum then 4 hourly for the next 24-48 hours then taper off drugs as per maternal improvement. Continue therapy with: 1. Magnesium sulfate for at least 24 hours postpartum. 2. Monitor strict intake and output for at least 24 hours postpartum with a Foley’s catheter in place. In case of end organ damage, refer for management in the specialized care units. Discharging antenatal patients preeclampsia. Patients with mild preeclampsia with no other co-morbidities or risk factors may be candidates for outpatient management. Patients should first be assessed for the severity of disease, once the patient’s blood pressure has been stabilized and there is no evidence of severe preeclampsia, the patient may be discharged home with weekly follow up High Risk OB clinic. Prior to discharge the patient must be educated to return to clinic for any of the following: 1. Danger signs of preeclampsia. 2. Performance of Fetal kick chart fore 10 movements in 12 hours and retur for decreased movement. 3. Danger signs of labour. 4. Home bed rest.

Reference. Moi Teaching and Refenal Hospital (MTRH) Protocols of the Dept. of Reproductive Health. Kenya, 2012.

C.3.17. TWIN GESTATION: MODE OF DELIVERY MANAGEMENT Depends on the presentation of the first twin: 1. First twin cephalic: Vaginal delivery should be attempted. Non-vertex presentation of the second twin is not a contraindication for vaginal delivery. 2. First twin breech presentation: Elective Cesarean delivery or vaginal delivery should be considered depending on provider comfort and careful patient selection. The patient must be informed of pertinent risks, including the possibility of «locked» twins. The incidence of «locked» twins is rare, occurring about 1:817 breech/vertex combination. 3. First twin transverse or oblique: If the first twin is transverse or oblique then, cesarean delivery is suggested. 4. Second twin cephalic – first twin delivered vaginally → Deliver vaginally unless in the case of foetal distress. 5. Second twin breech – first twin delivered vaginally → Vaginal delivery is suggested as long as the estimated foetal weight is between 1,500 g and 4,000 g and the health care provider is comfortable with and skilled in vaginal breech delivery. With the second twin as breech, a vaginal breech extraction is an acceptable option. (Consideration should be given to disparity in weight of the

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twins if the second twin is significantly larger. In the case of a second noncephalic twin weighing between 500 g and 1,500 g, there is no consistent evidence supporting either Cesarean delivery or vaginal delivery.) Second twin non-longitudinal – first twin delivered vaginally → If the second twin is non-longitudinal and weighs over 1,500 g, prompt external version or internal podalic version can be attempted. If these manoeuvres fail, cesarean section should be done. Trial of scar may be considered in patients with twins with one previous cesarean delivery.

INTRAPARTUM MANAGEMENT (Remember that a pregnancy with no ultrasound monitoring is at risk of being unrecognized twin pregnancy, so ‘always’ suspect!) a) First stage of labour. 1. Admit and manage as high risk pregnancy. 2. Establish intravenous access. 3. Take blood for: Hb, GXM. 4. The foetal lie, presentation and cardiac activity of each foetus should be assessed at admission by a bedside ultrasound in labour ward. 5. Foetal monitoring of both twins should be documented in the file. 6. Partograph should be kept accurately during labour. 7. Consider the use of the electronic foetal monitor if separate foetal heart rates cannot be distinguished. 8. Augmentation of labour: If protracted labour is encountered, augmentation of labour is an option. The same indications and methods are used as in a singleton pregnancy. b) Second stage of labour. 1. The ideal time limit in twin-to-twin delivery time should be within 15 min but with regular auscultation with fetoscope and reassuring foetal heart rate. 2. Make sure you are prepared for resuscitation of the second twin with a suction bulb, AMBU bag and additional nursing support. 3. Augmentation of labour after delivery of the first twin may be appropriate if there are inadequate contractions. 4. Following delivery of first twin, DO NOT administer IM oxytocin for AMTSL. Ascertain the lie, presentation and foetal heart rate of second twin by abdominal examination or ultrasound. If second twin is: • Vertex: proceed as first twin (facilitate AROM when necessary) or consider internal podalic version and breech extraction (if membranes intact) depending on comfort level of provider. • Breech: deliver using breech extraction. • Transverse lie with intact membranes: consider external version into longitudinal lie or internal podalic version followed by breech extraction, depending on comfort level of provider. • Transverse lie with ruptured membranes: will need a C/S for delivery if foetal survival is expected. Do vaginal exam to exclude cord prolapse.

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c) Third and Fourth stage of labour. 1. Twin delivery is an important risk factor for PPH. These patients should have AMTSL, empty bladder and fundal height checks every 15 min for the first 2 hours postpartum to ensure good uterine tone. 2. An intravenous infusion of 10 IU oxytocin/500 ml should be continued for 2 to 3 hours following delivery of the placenta to ensure the uterus stays well contracted.

POSTPARTUM MANAGEMENT 1. Recommend continued iron supplementation given the high risk of anaemia while breastfeeding twins. 2. Encourage long-term method of FP prior to discharge.

Reference. Moi Teaching and Refenal Hospital (MTRH) Protocols of the Dept. of Reproductive Health. Kenya. 2012.

C.3.18. MENDELSON’S SYNDROME CONCEPT This is due to the deep inhalation of liquid, acid and irritant gastric contents during general anaesthesia. It accounts for half of the obstetric anaesthetic deaths.

CLINICAL PRESENTATION 1. Cyanosis. 2. Tachycardia. 3. Bronchospasm. 4. Pulmonary oedema. 5. Shock in relation to general anaesthesia. 6. It may be confused with pulmonary oedema secondary to mitral stenosis, cardiac failure or amniotic fluid embolism.

MANAGEMENT 1. 2. 3. 4. 5. 6.

Tilt the patient head down. Turn her on one side and aspirate the pharynx. Give oxygen. Inject aminophylline 250 mg i.v. and hydrocortisone 1,000 mg i.v. and repeat as necessary. Suck bronchial tree clear through a bronchoscope (under GA). Prescribe broad-spectrum antibiotic.

Reference. Stirrat GM: Mendelson’s syndrome. In: Obstetrics (Pocket Consultant). London, 1981; 12.7: 210-211.

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PUERPERIUM

D.1.

PUERPERIUM ATTENDANCE

D.1.1.â&#x20AC;&#x201A; POSTPARTUM CARE CONCEPT The postpartum care are activities in health promotion and prevention, diagnosis and treatment planned with the purpose of achieving an appropriate return of the pregnant woman to her previous state and an appropriate development of the nursing.

CLASIFICATION The postpartum period or puerperium has different stages, each one with specific activities, which are: 1. Immediate puerperium: from childbirth to the first 24 hours. 2. Mediate puerperium: from the first 24 hours to the 7th day. 3. Late puerperium: from the 8th to the 42 th day. Objectives of postpartum care. 1. Facilitate the maternal adaptation to postpartum state. 2. Prevent complications during the puerperium. 3. Early detection of any complication. 4. Begin the appropriate treatment of possible complications in the puerperium. 5. Develop an appropriate maternal nursing. 6. Begin the contraception to achieve adequated intergenesic period.

IMMEDIATE PUERPERIUM I.

THE FIRST HOUR a) Clinical surveillance: 1. Transfer to postpartum service with permanent surveillance and trained personnel. 2. Control vital signs every 15 minutes (arterial pressure, heart and breaÂ thing frequency).

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Control the uterine involution: The uterine size should be below the navel, and the uterus must have hard consistency. 4. Control of the vaginal bleeding. b) Postpartum hemorrhage prevention: 1. Uterine massage. 2. Uterotonic drugs administration. Anyone of the following options can be used: • Oxitocin: 10 units in 500 ml saline solution to infuse intravenous in 20 min. • Metilergometrin: 0.2 mgs intramuscular. • Misoprostol: 400-600 mcgs rectal. 3. Intravenous solutions: there must be a permeable vein road to infuse liquids in case of hemorrhage persisting. c) Begin the nursing: after childbirth the mother should spend time with her newborn and begin their contact skin to skin, the appropriate technique for the breastfeeding should be given, except if the mothers or newborn’s clinical condition does not allow for it. II.

THE FIRST 24 HOURS a) Clinical surveillance: 1. The mother should stay in a postpartum service with trained personnel and adequate surveillance. 2. Control of vital signs every 4-6 hours, including temperature. 3. Control of skin and mucous coloration for anaemia detection. 4. Control of diuresis: there should be an urine production of 0.5 ml/kg/ hour, during the first days this may increase because of the redistribution and elimination of the corporal liquids that have increased during pregnancy. 5. Control of the uterine involution: a bladder globe can increase the perception of the uterus size, reason why it is necessary to observe the uterus after miction. 6. Control of vaginal bleeding: the quantity and aspect of the lochia should be observed, which is hematic during the first three days. 7. Control of milk production and the breast state, stimulating the production and the drainage. b) Specific care: 1. Perineal care: in case of episiotomy or perineal lacerations the mother should do adequated hygiene every 12 hours. In case of edema and inflammation apply locally ice. 2. Early walking: it should begin when the patient’s clinical condition allows for it, ideally between the first 2 and 4 hours; this helps to prevent thrombotics phenomenons, urinary retention and constipation. 3. Diet: the patient can receive a free diet, at her tolerance, with a high income of oral liquids. 4. Analgesics: they can be administered if need, but without influencing in the clinical monitorization, for example opiates non narcotics. 5. Stimulation of the nursing: insist in exclusive nursing and by demand of the newborn, avoiding the use of baby bottles. In case of delayed nursing feed the newborn with spoon or syringe.

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III. IN CAESAREAN SECTION BIRTH In general care is the same as vaginal birth, but there are special considerations and delayed ones: 1. Diet: it can begin with clear liquids at 6-8 hours, and according to tolerance give soft and normal diet after the 24 hours. 2. Endovenous liquids: as the blood lost is higher and the diet is restricted, the infusion of 2,000-2,500 ml should be ordered for 24 hours, until the patient has an appropriate oral income. 3. Diuresis: the bladder catheter should be maintained during the first 6-8 hours to watch over the urine volume; in case of normal being and tolerance to the oral income, it could help to improve early walking. 4. Surgical wound care: the wound should remain covered during the first 24 hours unless there is evidenced of active bleeding. 5. Walking; it should start early, but the difficulty that implies the surgical procedure makes it to be delayed for 6-8 hours depending on the tolerante walking. 6. Nursing: in this case the immediate beginning is not possible for the maternal impossibility of attending the newborn, but as soon as the maternal condition allows for the process of the maternal nursing it should be stimulated.

MEDIATE PUERPERIUM The clinical surveillance should persist for the early detection of complications, to emphasize tolerance of oral income and walking, and also for the newborn care. 1. Control of vaginal bleeding: the lochiaâ&#x20AC;&#x2122;s aspect change during the mediate puerperium, it is hematic during the first 72 hours, serohematic until the 5-7th day, and serous until disappearing around the 15th day. 2. Control of uterine involution: the uterine size decreases 2 cm per day, control throught abdominal wall until the 10th day. 3. Milk production: during the first 3 days the calostro appears and has a yellowish aspecto and contains more minerals and proteins (especially globulins), but less sugars and fat than the mature milk. This last level is reached from the 4-5 day arriving at its maximum maturity level at 4 weeks. 4. Prevention and treatment of postpartum anaemia. Iron supplementation is recommended with 30-60 mgs of elementary iron and 400 mcgs of folic acid, during the first two months of puerperium. 5. Education: during the first and second days postpartum the patient should receive information about the changes in puerperium, newborn care, maternal nursing, early detection of complications, sexual activity and contraception. Hospital discharge. The discharge time depends of the type of patient, includes tolerance to walking and oral income, appropriate maternal nursing, education in normal evolution of puerperium puericulture, and contraception. The minimum time of hospital stay for each particular patient depends on the childbirth type and the presence of risks. 1. Low risk vaginal birth: â&#x20AC;˘ Normal clinical surveillance during the first 24 hours postpartum. 2. High risk vaginal birth: includes patients with prolonged premature rupture of ovular membranes, prolonged labor, instrumental birth (forceps, vacuum, etc.), high risk pregnancies, etc.

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• Normal clinical surveillance during the first 48 hours postpartum. • Normal white cells count. Low risk caesarean birth: • Normal clinical surveillance during the first 48 hours postpartum. • Normal white cell count. High risk caesarean birth: • Normal clinical surveillance during the first 72 hours postpartum. • Normal white cells count.

LATE PUERPERIUM In this period, the clinical surveillance should continue for puerperium’s complications detection, insist in the maternal whole nursing by demand, and begin the contraceptive methods to achieve an appropriate intergenesic period to avoid perinatal complications.

Reference. Aguilar James NY, Ordoñez OE: Postpartum Care. In: Recommendations and Guidelines for Perinatal Medicine. Matres Mundi/WAPM; Barcelona 2007, 35: 301-311.

D.2.

PROCEEDINGS AND TECHNIQUES

D.2.1.â&#x20AC;&#x201A; INSPECTION OF PLACENTA AND MEMBRANES CONCEPT After the placenta has been delivered, it is necessary the inspection of the placenta umbilical cord and membranes for: 1. Diagnose the normality of the placenta, the insertion of the umbilical cord and the cord itself. 2. Screening for abnormalities. 3. To determine if the placenta and membranes were expelled completely. Main causes of maternal deaths. Structure of the mature placenta. 1. The mature placental disc shaped with a thickness of 3 cm and a diameter of 20 cm. A normal placenta weighs about 500 g. 2. The fetal side of the placenta is bright because of the amniotic membrane covering it. The fetal side is the insertion point of the umbilical cord in the chorionic plate and large placental branches of the umbilical arteries and vein that radiate from there. 3. The maternal side of the placenta is opaque and divided into 35 lobes. Inside each lobe there are several placental cotyledons, each of which consist of a main villus shaped trunk and its branches.

OBJECTIVES a) General objectives: 1. Increase the level of health of the puerperal woman. 2. Reduce the current numbers of maternal morbidity and mortality for postpartum haemorrhage. b) Specific objective: 1. Know if placenta is normal or with abnormalities. 2. Have a knowledge of the presentation and characteristics of the placenta and umbilical cord. 3. Know the expelled placenta and membranes.

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ACTIONS 1.

Once the placenta and membranes are outside, it paramount to review them; it is a must to always check whether the expulsion of the placenta and membranes has been completed. 2. This review is of particular importance and the midwife will do well to remind the doctor to do it or she will have to do it herself. 3. To check the placenta it is necessary to have good light and clean clothing. 4. Thus, with the reproduction and physiological shape of the uterine insertion, it is very easy to see the layout of the cotyledons and the possible lack of some of them, in which case we must check inside the uterus by hand to get them out. 5. Once reassured about the placenta integrity with the membranes compassing the placenta, control the umbilical cord, so that the fetal side of the camera facing us is well reviewed; then observe whether there is integrity of the membranes, and perceive the existence of an oval hole used by the fetus to emerge. 6. It is very important to examine the edge of the membranes and ensure that no vessel be directed to said edge causing it interruption. This is a sign of the «succenturiatas» or ancillary placentas that may be forgotten. Usually membranes are inserted around the placenta, and if they are not torn, they do not show other opening than the delivery outlet of the fetus. If there are two large holes, suspecte that one of them corresponds to a space left by a secondary placenta that may remain in the uterus. 7. The importance of this inspection is paramount, since the retention of placenta or accessory placenta fragments is invariably followed by bleeding and infection. Consequently, the existence of such debris, and even the suspicion of them, forces the doctor to introduce the hand into the uterus, even though the risk y operation, to ensure that the uterus is completely empty. 8. Retained membranes, however, do not require such radical manoeuvre, since they are spontaneously eliminated during the first week postpartum.

Reference. Carrera JM et al: Examen placentario postparto. In: Protocolos de Obstetricia y Medicina Perinatal del Instituto Universitario Dexeus. 3th Editon, Masson. Barcelona, 1995: 390.

D.2.2. INHIBITION OF THE BREAST-FEEDING BASIC CONCEPTS 1. The ideal food for the newborn is breast milk. However, there are certain circumstances, due to medical or social problems, in which the suppression of breastfeeding is necessary, one must go for artificial feeding; for example when breastfeeding is no longer required but a disadvantage and risk for the newborn (risk of HIV transmission). 2. The inhibition of postpartum lactation can be achieved with the use of na tural resources in 60-70 % of women. If an estrogen is administered success

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is achieved by an additional 10 % and with a combination estrogen-androgen it is reached in about 90 % of cases. The suppression of lactation inhibiting prolactin secretion, using a synthetic alkaloid from ergot, such as bromocriptine, is a highly effective procedure that achieves success in about 95 % of cases.

INDICATIONS 1. 2.

A small number of states of health of the newborn and the mother may justify recommending not to breastfeed temporarily or permanently. Whenever stopping breastfeeding is considered, one should weigh the risks of any of the diseases listed below in terms of the benefits that would accrue breastfeeding.

CHILDHOOD DISEASES Infants that should not receive breast milk or any other milk except a specialized formula: 1. Infants with classic galactosemia: a free special formula of galactose is needed. 2. Infants with the urine smell like maple syrup disease: a special formula free of leucine, isoleucine and valine is needed. 3. Infants with phenylketonuria: a free special formula of phenylalanine (some breastfeeding is allowed, under careful monitoring) is required. 4. Infants for whom breast milk remains the best feeding option but who may need other food for a limited period, in addition to breast milk: a) Infants born weighing less than 1.500 g (very low birth weight). b) Infants born before 32 weeks of gestation (very preterm). c) Newborns at risk for hypoglycaemia due to impaired metabolic adaptation or increased glucose demand as premature, small for gestational age or infants who have experienced significant hypoxic intrapartum and those diabetic sick mothers or children, if blood sugar is not controlled with breast or feeding expressed breast milk.

II.

MATERNAL DISEASES Mothers affected by any of the diseases mentioned below should receive treatment according to standard. 1. Maternal conditions that may justify avoidance of breastfeeding permanently: a) VIHb Infection: if replacement feeding is acceptable, feasible, affordable, sustainable and safe (AFASS). b) If these conditions are not met, exclusive breastfeeding in the first six months is advised. 2. Maternal conditions that may justify temporary avoidance of breastfeeding: a) Serious illness that prevents a mother from caring for her infant, for example septis. b) Herpes simplex type 1 (HSV-1): avoid direct contact between lesions in the breast and the baby’s mouth until all active lesions have resolved. 3. Maternal medication: a) Sedating psychotherapeutic drugs, antiepileptics and opioids and their combinations may cause side effects such as drowsiness and respiratory

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depression, which should be avoided if there are safer alternatives at hand. b) It is advisable to avoid the use of radioactive iodine-131 since there are safer options available; the mother can resume breastfeeding about two months after receiving this substance. c) Excessive use of topical iodine or iodophors (povidone-iodine), especially on open wounds or mucous membranes, may cause thyroid suppression or electrolyte abnormalities in the breastfed baby and should be avoided. d) The cytotoxic chemotherapy requires that a mother stops breastfeeding during therapy.

OBJECTIVES 1. 2.

Main goal. Provide guidelines for action aimed at informing professionals on the inhibition of breastfeeding. Secondary objectives. a) Educate and train all health personnel involved in assiting women who want to stop breastfeeding. b) Provide clear and effective guidelines to health professionals to ensure a good inhibition of breastfeeding for mothers that do not wish to breastfeed, their children but favor the bond. c) Provide information to primary care teams on nutritional development of healthy eating habits from the beginning of the childâ&#x20AC;&#x2122;s life.

TYPES DE WEANING 1.

Forced weaning. Weaning sometimes becomes inevitable for medical reasons or other. When weaning must be imposed by a fully justified reason, before the mother or child are prepared for it, both need support and understanding. However, before taking this decision, it is very important that the mother look for verified information on the need for the weaning, because too often we tend to inhibit lactation with no sound scientific justification. Good to know that really incompatible drugs with breastfeeding are very scarce and the diseases that are contraindication to breastfeeding even less. Volunteer weaning. Weaning can occur at the initiative of the mother or the child. In ideal situations it is desirable that weaning occurs by mutual agreement and is as satisfying and rewarding as the breastfeeding process, but this does not always happen. The decision on waning can have large variations from one child to another. Sometimes the mother may feel like stopping breastfeeding before her child is ready to accept it. Sometimes who decides to end it may be the child despite her/his mother does not have any problem in continuing. Whenever the moment one of the members of the nursing couple wants to put an end, or whatever the reasons, it is important to remember that this is a personal choice and that all are respectable.

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Weaning: a child initiative. If the weaning happens at the initiative of the child, she/he will be the one that sets the tone. Some children just decide one day they do not want to nurse any more. Others do it more slowly, they are gradually disinterested with breastfeeding, reducing demand until it ceases altogether. There are those who first suck only once a day, then once every few days, until they simply stop altogether. A new pregnancy may play a certain role in weaning the previous child. Due to mild changes during pregnancy (lower volume, distinct flavour) many children are waned at this time. Others prefer to continue sucking, and continue to do so after the birth of a new brother/sister. This situation of two children of different ages nursing at the same time is known as «tandem nursing». Weaning mother initiative. A mother may have various reasons for wishing that weaning takes place; from medical, emotional, family pressures, social reasons, etc. The time a mother begins to desire the cessation of breastfeeding is also very variable. Sometimes it may happen in a few days or months, in others after a some years. In any case it is preferable to stop weaning gradually. The latter can lead to breast engorgement (swollen, hard and painful breasts) and even mastitis (inflammation and infection of the breast usually after a duct obstruction due to the cessation of drainage), which would not occur if the adaptation of the breast is allowed to progressive decreased suction, as occurs during gradual weaning (the lower the suction, lower the milk production until it ceases altogether). From an emotional standpoint gradual weaning is also easier for the child. Weaning involves much effort, and mothers who have actively weaned their children often say they had no much free time, and they had to use it to distract their children otherwise. If children are weaned before overcoming their need to suck they may begin thumb sucking or pacifier use when it is offered, with breastfeeding substitutes that can provide some solace to a frustrated child. The night can be especially difficult for a little one waiting to suck that cannot understand the reluctance of the mother; at such a time not many in the family will be particularly rational and patient; the father can make the process better tolerated at night, providing night care to the child.

METHODS FOR INHIBITION OF THE BREAST-FEEDING 1. Natural weaning. Natural ways to suppress lactation are the simplest and oldest. They include avoiding infant suckling and breast manipulation, mechanical compression of the breasts with a breast band or bandage, and limiting fluid intake for 4872 hours. The most important measure is to avoid suction. When breast stimulation does not occur, it reduces reflection of milk removal and the stimulation of prolactin secretion necessary for its formation is reduced. Further distention of the cells drecreases milk secretion. Restricting fluid intake to the mother, although it is generally advisable it does not seem to influence lactogenesis. No changes were observed in the frequency of breast enforge

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ment and discomfort whether increased, maintained or decreased fluid intake. Pharmacological inhibition of breastfeeding. There are certain situations in which taking pills to cut milk is a good option, as it may happen when a woman has had few hours to dedicate to her baby and does not want to start breastfeeding again. In this case, cabergoline, which today is the most widely used drug for this purpose, cause a marked reduction in the level of prolactin in the blood, in most case (but not always), thus preventing rising milk production. However, it should be noted that: a) This medicine is not without risks, and often produces side effects such as dizziness, vomiting, headache and hypotension. These effects are generally attributed to post-partum period, and are mistaken with the «normal» state. b) All women should be informed of the possible risks of taking this medication, a priori and during the time they are taking it. As well as health hazards that means suppression of lactation, short and long term, for herself and her baby.

Situations that often occur: • Mastitis: in these cases it is especially dangerous weaning or stop pumping. It is necessary to continue extracting breast milk during the healing process, avoiding the formation of abscesses. This type of medication must be avoided especially in case of mastitis. • Abrupt weaning: when a woman expresses her desire to stop breastfeeding «here and now» for a thousand and one reasons, justified or not, it is usually prescribed cabergoline with the idea that milk production disappears immediately without any problems... Then seeing mothers with swollen breasts and mastitis risk of engorgement, along with possible side effects, the professional who prescribed the drug, along with the mother, often feel confused about what happened contrary to their expectations.

IDEAS AND SUGGESTIONS FOR SPEEDING WEANING 1. Do not offer, do not refuse. No guarantee can be prolonged while weaning. It is the least painful for the child. 2. Distraction. This is to identify times, places and circumstances where the child usually asks for the breast, and to anticipate alternatives to breastfeeding for the child to direct his attention to something new and attractive rather than to the loss of something endearing as nursing. 3. Replacing. Child food or drink is offered to prevent breast prompted by hunger. This is not to bribe him with treats to stop breastfeeding. It sucking only work when the child is hungry. Keep in mind that children also suck out of affection for his/her mother, to feel her closeness, for comfort if they are tired, frustrated or scared. 4. Postponement. With a child that already understands we can negotiate delaying a decision. The child should be mature enough to accept the wait. They can be offered something to keep them happy in the meantime. 5. Weaning by default, meaning that the mother is separated from the child for

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a few days. It is not recommended, because children not only are sharply deprived from their mother’s milk, but also of her presence, which is vital for affective and emotional health. Reference. Fabre E: Working Group on midwifery and birth outcomes. Perinatal Medicine Section of Spanish Society of Gynecology and Obstetrics. 2th Edition. Zaragoza (Spain), october 1995.

D.2.3. PUERPERAL CURETTAGE INDICATION Surgical evacuation of the uterus should be considered if retained placental tissue is suspected clinically or after ultrasound examination. Retained tissue is more likely if membranes were incomplete at delivery, primary PPH had occurred or if secondary PPH was judged to be heavy or moderate in volume.

PROCEDURE 1. Puerperal curettage should be done under ultrasound guidance. 2. A large aspiration cannula or a large blunt curette may be used. The suction canula, covers only a small area of the postpartum uterus, and its size and shape increase the likelihood of perforation. A large blunt curette, the «banjo» curette, is probably the safest instrument for curettage of the postpartum uterus. 3. Retained placental tissue is likely to be associated with infection and, therefore, broad spectrum intravenous antibiotics should be given in conjunction with surgical evacuation. 4. At the time of surgery, uterotonic agents such as Syntocinon, ergometrine and prostaglandins may be helpful to aid uterine contractility and control hemorrhage.

COMPLICATIONS 1.

Uterine perforation: The risk is much higher in postpartum uterine evacuation and may be even further increased if associated with endometritis. Perforation after cesarean section is more likely and, as these women have a lower risk of retained placental tissue, surgical evacuation in such instances should be considered very carefully. 2. Asherman’s syndrome: the risk is increased for postpartum uterine evacuation. The risk increase particularly if the uterus is infected. 3. The need for a second procedure due to incomplete evacuation of retained tissue may also occur. 4. Hysterectomy may be required to control bleeding in up to 5 % of cases. In view of these significant complications, women should always be fully coun seled on the risks and informed consent obtained. Surgery should be performed by experienced senior medical staff. Reference. Serra B, Mallafré J: Legrado puerperal. In: Protocolos de Obstetricia y Medicina Perinatal del Instituto Universitario Dexeus. 5th Edition, Elsevier-Masson. Barcelona, 2014: 438.

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D.2.4. POST-PARTUM HYSTERECTOMY

(Cesarean Hysterectomy)

a) The indications for postpartum hysterectomy include uterine atony that is unresponsive to massage, medication, or ligation of the uterine or hypogastric vessels; laceration of major vessels; severe cervical dysplasia or carcinoma in situ; and placenta accreta, increta, or percreta. b) Risks of the procedure include increased operative time, increased blood loss, increased rate of infection, and increased incidence of damage to the bladder and ureters when compared with nongravid hysterectomy or caesarean section alone. c) Technique. After delivery of the infant and the placenta, the uterine incision may or may not be approximated, depending on the degree of bleeding. The hysterectomy is performed in the standard fashion. If the hysterectomy is being performed because of bleeding, all pedicles may be clamped and cut and the uterus removed before suture ligation. 1. If a supracervical hysterectomy is performed, the uterus may be amputated from the cervix just below the level of the uterine vessels. The cervical stump is closed with interrupted sutures. 2. If a total hysterectomy is performed, it may be difficult to define the edges of the cervix if is dilated and effaced. An incision may be made in the lower uterine segment and a finger inserted into the incision to define the cervical edge. The glove on that hand should then be considered contaminated and discarded. After the cervix is removed, the vaginal vault is sutured using interrupted sutures or a continuous locking suture. Reference. Lich A, Witter F: Operative Deliveries and Procedures. In: The John Hopkins University. Ed. by Lambron NC, Morse AN and Wallach EE. Lippincott Williams and Wilkins; Baltimore, 1999: 24.

D.2.5. TREATMENT OF URINARY OBSTETRIC FISTULAS CONCEPT Fistula is a traumatic opening between the urinary tract and the outside. The soft tissues of the pelvis has been crushed by constant pressure of the fetal head, leading to an ischemic vascular injury and subsequent tissue necrosis.

GENERAL CONSIDERATIONS 1. 2.

Worldwide, the most common cause of fistulas is obstructed labor. Obstructed labor often occurs in rural areas where girls are married young (sometimes as early as 9 o 10 years of age) and where transportation is scarce and access to medical services is limited. 3. Women may be in labor as long as 5-6 days without intervention, and if they survive, they usually give birth to a stillborn infant. When this tissue sloughs, a vesico-vaginal fistula (VVF) or rectovaginal fistula develops.

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Many of these patients have complex or multiples fisulas, involving total destruction of the urethra and sloughing of the entire blade base. Frequently obstetric fistulas are as large as 5-6 cm. 5. After such fistulas develop, the lives of these young women (most of whom are younger then 20 years) are disrupted unless they can gain access to curative surgical services. 6. The constant, uncontrolled dribble of urine makes them offensive to their husbands and family members. They can no loner live with their families. Most of them eventually become destitute social outcasts- and yet these are otherwise healthy functional young women. 7. The social and economic costs of this problem are enormous. The morbidity associated with obstetric fistulas remains, along with the related problem of maternal mortality, one of the single most neglected issues in international women’s health care.

DIAGNOSE 1. History. 2. Physical examination. • The vulva and perineal area sould be carefully inspected. • Speculum examination. The differential diagnosis for the discharge of urine into the vagina includes single or multiple vesicovaginal, ure throvaginal, or ureterovaginal fistulas and fistula formation between the urinary tract and the cervix, uterus, vagina and vagina cuff. 3. Laboratory studies: • Concentration to determine urea, creatinine. 4. Imaging Studies. • An intravenous urogram is necessary to exclude ureteral injury or fistula because 10 % of VVFs have associated ureteral fistulas.

URINARY FISTULA TREATMENT I.

CONSERVATIVE TREATMENT For very small fistulae, an indewelling Foley catheter to remain in place for about 4 weeks may result in closure.

II.

SURGERY a) Transvesical approach. 1. This approach is usually done when the fistula is located at the level of the ureteral orifices or higher or if the vagina is stenotic. 2. After opening the bladder, ureteral stents are placed to identify the ureters. 3. The fistula is exposed, circumscribed and excised, thus allowing closure of the individual vaginal and bladder layers. Omentum can be useful to interpose between suture lines to improve healing rates. b) Vaginal approach. Decalogue of the basic principles: 1. Timing decision. If VVF is diagnosed within the first few days of surgery, a catheter sould be placed and maintained for up to 30 days. Small fistulas of 1 cm may

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resolve or decrease during this period if caution is used to ensure proper continuous drainage of the catheter. 2. Patient positioning. The patient is placed in a prone position with the knees spread and ankles raised in the air and supported by stirrups. Combining it with reverse Trendelenburg positioning enhances visualization with this technique. (Lawson position) 3. Techniques of repair. Instrumental. The best chance for a surgeon to achieve successful repair is by using the type of surgery most familiar. Long instrumental are adequate, blue methilene, Vicrye 1,000. 4. Exposure VVFs. Esposure and access to a VVF can be facilitated by catheterization of the fistula with a bulb catheter, such as a Fogarty Catheter. An uninflated catheter may thread the fistula where the bulb is inflated, then traction is placed on the catheter to draw the VVF into the field. A small VVf may be probed first with a lacrimal duct probe and dilated with cervical dilators to permit placement of a pediatric catheter/ureteral bulb catheter. 5. Vaginal cuff excision. The vaginal mucosa is denuded circumferentially for a radius of 3-5 mm from the vaginal cuff, including the fistula. This incision is then extended obliquely to the bladder wall so as to resect the fistula tract and vaginal cuff scar in a funnel-shaped specimen. 6. Mobilize the vagina. Dissect the anterior vaginal wall off the underlyng pubocervical fascia. 7. Close the fistula tract (bladder and vagina mucosa). Vertically using 3.0-absorbable sutures in a watertight fashion. Close the pubocervical fascia using 3.0-absorbable sutures horizontally. Excise the redundant vaginal mucosa. Aproximate the vaginal incision using 2.0-absorbable sutures, without causing an overlapping suture line. 8. Close tension-free. The bladder and vagina should be mobilized to enable tension-free. The bladder and vagina should be closed separately. The vaginal skin epithelia can be opposed either by minimal suturing to allow for drainage or closed more formally, but in either case haemostasis should be obtained. 9. Uretheral integrity. The uretheral integrity should be observed with cistoscopy or retrograde pyelogram. 10. Bladder drainage. The bladder should be drained with a size 16-18 catheter, 14 days.

POSTOPERATIVE DETAILS 1. Continue intravenous antibiotics until the patient is able to tolerate an oral diet. 2. To prevent bladder spasms, prescribe anticholinergics. 3. Remove pelvic drains when the output becomes minimal, usually prior to discharge.

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The cases where closure is difficult or tenuous, a Simonds-Knapsteir skin and fat pad (pedicle flap) may be harvested from the labia majora and interposed. A cylindrical bundle of bulbocavernous and pedicled fat are developed carefully, preserving the superior external pudendal artery. A capacious tunnel under the vaginal mucosa between the labia majora and the fistula site then is developed. The labial pedicle flap is brought through the vaginal mucosal tunnel and sutured to the edges of the fistula repair. Then the vaginal mucosa is closed over the labia skin. Reference. Devesa NR: Treatment of Obstetric Fistulas. In: Recommendations and Guidelines for Perinatal Medicine Matres Mundi/WAPM. Barcelona, 2007; 38: 327-330.

D.2.6. POST-PARTUM CONTRACEPTION BASICS CONCEPT 1.

Family planning is a strategy that allows couples to decide the number of children they want, as well as the right time to have them. It is also a human right, a public health strategy, a measure of family welfare and a condition that facilitates the socio-economic development and ensure sustainable de velopment. 2. The interval between pregnancies is important for the health of mothers, allowing them to recover from pregnancy and childbirth and the effort that requires the attention of children. The duration of breastfeeding and the interval between pregnancies are crucial to the quality of life of the newborns, especially in developing countries. Postpartum contraception helps to prolongo the interval between pregnancies. 3. Women and couples, properly informed, can decide about breastfeeding and contraception in the most convenient way for their situation and needs. It is important to consider that the fear of another pregnancy, the need for women to return to their paid work, their health and family, social or economic pressures influence the duration of breastfeeding and the decision of when to start a contraceptive method.

TYPES OF POSTPARTUM CONTRACEPTIVE METHODS 1.

2. 3.

Natural contraceptive methods. These are reversible contraceptive me thods, through which prevents pregnancy, planning sex and refraining from practice (periodic abstinence) in accordance with the fertile periods of the woman. Barrier methods. The use of temporary contraceptive methods that interfere with the fertilization mechanically or chemically. Hormonal contraceptives. Steroid substances or combination of substan ces administered by oral, intramuscular, subcutaneous and intrauterine way prevent pregnancy. Permanent contraceptive methods. Irreversible contraceptive methods

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that prevent the reproductive capacity of the individual or couple permanenthly, through a surgical procedure performed either in men or women.

ACTIONS Recommendations for the use of contraceptive methods described are different for breastfeeding women and women who do not breastfeed. I.

CONTRACEPTION FOR WOMEN WHO DO NOT BREASTFEED Fertility recovers quickly in women who do not breastfeed and first ovulation occurs between four weeks and two months after delivery. When a woman does not breastfeed, she can use any method of choice, if there are no health conditions that restrict their use. The Medical Eligibility Criterial of WHO for this group of women are: 1. Combined oral contraceptives should be started after 2 weeks postpartum to avoid risk of thrombosis. 2. Progestogen-only methods (pills, injections or implants) do not have this problem and can be initiated at any time. 3. IUDs can be inserted after four weeks postpartum, taking special precautions because of the condition of the uterus at this stage of involution. Inserting immediately after birth, just after the placenta delivered, is safe if practiced properly by trained personnel. The IUD should not be inserted between 48 hours and postpartum 4 weeks. General recommendations (categories 3 and 4) described in the section on IUD must be followed. 4. The use of barrier methods may be started at any time. Barrier methods, especially condoms, protect against pregnancy and sex transmitted infections. Since the contraceptive efficacy of these methods depends on the proper use in all sexual relationships, women and their partners should receive clear instructions on how to use and store. 5. Methods based on the recognition of the signs and symptoms of fertility, as the ovulation method, be can learned and used when menstrual cycles are restarted. 6. Surgical sterilization of women is a simples procedure in the early postpartum than during other stages of reproductive life, provided it is carried out with appropriate equipment for proper training conditions. It can be practiced in the first 7 days and after 42 days, but should be delayed between 7 and 42 days because there are more risks. It should also be postponed in severe pre-eclampsia; rupture of membranes for more than 24 hours, severe infections or bleeding; informed consent is required and guidance on this method when the election of women is made in good time, during pregnancy, and it must not be a decision made under the pressure of the circumstances surrounding the birth.

II.

CONTRACEPTION FOR WOMEN BREASTFEEDING In the case of breastfeeding women, there are additional considerations for the use of contraceptive methods; they should not interfere with lactation or growth of children. 1. Nonhormonal methods. Nonhormonal methods are considered the best option for breastfeeding women as they do not interfere with lactation or growth/lactating and do not involve transfer of steroids through milk.

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Lactation amenorrhea (LAM). Breastfeeding amenorrhea offers very high contraceptive protection for women who are exclusively breastfeeding; pregnancy rates are less than 1 % in the first six months postpartum. The provider service should be clear in that: a) The contraceptive effectiveness decreases rapidly after the first postpartum bleeding, with the introduction of supplementary feeding when six months postpartum are reached. When either of these conditions occurs, you must start using another method. b) Breastfeeding should be supported with a high frequency of suction to be successful, to maintain amenorrhea and to prevent supplementary feeding or nursing requirements. c) In addition to the contraceptive protection, lactation amenorrhea provides a period of several months during which the woman can start another method without fear of being pregnant (for example, an IUD can be inserted without waiting for the first bleeding). The assurance that women will not get pregnant in the first months postpartum, if in amenorrhea, also allows to postpone the start of hormonal contraception. Thus avoiding the passage of steroids to the infant, if this is the chosen contraception. Intrauterine devices (IUDs). The IUDs are one of the most reversible methods of contraceptive efficacy with lower pregnancy rates, of 1 % at the end of the year, which represents a great advantage in this period since a pregnancy can harm both the health of the mother and her child. a) The insertion is safe after four weeks postpartum, when completed uterine involution, during lactation amenorrhea or early postpartum periods. No need to wait the first period. One can also take in the post-partum period, taking into account the same considerations for the woman that does not breastfeed. b) It is important to remember that proper training is needed and special precautions taken with regards to the size and position of the uterus for insertion in this period, in order to avoid drilling. c) The inserts in breastfeeding women are less painful and women have fewer problems with bleeding and less discomfort during use, compared with insertions in women who do not breastfeed. The contraceptive efficacy and continuation rates are very good. Surgical sterilization. Surgical sterilization of women has negative consequences for breastfeeding, if prolonged separation of the mother and/lactating avoided. The postpartum period is also adequate for vasectomy because if the woman has breastfeeding amenorrhea the couple does not need additional protection during the three months after the procedure. Barrier methods and spermicides. a) Do not introduce synthetic hormones into a woman’s body and therefore do not interfere with milk production, a sound option in the first months. b) Contraceptive efficacy may be higher during lactation, as there is a partial reduction in fertility in the first postpartum cycle. Condom use protects against STIs/HIV since some women may be more vulnerable in this

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period. The diaphragm can be used after 6 weeks when the female anatomy has returned to normal, making measurements to determine the right size. Periodic abstinence. a) Recognition of the signs and symptoms of fertility, as with the ovulation method. One can learn during lactation amenorrhea how to apply when menstrual cycles are restarted. b) The interpretation of the basal body temperature and changes in cervical mucus may be more difficult during lactation. Some studies have found pregnancy rates somewhat higher after lactation amenorrhea, compared to the rates observed in women who do not breastfeed. Hormonal methods. The progestogen methods can only be administered after the first 6 weeks postpartum; pills, injections and implants can be used. a) These methods have no negative effect on breastfeeding or on the early growth and development of infants. Therefore, they are a good choice when nonhormonal methods represent a risk to the health of the mother or are not acceptable to her. b) They have a high contraceptive efficacy, with pregnancy rates of less than 1 % at the end of year of use and are well tolerated. c) When started during lactation, prolong the period of amenorrhea and women have longer cycles and less days of bleeding when menstrual cycles resume, which has a positive effect on haemoglobin levels. d) When these methods are used, a small amount of hormone passes to the milk, ranging from 10 mcg of MPA in case of injection to less than 100 ng with tablets containing the progestogen and implants. These hormones are active orally, and the effect they may have on long-term developments children is known. Therefore it is recommended to begin its use is six weeks after postpartum to prevent ingestion of the hormone by the baby in the stage and metabolic systems are immature blood-brain barrier. e) Progesterone is administered by vaginal rings, initiating their use at six weeks postpartum. It has been shown to be very effective as contraceptive without altering lactation or growth of infants. Progesterone prolongs the period of anovulation and amenorrhea postpartum, which help to strengthen the natural mechanisms of infertility associated with breastfeeding. Combined hormonal contraceptives. The ACO have a negative effect on the quantity and quality of milk, shortening the duration of breastfeeding and affecting infant growth. For these reasons, their use in the first six months postpartum is not recommended when women are breastfeeding, unless it is the only option. If this is the case, it should start as late as possible, delaying until after the first post-partum bleeding or until the introduction of supplementary feeding to/the infant. The same recommendation applies to injectable contraceptives containing estrogen, as this hormone is responsible for the negative effects on lactation.

Reference. Aguilar-Jaimes NY, Ordoñez OE: Postpartum Care. In: Recommendation and Guidelines for Perinatal Medicine. Matres Mundi/WAPM. Barcelona, 2007; 35: 309-311.

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D.2.7. KANGAROO MOTHER CARE CONCEPT Kangaroo Mother Care (KMC) is defined as early, prolonged and continuous skin to skin contact between a mother and her low birth weight infant (LBWI), both in hospital and after early discharge until at least the 40th week of postnatal gestational age. KMC does not need sophisticated equipment, and for its simplicity it can be applied almost everywhere including peripheral hospitals. Kangaroo Mother Care also contributes to the humanization of neonatal care an the containment of cost, for which reason it may also be attractive for neonatal units in highincome countries. The benefits of Kangaroo Mother Care. Many studies show that Kangaroo Mother Care offers the preterm infants many physical and emotional benefits, which include: 1. A stable heart rate. 2. More regular breathing. 3. Improved dispersion of oxygen throughout the body. 4. Prevention of cold stress and warming babies who are already in cold stress; Kangaroo transportation where there are no transport incubators to keep the warmth chain. 5. Longer period of sleep (during which the brain matures). 6. More rapid weight gain and earlier discharge from hospital. 7. Reduction of purposeless activity which simply burns calories at the expense of infant growth and health. 8. Decreased crying. 9. Opportunities to breast feed and enjoy all the healthful benefits of breast milk. 10. Earlier bonding. The KMC works so beautifully because of three factors concerning the infant: 1. It creates conditions similar to those with which the infant had become familiar in utero, such as the proximity of the mother’s heart beat sounds and her voice couple with the gentle rhythmic rocking of her breathing. 2. It provides containment and allows for flexion and prevents heat loss and provides heat from the skin to skin contact. 3. Protects the infant and offers him a reprieve from the stressful elements of NICU. When to discharge from Kangaroo position: TThe decision of discharging from Kangaroo position is made by the baby itself (at about the 40th week (gestational age 1 postnatal age) and weight of about 2,000 grams. The baby will be restless and the mother will not be able to maintain the Kangaroo position any more, so this is the time to get out of the kangaroo «pouch»

Reference. Standart Treatment Guideline for General Hospitals. Drug Administration and Control Authority of Etiopia Contents: 434-435.

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D.3.1. POSTPARTUM FEVER DEFINITION Postpartum fever (PPF) or puerperal fever is defined as an oral temperature of .38 °C in the first 10 days postpartum or $38.7 ºC during the first 24 hrs postpartum.

CAUSES 1. 2.

Benign fever. Urogenital infection. a) Endometritis. b) UTI. 3. Breast engorgement. 4. Mastitis/Breast abscess. 5. Prenumonia. 6. Wound infection (C/S, cervical, vaginal and or perineal lacerations, episiotomy, uterine rupture) Thrombophlebitis. 7. Deep Venous Thrombophlebitis. 8. Pulmonary Embolism (PE). 9. Septic pelvic vein thrombosis. 10. Pelvic abscess. 11. Pelvi-peritonitis. 12. Malaria. 13. Other causes of fever.

RISK FACTORS 1. 2. 3. 4. 5. 6. 7. 8.

Labor for $6 hours after ruptured membranes. Multiple pelvic examinations. Chorioamnionitis. Increased duration of active phase of labor. Retained placenta or membranes. Urethral catheterisation. Previous UTI. Operative vaginal delivery.

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9. Nipple fissure. 10. Long operative duration. 11. Anaemia. 12. Immunosuppressive therapy. 13. Immunodeficiency disorder. 14. Corticoid therapy. 15. Malnutrition.

SIGNS AND SYMPTOMS 1. Pelvic pain 2. Foul-smeeling lochia 3. Fever 4. Sweating, Tachypnea, Tachycardia 5. Chills 6. Headache 7. Malaise

COMPLICATIONS 1. Puerperal sepsis. 2. Peritonitis.

INVESTIGATIONS 1. FBC, CRP. 2. Urinary analysis with culture and sensitivity. 3. Wound swab for culture and sensitivity. 4. Blood cultures. 5. Cervical and uterine sample and sensitivity. 6. Ultrasound.

MANAGEMENT a) Non-pharmaceutical management. 1. Fluid management. 2. Oxygen therapy if necessary. b) Pharmaceutical management. 1. Antipyretics. • Paracetamol PO 1 g TDC or QOD not more than 6 g/day. 2. Antibiotics. • Ampicillin 2 g IV every 6 h for 3 days plus Gentamycin 160 mg OD for 5 days Plus Metronidazole 500 mg PO/IV q 8 h for 5 days. • If allergic to ampicillin; Erythromycine 500 mg PO every 8 h plus gentamycin plus metronidazole for 5 days. • Cefotaxim 1-2 g IV q 8 h for 3 days, plus metronidazole.

Reference. Ministry of Health of Rwanda: Clinical Protocols and Treatment Guidelines. Kigali, 2012: 117-120.

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D.3.2. POSTPARTUM HEMORRHAGE (PPH) CONCEPT Blood loss higher than 500 ml in vaginal birth, or 1,000 ml in Cesarean section Severe PPH when accompanied by hemodynamic unstability, or blood loss higher than 1,500 ml, or when there is a fall in the hematocrit of 10 % or Hemoglobin level in 4 gr % or more. It can be primary or early (first 24 hours) and secondary or late (after 24 hours). The PPH cause 25 % of maternal deaths in the world.

ETIOLOGY The main causes of PPH can be organized in 4 groups: 1. Contraction anormalities: a) Uterine overdistention: polihydramnios, multiple pregnancy and fetal macrosomy. b) Uterine muscle fatigue: prolonged labor, precipitate labor, and multiparty. c) Intraamniotic infection. d) Anatomical or functional distortion of the uterus like myomatosis, previous placenta, mullerian abnormalities, and medication (MgSO4, terbutalin, halagenous anesthetics). 2. Placental remains retention: tear of umbilical cord, placental retention, placental accretism. 3. Birth trauma: from the uterus to the perineum, it includes: a) Uterine rupture: primary or secondary, if a previous uterine surgery was made (Cesarean section, myomectomy or metroplasty). b) Uterine inversion. c) Histerotomy extension or Caesarean lacerations: they are usually presented when there is fetal advanced descent or malposition. d) Traume in cervix, vagina or perineum; they are frequent in instrumented births, precipitated birth and reveal low quality in birth attention. 4. Clotting abnormalities. These can be primary, such as von Willebrand disease or thrombocytopenic purple; or secondary, such as HELLP syndrome or Disseminated Intravascular clotting (fetal death, placental abruption, sepsis or amniotic fluid embolism).

PREVENTION 1. 2. 3. 4. 5.

Identification of risk factors. Prevention and treatment of anaemia during pregnancy. Practice the selective use of episiotomy. Make a whole physical exam of birth canal and placenta to detect lesions or retention of placental remais. Do active management of third stage of labor: prophylactic use of uterotonics (oxitocin, metilergometrine, misoprostol), controlled and sustained traction of umbilical cord and uterine massage before and after of childbirth.

TREATMENT a) Early diagnosis and timely reanimation: 1. Assure airway.

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2. 3.

Assure circulatory access: take two veins with catheters 14 F or 16 F. Continuous monitorization: arterial pressure, pulse, breathing frecuency and urine production. 4. Restore intravascular volume in 20-30 minutes with cristaloid infusions in relationship 3-4: 1 according to blood lost. 5. Laboratory samples for hemoglobin, hematocrit, hemoclassification, clotting test and crossed tests for transfusion. 6. Activate the alarm in the blood bank or transfusion unit. b) Management of a specific cause: 1. Contraction abnormalities. If uterus size is increased and not contracted: • Do a vigoruous bimanual uterine massage to stimulate the uterine muscle contraction and evacuate the intrauterine clots that can hinder the contraction. • Administer uterotonics. Oxitocin 10 to 40 units plus Saline solution 500 ml in 20-30 min, if necessary have caution with the hipotention that produce these doses; use metilergometrin 0.2 mgs intramus cular every 5 minutes with maximum 5 dose (1 mg), or Misoprostol 600-800 mcgs rectal, if there is hypotension, or oxitoxin is not available. 2. Retention of placental remains. • Check if the placenta came out completely. • Uterine manual revision or curettage with sedation or general anes thesy may be necessary. 3. Trauma on the birth day. • Make a systematic review of the birth canal. • Suture the wounded areas with absorbable sutures and hemostatic points. The uterine rupture should be corrected by laparotomy, and depending of the size could apply an emergency hysterectomy. • In case of uterine inversion the reduction of the uterus with the placenta in situ should be carried out, to extract it later on. 4. Clotting abnormalities. • Should have been corrected at the best level previous to childbirth, but if they appear again it is necessary to make the respective reinstatement of the altered blood component. c) Untractable postpartum hemorrhage. If after 20 minutes with the previous actions the hemorrhage does not stop: a) Blood transfusion. Begin with packed red globules (PRG) of the same patient’s group and Rh, but in case of no stock use group O and Rh ne gative. b) Uterine Tamponade. It is a transitory measure for the patient’s transport to an other institution or as an option in patients with suitable conservative treatment. It can be used in cases of uterine atony or placenta accrete. c) Antishock technology. It is used to improve the venous return and in cludes position changes (elevation of legs), and the use of pneumatic or non pneumatic suits. d) Surgical Procedures. To be applied by trained personnel only: • Trauma correction • Uterine or Hypogastric arteries ligature: the best result is achieved with the uterine arteries ligature (80-90 % Vs 50 %).

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•

Compresive uterine sutures: B-Linch, Hayman (transfixiant points) and Cho (multiple square points). • Emergency hysterectomy. • Abdominal packaging: Suitable when it cannot be maked hemostasy and clotting anomalies exist. e) Angiografic embolization. Used in some cases when there is difficult surgical access, or when in spite of the surgical procedures bleeding persists. f) Intensive care units. After surgical procedures and when stabilization and intensive monitorization are required.

Reference. Rueda S, Oros D, Fabre E: Postpartum Haemorrhage. In: Recommendations and Guidelines for Perinatal Medicine. Matres Mundi/WAPM. Barcelona, 2007; 35: 312-320.

D.3.3. POSTPARTUM ENDOMETRITIS CONCEPT Infection of the uterine cavity present after childbirth. It can extend to produce endomyometritis, pelvic abscess, septic pelvic trombophlebitis, sepsis and septic shock. It is characterized by polimicrobian aetiology, which comes mainly from the lower genital tract. There are Risk factors such as: 1. Bacterial vaginosis. 2. Prolonged premature rupture of ovular membranes (RPMO). 3. Prolonged labor. 4. More than 6 vaginal tacts in labor. 5. Caesaren section. 6. Internal fetal monitorization.

PREVENTION 1. Treat previous vaginal infections (Bacterial Vaginosis, Streptococcus agalactiae colonization, Trichomoniasis). 2. Induction of labour in PROM that does not need expectant management. 3. Appropriate control of labour. 4. Decrease of Caesarean section index.

DIAGNOSIS 1. Fever higher than 38 ºC. 2. Tachycardy. 3. Subinvoluted and painful uterus. 4. Odorous and hemopurulents lochias. 5. White cells count with leucocitosis and neutrophylia. 6. Differential diagnosis: urinary infection, infected haematoma, pelvic abscess, mastitis, viral infection.

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TREATMENT Antimicrobial therapy: wide spectrum schedules are used by parenteral way, until the patient remains asymptomatic 48 hours. a) Clindamicin 900 mg IV every 8 hours plus Gentamicin 5 mg/kg/day IV in single dose. b) Ampicilin- Sulbactam 1.5-3 gr IV every 6 hours. c) Crystalline G Penicillin 5,000,000 UI IV every 6 hours plus Gentamicin and Metronidazol 0.5-1 gr IV every 8 hours. d) Cefoxitin 2 gr IV every 6 hours. e) Piperacilin/Tazobactam 2-4 gr/0.25-0.5 gr every 6-8 hours IV. 2. Extraction of placental remains if there is retention evidence. 3. In case of Endomyometritis and/or pelvic abscess, laparotomy and hysterectomy should be done. 4. In case of septic pelvic trombophlebitis, heparin begin with a bolus of 5,000-10,000 UI and continue with 1,000 UI/hour with clotting control test every 6 hours. It is possible also to use low molecular weight heparins such as Enoxaparin or Nadroparin 1 mg/kg every 12 hours, or Dalteparin 200 UI/kg. 1.

Reference. Aguilar-James NY, Ordoñez OE: Postpartum Endometritis. In: Recommendations and Guidelines for Perinatal Medicine. Matres Mundi/WAPM. Barcelona, 2007; 35: 307-308.

D.3.4. THROMBOEMBOLISM IN PUERPERIUM CLASIFICATION 1. 2. 3.

Superficial trombophlebitis. Deep venous trombosis (DVT). Pulmonary thromboembolism (PTE).

DIAGNOSIS a) Superficial Trombophlebitis: 1. Pain and eritema along venous lap. b) Deep Venous Trombosis: 1. Deep pain in legs that improves with the elevation. 2. Increased leg circumference bigger than 2 cm compared to the contra lateral. 3. Positive Homan sign (muscular pain when foot dorsiflexion with extended leg). 4. Changes in skin coloration and delayed capillary fullness. 5. Venous Doppler shows flow obstruction. c) Pulmonary Thromboembolism: 1. Tachypnea, dysnea, pleuritic pain, cough and hemoptisis. 2. Electrocardiogram changes like tachycardia, inverted T wave, depressed ST, right branch blockade. 3. Hypoxemy and decreased oxygen saturation.

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RX of thorax shows increased heart silhouette, pulmonary condensation, increased pulmonary artery and pleural effusion. 5. Disbalance in ventilation/perfution gammagraphy. 6. Arteriography and Angiotomography show pulmonary arterial throm bosis.

TREATMENT a) Superficial Thrombophlebitis: 1. Bed rest and elevation of lower limb, with stockings or pressure ban dages. 2. Hot compresses with of Epson’s or England’s salt. 3. Paracetamol 500 mg VO as needed. 4. Early walking. b) Deep venous thrombosis. The abovementioned plus: 1. Anticoagulant therapy: Intravenous Heparin with a bolus of 5,00010,000 UI and continue with 1,000 UI/hour with clotting control test every 6 hours. Low molecular weight Heparin can also be used such as Enoxaparin or Nadroparin 1 mg/kg every 12 hours, or Dalteparin 200 UI/kg. When confirming the diagnosis continue with low molecular weight heparins or warfarin for maintenance therapy, for 6 weeks to 6 months depending on level of risk. c) Pulmonary Thromboembolism: 1. Transfer to intensive care unit. 2. Oxigen therapy with mechanical ventilation according to the clinical condition. 3. Opiate analgesics for management of pain. 4. Bed rest. 5. Anticoagulation therapy according to outline enunciated in point 2. 6. Inotropic drugs in the event of heart deficiency.

Reference. Aguilar-Jaimes NY, Ordoñez OE: Thromboembolic diseases. In: Recommendations and Guidelines for Perinatal Medicine. Matres Mundi/WAPM. Barcelona, 2007; 35: 308-309.

D.3.5. MASTITIS CONCEPT Infection in the breast caused by the incoming of germs into the galactic ductus or nipple fisures, facilitated by bad milk drainage and wrong cleaning of nipple. Generally produced by staphylococcus or streptococcus.

DIAGNOSIS 1. 2. 3.

Fever higher than 38 ºC. Pain, eritema, heat and tenderlness of breast. In case of mammary abscess, there is a fluctuating and painfus mass.

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TREATMENT a) General measures. 1. Effective milk removal. Continue the breast drainage white nursing with contralateral breast. 2. Massaging the breast during the feed with an edible oil on the fingers may also be hepful. 3. Alfer the feed, hand pressure or pump use may also increase milk drainage and hasten resolution of problem. 4. After feeding or expressing, cold packs can be applied to the breast in order to reduce pain and edema. 5. Paracetamol 500 mgs VO as needed according to level of pain. b) Antimicrobial therapy. If symptoms are not improving within 12 to 24 hours, or if the woman is acutely ill, antibiotics shoul be started. 1. Dicloxacilin 500 mg VO every 6 hours for 7-10 days, or if Penicillin allergy give Eritromicin 250 mg VO every 6 hours. 2. In case of no response to oral therapy for 72 hours or if there is a mammary abscess: oxacilin 2 grs. IV every 4 hours. c) Abscess drainage. It should be done with adequate anaesthesia, asepsis and antisepsis technics. If possible take samples of pus. Leave a gauze in cavity, to be removed at 24 hours. Wound’s cures 2 times at day. Reference. Aguilar-Jaimes NY, Ordoñez OE: Mastitis. In: Recommendations and Guidelines for Perinatal Medicine. Matres Mundi/WAPM. Barcelona, 2007; 35: 308.

D.3.6. PUERPERAL SEPSIS Puerperal sepsis is a kind of infection, that complicates delivery. It is caused by a number of microorganisms including gram positive, gram negative and anaerobes.

DIAGNOSIS 1. 2. 3.

Clinical. History of delivery with evidence of sepsis Laboratory. Anaemia, leucocytosis with neutrophilia, positive blood culture, pus culture. Untrasound. Evidence of retained products of conception, or evidence of abscess collection at tubo-ovarian complex, pelvic abscess or generalized peritonitis.

TREATMENT Requires hospitalization. Treatment includes: a) IV antibiotics until 48 hours after the fever has subsided followed by IM/PO dose for 10-14 days, Anti pyretics and analgesics should be used as required.

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Ampicillin, 1 gm IV QID. (For S/Es, C/Is and dosage forms.) PLUS Chloramphenicol. 1 gm IV QID. (For S/Es, C/Is and dosage forms.) OR Metronidazole, 500 mg IV QID. (For S/Es, C/Is and dosage forms.) OR Clindamycin, 600 mg IV QID. (For S/Es, C/Is and dosage forms.) PLUS Gentamicin, 80 mg IV TID until 48 hours after the fever has subsided. (For S/Es, C/Is and Dosage forms.) Followed by Ampicillin, 500 mg P.O. QID. (For S/Es, C/Is and dosage forms.) PLUS Gentamicin, 80 mg IV TID for 10-14 days. (For S/Es, C/Is and dosage forms.) PLUS Chloramphenicol, 500 mg P.O. QID. (For S/Es, C/Is and dosage forms.) OR Metronidazole, 500 mg P.O. TID. (For S/Es, C/Is and dosage forms.) Alternatives Ceftriaxone 1 gm IV QD. For 7-10 days. (For S/Es, C/Is and dosage forms.) PLUS Clindamycin, 450 mg IV QID. (For S/Es, C/Is and dosage forms.) OR Metronidazole, 500 mg P.O. TID. (For S/Es, C/Is and dosage forms.) b) Surgical treatment: • Evacuation of the uterus. • Laparotomy and drainage of abscess. • Salpigo-opherectomy and/or hysterectomy depending on the clinical situation. c) Additional treatment: Heparin 2,500-5,000 may be given in selected cases to prevent DIC (for dosage schedule, S/Es, C/Is and dosage forms).

Reference. Moi Teaching and Referral Hospital (MTRH). Protocols of the Dept. of Reproductive Health. Kenya, 2012.

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D.3.7. PUERPERAL PSYCHOSIS DEFINITION Puerperal psychosis is a depressive disorder that presents within 6 months after delivery.

CAUSES/RISKS FACTORS 1. 2. 3. 4. 5. 6. 7. 8.

Previous depression. Family history of depression. History premenstrual syndrome. Current history of abuse. Unwanted pregnancy. Alcohol or substance abuse. Vulnerability to hormonal change. Environmental stressors.

SIGNS AND SYMPTOMS Five signs of the following, most of the day, every day, for two weeks: 1. Depressed or irritable mood. 2. Inability to enjoy (anhedonia). 3. Changes in sleep: (cannot sleep when the baby is sleeping). 4. Changes in appetite. 5. Guilt. 6. Thought of death.

COMPLICATIONS 1. Suicide. 2. Infanticide.

INVESTIGATIONS 1. 2.

Thyroid test to rule out hypothyroidism. Investigation of cerebral tumor.

MANAGEMENT •

Medication and psychotherapy.

RECOMMENDATIONS 1. If any signs/symptoms of depression alert health facility. 2. Encourage breastfeeding.

Reference. Ministery of Health of Ruanda: Clinical Protocols and Treatment Guidelines. Kigali 2012: 123-124.

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E.1.

CLINICAL ATTENDANCE

E.1.1.â&#x20AC;&#x201A; NEONATAL ASSISTANCE IN DELIVERY ROOM GENERAL CONCEPT Maternal and fetal complications that require the presence in the delivery room of someone trained in neonatal resuscitation.

CONDITIONS REQUIRING THE AVAILABILITY OF A NEONATOLOGIST IN THE DELIVERY ROOM 1.

Fetal distress. a) Persistent dips II (late decelerations) or other serious anomalies of the FHR. b) The pH of the scalp is lower than 7.20. c) Meconium amniotic fluid. d) Cord prolapse. 2. Clear operative Obstructed labor (dystocia). a) Caesarea of repetition. b) Difficult instrumental extraction. 3. Bleeding in the third quarter/placental abnomalities. a) Placenta previa. b) Premature separation of the placenta from the uterus (placental abruption). 4. Multiple births. 5. Estimated weight lower than 2,000 grams/suspicion of serious intrauterine growth restriction (IUGR). 6. The estimated gestational age is equivalent to 34-35 weeks or less. 7. Difficult breech birth, prolonged labor or other conditions of the extraction and presentation of the fetus. 8. Insulin-dependent diabetes. 9. Rhesus isoimmunisation. 10. Severe hypertension-toxemia. 11. Severe or decompensated maternal disease (kidney, lung, heart, etc.). 12. Previous perinatal mortality, lack of prenatal care. Also when the obstetrician finds it necessary.

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CONDITIONS ADDITIONALLY REQUIRING, THE IMMEDIATE ASSISTANCE TO THE NEWBORN, STARTING A THERAPEUTIC OR DIAGNOSTIC PLAN 1. Major prenatally suspected fetal malformations or malformations identified in newborns at birth. 2. L/S Relation lower than 2 (or 3 in diabetics). Neonatal respiratory distress. 3. Apgar score lower than 5 in 5 minutes (with good previous Apgar score). 4. The pH in the cord is lower than 7.20. 5. Neonatal anoxia. 6. Signs of neonatal sedation. 7. Signs or suspicion of perinatal infection. a) Fever. b) Fetid amniotic fluid. c) Premature breakdown of membranes (more than 24 hours). d) Clinical-analytical signs of maternal infection. 8. Newborn from a diabetic mother. 9. Isoimmunized newborn. 10. Newborn from a mother with a probable or positive (autoimmune) etiology disease. 11. Newborn from a drug addict mother. 12. Oligoamnios or hidramnios of unknown cause. 13. Prematurity (less than 37 weeks). 14. Postmaturity or dysmaturity (more than 41.6 weeks or maturity not consistent with the gestational obstetric age). 15. Newborn with IURG or with signs of intrauterine malnutrition. 16. Other situations according to the opinion of the neonatologist. Reference. Carrera JM: Protocolos de Obstetricia y Medicina Perinatal del Instituto Universitario Dexeus. 4th Edition, Elsevier. Barcelona, 2006: 453-461.

E.1.2. NEONATAL EXAMINATION GENERAL CONCEPTS The staff in the neonatology section must evaluate the conditions of the newborn as soon as possible, even though the systematic exploration of a newborn in apparent good conditions can take a while. It has to be done during the first 12-18 hours, and later, at least every 3 days while the infant remains in the hospital, and a finally, in the 24 hours prior to dismissing the patient.

EXAMINATION SYSTEM The physical examination of the newborn should be done following proper gui delines.

COMPLEMENTARY EXAMS It is also necessary to complete: a) Determination of the pH of the umbilical artery right after birth.

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b) Determination of cord Rh. If both, mother and child have negative Rh it is recommended to perform a second test with blood from the heel. c) Hypothyroidism screening test. d) Screening of metabolic diseases (in our environment, fenilalaninemias, tyrosinemia, metabolic disorders of cystine, homocystine and histidine). Further determinations should be done according to the judgment of the neonatologist, particular pathologies and risks of the newborn. Reference. Carrera JM: Exploración normatizada del neonato. In: Protocolos de Obstetricia y Medicina Perinatal del Instituto Universitario Dexeus. 3rd Edition, Masson. Barcelona, 1995: 427-429.

E.1.3. BREAST-FEEDING ADVANTAGES OF BREAST MILK 1.

Antiinfective properties. a) Bifidus factor in breast milk protects against diarrhea by promoting proliferation of Lactobacillus bifidus in infant intestines, which discourages colonization by pathogens. b) Breast milk protects against respiratory infections, including respiratory syncytial virus (RSV) and otitis media. c) Breast milk protects against necrotizing enterocolitis. d) Breast milk promotes phagocytosis by macrophages and leukocytes. Antiallergic properties. a) A decreased incidence and severity of eczema has been demonstrated in breast-fed infants. b) Species-specific protein in breast milk delays introduction of foreign protein. Bonding. a) Breast-feeding promotes special closeness between mother and baby. b) The prolactin response increases maternal relaxation. c) Breast-feeding increases maternal self-confidence. d) Breast-feeding meets an infant’s need for safety, security, and cuddling.

CONTRAINDICATIONS 1. For women with breast cancer, the mother’s need for treatment takes precedence over lactation. 2. Women who have suffered acute HBV during pregnancy should not breastfeed; newborn infants of HBV- positive mothers who have received HBIG and vaccine, however, may be breast-fed. 3. Hepatitis C infection is a contraindication to breast-feeding. 4. Women with HIV infection should not breast-feed. 5. A life-threatening illness in the mother precludes breast-feeding. 6. Galactosemia in the infant is a contraindication to breast-feeding. 7. For women with herpes simplex virus (HSV) infection, breast-feeding is contraindicated in the presence of active breast lesions.

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HOW TO BREAST-FEED 1. Direct the mother to put the infant to breast as soon as feasible. 2. Encourage rooming in. Glycogen stores in full-term infants generally are sufficient initially; avoid supplemental feeding unless medically indicated. Frequent breast-feeding helps establish a mother’s milk supply, prevents excessive engorgement, and minimizes neonatal jaundice. 3. Positioning. a) Cradle position. The infant’s head rests in the mother’s antecubital fossa, with her body rotated so that the infant’s abdomen is against the mother’s chest; the infant’s lower arm is behind the mother, and his or her head, chest, abdomen, and knees are in a horizontal line at the level of the breast (pillows may be needed for support). b) Clutch (football) position. The infant’s body is positioned on pillows at the mother’s side, with hips flexed and the back of his or her neck supported by the mother’s hand. c) Side-ling position. The mother is positioned on her side in bed and the infant placed on his or her side facing the mother; the lower breast is offered first, then the mother rolls toward the baby or to her other side to offer the second breast. 4. Latch-on. a) The mother supports and lifts her breasts with her thumb on top and her fingers below, staying behind the areola; strokes the infant’s lips gently with her nipple; waits for the baby to open the mouth wide, then with the nipple directed toward the center of the mouth, the mother draws the baby in close. The tip of baby’s nose should touch the breast; the airway can be maintained by lifting up the breast if necessary. b) Appropriate latch-on and nutritive sucking are achieved when the infant’s jaw excursions are wide and swallows are audible. The infant’s tongue should be visible coming forward to the lower gum (visualized by holding down its lower lip), and the baby should not be pulled easily off the breast. The infant’s lips should be flanged outward and can be gently pulled out if necessary. c) If the baby latches on correctly and the mother does not report pain, there is no need for or benefit to limiting feeding time. Arbitrarily limiting feeding time can curtail intake by the infant as well as promote engorgement in the mother. d) Both breasts should be offered at each feeding; the breast offered should be alternated because the baby sucks more vigorously on the first breast at each feeding. e) The infant is removed from the breast by the mother’s finger, inserted in the corner of the baby’s mouth to release suction. f) The baby should be burped after each breast. g) To avoid drying and cracking of the nipple, a few drips of colostrums or mild should be extended onto the nipple and areola after feeding, followed by air drying for several minutes. Reference. Reddy U, Rossiter J: Breast-feeding. In: The John’s Hopkings manual of Gynecology and Obstetrics. Lippincott Williams and Wilkins. Ed. Lambrou NC, Morse AN Wallach EE. Philadephia, 1999; 1: 17-18.

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E.1.4. DRUGS CONTRAINDICATED DURING BREAST-FEEDING 1. Bromocriptine. 2. Cyclosporine. 3. Lithium. 4. Phenindione. 5. Marijuana. 6. Cocaine. 7. Doxorubicin. 8. Methotrexate. 9. Amphetamine. 10. Nicotina (smoking). 11. Cyclophosphamide. 12. Ergotamine. 13. Phencyclidine. 14. Heroin. 15. Certain radiopharmaceutical preparations. Reference. American Academy of Pediatrics (2010).

E.1.5. FETAL NECROPSY GENERAL CONCEPTS a) The term fetal «necropsy» refers to that set of postmorthem diagnostic procedures whose aim is to obtain as much information as possible about the pathological status of the fetus studied, and the cause(s) of death. b) In the prenatal area the main aim of necropsy is to specify the types of pathology suffered by the embryo or fetus, the findings being compared with the information provided by the various prenatal diagnostic techniques used and the presence of any othe abnormalities being ruled out. c) Necropsy examination of the product is essential not only to confirm or rule out a given pathology and clarify the cause of intrauterine death, but also to be able to offer appropriate reproductive counselling

AUTOPSY PROTOCOL a) The study protocol should include: 1. Photographic documentation of the fetus and placenta. 2. Radiographic study of the fetus and placenta. 3. External macroscopic examination of the fetus. 4. Internal macroscopic examination of the fetus. 5. Histological study of the fetus. 6. Examination of the placenta and adnexa (umbilical cord and membranes). 7. Cytogenetic study of the fetus and placenta. 8. Microbiological study (bacteriological and virological) of the fetus and placenta (optional).

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b) It is essential that the necropsy request be accompanied by an adequate clinical report of the case. c) Additional equipment used in fetal necropsy includes suitable dissection instruments, ophthalmic scissors, straight 6-inch Mayo forceps, 5 and 6-inch rounded forceps, blades and scalpels, various magnifying lenses and, if possible, a dissection microscope.

PHOTOGRAPHIC DOCUMENTATION a) Complete photographic documentation should include: 1. Overal view of the product’s phenotype (anterior, posterior and lateral views). 2. Dysmorphic features of particular diagnostic interest (facies, extremities, etc.), using various magnifications. 3. External malformations (from different angles). 4. View of the three body cavities. 5. Detailed view of the visceral morphological abnormalities. It is essential that a centimetre scale appear in all photopraphs. b) The instrumentation required to produce photographic documentation may be highly sophisticated (reprobit with accessories, etc.) or extraordinarily simple. A skilfully used Polaroid-type camera is often sufficient.

RADIOGRAPHIC STUDY a) Radiographic study should be a routine part of the study of the product from week 12 of gestation onwards. b) The main aims of radiographic study are as follows: 1. Assessment of the maturation, growth and development of the product, any abnormalities being established. Radiography enables these to be compared with the prenatal biometric data provided by ultrasound. 2. Confirmation or exclusion of skeletal abnormalities. When these are present, a careful radiographic study provides information of fundamental importance in making a diagnosis. 3. Full assessment of abnormalities or malformations, as well as their consequences for the various organs and systems. 4. When necropsy is not possible (absence of parental consent, etc.) ra diographic study provides valuable information about internal abnor malities. 5. Establish the cause of death, and the time it this took place in utero. c) The method of examination is as follows: 1. Complete anteroposterior radiography of the fetal body, including the cranium, thorax, abdomen and extremities. The upper extremities should be placed next to the fetal body, with the elbows flexed and the fingers extended. The lower extremities should be placed in abduction with the knees pointing forwards. 2. Complete radiography of the profile (lateral). In order to avoid skeletal structures being superimposed, the arms of the fetus should be extended in front of the thorax, as should its legs, the hip being flexed to different angles.

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3. Partial radiographs, which include structures of particular interest for the diagnosis. 4. Radiological studies with water-soluble contrast dyes in order to examine in detail the urinary system. 5. Radiology of dissected structures. In the case of skeletal dysplasia it may de worth carrying out an individual radiological study of one or more bones (e.g. the femur) after dissection.

EXTERNAL MACROSCOPIC EXAMINATION OF THE FETUS a) The most common methodology is as follows: 1. Weighing of the fetus and placenta. Both weight, should be compared with reference tables and/or curves. 2. Systematic examination of the fetal phenotype, looking not only for striking dysmorphic congenital defects (major malformations, disruptions, deformities, etc.) but also minor abnormalities or malformations. 3. Anthropometric assessment, which must include the following parametes: • Biparietal diameter (obtained with a compass). • Craniocaudal length (CCL) and head-to-heel length (HHL). • Cephalic circumference. • Thoracic circumference (at nipple level). • Abdominal circumference (at navel level). • Foot length. b) The measurements obtained should be compared with existing tables or curves of normality.

INTERNAL MACROSCOPIC EXAMINATION OF THE FETUS a) This should be done systematically in order to establish an accurate record of the position, relationship, connections and development of the various organs. b) The methodology commonly used is as follows: 1. Opening of the three body cavities: cranial, pleural and peritoneal. The incision technique will depend on the gestational age, the specific pathology and the individual preferences of the pathologist. 2. Removal of the organs and viscera in blocks. Four blocks are generally removed: central nervous sytem (CNS), thorax, abdomen and pelvic and retroperitoneal structures. 3. Examination of the whole organs and viscera (localization/relationship, structure, etc.) Some organs, such as the heart or those of CNS, require special examination procedures. 4. Measurement and weighing of the different organs, the results being compared with existing tables and/or curves of normality. 5. Detailed photographic documentation.

HISTOLOGICAL STUDY a) This is a fundamental stage of necropsy. Histological findings should be interpreted in the light of the gestational age and the degree of relative development of the various organs.

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b) The procedure differs from that of adult necropsy in terms of the way in which slices are taken and through the use of special study techniques. c) The fundamental stages are: 1. A series of slices of all the organs, which must be taken using different procedures from those for adults. This is due both to the different composition of fetal organs, which requires the use of special fixing tech niques. 2. Microscopic study of all the organs, especially those affected by mal formations. Obviously, in the case of intrauterine death the advanced maceration of the organs makes their histological study difficult, or even impossible.

EXAMINATION OF THE PLACENTA AND ADNEXA This involves both macroscopic and microscopic examination. a) Macroscopic examination. In addition to placenta weight, which should be compared with standard values for the gestational age, the diameter and length of the cord should also be measured. Macroscopic examination will include both the fetal and the maternal face. b) Microscopic examination. For microscopic examination of the placental and fetal adnexa (placental disk, umbilical cord and chorioamniotic membranes), it is essential that the placenta be sent as soon as possible, without fixing, to the pathological anatomy laboratory.

FINAL AIMS OF NECROPSY EXAMINATION The basic aims are: 1. To make a reliable diagnosis. 2. To enable proper reproductive counselling to be given. 3. To check the information provided by prenatal diagnosis. 4. To allow epidemiological study. Its additional advantages are that: 1. The practice of necropsy usually provides reassurance to the parents. 2. The procedure is legally accepted as «good medical practice». In contrast, failure to carry it out may be considered a case of negligence.

Reference. Carrera JM, Cusi V and Carrera M: Fetal Necropsy. In: Controversies in Perinatal Medicine. Ed. by JM Carrera, Frank A Chervenak and A. Kurjak. Parthenon Publishing. New York, 2003; 10: 107-129.

E.2.

PROCEEDINGS AND TECHNOLOGY

E.2.1. NEONATAL RESUSCITATION INTRODUCTION Approximately 10 % of deliveries will require some type of neonatal active resuscitation to attain a normal pattern of respiration.

GETTING READY FOR INTERVENTION IN THE DELIVERY ROOM I.

ANTICIPATION Caregivers should know «risk factors» in every pregnancy and/or delivery that may pose risk of resuscitation. High risk pregnancies should be transferred to an appropriate referral center fulfilling medical and equipment requirements.

II.

ATTENDING PERSONNEL 1. One attendant, trained to initiate basic neonatal resuscitation including positive pressure ventilation and chest compression, should take immediate care of the infant. 2. Another attendant trained in deep cardio-pulmonary resuscitation including tracheal intubation and drug administration should be easily accessible. 3. Deep resuscitation always requires 2 trained attendants: one for intubation and drug administration and the other for monitoring vital signs and, if necessary, to initiate chest compression. 4. The leader of the procedure will always be the most experienced attendant and will assume care of the respiratory airways.

III. DELIVERY ROOM Delivery room should be around 25 ºC, well illuminated, and include a flat surface under a radiant heater (37 ºC) for the newly born infant. Basic installations recommended. 1. Oxygen supply (with flow meter). 2. Air supply (with flow meter). 3. Oxygen-air blender (desirable). 4. Negative pressure source (with manometer desirable).

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Basic material recommended. 1. Suction catheter (FR 6, 8, 10, 12, 14). 2. Self-inflating bag (250-500 mL). 3. Facial mask (size for term and preterm). 4. Laryngoscope (size 0, 1). 5. Tracheal tubes (size 2.5; 3; 3.5 and 5 mm). Basic medication recommended. 1. Adrenaline (diluted 1:10,000 with normal saline). 2. Bicarbonate 1 M (diluted 50 % with distilled water). 3. Naloxone. 4. Normal saline (CINa 9 %). Material and medication should be easily accessible and reviewed daily.

IV. STEPS IN RESUSCITATION Term infant with vigorous cry and effective respiration, good tone and clear amniotic fluid do not need resuscitation. Dry gently with warm cloth and put to mother’s breast. If one of the previous conditions fails, the following steps should be performed. 1. Initial stabilization. 2. Ventilation. 3. Chest compression. 4. Drug administration. Allow 30 seconds for each step, re-evaluate respiration, FHR and color, and decide to go to the next step. a) Initial stabilization. 1. Maintain body temperature keeping the baby under a radiant heater and drying with warm towels. 2. Adequate supine position with slightly extended neck (neutral position). 3. Clean secretions with gauze or gentle aspiration with suction bulb syringe. 4. If obstruction of the upper respiratory airway is suspected aspirate with suction catheter and negative pressure mouth (first) and nostrils (max pres. 2100 mm Hg, 5 sec). Prolonged suction delays spontaneous respiration and may cause bradycardia and/or laryngeal spasm. 5. Respiration can be stimulated by gently rubbing while drying or stimulating back or feet sole. If unsuccessful initiate ventilation. 6. It the baby is not spontaneously breathing oxygen is useless, and positive pressure ventilation should be initiated. 7. Positive pressure ventilation can be initiated with room air if oxygen is not available. If oxygen is available and heart rate does not improve after 30 sec. FiO2 should be increased to 40 % and to 100 % thereafter with 30 sec intervals. b) Ventilation. • Positive pressure ventilation. –– Should be promptly initiated if after 30 sec of stabilization the baby exhibits: 1. Gasping or apnea. 2. Heart rate below 100 beats per minute (bpm). 3. Central cyanosis (with supplemental oxygen).

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––

Technique. 1. Free upper airway by aspirating secretions. 2. Put the baby supine with slightly extended head. 3. Choose the adequate facial mask and adjust it to impede leaking. 4. Connect mask to self-inflating bag (250 mL or 500 mL). 5. Set pressure limit (if possible) around 30-40 cm H2O. 6. First puffs should be performed using 30-40 cm H2O and prolonged inspiratory time to achieve an adequate FRC (functional residual capacity) Thereafter 20 cm H2O should be enough to maintain an adequate ventilation. 7. Respiratory rate should be kept between 30 (term) to 60 breaths (preterm) per min. 8. Efficacious ventilation will promptly increase heart rate and cause thoracic wall to expand. • Tracheal intubation. –– It should be always considered when: 1. Meconium-stained amniotic fluid is present in lower respiratory tract. 2. Unsuccessful bag and mask ventilation. 3. Cardiac massage is needed. 4. Need for tracheal administration of drugs. 5. Extreme prematurity (,1,000 g) or diaphragmatic hernia. –– Technique: 1. Mouth intubation is preferred in emergency situations. 2. Patient is put in neutral position. 3. Laryngoscope is introduced through the right side of the mouth and tongue is displaced to the left side. 4. Blade is forwarded until its tip is located within the vallecular crease. With a slightly vertical movement of the blade, the epiglottis is folded upwards to allow visualization of the vocal cords. 5. ETT is inserted between the vocal cords, and laryngoscope gently retired. 6. Adequate ETT size is essential for an adequate ventilation. Internal diameter: ,1 kg: 2.5 mm; 1-3 kg: 3.0 mm; .3 kg: 3.5 mm. 7. ETT is then connected to positive pressure device. –– Important. 1. To avoid hypoxemia the baby should be adequately ventilated with bag and mask before the procedure. 2. Intubation attempts should not last more than 30 sec. 3. If heart rate goes below 100 bpm procedure should be interrupted and allow baby to recover by bag and mask ventilation. 4. Effective ventilation should promptly increase heart rate. c) Chest compression. • Initiate if after 30 sec of effective tracheal ventilation heart rate stays ,60 bpm. • Technique: 1. Compression should be performed with both thumbs with the rest of the fingers encircling the chest and the lower third of the sternum. Avoid compression of the xyphoid process.

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2. Each compression should depress the sternum by one third of the anterior-posterior diameter of the chest. 3. Frequency should be of 90 bpm, with a ventilation interposed between 3 compressions. 4. HR and respiration should be continuously checked, and chest compression interrupted if heart rate . 60 bpm. 5. In rural areas with only one person present, chest compression should be performed with the index and middle finger of one hand, while the other hand fixes the face in the right position for doing mouth-to-mouth ventilation. d) Drug administration. 1. Drugs are very seldom used in newborn resuscitation. 2. Bradycardia is usually a consequence of hypoxemia, thus an adequate ventilation and oxygenation will solve most of one situations. 3. In rural areas drug administration is done seldom for no accessible venous route. –– Adrenaline. 1. Indicated in a-systolic infant or non-responsive bradycardia , 60 bpm. 2. Preferred by intravenous route (IV). Umbilical vein (UV) is preferred. Alternative intra-osseous (IO) route. Tracheal route has not been adequately evaluated. 3. Dose: 0.01-0.03 mg/kg/dose of a 1:10,000 solution; every 35 min. –– Volume expanders. 1. Indicated in fetal hemorrhage or suspicion of hypovolemic shock. 2. Crystalloid solution such as Normal Saline by UV is preferred. Seldom IO. 3. Dose: 10 mL/kg in 5 to 10 min; it may be repeated after 30 min if perfusion does not improve. 4. Very infrequently blood transfusion will be needed. –– Sodium bicarbonate. 1. Only exceptionally used for prolonged metabolic acidosis. 2. Mandatory: the baby is undergoing an adequate ventilation. 3. Use 1 M bicarbonate dilute 1:1 with distilled water. 4. Dose: 1-2 mEq/kg in 2-3 min IV. UV is preferred (seldom IO). –– Naloxone. 1. Very seldom used and only after adequate ventilation and heart rate normalization. 2. Never use in opiate addicted mothers. 3. Dose: 0.1 mg/kg IV (UV preferred) or IM (intramuscular). 4. Short half-life. Repeat every 2-3 min if respiratory depression persists. V.

RESUSCITATION IN SPECIAL SITUATIONS a) Presence of meconium stained amniotic fluid (SAF). 1. Risk of aspiration pneumonia at birth or during resuscitation. 2. Aspiration of pharynx before delivery is no longer recommended.

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3. 4.

In vigoruously crying Nwb just observe. In depressed Nwb creck trachea for the presence of SAF. If present, insert ETT connected to an intermittent suction catheter device. Aspirate while withdrawing ETT. Valid alternative is intubation with FR12-14 suction catheter. 5. Repeat procedure until suction catheter appears clean (keep HR . . 100 bpm). b) Premature infant. 1. 80 % of Low birth-weight infants (,1,500 g) or premature (,32 wks) will require resuscitation maneuvers. 2. Prone to hypothermia, respiratory depression, lung damage and intraventricular hemorrhage thus requiring expert personnel. 3. RECOMMENDED: Transfer the mother to the REFERRAL CENTER with Neonatal Intensive Care. 4. If ventilation is needed use of low tidal volume with positive inspiratory pressure (PIP) with pressure limitation valve adjusted at 20 cm H2O, and positive end expiratory pressure (PEEP) adjusted 3-4 cm H2O. Both of these protect lung and improve compliance and gas exchange. 5. If prolonged ventilation is needed add PEEP valve to the self-inflating bag. 6. In spontaneously breathing, continuous positive airway pressure (CPAP) prompts respiratory stabilization and reduces oxygen requirements. 7. It is highly recommended the use of Pulse Oxymeter with saturations kept within 85-92 % range. If not possible keep oxygen as low as possible (check central color and HR frequently). 8. Avoid loss of heat (use radiant heater and polyethylene bag if possible). VI. ETHICAL ASPECTS − Show the highest respect for religious and cultural background of the parents. They usually want to have an active participation and therefore information should be clear and understandable. − In extreme cases (,400 g; ,23 wks; severe congenital anomalies e.g.: anencephaly, 13 or 18 trisomy) resuscitation may not be initiated.

Reference. Gimeno A, Escrig R. Brugada M, Saenz P, Izquierdo I, Vento M: Resuscitacion and Neonatal Arphyxia. In: Recommendations and Guidelines for Perinatal Medicine. Matres Mundi/WAPM. Barcelona, 2007; 4: 348-356.

E.2.2. RESPIRATORY THERAPY IN THE NEWBORN CONCEPT Many neonates are ill during the first days alter birth and require some level of respiratory support. Infants may have impairment of oxygenation or of CO2 elimination or a combination of both.

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OXYGEN THERAPY Infants with central cyanosis and/or documented low levels of oxygen saturations require oxygen supplementation. Term infants should have saturations $ 95 %. In preterm infants, saturations of 85 to 95 % are usually acceptable. Oxygen can be delivered in several ways: 1. Hood. An oxygen hood is a simple and effective way of delivering a precise amount of oxygen supplementation. Oxygen can be appropriately warmed and humidified as necessary. 2. Nasal cannula. Oxygen nasal cannula is an acceptable method for delivery of oxygen although the actual inspired oxygen level varies markedly. In lowresource countries, this is the preferred method of delivery of oxygen because of its simplicity and low cost. 3. Bag and mask. A bag and mask can be used to delivery oxygen during emergencies with or without positive pressure. 4. Continuous positive airway pressure (CPAP). CPAP can be used to delivery oxygen when a constant pressure is also necessary. CPAP can be provided by nasal prongs but also can be provided by nasopharangeal prongs and by other means. 5. Mechanical ventilation. Mechanical ventilation is used to deliver oxygen when ventilation is necessary.

VENTILATORY SUPPORT The ventilatory needs of a patient depend largely on the mechanical properties of the respiratory system and the type of abnormality in gas exchange. a) Gas exchange. The pathophysiologic mechanisms responsible for hypoxemia in order of relative importance in neonates are: ventilation-perfusion mismatch, shunt, hypoventilation, and diffusion limitation. 1. Ventilation-perfusion (V/Q) mismatch is an important cause of hypo xemia in newborns. Supplemental oxygen can largely overcome the hypoxemia resulting from V/Q mismatch. 2. Shunt is a common cause of hypoxemia in newborns. A shunt may be physiologic, intracardiac (e.g., PPHN, congenital cyanotic heart disease), or pulmonary (e.g., atelectasis). It can be thought of as a V/Q 5 O and supplemental O2 cannot reverse the hypoxemia. 3. Hypoventilation results from a decrease tidal volume or respiratory rate. During hypoventilation, the rate of oxygen uptake from the alveoli exceeds its replenishment. Thus, alveolar PO2 falls and PaO2 decreases. It can be thought of as low V/Q and supplemental O2 can overcome the hypoxemia easily. Causes of hypoventilation include: depression of respiratory drive, weakness of the respiratory muscles, restrictive lung disease, and airway obstruction. 4. Diffusion limitation is an uncommon cause of hypoxemia, even in the presence of lung disease. Diffusion limitation occurs when mixed venous blood does not equilibrate with alveolar gas. Supplemental O2 can overcome hypoxemia secondary to diffusion limitation. Oxygenation may be largely dependent on lung volume, which in turn depends on mean airway pressure. On a pressure ventilator any of the following

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will increase mean airway pressure: increasing inspiratory flow, increasing peak inspiratory pressure (PIP), increasing the inspiratory to expiratory (I:E) ration or increasing positive end expiratory pressure (PEEP). b) Ventilator parameters and their effects on gas exchange. 1. Peak Inspiratory Pressure (PIP). PIP partially determines the pressure gradient between the onset and end of inspiration, and thus, affects the tidal volume and minute ventilation. During volume ventilation an increase in tidal volume corresponds to an increase in PIP during pressure ventilation. If tidal volume is not measured, initial PIP can be selected based on observation of the chest wall movement and magnitude of the breath sounds. An increase in PIP will increase tidal volume, increase CO2 elimination, and decrease PaCO2. An increase in PIP will increase mean airway pressure, and thus improve oxygenation. An elevated PIP may increase the risk of barotrauma, volutrauma, and bronchopulmonary dysplasia/chronic lung disease. There is increasing evidence that lung injury is primarily caused by large tidal volume delivery and lung overdistention. Thus, it is important to adjust PIP based on lung compliance, and ventilate with relatively small tidal volumes. (e.g., 3-5 mL/kg) 2. Positive End Expiratory Pressure (PEEP). PEEP partially determines lung volume during the expiratory phase, improves ventilation/perfusion mismatch, and prevents alveolar collapse. PEEP contributes to the pressure gradient between the onset and end of inspiration, and thus, affects the tidal volume and minute ventilation. A minimum «physiological» PEEP of 2-3 cm H2O should be used in most newborns. An increase in PEEP increases expiratory lung volume (functional residual capacity) during the expiratory phase, and thus, improves ventilation/perfusion matching and oxygenation in patients whose disease state reduces expiratory lung volume. An increase in PEEP will increase mean airway pressure, and thus, improve oxygenation in patients with this type of disease. An increase in PEEP will also reduce the pressure gradient during inspiration, and thus, reduce tidal volume, reduce CO2 elimination, and increase PaCO2. An elevated PEEP may overdistend the lungs and lead to decreased lung compliance, decreased tidal volume, less CO2 elimination, and an increase in PaCO2. While use of low-to-moderate PEEP may improve lung volume, a very high PEEP may cause overdistention and impaired CO2 elimination secondary to decreased compliance and gas trapping. Furthermore, a very high PEEP may decrease cardiac output and oxygen transport. 3. Frequency. The ventilator frequency (or rate) partially determines minute ventilation, and thus, CO2 elimination. Ventilation at high rates (60/min) frequently facilitates synchronization of the ventilator with spontaneous breaths. Spontaneous breathing rates are inversely related to gestational age and the time constant of the respiratory system. Thus, infants with smaller and less compliant lungs tend to breathe faster.

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Inspired Oxigen Concentration (FIO2). Changes in FiO2 alter alveolar oxygen pressure, and thus, oxygenation. Because both FiO2 and mean airway pressure determine oxygenation, the most effective and less adverse approach should be used to optimize oxygenation. When FiO2 is above 0.6-0.7, increases in mean airway pressure are generally warranted. When FiO2 is below 0.3-0.4, decreases in mean airway pressure are generally preferred. FiO2 directly determines alveolar PO2 and thus PaO2. A very high FiO2 can damage the lung tissue, but the absolute level of FiO2 that is toxic has not been determined. Flow. Changes in flow rate have not been well studied in infants, but they probably impact arterial blood gases minimally as long as a sufficient flow is used (which is generally the case with most ventilators). In summary, depending on the desired change in blood gases, the following ventilator parameter changes can be performed. Desired Blood Gas Goal and Corresponding Ventilator Parameter Changes.

DESIRED GOAL

PIP

PEEP

FREQUENCY

I:E RATIO

FLOW

To decrease PaCO2

↑

↓

↑

—

6↑

To increase PaCO2

↓

↑

↓

—

6↓

To decrease PaCO2

↓

—

↓

6↓

To increase PaCO2

↑

—

↑

6↑

Desired Blood Gas Goal and Corresponding Ventilator Parameter Changes.

Reference. Carlo W: Respiratory Theraphy in the Newborn. In: Recommendations and guidelines for Perinatal Medicine, Matres Mundi/WAPM. Barcelona, 2007; 42: 356-362.

E.2.3. OCULAR PROFILAXIS (OP) For the ocular profilaxis, it is recommended to use: 1. Oftalmic pomade of Eritromicin 0.5 % or oftalmic pomade of Tetraciclin 1 % (applyng a similar quantity to a grain of rice in each eye, or. 2. Eye drops of Eritromicin or Tetraciclin (one o two drops per eye directly to the lower conjunctival sac). This measure is particularly effective for the profilaxis of conjunctivitis caused by Chlamydia trachomatis, and also very usefull for the Neisseria Gonorrea. 3. If the mother is positive for Neisseria Gonorrea, it is necessary to administer a dosis of Peniciline G sodic by parenteral injection (25,000-50,000) U/kg).

Reference. Carrera JM: Procedimientos básicos disponibles en una sala de recién nacidos. In: Protocolos de Obstetricia y Medicina Perinatal del Instituto Universitario Dexeus. 3th Edition, Masson. Barcelona, 1995: 433.

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E.2.4. VITAMIN K PROPHYLAXIS In order to prevent hemorrhagic disease in the newborn, provide from 0.5 to 1 mg of vitamin K1 (phytomenadione) intramuscularly in the thigh during the first hour of life. Extreme premature infants and epileptic mother under treatment with Phenobarbital might require an extra dose.

E.2.5. NEONATAL TRANSPORT GENERAL CONCEPTS 1.

Neonatal transport should be considered when the human and technical resources immediately available are not the most appropriate for the attention to a new born according to its present and future condition and from the medical and surgical point of view. 2. The decision should be made by an experienced paediatrician or neonatologist who should be part of the staff during the transfer, taking care of all the required measures and avoiding unnecessary transfers. 3. The newborn should be transferred to a reference hospital, according to the care required. The center must be previously informed in order to allow the admission. There should be a fluent and constant communication between centers. 4. In serious situations, maternal-fetal transfer must be considered.

INDICATIONS The following conditions might require specific treatment and transportation. For this reason, this indication should be taken only as a guide, conditioned to variations depending of the situation of each center: 1. Less than 34 weeks of gestation or weight less than 2,000 g. 2. Neonatal sepsis or high risk or infection. 3. Respiratory difficulties and metabolic acidosis persistent after the first two hours of life and in case the center lacks equipment to provide a therapy with monitored oxygen or assisted ventilation. 4. Neonatal bleeding. 5. Hypoglycemia. 6. Hemolytic disease of the newborn. 7. Drug addict mother. 8. Diabetic mother. 9. Neonatal convulsions. 10. Meningitis. 11. Congenital malformations requiring surgical care or special observation. 12. Neurological signs, neonatal anoxia after the birth, persisting for more than 2 hours. 13. Congenital heart disease with persistent cyanosis or heart failure. 14. Progressive respiratory difficulty syndrome. 15. Any condition requiring mechanical ventilation for more than 1 hour.

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16. Newborn requiring more than a routine observation. 17. Shock.

ASSISTANCE OF THE NEWBORN PRIOR TO TRANSPORT 1.

2. 3.

Stabilization. The most critical hours of the newborn are those before the transport. For this reason, the newborn must be checked carefully in the hospital of origin regarding to primary diagosis and its complications, as well as being stabilized properly. This actions minimize the subsequent deterioration and avoid intricacies during transport. Temperature. The newborn must be in a neutral thermal environment suitable for its age and birth weight. Hypoglycemia prevention. The majority of premature infants, too young for their gestational age, and newborns with serious affectations have a high risk of hypoglycaemia. For this reason, they should be monitored in time and periodically and in many cases perform an intravenous perfusion providing glucose. Umbilical catheters are only advised in serious conditions. Oxygen saturation. a) The blood gases must be monitored. If it is not possible, oxygen must be supplied in minimum quantities to prevent cyanosis. b) If it is not possible to maintain a rose skin-color, assisted ventilation must be initiated. c) In most cases control and attendance of an appropriate oxygenation, keeping a proper thermal environment and the prevention of hypogly caemia, should be enough.

INDICATIONS AND EQUIPMENT DURING THE TRANSFER 1.

In case of a sick or high risk newborn, an experienced neonatologist or a paediatrician should be in charge. If not possible, then a trained nurse may do it, making sure that the equipment remains in good conditions. 2. The equipment varies and depends on the resources available. It is necessary to have, at least, a portable incubator and a monitoring system, given the difficulties to perform an auscultation with stethoscope. Also an oxygen source allowing for a precise concentration.

NEWBORN WITH SPECIAL NEEDS a) Too small newborns are a big challenge during a transfer mainly because it is difficult to maintain their body temperature, fundamental aspect for their stability. In order to avoid the decreasing of the temperature, aluminized fabrics, plastic covers or preheated blanquet. b) Surgical newborns: 1. Diaphragmatic hernia: Easier to move with the head up, the affected area on the lower side and a nasogastric catheter. Avoid ventilation with Ambu and mask. In case of breathing difficulties perform an intubation prior the transfer. 2. TEF: Maintain the head in a high position and with a thick catheter aspirating softly and frequently.

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3. Omphalocele or gastroschisis: Thermal regulation is vital fiven the large amount of intestinal surface exposed. Coat the injury with compresses soaked in sterile isotonic saline solution, wrapped in gauzes and covered with an sterile plastic, trying not to compromise the exposed intestine. It is also necessary to use a nasogastric tube and an intravenous infusion. 4. Myelomeningocele: Transport in a prone position, covering the injury with a sterile compress, avoiding contamination with urine and feces.

Reference.â&#x20AC;&#x201A; Carrera JM: Transporte neonatal. In: Protocolos de Obstetricia y Medicina Perinatal del Instituto Universitario Dexeus. Masson. Barcelona, 1995: 439.

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E.3.

NEONATAL PATHOLOGY

E.3.1. PRETERM INFANT: CLINICAL CARE THERMAL CARE OF THE PRETERM INFANT a) Preterm infants are susceptible to heat loss because: 1. Low body weight to surface ratio. 2. High transepidermal evaporative water loss due to poorly keratinised stratum corneum. 3. Poor glycogen and brown adipose tissue stores (which metabolise to produce thermogenesis). 4. Immature behavioural and physiological responses to heat loss. Temperature can drop by 0.1-0.3 ºC per minute unless interventions to prevent this are put in place immediately. b) Hypothermia in the newborn infant has been shown to. 1. Increase severity of illness. 2. Decrease survival. 3. Decrease rate of growth. An infant should therefore be nursed in a thermo-neutral environment so that excess energy is not wasted on maintaining body temperature. c) Interventions at delivery to prevent heat loss. 1. Maintain delivery room temperature at 25 ºC. 2. Pre-warm all contact surfaces. 3. Eliminate all drafts. 4. Use a pre-warmed radiant heater during resuscitation. 5. Dry infants .28 weeks gestation thoroughly, especially the head. 6. Remove any wet towels/blankets. 7. Put cap on baby. d) Gestational age. 1. Infants ,28 weeks gestation place immediately into plastic bag. • Do not dry infant. • Place entire body to neck into bag. • Auscultation and colour can be assessed though the bag. • If acces required to umbilical cord vessels, small holes may be made in bag and then occluded when no longer required. 2. Infants ,28 weeks or ,1,500 g to be placed on transwarmer mattress.

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INTERVENTIONS FOR HYPOTENSION a) Definition. Hypotension is a common complication of prematurity. The definition varies in the literature; it may be defined as: 1. ,30 mm Hg. 2. ,10th centile of a birth weight and age-specific range. 3. Mean arterial pressure (MAP) , number of completed weeks of gestation of the infant. b) Hypotensión is associated with: 1. Increased rate of intraventricular haemorrhage. 2. Poor long term neurodevelopmental outcome. c) Treatment. 1. Volume expansion. • The use of intravenous volume expander (normal saline preferred to albumin) is common. • There is no evidence to support or refute the routine use of volume expansion in hypotensive newborn infants. 2. Inotropes: • Dopamine and dobutamine are most commonly used. • Other inotropes (adrenaline, noradrenaline and isoprenaline) are less frequently used in severe resistant hypotension. 3. Systemic steroids: • Meta-analysis shows that a single dose of dexamethasone is effective in treating infants with refractory hypotension. • Post-natal dexamethasone used to prevent chronic lung disease suggests it is associated with a poor neurodevelopmental outcome. • Subsequently hydrocortisone has been used with no long-term adverse effects yet evident.

PATENT DUCTUS ARTERIOSUS (PDA) a) Concept. Patent ductus arteriosus is associated with an increased risk of: 1. IVH. 2. NEC. 3. CLD. 4. Death. b) Treatment. Standard treatment has been indomethacin. More recently ibuprofen has been used and shown to: 1. Close PDA. 2. No reduction in cerebral, intestinal or renal circulation. 3. Enhance cerebral blood flow auto regulation. 4 Protect neurological functions following an oxicative stress in a piglet model. c) Consequences. Side effects include: 1. Decreased cerebral blood flow. 2. Decreased cerebral oxygen delivery.

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3. Transient renal failure. 4. Isolated bowel perforation. 5. Decreased cerebral blood volume. 6. Oliguria. 7. Necrotizing enterocolitis. 8. Gastrointestinal hemorrhage.

FEEDING THE LBW INFANT Breast milk is the recommended nutritional source for full term infants but for preterm infants human milk supplies insufficient quantities of protein, calcium, phosphorus and sodium to meet demand. Multicomponent human milk fortifiers are available that contain protein, carbohydrate, calcium, phosphorus, vitamins and trace minerals. Preterm infants fed human milk compared with infants fed term or preterm formulae have: 1. ↓ Weight gain. 2. ↓ Bone mineralization. 3. ↓ Risk of necrotising enterocolitis. 4. ↑ Neurodevelopmental outcome.

GERMINAL MATRIX-INTRAVENTRICULAR HAEMORRHAGE (GMH-IVH) a) Incidence. 1. Decreases over the last 30 years. 2. About 20 % of preterm infants have evidence of GMH-IVH. 3. The majority occur in the first 72 hours may extend over 24-48 hour. b) Pathology. 1. GMH-IVH usually arise form the germinal matrix. 2. Fragile, highly vascular capillary bed over the head of caudate nucleus. 3. Most abundant at 24-34 weeks; almost entirely involuted by term. 4. Venous drainage of deep white matter is through the germinal matrix: If venous drainage is impaired periventricular venous infarction may evolve. c) Diagnosis. 1. Most frequently the onset of GMH-IVH is asymptomatic. 2. Rarely catastrophic deterioration e.g. increased ventilation, hypotension etc. d) Confirmation of the diagnosis. 1. With ultrasound. 2. There are classification systems but perhaps it is more reliable to describe the ultrasound appearances accurately when reporting to avoid confusion. GMH-IVH may be. • Small and confined to the GMH. • Larger with blood filling the ventricle. • Blood filling the ventricle and ventricular dilatation. • Large GMH-IVH with periventricular venous infarction. e) Complications. Complications may occur, particularly with the larger GMH-IVH.

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Post-haemorrhagic ventricular dilatation (PVHD) may occur causing hydrocephalus: 1. This may occur 2-3 weeks post GMH-IVH. 2. Symptoms include apnoea, feed intolerance and seizures. 3. Assessment is by serial ultrasound measurement of the ventricular size and head circumference. 4. Measurement of cerebrospinal fluid (CSF) pressure at lumbar puncture should be done if there is ventriculomegaly. 5. Drainage should be considered if symptoms are present, CSF pressure is .10 cm or head circumference is rapidly increasing. 6. Measures to decrease the incidence of PHVD such as fibrinolytic therapy or acetazolamide have been shown to be harmful. Prevention. The following methods have been shown to reduce the incidence of GMHIVH: 1. Antenatal corticosteroids. 2. Indomethacin.

Reference. McKechnie L, Levene JM: Clinical Care of the Preterm Infant. In: Recommendations and Guidelines for Perinatal Medicine. Matres Mundi/WAPM. Barcelona, 2007; 40: 340-347.

E.3.2. NEONATAL ASPHYXIA GENERAL CONCEPTS Failure to perform an adequate fetal to neonatal transition due to absence of an adequate oxigenation and/or perfusion lends to: 1. Bradycardia, hypotonia, hypo-responsiveness to stimuli, respiratory depression and cyanosis as defined by Apgar score # 3 at 5 min. 2. Metabolic acidosis as detected in blood gases performed in umbilical artery (pH , 7.0; base excess $ 12 mEq/L). 3. Multiple organ damage (especially brain, kidney and heart). 4. In the absence of neurological manifestations the presence of an asphyctic episode cannot be ascertained. Apgar score SCORE

Heart rate

Absent

,100 bpm

.100 bpm

Respiratory effort

Absent

Slow (irregular)

Good cryng

Muscle tone

Limp

Some flexion extremities

Active motion

Reflex irritability

No response

Grimace

Cough or sneeze

Color

Blue, pale

Pink body, blue extremities

Full pink

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CRITERIA FOR ORGAN FAILURE 1.

Central Nervous system: a) Variability in clinical condition moving from inability for arousal, hy potonia, hyporreflexia and seizures in the first 24-72 hrs to hypertonia, hyperreflexia, and difficulty for feeding thereafter. b) Increased S100 protein and neuronal specific enolase in CSF. c) Low voltage base line, burst-suppression, absence of arousal-sleep, seizures present in amplitude integrated EEG (Cerebral Brain Monitor). d) Ultrasound: diffuse increase in ecogenicity in hemispheres and collapsed ventricles due to brain edema. 2. Renal: −− Anuria/oliguria (,1 mL/kg/h) for $24 hr and/or creatine . 125 mmol/L. 3. Cardiovascular: −− Hypotension treated with an inotrope . 24 hr and/or ECG with transient myocardial ischemia. 4. Pulmonary: −− Need for respiratory support with oxygen requirement .40 % for at least 4 hour after birth. 5. Hepatic: −− Aspartate amino-transferase . 100 Ul/L or alanine amino-transferase . . 100 Ul/L at any time during the first week of life

TREATMENT 1. 2. 3. 4.

Adequate maintenance of vital signs and metabolic status. Treat seizures initially with Phenobarbital (no prophylactic use). Avoid hyperthermia and hypercapnia. Close follow-up.

Reference. Gimeno A, Escrig R. Brugada M, Sáenz P, Izquierdo I, Vento M. In: Recommendations and Guidelines for Perinatal Medicine. Matres Mundi/WAPM. Barcelona, 2007, 41: 354-356.

E.3.3. NEONATAL SEPSIS CONCEPT Neonatal sepsis is defined as bacteriemia with systemic manifestation in the absence of other primary systemic problems during the first 28 days of life. Diagnosis is clinical and blood culture.

SUBTYPES 1.

Early onset sepsis. Occurs with in the first 72 hours of life. It is caused by organisms prevalent in the genital tract of the mother or in the labour room, which includes mainly group B streptococci and E. coli. Majority of the neonates with early onset sepsis clinically manifest with respiratory distress due

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to intrauterine pneumonia. Early onset sepsis has usually fulminant course and high mortality. Late onset sepsis. The onset is delayed for a minimum of four days in most cases symptoms appear by the end of first week of life. About 2/3 cases of late onset septicaemia are caused by gram negative bacilli while the rest are contributed by gram positive organisms. Meningitis is quite frequent.

DIAGNOSIS Clinical and laboratory.

TREATMENT 1.

Non-Drug treatment. Supportive care which includes maintenance of normal body temperature including Kangaroo care, adequate calorie and fluid supply, and correction of associated metabolic abnormalities. Drug treatment. Until the culture report is collected start with broad-spectrum antibiotics, which includes penicillin and amino glycoside. • Ampicillin, 100 mg/kg/day every 6-8 hours i.m. for 10 days. • Gentamicin, 5 mg/kg/day IM TID for 10 days. Alternative: • Penicillin G. Sodium Crystalline 50,000 IU/kg QID for ten days. • Gentamicin, 5 mg/kg/day IM TID for 10 days.

Reference. Standard Treatment Guidelines for General Hospitals. In: Drug Administration and Control Authority of Ethiopia Content. Addis Abeba, 2010: 220-221.

E.3.4. NEONATAL TETANUS CONCEPT Neonatal tetanus is caused by the neurotoxin tetano-spasmin produced by Clostridium tetani, which infects the umbilical stump. The incubation period is 5 to 14 days. Affected infants develop difficulty in sucking and swallowing, «lockjaw», generalized hypertonicity spasms and opisthotonus. Once signs develop the disease progresses to a fatal out come in 60-70 % of cases. Neonatal disease may occur if maternal immunity is lacking and infection is introduced at the time of delivery.

DIAGNOSIS Mainly clinical.

PREVENTION The administration of the toxoid vaccine to all mothers prior to pregnancy and proper newborn umbilical hygiene can effectively prevent this disease.

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DRUG TREATMENT • • • •

Tetanus immune globulin (TIG), 500-3,000 IU IM should be given. Dosage forms: Injection, 3,000 IU. Penicillin G Sodium Crystalline, 50,000 IU/kg/24 hrs QID for ten days. Chlorpromazine, 1.6 mg/kg/24 hours divided in to 4 doses IV/IM.

Reference. Standard Treatment Guidelines for General Hospitals. In: Drug Administration and Control Authority of Ethiopia Content. Addis Abeba, 2010.

E.3.5. NEONATAL SEIZURES CONCEPT Seizures can be the most dramatic indication of neurologic abnormality in the newborn, yet most neonatal seizures are subtle or even silent. Types: there are five types of neonatal seizures: subtle seizures (presenting with apnea, starring, lip smacking, chewing or eye blinking); focal clinic; multifocal clonic; tonic, and myoclonic seizures. The causes of neonatal seizures include metabolic, toxic structural and infectious diseases.

DIAGNOSIS Clinical

DRUG TREATMENT •

Phenobarbital, I.M/I.V/P.O. 4-6 mg kg/day loading dose, followed by 5 mg/kg in two divided doses. Alternative. • Phenytoin, I.M/.I.V/P.O. 4-6 mg kg/day loading dose, followed by 5 mg/kg in two divided doses. If seizures are associated with: 1. Hypocalcaemia (Hypocalcaemic tetany): Calcium gluconate solution, 10 % 1-2 ml/kg/; repeat PRN after 6 hours. S/Es: bradycardia, cardiac arrest, extra vascular leakage may cause local necrosis. 2. Hypoglycemia: Glucose 10 %, (For dosage schedule, see under Hypoglycemia). 3. Vitamin B & deficiency: Vitamin B 6 (pyridoxine), 50 mg IM as single dose.

Reference. Standard Treatment Guidelines for General Hospitals. In: Drug Administration and Control Authority of Ethiopia Content. Addis Abeba, 2010: 221.

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E.3.6. CONGENITAL SYPHILIS CONCEPT Syphilis is a chronic systemic infection caused by Treponema pallidum, a sexuallytransmitted disease. In case of pregnancy, T. pallidum may be transmitted to the unborn child, via the placenta. Infants born to mothers with syphilis refer to a newborn whose mother has positive serological tests for syphilis independently of the clinical stage of the disease. Nearly all cases of syphilis are acquired by sexual contact with infectious lesions.

DIAGNOSIS IN THE PREGNANT WOMAN 1.

2. 3. 4.

Clinical. Detection of the typical chancre associated with regional lymphadenopathy in early primary syphilis. Serological tests may be negative (window period). Serological. Diagnosis is frequently established by serological tests during control of pregnancy. Non-specific (reagin) antibody tests. Rapid plasma reagin (RPR) and Venereal Disease Reference Test (VDRL) with quantification. Specific treponemal antibody tests. FTA-Abs and MHA-TP (TPHA).

DIAGNOSIS IN THE NEWBORN 1.

Clinical diagnosis. Characteristic clinical features of congenital syphilis include rhinitis, palmoplantar pemphigous, hepatosplenomegaly, and bone anomalies (periostitis and osteochondritis). Bullae and vesicles of syphilitic pemphigous are very contagious. With regard to treatment, the following clinical forms should be differentiated: a) Multiorgan involvement (hydrops, hepatitis, pemphigous, etc.). b) Exclusive bone involvement. c) Asymptomatic with positive serology. d) Neurosyphilis. Serological tests. Infection is diagnosed in the presence of a fourfold increase of serum titers in comparison with maternal titers. Specific treponemal antibody tests include IgM-FTA-Abs, TPHA, and specific IgM antibodies. Diagnosis of neurosyphilis is established by VDRL reactivity in the CSF. Radiographic studies of long bones to assess the presence of periostitis and osteochondritis.

TREATMENT OF THE NEWBORN 1.

Congenital syphilis with multiorgan involvement but without involvement of the central nervous system (CNS): penicillin G sodium 50,000 IU/kg every 12 h i.v. during the first week (every 8 h after the first week) during 1014 days. The Herxheimer reaction may occur in patients with systemic inv olvement, and it may be advisable to increases the doses of penicillin progressively: 1,000-5,000-10,000-20,000 and 50,000 IU/kg/day. Strict isolation measures should be implemented in infants with syphilitic pemphigous.

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Syphilis with CNS infection (pleocytosis, increase of proteins or positive VDRL), the same regimen of penicillin G sodium but for 3 weeks. 3. Exclusive bone disease or asymptomatic with positive serology, penicillin G procaine 50,000 IU/kg/day i.m. during 10-14 days. 4. Asymptomatic infants born to mothers with syphilis should be treated in the following conditions: a) Infants born to mothers treated before or during pregnancy whose serum titers do not decrease up to ¼ of the previous pre-treatment value in 3 months. b) Infants born to mothers who had not received treatment during the last month, with negative assessment at birth. c) Infants born to mothers treated during pregnancy with a non-penicillin antibiotic (e.g., erythromycin). d) Infants born to untreated mothers, mothers insufficiently treated, or who had sexual contact with an infected person. e) HIV-infected mothers whose treatment had been inferior to that for neurosyphilis. Treatment: penicillin G benzathine 50,000 IU/kg i.m. (single dose). 2.

Reference. Botet F, Figueras Aloy J, Carbonell Estrany X: Congenital Syphilis and Infant Born to a Mother with Syphilis. In: Recommendations and Guidelines for Perinatal Medicine. Matres Mundi/WAPM. Barcelona, 2007; 48: 416-417.

E.3.7. CONGENITAL MALARIA CONCEPT Congenital malaria is generally defined as malaria acquired by the fetus or newborn directly from the mother, either in utero or during delivery. The majority of neonates with a congenital infection are asymptomatic. Onset may be as early as 14 h of age to as late as 8 weeks but on an average it is between 10 to 28 days of life.

DIAGNOSIS 1. Clinical diagnosis. Fever, irritability, feeding problems, anaemia, thrombocytopenia, reticulocytosis, loose motions, failure to thrive, jaundice, hepatosplenomegaly and respiratory distress may occur. 2. Malaria parasites. To assess the presence of parasites in adults or children, peripheral blood should be examined for parasites by a Giemsa-stained thick or thin film. This technique remains the «gold standard» for laboratory confirmation on malaria. 3. Antigen detection. Various rapid test kits are commercially available to detect antigens derived from malaria parasites and may offer a useful alternative to microscopy in situations where reliable microscopic diagnosis is not available. It is especially useful in the diagnosis of malaria infection in non-immune patients due to the frequently low parasite density and low reliability of microscopy.

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4. Serology: Serology detect antibodies from malaria parasites, but only detects a past and not a current infection. It is useful to assess the level of exposure and to do seroepidemiological studies.

TREATMENT All newborn with positive haematological examination or with risk factors (ma larial parasite demonstrated in mother during pregnancy) and neonates with suggestive disturbances need treatment. 1. Mild infections or parasitemias by P. vivax, P. ovale, P. malariae and chloroquine sensitive P. falciparum should be treated with chloroquine orally 10 mg/ kg initially, followed by 5 mg/kg after 6 h and then once a day for the next 2 days. Primaquine is not required for treatment as the tissue phase is absent in congenital malaria. 2. Severe infection should be treated with quinine initially 20 mg/kg i.v. in 5 % dextrose over 4 h followed by 10 mg/kg every 8 h. i.v. until oral treatment is possible, for a total duration of 7 days. 3. Chloroquine-resistant cases (most frequent with P. falciparum) should be treated with quinine give parenterally until oral treatment is possible: a) Duration of treatment: 7 days. b) Add clindamycin: 20-40 mg/kg/day every 8 h for 5 days. 4. Quinine-resistant cases: Halofantrine-based therapies may be used. 5. Exchange transfusion may be required when parasitema exceeds 10 %. Supportive management for fever, fluids, calories and electrolytes need to be supervised. 6. Only very small concentration of antimalarial drugs is detected in breast milk, the amount is neither harmful nor protective against malaria.

Reference. Botet F, Figueras, Aloy J, Carbonell-Estany X: Malaria. In: Recommendations and Guidelines for Perinatal Medicine. Matres Mundi/WAPM. Barcelona, 2007; 48: 421-422.

E.3.8. HUMAN IMMUNODEFICIENCY VIRUS (HIV)

IN NEWBORN

CONCEPT The infection caused by the human immunodeficiency virus (HIV) productes a long-standing immunodeficiency syndrome. Infants become infected by vertical transmission during gestation (last 6 weeks), at the time or delivery of by breastfeeding, which represents an added risk for acquiring HIV infection.

DIAGNOSIS IN THE NEWBORN Serological test and measurement of the viral load at the first hours of life and again after 2 weeks. If in both assessments the viral load is negative, vertical transmission can be excluded.

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TREATMENT OF THE NEWBORN 1. 2.

Invasive procedures should be avoided (vitamin K i.m.) until the end of bath. Artificial feeding. Zidovudine starting at 8-12 of life, 2 mg/kg every 6 h. orally, until 6 weeks of life. Serial blood cells counts to assess the appearance of anaemia and neutropenia are necessary. In the presence of risk factors (no maternal treatment), nevirapine 120 mg/m2 in 48 h should be administered.

Reference. Botet F, Figueras Aloy J, Carbonell-Extrany X: Human Immunodificiency. Virus (HIV). In: Recommendations and Guidelines for Perinatal Medicine. Matres Mundi/WAPM. Barcelona, 2007; 48: 420-421.

E.3.9. INFANT BORN TO A MOTHER WITH HEPATITIS B VIRUS

(HBV) INFECTION

CONCEPT Infection caused by hepatitis B virus may show a clinical course towards resolution or, frequently, towards carrier states in which there is persistence of HBV. Chronic HBV carriers may transmit the infection to the fetes through the placenta or to the newborn at the time of delivery.

DIAGNOSIS HBV- infected pregnant women are asymptomatic. The diagnosis is established by serological controls, including systematic hepatitis B surface antigen (HBsAg) and hepatitis B virus core antigen (HBeAg)

TREATMENT OF THE NEWBORN 1. Invasive procedures during labor should be minimized. Postpartum secretions should be cleansed before punctures and blood sampling. 2. Anti-HB hyperimmune gamma globulin 0.5 mL (100 IU) i.m. together with specific hepatitis B vaccine 0.5 mL (5 ug) i.m. in the anterolateral aspect of both thighs should be administered, preferably during first 12 h of life, followed by the vaccination schedule with doses at 1 month and 6 months. 3. The administration of anti-HB hyperimmune gamma globulin and specific hepatitis B vaccine do not influence upon serological results (HBsAg). 4. In HBsAg-positive infants, vaccination is not indicated. 5. Infants born to HBeAg-positive mothers are at higher risk of infection. 6. Breastfeeding is not contraindicated. Reference. Botet F, Figueras Aloy J, Carbonell-Extrany X: Infant Born to a mother with Hepatitis B Virus (HBV) infection. In: Recommendations and Guidelines for Perinatal Medicine. Matres Mundi/WAPM. Barcelona, 2007; 48: 419-420.

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E.3.10. INFANT BORN TO A MOTHER

WITH HEPATITIS C VIRUS (HCV) INFECTION

CONCEPT The infection is transmitted by the parenteral route. Vertical transmission occurs in HCV positive mothers during pregnancy or at labor. Blood transfusion is another route of infection.

DIAGNOSIS a) Clinical. HCV infection may present as an acute hepatitis with jaundice. The course of the disease may be self-limited or may show progression to cirrhosis or hepatocarcinoma. b) Laboratory. The diagnosis is established by positive HCV antibodies and HCV RNA PCR. Transient or persistent increases of serum aminotransferases are observed.

TREATMENT OF THE NEWBORN Invasive procedures during labor should be avoided. Postpartum secretions should be cleansed before punctures and blood sampling. Breastfeeding is allowed.

E.3.11. SCREENING OF SURGICAL DISEASE

IN NEONATAL PERIOD

A. CHOANAL ATRESIA (CA) a) Concept. Due to lack of communication between nasal fossa and nasopharynx; the malformation might be uni or bilateral. b) Diagnosis. 1. Clinic. The unilateral shape is normally asymptomatic; the bilateral produces a severe cyanosis and respiratory difficulty. It gets better when the baby opens his mouth and cries. Etiologic. Due to a membrane or septum. 2. Complementary studies. The clinical gives us the diagnosis in most cases. In the unilateral type; the alternative comprenssion of the nasal fosses with the mouth closed shows the lack of ventilation on the damaged side. Through direct visual

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inspection by otoscopy or through the frailed probe, we can verify this malformation. c) Treatment. Immediately. Placement of a Mayo Tube. Once the patient has recovered, the atresia is perforated a with a trocar or laser via nasal.

B. GLOSSOPTOSIS a) Concept. The most characteristic is the Pierre Robin Syndrome. This is characterized by glossoptosis, microrretrognatia, and cleft palate (in the less severe cases ojival palate). The tongue lies posteriorly and obstructs the air entrance. b) Diagnosis. 1. Clinic. Distress respiratory syndrome, cyanosis and apnea that get better in upside down position. c) Treatment. Prone position in the mild cases. In severe condition, placement of a Mayo tube, traqueal intubation or surgical techniques (glosopexias). Feeding will be given orally or through nasogastric tube.

C. CONGENITAL DIAPHRAGMATIC HERNIA a) Concept. Congenital diaphragmatic hernia (CDH) is a malformation characterized by a defect in the posterolateral diaphragm, the forament of Bochdalek, through which the abdominal viscera migrate into the chest during fetal life. b) Diagnosis. 1. Ultrasonography. Widespread use of obstetric sonography has led to an increase in the frequency of antenatal diagnosis of CDH, which is established by demonstration of the abdominal viscera in the chest. 2. Clinic the symptoms of a CDH appear soon after the baby is born and include: dyspnea, fast breathing, tachycardia, cyanosis, abnormal chest development, with one side being larger than the other, abnormal abdominal shape (concave) Complementary studies: chest x-ray shows the abnormalities of the lungs, diaphragm and intestine. c) Treatment. 1. The surgery to repair the diaphragm is not an emergency and the baby should be as stable as possible before it; this may take days to weeks. 2. At the time of surgery the stomach, intestine and other abdominal organs are moved from the chest cavity back to the abdominal cavity. 3. The diaphragmatic defect is repaired by direct suture (stitches); sometimes it may require the use of plastic piece or mesh. 4. Many babies will need to remain in the NICU for a while after surgery.

D. CONGENITAL CYSTIC ADENOMATOID MALFORMATION (CCAM) a) Concept. CCAM is a developmental hamartomatous abnormality of the lung with adenomatoid proliferation of cysts resembling bronchioles.

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b) Types. CCAM is subdivided into 3 major types. 1. Type I lesions, the most common, are composed of 1 or more large cysts measuring 2-10 cm in diameter. 2. Type II lesions are characterized by small relatively uniform cysts resembling bronchioles. The cysts generally measure 0.5-2 cm in diameter. 3. Type III lesions consist of microscopic, adenomatoid cysts, and are grossly a solid mass without obvious cyst formation. Microscopic adenomatoid cysts are present. 4. Type II and III lesions can occasionally coexist with extralobar seques tration. c) Diagnosis. 1. Clinic. In the newborn, 80 % of CCAMs present with some degree of respiratory distress secondary to mass effect and pulmonary compression or hypoplasia. 2. Complementary studies. CCAM may be initially detected during prenatal ultrasonography. 3. After birth, chest radiography shoul be perormed first. Although lesions remain filled with fluid, postnatal sonography can be used for a more detailed assessment, particularly in type III lesions. Once lesions are air-filled. CT scanning is necessary for determination of the type and extent of the lesions.

E. CONGENITAL LOBAR EMPHYSEMA (CLE) a) Concept. Congenital lobar emphysema presents with overexpansion of a pulmonary lobe and compression of the remaining ipsilateral lung. The abnormality is related to intrinsic bronchial narrowing. In these cases, there is weakened or absent bronchial cartilage. During inspiratory air enters but collapse of the narrow bronchial lumen occurs during expiration. This bronchial defect results in lobar air trapping. CLE almost always involves one lobe (Left upper lobe 41 %). b) Diagnosis. 1. Clinical. Approximatetly half of patients develop respiratory distress within the newborn period while the remainder is delayed till 4 to 6 months of age or later. Presenting sings are those of respiratory embarrassment, including dyspnea, tachypnea, agitation and wheezing. 2. Complementary studies. Usually, chest X-radiography shows marked overdistention of an upper lobe with mediastinal shift to the other side. Computed tomography scanning can provide details about the involved lobe and its vascularity, as well as information about the remaining lung. c) Treatment. Emergency surgical lobectomy was once considered the only treatment for CLE, but appropriate care may be nonsurgical in infants with only moderate respiratory distress.

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F. OESOPHAGEAL ATRESIA a) Concepts. 1. Oesophageal atresia is defined as an interruption in the continuity of the oesophagus with or without fistula to the trachea. The most frequent type is the form with a distal tracheoesophageal fistula , 85 %). 2. Oesophageal atresia is associated frequently with other anomalies, such as imperforate anus, skeletal abnormalities or cardiac malformations that can be evident on physical examination. 3. Up to 10 percent of infants with esophageal atresia have the VATER syndrome. The acronym VATER, or VACTERL (vertebral defect, anorectal malformation, cardiac defect, tracheoesophageal fistula, renal anomaly, radial dysplasia and limb defects), has been used to describe the condition of multiple anomalies in these infants. b) Diagnosis. 1. Clinic. Postnatal presentation is characterized by drooling of saliva and cyanotic attack. If a fistula between the esophagus and the trachea is present, abdominal distention develops as air builds up in the stomach. The abdomen will be scaphoid if no fistula exists. If passage of 12 F feeding tube into the stomach is not possible, oesophageal atresia is almost certain. 2. Complementary studies. • The prenatal ecography may show polyhydramnios in the second half of pregnancy. • The chest radiograph provides information about the cardiac silhouette, the location of the aortic arch and the presence of vertebral and rib anomalies. Contrast studies are seldom necessary to confirm the diagnosis. c) Treatment. Once a diagnosis of esophageal atresia is established, preparations should be made for surgical correction. The oral pharynx should be cleared, and a 8 French sump tube placed to allow for continuous suctioning of the upper pouch. Gastrostomy for gastric decompression is reserved to patients with great operatory risk.

G. DUODENAL OBSTRUCTION a) Concepts. 1. Congenital duodenal atresia is one of the more common intestinal anomalies treated by pediatric surgeons. 2. Duodenal obstruction may be complete or incomplete. Duodenal atresia is a complete intrinsic obstruction. Duodenal stenosis is an incomplete intrinsic abnormality; however, duodenal extrinsic stenosis can occur in association with malrotation, annular pancreas or a preduodenal portal vein. b) Diagnosis. 1. Clinic. Prenatal diagnosis can be suspected by polyhydramnios and the distension of the stomach and the first portion of the duodenum with swallowed

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amniotic fluid. In the postnatal period, duodenal atresia is typically characterized by onset of vomiting within hours of birth. While vomits are most often bilious, it may be nonbilius because 15 % of defects occur proximal to the ampulla of Vater. 2. Complementary studies. RX a characteristic finding of duodenal obstruction is the double bubble image of an air-filled stomach proximal to an air-filled first portion of the duodenum. Absence of gas in the remaining small and large bowel suggests atresia. Whereas scattered amounts of gas distal to the obstruction suggests stenosis or malrotation. c) Treatment. The definitive intervention to correct the anomaly is surgical and consists of duodenostomy in the newborn period.

H. JEJUNO-ILEAL ATRESIA a) Concepts. 1. Defects in the continuity of the small bowel can morphologically be di vided into stenosis or atresia and represent one of the most common causes of neonatal intestinal obstruction. 2. The most accepted theory regarding the etiology is that of an inatrauterine vascular accident resulting in necrosis of the affected segment, with subsequent resorption. 3. One third is premature or small-for-date. Four types of jejunoileal atresias are described. 4. The different types represent a spectrum of severity, from a simple web to multiple atresias with loss of bowel length. b) Diagnosis. 1. Clinic. • Clinically, the neonates with a proximal atresia develop bilious emesis within hours, whereas the patients with more distal lesions may take longer to begin vomiting. • A normal or scaphoid like abdomen in a neonate with bilious emesis should be considered indicative of a proximal obstruction until proven otherwise. • Abdominal distension is more pronounced with distal lesions. 2. Complementary studies. • Radiography is helpful to confirm the diagnosis. The more proximal the atresia develops, the fewer air-fluid levels are evident, with no apparent gas in the lower part of the abdomen. Distal lesions demonstrate more air-fluid levels, although the distal intestine remains gasless. • A barium enema may be used to define a microcolon indicative of a distal small-bowel obstruction; it is also capable of establishing the diagnosis of other causes of lower obstruction, such as Hirschsprung disease or a meconium plug. c) Treatment. 1. Gastric decompression and fluid resuscitation. The dilated proximal bulb generally does not have a normal function and, as a result, should be re-

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sected up to a more suitable size to avoid problems with abnormal peristalsis postoperatively. 2. If the bowel length is limited, a tapering enteroplasty should be consi dered rather than resection. An end-to-end anastomosis can then be performed.

I. ANORECTAL MALFORMATIONS (MAR) a) Concepts. 1. Anorectal malformations are a complex group of malformations diag nosed at the time of birth because of the absence or an ectopic location of the anus. 2. 85 % of MAR present with fistulas: genitourinary tract, vagina or perineum. 3. Clasification MARS (Krieckenbeck): perineal fistula, rectourethal fistula (bulbar, prostatic), rectovesical fistula, vestibular fistula and cloaca. No fistula. Anal stenosis. 4. The cases without fistula are associated to Dow syndrome in 50 % of the cases. b) Diagnosis. 1. Clinic. Absence of meconium evacuation or meconium emission through the fistula, abdominal distention. Physical exploration: Absence or abnormal position of the anus. Proper classification of most MAR can be usualy made. 2. Complementary studies. A lateral pelvis radiograph obtained with the baby in prone position (between 18 and 24 hours to allow time for gas or meconium to appear in the perineum) and the hips raised usually suffice. A gap of 1 cm or greater between gas shadow and skin usually represents a significant anomaly. Ultrasonography can provide the same type of information. 3. The rest of physical examination is directed toward detecting associated malformations that are present to in 70 percent of patients (digestive, cardiac, vertebral, genitourinary, chromosomic...). c) Treatment. 1. Terminal colostomy in descending colon in case of insufficient fistula. 2. Posterior surgical anorectoplasty (ARPS) according to Peña (from the 4th month of life on).

J. MECONIUM ILEUS a) Concepts. 1. Meconium ileus (MI) is one of the most common causes of intestinal obstruction in the newborn. 2. MI could be the first clinical manifestation of cystic fibrosis (CF) and occurs as either simple or complicated in approximately 8-10 % of patients who have CF. 3. MI may also occurs in patients without this disease.

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b) Diagnosis. 1. Clinical. • Prenatally, may be confirmed the development of atresias, perforation or peritonitis. Patients with simple MI usually present with abdominal distension at birth, eventually leading to failure to excrete meconium, bilious vomiting, and progressive abdominal distension. • Often, examination reveals dilated loops of bowel with a doughy character. The rectum and anus usually are narrow; a finding possibly misinterpreted as anal stenosis. • Patients with complicated MI present more dramatically at birth with severe abdominal distension, sometimes accompanied by abdominal wall erythema and edema. • Diagnosing CF during the neonatal period is difficult, since the sweat test can only give us relevant information from the 3rd or 4th month of life on. • Altered levels of trypsinogen, a pancreatic enzyme, can identify patients with CF in an early age. 2. Complementary studies. • Abdominal radiographs may reveal a distended bowel, few airfluid levels and, in the right lower abdomen, meconium mixed with air, which has a ground-glass appearance on plain film. The presence of calcifications, free air or very large air-fluid levels suggests complications. • Contrast enema radiographic examination demonstrates a microcolon, often with no bowel contents. Reflux of contrast into the small bowel reveals the plugs. The small bowel is of narrow calibre below the plug and dilated above the plug. c) Treatment. 1. Simple meconium ileus may be successfully treated by administration of a diatrizoate meglumine (Gastrografin) enema with fluoroscopic control and plenty of intravenous fluid. 2. If the Gastrografin enema is unsuccessful operative evacuation of the obstructing meconium by irrigation will be necessary. 3. Complications such as atresia, perforation and meconium peritonitis always require immediate surgery, including resection, intestinal anastomosis and ileostomy.

K. SERIOUS DEFECTS OF THE ABDOMINAL WALL: GASTROSCHISIS AND OMPHALOCELE a) Concepts. 1. Gastroschisis. The defect usually occurs on the right side of the umbilical cord, with a healthy piece of skin between both; the herniated bowel loops are not covered by peritonreum, and they are swollen, matted, adhered among themselves and covered with a thick fibrinous peel around the intestine. Zones of infarction and one or more zones of atresia or stenosis may be found as a result of intrauterine intestinal infarcts, with a high risk of obstruction and intestinal perforation.

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Omphalocele. It may be associated with other congenital anomalies as a polimalfor mative syndrome in more than 50 % of the cases (cardiopathies, trisomies 13 or 18, etc.). The size of the defect can vary from a simple umbilical hernia to great defects that even affect the anterior region of the thorax and the pelvis. An amniotic sac covers the abdominal content. When the defect is large, the peritoneal cavity usuall is too smalt to contain the herniated visceral organs. b) Treatment. 1. The primary closing of all the layers of the abdominal wall is the objective of the surgical treatment of both abnormalities, bur it is not always possible, at least at the first time. 2. In big omphaloceles, when peritoneal cavity is too small to contain the herniated organs, the Schuster technique may be used; organs are convered with a coat os silastic mesh, as a tempory housing for the intestine. 3. Later, the intestines can be returned to the abdomen graduallyby gentle pressure and placing the string that ties off the top of the silastic oat lower. 4. Once the intestines are almost back inside, the silastic sac is removed and the abdominal defect closed. 5. In gastroschisis, a direct closing is usually possible but when the intestine could not be completely placed back into the abdomen, the technique of Schuster may be also used. 2.

L. HIRSCHSPRUNG DISEASE (CONGENITAL MEGACOLON) a) Concepts. 1. The disease result from the absence of parasympathetic ganglion cells in the myenteric and submucosal plexus of a segment of the intestine, usually rectum and/or sigmoid colon (75 % of cases). This segment is spastic and noncontractile. 2. The proximal intestine becomes partially or completely functionally obstructed, and begins to dilate. b) Diagnosis. 1. Clinical. • In half of the cases manifestations begins in the neonatal period with intestinal obstruction or chronic constipation since birth. • The main symptoms are delayed passage of meconium, abdominal distension and vomiting. • In the unweaned baby, disease is usually manifested by a persistent constipation, mostly related to a nourishing change like substitution of breastfeeding for bottle-feeding or introduction of a complementary feeding. 2. Complementary examinations. • Plain abdominal radiography of abdomen shows important bowel distension with a speckled aspect of the bowel content because of trapped air inside of retained meconium. • Findings of single-contrast barium or gastrografin enema in newborns can be difficult to interprete. A delayed evacuation of barium

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Neonatal pathology E.3.

and a transition zone between a narrowed aganglionic segment and a dilated and normally innervated segment may be observed. • Accuracy of rectal manometry can be of 85 %. Children with Hirschsprung disease fail to demonstrate the reflex relaxation of the internal anal sphincter in response to inflation of a rectal balloon. However, this reflex is not developed in newborn, so the test is not helpful at this age. • The definitive diagnosis of Hirschsprung disease has to be done with the on histological review of rectal biopsies. Specimens are carefully examined for the presence or absence of ganglion cells in the myenteric plexuses and for increased acetylcholinesterase activity by histochemical study. 3. Differential diagnosis. Is should be considered with other problems that show neonatal intestinal obstruction: meconium plug syndrome, left colon hypoplasia syndrome, septic problems and cerebral palsy. c) Treatment. 1. Nursing: Normal saline irrigations through a rectal tube placed beyond the aganglionic segment. 2. Colostomy: If the nursing management is not helpful, a loop colostomy, performed over healthy colon, proximal to aganglionic zone, is indicated. 3. A surgical pull-through procedure is the definitive treatment.

M. PERFORATION OF HOLLOW VISCUS (PNEUMOPERITONEUM) a) Concept. The pneumoperitoneum is due to an intestinal or gastric perforation. b) Diagnosis. 1. Clinical course. Severe abdominal distention, tenderness, shock and respiratory distress. Tympanic abdominal percussion. 2. Etiology. • Gastric perforation can be spontaneous during reanimation maneuvers in perinatal hypoxia or while introducing a nasogastric tube improperly. Duodenal perforation can be because of a stress ulcer or gastroduodenal tube maintained during a long period. • Other perforations along the rest of the bowels might be due to previous pathology (NEC, Hirschsprung disease, meconium ileus). 3. Complementary studies. • Erected plain films show the free air in abdominal cavity located between the diaphragm and the liver. If the patient is supine, plain films with horizontal ray show free air under umbilicus. • Peritoneal lavage can help to determine the presence of enzymes and germs. Differential diagnosis: pneumoperitoneum could be ori ginated in the thorax when there is air migration through lymphatic vessels.

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c) Treatment. Emergency laparotomy in other to close the perforation, excision of an extended affected area and ostomies if necessary.

N. SOLID ORGANS INJURY (HEMOPERITONEUM) a) Concept. Solid organs injury can occur during delivery and can cause hemoperitoneum. The most frequent affected organ is the liver followed by the spleen.

O. HEPATIC RUPTURE a) Concept. It is a severe lesion with a high mortality rate (60-70 %) due to the hypovolemic shock. b) Diagnosis. 1. Clinical course. • Acute anaemia and hypovolemic shock. • The newborn presents pallor, deficient peripheric vascularisation with hypothermia, tachycardia with progress to bradycardia, hypotension with a decrease of central venous pressure. • The onset of hepatic rupture can be critic or slow in case of integrity of Glisson capsule, causing hepatomegaly and chronic anaemia. 2. Etiology. • Obstetric procedures. Immaturity, breech presentation, perinatal asphyxia and fetal macrosomia are predisposing factors. • Postnatal, reanimation maneuvers, cardiac massage, etc. 3. Complementary studies. a) Progressive anaemia. • Ultrasonography can show a subcapsular hemorrhage of the liver and later an intra-abdominal hemorrhage. • The goal of the peritoneal lavage is to determine if there is blood in the free peritoneal cavity. • Abdominal plain films provide valuable information such as hepa tomegaly and intra-abdominal hemorrhage signs (generalized ground-glass appearance to a largely gassless abdomen, blur the liver edges). c) Treatment. Fluid resuscitation sufficient to restore promptly and maintain adequate circulatory volume is an absolute priority. Surgery is indicated in case there is an ongoing blood loss that out of control.

P. SPLEEN RUPTURE It normally occurs in pathologic spleens due to a blunt trauma during delivery or after an exanguintransufion. Mortality rate is high.

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Q. PENUMOTHORAX AND PNEUMOMEDIASTINUM a) Concepts. 1. Accumulation of air or gas in the pleural cavity or mediastinum occurring as a result of alveolar breakage mainly because of interstitial pulmonary emphysema. 2. The air infiltrates the bronchovascular spaces and then reaches at the mediastinum, pleural cavity and subcutaneously (subcutaneous emphysema). b) Diagnosis. 1. Clinic. • In laminary pneumothorax symptoms are very slight and many are asymptomatic. • Tension pneumothorax starts abruptly with acute severe respiratory insufficiency, cyanosis, tachypnea, and tachycardia with low response to oxygen therapy. • Bilateral pneumothorax is a very severe situation that presents with interstitial and subcutaneous emphysema, pneumomediastinum, pneumopericardium and pneumoperitoneum. 2. Etiology. Iatrogenic cardiopulmonary resuscitation, obstructions (foreign bodies, mucus, etc). meconial aspiration, neonatal respiratory distress, congenital lobar emphysema, etc. 3. Complementary exams. X-Ray is diagnostic. Pneumothorax: Lung collapse with peripheral air image without pulmonary density. Pneumomediastinum. Air density along the cardiac silhouette and great vessels. Subcutaneous emphysema: air bubbles in the subcutaneous tissue with smooth bulging of the skin. Pneumopericardium: hyperclarity only along de cardiac silhouette. c) Treatment. 1. Pneumothorax. Needle puncture and aspiration only in emergency situations. Catheter place in the medial axilar line, not involving the mammary gland, with continuous aspiration (10-15 H20 cm) or just water seal. Catheter is removed when the underling disease is controlled. First, the catheter has to be closed for 24 h and a new X-Ray done in order to verify that no pneumothorax is formed again. Pneumomediastinum: some severe cases may need drainage. 2. Pneumopericardium. If cardiac tamponade is associated, immediate pericardiocentesis, needle evacuation of the fluid and lowering of the pericardial pressure, and then treatment of the underlying cause, has to be done. If possible, echocardiography may be helpful. 3. Pneumoperitoneum originated in the thorax is usually spontaneously resolved with no need of external intervention.

R. INGUINAL HERNIA a) Concepts. 1. Congenital indirect inguinal hernias develop because the processes vaginalis remains patent after birth.

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Inguinal hernia is more common in males than is females 5:1. Of all inguinal hernias, 60 % occurs on the right side, 25-30 % on the left, and 10-15 % are bilateral. b) Diagnosis. 1. Clinic. • The most common presentation of inguinal hernia in a child is a groin bulge, extending towards the top of the scrotum. • Complication: Sometimes a portion of the intestine is trapped in the scrotum (incarceration); this can cut off the intestine’s blood supply (strangulation). • Strangulated intestines may become gangrenous within hours. 2. Diagnosis difference. Cyst in the high cord, transparency by translumination, in front of the strangulated hernia opacity will help us decide the diagnosis. The adenitis or inguinal adenophlegmon of the ganglion inguinal packages. c) Treatment. The main treatment for inguinal hernia is surgery to repair the opening in the muscle wall.

S. TESTICULAR TORSION a) Concepts. 1. The spermatic cord that provides the blood supply to a testicle is twisted, cutting off the blood supply, often causing orchalgia. Prolonged testicular torsion will result in the death of the testicle and surrounding tissues. 2. It is also believed that torsion occurring during fetal development can lead to the so-called neonatal torsion. Left testicle is more commonly affected. Testicular torsion can be extra or intravaginal (in between the testicle and the epididymis). Extravaginal torsion is the most common from among neonates. b) Diagnosis. 1. In the newborn we can find swelling within one side of the scrotum, a blackish testicular mass associated with fever and in some cases nausea or vomiting. 2. Differential diagnosis has to be done with inguinal hernia. Doppler shows normal blood flux in the normal testicle with low or absence in the torsionated one.

T. HYDRONEPHROSIS a) Concepts. 1. Pelvi-ureteric junction obstruction (PUJ) is the most common cause of hydronephrosis detected antenatally. 2. Controversy continues on the optimal timing of surgical intervention in children with antenatal detected hydronephrosis. 3. Recognition is important to prevent irreversible damage to the kidneys.

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Neonatal pathology E.3.

b) Diagnostic. 1. Clinic. Before the routine fetal ultrasonography, the commonest presentation was with abdominal flank mass. Some patients present with urinary tract infection, irritability, vomiting and failure too thrive. 2. Complementary examinations. Radionuclide studies (diethylenetriaminepentaacetic acid DTPA and mercaptocetyltriglycine MAG3) are undertaken when the child is 68 weeks old in order to asses renal function and rule out obstruction. c) Treatment. The decision of surgical intervention is complex because spontaneous resolution of antenatal and neonatal upper urinary tract dilatations is well known. Currently surgery is undertaken only in infants with deteriorating renal function.

Reference. Castañon M: Screening of surgical discase in neonatal period. In: Recommendations and Guidelines for Perinatal Medicine. Matres Mundi/WAPM. Barcelona, 2007; 45: 381-392.

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SUBJECT INDEX

A Abbreviations, 7, 27 Abdominal Trauma, 93, 94, 100, 165, 166 Abo/Rh Screening, 101 Abruptio Placenta, 93, 94, 116, 222 Abscess Drainage, 269 Abscess/Seroma, 202 Acceleration Pattern, 186 Acquired Cervical Incompetence, 85 Acupuncture, 207 Acute Fatty Degeneration of the Liver, 137 Ccute Pyelonephritis, 143, 144 Alcohol, 24, 29, 41, 45, 57, 59, 97, 136, 271 Amniocentesis, 7, 55, 56, 57, 58, 59, 68, 83, 91, 92, 99, 100, 102 Amnioscopy, 7, 58 Amniotic Fluid Embolism, 223, 228, 229, 239, 264 Amniotic Fluid Index, 7, 27, 67 Amniotomy, 27, 119, 183, 184 Anaemia in Pregnancy, 121, 122 Anaemia Macrocytic, 121, 122 Anaemia Microcytic, 121, 122 Anaemia Normocytic, 121 Anatomical Cervical Incompetence, 85 Android Pelvis, 64 Angiografic Embolization, 266 Anorectal Malformations, 31, 310

Antenatal Period, 39, 96 Antepartum Care, 7, 39, 43 Antepartum Haemorrhage, 8, 27, 93 Anthropoid Pelvis, 64 Antibiotic Prophylaxis, 58, 129, 154, 211, 212 Antibiotic Use in Obstetrics Surgery, 9, 211 Anticonvulsants, 139 Anti-D Ig, 100, 101, 102 Antimicrobial Therapy, 267, 269 Antiretrovial Drugs, 162, 163 Apgar Score, 276, 297 Arrhythmias, 115, 128, 129 Ashermanâ&#x20AC;&#x2122;s Syndrome, 253 Aspiration Pneumonia, 286 Assistance of the Newborn Transport, 292 Asymptomatic Bacteriuria, 134, 142 Atrial Fibrillation, 129 Atrial Tachycardia, 129 Autopsy Protocol, 279

B Bacteriuria, 41, 42, 134, 142, 143, 163 Ballistic Trauma, 166 Barrier Methods and Spermicides, 259 Baseline Bradycardia, 185 Baseline Irregularity, 185, 186 Baseline Tachycardia, 186 Betamimetic Drugs, 89

CLINICAL GUIDELINES FOR MATERNITY HOSPITALS

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Subject Index

Birth Trauma, 26, 130, 264 Bishop’s Score, 182 Blighted Ovum, 73 Blood Products, 9, 204, 206, 207 Blood Transfusion, 123, 205, 265, 305 Blood Transfusion in Pregnancy, 205 Brachial Plexus Injury, 216, 217, 218 Breast-Feeding, 9, 40, 41, 47, 135, 150, 248, 251, 277, 278, 279 Breastfeeding, 39, 47, 120, 124, 138, 139, 155, 164, 232, 233, 239, 244, 248, 249, 250, 251, 252, 257, 258, 259, 260, 271, 303, 304, 305, 312 Breast-Feeding Contraindicated Drugs, 279 Breast Milk, 155, 164, 248, 249, 252, 261, 277, 296, 303 Breast Stimulation, 182, 251 Breech Delivery, 40, 193, 223, 224, 237 Breech Presentation, 9, 42, 43, 54, 66, 185, 186, 195, 220, 221, 222, 223, 230, 237, 314 Bronchial Asthma, 123 Brow Presentation, 191, 219, 220, 221 Buddha Position, 118 Burns, 167, 261

C Caesarean Elective, 194, 211, 215, 218, 237 Caesarean Intrapartum, 194, 195 Caesarean Section, 9, 25, 26, 40, 42, 84, 128, 130, 140, 148, 166, 167, 168, 176, 177, 178, 182, 184, 187, 194, 195, 197, 199, 205, 209, 218, 219, 222, 223, 224, 225, 228, 230, 234, 245, 254, 266 Caesarean Surgery Technique, 198 Caesarean Technique, 197 Caesarean Urgent, 194 Caffeine, 45 Calcium Gluconate, 105, 112, 229, 300 Cardiac Disease, 8, 9, 22,23, 129, 234 Cardiac Disease in Pregnancy, 8, 127 Cardiac Diseases, 24 Cardiac Failure, 69, 128, 239 Cardiotocographic Prenatal Monitoring, 60 Cardiotocography, 28, 60, 210

Cephalo-Pelvic Disproportion, 28, 65, 195, 196, 216 Cephalopelvic Disproportion, 112, 176, 177, 191, 219, 221 Cerclage Technique, 7, 62 Cervical Incompetence, 62, 85, 86 Cesarean Hysterectomy, 10, 254 Chagas’ Disease, 8, 164 Chlamydia, 62, 145, 146, 147, 149, 290 Chlamydia Trachomatis, 62, 146, 290 Choanal Atresia, 305 Chorioamnionitis, 28, 56, 64, 87, 89, 90, 92, 116, 118, 119, 181, 212, 218, 262 Choriocarcinoma, 76, 77, 78, 79 Chromosomal Abnormalities, 69, 73, 98, 99, 115 Chronic Anaemia, 204, 314 Chronic Diabetes, 232 Chronic Hbv Carriers, 61, 304 Chronic Hypertension, 25, 102, 103, 120 Chronic Hypertension in Pregnancy, 102, 108 Classification of Fetal Risk, 23 Clement’s Test, 59 Clinical Dating, 52 Clinical Diabetes, 131 Clinical Pelvimetry, 7, 64, 177 Coagulation Defects, 9, 228 Combined Cerclage of Carrera, 63 Combined Hormonal Contraceptives, 260 Complete Abortion, 74 Complete Breech, 197, 221, 222 Complete Miscarriage, 73 Complete Mole, 76 Congenital Cervical Incompetence, 85 Congenital Cystic Adenomatoid Malformation (CCAM), 306 Congenital Defects, 7, 26, 68, 70, 99, 281 Congenital Diaphragmatic Hernia, 28, 306 Congenital Lobar Emphysema, 28, 307, 315 Congenital Malaria, 10, 302, 303 Congenital Malformations, 48, 50, 115, 132, 139, 291 Congenital Megacolon, 312 Congenital Rubella Syndrome, 61 Congenital Syphilis, 10, 117, 145, 301, 302

CLINICAL GUIDELINES FOR MATERNITY HOSPITALS

Subject Index

Continuous Positive Airway Pressure (CPAP), 288 Continuous Recording of the FHR, 184 Contraceptive Methods, 246, 257, 258 Control of FHR, 174 Cord Prolapse, 9, 181, 183, 197, 221, 222, 224, 230, 238, 275 Cord Prolapse: Emergency Measures, 230 Cystic Hygroma, 28, 69, 70 Cystitis, 142, 143 Cytomegalovirus, 8, 28, 62, 117, 149, 150, 155, 152, 161

D Deep Vein Thrombosis, 29, 140 Deep Venous Trombosis, 267 Defibulation, 41, 228 Deflected Presentations, 195, 196 Delivery of the Placenta, 174, 225, 239 Delivery Room, 10, 29, 66, 172, 205, 275, 283, 294 Depressive Disorder, 271 Depressive Illness, 135 Dexeus Test, 60, 61 Diabetes and Pregnancy, 8, 131, 135 Diabetes: Intrapartum Management, 9, 231 Diaphragmatic Hernia, 28, 285, 292, 306 Dilatation Period, 172, 195 Dinoprostone, 183 Disease Reference Test, 301 Drainage of Abscess, 270 Drug Abuse and Pregnancy, 136 Drugs and Radiations in Perinatal Period, 48 Duodenal Obstruction, 308, 309 Dysfunctional Cervix, 85 Dystocia, 8, 9, 34, 40, 95, 112, 175, 178, 194, 195, 209, 216, 217, 218, 275

E Early Decelerations, 61, 186 Early Neonatal Mortality, 21 Early Neonatal Period, 20 Early Onset Sepsis, 298, 299 Eclampsia, 8, 9, 25, 40, 89, 102, 103, 106, 111, 197, 209, 236

Eclampsia Mamagement, 111 Eclamptic Seizures, 103, 104 Ectopic Pregnancy, 7, 24, 74, 75, 77, 102 Effects of Diagnostic Radiation, 51 Endomyometritis, 266, 267 Endotoxic Shock, 228 Epidural Analgesia, 119, 210, 211 Epidural Analgesia: Complications, 210 Epilepsy, 8, 22, 40, 72, 139, 140, 209 Episiotomy, 9, 29, 119, 174, 188, 189, 192, 194, 196, 208, 214, 215, 223, 227, 228, 244, 262, 264 Epistomy Mediolateral, 188 Epistomy Midline, 188 Epithelioid Trophoblastic Tumour, 29, 76, 79 Evacuation of the Uterus, 102, 253, 270 Exercise, 45, 46, 233 Expulsion Period, 173 External Cephalic Version, 7, 42, 43, 65, 102, 222 Extremely Low Birth Weight, 19

F Face Presentation, 53, 193, 219, 220, 221 False Labour, 176 Family Planning, 201, 203, 233, 235, 257 Fascial Dehiscence, 202 Female Genital Mutilation, 29, 41, 226 Female Genital Mutilation Classification, 226 Female Genital Mutilation: Consequences, 227 Female Genital Mutilation: During Labour, 227 Fetal Blood Samples, 187 Fetal Blood Sampling, 186 Fetal Control, 130, 172 Fetal Death, 21, 29, 61, 83, 98, 100, 114, 116, 117, 118, 119, 120, 130, 136, 168, 181, 264 Fetal Demise, 8, 31, 83, 89, 116, 117, 118, 120 Fetal Demise: Etiology, 117 Fetal Demise: Potential Complications, 118

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Subject Index

Fetal Heart Rate, 29, 43, 49, 84, 88, 96, 106, 107, 109, 113, 181, 183, 185, 223, 236 Fetal Lung Maturity, 59 Fetal Necropsy, 10, 279, 280, 282 Fetal Period, 20, 21 Fetal PH, 173, 185, 186, 187 Fetal Respiratory Reverse, 33, 60 Fetal Resuscitation, 284 Fetal Resuscitation in Special Situations, 286 Fetal Scalp PH, 184 Fetal Ubication, 7, 53 Fetal Well Being, 93, 103, 106, 108 Fistula, 34, 35, 189, 254, 255, 256, 257, 308, 310 Fistula: Postoperative Details, 256 Fistula Tract, 256 FLU (Influenza), 152 Foetal Distress, 197, 236, 237 Folley Catheter, 182 Forceps, 9, 31, 40, 128, 174, 175, 178, 186, 189, 190, 192, 193, 194, 195, 219, 224, 230, 245, 280 Fourth-Degree Episiotomy, 189 Frank Breech, 220, 221 Fundal Height, 97, 106, 113, 216, 239

G Gas Exchange, 287, 288, 289 Gastroschisis, 115, 293, 311, 312 General Analgesia, 208 Genetic Amniocentesis, 55 Genital Mutilation, 9, 29, 41, 226 Germinal Matrix-Intraventricular Haemorrhage, 296 Gestational Age, 19, 20, 31, 34, 42, 43, 52, 54, 55, 56, 60, 73, 76, 77, 83, 84, 86, 87, 88, 89, 90, 95, 97, 98, 102, 103, 113, 114, 156, 158, 182, 223, 249, 261, 275, 281, 282, 289, 292, 294 Gestational Diabetes, 8, 9, 23, 24, 25, 30, 40, 41, 129, 131, 232, 233 Gestational Hypertension, 103 Gestational Trophoblastic Neoplasia/ Tumour, 7, 76, 78 Glossoptosis, 306

Glucose Monitoring, 130, 231, 232 Glucose Tolerance Test, 30, 32, 131, 233 Gonorrhoea, 145 Gynecoid pelvis, 64

H Haemorrhages of the First Term, 77 HBV-Infected Pregnant Women, 304 Health Care During Pregnancy, 44 Health Education During Pregnancy, 7, 44, 47 Hellp Syndrome, 103, 264 Hemoperitoneum, 166, 314 Heparin, 120, 141, 142, 187, 200, 209, 229, 230, 267, 268, 270 Hepatic Rupture, 314 Hepatitis, 10, 23, 30, 40, 61, 136, 137, 147, 150, 152, 162, 277, 301, 304, 305 Hepatitis, 304, 305 Hepatitis B Virus, 10, 30, 61, 304 Hepatitis C Virus (Hcv) Infection, 305 Herpes Simplex, 30, 147, 150, 161, 249, 277 Herpesvirus, 147 High Forceps, 193 High Risk Delivery, 195 High-Risk Pregnancy, 23 Hirschsprung Disease, 309, 312, 313 HIV/Aids in Pregnancy, 8, 158 HIV Clinical Scenarios, 159 HIV Disease: Clinical Staging, 161 HIV Prevention, 159 Hormonal Contraceptives, 257, 260 Hormonal Methods, 260 HSV-1, 147, 249 HSV-2, 147 Human Immunodeficiency Virus, 10, 62, 158, 303 Human Papillomavirus, 30, 148 Hydatidiform Moles, 76 Hydralazine, 104, 111 Hydronephrosis, 316 Hygroscopic Dilator, 182 Hyperemesis Gravidarum, 71, 72 Hypertensive Emergencies, 104 Hypnosis, 207 Hypocalcaemia, 300 Hypothermia in the Newborn, 294

CLINICAL GUIDELINES FOR MATERNITY HOSPITALS

Subject Index

Hypothyroidism, 73, 122, 138, 139, 271, 277 Hypoxic-Ischamic Encephalopathy, 217

I Ideal Pelvis, 65 III, 54 Illegal Drugs, 45 Immediate Puerperium, 243 Immunodeficiency Syndrome, 27, 158, 160, 303 Inadequate Uterine Activity, 176, 177 Incomplete Abortion, 74 Incomplete Breech, 197, 221, 222 Incomplete Miscarriage, 73, 101 Indirect Coombs Test, 101 Indomethacin, 90, 116, 295, 297 Induction of Labour, 106, 107, 113, 181, 182, 183, 184, 235, 236, 266 Infection in the Breast, 268 Infections Diseases in Pregnancy, 8, 144 Infective Endocarditis, 129 Inguinal Hernias, 315, 316 Inhalatory Analgesia, 208 Inhibition of Breastfeeding, 250, 252 Inhibition of the Breast-Feeding, 9, 248, 251 Injuries During Pregnancy, 8, 165 Inspection of Placenta, 9, 247 Inspired Oxigen Concentration, 29, 290 Insulin Therapy, 130, 133 Intercurrent Jaundice in Pregnancy, 137 Intermittent Recording of FHR, 184 International School of Perinatal Medicine For Africa, 1, 3, 5 Intraamniotic Infection, 8, 30, 90, 91, 92, 264 Intrahepatic Cholestasis, 137 Intrapartum Defibulation, 41, 228 Intrapartum Fetal Monitoring, 9, 184 Intrapartum Management, 9, 115, 231, 233, 234, 238 Intrauterine Devices, 259 Intrauterine Growth Restriction, 8, 24, 26, 31, 45, 97, 114, 125, 134, 153, 223, 275 Iron Deficiency, 122, 123

Isoimmunization, 8, 24, 57, 100, 101, 102, 115, 116, 117 Ispema, 1, 5, 11, 13, 15, 30 IUD, 31, 54, 134, 233, 258, 259 Iugr Diagnosis Type I, 54, 97, 98 Iugr Diagnosis Type II, 54, 97, 98 Iugr Diagnosis Type III, 54, 97

J Jaundice, 8, 136, 137, 138, 150, 278, 302, 305 Jaundice Caused By Pregnancy, 137 Jaundice Complicating Pre-Eclampsia, 137 Jejuno-Ileal Atresia, 309

K Kangaroo Mother Care, 10, 261 Kehrerâ&#x20AC;&#x2122;s Sign, 118

L Labetolol, 104, 111 Labour Attendance, 8, 171 Labour Dystocia, 195 Lactation Amenorrhea, 31, 259, 260 Late Deceleration, 61, 172, 186, 275 Late Neonatal Mortality, 21, 22 Late Neonatal Period, 20 Late Onset Sepsis, 299 Late Puerperium, 243, 246 Leopoldâ&#x20AC;&#x2122;s Manoeuvres, 7, 53 Lifestyle, 44, 45, 233, 234 Lifetime Births Per Woman, 22 Listeria Monocytogenes, 154 Listeriosis, 8, 117, 154 Live Birth, 19, 21, 40 Local Analgesia, 191, 208 Low Birth Weight, 19, 31, 40, 81, 157, 261 Low-Molecular-Weight-Heparin (LMWH), 141

M Macdonald Operation, 63 Macrocytic Anaemia, 122

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324

Subject Index

Macrosomia, 9, 112, 116, 130, 132, 134, 216, 214, 216, 217, 218, 221, 223, 314 Magnesium Sulfate, 31, 104, 105, 111, 107, 236, 237 Magnesium Toxicity, 105, 107, 112, 236 Malaria Diagnosis, 157 Malaria in Pregnancy, 8, 157 Malaria Parasites, 302, 303 Malaria Prevention, 157 Malaria Treatment, 157 Malpresentations, 9, 195, 196, 218 Management of Dystocia, 8, 175 Maneuver of Bracht, 224 Maneuver of Deventer-MĂźller, 224 Maneuver of Mauriceau-Veit-Smellie, 224 Marginal Placenta Previa, 94, 96 Mastitis, 10, 251, 252, 262, 266, 268, 269 Maternal Mortality, 22, 24, 25, 124, 157, 167, 180, 255 Matres Mundi, 3, 4, 5, 11, 13, 15, 22, 26, 43, 47, 51, 70, 74, 75, 77, 84, 87, 120, 135, 153, 155, 157, 158, 164, 184, 188, 199, 208, 211, 218, 224, 228, 246, 257, 260, 266, 267, 268, 269, 287, 290, 297, 298, 302, 303, 304, 305, 317 Mc Twins, 82, 83, 84 Mechanical Ventilation, 34, 268, 291 Meconium Ileus, 310, 311, 313 Meconium Stained Amniotic Fluid, 286 Medial Forceps, 193 Mediate Puerperium, 243, 245 Medical History, 40 Membrane Sweeping, 183 Mendelsonâ&#x20AC;&#x2122;s Syndrome, 9, 239 Methotrexate (MTX) Treatment, 75 Microcytic Anaemia, 122 Mild Preeclampsia, 105, 106, 107, 109, 236, 237 Miscarriage, 7, 22, 45, 49, 50, 72, 73, 74, 77, 101 Misoprostol, 74, 180, 183, 236, 244, 264, 265 Missed Miscarriage, 73 Molar Pregnancy, 7, 76, 77 Multifetal Pregnancy Reduction, 31, 82 Multiple Pregnancies, 8, 81, 84 Mycotic Infection, 149

N Nasal Bone, 32, 70 Natural Contraceptive Methods, 257 Natural Weaning, 251 Necropsy Examination, 279, 282 Neisseria Gonorrhoeae, 62, 145, 146 Neonatal Asphyxia, 10, 297 Neonatal Assistance, 10, 275 Neonatal Examination, 10, 276 Neonatal Mortality, 19, 21 Neonatal Period, 20, 21, 305, 311, 312, 317 Neonatal Resuscitation, 10, 275, 283 Neonatal Seizures, 10, 300 Neonatal Sepsis, 10, 154, 291, 298 Neonatal Tetanus, 10, 299 Neonatal Transport, 10, 215, 291 Newborn, 10, 19, 21, 26, 40, 45, 47, 50, 97, 100, 114, 148, 150, 153, 155, 163, 164, 183, 192, 198, 215, 216, 244, 245, 248, 249, 276, 277, 286, 287, 288, 289, 290, 291, 292, 294, 295, 299, 300, 301, 302, 303, 304, 305, 307, 309, 310, 312, 313, 314, 316 Nifedipine, 89, 104 Non-Stress Test, 60, 223 Normal Labour, 8, 53, 171 Normocytic Anaemia, 122 Nuchal Fold, 32, 69, 70 Nuchal Translucency, 32, 69, 82 Nutrition, 33, 34, 39, 44, 46, 47, 54, 71, 137, 159

O Obstetrical Ultrasonography, 7, 53 Obstetric Anaesthesia, 207, 208 Obstetric Analgesia, 207, 208, 210, 211 Obstetric History, 24, 40, 130, 134, 185, 222 Obstructed Labor, 254, 275 Occiput Posterior Position, 214, 218, 219 Occiput Transverse Position, 219 Ocular Profilaxis, 10, 32, 290 Oesophageal Atresia, 308 Oligoamnios, 8, 24, 67, 114, 276 Oligoamnios Clinical Management, 114 Oligohydramnios, 8, 86, 90, 110, 114, 115, 185, 222

CLINICAL GUIDELINES FOR MATERNITY HOSPITALS

Subject Index

Operative Vaginal Delivery, 9, 96, 112, 181, 190, 262 Ophthalmia Neonatorum, 146 Oral Contraceptives, 233, 258 Oxygen Therapy, 263, 288, 315

P Palmer Operation, 63 Paracervical Block, 208 Parenteral Analgesia, 208 Parotiditis, 152 Partial Mole, 76 Partial Placenta Previa, 94 Parvovirus, 116, 117, 150, 152 Patent Ductus Arteriosus, 32, 295 Peak Inspiratory Pressure, 33, 289 Pelvic Abscess, 262, 266, 267, 269 Pelvic Fractures, 167 Pelvi-Ureteric Junction Obstruction, 316 Penetrating Abdominal Trauma, 166 Penumothorax, 315 Perforation of Hollow Viscus, 313 Perimortem Caesarean, 168 Perinatal Mortality, 21, 26, 33, 112, 275 Perinatal Mortality Rate, 21 Perinatal Period, 20, 21, 48, 51, 150 Perineal Lacerations, 9, 214, 244, 262 Periodic Abstinence, 257, 260 Peri-Operative Blood Loss, 204 Permanent Contraceptive Methods, 257 Placenta Accreta, 95, 96, 254 Placental Abruption, 40, 94, 117, 118, 119, 165, 166, 195, 223, 224, 228, 229, 264, 275 Placental Trophoblastic Tumour, 79 Placenta Previa, 24, 54, 66, 93, 94, 95, 96, 100, 102, 118, 182, 197, 222, 275 Plasmodium, 157 Platypelloid pelvis, 64 Pneumonia, 32, 91, 124, 153, 161, 202, 286, 299 Pneumoperitoneum, 313, 315 Poliomyelitis, 149, 153 Polyhydramnios, 8, 93, 115, 116, 132, 134, 155, 308 Polyhydramnios Treatment, 116

Positive End Expiratory Pressure, 287, 289 Positive Pressure Ventilation, 283, 284 Postoperative Care, 9, 199 Post-Operative Complications, 202 Postpartum Blues, 135 Postpartum Care, 9, 243, 246, 260 Post-Partum Contraception, 10, 257 Postpartum Fever, 10, 33, 262 Postpartum Hemorrhage, 10, 25, 33, 107, 205, 217, 236, 244, 265 Post-Partum Hysterectomy, 10, 254 Postpartum Revision, 9, 203, 248 Post-Term, 20, 84 Postterm Pregnancy, 8, 9, 112, 113, 118, 235 Postterm Pregnancy Diagnosis, 112 Potential Diabetes, 131 Pre-Conception Visit, 44 Preeclampsia, 8, 9, 25, 89, 97, 102, 103, 104, 105, 106, 107, 108, 109, 110, 114, 117, 120, 134, 197, 209, 222, 236, 237 Preeclampsia Management, 103 Pregnancy Dating, 7, 52, 112 Premature Infants, 145, 155, 287, 291, 292 Premature Rupture of Membranes, 8, 63, 66, 67, 86, 92, 93, 121, 165, 221, 222 Prematurity: Hypotension, 295 Prenatal Attendance, 7, 39 Prenatal Care, 25, 44, 47, 52, 79, 101, 275 Pre-Term, 20, 86, 124, 137, 185 Preterm Delivery: Assistance, 9, 215 Preterm Infant: Clinical Care, 10, 294 Preterm Labor, 8, 25, 26, 33, 56, 88, 90, 91, 92, 116, 165 Pre-Term Prom, 86 Primary Syphilis, 145, 301 Progress of Labour, 175, 176 Prolonged Active Phase, 176, 177 Prolonged Expulsive Phase, 176, 178 Prolonged Latent Phase, 176 Prostaglandins, 74, 90, 91, 115, 176, 183, 184, 253 Psichoprophilaxis, 207 Psychiatric Disorders, 8, 135 Psychotropic Drugs in Pregnancy, 136 Pudendal Block, 208 Puerperal Curettage, 9, 253

325

CLINICAL GUIDELINES FOR MATERNITY HOSPITALS

326

Subject Index

Puerperal Fever, 262 Puerperal Psychosis, 10, 135, 271 Puerperal Sepsis, 10, 40, 198, 263, 269 Pulmonary Congestion, 128 Pulmonary Embolism, 140, 141, 142, 199, 262 Pulmonary Oedema, 127, 128, 234, 235, 239 Pulmonary Thromboembolism, 267, 268 Pulmonary Tuberculosis, 124, 161

R Radiations in Pregnancy, 50 Radiotherapy during Conception, 51 Rapid Plasma Reagin, 301 Rectovaginal Fistula Develops, 254 Recurrent Miscarriage, 73 Recurrent Stillbirth: Prevention, 120 Respiratory Diseases in Pregnancy, 8, 123 Respiratory Therapy in the Newborn, 10, 287 Resuscitation Measures, 165 Revision of the Canal, 203 Rheumatic Heart Disease in Pregnancy, 8, 124 RH Isoimmunization, 8, 100 RH Negative Mothers, 100 Risk Factors For Adverse Perinatal Outcomes, 25 Risk Factors For Maternal Morbidity, 24 Risks of Diabetes in Pregnancy, 132 Rooming, 278 Rotation Dystocia, 218 Routine Monitoring of Gestation, 54 Rubella, 31, 61, 62, 117, 150, 153

S Scalp PH, 184 Secondary Syphilis, 145 Septic Pelvic Trombophlebitis, 266, 267 Serological Tests, 114, 301 Severe Preeclampsia, 89, 103, 104, 105, 106, 107, 108, 109, 110, 120, 236, 237 Sexually Transmitted Infections, 41, 91, 144

Shake-Test, 59 Shirodkar Operation, 63 Short Femur and Humerus, 70 Shoulder Dystocia, 9, 34, 216, 217, 218 Sign of Ahlfeld, 175 Sign of KĂźstner, 174 Sodium Bicarbonate, 286 Solid Organs, 314 Spaldingâ&#x20AC;&#x2122;s Sign, 118 Spatulas, 9, 190, 193 Special Ultrasound Techniques, 54 Speeding Weaning, 252 Spinal Analgesia, 9, 208, 209, 210 Spleen Rupture, 314 Status Epilepticus, 140 Stillbirth, 17, 21, 45, 25, 140, 49, 54, 101, 112, 116, 117, 120, 227 Stillbirth Mortality Rate, 21 Stillborn: Evaluation, 119 Streptococcus Agalactiae, 163, 171, 266 Streptococcus Agalactiae Detection of Carriers, 163 Superficial Trombophlebitis, 267 Superimposed Preeclampsia, 103, 108 Surgical Disease, 10, 305 Surgical Sterilization, 258, 259 Surgical Sterilization of Women, 258, 259 Symtomatic Bacteriuria, 142 Syphilis, 10, 34, 41, 43, 116, 117, 136, 144, 145, 159, 301, 302 Szendi Operation, 63

T Term, 20 Terminology in Perinatal Medicine, 7, 19, 22 Testicular Torsion, 316 Tetanus, 10, 43, 165, 299 300 Third-Degree Episiotomy, 189 Third-Trimester Amniocentesis, 56 Threatened Miscarriage, 73 Thromboembolism, 8, 10, 140, 142, 267, 267, 268 Thromboembolism in Puerperium, 10, 267 Thrombophlebitis Superficial, 140 Thyroid Disorders, 8, 138, 139

CLINICAL GUIDELINES FOR MATERNITY HOSPITALS

Subject Index

Thyroidectomy, 138 Tocolytic Therapy, 87, 89, 95 Total Placenta Previa, 94 Toxicologic Examination, 62 Toxoplasma Gondii, 156 Toxoplasmosis, 8, 62, 156, 161 Tracheal Intubation, 283, 285 Traditional Birth Attendant, 9, 179, 180 Transfer: Equipment, 292 Transfusion of Fresh Blood is Ideal, 229 Transfusion Procedures, 206 Treponema Pallidum, 31, 62, 301 Trichomoniasis Infection, 149 Tripanosoma Cruzi, 164 Tuberculosis, 31, 34, 39, 40, 62, 117, 124, 161 Twin Gestation: Mode of Delivery, 9, 237 Twins: Intrapartum Management, 238 Types of Miscarriage, 73 Types of Pelvises, 64

U Ultrasonic Screening and Diagnosis, 68 Ultrasound Dating, 20, 52 Untractable Postpartum Hemorrhage, 265 Urethritis, 143, 146, 147 Urinary Fistula: Treatment, 255 Urinary Obstetric Fistulas, 10, 254 Urinary Tract Infections, 8, 142, 227 Us FDA Risk Classification in Pregnancy, 48 Us Markers, 69 Uterine Inversion, 225, 264, 265 Uterine Muscle Fatigue, 264 Uterine Overdistention, 264 Uterine Perforation, 253

Uterine Revision, 203 Uterine Rupture, 25, 118, 165, 166, 181, 182, 195, 198, 217, 223, 224, 262, 264, 265 Uterine Scars, 195 Uterine Tamponade, 265

V Vacuum, 9, 32, 40, 128, 178, 189, 190, 191, 192, 195, 196, 245 Vacuum Assisted Delivery, 190 Vaginal Delivery, 84, 93, 95, 178, 196, 237 Vaginitis, 132, 149 Valvular Heart Disease, 125, 234, 235 Variable Deceleration, 186 Varicela, 62, 153 Vasa Previa, 96, 118 Venoclisis Oxytocin, 174 Ventilatory Support, 288 Very Low Birth Weight, 19, 249 Vesico-Vaginal Fistula, 35, 199, 199 Viral Infection, 62, 149, 155, 266 Vitamin K Prophylaxis, 10, 291 Vomiting in Pregnancy, 7, 71

W Weaning, 136, 250, 251, 252 Womenâ&#x20AC;&#x2122;s Health Dexeus, 3, 5 Work, 46 Work in pregnant, 46 Wound Infection, 25, 199, 202, 262

Z Zidovudine, 35, 162, 163, 304

327