Ijcp December 2013

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Volume 24, Number 7

December 2013, Pages 601-700

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Dr KK Aggarwal Group Editor-in-Chief Dr Veena Aggarwal MD, Group Executive Editor

IJCP Editorial Board Obstetrics and Gynaecology Dr Alka Kriplani Dr Thankam Verma, Dr Kamala Selvaraj Cardiology Dr Praveen Chandra, Dr SK Parashar Paediatrics Dr Swati Y Bhave Diabetology Dr CR Anand Moses, Dr Sidhartha Das Dr A Ramachandran, Dr Samith A Shetty ENT Dr Jasveer Singh Dr Chanchal Pal Dentistry Dr KMK Masthan Dr Rajesh Chandna Gastroenterology Dr Ajay Kumar Dr Rajiv Khosla Dermatology Dr Hasmukh J Shroff Dr Pasricha Dr Koushik Lahiri Nephrology Dr Georgi Abraham Neurology Dr V Nagarajan Dr Vineet Suri Journal of Applied Medicine & Surgery Dr SM Rajendran, Dr Jayakar Thomas Orthopedics Dr J Maheshwari

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Volume 24, Number 7, December 2013 FROM THE DESK OF THE GROUP EDITOR-IN-CHIEF

605 Some HIV Prevention Messages for World AIDS Day to be Displayed in Your Clinic

KK Aggarwal

AMERICAN FAMILY PHYSICIAN

607 Seasonal Affective Disorder

Stuart L. Kurlansik, Annamarie D. Ibay

611 Practice Guidelines 613 Photo Quiz ANESTHESIOLOGY

615 Control of Hazards in Operation Theater

Sen J, Sen B

CARDIOLOGY

620 Role of Atorvastatin in Dyslipidemia: A Clinical Study

Pooja BA, Bhatted S, Chaturvedi N, Deekshit S, Bhojani MK

COMMUNITY MEDICINE

623 Causes of Adult Deaths by Verbal Autopsy in an Urban Slum of Ludhiana

Alexander SA, Sengupta P, Benjamin AI

DERMATOLOGY

626 Penicillin-Induced Stevens–Johnson Syndrome: A Case Report

Patil JR, Motghare VM, Deshmukh VS, Jaykare SC, Pise HN

ENT

628 Facial Necrotizing Fasciitis: A Rare Complication of Maxillary Sinusitis

Gupta N, Varshney S, Gupta P

631 Acinic Cell Carcinoma of the Parotid

Easweran SV, Lokesh, Raghvendra U, Yuvraj, Manjula

636 A Unique Case in the Field of Medicine

Thakkar H

GASTROENTEROLOGY

640 Chylous Ascites Due to Tuberculosis: A Case Report and Review of Literature

Kumar P, Chandra K

HEMATOLOGY

646 Thrombotic Thrombocytopenia Purpura Refractory to Plasmapheresis Treated Successfully with Rituximab

Shah VH, Patel A, Chavda RK

INFECTIOUS DISEASES

649 “Buffalo Hump” in a Female on Zidovudine-Based Antiretroviral Therapy: A Case Report

Agrawal P, Gautam A, Chandra S, Aneez A, Gupta A

OBSTETRICS AND GYNECOLOGY

651 A Study of Outcome of Induction of Labor: Medical Versus Surgical

Kaur P, Kaur M, Kaur K, Manjit MK, Goel P

OBSTETRICS AND GYNECOLOGY Published, Printed and Edited by Dr KK Aggarwal, on behalf of IJCP Publications Ltd. and Published at E - 219, Greater Kailash, Part - 1 New Delhi - 110 048 E-mail: editorial@ijcp.com

655 Mullerian Agenesis: An Unusual Presentation as Hematometra and Bilateral Hematosalpinx

Gupta S, Kumari A

657 Outcome of Prelabor Rupture of Membranes in a Tertiary Care Center in West Bengal

Printed at New Edge Communications Pvt. Ltd., New Delhi E-mail: edgecommunication@gmail.com

Chakraborty B, Mandal T, Chakraborty S

663 A Comparative Study between Cleavage Stage Embryo Transfer at Day 3 and Blastocyst Stage Transfer at Day 5 in IVF/ICSI on Clinical Pregnancy Rates

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Kaur P, Swarankar ML, Maheshwari M, Acharya V

668 Randomized Control Study of Oral Versus Vaginal and Sublingual Misoprostol with Mifepristone for First-Trimester MTP

Sahu RR, Soni AA, Raut VS

ONCOLOGY

Editorial Policies

674 Immature Teratoma with Somatic Tumor-Type Sarcoma:

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A Case Report

Chandoke RK, Verma AK, Kaur O, Yadav N, Agarwal S, Bhushan B, Mehra P

OPHTHALMOLOGY

678 Marcus Gunn Jaw-Winking Phenomenon: Brief Communication

Jhagta HS

PEDIATRICS

680 A Case of Biotinidase Deficiency Presenting as Quadriparesis

Thapar R, Venkatnarayan K

MEDILAW

684 Medicolegal Cases in Injury Patients and Indian Law

Aggarwal KK

MEDIFINANCE

686 FAQs in Income Tax Planning eMEDI QUIZ

687 Quiz Time

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FROM THE DESK OF THE GROUP EDITOR-IN-CHIEF

Dr KK Aggarwal

Padma Shri and Dr BC Roy National Awardee Sr. Physician and Cardiologist, Moolchand Medcity, New Delhi President, Heart Care Foundation of India Group Editor-in-Chief, IJCP Group and eMedinewS National Vice President Elect, IMA Member, Ethics Committee, MCI Chairman, Ethics Committee, Delhi Medical Council Director, IMA AKN Sinha Institute (08-09) Hony. Finance Secretary, IMA (07-08) Chairman, IMA AMS (06-07) President, Delhi Medical Association (05-06) emedinews@gmail.com http://twitter.com/DrKKAggarwal Krishan Kumar Aggarwal (Facebook)

Some HIV Prevention Messages for World AIDS Day to be Displayed in Your Clinic ÂÂ Acquired immunodeficiency syndrome (AIDS) is caused by the human immunodeficiency virus (HIV), which ÂÂ ÂÂ ÂÂ ÂÂ ÂÂ ÂÂ ÂÂ ÂÂ ÂÂ ÂÂ ÂÂ ÂÂ ÂÂ ÂÂ ÂÂ ÂÂ ÂÂ ÂÂ

ÂÂ ÂÂ ÂÂ ÂÂ

damages the body’s defense system.

AIDS is the late stage (stage 4) of HIV infection.

AIDS virus destroys certain kind of cells that normally help the body to fight disease. With the destruction of these cells, the body cannot defend itself against infections.

People who have AIDS grow weaker and fall ill because their bodies lose the ability to fight off illnesses.

Progression from HIV infection to AIDS, if untreated, may take 8–10 years. In young children, it usually develops much faster.

People with silent HIV-positive state may live for years without any signs of the disease but they can still pass on the virus to others.

AIDS is a chronic manageable disease, but it is better to prevent it. One can live a near normal life.

HIV is not caused by witchcraft and it cannot be cured by having sex with a virgin.

HIV spreads through unprotected sex with an HIV-positive person.

HIV spreads through transfusions of unscreened (HIV-positive) blood.

HIV can spread from an infected woman to her child during pregnancy and childbirth.

HIV infection can be passed from a mother to her child through breastfeeding.

HIV can spread by unsterilized infected needles or syringes, especially those used for injecting drugs.

Used infected razor blades, knives, or tools that cut or pierce the skin also carry some risk of spreading HIV. It is not possible to get HIV/AIDS from touching those who are infected.

Hugging, shaking hands, coughing, and sneezing do not spread the disease.

HIV/AIDS cannot be transmitted through toilet seats, telephones, plates, glasses, eating utensils, towels, bed linen, swimming pools, or public baths.

HIV does not spread by mosquitoes or other insects.

The risk of getting HIV through sex can be reduced if people reduce the number of sex partners, if uninfected partners have sex only with each other, or if people practice safe sex (sex without penetration or while using a condom).

Correct and consistent use of condoms can save lives by preventing the spread of HIV. All pregnant mothers should get HIV test done.

Blood banks now test all donated blood and discard all units that test positive.

All people, including children, are at risk for HIV/AIDS.

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FROM THE DESK OF THE GROUP EDITOR-IN-CHIEF ÂÂ People who have a sexually transmitted infection (STI) are at greater risk of getting HIV and of spreading HIV

to others.

ÂÂ People with STIs should seek prompt treatment and avoid sexual intercourse or should practice safe sex (nonÂÂ ÂÂ

ÂÂ ÂÂ ÂÂ

ÂÂ ÂÂ ÂÂ ÂÂ ÂÂ ÂÂ ÂÂ ÂÂ ÂÂ ÂÂ ÂÂ ÂÂ ÂÂ ÂÂ ÂÂ ÂÂ ÂÂ ÂÂ ÂÂ ÂÂ ÂÂ ÂÂ ÂÂ ÂÂ ÂÂ

606

penetrative sex or sex using a condom).

The more sex partners people have, the greater the risk that one of them will have HIV/AIDS and will pass it on.

Internal secretions, which can harbor HIV virus, are blood (including menstrual blood), semen, vaginal secretions, breast milk, peritoneal fluid, brain fluid, pleural lung fluid, pericardial heart fluid, etc. These secretions when mixed with secretions of another person infected with HIV transmit HIV. External secretions that do not harbor the HIV virus are saliva, tear, sweat, urine, and feces. The mixing of these secretions with secretions of an HIV-positive person does not transmit HIV. High-risk behaviors are anal intercourse without condom, vaginal intercourse without condom, sexual activity that causes bleeding or injury, and oral sex on a man without condom.

No-risk or low-risk sexual behaviors are hugging and rubbing bodies together, wet kissing with your open lips, masturbating yourself, using sex toys or talking sex, vaginal intercourse using condom, and anal intercourse using condom.

A blood test is the most accurate way to tell if someone is infected with HIV. Most of the tests for HIV/AIDS check for the presence of antibodies to the virus.

If the result of an HIV/AIDS test is negative, it means the person tested is not infected or it is too early to detect the virus.

The HIV blood test may not detect infection up to the first few weeks to few months.

Even if the first test is negative, the test should be repeated 6 months after any possible exposure to HIV infection to confirm the status.

The time period when an infected person does not come as HIV positive in the blood test is referred to as window period.

Since an infected person can transmit the virus at any time, it is important to use a condom during sex or to avoid penetration.

HIV counseling and testing can help in the early detection of HIV infection, to get the support services for those who are infected.

Counseling helps to manage other infectious diseases they might have and learn about living with HIV/AIDS and how to avoid infecting others.

Counseling and testing can also help those not infected to remain uninfected through education about safer sex.

A condom should always be used during all penetrative sex, unless it is absolutely certain that both partners are free of HIV infection.

A person can become infected through even one occasion of unprotected penetrative sex (sex without a condom).

Condoms with lubrication (slippery liquid or gel) already on them are less likely to tear during handling or use.

If the condom is not lubricated enough, a “water-based” lubricant, such as silicone or glycerine, should be added.

If such lubricants are not available, saliva can be used.

Drinking alcohol or taking drugs interferes with judgment. Even those who understand the risks of AIDS and the importance of safer sex may become careless after drinking or using drugs.

Young people need to be informed that there is no vaccination and no cure for HIV/AIDS. Prevention is the only protection against HIV/AIDS. Persons suffering from STI have a 5–10 times higher risk of becoming infected with HIV if they have unprotected sexual intercourse with an HIV-infected person.

If both partners are not treated for an STI, they will continue infecting each other with the STI. Most STIs are curable.

Be faithful to your partner for safe sex.

Do not have sex without condom whether it is a one-time sex or a long-time relationship.

ABC for safe sex: Abstain, Be faithful to your partner, and, if you cannot, use Condoms.

Girls and women have the right to refuse unwanted and unprotected sex.

Indian Journal of Clinical Practice, Vol. 24, No. 7, December 2013

AMERICAN FAMILY PHYSICIAN

Seasonal Affective Disorder STUART L. KURLANSIK, ANNAMARIE D. IBAY

ABSTRACT Seasonal affective disorder is a combination of biologic and mood disturbances with a seasonal pattern, typically occurring in the autumn and winter with remission in the spring or summer. In a given year, about 5 percent of the U.S. population experiences seasonal affective disorder, with symptoms present for about 40 percent of the year. Although the condition is seasonally limited, patients may have significant impairment from the associated depressive symptoms. Treatment can improve these symptoms and also may be used as prophylaxis before the subse­quent autumn and winter seasons. Light therapy is generally well tolerated, with most patients experiencing clinical improvement within one to two weeks after the start of treatment. To avoid relapse, light therapy should continue through the end of the winter season until spon­taneous remission of symptoms in the spring or summer. Pharmacotherapy with antidepres­sants and cognitive behavior therapy are also appropriate treatment options and have been shown to be as effective as light therapy. Because of the comparable effectiveness of treatment options, first-line management should be guided by patient preference.

Keywords: Seasonal affective disorder, depressive symptoms, light therapy, antidepres­sants, cognitive behavior therapy

S

easonal affective disorder (SAD) is a combination of biologic and mood disturbances with a seasonal pattern. It typically occurs in the autumn and winter with remission in the spring or summer, but it may also occur at other times of the year.1

INCIDENCE Community-based studies estimate that the prevalence of SAD approaches 10 percent in northern latitudes.1 With strict application of criteria from the Diagnostic and Statisti­ cal Manual of Mental Disorders, 4th ed., text revision (DSM-IV–TR),2 the prevalence of SAD is approximately 1 to 2 percent in the United States and approximately 2 percent in Canada. In a given year, about 5 percent of the U.S. population experiences SAD, with symptoms lasting approximately 40 percent of the year.3 Because of its recurrence and duration, SAD is considered a serious mental health problem.3 The symptoms can have a sub­stantial impact on patients’ families and employment. SAD tends to be predominant in women, particularly during childbear­ing years, with a reported female-to-male ratio of 4:1.4 Rates of SAD have been shown to decline among older persons, with

STUART L. KURLANSIK, PhD, is a psychologist and behav­ioral medicine faculty member at Virtua Family Medicine Residency in Voorhees, N.J. ANNAMARIE D. IBAY, MD, is associate director of Virtua Family Medicine Residency and lead physician at Virtua Family Medicine Center in Lumberton, N.J. Source: Adapted from Am Fam Physician. 2012;86(11):1037-1041.

older men and women equally susceptible.1 Older children also are susceptible to SAD. In a large study examining parents’ and children’s report of seasonal depression in children six to 18 years of age, there was no compelling evidence showing seasonally tied symptoms of depression in children six to 15 years of age.5 However, parents in this study rated the degree of depression as significantly more severe in 16- to 18-year-olds than in six- to 15-year-olds, although only when they were assessed in autumn and winter. The level of depression in patients 16 to 18 years of age was found to be more severe in autumn and winter than in spring and summer.5 ETIOLOGY AND PATHOPHYSIOLOGY There may be several biologic mechanisms underlying SAD,3 including circadian phase delay or advance (the phase shift hypothe­sis), which tends to appear as the chief cause in the literature. Additional contributing mechanisms may include retinal sensitiv­ity to light, neurotransmitter dysfunction, genetic variations affecting circadian rhythms, and serotonin levels.

Researchers propose that the syndrome is best viewed as a complex disorder resulting from a combi­nation of factors.6,7 Physicians must also consider the presence of psychological mechanisms, such as vul­nerability to stress, when treating patients with SAD.2 Other risk factors include living in northern latitudes, and having a first-degree relative who has manifested symp­toms of depression.1,6

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AMERICAN FAMILY PHYSICIAN TYPICAL PRESENTATION Patients with SAD typically present with symptoms consistent with some form of depression. When depression is suspected, the physician should consider SAD if there is a history of a seasonal pattern to the depression and if it aligns with the current season.

Often-noted concomitants of SAD not considered to be specific criteria for other depressive disor­ders are carbohydrate craving and hyperpha­gia, with resulting weight gain. However, the presence of these symptoms is not diagnostic for SAD; seasonality is required, with other symptoms of clinical depression.

DIAGNOSIS If SAD is suspected, a full evaluation using current DSM-IV–TR depression criteria is needed. A number of instruments can be used to screen for depression and determine its severity. These instruments can be used instead of, or in addition to, a clinical inter­view. Two of the most commonly used tools are the Beck Depression Inventory and the Hamilton Rating Scale for Depression.

Evaluation for comorbid psychological problems is important. Because there may be a seasonal component in bipolar or cyclothy­ mic disorders, it is important to determine the presence of a cyclical pathology in addition to symptoms of major depressive disorder.

Treat­ment considerations for these conditions vary.

Diagnostic Criteria Diagnostic criteria for SAD are listed in Table 1.2 As of yet, there are no significant changes to the criteria in the upcoming edi­tion of DSM-V.8

Differential Diagnosis The differential diagnosis of SAD includes the following: major depressive disorder, bipolar I and II disorders that do not have a seasonal pattern, cyclothymic disorder, dysthymic disorder, premenstrual dys­phoric disorder, chronic fatigue syndrome, hypothyroidism, and drug or alcohol abuse. There may be other, less likely pathologic causes of depression, which should be inves­tigated after ruling out these diagnoses.9 TREATMENT Studies have shown that light therapy, pharmacotherapy, and cognitive behavior therapy (CBT) are appropriate options for treating SAD, but no treatment, or combi­ nation of treatments, has been found to be superior.

For this reason, treatment choice should be guided by patient preference.

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Table 1. Diagnostic Criteria for Seasonal Affective Disorder Seasonal affective disorder is currently classified under major depressive disorder, recurrent, as well as bipolar I or II disorder.

The disorder is assigned a seasonal pattern specifier if there is a regular recurrence of the major depressive episode at a particular time of year.

Psychosocial stressors associated with a particular season resulting in a major depressive episode do not qualify for the seasonal pattern specifier.

Full remission, or a change from major depression to mania or hypomania, must also occur at a particular time of year.

To demonstrate the temporal seasonal relationship, two major depressive episodes must have occurred in the past two years.

Nonseasonal major depressive episodes must not have occurred during the same period of time.

Seasonally related major depressive episodes must outnumber the nonseasonal major depressive episodes that may have occurred over a person’s lifetime.

Information from reference 2.

Light Therapy Many published studies on the effects of light therapy in persons with SAD do not meet recognized standards for rigorous clinical trial design because of inherent difficulties in creating an acceptable placebo. How­ ever, multiple systematic reviews and meta-analyses evaluating the available data sup­port the use of light therapy as an effective treatment for SAD.6,10 Clinical practice guidelines have out­lined the standard protocol for light therapy (Table 2).11 Patients should be positioned about 12 to 18 inches from a white, fluo­ rescent light source at a standard dosage of 10,000 lux for 30 minutes per day in the early morning. They must be awake with their eyes open, but are not required to look directly into the light (i.e., eating or reading during the treatment is acceptable as long as the light enters the pupil). Ultraviolet wave­lengths have not shown statistically signifi­cant improvement of depressive symptoms and should be avoided because of the poten­ tially harmful effects.12 Statistically significant clinical improve­ment has been observed after one to two weeks of light therapy, but when treatment is discontinued, most patients relapse after a similar period; therefore, treatment should be continued until the time of usual sponta­ neous 6,13 remission in the spring or summer. After remission, patients can individual­ize their dosing by reducing daily exposure time or using the therapy on weekdays only, as long as they maintain control of symp­toms.

AMERICAN FAMILY PHYSICIAN Table 2. Light Therapy Guidelines for Seasonal Affective Disorder Patients should be positioned about 12 to 18 inches from a source of 10,000 lux of white, fluorescent light without ultraviolet wavelengths.

Therapy should last for 30 minutes daily in the early morning.

Eyes must be open, although it is not necessary to stare at the light.

After remission, dosing may be individualized for the rest of the winter season.

In subsequent years, treatment may begin in early autumn to avoid relapse.

Information from reference 11.

To avoid relapse in subsequent years, patients may start light therapy in the early autumn before the onset of symptoms.14 Light therapy is generally well tolerated. Adverse effects may include headache, eye strain, nausea, agitation, and blurred vision, but these are usually mild and transient.6,13,15 There is no evidence that light therapy is associated with ocular or retinal damage.16 Ophthalmologic examinations before start­ ing light therapy and at regular follow-up intervals are recommended only for patients with preexisting retinal disease or systemic diseases involving the retina and for those taking photosensitizing medication.6 Like antidepressants, light therapy may precipi­tate hypomanic or manic episodes in suscep­tible patients with bipolar disorder.17 Light therapy units may be purchased from online retailers, drug stores, and some hardware stores. Units range from $180 to $500, with most costing less than $250. Reimbursement by health insurers is incon­sistent; some companies may cover the cost if the physician provides a prescription or letter of necessity.

Pharmacotherapy Results from most randomized controlled trials depressants (i.e., indicate that second-generation anti­ selective serotonin reuptake inhibitors and serotoninnorepinephrine reuptake inhibitors) are superior to placebo in reducing depression scores and remission rates.6 Selective serotonin reuptake inhibitors have the best evidence for effec­tiveness, with fluoxetine (20 mg per day) being the most investigated drug.13,18-22 A 2011 Cochrane review, however, determined that the low overall quality of the studies precludes the ability to draw any con­ clusions about the use of secondgeneration antidepressants for the treatment of SAD.23

Light Therapy Versus Pharmacotherapy Few trials have compared the effectiveness of light therapy versus pharmacotherapy. One double-blind randomized controlled trial assigned 96 patients to one of two regimens: (1) eight weeks of 10,000 lux light therapy for 30 minutes daily as soon as possible after waking plus a placebo capsule, or (2) eight weeks of 20-mg fluoxetine per day plus 100 lux light therapy (placebo) for 30 minutes daily.13 Clinical response and remission rates for the two groups were similar, but the group receiving light therapy at the higher dosage had an earlier response and slightly lower rate of adverse effects compared with the fluox­etine group. The authors concluded that light therapy and fluoxetine are comparably effec­tive and well tolerated, and that other clinical factors, including patient preference, should guide the selection of treatment.

Cognitive Behavior Therapy CBT is an empirically validated treatment for nonseasonal depression. One group of researchers developed and pilot tested a ver­sion of CBT tailored for patients with SAD that involved 90-minute sessions twice per week over a period of six weeks.24 The small (n = 23) uncontrolled feasibility study found that standard light therapy, SAD-tailored CBT, and a combination of light therapy and CBT all led to comparable reductions in depressive symptoms and good remis­sion rates, both of which were statistically significant for all three groups. Combined treatment had the highest remission rate but was not statistically superior to the other treatments alone. The authors subsequently published a larger (n = 61) randomized con­ trolled trial that also demonstrated statisti­ cally significant and similar improvements in depression severity in all three treatment groups, compared with the control group.25 Treatment with CBT, with or without adjunct light therapy, was associated with a statistically significant reduction in recur­rences of depression during the following winter compared with light therapy alone.26 Additionally, persons in the CBT group, but not the combination group, demonstrated a statistically significant decrease in depres­sion severity at one year compared with persons in the light therapy group, based on two depression severity scales.26 The authors postulated that CBT for treating SAD may be prophylactic.

PREVENTION Because of its predictable pattern of recur­rence, patients with SAD may begin light therapy in the early autumn before the onset of symptoms.21 CBT may reduce the recur­rence and severity of depressive

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AMERICAN FAMILY PHYSICIAN symptoms.26 One study showed that patients with a history of SAD who were randomized to take bupro­ pion XL (300 mg per day) starting in the early autumn had lower recur­rence rates than those in the placebo group; however, results did not reach statistical sig­ nificance because the recurrence rates were low overall, even in the placebo group.27 Some experts recommend certain lifestyle adjust­ments to prevent SAD symptoms, including exercising more often, increasing light in the home, practicing relaxation and stress man­agement techniques, spending more time out­side, and visiting sunnier, warmer climates.28 REFERENCES 1. Byrne B, Brainard GC. Seasonal affective disorder and light therapy. Sleep Med Clin. 2008;3(2):307-315.

2. American Psychiatric Association. Diagnostic and Statis­ tical Manual of Mental Disorders. 4th ed., text revision.

Washington, DC: American Psychiatric Association; 2000.

3. Rohan KJ, Roecklein KA, Haaga DA. Biological and psychological mechanisms of seasonal affective dis­ order: a review and integration. Curr Psychiatry Rev. 2009;5(1):37-47.

4. Jepson TL, Ernst ME, Kelley MW. Current perspectives on the management of seasonal affective disorder. J Am Pharm Assoc (Wash). 1999;39(6):822-829.

5. Nillni YI, Rohan KJ, Rettew D, Achenbach TM. Seasonal trends in depressive problems among United States children and adolescents: a representative population survey. Psychiatry Res. 2009;170(2-3):224-228.

6. Westrin A, Lam RW. Seasonal affective disorder: a clini­cal update. Ann Clin Psychiatry. 2007;19(4):239-246.

7. Levitan RD. The chronobiology and neurobiology of winter seasonal affective disorder. Dialogues Clin Neu­ rosci. 2007;9(3):315-324.

8. American Psychiatric Association. DSM-5: the future of psychiatric diagnosis. http://www.dsm5.org/Pages/ Default.aspx. Accessed August 30, 2012.

9. BMJ Best Practice. Seasonal affective disorder. http:// bestpractice.bmj.com/best-practice/monograph/985/ diagnosis/differential.html (subscription required).

Accessed January 16, 2012.

10. Golden RN, Gaynes BN, Ekstrom RD, et al. The efficacy of light therapy in the treatment of mood disorders: a review and meta-analysis of the evidence. Am J Psychia­ try. 2005;162(4):656-662.

11. Lam RW, Levitt AJ, eds. Canadian Consensus Guide­ lines for the Treatment of Seasonal Affective Disorder.

Vancouver, British Columbia, Canada: Clinical and Aca­ demic Publishing; 1999.

12. Lee TM, Chan CC, Paterson JG, Janzen HL, Blashko CA. Spectral properties of phototherapy for seasonal affective disorder: a meta-analysis. Acta Psychiatr Scand.

1997;96(2):117-121.

13. Lam RW, Levitt AJ, Levitan RD, et al. The Can-SAD study: a randomized controlled trial of the effective­ness of light

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therapy and fluoxetine in patients with winter seasonal affective disorder. Am J Psychiatry. 2006;163(5):805-812.

14. Partonen T, Lönnqvist J. Prevention of winter seasonal affective disorder by bright-light treatment. Psychol Med. 1996;26(5):1075-1080.

15. Terman M, Terman JS. Bright light therapy: side effects and benefits across the symptom spectrum. J Clin Psy­ chiatry. 1999;60(11):799-808.

16. Gallin PF, Terman M, Remé CE, Rafferty B, Terman JS, Burde RM. Ophthalmologic examination of patients with seasonal affective disorder, before and after bright light therapy. Am J Ophthalmol. 1995;119(2):202-210.

17. Chan PK, Lam RW, Perry KF. Mania precipitated by light therapy for patients with SAD [letter]. J Clin Psychiatry.

1994;55(10):454.

18. Lam RW, Gorman CP, Michalon M, et al. Multicenter, placebo-controlled study of fluoxetine in seasonal affec­ tive disorder. Am J Psychiatry. 1995;152(12):1765-1770.

19. Moscovitch A, Blashko CA, Eagles JM, et al.; Interna­ tional Collaborative Group on Sertraline in the Treat­ ment of Outpatients with Seasonal Affective Disorders.

A placebo-controlled study of sertraline in the treat­ ment of outpatients with seasonal affective disorder.

Psychopharmacology (Berl). 2004;171(4):390-397.

20. Martiny K, Lunde M, Simonsen C, et al. Relapse pre­ vention by citalopram in SAD patients responding to 1 week of light therapy. A placebo-controlled study. Acta Psychiatr Scand. 2004;109(3):230-234.

21. Partonen T, Lönnqvist J. Prevention of winter seasonal affective disorder by bright-light treatment. Psychol Med. 1996;26(5):1075-1080.

22. Ruhrmann S, Kasper S, Hawellek B, et al. Effects of fluox­ etine versus bright light in the treatment of seasonal affective disorder. Psychol Med. 1998;28(4):923-933.

23. Thaler K, Delivuk M, Chapman A, Gaynes BN, Kaminski A, Gartlehner G. Second-generation antidepressants for seasonal affective disorder. Cochrane Database Syst Rev. 2011;(12):CD008591.

24. Rohan KJ, Lindsey KT, Roecklein KA, Lacy TJ. Cognitivebehavioral therapy, light therapy, and their combination in treating seasonal affective disorder. J Affect Disord.

2004;80(2-3):273-283.

25. Rohan KJ, Roecklein KA, Tierney Lindsey K, et al. A randomized controlled trial of cognitive-behavioral therapy, light therapy, and their combination for seasonal affective disorder. J Consult Clin Psychol. 2007;75(3): 489-500.

26. Rohan KJ, Roecklein KA, Lacy TJ, Vacek PM. Win­ter depression recurrence one year after cognitive-behavioral therapy, light therapy, or combination treat­ment. Behav Ther. 2009;40(3):225-238.

27. Modell JG, Rosenthal NE, Harriett AE, et al. Seasonal affective disorder and its prevention by anticipa­ tory treatment with bupropion XL. Biol Psychiatry.

2005;58(8):658-667.

28. Mayo Clinic. Seasonal affective disorder (SAD). http:// www.mayoclinic.com/health/seasonal-affective-disorder/ DS00195. Accessed January 8, 2012.

AMERICAN FAMILY PHYSICIAN

Practice Guidelines ACP RELEASES BEST PRACTICE ADVICE ON COLORECTAL CANCER SCREENING

Table 1. American College of Physicians Best Practice Advice on Colorectal Cancer Screening

Although the incidence of colorectal cancer in the United States has been declining by 2 to 3 percent per year over the past 15 years, it is the second leading cause of cancer-related death in the country. The disease is rare before 40 years of age, with 90 percent of cases occurring in those older than 50 years. Appropriate screening is important because detection and removal of premalignant adenomas or localized cancer can prevent the development of cancer.

Indications for screening

The American College of Physicians (ACP) recently reviewed available guidelines from the American Cancer Society/U.S. Multi-Society Task Force on Colorectal Cancer/American College of Radiology, Institute for Clinical Systems Improvement, U.S. Preventive Services Task Force, and the American College of Radiology. Based on the evidence from these guidelines, the ACP has published best practice advice, which is summarized in Table 1.

Endoscopic and radiologic tests

GUIDANCE STATEMENTS Clinicians should perform individualized assessment of risk for colorectal cancer in adults.

This assessment can help determine when screen足 ing should begin. Risks include age, race, and family history (e.g., history of colorectal cancer, especially in a first-degree relative diagnosed before 50 years of age; hereditary nonpolyposis; or familial adenomatous polyposis). Blacks have the highest incidence of cancer compared with other races.

Clinicians should screen for colorectal cancer in average-risk adults starting at 50 years of age, and in high-risk adults at 40 years of age or at 10 years younger than the age at which colorectal cancer was diagnosed in the youngest affected relative.

Evidence shows that screening identifies premalig足 nant lesions, allowing for early treatment and reduced mortality. The benefits of screening outweigh the risks in these adults.

Source: Adapted from Am Fam Physician. 2012;86(12):1153-1154

Average-risk adults starting at 50 years of age High-risk adults starting at 40 years of age, or at 10 years younger than the age at which colorectal cancer was diagnosed in the youngest affected relative Black adults starting at 40 years of age See Table 2 for screening intervals of the different testing options Harms of unnecessary screening Optical colonoscopy: costly and limited availability (facilities and clinicians), postpolypectomy bleeding, perforation/ bleeding, cardiopulmonary complications, diverticulitis, severe abdominal pain, death, false-negative results Flexible sigmoidoscopy: perforation/bleeding, false-negative results Double-contrast barium enema: perforation/bleeding (low risk), false-positive results, false-negative results Computed tomography colonography: low-dose radiation exposure, additional diagnostic testing and procedures for lesions that might not be clinically significant, false-negative results Stool-based tests: few known harms other than false-positive results, false-negative results High-value, cost-conscious care Clinicians should not screen adults who are older than 75 years or who have a life expectancy of less than 10 years (e.g., those with significant comorbid conditions such as diabetes mellitus, cardiopulmonary diseases, or stroke); harms of screening seem to outweigh the benefits in most of these patients 10 years is usually regarded as a safe interval for optical colonoscopy screening

Stool-based tests, flexible sigmoidoscopy, or optical colo足 noscopy should be used for screening average-risk adults.

Test selection should be based on benefits versus harms, availability, and patient preference.

Because colorectal cancer screening tests have similar effectiveness, the patient should be counseled about the benefits, harms, effectiveness data, and costs of the different options (Table 2). Optical colonoscopy is generally considered the preferred screening test; however, it has a false-negative rate of 10 to 20 per足cent,

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AMERICAN FAMILY PHYSICIAN Table 2. Screening Tests for Colorectal Cancer Test

Sensitivity

Specificity Cost

Interval

Requirements

Computed tomography colonography

Medium

Medium

5 years

Complete bowel preparation

High

Double-contrast barium enema

Low

Low

Low

5 years

Complete bowel preparation

Flexible sigmoidoscopy*

Medium

Medium

High

5 years

Complete bowel preparation

Guaiac-based fecal occult blood test*

Variable

Variable

Low

Annual

Two samples from three consecutive stools at home

Immunochemical-based fecal occult blood test*

Variable

Variable

Medium

Annual

Stool sample Complete bowel preparation

Optical colonoscopy

High

High

High

10 years

Stool DNA panel*

Variable

High

High

Uncertain Adequate stool sample (30-g minimum)

Note: Positive results from noncolonoscopic tests require follow-up with colonoscopy. Specific risks of the tests are listed in Table 1. *Low-risk test.

and evidence on the optimal frequency of the screening is unclear. Although colonoscopy screening every 10 years is regarded as safe in average-risk per­sons, highrisk persons should be screened every five years. If a noncolonoscopic test is used, patients with a positive result should receive follow-up colonoscopy screening. raphy is an Although computed tomography colonog­

option for average-risk patients older than 50 years, the U.S. Preventive Services Task Force found insufficient evidence to determine the benefits and harms of the test.

Screening should end after 75 years of age or if the patient’s life expectancy is less than 10 years.

The harms of screening seem to outweigh the benefits in these patients.

■■■■

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AMERICAN FAMILY PHYSICIAN

Photo Quiz RASH IN AN EIGHT-YEAR-OLD BOY An eight-year-old boy presented with blis­ ters on his lower lip and tongue that had appeared two days earlier. One day after the blisters appeared, a nonpruritic, bilateral rash developed on his palms and soles. The patient recently had swum at a community pool, after which he reported fatigue. He had no fever, chills, nausea, vomiting, rhinor­rhea, cough, or history of recent travel. His activity levels and appetite were normal. The patient’s immunizations were up to date, and he had no significant medical history.

Physical examination demonstrated ery­thematous, 2-mm ulcers in the oral mucosa of his lower lip (Figure 1), an erythematous pharynx, and tender vesicles on the hard palate and tongue. The skin examination

Figure 1.

Figure 2.

revealed erythematous papules and vesicles with a surrounding rim of erythema on both of the palms and soles (Figures 2 and 3).

Question Based on the patient’s history and physical examination findings, which one of the fol­lowing is the most likely diagnosis?

A. Aphthous stomatitis.

B. Hand-foot-and-mouth disease.

C. Herpangina.

D. Herpes labialis.

E. Rocky Mountain spotted fever.

Figure 3.

SEE THE FOLLOWING PAGE FOR DISCUSSION.

Source: Adapted from Am Fam Physician. 2012;86(12):1141-1142.

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AMERICAN FAMILY PHYSICIAN DISCUSSION

Summary Table

The answer is B: hand-foot-and-mouth dis­ease.

Condition

Characteristics

This disease is caused by enterovi­ruses, most commonly coxsackievirus A5, A7, A9, A10, A16, B2, or B5, and enterovirus 71.1 Hand-foot-and-mouth disease usually occurs in children younger than 10 years. The infection is spread by direct contact with infected nasal discharge, saliva, blister fluid, or stool. The virus can remain in the body for several weeks after symptoms resolve.

Aphthous stomatitis

Painful oral ulcers measuring approximately 2 to 8 mm in diameter; affects nonkeratinized mucosa

Hand-footand-mouth disease

Viral prodrome and rash on the palms and soles or the groin and buttocks; painful oral lesions begin as erythematous macules and evolve into tender, 3- to 5-mm vesicles on an erythematous base

The typical clinical presentation is painful oral lesions, and a nonpruritic rash on the palms and soles or the groin and buttocks. Oral lesions begin as erythematous macules that evolve into tender, 3- to 5-mm vesicles drome of on an erythematous base.1,2 A one-day pro­ low-grade fever (in some patients), anorexia, malaise, abdominal pain, and upper respiratory tract symptoms may also be present. ment that Aphthous stomatitis is a common oral ail­ typically appears in childhood, disappearing around 30 years of age.1 The disease leads to painful oral ulcers, which are typically covered by a white to yellow pseudomembrane measuring 2 to 8 mm in diameter.

They usually affect nonkeratinized mucosa, such as the labial and buccal mucosa and the floor of the mouth or the ventral surface of the tongue, and are surrounded by an erythematous halo.3,4 Herpangina is an acute viral illness appearing between three and 10 years of age, although infection can occur in adults and neonates.

The incidence is highest in one- to seven-year-olds.5 It is caused by enteroviruses (cox­sackievirus A16 or B, and enterovirus 71).5 Herpangina is most common during the fall and summer. Clinical manifestations can vary but may include high fever and odynophagia, which leads to decreased appetite. The vesicles, which may persist for up to one week, are approximately 1 to 4 mm in diameter and tender. They are surrounded by erythematous rings and appear on the soft palate, uvula, and anterior tonsillar pillars.2 Herpes labialis is caused by herpes simplex virus type 1. Primary infection usually occurs through non­ sexual contact during childhood, usually appearing two to 20 days after contact with an infected person.2 Transmission involves mucous membranes and open or abraded skin. Symptoms may include a prodrome of fever, followed by tender oral lesions and lymphade­ nopathy. The classic oral lesions appear as a cluster of small vesicles on an erythematous base at the vermilion border of the lip. The lesions spontaneously heal within two weeks.2,4 Rocky Mountain spotted fever is a tick-borne disease caused by Rickettsia rickettsii. It is typically charac­terized by fever, myalgias, arthralgias,

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Herpangina Tender, 1- to 4-mm vesicles surrounded by an erythematous ring on the soft palate, uvula, and anterior tonsillar pillars; may be associated with high fever and odynophagia, which leads to decreased appetite Herpes labialis

Cluster of tender vesicles on an erythematous base appearing at the vermilion border of the lip

Rocky Mountain spotted fever

Small, blanching, pink macules measuring 1 to 4 mm in diameter initially on the ankles and wrists; spreads centrally to the palms and soles, sparing the face, and evolves into macules, papules, and petechiae; ultimately coalesces into large ecchymoses and ulcerations; usually associated with fever, myalgias, arthralgias, fatigue, and travel to endemic regions

fatigue, and a petechial rash, and is associated with travel to endemic regions. The rash usually develops two to four days after onset of fever,6 and typically appears as small, blanching, pink macules measuring 1 to 4 mm in diameter, initially on the ankles and wrists.

The rash spreads centrally to the palms and soles, sparing the face, and evolves into macules, papules, and petechiae. Ultimately, the rash will coalesce into large ecchymoses and ulcerations.7 REFERENCES 1. Ng JJ, Jeremiah J. Hand foot mouth disease. In: Ferri FF, ed. Ferri’s Clinical Advisor 2012: Instant Diagnosis and Treatment. St. Louis, Mo.: Elsevier Mosby; 2011:426.

2. Usatine RP, Tinitigan R. Nongenital herpes simplex virus.

Am Fam Physi­cian. 2010;82(9):1075-1082.

3. Scully C. Aphthous ulceration. N Engl J Med. 2006;355(2):165-172.

4. Gonsalves WC, Chi AC, Nelville BW. Common oral lesions: part 1. Superficial mucosal lesions. Am Fam Physician. 2007;75(4):501-507.

5. Rotbart HA, Hayden FG. Picornavirus infections: a primer for the prac­titioner. Arch Fam Med. 2000;9(9):913-920.

6. Chapman AS, Bakken JS, Folk SM, et al.; Tickborne Rickettsial Diseases Working Group; CDC. Diagnosis and management of tickborne rickettsial diseases: Rocky Mountain spotted fever, ehrlichiosis, and anaplasmosis— United States: a practical guide for physicians and other health-care and public health professionals. MMWR Recomm Rep. 2006;55(RR-4):1-27.

7. Bratton, RL, Corey R. Tick-borne disease. Am Fam Physician. 2005;71(12):2323-2330.

ANESTHESIOLOGY

Control of Hazards in Operation Theater SEN J*, SEN B†

ABSTRACT The operation theater (OT) environment is charged with multiple inherent risks. So, the team in the OT and the patient brought for surgical treatment may come across various hazards that can be classified as: (a) physical and accidental hazards, (b) chemical hazards, (c) biological hazards, (d) fire hazards, and (e) other hazards, such as organizational, psychological, and atmospheric.

Inadequate safety measures thus can result in multiple ill effects. Constant vigilance, awareness with timely intervention, maintenance of a specific operative procedure, and an educated team culture can make the OT environment a safe haven for the patient as well as for the theater team. The aim of this article is to identify and categorize the hazards that occur in the OT during surgery, and the related precautionary measures taken thereof for the safety of both the operating team and the patients who have the right to be treated with dignity and respect.

Keywords: Hazards, operation theater, patients, precaution

O

peration theater (OT) is a specialized world where ignorance or inadequate safety measures may cause many hazards that can affect the patient and the operating team as well. Recognition of these potential hazards through awareness and constant vigilance can control the OT environment and make it a safe haven.

ÂÂ

Easy movement of the team personnel.

ÂÂ

Sufficient space for necessary equipments.

ÂÂ

Audiovisual arrangements to communicate with the concerned specialities as follows: zz

Radiology/Pathology outside: This reduces traffic inside the OT and thus lessens contamination and risk of infection to the patient.

DISCUSSION

zz

The hazards can be classified as: (a) physical and accidental hazards, (b) chemical hazards, (c) biological hazards, (d) fire hazards, and (e) other hazards.

Temperature: Inside the OT, it is ideally to be maintained at 18°C–21°C with a relative humidity of 50%–55% to prevent the patient from the possible occurrence of hypothermia.

zz

Anesthesia and the patient: International Standard Organization described “gas pathways in direct connection with the patient” that incorporates different components of anesthesia machine, ventilator and resuscitator, where misconnections may lead to life-threatening hazards.3,4

Physical and Accidental Hazards It can be divided into the following types.

Architectural Room design design1,2

Modern architectural emphasizes on nonporous floor, wall, and ceiling. OTs are now designed for:

*Associate Professor

Dept. of Anesthesiology, Goldfield Institute of Medical Sciences and Research Chhainsa, Faridabad †PG Aspirant Address for correspondence Dr Jayashree Sen Dept. of Anesthesiology Goldfield Institute of Medical Sciences and Research Chhainsa, Faridabad, Haryana E-mail: jayashree_sen@rediffmail.com

Precaution ÂÂ

Thorough pre-use checkup and cross checkup of the anesthetic equipments and the drugs to be administered should be done by another competent personnel. As per studies, human error is not infrequent than equipment failure.5,6

ÂÂ

Periodical equipment maintenance is mandatory.

ÂÂ

To prevent hypothermia to the patient, warm intravenous fluid and warm water mattresses are recommended.

Lighting Arrangement Use of head lamps with fiber-optic lighting for confined space surgery makes room in the operation table area.7

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ANESTHESIOLOGY Adjustable ceiling OT lights, which are free of glare and are nonreflective,8 should be kept at a height that can give proper illumination to the surgical field and does not cause head injury to any personnel while moving around.

Airflow Unidirectional laminar airflow into the OT is ideal that, at the entry point, gets filtered by high-efficiency particulate air filter. Hygiene of OT should be maintained by an efficient gas scavenger system.

Nonionizing Radiation It is produced by laser. The fume is infrared/UV or visible. It is harmful because of its intensity and the substance released during the treatment. Chances of eye injury by direct or reflected radiation are there to the person operating it.

Precaution ÂÂ

Keep suction close to the fume generated. The National Institute for Occupational Safety and Health (NIOSH) recommends a suction system that is positioned within 2 inches of the surgical site having a capture velocity of 100–150 ft/min at the inlet nozzle and can pull 50 cubic ft/minute.12

ÂÂ

Use protective eyeshield with permitting vision.

Electrical Hazards It consist of macro-shock, micro-shock, and burn.

Macro-shock to any OT personnel may occur due to faulty electrical connections. Micro-shock or skin burn to the patient may occur due to inadequate diathermy machine grounding or defect in insulation.9 This can even cause ventricular fibrillation when the electric current instead of the grounding pad travels through electrogadiography leads or pacemaker catheter.10

UV ray is another source of radiation in modern orthopedic OT where it is used to decrease the bacteria in the environment during joint replacement surgery.

The ray is harmful.

Precaution

Precaution ÂÂ Check all extension cords and electric connections at intervals as long as the OT work continues. ÂÂ Use of bipolar electric cautery should be undertaken wherever possible. ÂÂ Document of the pacemaker, appropriate resuscitative equipment, and magnet should be at hand. ÂÂ In case of robotic surgery, cautery tip should be well coated.

Protective shield should be used both for the patient and the team.

Radiation

Precaution

The potential radiological hazards can be categorized into thermal, as in lasers, radioactive isotopes, as in brachytherapy and radioimmunoscintigraphy procedures, and electromagnetic radiation as in X-ray, gamma, and ultraviolet (UV) radiation.

Acoustical More the noise, more stress for the team. Significant hearing loss during orthopedic procedures13 in orthopedic surgeons is associated with elevated noise level that may go even higher than the intensity of normal conversation which is 50 dBA. ÂÂ

Architectural construction of OT should have minimum reverberation.

ÂÂ

Quieter movement of the personnel during surgical procedures.

ÂÂ

Instruments made of heat-resistant plastic material should be used for no clatter.

ÂÂ

Mobile phones should be in silent mode.

ÂÂ

Least possible verbal communication.

Ionizing Radiation “National Council on Radiation Protection and Measurement” established a maximum limit of X-ray for occupational exposure to be 5 rem/year10,11 except for any personal medical requirement.

Precaution Lead aprons with a material of 0.25 mm reduces radiation by 90% and 0.5 mm by 99% as per as the occupational exposure is concerned. But the best way is physical separation because the intensity of scattered radiation is inversely proportional to the square of the distance from the source. A recommended distance is 3 feet from the source.

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Occupational Safety and Health Administration (OSHA) recommends protective devices where exposure of continuous sound intensity is at least 80 dBA and the duration is 8 h.

Accidental Hazards Related to Patient The possibilities are faulty operative procedures, fall from OT table, injury due to improper positioning, and wrong patient having identical names.

ANESTHESIOLOGY Related to Team

Biological Hazards

Slip and fall on wet floor, cuts from blades, needle prick, and pain due to long hour of standing or handing of patients.

Related to Patient

Precaution ÂÂ

Proper identification of the patient and the surgical procedure is a must.

ÂÂ

Check for patient’s comfort in the intended position of surgery before induction of anesthesia whenever practical.14,15

ÂÂ

A caution sign for wet floor, slip-resistant shoes to prevent against fall.

ÂÂ

Disposal of wastes in earmarked containers.

ÂÂ

Use of personal protective equipments.

ÂÂ

Squeeze blood from the needle pricked part, use first aid, and report to the hospital’s infection control committee.

Chemical Hazards HAZMAT or hazardous materials are the substances that on contact cause harm to a person or the environment.

Chemical hazards form the broadest category among the potential hazards in the OT. These hazards can be the following: ÂÂ

Solid: found primarily in the chemical disinfectants.

ÂÂ

Liquid: used as medication, for tissue preservation, as agents in sterilization process.

ÂÂ

Gas/vapor: usage is associated with anesthesia, sterilization, and disinfection process of both the surgical equipment and the OT.

For the Patient Faulty connection or labeling of anesthetic gas cylinders16 and wrongly calculated dose of anesthetic agents.

For the Team Dermatitis and eczema to the extent of T–cell-mediated delayed type IV or IgE-mediated type I reaction with gloves powder, handwashing sterilizing agents, local anesthetics as procaine, xylocaine, and tetracaine solution, and cement or acrylic monomer used in joint replacement surgery.

Precaution ÂÂ

Repeated pre-use verification of all anesthetic equipments and drugs.

ÂÂ

NIOSH recommends steps against latex gloves use.

ÂÂ

Avoid all agents that cause itching on contamination.

Nosocomial infection from a carrier in the OT team or seedling of microflora from the OT environment can cause postoperative surgical site infection.17 Patient may acquire infection of HIV, HbsAg, HCV, and even Legionella pneumophila present on air-conditioner duct from OT itself.

Related to Team Blood-borne diseases such as HbsAg, HCV, and HIV can be caused from known infected patient through accidental needle prick.18 New strains of tuberculosis, vancomycin and methycillin-resistant bacteria, and prion disease protein, which are resistant to standard sterilization processes, are threats to the team. Increased incidence of miscarriage among lady personnel is also recorded.19 Precaution ÂÂ

Since the emergence of AIDS in the mid-1980s, the practice of universal precautions for protection from fluid and blood-borne pathogens has been recommended by the Centre for Disease Control in 1985 and implemented by OSHA in 1991.

ÂÂ

Linen and contaminated theater clothes must be changed at the end of case and sent for proper disposal or decontamination.

ÂÂ

The endoscope and accessories are to be sent to a central reprocessing unit following use.20,21

ÂÂ

Periodic surveillance22 and OT fumigation and sterilization with recommended agents at regular intervals and swab culture confirmation for no contaminant help in early detection of any organism.

Fire Hazards Operating room fire is defined as fire that occurs on or near patients who are under anesthesia care. It includes surgical fire, airway fire, and fire within the airway circuit. A surgical fire is defined as a fire that occurs on or in a patient. An airway fire is a specific type of surgical fire that occurs in a patient’s airway. Airway fires may or may not include fire in the attached breathing circuit. Adverse outcomes associated with OT fires may include major or minor burns, inhalation injuries, infection, disfigurement, and death. Related adverse outcomes may include psychological trauma, prolonged hospitalization, delay or cancellation of surgery, additional hospital resource utilization, and liability.

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ANESTHESIOLOGY Precaution ÂÂ

Minimizing or avoiding an oxidizer-enriched atmosphere near the surgical site.

ÂÂ

Safe management of ignition sources and fuels.

ÂÂ

Equipment for managing a fire should be readily available in every procedural area where a fire triad consisting of fuel, oxygen, and ignition may exist.23

ÂÂ

Formation of a safety code.

ÂÂ

Education of the OT personnel about the safe and proper use of electrical goods.

ÂÂ

Mock fire drill that is defined as a formal and periodic rehearsal of the OT team’s planned response to a fire.

Other Hazards Other hazards consist of the following.

Organizational

ÂÂ

Studies have demonstrated that where scavenging systems are used, trace concentrations of waste anesthetic gases do not have adverse effect on the personnel in operating rooms.30

ÂÂ

Practice of yoga and training of the team for psychological stress release is recommended.31

CONCLUSION It is better to be safe than to be sorry. So the standard operative procedure for OT etiquette is to be followed precisely to minimize the risk of random inappropriate practice. A checklist for potential hazards to be prepared and followed up through meetings at a regular interval for the betterment. Well-designed plans and staff education will prepare the healthcare personnel to reduce the probability of unwanted incidents and permit safe, efficient, effective, and high standards of care to all patients at all times thus controlling hazards in OT.

Heavy operational theater workload, long working hours, night shift and sleep deprivation, fatigue from handling the patients, and stress on managing the very sick patients are the occupational hazards that can have adverse effect on mental skill and reaction time, vigilance, and interpersonal relationship among the OT personnel.

REFERENCES

Psychological

4. Dinnick OP. Hazards in the operating theatre; hazards of respiratory circuits. Ann R Coll Surg Engl 1973;52(6):

Exposure to severely traumatized patients, irreversible cardiac arrest of a patient may lead to postoperative stress syndrome to the caregivers of the OT. Atmospheric Debris or the fumes and small particles produced using carbon dioxide laser ray can cause pulmonary lesions in experimental animals. HIV provirals have been demonstrated in the HIV-positive laser smoke.24

1. Laufman H. Surgical hazard control: effect of architecture and engineering. Arch Surg 107;552:1973.

2. Laufman H (editor). Hospital Special Care Facilities Planning for User Needs. New York: Academic Press 1981.

3. Whitten MP, Wise CC. Design faults in commonly used carbon dioxide absorbers. Br J Anaes 1972:44(5):535-7.

349-54.

5. Short TG, O’Regan A, Jauyasuriya JP, et al.

Improvements in anaesthetic care resulting from a critical incident reporting programme. Anaesthesia 1996;51:615-21.

6. Caplan RA, Vistica MF, Posner KL, et al. Adverse anaesthetic outcomes arising from gas delivery equipment. A closed claims analysis. Anesthesiology 1997;87:741-8.

Release of waste anesthetic gases inside OT can cause decreased mental alertness and motor skill, tiredness, and slowing of reflexes of the OT personnel.25,26 Teratogenicity in OT team member and malignancy of reticuloendothelial system, liver and kidney disorder have been reported.27,28

7. Beck WE, Heimburger RF. Illumination hazard in the operating room. Arch Surg 1973;107:560.

Use of flammable anesthetic gases such as diethyl ether, ethylene, and fluroxane are no longer continued.29

10. Hull CJ. Electrocution hazards in the operating theatre. Br J Anaesth 1978;50(7):647-57.

Precaution ÂÂ

618

NIOSH has recommended the upper limit of nitrous oxide as 25 ppm and for halogenated anesthetics as 2 ppm in the OT atmosphere.

Indian Journal of Clinical Practice, Vol. 24, No. 7, December 2013

8. Verrinder J. Use of right lighting levels essential. Health Estate 2007;61(6):31-2.

9. Phelps JA. Electrical hazards in the operating room. J Ky Mod Assoc 1975;73:93.

11. Day JL, Lightfoot DA. OR radiation hazards. AORN J 1974;20:249.

12. AORN Recommended Practices Committee.

Recommended practices for electrosurgery. AORN J 2005;81:616-8, 621-6, 629-32.

ANESTHESIOLOGY 13. Willett KM. Noise-induced hearing loss in orthopaedic staff. J Bone Joint Surg Br 1991;73:113-5.

14. Egan MT, Sandberg WS. Auto identification technology and its impact on patient safety in the operating room of the future. Surg Innov 2007;14:41-50, 51.

23. Kalkman CJ, Romijn C, van Rheineck Leyssius AT. Fire and explosion hazard during oxygen use in operating rooms. Ned Tijdschr Geneeskd 2008;152(23):1313-6.

15. Christian CK, Gustafson ML, Roth EM, et al. A prospective study of patient safety in the operating room. Surgery 2006;139:159-73.

24. Hill DS, O’Neill JK, Powell RJ, Oliver DW. Surgical smoke – a health hazard in the operating theatre: a study to quantify exposure and a survey of the use of smoke extractor systems in UK plastic surgery units. J Plast Reconstr Aesthet Surg 2012;65(7):911-6.

16. Feeley TW, Bancroft ML, Brooks RA, Hedley-White J. Potential hazards of compressed gas cylinders: a review.

Anesthesiology 1978;48:72.

25. Feeley TW, Bancroft ML, Brooks RA, Hedley-White J. Potential hazards of compressed gas cylinders: a review.

Anesthesiology 1978;48:72.

17. Altemeier WA, Burke JF, Pruitt BA, Sandusky W (editors).

Manual of Control of Infection in Surgical Patients.

Philadelphia: JB Lippincot Co. 1976.

26. Bruce DL, Bach MJ, Arbit I. Trace anesthetic effects on perceptual cognitive and motor skills. Anesthesiology 1974;40:453.

18. Pattison CP. Epidemiology of hepatitis B in hospital personnel. Am J Epidemiol 1975;101:59.

27. Cullen BF. An evaluation of health hazards in the operating room. Proc Inst Med Chic 1978;32:49.

19. Spence AA, Cohen EN, Brown BW, Knill-Jones RP, Himmelberger DU. Occupational hazards for operating room-based physicians. JAMA 1977;238(9):955-9.

28. Spence AA, Cohen EN, et al. Occupational hazards for operating room-based physicians. JAMA 1977;238(9):955-9.

20. Fraise AP, Bradley C (editors). Ayliffe’s Control of Healthcare-Associated Infection, 5th Edition. London: Hodder Arnold 2009.

21. WHO Guidelines for Safe Surgery. World Health Organisation, 2009. Available at: http://www.who.int/ patientsafety/safesurgery/en/ 22. Beck WC. The Surgeon’s Role in Device Standardization.

Am J Surg 1979;137:t49.

29. Fineberg HV, Pearlman LA, Gabel RA. The case for abandonment of explosive anesthetic agents. N Eng J Med 1980;303(11):613-7.

30. McGregor DG. Occupational exposure to trace concentrations of waste anesthetic gases. Mayo Clin Proc 2000;75:273-7.

31. Lanza ML, Zeiss RA, Rierdan J. Nonphysical violence: a risk factor for physical violence in health care settings.

AAOHN J 2006;54:397-402.

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Equipment-Related Failures Common in Operation Theater As per a study published in BMJ Quality and Safety July Edition, equipment-related errors are responsible for 20% of all errors that occur in the operating room.

Commenting on the subject, Padma Shri & Dr. BC Roy National Awardee, Dr. K K Aggarwal, President Heart Care Foundation of India, said that lack of equipments availability accounted for 38% of all failures and direct malfunctioning of the equipment accounted for 34%.

Many cases of equipment failure have also been reported in Indian circumstances although most of them go unnoticed. It is not unusual for the patient under anesthesia to wait for procurement of a particular device or nonavailability of the right size of the interventional device.

In the study, 21% of all errors were serious errors with equipment problem, communication failure, and technical fault amounting to 21% and 13% of major failures, respectively.

Assessing a checklist specifically including an equipment check, the error can be reduced by up to 60%.

In the US, such an error would lead to a malpractice suit and in India it is considered either as a deficiency of service or a medical accident as the case may be.

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CARDIOLOGY

Role of Atorvastatin in Dyslipidemia: A Clinical Study POOJA BA*, BHATTED S†, CHATURVEDI N‡, DEEKSHIT S‡, BHOJANI MK¶

ABSTRACT This clinical study aimed to see the efficacy of atorvastatin in the management of dyslipidemia. It was a randomized observational clinical study involving 30 patients diagnosed with dyslipidemia. The patients were administered atorvastatin 10 mg tablet once-daily at bedtime and followed up for 12 weeks. This drug achieved the desired lipid profile at the end of the 12th week.

Statistically strongly significant results were obtained in all the lipid profile levels. Thus, the present study showed this drug to be effective in the treatment of dyslipidemia.

Keywords: Dyslipidemia, atorvastatin

D

yslipidemia, defined as an abnormal amount of lipids (e.g., cholesterol and/or fat) in the blood,1 is an important risk factor for coronary heart disease and stroke (cerebrovascular disease). In developed countries, most dyslipidemias are hyperlipidemias often due to faulty diet and lifestyle. Dyslipidemia can be caused due to prolonged elevation of insulin levels and also due to increased levels of O-linked N-acetylglucosamine (O-GlcNAc) transferase.

The data from the US National Health and Nutrition Examination Survey conducted from 1999 to 2000 reported that 25% of adults either had total cholesterol greater than 239.4 mg/dL or were taking a lipidlowering medication.2 According to the World Health Report 1999, ischemic heart disease was the leading single cause of death in the world, the leading single cause of death in high-income countries, and second only to lower respiratory tract infections in low- and middle-income countries. In 1998, it was the leading cause of death, with nearly 7.4 million estimated deaths per year in member states of the World Health

Organization, and caused the eighth highest burden of disease in low and middle-income countries (30.7 million disability-adjusted life years).

Lifestyle modifications should always be part of the treatment regimen for patients with dyslipidemia, regardless of pharmacologic intervention. There are four main classes of lipid-lowering drugs: The bile acid sequestrants (resins), niacin/nicotinic acid, fibric acid derivatives (fibrates), and the 3-hydroxy3-methylglutaryl-coenzyme A (HMG-CoA) reductase inhibitors (statins).

The statins, or HMG-CoA reductase inhibitors, have taken a major role in the management of dyslipidemia.

More specifically, this family of agents is considered first-line for the treatment of hypercholesterolemia in patients who have failed to adequately respond to dietary therapy.3 The statins are well-tolerated and there does not appear to be major differences in toxicity or adverse effect profiles.4,5 Hence, this study was undertaken to see the efficacy and tolerability of atorvastatin (a statin) in the treatment of dyslipidemia.

METHODS

*PhD Scholar †Associate Professor Dept. of Panchakarma National Institute of Ayurveda, Jaipur, Rajasthan ‡Assistant Professor Dept. of Cardiology SMS Medical College and Hospital, Jaipur, Rajasthan ¶Professor Government Ayurvedic Medical College, Junagadh, Gujarat Address for correspondence Dr Pooja BA Dept. of Panchakarma National Institute of Ayurveda, Jaipur, Rajasthan E-mail: drpoojaba@gmail.com

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The present study was a randomized observational clinical trial carried out at the Sawai Mansingh Medical College and Hospital, Jaipur, Rajasthan, over a period of 6 months. The study protocol was approved by the Ethical Committee of the National Institute of Ayurveda, Jaipur. After obtaining written informed consent, 30 patients of either sex in the age group of 20–60 years with newly detected dyslipidemia were selected for the study. Patients with the following conditions were excluded from the study: pregnant and

CARDIOLOGY lactating women, and patients with history or evidence of systemic disorders like cardiac, hepatic, renal, or neurological diseases. A detailed medical history, clinical examination, anthropometric measurements, and baseline laboratory investigations were carried out.

Patients fulfilling the study criteria were administered with atorvastatin 10 mg tablet once daily at bedtime for 90 days (12 weeks). The lipid profile was recorded at baseline and after the 12th week. The patients were monitored for adverse events throughout the study period.

Laboratory investigations like Hb%, fasting blood sugar, lipid profile, renal function tests, liver function tests, urine analysis, and electrocardiography were done at baseline and at the end of the 12th week.

The data were expressed in percentages and mean ± standard deviation (SD). ANOVA was used to find the significance of treatment on the lipid profile.

RESULTS Out of 30 patients, 24 were men and 6 were women.

The mean age was 45 ± 8.0 years. Ninety-two percent of patients were from urban and the remaining 8% were from rural areas.

The most comorbid condition, obesity (BMI ≥ 25 kg/m2) was observed in 26.66% (n = 8) of patients.

Table 1 reveals that the mean cholesterol level was 303.33 ± 26.31 at baseline and 223.33 ± 34.77 after 12th week with p < 0.001**, which is statistically strongly significant. Mean triglyceride (TG) level was 232.00 ± 23.98 at baseline that reduced to 159.67 ± 23.27 at 12th week with p < 0.001**, which is strongly significant. The mean high-density lipoprotein (HDL) level was 50.37 ± 6.24 at baseline and 49.70 ± 5.86 at 12th week with p = 0.094†, which is significant. At the baseline, mean low-density lipoprotein (LDL) was 206.57 ± 24.71 and at 12th week it was 142.03 ± 32.74 with p < 0.001** showing Table 1. Lipid Profile Analysis Between Basal and 12th Week Values Lipid Profile Basal Value in Mean ± SD

12th Week Value p Value in Mean ± SD

Serum cholesterol

303.33 ± 26.31

223.33 ± 34.77

<0.001**

Serum TG

232.00 ± 23.98

159.67 ± 23.27

<0.001**

Serum HDL

50.37 ± 6.24

49.70 ± 5.86

0.094†

Serum LDL

206.57 ± 24.71

142.03 ± 32.74

<0.001**

31.93 ± 4.65

<0.001**

Serum VLDL 46.40 ± 4.80

Table 2. Adverse Events During Study Symptoms

Number of Patients

Constipation

3

Fatigue

2

Abdominal discomfort

4

Myalgia

3

statistically strongly significant result. The mean verylow-density lipoprotein (VLDL) level was 46.40 ± 4.80 at baseline and 31.93 ± 4.65 after 12th week with p < 0.001**, which is statistically strongly significant.

All other laboratory parameters, both at baseline and at the end of 12th week, were within normal limits.

Adverse events like constipation and myalgia were encountered in three patients; abdominal discomfort and fatigue was observed in four and two patients, respectively (Table 2). All these symptoms were mild, transient, and did not require any treatment, discontinuation of medication, or withdrawal from the study.

DISCUSSION In this study, reduction in cholesterol level by 26.37%, TGs level by 31.17%, HDL level by 1.33%, LDL level by 31.24%, and VLDL level by 31.18% was achieved at 12th week when compared with baseline values. Statistically, the results were showed strongly significant.

Atorvastatin calcium is a synthetic lipid-lowering agent and is an inhibitor of HMG-CoA reductase, which catalyzes the conversion of HMG-CoA to mevalonate.

Inhibition of HMG-CoA reductase leads to upregulation of LDL cholesterol (LDL-C) receptors in the liver,6 mediated by activation of sterol regulatory elementbinding proteins resulting in enhanced clearance of LDL from the circulation, thus playing an important role in preventing atherosclerosis.

In the present study, mild adverse events like constipation and fatigue were observed in few patients, which are considered as the common adverse reactions of atorvastatin. The patients did not require any medication to treat the same.

CONCLUSION Dyslipidemia is a common high-risk factor of cardiovascular disease. Despite the widespread availability of safe and efficacious medications, the management of this condition is far from optimal.

Indeed, epidemiological studies have indicated that 90% of patients with dyslipidemia fail to achieve their

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CARDIOLOGY therapeutic targets. Moreover, the optimal goal in patients with risk factors has been steadily declining, necessitating the treatment of bigger population subsets.

Statin group of drugs have excellent efficacy and safety profiles for the treatment of dyslipidemia. The present study also suggested that atorvastatin is effective in controlling the lipid profile at the end of 12th week and is tolerated with few minor adverse symptoms.

REFERENCES 1. Harrison TR. Harrison’s Principles of Internal Medicines, 12th International Edition. In: Braunwald E, Fanci AS, Hauser SL, Kasper DL, Longo DL, Jameson JL (editors).

New York: McGraw-Hill Medical Publishing Division, Vol. I, 2002.

2. Rosamond W, Flegal K, Furie K, et al. Heart disease and stroke statistics – 2008 update: a report from the American Heart Association Statistics Committee and Stroke Statistics Subcommittee. Circulation 2008;117(4):e25-e146.

3. Heart Protection Study Collaborative Group. MRC/BHF Heart Protection Study of cholesterol lowering with simvastatin in 20,536 high-risk individuals: a randomised placebo-controlled trial. Lancet 2002;360(9326):7-22.

4. Sever PS, Dahlof B, Poulter NR, et al. Prevention of coronary and stroke events with atorvastatin in hypertensive patients who have average or lowerthan-average cholesterol concentrations, in the AngloScandinavian Cardiac Outcomes Trial–Lipid Lowering Arm (ASCOT-LLA): a multicentre randomised controlled trial. Lancet 2003;361(9364):1149-58.

5. Pearson TA, Laurora I, Chu H, Kafonek S. The lipid treatment assessment project (L-TAP): a multicenter survey to evaluate the percentages of dyslipidemic patients receiving lipid-lowering therapy and achieving low-density lipoprotein cholesterol goals. Arch Intern Med 2000;160(4):459-67.

6. Delsing DJ, Jukema JW, van de Wiel MA, et al. Differential effects of amlodipine and atorvastatin treatment and their combination on atherosclerosis in Apo E* 3-Leiden transgenic mice. J Cardiovasc Pharmacol 2003;42(1): 63-70.

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Radial access for percutaneous coronary interventions (PCI) appears to be as safe as femoral approach even for women, who are disadvantaged by smaller artery size, as reported at the Transcatheter Cardiovascular Therapeutics meeting. In a trial of 1,787 women, the bleeding rate for those randomized to transradial PCI was 2.9% versus 1.2% (p = 0.12) for those whose physicians used the femoral approach, which led the data safety monitoring board for the SAFE–PCI trial to conclude after just 1,120 patients were randomized and 446 had undergone the procedure that the trial was “unlikely to show a difference at the planned sample size."

According to a research presented at the 53rd Interscience Conference on Antimicrobial Agents and Chemotherapy, corticosteroids might reduce the risk for Clostridium difficile–associated diarrhea, report researchers studying patients with chronic obstructive pulmonary disease (COPD) treated with antibiotics. This finding contradicts previous research suggesting no apparent benefit of steroids.

5 Steps to Lower Alzheimer’s Risk ÂÂ

Maintain a healthy weight.

ÂÂ

Check your waistline.

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Eat mindfully. Emphasize colorful, vitamin-packed vegetables and fruits; whole grains; fish, lean poultry, tofu, and beans and other legumes as protein sources; plus healthy fats. Cut down on unnecessary calories from sweets, sodas, refined grains like white bread or white rice, unhealthy fats, fried and fast foods, and mindless snacking. Keep a close eye on portion sizes, too.

ÂÂ

Exercise regularly. Aim for 2½ to 5 hours weekly of brisk walking (at 4 mph). Or try a vigorous exercise like jogging (at 6 mph) for half that time.

ÂÂ

Keep an eye on important health numbers. In addition to watching your weight and waistline, keep a watch on your cholesterol, triglycerides, blood pressure, and blood sugar numbers.

–Healthbeat

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COMMUNITY MEDICINE

Causes of Adult Deaths by Verbal Autopsy in an Urban Slum of Ludhiana ALEXANDER SA*, SENGUPTA P†, BENJAMIN AI†

ABSTRACT Twenty-three of the world’s 192 countries have high-quality death registration data and 75 have no cause-specific mortality data at all. Verbal autopsy (VA), an alternative method for collecting mortality data, enables investigators to establish the cause of death retrospectively. VA carries information on circumstances, events, signs, and symptoms of illness experienced by the deceased before death. It can ascertain the leading causes of death, reduce the misclassification of causes, reduce the proportion of adult (age 25 or older) deaths attributed to unspecified or unknown causes (from 54% to 23% in urban areas and from 41% to 26% in rural areas). A study was undertaken in a urban slum of Ludhiana, to find the cause specific mortality of adult deaths and get an insight into the mortality pattern of this sample population.

Keywords: Verbal autopsy, adult deaths, urban slum

T

wenty-three of the world’s 192 countries have high-quality death registration data and 75 have no cause-specific mortality data at all.1 Verbal autopsy (VA), an alternative method for collecting mortality data, enables investigators to establish the cause of death retrospectively.2 This method is used by the Registrar General of India’s Sample Registration System, the country’s primary system for collecting demographic data. VA carries information on circumstances, events, signs, and symptoms of illness experienced by the deceased before death and hence the expensive process of sending professionally trained individuals for routine investigation of deaths is done away with.

Studies carried out in Tamil Nadu3,4 showed that VA can ascertain the leading causes of death, reduce the misclassification of causes, reduce the proportion of adult (age 25 or older) deaths attributed to unspecified or unknown causes (from 54% to 23% in urban areas and from 41% to 26% in rural areas), derive the

*MBBS Student †Professor (Community Medicine) Dept. of Community Medicine Christian Medical College, Ludhiana, Punjab Address for correspondence Dr Paramita Sengupta Dept. of Community Medicine Christian Medical College, Ludhiana, Punjab E-mail: drparamita2425@gmail.com Source of Funding: This study was funded by the Indian Council of Medical Research (STS-2012) – ID-2012-02674.

probable underlying cause of death when it has not been reported, and yield a broad classification of the underlying causes in 90% of deaths before age 70.

This study was undertaken to find the cause specific mortality of adult deaths and get an insight into the mortality pattern of this sample population.

METHODS This cross-sectional study was conducted from June 1, 2011 to May 31, 2012. All the adult deaths (deaths in 15 years or older) in the 30,000 population of the urban field practice area of the Dept. of Community Medicine of a medical college in Ludhiana were studied. One hundred thirty-five total deaths were reported from these areas in this 12-month period. There were 16 childhood deaths and 13 others who either met the exclusion criteria or did not give consent. Participating next of kin were interviewed with the help of a standard VA tool, previously used and validated in a study in Andhra Pradesh.5 Overall, the causes of death were divided into three broad disease categories: Group I– communicable diseases, maternal causes, conditions arising in the perinatal period, and nutritional deficiencies; Group II – noncommunicable diseases; and Group III – injuries).6 The causes of death were then coded according to the International Statistical Classification of Diseases and Related Health Problems, 10th revision (ICD-10).7 Algorithms for selected adult causes of death as previously developed was used to come to a diagnosis of the probable cause of death.

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COMMUNITY MEDICINE The data was then entered in Microsoft Excel and analyzed in Epi-Info Version 6 software. Statistical analysis was done using simple proportions and percentages.

Chi-square test was applied where appropriate.

RESULTS More than half of all deaths were in the geriatric age group (59.4%), more in males (61.3%), with 89.6% of the respondents being present with the deceased at the time of death. Majority (63.2%) of the deaths took place at home.

Table 1. Categorization of Deaths According to Global Burden of Disease Class No. of Males (%)

No. of Females (%)

Total No. (%)

Group I

15 (23.1)

18 (43.9)

33 (31.1)

Group II

44 (67.7)

20 (48.8)

64 (60.4)

Group III

6 (9.2)

3 (7.3)

9 (8.5)

65 (100.0)

41 (100.0)

106 (100.0)

Ď&#x2021;2 = 5.10; df = 2; p = 0.078

Table 2. Causes of Deaths Identified Through VA in Comparison with Medical Record Data Cause of Death as Per ICD-10

VA

MR

A00-B99: Certain infectious and parasitic diseases

9 (8.5)

10 (9.4)

C00-D48: Neoplasms

9 (8.5)

5 (4.7)

E00-E90: Endocrine, nutritional, and metabolic diseases

4 (3.8)

3 (2.8)

G00-G99: Disease of the nervous system

18 (17.0)

4 (3.8)

I00-I99: Diseases of the circulatory system

27 (25.5)

23 (21.7)

J00-J99: Disease of the respiratory system

7 (6.6)

3 (2.8)

K00-K93: Diseases of the digestive system

5 (4.7)

9 (8.5)

N00-N99: Diseases of the genitourinary system

2 (1.9)

0 (0.0)

16 (15.1)

7 (6.6)

9 (8.5)

2 (1.9)

R00-R99: Symptoms, signs, and abnormal clinical findings V01-Y98: External causes of morbidity and mortality Unknown (missing data) Total

624

As per the available medical records, 37.7% of the deaths had missing data and another 6.6% were not given a specific cause of death. In comparison, although there was no missing data in the case of VA, 15.1% could not be assigned a specific cause (p = 0.0000) and were coded into R00-R99 of ICD-10 classification (Table 2).

DISCUSSION

Global Burden of Disease Class

Total

Group II conditions contributed to the majority of deaths (60.4%). Group I conditions contributed for 31.1% of the deaths and only 8.5% of the deaths were due to Group III conditions. There were no significant gender differences in the deaths according to global burden of disease class (Table 1).

0 (0.0)

40 (37.7)

106 (100.0)

106 (100.0)

Indian Journal of Clinical Practice, Vol. 24, No. 7, December 2013

There were total 135 deaths in the 1-year period from June 1, 2011 to May 31, 2012, with the crude death rate being 4.5/1,000 population8 of which 119 were in the age group of 15 years and above. VAs were done for 106 of the deaths in this age group (89.1%), hence, the nonresponse rate was 10.9%. Yang et al9 reported a nonresponse rate of 6.5%, mostly in Beijing, Shanghai, and Guangzhou.

The majority of the deaths were in the geriatric age group (59.4%) and there were more deaths in males (61.3%) as compared to females (38.7%). Similar findings were observed by Joshi,10 Kanungo et al,11 and Gajalakshmi et al.3 In 89.6% of deaths, the death occurred in the presence of the respondent. This facilitates the correct reporting of the chain of events leading to death and hence a proper VA report. Nearly, two-thirds of the deaths in the area took place at home (63.2%).

It is estimated that nearly half the disease burden in low- and middle-income countries is from noncommunicable diseases and more than 21% of deaths in such countries are due to cardiovascular diseases.12 In the present study also, noncommunicable diseases contributed to the majority of deaths (60.4%) that is similar to the findings of Kanungo et al11 who also found Group II conditions6 to be responsible for 66% of the deaths, with cardiovascular conditions leading. Joshi10 also reported a preponderance of chronic and noncommunicable causes of death in their study villages.

According to ICD-10, the most common cause of death in this area was found to be diseases of the circulatory system (25.5%), which was more common in males than females. Joshi10 also reported a preponderance of diseases of the circulatory system (32%), with more deaths in men. Out of these, it was not possible to

COMMUNITY MEDICINE assign a specific cause for 15.1% of deaths. These deaths were found to be due to some abnormal clinical or laboratory finding and were given codes R00-R99. Chandramohan8 reported that 22% of their diagnoses were not confirmed, Joshi10 could not assign a specific cause for 18% of deaths, while Gajalakshmi et al3 reported this figure as 10% and Kanungo et al11 as 11%.

study can be incorporated in healthcare systems while ascertaining the cause of death.

Missing data was found in 37.7% of the medical records even in a set-up where routine healthcare was provided to the population and all the vital events were recorded in a computerized database. Moreover, 6.6% of the deaths could not be listed under a specific cause of death in the medical records. Missing data in the VA method was not found as the symptom checklist used helped in procuring most of the data in the field. The VA tool could not ascertain a specific cause of death for 15.1% of deaths, whereas this was 44.3% in the medical records (p = 0.0000). Hence, the symptom checklist used in the VA tool was found to be more sensitive in identifying the cause of death as compared to the routine medical records data maintained in the health center.

2. World Health Organization. WHO Technical Consultation on Verbal Autopsy Tools. Geneva: WHO, 2005.

REFERENCES 1. Mathers CD, Fat DM, Inoue M, Rao C, Lopez A. Counting the dead and what they died from: an assessment of the global status of cause of death data. Bull World Health Organ 2005;83(3):171-7.

3. Gajalakshmi V, Peto R, Kanaka S, Sivagurunathan B. Verbal autopsy of 48,000 adult deaths attributable to medical causes in Chennai (formerly Madras), India. BMC Public Health 2002;2:7.

4. Gajalakshmi V, Peto R. Verbal autopsy of 80,000 adult deaths in Tamilnadu, South India. BMC Public Health 2004;4:47.

5. Joshi R. Causes of Death in Rural Andhra Pradesh, India (Thesis submitted for Doctor of Philosophy), University of Sydney, Sydney, Australia, June 2006.

6.

CONCLUSION This study showed that the majority of the deaths were in the geriatric age group and there were more deaths in males in this area. Noncommunicable diseases contributed to the majority of the deaths, with diseases of circulatory system as the leading cause of death.

Although, the primary healthcare delivery in this area was less well equipped to deliver care and prevention for chronic diseases, the VA reduced the proportion of deaths attributed to unspecified medical causes and unknown causes from 44.3% down to 15.1%. VA identified 40 deaths in more than 15 years old that were not registered in the health center’s mortality database. This study demonstrated the possibility of ascertaining at least the leading causes of death, reducing the misclassification of cause of death, and deriving the probable underlying cause of death when it has not been reported. Since, the proportion of people who die while under medical care is low, about two-thirds of the deaths taking place at home, VA can be of substantial help in assessing the underlying cause of death. The VA tool used in this

Murray CJL, Lopez AD. Estimating causes of death: new methods and global and regional applications for 1990. In: Murray CJL, Lopez AD (editors). The Global Burden of disease – a comprehensive assessment of mortality and disability from diseases, injuries, and risk factors in 1990 and projected to 2020. Boston: Harvard School of Public Health;1996:117‐200.

7. World Health Organization. International Statistical Classification of Diseases and Related Health Problems, 10th revision. Geneva: WHO;2003.

8. Chandramohan D, Maude D, Rodrigues LC, Hayes RJ. Verbal autopsies for adult deaths: their development and validation in a multicentre study. Tropic Med Int Health 1998;3:436-46.

9. Yang G, Rao C, Ma J, Wang L, Wan X, Dubrovsky G, et al.

Validation of verbal autopsy procedures for adult deaths in China. Int J Epidemiol 2006;35:741-8.

10. Joshi R, Cardona M, Iyengar S, Sukumar A, Raju CR, Raju KR, et al. Chronic diseases now a leading cause of death in rural India – mortality data from the Andhra Pradesh Rural Health Initiative. Int J Epidemiol 2006;35:1522-9.

11. Kanungo S, Tsuzuki A, Deen JL, Lopez AL, Rajendran K, Manna B, et al. Use of verbal autopsy to determine mortality patterns in an urban slum in Kolkata, India. Bull World Health Organ 2010;88:667-74.

12. Lopez AD, Mathers CD, Ezzatti M, Jamison DT, Murray CJL. Global and regional burden of disease and risk factors, 2001: systematic analysis of population health data. Lancet 2006;367:1747-57.

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DERMATOLOGY

Penicillin-Induced Stevens–Johnson Syndrome: A Case Report PATIL JR*, MOTGHARE VM†, DESHMUKH VS‡, JAYKARE SC*, PISE HN*

ABSTRACT Stevens–Johnson syndrome (SJS) is one of the manifestations of severe form of cutaneous adverse drug reactions (CADRs).

Penicillin group of antibiotics is well-known to cause the CADRs. Few cases of amoxicillin and only one case of dicloxacillininduced SJS have been reported. To the best of our literature search, we have not come across a single case of amoxicillin– dicloxacillin-induced SJS. Here, we report a case of amoxicillin–dicloxacillin-induced SJS in a 28-year-old female patient.

The rationality of amoxicillin–dicloxacillin fixed drug combination is doubtful. Hence, prescribing rational drug therapy and promptly reporting the adverse drug reactions is essential so that noncompliance to treatment with resultant therapeutic failure and augmented antimicrobial resistance can be avoided.

Keywords: Amoxicillin–dicloxacillin, CADRs, Stevens–Johnson syndrome, rational drug therapy

C

utaneous eruption is one of the common forms of adverse drug reaction manifestations. Stevens– Johnson syndrome (SJS) is one such manifestation that represents severe form of cutaneous eruptions.

It is characterized by severe purulent conjunctivitis, severe stomatitis with extensive mucosal necrosis, and purpuric macules. Evidently, the etiology is linked to the use of drugs rather than other etiologic factors.

The common culprits are antimicrobials like sulfonamide followed by nonsteroidal anti-inflammatory drugs (NSAIDs), anticonvulsant drugs, and anti-gout drugs.1 Here, we report a case of SJS-induced by penicillin.

CASE REPORT A 28-year-old female presented to our hospital’s emergency department with complaint of rashes all over the body since 3 days. She was apparently alright 3 days back when she had history of drug ingestion for fever. After ingestion of medicine, rashes appeared

*Junior Resident II †Professor and Head ‡Assistant Professor Dept. of Pharmacology Swami Ramanand Teerth Rural Govt. Medical College Ambajogai, Beed, Maharashtra Address for correspondence Dr Jyoti R Patil Dept. of Pharmacology Third Floor, College Building Swami Ramanand Teerth Rural Govt. Medical College Ambajogai, Beed, Maharashtra E-mail: drjyotipatil777@gmail.com

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Indian Journal of Clinical Practice, Vol. 24, No. 7, December 2013

all over her body that initially appeared over face and spread rapidly to the neck, chest, back, abdomen, upper and lower extremities, within 24 h. On examination, the lady was ill-looking; the rashes were typically erythematous and vesicular in nature with blisters spreading all over the body. There was involvement of mucosal areas as well in the form of vesicular lesions over eyes, tongue, buccal mucosa, and genitalia (Fig. 1). Systemic examination, otherwise, did not reveal any other significant findings. On detailed inquiry, the patient gave a history of ingestion of capsule dicloxacillin prescribed by a general practitioner for fever, following which she developed swelling over lips and rashes all over the body. Considering the history, clinical examination, and laboratory findings, the patient was diagnosed as a case of penicillininduced SJS. The patient was managed aggressively with parenteral antibiotics, steroids, antihistamines, local treatment of lesions, and nutritional supplements.

On causality assessment using Naranjo’s causality algorithm, association was probable for both the drugs.

DISCUSSION Cutaneous adverse drug reactions (CADRs) are very commonly encountered in the dermatology outpatient department. SJS or toxic epidermal necrolysis (TEN) is one of the dermatologic conditions that can be potentially fatal. SJS/TEN are considered as a spectrum of the same disease; in SJS, the extent of total skin surface involvement is less than 10%; more than 30% skin involvement is termed as TEN, while 10%–30%

DERMATOLOGY

a Figure 1. Mucosal lesions. (a) Ocular. (b) Oral.

is designated SJS/TEN overlap syndrome.2 In both the conditions, there is a development of acute rash with mucocutaneous involvement that is typically associated with vesicles and blisters. In severe cases, there is extensive necrosis of the epidermis and mucous membrane. Although the exact etiology of SJS/TEN is not fully understood, it is believed to be a immunemediated hypersensitivity reaction in which cytotoxic T lymphocytes play a role in the pathogenesis.2 In clinical practice, often, these reaction are manifestations of drug-induced hypersensitivity. The etiological factors of SJS can be range from viral infections to various pharmacological agents. The commonly associated drugs are antimicrobials (sulfonamide and other nonsulfonamide antibiotics such as aminopenicillins, cephalosporins, and quinolones), anticonvulsants (carbamazepine, phenytoin, phenobarbitone, and valproic acid), NSAIDs of the oxicam type, and allopurinol.1,3 As stated earlier, penicillin group of antimicrobials are common antimicrobial agents known to cause cutaneous drug eruptions. Patel et al4 reported that penicillins are one of the antimicrobials frequently causing severe CADRs in the Indian population.

Till date, few cases of amoxicillin-induced SJS/TEN have been reported.3,5 In our case, patient consumed amoxicillin–dicloxacillin combination that caused SJS. After meticulous literature search, we have come across only one case of dicloxacillin-induced SJS (reported

by Li et al),6 while no case caused by amoxicillin– dicloxacillin fixed-dose combination (FDC)-induced SJS/TEN has been reported yet. The FDC of amoxicillin + cloxacillin is considered irrational as they do not provide any additive effect and, on the contrary, adds to the cost of the therapy and accelerates the chances of emergence of drug-resistant strains.7 As dicloxacillin belongs to the same class as that of cloxacillin, the rationality of amoxicillin–dicloxacillin FDC is doubtful.

Prescribing irrational drug combinations is rampantly followed in clinical practice, which needs rectification.

Also, when an ADR occurs due to a drug combination,

b Figure 2. Fading lesions over lower limbs.

it is difficult to attribute it to any particular entity, as in the present case.

CONCLUSION Beta-lactam group of antimicrobials are frequently associated with severe CADRs like SJS and TEN. Although these CADRs are predominantly mild in nature, they can be at times, severe in manifestation.

In developing countries like India, where the infectious diseases are widely prevalent, the frequent use of betalactam antimicrobials and the subsequent ADRs cannot be avoided. Thus, rational drug therapy and promptly reporting the ADRs is essential so that noncompliance to treatment with resultant therapeutic failure and augmented antimicrobial resistance can be avoided.

REFERENCES 1. Jaykare S, Motghare V, Patil J, Pise H. Nimesulide induced Stevens Johnson syndrome: a case report.

Indian J Med Case Rep 2012;1:1-3.

2. Harr T, French LE. Toxic epidermal necrolysis and Stevens-Johnson syndrome. Orphanet J Rare Dis 2010;5:39.

3. Sanmarkan AD, Sori T, Thappa DM, Jaisankar TJ. Retrospective analysis of Stevens-Johnson syndrome and toxic epidermal necrolysis over a period of 10 years. Indian J Dermatol 2011;56(1):25-9.

4. Patel TK, Barvaliya MJ, Sharma D, Tripathi C. A systematic review of the drug-induced StevensJohnson syndrome and toxic epidermal necrolysis in Indian population. Indian J Dermatol Venereol Leprol 2013;79(3):389-98.

5. Roujeau JC, Kelly JP, Naldi L, Rzany B, Stern RS, Anderson T, et al. Medication use and the risk of Stevens-Johnson syndrome or toxic epidermal necrolysis. N Engl J Med 1995;333(24):1600-7.

6. Li TH, Chan C, Sun CC. Erythema multiforme, Stevens Johnson syndrome and toxic epidermal necrolysis – antecedent drug exposures in 99 hospitalized patients.

Dermatol Sinica 1996;14:119-25.

7. Jadav SP, Parmar DM. Critical appraisal of irrational drug combinations: a call for awareness in undergraduate medical students. J Pharmacol Pharmacother 2011;2(1):45-8.

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ENT

Facial Necrotizing Fasciitis: A Rare Complication of Maxillary Sinusitis GUPTA N*, VARSHNEY S†, GUPTA P‡

ABSTRACT Necrotizing fasciitis is an uncommon infection of the fascia and subcutaneous tissue, which is extremely rare in head and neck region because of high vascularity. Necrotizing fasciitis arising as a complication of maxillary sinusitis is exceptionally rare.

We present the case of a 50-year-old female patient who was immunocompetent and developed facial necrotizing fasciitis as a sequel of maxillary sinusitis. She was effectively managed by surgical debridement and antibiotics. To the best of our knowledge, this is the second case report in English literature presenting as necrotizing fasciitis secondary to maxillary sinus infection.

Keywords: Maxillary, sinusitis, facial, necrotizing, fasciitis

M

axillary sinus lies close to the orbit superiorly, nasal cavity medially, teeth inferiorly, pterygopalatine fossa posteriorly, and facial skin anteriorly. Complications occurring as a sequelae of maxillary sinusitis can involve all these structures but with the advent of highly effective antibiotics, it is rare to see them in the modern era.1 Necrotizing fasciitis of facial region is even a rarer occurrence, especially in an immunocompetent patient. The most common causes of cervicofacial necrotizing fasciitis are of odontogenic origin.2 Maxillary sinusitis is an uncommon cause of necrotizing fasciitis. The onset is often insidious in the form of nonspecific regional facial swelling, erythema, and fever. Thus, clinical distinction from more benign inflammatory conditions of the neck, such as cellulitis, may be impossible at an early stage. Without immediate surgical treatment, however, necrotizing fasciitis of the head and neck invariably leads to mediastinitis and fatal sepsis.3 Therefore, it is important to establish the correct diagnosis at an

*Assistant Professor Dept. of ENT Government Medical College and Hospital, Chandigarh, Punjab †Professor and Head Dept. of ENT All India Institute of Medical Sciences, Rishikesh, Uttarakhand ‡Lecturer Dept. of Orthodontics Subharti Dental College, Meerut, Uttar Pradesh Address for correspondence Dr Nitin Gupta Dept. of ENT Government Medical College and Hospital, Sec 32, Chandigarh, Punjab E-mail: nitinent123@gmail.com

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early stage. Contrast-enhanced computed tomography (CECT) scan is the investigation of choice to evaluate the extent of the disease. The diagnosis of necrotizing fasciitis should be suspected if the inflammatory signs on CT scan are not limited to cellulitis, but include widespread fasciitis of the superficial and deep fascia.4 Antibiotic treatment alone is insufficient; prompt and aggressive surgical exploration and debridement are imperative to prevent a fatal outcome.

CASE REPORT A 50-year-old female presented in the ENT OPD with swelling over right cheek and upper lip for the last 3 days. Swelling was sudden in onset, rapidly progressive in size, associated with severe pain and fever for 2 days and black discoloration of the skin.

Patient also complained of obstruction and purulent discharge in right nasal cavity. There was no history of diabetes, any drug reaction, or insect bite. There was swelling and pain over right eyelid. Examination of the patient revealed temperature of 100.3°F, tachycardia (pulse rate 104/min). On local examination, there was a swelling on right cheek, upper lip, and partly extending to lower lip with patchy black discoloration.

Swelling was tender, 4 × 6 cm in size and temperature over surface raised, diffused with ill-defined margins, soft in consistency, and nonfluctuant (Fig. 1). There was edema over the right eyelid while the left eyelid was normal in texture and function. Anterior rhinoscopy and diagnostic nasal endoscopy were suggestive of purulent discharge in middle meatus of right nasal cavity. Vision and examination of cranial nerves was

ENT

Figure 2. CECT scan of the nose and PNS showing features of acute right-side sinusitis and soft tissue swelling of right cheek with marked thickening of fascia.

Figure 1. Patient showing diffuse swelling over right cheek and lips.

normal except for hypoesthesia over right cheek. The patient was hospitalized and started on broad-spectrum intravenous antibiotics (Ceftriaxone, Gentamycin, and Metronidazole) along with analgesics, antipyretics, and nasal decongestants. Pus was sent for culture and sensitivity. Routine blood examination was suggestive of leukocytosis while other tests (urine, random blood sugar, and serum creatinine) were within normal range.

Enzyme-linked immunosorbent assay (ELISA) test for human immunodeficiency virus (HIV) was negative.

CECT scan of the nose and paranasal sinus (PNS) was done, which revealed air–fluid level in right maxillary sinus along with mucosal thickening in bilateral maxillary, ethmoid, and frontal sinuses, and a soft tissue swelling of right cheek extending to temporal region.

There was marked thickening of superficial and deep fascia of this region (Fig. 2). Considering the clinical and CT scan findings, a diagnosis of necrotizing fasciitis was made. The patient was posted for emergency surgery where debridement of the wound and followup wound care was done. Pus culture revealed growth of b-hemolytic streptococci Group A, Pseudomonas spp., and Staphylococcus aureus that were sensitive to the prescribed antibiotics. Surgery and postoperative period was uneventful. Pain and swelling subsided considerably after 48 h. Histopathological examination of the tissue was suggestive of acute abscess.

A postoperative CT scan done 5 days after surgery was normal and had no inflammatory signs (Fig. 3).

The patient was discharged on the sixth postoperative day. Patient has been on a regular follow-up for the last 4 months with no recurrence of disease.

DISCUSSION The term “necrotizing fasciitis” is used to describe a severe, acute, and potentially life-threatening inflammatory condition caused by streptococcal or mixed bacterial infection and propagating continuously within soft tissues.5 Necrotizing fasciitis is a rare infection of the fascial planes, which is less common in head and neck because of higher vascularity in the region. The most common causes of necrotizing fasciitis are dental infections (dental abscess, gingivitis, and pulpits), blunt trauma, radiotherapy, and tonsillitis.6 Maxillary sinusitis is an uncommon cause of necrotizing fasciitis. The predisposing factors for the development of necrotizing fasciitis are diabetes, hypertension, obesity, malnutrition, peripheral vascular diseases, severe liver disease, alcoholism, and acquired immunodeficiency syndrome (AIDS).7 Although necrotizing fasciitis has been described mainly in elderly and immunocompromised patients, it recently has been observed increasingly in young, otherwise healthy, individuals. Normally, infection progresses rapidly and can involve the vascular structures causing small vessel thromboses. The most common clinical presentations are painful edema, erythema, warmth, tenderness, and crepitation. Patients can develop mediastinitis and consequent septic shock.8

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ENT some authors.9 The morbidity and mortality seems to be related to the promptness of medical and surgical intervention. The mortality rate reported in the literature ranges from 19% to 40%.5 The higher mortality rate is related to pre-existing systemic illness, late surgical intervention, septicemia within 24 h, old age, and mediastinal and thoracic extension of the infection.

REFERENCES 1. Stamenkovic I, Lew D. Early recognition of potentially fatal necrotizing fasciitis. The use of frozen-section biopsy N Engl J Med 1984;310(26):1689-93.

2. Raboso E, Llavero MT, Rosell A, Martinez-Vidal A. Craniofacial necrotizing fasciitis secondary to sinusitis.

J Laryngol Otol 1998;112(4):371-2.

3. Banerjee AR, Murty GE, Moir AA. Cervical necrotizing fasciitis: a distinct clinicopathological entity? J Laryngol Otol 1996;110(1):81-6.

Figure 3. Postoperative CT scan showing normal nose and PNS.

CT scan has been advocated for detecting gas, identifying the spread of infection in vascular sheaths, and detecting the extension of infection to remote areas (mediastinitis and pleural or pericardial effusions).

Necrotizing fasciitis is a polymicrobial infection; the most common pathogens are Streptococcus spp., but S. aureus and anaerobes are also present in large proportion of cases. Effective treatment and management of necrotizing fasciitis is based on early recognition aggressive surgical intervention, use of broad-spectrum antibiotics, and supportive therapy. It is important to explore and drain all involved fascial planes. Hyperbaric oxygen was found to be useful by

4. Becker M, Zbären P, Hermans R, Becker CD, Marchal F, Kurt AM, et al. Necrotizing fasciitis of the head and neck: role of CT in diagnosis and management. Radiology 1997;202(2):471-6.

5. Bahu SJ, Shibuya TY, Meleca RJ, Mathog RH, Yoo GH, Stachler RJ, et al. Craniocervical necrotizing fasciitis: an 11-year experience. Otolaryngol Head Neck Surg 2001;125(3):245-52.

6. Krespi YP, Lawson W, Blaugund SM, Biller HF. Massive necrotizing fasciitis infections of the neck. Head Neck Surg 1981;3(6):475-81.

7. Zbaren P, Rothen HU, Läng H, Becker M. Necrotizing fasciitis of soft tissues of the face and neck. HNO 1995; 43(10):619-23.

8. Vaid N, Kothadiya A, Patki S, Kanhere H. Necrotizing fasciitis of the neck. Indian J Otolaryngol Head Neck Surg 2002;54(2):143-5.

9. Kantu S, Har-El G. Cervical necrotizing fasciitis. Ann Otol Rhinol Laryngol 1997;106(11):965-70.

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Harvard Six Ways to Ease Neck Pain ÂÂ

Don’t stay in one position for too long.

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Make some ergonomic adjustments. Position your computer monitor at eye level so you can see it easily. Use the hands–free function on your phone or wear a headset. Prop your touch–screen tablet on a pillow so that it sits at a 45° angle, instead of lying flat on your lap.

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If you wear glasses, keep your prescription up-to-date.

ÂÂ

Don’t use too many pillows.

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Know your limits. Before you move a big armoire across the room, consider what it might do to your neck and back, and ask for help.

ÂÂ

Get a good night’s sleep.

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ENT

Acinic Cell Carcinoma of the Parotid EASWERAN SV*, LOKESH†, RAGHVENDRA U‡, YUVRAJ¶, MANJULA‖

ABSTRACT Acinic cell carcinoma, also known as acinar/acinous cell carcinoma is a rare salivary gland cancer (6-10%). Around 3-13% malignancies involve the parotid; it arises to also from other glands namely submandibular, minor salivary gland, rarely parapharyngeal spaces,1,2 pancreas and lung (which it, usually metastasizes). Acinic cell carcinoma usually occur bilaterally, it presents in younger median age. It is a slow growing, painless tumor. It affects females more than males. Facial nerve is spared.

If it metastatizes, it does so to the lung, bone, CNS, mediastinum, liver and brain.

Keywords: Acinic cell, parotid

A

cinic cell carcinoma is a rare salivary gland cancer.3 In the past, the malignant nature of this cancer was disputed and hence it was classified as an ‘acinic cell tumor’/benign ‘adenoma’; later due to high potential to recur and metastatize it came to be known as a malignant carcinoma (WHO). Acinic cell carcinoma are typically slow growing, low-grade (highly differentiated) neoplasms. Recurrences (8-60%), metastasis (7-29%) after 3-10 years are uncommon.

Patients with lung metastasis have poor prognosis.

CASE REPORT A 25-year-old male presented to the ENT OPD with history of swelling of the left side of the cheek since 2-3 years, which gradually kept on increasing to attain the present size (Fig. 1a and b). Patient had no evidence of the facial nerve abnormality.

a

On Examination Swelling present on the left side of the cheek. Soft to firm on palpation, mobile, no rise of local temperature, facial nerve was normal.

Investigation Blood Examination Hemoglobin (Hb): 9.2 g/dl, WBC: TC: 5,100 cells/mm3, DC:N-50%, L-40%, E-8%, M-2%, erythrocyte

*ENT Specialist †General Surgeon ‡Anesthesiologist Pandit General Hospital, Sirsi, North Karnataka ¶Radiologist ‖Pathologist Sirsi Scan Center, North Karnataka

b Figure 1. (a and b) Swelling on the left side of the cheek.

sedimentation rate (ESR)-31 mm/1st hour, BT-1 minute 30 second, CT-3 minute 15 second, RBS-122 mg/dl, HIV-negative, HBS-negative.

Ultrasound A well-defined rounded more predominantly cystic lesion of size 4.3 × 2.7 cm seen involving left parotid

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ENT

a a

b Figure 2. (a and b) A well-defined rounded more predominantly cystic lesion of size 4.3 × 2.7 cm on ultrasound.

b

gland with internal solid component and internal septae (Fig. 2). Soft tissue cystic neoplasm involving parotid gland, possibly benign.

FNAC ÂÂ

Gross: Three milliliter of slight reddish fluid aspirated.

ÂÂ

Microscopy: Blood-stained smears shows many scattered lymphocytes, few neutrophils and ductal epithelial cells, few acini and cystic macrophages on background of proteinaceous material. c

Steps of Surgery Patient intubated. Part cleaned and draped. A lazy S incision taken on the affected side after giving local as infiltration. Layers dissected, a cystic swelling indentified in the matter of superficial part of the parotid. Swelling and the superficial parotid gland excised and sent for histopathology. Facial nerve identified and preserved.

Branch of the greater auricular nerve inadvertently

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Figure 3. (a–c) Steps of surgery.

cut. Suturing done in layers (Fig. 3). Drain kept at the operated site for the next 3 days. Patient tolerated ID gland tumor procedure well. Postoperatively period patient put on injectable antibiotics, painkillers and antacids. Patient discharged on 4th postoperative day.

ENT Histopathological Report ÂÂ

Gross: Partly opened cystic mass, measuring 4 × 3 × 0.4 cm with bosselated surface. The cut surface reveals, focally an irregular thickened and small cystic spaces contain blood clot. No evidence of solid areas.

ÂÂ

Microscopy: Multiple sections show parotid tissue with focally microcystic and papillary cystic glands lined by acinic cells displaying granular cytoplasm

and focally clear, vacuolated cells, surrounding stroma contains lymphoid aggregates, hemorrhage and hemosiderin pigments. Few areas show laminated concretions like psammoma bodies within the lumina (Fig. 4). There is 0-1 mitotic activity/hpf.

Impression Features are suggestive acinic cell cacinoma with marked cystic degeneration.

Follow-up Patient has been following-up since two months postdischarge (Fig. 5). Patient was advised follow-up for first 3 months and then 3–6 month yearly.

DISCUSSION Acinic cell carcinoma is a rare salivary gland cancer3 accounting for 6%-10% of all salivary gland carcinomas and 2%-13% of all malignant parotid gland tumors. a

b

c

10X

a

20X

b 20X

Figure 4. (a–c) Histopathological finding of the tumor mass.

Figure 5. (a and b) Patient at 2 months follow-up postdischarge.

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ENT It arises more frequently in the parotid gland, other sites being submandibular gland, minor salivary gland.

It is usually seen bilaterally. On rarer occasions it also presents itself in the pancreas and the lung and if it does it usually metastasizes. It is seen in the younger age group. It is a slow-growing tumor; it’s painless and spares the facial nerve.

The sites of its metastasis are lungs, bone, central nervous system (CNS) and liver. In the past, it was considered a benign lesion now it’s considered by WHO as malignant due to its recurrence potential and metastases, recurrences and metastasis after 3-10 years are common. Local recurrences 8-60%, metastasis 7-29%, death-1-26%. Lung metastasis has poorer prognosis.

Acinic cell carcinoma is least aggressive of salivary gland cancers. High grade variants of acinic4 cell carcinoma are papillocytic carcinoma or carcinomas with undifferentiated cells in medullary pattern. It belongs to the family of adenocarcinomas. Pancreatic form of acinic cell carcinoma is a rare subtype of exocrine pancreatic cancer which include ductal and acinar cell tumors, seen commonly in males.

Treatment compromises of surgery and or postoperative radiation.5 Complete and total removal is a must to avoid recurrence, incomplete excision is associated with lower chance of survival, if complete and total tumor removal is not achieved then radiation using fast neutron beam6 is given, conventional radiation7 is used to treat high grade and residual disease after surgery. Chemotherapy has been considered in

effective and is used only for pain relief. Acinic cell carcinoma is considered chemo-resistant in literature.

Its pancreatic version is treated using intra-arterial infusion chemotherapy.

REFERENCES 1. Yokoyama M, Nomura Y, Semba T. Acinic cell carcinoma of the parapharyngeal space: case report. Head Neck 1993;15(1):67-9.

2. Askin FC, Westra WH. Pathologic Diagnosis: Acinic cell carcinoma of the deep lobe of the parotid gland involving the right parapharyngeal space.

Arch Otolaryngol Head Neck Surg 1999;125(6): And Archives of Otolaryngology online: Head and Neck Surgery Diagnosis Pathologic Quiz Case / http://archotol. ama-assn.org/issues/v125n6/ffull/orp0699-1b.html.

3. Rare and Exotic Cancers website, 2002 http://home. pacbell.net/markmcc/RARE_CANCERS/rare.html 4. Lewis JE, Olsen KD, Weiland LH. Acinic cell carcinoma.

Clinicopathologic review. Cancer 1991;67(1):172-9.

5. North CA, Lee DJ, Piantadosi S, Zahurak M, Johns ME. Carcinoma of the major salivary glands treated by surgery or surgery plus postoperative radiotherapy. Int J Radiat Oncol Biol Phys 1990;18(6):1319-26.

6. Buchholz TA, Laramore GE, Griffin BR, Koh WJ, Griffin TW. The role of fast neutron radiation therapy in the management of advanced salivary gland malignant neoplasms. Cancer 1992;69(11):2779-88.

7. Leborgne F, Zubizarreta E, Fowler J, Ortega B, Mezzera J, Deus JL, et al. Improved results with accelerated hyperfractionated radiotherapy of advanced head and neck cancer. Int J Cancer 2000;90(2):80-91.

■■■■

Excessive noise pollution can cause hearing loss. One should wear ear plugs to avoid noise-related ear injury. Noise pollution can also cause high blood pressure and mental irritation.

Coronavirus is Not a Global Emergency As per an alert by World Health Organization (WHO), Middle East respiratory syndrome coronavirus (MERS) is not a public health emergency of international concern. So far the deadly SARS-like virus has infected 82 people and killed 45 of them. WHO said that the current situation is serious and of great concern but does not constitute the public health emergency of international concern at this moment. Cases so far has been reported in Jordan, Kuwait, United Arab Emirates, Britain, France, Italy and Tunisia. Millions are expected to travel to Mecca for Hujj pilgrimage but Saudi Authorities have cut the number of VISAs this year citing safety concern over expansion work at the Mosque site.

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ENT

A Unique Case in the Field of Medicine THAKKAR H

ABSTRACT Chronic cough fever and off and on difficulty in breathing in a 10-year-old male patient was not responding to drugs. Here we present a case of undiagnosed foreign body since 7 years in airway.

Keywords: Bronchoscopy, mucopus

R

ecently, I had a very unique and most probably a very rare case in the history of medicine â&#x20AC;&#x201C; a case of a foreign body (a plastic whistle) that was stuck in the air passage of a 10-year-old boy since 7 years (Fig. 1). We do get foreign bodies in airways frequently and we have to remove it by bronchoscopy.

However, such foreign bodies are usually a few hours or days or few months old accidents happening in the life of many young children who swallow small things inadvertently. This case is unique because this foreign body went undetected for a period of 7 years; although the kid had consulted scores of doctors during this time period, it was treated as a case of bronchial asthma and tuberculosis. The patient had complaints of difficulty in breathing off and on and also history of cough and fever for which he was admitted to the local hospitals for number of times. There was a history of plastic whistle swallowed at the age of 3 years and thereafter the patient had complaints of fever, chronic cough, and difficulty in breathing. This proved that the boy had the whistle sticking in his right-side bronchus in the wind pipe for nearly 7 years, which is so unique about it. The patient belonged to a village named Matana, Gir Somnath, Sutrapada, Gujarat, India. The boy had swallowed the plastic whistle when he was 3 years old, and he visited us at Rajkot when he was of 10 years.

INVESTIGATION Routine investigations included chest X-ray which revealed prominent bronchovascular markings; routine blood investigations done many times were suggestive

ENT Surgeon Honorary Secretary, IMA, Rajkot, Gujarat Address for correspondence Dr Himanshu Thakkar IMA, Rajkot, Gujarat E-mail: drhimanshuthakkar@gmail.com

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Figure 1. Patient named Vismay (M/10).

of anemia and sometimes raised ESR up to 40 mm in the first hour, and raised total WBC was noted in some readings. CT scan of the thorax suggested a cylindrical foreign body involving the right lower lobe bronchus (Figs. 2 and 3). On examination, decreased air entry on the right side and few basal crepts were found with SpO2 of 97%.

PROCEDURE We did rigid bronchoscopy under general anesthesia and found that a foreign body was stuck to the right side of the bronchial wall.1â&#x20AC;&#x201C;3 There was plenty of mucopus and granulation tissue all around the foreign body as it was 7 years old.

The procedure was very risky as there were chances of bleeding and also chances of pneumothorax, but there was no complication. We successfully managed to remove the whole plastic whistle with all its three parts and the patient was absolutely fine after the operation, which lasted for 20 minutes. The patient was discharged from the hospital the next day.

ENT

Figure 4. Plastic whistle.

Figure 5. Three parts of the plastic whistle.

ÂÂ

Initial period: This lasts for a short period, and can lead to choking, gagging, and wheezing. During this period, the foreign body may be coughed out or it may lodge in the larynx or tracheobronchial tree.

ÂÂ

Symptom-free interval: Respiratory mucosa adapts to the presence of the foreign body. This period varies with the size and nature of the foreign body.

ÂÂ

Late phase: During this phase, the symptoms are caused by obstruction to the airway and inflammation or trauma induced by the foreign body. Most foreign bodies enter the right bronchus because it is wider and more in the line with the tracheal lumen.

Figure 2. CT scan of thorax.

CONCLUSION

Figure 3. CT scan showing cylindrical foreign body involving the right lower lobe bronchus.

DISCUSSION Removing foreign body from the respiratory passage is more challenging in pediatric patients. The reasons are more than one: ÂÂ

Small size of the air passage

ÂÂ

Compromised state of the patient

ÂÂ

General anesthesia physiology

and

pediatric

patient’s

In view of the above circumstances, time taken for the entire procedure was a very critical factor. Shorter the time taken, better would be the outcome. Symptoms produced by these foreign bodies vary in terms of their size, composition, location, and duration. In the air passage, the foreign body can migrate from right to left bronchus. Symptoms of the foreign bodies are divided into three stages:

In pediatric patients, the history is as important as investigations, as investigations are generally normal.

Clinical examination and history plays a very important role. After removing the foreign body, inspect both bronchus (left and right) of the airway again and always for: ÂÂ

The remnants of the foreign body

ÂÂ

Another foreign body

ÂÂ

Foreign body at another site

Pediatric patients with chronic cough and fever not responding to conventional medical line of treatment should be checked for the presence of foreign bodies.

REFERENCES 1. Jackson C, Jackson CL. Disease of air and food passage of foreign body origin. Philadelphia: Saunders, 1950: 13-34.

2. Holinger PH, Holinger LD. Use of open tube bronchoscope in the extraction of foreign bodies. Chest 1978;73 (Suppl 5):721-4.

3. Harboyan G, Nassif R. Tracheobronchial foreign bodies: a review of 14 years experience. J Laryngol Otol 1970;84: 403-12.

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GASTROENTEROLOGY

Chylous Ascites Due to Tuberculosis: A Case Report and Review of Literature KUMAR P*, CHANDRA K†

ABSTRACT Chylous ascites (CA) is an uncommon clinical condition and occurs as a result of disruption of abdominal lymphatics either due to trauma or secondary to obstruction. We report a case of CA associated with disseminated tuberculosis.

Keywords: Chylous ascites, disseminated tuberculosis, ascites in tuberculosis

C

hylous ascites (CA) is the extravasation of milky chyle into the peritoneal cavity. The incidence of CA in 1950 was 1 case in 1,87,000 hospital admissions but in 1980s the incidence increased to 1 case in 11,584 hospital admission; this increase in cases was probably due to aggressive retroperitoneal and cardiothoracic surgery and longer survival of cancer patient.1,2 CA commonly affects adults in 50–60 years of age but can even occur in pediatric populations.3 It affects male and female equally but a study conducted on 28 patients of CA at Massachusetts General Hospital found 75% affection to females.3 In adults, the most common causes are abdominal malignancies and cirrhosis which account for more than two-thirds of the cases in developed countries, whereas infectious diseases such as tuberculosis and filariasis are prevalent in developing countries.4–6 Other causes include congenital, inflammatory, postoperative, traumatic, and miscellaneous disorders.3 CASE REPORT A 52-year-old man of Uttarakhand was admitted in our hospital with complaints mainly of fever and cough

*Associate Professor Dept. of General Medicine Shri Ram Murti Smarak Institute of Medical Science Bhojipura, Bareilly, Uttar Pradesh †Associate Professor Dept. of Pathology Shri Ram Murti Smarak Institute of Medical Science Bhojipura, Bareilly, Uttar Pradesh Address for correspondence Dr Praveen Kumar Dept. of General Medicine Shri Ram Murti Smarak Institute of Medical Science, Bhojipura, Bareilly - 243 202, Uttar Pradesh E-mail: praveen_kmr_23@yahoo.co.in

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for 5 months and distension of abdomen for 4 months.

He was apparently alright 5 months back when he developed continuous low-grade fever and cough. He was diagnosed as a case of pulmonary tuberculosis and directly observed treatment strategy (DOTS) regime for tuberculosis started. The patient had partial relief in fever and cough but he developed ascites. He was revaluated and ascitic fluid showed total count (TC) – 1700 cells/mm3, differential count (DC) – N10L90 RBC+, protein – 3.6 g/dL, sugar – 100 mg/dL, and adenosine deaminase level (ADA) – 179 IU/L. He was labeled as a case of disseminated tuberculosis and DOTS regime for tuberculosis continued. But his ascites progressed gradually with mild relief in fever and cough. There was no significant past, personal, and family history.

On examination, he was febrile with scattered crepitations in respiratory system and evidence of free fluid in the abdomen. Laboratory investigation reports were as follows: hemoglobin (Hb) – 12.8 g/dL, total leukocyte count (TLC) – 3,000/mm3, differential leukocyte count (DLC) – N65L33E1M1, platelets – 2.95 lakhs, prothrombin – N, partial thromboplastin time – N, erythrocyte sedimentation rate (ESR) – 44 mm/h, total protein – 6.0 mg% with A/G ratio of 0.9 mg%, S bilirubin – 0.4 mg%, aspartate aminotransferase (AST) – 38 IU/L, alanine aminotransferase (ALT) – 16 IU/L, S alkaline phosphatase – 162 IU/L, S cholesterol – 178 mg/dL, and S triglyceride – 148 mg/dL. Enzyme-linked immunosorbent assay test for human immunodeficiency virus (HIV) and hepatitis B surface antigen (HBsAg) were nonreactive. Analysis of ascitic fluid revealed grossly milky fluid with glucose level of 146 mg/dL, total protein – 6.3 g/dL, amylase – 62 IU/L, triglycerides – 1,576 IU/L, cholesterol – 120 mg/dL, and an ADA level of 27 IU/L. The cell count of ascitic fluid was

GASTROENTEROLOGY 850 cells/mm3 with a DC of 98% lymphocytes and 2% polymorphs. Culture of fluid was sterile and cytological examination was negative for malignant cells. Contrastenhanced computed tomography (CECT) of the chest showed clustered nodular opacities in bilateral lung fields with minimal left pleural effusion and small area of consolidation in the left lung. CECT abdomen showed gross ascites with mild omental thickening and few discrete lymph nodes in pre/left para-aortic region, the largest measuring 14 mm. Diagnostic laparoscopy was done that showed gross CA but mesenteric lymphadenopathy/omental thickening was not seen. The patient was started on daily regime of antitubercular drug. The patient was further managed by large-volume paracentesis, diuretics, and lowsalt diet. He was discharged and was later called for follow-up. The patient received a total of 9 months of antitubercular treatment (ATT) with full clinical response and complete recovery.

DISCUSSION CA is defined as the extravasation of milky or creamy appearing peritoneal fluid rich in triglycerides, caused by the presence of thoracic or intestinal lymph in the abdominal cavity.7 It is a manifestation of underlying pathology and is not a disease by itself.

Morton, in 1691, performed paracentesis in an 18-month-old boy with disseminated tuberculosis and noted the presence of CA.8 Trauma was recognized as the most common cause in the 17th century. Later on multiple causes have been described; these are abdominal surgery, blunt abdominal trauma, malignant neoplasm, spontaneous bacterial peritonitis, cirrhosis, pelvic irradiation, peritoneal dialysis, abdominal tuberculosis, carcinoid syndrome, and congenital defects of lacteal formation. In tropical countries, tuberculosis and filariasis are the leading causes.

Congenital abnormalities of the lymphatics system and trauma should be considered as the most important etiological factor in children.2,4,5 A study was conducted on 35 patients to know the etiology and prognosis of CA. More than 90% cases were due to malignancy that included mainly lymphomas and abdominal carcinoma, cirrhosis, and retroperitoneal surgery. These cases of malignant CA chiefly presented with extensive tumor dissemination with 1-year mortality rate of 80%. Cases of CA with cirrhosis were having refractoriness to treatment in 13 out of 15 cases with mortality rate 69%.9 Mycobacteria spp. is the most common cause of CA in HIV-infected patients.5,10,11

The possible mechanisms of CA are lymph node fibrosis or infiltration by malignancy obstructing the flow of chyle, leaking of chyle through a fistula into the peritoneal cavity due to congenital lymphangiectasis, and acquired thoracic duct obstruction with a lymphoperitoneal fistula causing chyle leakage from subserosal lymphatics.8 Paradoxical immune reconstitution inflammatory syndrome (IRIS) has also been documented in the development of CA.12 Fibrosis of lymph node secondary to tuberculosis was the possible mechanism in our case. But as the CA developed and progressed even after DOTS regime for tuberculosis in early stage, paradoxical IRIS may also be a possible contributory mechanism of development of CA in our case.

The clinical presentation of CA is characterized by progressive and painless abdominal distension, weight gain, sign of malnutrition along with symptoms, and signs of underlying conditions. Patient may also have chylothorax due to reflux of chyle across the diaphragm into the pleural cavities. Rarely, patients may have acute onset of CA with rapid weight gain and dyspnea especially in a patient who has undergone abdominal and thoracic surgery.13,14 Patients of CA should be advised for complete blood count, renal function tests, liver function tests, triglycerides, cholesterol, amylase, lipase, and lactate dehydrogenase (LDH). Ascitic fluid examination such as total and differential counts, biochemical examination, cytology for malignant cell, triglycerides level, cholesterol level, LDH, serum ascitic albumin gradient (SAAG) ratio, Gramâ&#x20AC;&#x2122;s staining, ADA, and acid-fast bacilli (AFB) and mycobacterial 15,16 culture.

CT of the abdomen is useful in identifying pathological intra-abdominal lymph nodes and masses. Lymphangiography is the gold standard to define causes of lymphatic obstruction, abnormal retroperitoneal nodes, leakage from dilated lymphatics, and fistulization but has several complications related to the volume and type of contrast used. Lymphoscintography is a less-invasive alternative to lymphangiography and can confirm an active lymphatic leak into the peritoneal cavity. These tests may be useful in selecting patients for surgery.17 Other investigations that are useful in CA are lymph node biopsy, laparoscopy, or laparotomy, bone marrow examination, and intravenous pyelography.3,13 Chyle is grossly milky in appearance similar to the peripheral lymph. In vitro characteristics of chylous fluid are its separation into a creamy layer on standing, alkaline pH, specific gravity between 1.010 and 1.054,

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GASTROENTEROLOGY total protein that varies from 1.4 to 6.4 g/dL, fat content of 0.4%–4%, total solids 14%, positive staining of fat globules with Sudan red stain, and normal glucose, amylase, and cholesterol.18 CA contain high triglycerides usually higher than 200 mg/dL, although some use a cut-off value of 110 mg/dL.2,7,15 Some authors have identified an elevated ascites, plasma triglyceride ratio between 2:1 and 8:1, as being indicative of CA.4 CA is differentiated from pseudochyle and chyliform ascites by the presence of high triglyceride content that is low in pseudochyle and chyliform ascites.19 Chyliform ascites contain lecithin–globulin complex due to fatty degeneration of cells and pseudochylous ascites fluid is milky in appearance due to the presence of pus.3,13 Casafont et al20 conducted a study on 22 patients of CA (11 cirrhotic and 11 noncirrhotic) to know the characteristic of fluid in cirrhotic and noncirrhotic patients. The cirrhotic patients with CA showed lower protein (1.3 ± 0.74 mg/dL; p = 0.002) and cholesterol concentration (46.0 ± 45.2 mg/dL; p = 0.02) in ascitic fluid than noncirrhotic patients (3.1 ± 1.09 mg/dL and 100.85 ± 41.7 mg/dL, respectively). In addition, the cellularity in the ascitic fluid was also lower in cirrhotic patients ([209.09 ± 113.96 cell/mm3] vs [831.8 ± 945.08 cell/mm3; p < 0.05]). This difference was proposed because of dilutional mechanism due to the combination of “clear” ascites secondary to portal hypertension and CA. Four patients (18.18%) presented high ADAs in the ascitic fluid in the absence of tuberculous peritonitis.

Furthermore, CA could be the cause of an elevation in ADA in the absence of tuberculous peritonitis.20 CA can be managed by treating the underlying cause, nonpharmacological treatment, pharmacological treatment, and surgical treatment. In most conditions, management of underlying condition especially infective, inflammatory, or hemodynamic causes results in complete resolution of CA. Nonpharmacological treatments include dietary modification with salt and water restriction, elevation of legs, and stocking.

Dietary modifications include high-protein diet and use of a low-fat diet with medium-chain triglyceride supplementation that reduces the production and flow of chyle. This is because medium-chain triglycerides are absorbed directly into the intestinal cells and transported as fatty acids and glycerol directly to liver via the portal vein, whereas long-chain triglycerides need conversion to monoglycerides and free fatty acids that are transported as chylomicrons to the intestinal lymph ducts.21–23 Orlistat can be tried when patient have difficulty in complying with a low-fat diet.24 Dietary

modification is effective in 50% cases and should be maintained for several months after resolution of CA. If CA persists despite dietary management, the next step may involve bowel rest and the institution of total parenteral nutrition (TPN). Bowel rest and TPN are postulated to be beneficial in patients with posttraumatic or postsurgical CA and are effective by fulfilling the nutritional requirement of these patients and decreasing the production of lymph and allowing bowel rest. TPN is effective in 60%–80% cases of CA not responding to dietary modification and should be given for 2–6 weeks.23,25 Pharmacological management includes diuretics, somatostatin or octreotide, and etilefrine. Somatostatin or octreotide have been reported to be useful in some cases and help in closing fistula more rapidly; they also help in inhibition of lymph fluid excretion through specific receptor found in the normal intestinal wall of the lymphatic vessels.19 Mincher et al reported 100% resolution of CA in seven patients treated with subcutaneous octreotide and a fatfree diet.18 Etilefrine, a sympathomimetic drug that acts by contracting the smooth muscle of the thoracic duct thereby decreasing the flow of the chyle, is also effective in the management of CA.26 Embolization of cisterna chyle by fibered endovascular coil, gelatin, sponge, and doxycycline can be tried for management of CA.27 Surgery is beneficial in patients with postoperative, neoplastic, and congenital causes after identifying the site of leakage or the presence of fistula by a lymphangiogram or lymphoscintigraphy.4,28 Aalami et al conducted a study on 51 cases and found 41% effectivity of surgical management that is dependent on accurate localization of the defect.4 The optimal timing of surgery remains controversial, but most authors recommend a trial of conservative measures for at least 4–8 weeks before surgical intervention.

Paracentesis should be performed to relieve abdominal discomfort in large and symptomatic ascites and can be repeated as needed especially in end-stage disease not amenable to medical or surgical management. But, paracentesis has been implicated in prolongation of leaks, worsening of protein loss, nutritional depletion, and infectious complications.29 Peritoneovenous shunt (LeVeen or Denver shunt) is indicated in patients of refractory CA who are too ill to undergo surgical exploration for direct repair, but this is associated with high rate of complications such as sepsis, disseminated intravascular coagulopathy, electrolyte imbalance, small bowel obstruction, risk for air embolism, and high rate of shunt closure in majority of cases because of the high viscosity of the chyle.30,31

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GASTROENTEROLOGY So, management of CA gradually increases in invasiveness, escalating from dietary manipulation to radiographic intervention and, ultimately, surgical options. In a large review of 156 cases, 67% resolved after conservative measures and 33% required surgery.32 CA is associated with nutritional depletion, immunological depletion, and septicemia out of which sepsis is the most common complication leading to sudden death of patient.

CONCLUSION CA is a challenging clinical condition commonly associated with abdominal malignancy and cirrhosis in developed countries and tuberculosis and filariasis in developing countries. It is associated with high morbidity and mortality due to the associated comorbid condition. The outcome depends on early diagnosis and prompt treatment of underlying condition especially in the context of treatable cause such as tuberculosis that is very common in our country.

Acknowledgment The first author would like to extend his gratitude and sincere thanks to all those who helped him to complete this study.

He would also like to thank the departments of medicine, surgery, pulmonology, pathology, microbiology, biochemistry, and radiology for providing him adequate facility that helped him to carry out this study. He owes great sense of indebtedness to the Dean, SRMS-IMS, Bhojipura, Bareilly, for permitting him to carry out this study.

REFERENCES 1. Nix JT, Albert M, Dugas JE, Wendt DL. Chylothorax and chylous ascites: a study of 302 selected cases. Am J Gastroenterol 1957;28(1):40-53.

2. Press OW, Press NO, Kaufman SD. Evaluation and management of chylous ascites. Ann Intern Med 1982;96(3):358-64.

3. Wolf DC, Katz J. Chylous Ascites. Available at: http:// emedicine.medscape.com/article/18777-overview 4. Aalami OO, Allen DB, Organ CH Jr. Chylous ascites: a collective review. Surgery 2000;128(5):761-78.

5. Sathiravikarn W, Apisarnthanarak A, Apisarnthanarak P, Bailey TC. Mycobacterium tuberculosis associated chylous ascites in HIV-infected patients: case report and review of the literature. Infection 2006;34(4):230-3.

6. Manson-Bahr PEC, Bell JR. Filariasis. In: Manson Bahr’s Textbook of Tropical Disease. ELBS:London;1977.

7. Frick E, Scholmerich J. Etiology, diagnosis and management of noncirrhotic ascites. In: Ascites and Renal Dysfunction in Liver Disease. Arroyo V, Gines P, Rodes J, Schrier RW (Eds.). Blackwell Science: Malden 1999:116-25.

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8. Browse NL, Wilson NM, Russo F, Hassan HA, Allen DR. Aetiology and treatment chylous ascites. Br J Surg 1992;79:1145-50.

9. Sultan S, Pauwels A, Poupon R, Levy VG. Chylous ascites in adults: etiological, therapeutic and prognostic aspects.

Apropos of 35 cases. Ann Gastroenterol Hepatol (Paris) 1990;26(5):187-91.

10. Keaveny AP, Karasik MS, Farber HW. Successful treatment of chylous ascites secondary to Mycobacterium avium complex in a patient with the acquired immune deficiency syndrome. Am J Gastoenterol 1999;94:1689-90.

11. Ekwacani CN. Chylous ascites, tuberculosis and HIV/ AIDS: a case report. West Afr J Med 2002;21:170-2.

12. Rabie J, Lomp A, Goussard P, Nel E, Cotton M. Paradoxical tuberculosis associated immune reconstitution inflammatory syndrome presenting with chylous ascites and chylothorax in a HIV-1 infected child. J Trop Pediatr 2010;56(5):355-8.

13. Cárdenas A, Chopra S. Chylous ascites. Am J Gastroenterol 2002;97(8):1896-900.

14. Vettoretto N, Odeh M, Romessis M, Pettinato G, Taglietti L, Giovanetti M. Acute abdomen from chylous peritonitis: a surgical diagnosis. Case report and literature review. Eur Surg Res 2008;41:54-7.

15. Runyon BA. Care of patients with ascites. N Engl J Med 1994;330:337-42.

16. Uriz J, Cárdenas A, Arroyo V. Pathogenesis, diagnosis and treatment of ascites in cirrhosis. Baillieres Best Pract Res Clin Gatroenterol 2000;14:927-43.

17. Pui MH, Yueh TC. Lymphoscintigraphy in chylurea, chyloperitoneum and chylothorax. J Nucl Med 1998;39:1292-6.

18. Dreznik Z, Dinbar A, Wolfstein I, Tulchinsky DB. Acute chylous peritonitis: a case report with a review of the literature. Isr J Med Sci 1973;9:89-91.

19. Nakabayashi H, Sagara H, Usukura N, Yashimitsu K, Imamura T, Leta T, et al. Effect of somatostatin on the flow rate and triglyceride levels of thoracic duct lymph in normal and vagotomised dogs. Diabetes 1981;30(5):440-5.

20. Casafont F, Lopez-Arias MJ, Crespo J, Duenas C, SanchezAntolin G, Rivero M, et al. Chylous ascites in cirrhotic and non-cirrhotic. Gastroenterol Hepatol 1997;20(6):291-4.

21. Weinstein LD, Scanlon GT, Hersh T. Chylous ascites.

Management with medium-chain triglycerides and exacerbation by lymphangiography. Am J Dig Dis. 1969;14(7):500-9.

22. Leibovitch I, Mor Y, Golomb J, Ramon J. The diagnosis and management of postoperative chylous ascites. J Urol 2002;167(2Pt.1):449-57.

23. Baniel J, Foster RS, Rowland RG, Bihrle R, Donohue JP. Management of chylous ascites after retroperitoneal lymph node dissection for testicular cancer. J Urol 1993;150:1422-4.

24. Chen J, Lin RK, Hassanein T. Use of orlistat (xenical) to treat chylous ascites. J Clin Gastroenterol 2005;39(9):831-3.

GASTROENTEROLOGY 25. Petrasek AJ, Ameli FM. Conservative management of chylous ascites complicating aortic surgery: a case report.

Cab J Surg 1996;39(6):499-501.

26. Shah SS, Ahmed K, Smith R, Mallina R, Akbari P, Khan MS. Chylous ascites following radical nephrectomy: a case report. J Med Case Rep 2008:2:3.

27. Cope C. Diagnosis and treatment of postoperative chyle leakage via percutaneous transabdominal catheterization of the cisterna chyli: a preliminary study. J Vasc Interv Radiol 1998;9(5):727-34.

28. Bauwens K, Jacobi CA, Gellert K, Aurisch R, Zieren HU. Diagnosis and therapy of postoperative chyloperitoneum.

Chirurg 1996;67(6):658-60.

29. Pabst TS 3rd, McIntyre KE Jr, Schilling JD, Hunter GC, Bernhard VM. Management of chyloperitoneum after abdominal aortic surgery. Am J Surg 1993;166(2): 194-9.

30. Ablan CJ, Littoy FN, Freeark RJ. Postoperative chylous ascites: diagnosis and treatment. A series report and literature review. Arch Surg 1990;125:270-3.

31. Voros D, Hadziyannis S. Successful management of postoperative chylous ascites with a peritoneo-jugular shunt. J Hepatol 1995;22:380.

32. Leibovitch I. Postoperative chylous ascites – the urologist’s view. Drug Today (Barc) 2002;38:687-97.

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India Has Too Few Postgraduate Specialists Postgraduates (PG) seats in India are much less than in the US. The distribution is Cardiology 250 (US 781); Diabetology/Endocrinology 50 (US 251); Gastroenterology 93 (US 433); Hematology 13 (US 523); Nephrology 84 (US 416); Neurology 159 (US 592) and Oncology 48 (508).

Only 250 new cardiologists are added to the pool in India with largest number of heart patients in the world.

It’s worse for diabetics. Even when the country is heading towards becoming the diabetes capital of the world, we have only 50 PG seats in endocrinology. The US, on the other hand, has 250 PG seats in this subject.

Tuberculosis is the sixth highest contributor to the number of deaths in India but the country has only 307 specialized doctors graduating in pulmonary medicine every year.

Cancer the most feared disease has only 47 seats in India. In contrast, the US has 508 seats.

While a mother dies every 10 minutes in India, we have only around 1,400 obstetrics and gynecology seats. There are about 93 seats in gastroenterology, as against 433 in the US, even when diarrheal diseases are the second highest contributor to deaths in India.

On the other hand, there are 5,833 para-clinical PG seats in the country. Pathology tops with 1,201 MD seats, microbiology has 724 and community medicine 736, biochemistry has been allotted 481 seats and physiology 672.

Doctors say every unit in a medical college in the country can accommodate upto five PG students, according to MCI norms. If that’s the case, the number of PG seats can go upto 38,390 in the current scenario, but will that happen?

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HEMATOLOGY

Thrombotic Thrombocytopenia Purpura Refractory to Plasmapheresis Treated Successfully with Rituximab SHAH VH*, PATEL A†, CHAVDA RK‡

ABSTRACT Thrombotic thrombocytopenia purpura (TTP) is a rare hematological disease and only 20%–30% of patients present with classic pentad. About 20% of patients with TTP are resistant to plasma exchange. We have described a 28-year-old female patient with TTP who did not have classic pentad of TTP. We ruled out all other differential diagnosis. She was refractory to plasmapheresis and was treated successfully with rituximab. It was thus concluded that on the basis of the literature review, rituximab should be considered in TTP patients who fail to respond after 7–14 days of standard treatment with daily plasmapheresis and glucocorticoids.

Keywords: TTP, plasmapheresis, rituximab, thrombocytopenia

T

hrombotic thrombocytopenia purpura (TTP) is caused by the development of hyaline thrombi in the microvasculature resulting in thrombocytopenia, microangiopathic hemolytic anemia, and organ dysfunction. Classic pentad includes microangiopathic hemolytic anemia, thrombocytopenia, fever, neurological abnormalities and renal failure.

However, many patients have neither neurologic nor renal function abnormalities.

All such patients are diagnosed via the presence of thrombocytopenia and microangiopathic hemolytic anemia without another clinically apparent cause for the same. About 20% of TTP are resistant to plasma exchange (PE). We describe a patient presenting with a first episode of acute refractory TTP in whom remission was not achieved by plasmapheresis and steroids.

He was successfully treated with rituximab. We also review the literature on the role of rituximab in a first episode of acute refractory idiopathic TTP.

CASE REPORT A 28-year-old female patient was diagnosed and treated for TTP in a private hospital and was referred

*Third Year Resident †Second Year Resident ‡Professor and Head Dept. of Medicine Government Medical College, Surat, Gujarat Address for correspondence Dr Vitrag Shah 3-4, Kailash Nagar, Beside Jogani Nagar, Anand Mahal Road, Surat - 395 009, Gujarat E-mail: dr.vitrag@gmail.com

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to our hospital for plasmapheresis after 2–3 months.

The patient had history of cesarean section and healthy twin babies were delivered uneventfully. After 4–5 days of delivery, she complained of low-grade fever and bruises at various sites of venipuncture. Laboratory reports showed anemia and thrombocytopenia and peripheral smear showed schistocytes, suggestive of microangiopathic hemolytic anemia, and raised serum lactate dehydrogenase (S-LDH); no other features were suggestive of classic pentad of TTP, no other specific investigations were done, and the patient was started with steroids and five cycles of plasmapheresis were given in the private hospital. Platelet count before starting treatment was 28,000/mm3 and S-LDH was 1,180; after five cycles of plasmapheresis, platelet count was 35,000/mm3 and S-LDH was 855.

The patient was then referred to our hospital for further cycles of plasmapheresis, but as the patient had no improvement with five cycles of plasmapheresis and steroids, we also investigated for all possible differential diagnosis.

The patient had no significant past or family history and no significant drug history.

The patient was diagnosed to have hypertension during third trimester of her pregnancy and she complained of pedal edema since last trimester; urine albumin was 1+ to 2+, HELLP syndrome could have presented similarly but liver enzymes were normal; it has been three months since delivery, yet the platelet count did not improve, so we ruled out HELLP syndrome.

HEMATOLOGY Since blood pressure was 140/90 mmHg and fundus was normal, malignant hypertension leading to similar presentation was also ruled out.

Platelet count after 24 h of first dose of rituximab injection and two doses of vincristine was 1,28,000/mm3, and S-LDH was 628.

Chest X-ray and ultrasonography of the abdomen were normal. Electrocardiography was normal. Reticulocyte count was 4.5%. On admission, Hb was 9.9 g%, TC was 8,800/mm3, platelet count was 32,000/mm3, and MCV 101 µm3. S-TSH was normal. RFT and LFT were normal.

HIV, HbsAg, and HCV were negative. RA and CRP were negative. WBC count was normal and since there was no sign suggestive of sepsis, it was also ruled out.

After 24 h of four doses of vincristine and rituximab injections, the patient’s platelet count was 2,2,8,000/mm3 and S-LDH was 355. We discharged the patient and on follow-up after one month, the platelet counts were 2,58,000/mm3 and S-LDH was 245.

FBS was 170, PP2BS was 230, and HbA1c was 5.3, therefore patient was having steroid-induced impaired glucose tolerance and impaired fasting hyperglycemia.

PT and aPTT was normal, FDP was negative, and there was no history of stillbirth and abortion, therefore antiphospholipid antibody syndrome and disseminated intravascular coagulation was also ruled out. ICT and DCT were negative, so Evans syndrome was also ruled out. ANA was negative, so we ruled out systemic lupus erythematosus too.

S-Vit B12 was 156 pg/mL and the patient was not on any Vit B12 and folic acid supplements, so we started Vit B12 injection and folic acid tablet as megaloblastic anemia can also be associated with TTP or itself can also present as anemia, thrombocytopenia, and raised S-LDH and reticulocyte counts.

While ruling out other causes, we continued steroids and plasmapheresis, but again even after further five cycles of daily plasmapheresis and Vit B12 injection and folic acid tablet, platelet count was 30,000/mm3; the patient further developed transfusion-related acute lung injury (TRALI) during fifth cycle of plasmapheresis and recovered from TRALI within 48 h with noninvasive ventilator support. So, we stopped plasmapheresis and tapered and stopped steroids too.

We also went for bone marrow examination to rule out any malignancy or leukemia, but bone marrow aspiration and biopsy was absolutely normal except mild megaloblastic changes.

So we considered it as TTP refractory to steroids and plasmapheresis with megaloblastic anemia. We then started giving vincristine injection 1.4 mg/m2 (2 mg) to the patient on days 1, 4, 7, and 10.

Platelet count did not improve significantly after first two doses of vincristine injection, so we started giving rituximab injection 375 mg/m2 (500 mg) per dose to the patient once every week for 4 weeks.

DISCUSSION TTP is a rare disease and diagnosis of TTP is clinical.

Patients with TTP have unusually large multimers of von Willebrand factor (vWF) in their plasma. Patients with TTP lack a plasma protease (ADAMTS13) that is responsible for the breakdown of these ultralarge vWF multimers or inhibitor (antibody), so steroids and immunosuppressive agents like rituximab are useful in TTP. However, measurement of ADAMTS13 activity is not required for diagnosis or starting treatment.

Many patients have neither neurologic nor renal function abnormalities. For example, approximately 50% of patients with TTP-hemolytic uremic syndrome (TTP-HUS) associated with a severe (i.e., <10%) deficiency of ADAMTS13 activity had no or minimal neurologic abnormalities and no evidence for renal failure.

However, all such patients are diagnosed via the presence of thrombocytopenia and microangiopathic hemolytic anemia without another clinically apparent cause for the same.

TTP usually responds well to PE treatment in the majority of patients. Although there is no generally accepted definition of refractory disease, escalation of therapy should be considered after 7–14 days of adequate treatment with daily PE and corticosteroids if the clinical course deteriorates during that time.

In such cases, intensification of PE or the addition of immunosuppressive drugs such as vincristine, cyclophosphamide, or cyclosporine has been recommended.

Treatment with rituximab, a chimeric monoclonal antibody directed against the CD 20 antigen present on B lymphocytes, leads to clearance of B lymphocytes responsible for antibody production by complementdependent cytotoxicity, antibody-dependent cellular cytotoxicity, or directly by inducing apoptosis. So, it has a role in the treatment of acute refractory and relapsing autoimmune TTP due to ADAMTS-13 inhibitory antibodies.

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HEMATOLOGY We report on a patient with acute TTP in whom remission was not achieved by initial treatment consisting of PE, plasma infusion, and corticosteroids, followed by vincristine and the patient had also complication of plasma infusion in the form of TRALI. So, we started rituximab injection on the patient.

Treatment with rituximab appears to be both effective and safe, possibly leading to a significant reduction in plasma requirement and complications of FFP transfusion like TRALI and TACO, or transmission of infection.

CONCLUSION This case emphasized the importance of ruling out other differential diagnosis before treating TTP if classic pentad is not present as it is a rare disease. We also looked for associated diseases – other causes of anemia and thrombocytopenia (S-Vit B12 deficiency in this case). Bone marrow examination should be done in all cases prior to starting secondary treatment of TTP (immunosuppressants) to rule out associated disorders or malignancy or leukemia.

We conclude that on the basis of the literature review, rituximab should be considered in TTP patients who fail to respond after 7–14 days of standard treatment with daily plasmapheresis and glucocorticoids. In future, rituximab may be considered as primary treatment of choice too considering hazards of PE with infusion and variable response rate.

REFERENCES 1. Rüfer A, Brodmann D, Gregor M, Kremer Hovinga JA, Lämmle B, Wuillemin WA. Rituximab for acute plasma-

refractory thrombotic thrombocytopenic purpura. Swiss Med Wkly 2007;137:518-24.

2. George JN. How I treat patients with thrombotic thrombocytopenic purpura. Blood 2010;116:4060.

3. Scully M, Hunt BJ, Benjamin S, et al. Guidelines on the diagnosis and management of thrombotic thrombocytopenic purpura and other thrombotic microangiopathies. Br J Haematol 2012;158:323.

4. Fakhouri F, Vernant JP, Veyradier A, Wolf M, Kaplanski G, Binaut R, et al. Efficiency of curative and prophylactic treatment with rituximab in ADAMTS13-deficient thrombotic thrombocytopenic purpura: a study of 11 cases. Blood 2005;106(6):1932.

5. Ahmad A, Aggarwal A, Sharma D, Dave HP, Kinsella V, Rick ME, et al. Rituximab for treatment of refractory/ relapsing thrombotic thrombocytopenic purpura (TTP).

Am J Hematol 2004;77(2):171.

6. Froissart A, Buffet M, Veyradier A, Poullin P, Provôt F, Malot S, et al. Efficacy and safety of first-line rituximab in severe, acquired thrombotic thrombocytopenic purpura with a suboptimal response to plasma exchange.

Experience of the French Thrombotic Microangiopathies Reference Center. Crit Care Med 2012;40(1):104-11.

7. Jasti S, Coyle T, Gentile T, Rosales L, Poiesz B. Rituximab as an adjunct to plasma exchange in TTP: a report of 12 cases and review of literature. J Clin Apher 2008; 23(5):151.

8. Rock G, Porta C, Bobbio-Pallavicini E. Thrombotic thrombocytopenic purpura treatment in year 2000.

Haematologica 2000;85:410-9.

9. Wun T, Besa EC. Thrombotic thrombocytopenic purpura.

MedScape.

10. Kaplan AA, George JN. Treatment and prognosis of thrombotic thrombocytopenic purpura: hemolytic uremic syndromes in adults. UpToDate, Wolters Kluwer.

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Travel More Than Doubles Risk of Blood Clots Long–distance travel can lead to potentially fatal blood clots in some people and the risk grows with the length of the trip. Those at increased risk of blood clots include cancer patients, people who have recently had major surgery such as a joint replacement and women on birth control pills.

In general, travel is associated with a nearly 3–fold increase in the risk of venous thromboembolism (blood clots that form in the veins), often in the legs. If such a clot dislodges and travels to the lungs, it can cause a potentially fatal condition, called pulmonary embolism.

A combination of factors including dehydration and hours of sitting in cramped conditions explains why some people develop blood clots.

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INFECTIOUS DISEASES

“Buffalo Hump” in a Female on Zidovudine-Based Antiretroviral Therapy: A Case Report AGRAWAL P*, GAUTAM A*, CHANDRA S*, ANEEZ A†, GUPTA A†

ABSTRACT We report a case of a 35-year-old HIV-positive female patient without any other premorbid illness on antiretroviral therapy (zidovudine, lamivudine, and nevirapine) presenting to us with cervical lipomatosis (“buffalo neck”), which is an uncommon side effect of zidovudine-based regimens while it is not an uncommon side effect of stavudine-based regimens.

Keywords: Antiretroviral therapy, cervical lipomatosis, side effect CASE REPORT A 35-year-old female came to our OPD with the complaint of swelling behind the neck for 2 months that was progressive and not painful. She was diagnosed human immunodeficiency virus (HIV) positive 2 years back for which antiretroviral therapy (ART) (zidovudine, lamivudine, and nevirapine) was started.

There were no other medications. There was no history of fever, significant weight loss, cough, loose stools, or oral ulcerations. Menstrual cycles were normal.

On examination, the patient was moderately built, well-nourished, and afebrile with stable vitals. Pallor, clubbing, or pedal edema was not found. Systemic examination was within normal limits. On local examination of the neck, there was a soft 10 × 6 cm diffuse swelling in the nape of neck without any erythema, cough impulse, nontender, fluctuant, and nonreducible; no similar swelling was found elsewhere (Fig. 1).

Investigations showed mild normocytic normochromic anemia (hemoglobin [Hb]: 10.4), erythrocytes sedimentation rate (ESR): 21 mm/h, liver functional test (LFT), renal function test (RFT): Normal, CD4

*Assistant Professor †Junior Resident (Third Year), Postgraduate Dept. of Medicine, Sarojini Naidu Medical College Agra, Uttar Pradesh Address for correspondence Aneez A Postgraduate Dept. of Medicine Sarojini Naidu Medical College, Agra, Uttar Pradesh E-mail: aneeza110@gmail.com

count: 286 cells/dL, and Venereal Disease Research Laboratory (VDRL): Negative; chest X-ray was within normal limits and lipid profile showed TG: 170 mg%, cholesterol: 122 mg%, and very low-density lipoprotein (VLDL): 34 mg%.

DISCUSSION Lipodystrophy is a disorder of fat metabolism that may be clinically evident as adipose tissue accumulation (in intra-abdominal, cervical, or breast and lipomas), lipoatrophy (loss of fat in the face, limbs, and buttocks), and metabolic abnormalities (e.g., insulin resistance, diabetes, dyslipidemia, or lactic acidosis). 1 The body composition changes in HIV-associated lipodystrophy include subcutaneous fat atrophy (facial fat atrophy, gluteal fat wasting, peripheral fat atrophy, and subcutaneous abdominal fat atrophy), visceral abdominal fat hypertrophy, dorsocervical fat hypertrophy, breast hypertrophy, and submandibular hypertrophy.2 Protease inhibitors (PIs) have been associated with fat accumulation and the nucleoside analog reverse transcriptase inhibitors (NRTIs) stavudine, didanosine, and zidovudine have been associated with fat loss (lipoatrophy).3,4 The pathogenesis of lipodystrophy in HIV-infected patients is multifactorial and includes host factors, direct effects of ART, fat redistribution syndrome, direct effects of HIV infection (increased TGs and decreased HDL), and insulin resistance.

NRTIs inhibit mitochondrial DNA polymerase and cause mitochondrial toxicity by interfering with respiratory chain complexes. This result is impaired fatty acid oxidation and intracellular accumulation

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INFECTIOUS DISEASES

Figure 1. A soft diffuse 10 × 6 cm swelling in the nape of neck.

of TGs and lactate.5 The frequency of this side effect among NRTIs is zalcitabine > didanosine > stavudine > lamivudine > zidovudine. PIs inhibit maturation of sterol response element-binding proteins and affects intracellular fatty acid and glucose metabolism and adipocyte differentiation; they also downregulate peroxisome proliferator-activated receptor gamma necessary for adipocyte differentiation and function.

Risk factors include old age, female sex, and race.

Strategies to minimize lipodystrophy include switching to treatment with regimens that include drugs associated with lower risk of lipoatrophy (tenofovir, abacavir, lamivudine, and emtricitabine).4 Treatment modalities to reverse fat redistribution include exercise, metformin liposuction, and fat transplantation.

clinical and treatment is by exercise and metformin liposuction.

REFERENCES 1. Lo JC, Mulligan K, Tai VW, Algren H, Schambetan M. “Buffalo hump” in men with HIV infection. Lancet 1998;351(9106):867-70.

2. Gervasoni C, Ridolfo AL, Trifiro G, Santrambrogio S, Norbiato G, Musicco C. Redistribution of body fat in HIV infected women undergoing combined antiretroviral therapy. AIDS 1999;13(4):465-71.

3. Nolan D, Hammond E, James I, McKinnon E, Mallas S. Contribution of nucleoside-analogue reverse transcriptase inhibitor therapy to lipoatrophy from the population to the cellular level. Antivir Ther 2003;8(6):617-26.

CONCLUSION

4. Sattler FR. Pathogenesis and treatment of lipodystrophy: what clinicians need to know. Top HIV Med 2008;16(4): 127-33.

Buffalo hump is a common side effect of ART but is uncommonly seen with zidovudine. The diagnosis is

5. Mallewa JE, Wilkins E. HIV-associated lipodystrophy: a review of underlying mechanisms and therapeutic options. J Antimicro Chemother 2008;62:648–60.

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OBSTETRICS AND GYNECOLOGY

A Study of Outcome of Induction of Labor: Medical Versus Surgical KAUR P*, KAUR M*, KAUR K†, MANJIT MK‡, GOEL P§

ABSTRACT The aim of this article is to study the outcome of induction of labor using medical and surgical methods. Two hundred and twelve patients with >28 weeks pregnancy requiring induction of labor were studied for a period of 1 year in the Government Medical College and Rajindra Hospital, Patiala, Punjab. In 25 patients (Group 1), artificial rupture of membranes was done to induce labor, 52 patients were induced with oxytocin, and 83 patients were induced with misoprostol (Group 2). In 52 patients (Group 3), medical and surgical methods were used in combination. The incidence of labor induction came out to be 13.86%.

The induction delivery interval was shortest in Group 3 (85.42% delivered within 12 h) compared to 62.72% and 64.60% in Groups 1 and 2, respectively. The lower segment cesarean section rate was least in Group 3 (7.69% vs 12% and 16.30%, respectively).

Postpartum hemorrhage and maternal pyrexia were observed more in Group 1 (20% and 8%) than in Group 2 (2.96% and 0.74%) and Group 3 (5.77% and 3.85%). All methods were equally effective in induction of labor in terms of induction delivery interval and mode of delivery.

Keywords: Induction of labor, misoprostol, oxytocin

I

nduction of labor (IOL) implies stimulation of uterine contractions before the spontaneous onset of labor with or without ruptured fetal membranes for the purpose of accomplishing delivery.1 IOL is indicated when the benefit to either the mother or fetus outweighs that of continuing the pregnancy.2 However, all inductions are not successful and some may develop complications. In nullipara with an unfavorable cervix undergoing labor induction, cesarean delivery rate is more than 30%.3 This study was carried out to find out the incidence of IOL in our institution, to find the indications for which IOL is performed, to find out the most effective method for IOL, to study the complications of induced labor, and to find out the failure rate of IOL.

*Associate Professor †Professor ‡Professor and Head §Junior Resident Dept. of Obstetrics and Gynecology Government Medical College and Rajindra Hospital, Patiala, Punjab Address for correspondence Dr Parneet Kaur House No. 151, Punjabi Bagh Near Klair Orthopedic Centre Patiala 147 001, Punjab E-mail: parneetkd@yahoo.co.in

METHODS The present study was conducted for a period of 1 year from January 1, 2009 to December 31, 2009 in the labor room of the Dept. of Obstetrics and Gynecology, Government Medical College and Rajindra Hospital, Patiala. A total of 212 patients were studied and were divided into three groups according to the method of induction employed. ÂÂ

Group 1: Cases in which mechanical or surgical IOL, that is, artificial rupture of membranes (ARM) was done on 25 patients. Patients in this group were less as in most patients either the os was closed or the head was high up; therefore, induction by ARM could not be done.

ÂÂ

Group 2: Cases in which medical induction was done. This group was subdivided into two subgroups: (A) Oxytocin by intravenous infusion in 52 patients. (B) Misoprostol sublingual or per vaginum given in 83 patients.

ÂÂ

Group 3: Cases in which medical and surgical methods were used in combination 52 patients.

This study was performed based on two criteria: ÂÂ

Inclusion criteria: Cases with singleton pregnancy, of >28 weeks gestation and parity ≤ 4 were included in this study.

ÂÂ

Exclusion criteria: Included cases with previous cesarean section, myomectomy, hysterotomy,

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OBSTETRICS AND GYNECOLOGY or any other scar on the uterus, contracted pelvis, cephalopelvic disproportion (CPD), malpresentation, active herpes simplex infection, and placenta previa; any clinical evidence of fetal distress, or history of allergy to prostaglandins.

On admission of the patient to the hospital, the particulars of the patient, such as name, age, parity, detailed history of pregnancy, menstrual history with last menstrual period and obstetric history, were recorded. Family history, past history, and drug history were also noted. A thorough general physical examination was done followed by local examination, which included per abdomen examination and per vaginal examination. The indication for IOL of each case was noted and the method of induction was chosen according to the individual case. In cases where the Bishop Score was five or less, that is, unfavorable cervix, ripening of cervix was done by intracervical (0.5 mg)/intravaginal (1 mg) instillation of prostaglandin gel or intravenous oxytocin drip. Cervical scoring was

repeated after 6 h. In cases where cervix was ripe, IOL was started by any of the method described above.

In those cases where cervix was unripe even after 12 h of first instillation, second dose of prostaglandin was instilled. Time of onset of regular painful uterine contractions was taken as time of initiation of labor.

OBSERVATIONS The following observations were made in all the cases: (1) progress of labor, (2) mode of delivery, and (3) any maternal complications. The observations were recorded and analyzed, and conclusions were drawn.

The incidence of IOL in the present study group was 13.86%.

The most common indications for IOL (Table 1) were postdated pregnancy (29.72%) and hypertensive disorders of pregnancy (28.77%).

Table 2 shows that maximum number of patients (85.42%) in Group 3 were delivered vaginally within

Table 1. Indications for Induction of Labor Group 1

Group 2

Group 3

Total

%age

HDP

10

40

11

61

28.77

Postdated pregnancy

4

38

21

63

29.72

PROM/LPV

2

30

–

32

15.09

APH

6

1

6

13

6.13

Congenital malformation

–

5

5

10

4.72

BOH

1

1

5

7

3.30

Nonreactive NST

–

2

2

4

1.89

Hydraminos

2

–

2

4

1.89

IUD

–

18

–

18

8.49

Total

25

135

52

212

100

BOH, bad obstetric history; HDP, hypertensive disorders of pregnancy; IUD, intrauterine death; LPV, leaking per vaginum; NST, nonstress test; PROM, premature rupture of membranes.

Table 2. Induction–Delivery Interval Induction–delivery interval (in Hours)

Successful no. of patients (%age) (vaginal delivery) Group 1

Group 2

Group 3

0–6

10 (45.45)

25 (22.12)

21(43.75)

6–12

6 (27.27)

48 (42.48)

20(41.67)

12–18

3 (13.64)

21 (18.58)

4(8.33)

18–24

2 (9.09)

12 (10.62)

3(6.25)

>24

1 (4.54)

7 (6.19)

0(0)

Total

22

113

48

χ2 = 2.87; p = 0.5798 (not significant).

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OBSTETRICS AND GYNECOLOGY 12 h, 14.58% were delivered in 12–24 h, and none had induction–delivery interval >24 h. In Group 1 and Group 2, delivery within 12 h was accomplished in 62.72% and 64.60% cases, respectively, while 22.73% and 29.2%, respectively, took 12–24 h to deliver; but this difference was not statistically significant.

The maximum number of patients (90.39%) delivered vaginally were in Group 3, whereas 88% and 82.22%

of the patients were delivered vaginally in Group 1 and Group 2, respectively; but the difference was not statistically significant. The LSCS rate in Group 1, Group 2, and Group 3 was 12%, 16.30%, and 7.69%, respectively (Table 3).

In the present study, the most common maternal complication was PPH that occurred in 5.66% of the patients (Table 4).

Table 3. Mode of Delivery Mode of delivery

Group 1

Spontaneous vaginal delivery

22 (88%)

Outlet forceps delivery

Group 2

Group 3

111 (82.22%)

47 (90.39%)

Total No. of patients

%age

180

84.90

–

2 (1.48%)

1 (1.92%)

4

1.89

LSCS

3 (12%)

22 (16.30%)

4 (7.69%)

29

13.68

Total

25

135

52

212

100

χ2 = 2.87; p = 0.5798 (not significant).

LSCS, lower segment cesarean section.

Table 4. Maternal Complications in Different Study Groups Maternal complications

PPH Retained placenta Maternal pyrexia

Group 1

Group 2

Group 3

Total No. of patients

%age

5 (20%)

4 (2.96%)

3 (5.77%)

12

5.66

–

1 (0.74%)

2 (3.85)

3

1.42

2 (8%)

1 (0.74%)

2 (3.85%)

5

2.36

Cervical tear

–

4 (2.96%)

1 (1.92%)

5

2.36

Cesarean hysterectomy

–

–

–

–

–

Total

7

10

8

25

11.80

PPH, postpartum hemorrhage.

Table 5. Indications for Cesarean Section in Cases of Induced Labor Maternal complication

Group 1

Group 2

Group 3

Total No.

%age

Cervical dystocia

0

1

0

1

0.47

NPOL

2

1

0

3

1.42

Failed induction

0

2

0

2

0.94

Undiagnosed CPD

0

1

0

1

0.47

Fetal distress

1

13

3

17

8.02

Malposition

0

1

1

2

0.94

Abnormal uterine action

0

2

0

2

0.94

HELLP

0

1

0

1

0.47

Total

3

22

4

29

13.68

APH, antepartum hemorrhage; HELLP, hemolysis, elevated liver enzymes, low platelet count; NPOL, nonprogress of labor.

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OBSTETRICS AND GYNECOLOGY The most common indications for LSCS were fetal distress (8.02%) and NPOL (1.42%). The rate of failed induction was 0.94% (Table 5).

5.66% and 2.36%, respectively, whereas the study by Tan et al6 reported PPH and maternal pyrexia in 13.3% and 21%, respectively.

DISCUSSION

CONCLUSION

IOL is a valuable procedure in obstetrics, often undertaken in the interest of the mother or of the fetus or both. An ideal method of induction must be cost effective, must ensure efficacy and safety for the mother and the fetus with minimal induction delivery interval, and should be convenient for the patient and the medical staff.

All methods were equally effective in IOL in terms of induction delivery interval and mode of delivery but the combined method, that is, medical and surgical, had the best results.

The incidence of IOL in the present study (13.86%) is higher as compared to that reported by Arulkumaran et al (10% and 9.8%).4 In the present study, the most common indications for IOL were postdated pregnancy (29.72%) and HDP (28.77%). Boulvain et al5 also reported these two as the most common indications for IOL. In the present study, medical and surgical methods when used in combination gave the best results in terms of both induction–delivery interval (85.42% of the patients delivered within 12 h) and successful vaginal delivery (92.31%) as compared to when either of these methods were used individually; 72.72% and 65.18% of the patients were delivered within 12 h when induced by surgical methods and medical methods, respectively, and 88% and 83.7% of the patients delivered vaginally when induction was done by surgical and medical methods, respectively.

Out of total, 86.32% of the patients delivered vaginally and 13.68% underwent cesarean section, which is comparable to the study of Boulvain et al5 who reported vaginal delivery and cesarean in 87.88% and 12.12% of the patients, respectively.

PPH and maternal pyrexia were the most common maternal complications observed and occurred in

ACKNOWLEDGMENT The authors would like to thank Dr Surjit Kaur Bajwa, our Ex-Professor and Head, for her continuous guidance and support during the study.

REFERENCES 1. American College of Obstetricians and Gynecologists.

Technical Bulletin Number 157-July 1991. Induction and augmentation of labor. Int J Gynecol Obstet 1992;39:139.

2. Abramovici D, Goldnasser S, Mabie BC, Mercer BM, Goldwasser RN, Sibai BM. A randomized comparison of oral misoprostol versus Foley catheter and oxytocin for induction of labor at term. Am J Obstet Gynec 1999;181:1108-12.

3. Johnson DP, Davis NR, Brown AJ. Risk of cesarean delivery after induction at term in nulliparous women with an unfavourable cervix. Am College Obstet Gynecol 2003;188:1565-9.

4. Arulkumaran S, Gibb DM, Tambyraja RL, Heng SH, Ratnam SS. Failed induction of labor. Aust N Z J Obstet Gynaecol 1985;25(3):190-3.

5. Boulvain M, Fraser WD, Marcoux S, Fontaine JY, Bazin S, Pinautt JJ, et al. Does sweeping of the membranes reduce the need for formal induction of labor? A randomized controlled trial. Br J Obstet Gynecol 1998;105:34-40.

6. Tan PC, Valiapan SD, Tay PYS, Omar SZ. Concurrent oxytocin with dinoprostone pessary versus dinoprostone pessary in labor induction of multiparas with infavourable cervix: a randomized placebo-controlled trial. Br J Obstet Gynaec 2007;114:824-32.

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OBSTETRICS AND GYNECOLOGY

Mullerian Agenesis: An Unusual Presentation as Hematometra and Bilateral Hematosalpinx GUPTA S*, KUMARI A†

ABSTRACT A case of hematometra with bicornuate uterus and bilateral hematosalpinx in a 15-year-old girl complicated by vaginal agenesis and absent cervix is presented. She was managed by abdominal hysterectomy and bilateral salpingectomy. Bilateral ovaries were conserved.

Keywords: Mullerian agenesis, hematometra, hematosalpinx

M

ullerian agenesis occurs in 1 out of every 4,000–10,000 females.1 The independent occurrence of congenital hematometra without hematocolpos is a rare mullerian duct anomaly that results from a noncommunicating rudimentary horn with functioning endometrium or primary cervical atresia and absent upper vagina.2–4 Women affected by this disorder often have accompanying renal, skeletal, and other anomalies.5

We report a case of bicornuate uterus with hematometra and bilateral hematosalpinx in a 15-year-old girl who presented with acute abdominal pain and 6 × 4 cm pelviabdominal mass (Fig. 1).

CASE REPORT A 15-year-old unmarried female presented with complaint of primary amenorrhea with cyclical abdominal pain for past 12 months. Pain was relieved by oral analgesics. There were no bladder or bowel complains. Her general and systemic examinations were within normal limits. Examination per abdomen revealed a firm, well-defined, nontender, noncompressible, and nonreducible mass measuring 6 × 4 cm in left iliac fossa. Per rectal examination was

*Antenatal Medical Officer and Lecturer †Senior Resident Dept. of Obstetrics and Gynecology BRD Medical College Gorakhpur, Uttar Pradesh Address of correspondence Dr Ankita Kumari H. No. 727, Anand Vihar Colony Rapti Nagar, Arogya Mandir Gorakhpur, Uttar Pradesh-273 003 E-mail: drankita09@gmail.com

noncontributory. Per vaginal examination was not carried as she was unmarried.

All routine examinations revealed no obvious abnormality. An ultrasound scan of pelvis and abdomen revealed hematometra with bilateral hematosalpinx.

Computed tomography scan showed thick-walled cystic lesion in left lumbar region continuous with hematometra. Examination under anesthesia revealed a blind lower vagina of 2 cm. On rectal examination, tense and firm mass was felt.

A diagnostic laparoscopy was performed that revealed a bicornuate uterus with hematometra; bilateral fallopian tubes were distended and bluish in color suggestive of hematosalpinx. Both ovaries were normal. Stick-like band was seen between lower half of both mullerian ducts.

Figure 1. Intraoperative photograph showing bicornuate uterus with hematometra and bilateral hematosalpinx.

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OBSTETRICS AND GYNECOLOGY On laparotomy, bilateral hematosalpinx with bilateral normal ovaries and distended bicornuate uterus was found. The lower part of uterus, cervix, and upper three-fourth of vagina were not formed. Routine hysterectomy along with removal of both fallopian tubes was done. Both ovaries were conserved. The patient had an uneventful postoperative recovery. Her stitches were removed on the eight postoperative day and she was allowed to go home the same day.

DISCUSSION Complete cervicovaginal agenesis with a functioning endometrium in a bicornuate uterus is an extremely rare mullerian duct malformation.6 Only few cases of such abnormality have been reported along with their surgical procedures.

This 15-year-old girl had cyclical abdominal pain for last 12 months. As she was in perimenarchal age and presented with an abdominal mass, it was suspected to be due to cryptomenorrhea resulting from entrapped menstrual blood in the uterine cavity causing pain.

A pelviabdominal ultrasound showed hematometra.

Diagnostic laparoscopy confirmed bicornuate uterus with bilateral hematosalpinx with absent cervix and upper vagina.

Our case emphasizes that mullerian anomalies should be considered among the differential diagnosis of cyclical abdominal pain that responds poorly to analgesics. As developmental anomalies of urinary and mullerian tracts are commonly associated, the former anomalies should be specifically investigated before elective surgery is carried out.

The general consensus of treatment of these patients has been to remove the mullerian structures during initial operation so as to avoid postoperative complications.

The same principle of treatment was applied in the case described.

CONCLUSION When one encounters blocked uterus, it should be thoroughly evaluated especially in adolescents with relevant investigations keeping in mind the rare possibility of mullerian anomaly. Early diagnosis and prompt treatment is recommended in these patients to avoid future gynecological and obstetrical complications. Although technical advances favor reconstructive surgery for cervicovaginal agenesis, it must be emphasized that these complex procedures are not without complications resulting in recurrence of hematometra ultimately requiring hysterectomy. In this patient, the decision for hysterectomy was considered most appropriate to suit her social circumstances.

REFERENCES 1. Envans TN, Poland ML, Boving RL. Vaginal malformations.

Am J Obstet Gynaecol 1981;141:910-20.

2. Rana A, Gurung G, Begum SH, Adhikari S, Neupane BB. Hysterectomy for hematometra in a 15 years-old mentally handicapped girl with congenital cervicovaginal agenesis and concomitant ovarian adenoma. J Obstet Gynaecol Res 2008;34(1):105-7.

3. Garat JM, Martinez E, Aragona F, Gosalbez R. Cervical urinary atresia with hematometra: a rare case of urinary retention in a girl. J Urol 1984;132(4):772-3.

4. Khunda SS, Al-omari S. A new approach in the management of lower mullerian atresia. J Obstet Gynaecol 1998;18(6):566-8.

5. Miller PB, Forstein DA. Creation of a neovagina by the Vecchietti procedure in a patient with corrected high imperforate anus. JSLS 2009;13(2):221-3.

6. Gurbuz A, Karateke A, Haliloglu B. Abdominal surgical approach to a case of complete cervical and partial vaginal agenesis. Fertility Sterility 2005;84(1):217.

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OBSTETRICS AND GYNECOLOGY

Outcome of Prelabor Rupture of Membranes in a Tertiary Care Center in West Bengal CHAKRABORTY B*, MANDAL T†, CHAKRABORTY S‡

ABSTRACT The etiology is unknown in majority of cases though bacterial infection, cervical incompetence, hypertensive disease, recent coitus, malpresentation, antepartum hemorrhage (APH), malnutrition are recognized causes of prelabor rupture of membranes (PROM). A study was conducted in our institution in 2011, where 478 cases out of a total obstetric admission of 9,637 presented with PROM. Spontaneous rupture of membranes after 28 weeks of gestation before the onset of labor is called PROM. When it occurs before 37 completed weeks of gestation it is called preterm PROM (pPROM). The term PROM cases were induced after waiting for 24 hours for a spontaneous onset of labor. The preterm population were divided in three groups and were given treatment as; Group A: with beta-mimetic, antibiotic, steroid, iron and folic acid (IFA); Group B: With steroid, antibiotic, natural progesterone and IFA; Group C: With only antibiotic and IFA. Observed neonatal mortality in the very preterm group (<34 weeks) was 10% as compared to 5.8% in preterm (34-37 weeks) and nearly 3% among term pregnancies. Treatment of pPROM cases with steroid and antibiotic compared with addition of natural progesterone with or without beta-mimetic did not show any significant difference in terms of Apgar score, need for resuscitation in absence of maternal infection. Elective lower segment cesarean section (LSCS) showed a zero neonatal mortality, better Apgar score and significantly lesser requirement of neonatal resuscitation compared to emergency LSCS. It was concluded that gestational age at the time of delivery is the main determinant of neonatal body weight as well as survival among PROM cases. Beta-mimetics and progesterone showed no role to prolong pregnancy in PROM cases.

Keywords: PROM, pPROM, Apgar score, neonatal mortality

P

relabor rupture of membranes (PROM) is defined as the spontaneous rupture of membranes any time beyond 28th week of pregnancy but before the onset of labor.1 Premature prelabor rupture of membranes (pPROM) is defined as the spontaneous rupture of membranes during the period from viability to 37 completed weeks prior to the onset of labor.2 PROM complicates 5-10% of all pregnancies. At least 60% cases of PROM occurs at term.3

neonatal respiratory distress syndrome (RDS) are the complications of PROM. Fetal pulmonary hypoplasia, especially in preterm PROM is a real threat when associated with oligohydramnios.1

PROM is one of the important causes of preterm labor and prematurity. Chance of ascending infection in PROM is more if labors fails to start within 24 hours.1 Chorioamnionitis, cord prolapse, dry labor and

REVIEW OF LITERATURE

*Associate Professor †2nd Year Student ‡Rotating House Physician Dept. of Obstetrics and Gynecology Bankura Sammilani Medical College and Hospital, Bankura, West Bengal Address for correspondence Dr Barunoday Chakraborty Associate Professor Dept. of Obstetrics and Gynecology G-5/26, College Quarter, Bankura Sammilani Medical College Bankura - 722 102, West Bengal E-mail: c.subhankar@gmail.com

The current study was conducted to investigate the efficacy of three different management protocols in cases with pPROM and to know the fetomaternal outcome.

Review of available literature shows that rupture of membranes is related not only to bacterial infection but also to cervical incompetence, hypertensive disease, recent coitus, malpresentation, antepartum hemorrhage (APH), and inappropriate nutrition. PROM is also found more commonly in low socioeconomic class with inadequate prenatal care and inadequate weight gain during pregnancy.4,5 The etiology of pPROM is uncertain though probably multifactorial. The final common pathway usually involves a subclinical chorioamnionitis, which is facilitated via cervical changes leading to a loss of integrity of the canal or particular organisms being

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OBSTETRICS AND GYNECOLOGY present in the vagina allowing overgrowth of unwanted organisms. The effect is a cascade of biochemical changes in the fetal membranes and decidua which ultimately lead to prostaglandin and cytokine release and up regulation of intracellular messengers. In turn these changes lead to cervical ripening and membrane disruption. Increased uterine activity is often not far behind.3 The history of leaking fluid or gushing of water from vagina is diagnostic in over 90% cases. Different tests like nitrazine test, fern test, evaporation and diamine oxidase tests are done to confirm PROM. Now-a-days, ultrasound examination is also a popular method of diagnosis of PROM.5 On examination, the fetal presentation needs to be assessed as there is high chance it may not be cephalic. A sterile speculum examination should be performed and high vaginal swab (HVS) to be taken. Per vagina (PV) examination should be avoided.

Liquor is usually clear and colorless, though it may be pink. White cell count and C-reactive protein (CRP) have been investigated as possible better predictors of evolving chorioamnionitis but are not reliable.3 The microorganisms most commonly identified in the membranes and amniotic fluid of pregnancies complicated with spontaneous preterm labor with intact membranes are Ureaplasma urealyticum, Mycoplasma hominis, Gardnerella vaginalis, Mobiluncus, and bacteroides. The microorganisms most commonly associated with clinical chorioamnionitis and fetal infection after rupture membrane are Group B-streptococci (GBS) and Escherichia coli. However, the association between preterm labor and lower genital tract colonization with these organisms is less clear.

Upto 30% of pregnant women are colonized with GBS. GBS is the leading cause of neonatal sepsis and a substantial number of neonatal sepsis occurs among preterm infants.6 Birth asphyxia is the most common neonatal morbidity seen among PROM and reaches upto 40% followed

by RDS seen nearly among 28% cases. Study carried out in West Bengal, India showed that 68% babies were healthy, 27% were asphyxiated and revived, 3.5% were asphyxiated and could not be revived and 1.5% were stillborn. The incidence of neonatal morbidity increases as duration of PROM increases. Apart from infection (pneumonia, meningitis, sepsis), pulmonary hypoplasia, limb and body deformities, umbilical cord compression or prolapse and abruptio placentae are occasional complications of PROM.5

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The optimum management of PROM would be that, which minimizes the risk of both RDS and maternal and perinatal infection.4 The Cochrane review of over 6,000 randomized women shows that there is no difference in neonatal outcome from immediate induction of labor or waiting upto four days.

There is no evidence that routine use of antibiotics improve neonatal outcome in absence of an indication for GBS prophylaxis.3 Random treatment of pregnant women of third trimester with oral erythromycin or placebo continuously for 10 weeks to treat GBS colonization, chlamydia and U. urealyticum resulted in no significant improvement of preterm delivery in pPROM. Majority of randomized control trials with antibiotic treatment of lower genital tract infections in cases of bacterial vaginosis (BV) have failed to show any significant benefit in terms of preterm labor and neonatal body weight. However, there is significant heterogeneity between studies. The Center for Disease Control (CDC) in USA notes in its guideline that evaluation of BV be conducted at the first prenatal visit for asymptomatic woman who are at risk of preterm labor. But current evidence does not support routine testing for BV.6 The practice in our center is to treat an woman with PROM with antibiotics e.g. amoxycillin, which aims at preventing neonatal sepsis and maternal postnatal morbidity.

The use of progesterone administration to improve pregnancy outcome in threatened preterm labor dates back to as early as 1950s. The results of these early trials were summarized in two meta-analyses published in 1989 and 1990. One of these meta-analyses found positive efficacy of progesterone in reducing preterm delivery; whereas, the other did not find any. Erny et al in 1986 used 400 mg of micronized progesterone orally or a placebo in their patients with 30-36 weeks of gestation who were at risk of preterm labor. After one hour all their patients received intravenous ritodrine for tocolysis. The frequency of uterine contractions decreased in 76% of the progesterone group and 43% of the placebo group. Although progesterone treatment to prevent preterm delivery is not considered standard of care now-a-days, many clinicians may, in their wisdom decide to use this drug for these specific groups of women.6 Although it is generally accepted that antenatal glucocorticoids reduce RDS in preterm pregnancies with intact membranes their use in pregnancies with PROM has been studied in limited number of prospective trials with conflicting results.7,8

OBSTETRICS AND GYNECOLOGY In absence of fetal and maternal compromise, where the presentation is cephalic, vaginal delivery is usually indicated. Where the presentation is breech there is no evidence to suggest that cesarean section improves neonatal outcome. Generalization is difficult and decision needs to be individualized. Generally, outcome is related to the period of gestation, birth weight and fetal sex as with all preterm births. In pPROM particularly, fetal/neonatal sepsis will result in worse outcome.3 AIMS AND OBJECTIVES The objectives of the study were ÂÂ

ÂÂ

To observe the perinatal and maternal outcome in PROM treated with

Isoxsuprine + antibiotic + iron and folic acid (IFA)

Natural progesterone + antibiotic + IFA

Only antibiotic + IFA

To note the perinatal outcome in different modes of delivery in PROM cases, e.g.

admission of 9,637 mothers. All the participant mothers gave informed consents.

Detailed history was taken from every case and period of gestation was noted. On clinical examination, we noticed maternal height, weight pulse, blood pressure temperature and condition of heart, lung, liver and spleen. We also noticed fetal heart rate and whether patient was in labor or not by per abdominal examination.

Internal examination was done by a consultant or a senior resident to exclude any cord prolapse. A high vaginal swab was taken for bacteriological examination. Hematological investigations were done for Hb%, ABO and Rh-typing. Blood sugar estimation and VDRL testing were also done. Routine and microscopic urine examinations were also performed.

Anaerobic culture specific for GBS is not a routine practice in our institution. Hence special arrangements to do the same failed due to official delay in face of a short notice and also prohibitive cost of the detection kit. Ultrasonography was prescribed in every case to determine feto-placental profile and liquor volume.

Elective lower segment cesarean section (LSCS)

Emergency LSCS after a failed induction of labor after six hours

Regarding treatment, we waited for 24 hours for spontaneous onset of labor in term PROM cases (e.g.

37 weeks of gestation). But in preterm cases we divided the study population in three groups for three different management protocols as namely

Vaginal delivery

ÂÂ

Group A: Isoxsuprine (10 mg TDS) + antibiotic (cap amoxycillin 500 mg TDS) + betamethasone (12 mg IM 12 hourly two such for 24 hours) + IFA

ÂÂ

Group B: Natural progesterone (200 mg orally at bed time) + betamethasone (12 mg IM 12 hourly two such for 24 hours) + antibiotic (amoxycillin 500 mg cap TDS) + IFA

ÂÂ

Group C: Only antibiotic + IFA

MATERIAL AND METHODS The study was conducted at “Bankura Sammilani Medical College and Hospitals,” which is a tertiary care center in a district town in West Bengal. The duration of the study was six months during April to September, 2011. All the patients presented with PROM to the Dept. of Obstetrics and Gynecology, during that period were admitted. Then considering the previously set criteria mothers suitable for the study were included in the study population. The exclusion criteria were ÂÂ Patient in labor ÂÂ Pre-eclampsia/Pregnancy-induced hypertension (PIH) ÂÂ Multiple pregnancy ÂÂ Patients already suffering from fever ÂÂ Intrauterine fetal death ÂÂ Diagnosed cases of placenta previa and accidental hemorrhage ÂÂ Fetal congenital anomaly As per the said design we got 478 pregnant mothers complicated with PROM out of a total obstetric

But most of the consultants working here disagreed to prescribe isoxsuprine and natural progesterone and preferred only antibiotic.

We followed up the cases till the onset of labor or termination by induction and subsequent events. The different modes of delivery i.e., spontaneous vaginal delivery, vaginal delivery following induction of labor and LSCS were noted in each case. Birth weight of the babies and Apgar score were recorded. Birth weight <1.5 kg and/or Apgar score <7 babies were sent to sick neonatal care unit (SNCU) attached to the same building. Any resuscitation measure undertaken on the neonate was recorded. We could not follow the mothers for three days following vaginal delivery due to heavy patient load and shortage of bed. Here, the practice is

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OBSTETRICS AND GYNECOLOGY to discharge the patients with vaginal delivery after 24 hours. But, we followed mothers for seven days following cesarean section.

RESULTS During our study, we followed 9,637 pregnant mothers admitted in our department. Out of them, 478 mothers were included in our study as they fulfilled the inclusion criteria.

Table 1 shows the distribution of PROM at different gestational periods. Thirty mothers (n1) were in between 28-34 weeks; 34 mothers (n2) were in between 34-37 weeks and finally 414 mothers (n3) presented beyond 37 completed weeks. There was three neonatal deaths in the first group; 2 neonatal deaths occurred in group n2 and 13 deaths occurred in group n3. The neonates born to group n1 mothers had birth weights ranging from 0.7 to 2.6 kg. The second group of mothers (n2) had the neonates ranging from 2.2 kg to 3.1 kg and finally the n3 group had their neonatal birth weights ranging in between 2.75 kg to 3.3 kg.

Table 2 shows the perinatal events among the 64 mothers (n1+ n2) who had a PPROM and received treatment according to previously set protocol, e.g. ÂÂ

Group A: Treated with isoxsuprine + antibiotic

ÂÂ

Group B: Treated with natural progesterone + antibiotic

ÂÂ

Group C: Treated with only antibiotic

Group A consisted of 10 cases; their neonatal body weights varied in between 1.5-2.6 kg. Apgar score varied in between 4-7. Baby resuscitation was necessary in nine cases with bag mask ventilation (BMV) and oxygen inhalation. There were two neonatal deaths. Group B consisted of 14 cases with pPROM; their baby weights were in between 2.3-3 kg; Apgar score in between 4-8 and four babies required resuscitation in the form of BMV and oxygen and there was no perinatal mortality.

Group C consisted of 40 cases, where the birth weights were in between 0.7-3.1 kg; Apgar scores between 2-9; baby resuscitation was necessary in 28 cases and there were nine neonatal deaths. Records regarding perinatal

outcome in different modes of delivery has been tabulated in Table 3. Total number of vaginal delivery performed were 351 among 478 study cases (73.4%) and rest (i.e., 127 among 478 cases) had been delivered by LSCS. Among these 127 cases, 46 mothers had been operated electively (36.22%) and rest 81 mothers had undergone emergency LSCS. The electively operated mothers had their neonatal body weights ranging between 1.75-3.1 kg, Apgar scores varied between 4-7 and 13 neonates in this group required resuscitation in the form of BMV and/or oxygen inhalation. There was no neonatal mortality. In emergency LSCS cases, neonatal body weights varied in between 1.2-3.0 kg, Apgar scores varied in between 2-7 and 32 neonates required resuscitation measures. There were eight neonatal deaths in this group. On the other hand, the 351 mothers who delivered vaginally had their babies with body weights ranging in between 0.7-3.3 kg, Apgar scores in between 2-10 and 48 newborns among them required neonatal resuscitation. Twenty neonatal death were recorded in this group.

OBSERVATIONS AND DISCUSSION Table 1 shows the distribution of neonatal body weights at different gestational ages. The number of cases under the term PROM (414) was considerably larger than the other two groups e.g. preterm (34-37 weeks - 34 cases) and very preterm (<34 weeks - 30 cases only). It is also obvious that gestational ages at delivery has shown the main impact on neonatal body weights, neonatal mortality and need for neonatal resuscitation.

Observed neonatal mortality of 10% in the very preterm group against 5.8% in preterm and nearly 3% among term pregnancies when compared in pairs did not show any significance but there was much higher incidence of neonatal resuscitation among preterm neonates against their term counterparts - 90% in very preterm, 60% in preterm and only 11.8% among term neonates. One reason for this might be nonavailability of electronic fetal monitoring (EFM) in all cases, which could have indicated the optimum timing for a caesarean section. Morales et al in their study, observed

Table 1. Distribution of PROM of Different Gestational Periods Ge stational Age Criteria

28-34 weeks (n1 = 30)

34-37 weeks (n2 = 34)

>37 weeks (n3 = 414)

Baby weight (kg)

0.7-2.6

2.2-3.1

2.75-3.3

Neonatal mortality

3 (10%)

2 (5.8%)

13 (3.14%)

Neonatal resuscitation required

27 (90%)

21 (61.7%)

49 (11.8%)

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Indian Journal of Clinical Practice, Vol. 24, No. 7, December 2013

OBSTETRICS AND GYNECOLOGY Table 2. Perinatal Events Among Mothers who Received Treatment for PROM Treatment Protocol Groups Criteria

Group A

Group B

Group C

10

14

40

1.5-2.6

2.3-3.0

0.7-3.1

No. of cases Neonatal body weight (kg) Apgar score

4-7

4-8

2-9

Baby resuscitation

9

4

28

Neonatal mortality

2 (20%)

–

9 (22.5%)

Table 3. Comparative Results of Elective and Emergency LSCS Modes of Delivery Perinatal Outcome Neonatal body weight (kg) Apgar score Neonatal mortality Resuscitation required

Elective Cesarean Section (n = 46)

Emergency Cesarean Section (n = 81)

Vaginal Delivery (n = 351)

1.75-3.1

1.2-3.0

0.7-3.3

4-7

2-7

2-10

–

8 (9.8%)

20 (5.7%)

13 (28.3%)

32 (39.5%)

48 (13.6%)

a neonatal mortality of 5%-12% among preterm rupture of membrane below 34 weeks.4 Table 2 shows that addition of isoxsuprine with steroid and antibiotic (Group A) or isoxsuprine, steroid and natural progesterone with antibiotic (Group B) did not show any significant benefit in terms of Apgar score, need for neonatal resuscitation. There was no incidence of neonatal mortality in the natural progesterone group, which was obviously due to higher birth weights (2.3-3.0 kg) as compared to other two groups-the finding that reinforces our claim that it is the birth weight in absence of maternal infection that is the major determinant of neonatal survival. Paul J Meis and Ngina Connors in their review “Progesterone Treatment to Prevent Preterm Birth” have concluded that all the successful trials reported have indicated therapy relatively early in gestation (at <24 weeks) in women who showed no symptoms of preterm labor.

Trials of progesterone compounds to aid in halting the progression of labor have not been successful and the use of progesterone in women who have had symptoms or signs of labor should be discouraged.6 Table 3 indicates that planned elective LSCS showed a zero neonatal mortality, better Apgar score and significantly lesser requirement of neonatal resuscitation compared to emergency LSCS (28.3% against 39.5%).

Hassan et al in their study at Lahore found nearly 30% neonatal intensive care admission after emergency LSCS and nearly 13% after elective LSCS.9 Compared to this a mild but significant higher resuscitation rate in

our study may allude to greater degree of prematurity and lack of universal EFM. CONCLUSION The study clearly indicates that gestational age at the time of delivery is the main determinant of neonatal body weight as well as survival among PROM cases.

Having said that obstetrician should consider elective LSCS in appropriate cases to avoid unnecessary emergencies to save a valuable child thanks to NICU support and antibiotic prophylaxis. Beta-mimetics and progesterone have no role to prolong pregnancy in PROM cases. Continuous EFM can help to decide an optimum timing of LSCS terminating a trial of vaginal delivery.

REFERENCES 1. DC Dutta. Textbook of Obstetrics. 6th edition, New Central Book Agency (P) Ltd.8/1 Chittaranjan Das Lane, Calcutta 700009. Page 317.

2. Duff P. Premature rupture of the membranes at term. N Engl J Med 1996;334(16):1053-4.

3. Parry E. Managing PROM and PPROM. Obstet Gynecol 2006;8(4):35-8.

4. Gershenson DM, Kavanagh JJ, Copeland LJ, Stringer CA, Morris M, Wharton JT. Re-treatment of patients with recurrent epithelial ovarian cancer with cisplatin-based chemotherapy. Obstet Gynecol 1989;73(5 Pt 1):798-802.

5. Shrestha SR, Sharma P. Fetal outcome of pre-labour rupture of membranes. Nepal J Obstet Gynaecol 2006;1(2): 19-24.

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OBSTETRICS AND GYNECOLOGY 6. Clinical Obstetrics and Gynecology; Indian Edition, Prevention of Preterm Birth, by Paul J. Meis, Lippincott Williams & Wilkins, April 2005/volume1/Number2; p.203-09.

7. Sanyal MK, Mukherjee TN. Premature rupture of membranes an assessment from a rural medical college of West Bengal. J Obstet Gynaecol India 1990;40(5): 623-8.

8. Morales WJ, Diebel ND, Lazar AJ, Zadrozny D. The effect of antenatal dexamethasone administration on the prevention of respiratory distress syndrome in preterm gestations with premature rupture of membranes. Am J Obstet Gynecol 1986;154(3):591-5.

9. Hassan S, Javaid MK, Tariq S. Emergency Cesarean section: a comparative analysis. Professional Med J 2008;15(2):211-5.

■■■■

ÂÂ

Updated opinion statement of the American College of Obstetricians and Gynecologists (ACOG) states that physicians should carefully counsel women who are considering elective surgery that is not traditionally recommended and, ideally, jointly make the decision with them. The statement is published in the November issue of Obstetrics and Gynecology. As per the authors, after the physician has provided information and careful counseling, the patient and physician will often reach a mutually acceptable decision. If the patient and physician cannot reach an agreement, then referral or second opinion may be appropriate.

ÂÂ

Data from a prospective cohort study of more than 66,000 older adults in Washington state and published in the December issue of the American Journal of Hematology found that women with any airborne allergen had a 47% increase in risk for a hematologic cancer than men. Also, women who hit the allergy trifecta of sensitivity to plants, grass and trees had a 73% greater chance of developing a mature B–cell lymphoma or related disorder.

ÂÂ

Individually targeted lifestyle changes may increase the likelihood nulliparous women will have normal pregnancies, according to results from a large, newly published cohort study published their study in November current issue of BMJ. The changes identified include normalizing maternal weight, increasing consumption of fruits before pregnancy, reducing blood pressure, and avoiding use of drugs.

ÂÂ

New research conducted separately in 2 countries with different healthcare systems — Israel and the United Kingdom indicates that there is much room for improvement in the medical care of women with diabetes before they conceive and during pregnancy. This neglect gives rise to poor outcomes, with a significantly higher rate of stillbirth and infant death than is seen in the general population.

ÂÂ

Traditional tools for diagnosing depression fail to include symptoms common in men, which may explain why they are diagnosed with the disorder half as often as women, according to a study reported in the Aug. 28 issue of JAMA Psychiatry.

What Are the Psychological Effects of a Multiple Pregnancy on a Family? ÂÂ

662

Many women with a multiple pregnancy do well; their families may experience significant stress. Even if medical problems are overcome and the infants survive without disability, the effect of multiple births on family life is profound and life–altering. The impact of a multiple birth clearly affects the parents, but also the babies, other siblings, and the extended family. Financial stresses may be overwhelming. Obvious additional costs include feeding, clothing, housing, and caring for multiple children.

Indian Journal of Clinical Practice, Vol. 24, No. 7, December 2013

OBSTETRICS AND GYNECOLOGY

A Comparative Study Between Cleavage Stage Embryo Transfer at Day 3 and Blastocyst Stage Transfer at Day 5 in IVF/ICSI on Clinical Pregnancy Rates KAUR P*, SWARANKAR ML†, MAHESHWARI M†, ACHARYA V†

ABSTRACT Objective: To evaluate the efficacy of blastocyst transfer in comparison with cleavage stage transfer. Study design: A randomized, prospective study was conducted in Infertility Clinic, Dept. of Obstetrics and Gynecology, Mahatma Gandhi Hospital, Jaipur on 300 patients aged 25-40 years undergoing in vitro fertilization/intracytoplasmic sperm injection (IVF/ ICSI) cycle from May 2010 to April 2011. When three or more Grade I embryos were observed on Day 2 of culture, patients were divided randomly into two study groups, cleavage stage transfer and blastocyst transfer group having 150 patients each. Primary outcomes evaluated were, clinical pregnancy rate and implantation rate. The results were analyzed using proportions, standard deviation and Chi-square test. Results: Both the groups were similar for age, indication and number of embryos transferred. Clinical pregnancies after blastocyst transfer were significantly higher 66 (44.0%) compared to cleavage stage embryo transfer 44 (29.33%) (p < 0.01). Implantation rate for blastocyst transfer group was also significantly higher (p < 0.001). Conclusion: Blastocyst transfer having higher implantation rate and clinical pregnancy rate leads to reduction in multiple pregnancies.

Keywords: Blastocyst transfer, embryo transfer, in vitro fertilization, clinical pregnancy rates, intracystoplasmic sperm injection

A

dvances in the dynamics of embryo culture allow us to culture embryos to the blastocyst stage. Prolonging the duration of culture to Day 5 allows chromosomally competent embryos to develop to the blastocyst stage and permits selection of embryos that have the potential for continued development under embryonic genomic control.1 In addition, selection of Day 5 embryos has the advantage of physiological synchronization with the uterine endometrium, thereby resulting in better pregnancy rates.2 The introduction of sequential media that takes into account the changing metabolic requirement of the embryo, as it develops from the zygote to the blastocyst stage, allows extended culture.3,4

Blastocyst transfer should enable transfer of fewer but higher quality embryos resulting in increased implantation rates. This would maintain a high pregnancy rate while controlling the multiple pregnancy rate.5 Reasons for higher success rates with blastocysts are mainly related to embryo selection process. Embryos selected for transfer on Day 5 are healthier and carry a lower risk of being aneuploid, thereby increasing patient’s chance of achieving an ongoing pregnancy.6 Although blastocyst transfer has been shown to be beneficial in good prognosis patients, similar benefits were not seen in an unselected group. The aim of our study was to evaluate the efficacy of blastocyst transfer in comparison with Day 3 embryo transfer.

MATERIAL AND METHODS

*Resident †Professor Dept. of Obstetrics and Gynecology Mahatma Gandhi Medical College and Hospital, Jaipur Address for correspondence Dr Prabhleen Kaur A-2/93 Janak Puri, New Delhi - 110 058 E-mail: dr.prabhleenahuja@gmail.com

Three hundred patients aged 25-40 years undergoing in vitro fertilization/intracytoplasmic sperm injection (IVF/ICSI) cycle between May 2010 and April 2011 were included in our study, meeting the inclusion criteria set namely, 2-20 years of infertility, having minimum five

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OBSTETRICS AND GYNECOLOGY oocytes at oocyte pick up and endometrial thickness of 7 mm and more indicating good ovarian response, having normal uterine cavity and basal folliclestimulating hormone (FSH) (<10 mIU/ml). Complete patient work-up, baseline routine investigations and hormonal analysis was done and postmenstrual diagnostic hysteroscopy was done. Patients were put on long protocol, gonadotropin-releasing hormone (GnRH)-agonists started on cycle Day 21 daily doses given subcutaneously till Day 3 of next cycle. Hormonal evaluation: Serum FSH, luteinizing hormone (LH), estradiol (E2) and transvaginal sonography was done on Day 3 to confirm down regulation. Induction with recombinant FSH (rFSH) was started once pituitary down regulation was confirmed. The dose schedule was modified according to parameters like body mass index (BMI), previous response and ovarian reserve estimates and was given for five days (Day 3-7).

Follicular monitoring was initiated on Day 8 of cycle and further doses of rFSH were given according to follicle size and continued till Day 11. Women were scheduled for oocyte retrieval when at least three follicles reached 18 mm size and injection human chorionic gonadotropin (hCG) 10,000 IU was given. Transvaginal sonography guided oocyte retrieval was then planned 36 hours after hCG, which was performed under short general anesthesia.

The retrieved oocytes were then incubated for 3-4 hours in IVF-30 media and then, depending on maturity of oocytes and previous IVF performance, IVF or ICSI was performed. Short incubation insemination for two hours and group culture was followed for IVF. Denudation of oocytes was carried out mechanically before ICSI was performed. Oocytes were incubated overnight in IVF-30 media in a carbon dioxide (CO2) incubator and observed after 16-18 hours postinsemination for fertilization. The fertilized oocytes were then transferred into a cleavage medium and incubated. Embryos were observed on Day 2 and transfer was scheduled according to random allocation of patients into two groups based on availability of minimum three good quality embryos: Group 1: Included patients undergoing embryo transfer on Day 3.

Group 2: Included patient in which extended culture till Day 5 was done in G2 plus media and blastocysts were transferred on Day 5.

Random allocation of patients was done equally so that study population in both groups was comparable.

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The number of blastocysts/embryos transferred was determined by the availability of embryos, patients age and previous clinical history. Not more than three embryos/blastocysts were transferred on any occasion.

All transfers were performed using Edward-Wallace catheter. Luteal support was given in form of micronized vaginal progesterone in a dose of 200 mg thrice-daily for 18 days post retrieval. In addition, injection hCG 2,000 IU was given intramuscular on Days 5, 8 and 11 after retrieval. Serum b-hCG was performed on Day 15 following embryo transfer and if positive then transvaginal sonography was performed 15 days later to detect and confirm intrauterine pregnancy. Positive cases were followed till six weeks to check for fetal cardiac activity.

Outcome Measures Primary outcome ÂÂ

Implantation rate

ÂÂ

Clinical pregnancy rate

Secondary outcome ÂÂ

Fertilization rate

ÂÂ

Cleavage rate

ÂÂ

Multiple pregnancy rate

ÂÂ

Mean number of embryos/blastocysts transferred.

Implantation rate: Defined as the number of gestational sacs determined by ultrasound by number of embryos transferred.

Clinical pregnancy rate: Defined as presence of gestational sac with a fetal pole with cardiac activity on transvaginal ultrasound at six weeks.

Fertilization rate: Defined as total number of fertilized oocytes by total number of mature oocytes retrieved.

Cleavage rate: Total number of Day 3 embryos by total number of fertilized oocytes.

Study Analysis The results were analyzed by using proportions, standard deviation (SD) and Chi-square test.

RESULTS Total 300 patients were randomized for the study and allocated into two groups of 150 patients each. As shown in Table 1 no significant difference were found for age, duration of infertility, type of infertility, ratio of ICSI:IVF cases and mean E2 level at hCG injection.

Table 2 shows that no significant difference between both the study groups in term of indication for IVF.

OBSTETRICS AND GYNECOLOGY Table 1. Demographic Profile Variable

Day 3 Transfer (n = 150)

Day 5 Transfer (n = 150)

32.46 ± 4.3

32.04 ± 4.4

25-40

25-40

8.9 ± 5.2

7.7 ± 4.7

Primary

101

100

Secondary

49

50

No. of cases with ICSI

46

55

No. of cases with IVF

104

95

1158.3 ± 890.2

1327.52 ± 917.62

Age (years, mean ± SD) Range Duration of infertility (years) Type of infertility

Estradiol at hCG injection (pg/ml, mean ± SD)

No statistically significant difference was demonstrated between the two groups.

Table 2. Clinical Profile of Patients Infertility Indication (n)

Day 3 Transfer (n = 150)

Day 5 Transfer (n = 150)

Tubal

53

42

Endometriosis

10

9

Anovulation

15

21

Male

42

44

Mixed

15

19

Unexplained

15

15

No statistically significant difference was demonstrated between the two groups.

Table 3. Results After Oocyte Aspiration with Respect to Number of Oocytes and Embryos Variable

Day 3 Transfer (n = 150)

Day 5 Transfer (n = 150)

Oocytes at OR (n)

1,094

1,141

Mature oocytes (n)

922

1,007

Fertilized oocytes (n)

599

658

Total Day 3 embryos (n)

447

549

Embryos transferred (n)

309

290

No. of oocytes at OR (mean ± SD)

7.3 ± 2.1

7.6 ± 2.3

No. of mature oocytes (mean ± SD)

6.1 ± 1.6

6.6 ± 2.1

No. of two-pronucleate embryos (mean ± SD)

3.9 ± 1.7

4.3 ± 1.5

2.04 ± 0.74

1.93 ± 0.48

Fertilization rate (%)

64.96

65.34 (p > 0.05) NS

Cleavage rate (%)*

74.62

83.43 (p < 0.001) HS

No of embryos per transfer (mean ± SD)

No statistically significant difference was demonstrated between the two groups.

NS = Not significant; HS = Highly significant. *Cleavage rate was significantly higher in blastocyst transfer.

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OBSTETRICS AND GYNECOLOGY Table 4. Results After Oocyte Aspiration with Respect to Outcome Variable

Day 3 Transfer (n = 150)

Day 5 Transfer (n = 150)

Positive b-hCG

48

68

Percentage per OR

32

45.33

Clinical pregnancies (n)

44

66

29.33

44

Embryos transferred (n)

309

290

Total gestational sacs on USG (n)

66

102

21.35

35.17

Clinical pregnancy rate (%)

Implantation rate Total multiple pregnancies Multiple pregnancy rate

14

32

31.81

48.48

c2

df

p Value

5.6

1

<0.01 (S)

6.3

1

<0.01 (S)

14.12

1

<0.001 (HS)

2.36

1

>0.05 (NS)

S: Significant; HS: Highly significant; NS: Not significant.

Table 5. Pregnancy Outcome Variable

Day 3 Transfer (n = 150)

Day 5 Transfer (n = 150)

48

68

44 (29.33%)

66 (44%)

Missed

3 (2%)

2 (1.33%)

Ectopic

1 (0.66%)

0

Single

30

34

Twin

10

30

Triplets

4

2

Positive b-hCG Clinical pregnancies

c2 =

5.20; df = 1; p < 0.01 (significant).

Hence, women in blastocyst transfer group had significantly higher clinical pregnancy rates, implantation rate and cleavage rates.

DISCUSSION Blastocyst transfer is gaining popularity nowadays due to its higher clinical pregnancy rates and implantation rates. In this study, no significant difference was found between both the study groups in terms of age, duration of infertility, indication of infertility and type of infertility. This was in agreement with the study conducted by Van der Auwera et al.7 The mean number of embryos transferred in both groups showed no significant difference (2.04 and 1.93, p > 0.05).

Table 4 shows higher clinical pregnancies per oocyte retrieval was observed in blastocyst transfer group than in Day 3 embryo transfer group (44% and 29.33%) (p < 0.01), and higher implantation rate per embryo transfer in blastocyst transfer group (35.17%) than in Day 3 embryo transfer group (21.35%) (p < 0.01).

In our study, the proportion of clinical pregnancies occurring as the result of blastocyst transfer was higher 66 (44%) as compared to embryo transfer, which was 45 (30%), the association was statistically significant and similar results were seen in the study by Van der Auwera et al7 and Mangalraj et al.8 Although, the fertilization rate was higher with blastocyst transfer (65.34%) compared to Day 3 embryo transfer (64.96%) in our study, but association was not significant (p < 0.05) and same association was observed in study of Mangalraj et al.8

Table 5 shows that although multiple pregnancy rate in blastocyst transfer group were higher than Day 3 embryo transfer group, association was not significant (48.48% and 31.81%) (p > 0.05). Pregnancy rate in blastocyst transfer group was significantly higher than Day 3 embryo transfer group (44% and 29.33%). Day 3 embryo transfer group reported 2% of pregnancies as missed abortions and 1% as ectopic, while Day 5 blastocyst transfer group had no ectopic pregnancy and 1.33% pregnancies ended up as missed abortions.

Amongst both the study groups, cleavage rates (74.62% and 83.43%) and implantation rates (21.35% and 35.17%) were significantly higher in blastocyst transfer/Group 2 over Day 3 embryo transfer/ Group 1. The results of our study were similar to the study by Van der Auwera et al7 and Mangalraj et al.8 Although, the proportion of multiple pregnancy in our study was higher with blastocyst transfer (48.48%) than with embryo transfer (31.81%), but the association was not significant (p > 0.05).

As shown in Table 3, both the groups had a comparable mean number of oocytes at retrieval, same proportion of mature oocytes and fertilized oocytes and a comparable mean number of embryos per transfer.

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OBSTETRICS AND GYNECOLOGY Thus in younger women with good ovarian response and with three or more Grade I embryos on Day 3, extended culture can be offered. The good clinical pregnancy and implantation rates observed will confidently allow transfer of not more than two good quality blastocysts and allow women to enjoy benefits of limiting numbers for transfer. Hence, by transferring fewer embryos at blastocyst stage in selected group of good prognostic patients, physicians are practicing preventive medicine, as there are fewer multiple gestations and ultimately greater pregnancy success is achieved.

CONCLUSION In conclusion, this study has shown that in younger patients with good ovarian response, extended culture to Day 5 can be offered, as blastocyst transfer is found to have good clinical pregnancy rates. The good clinical pregnancy and implantation rates observed will confidently allow transfer of not more than two good quality blastocysts and allow women to enjoy the benefits of limiting numbers for transfer.

REFERENCES 1. Racowsky C, Jackson KV, Cekleniak NA, Fox JH, Hornstein MD, Ginsburg ES. The number of eight-cell embryos is a key determinant for selecting day 3 or day 5 transfer. Fertil Steril 2000;73(3):558-64.

2. Alper MM, Brinsden P, Fischer R, Wikland M. To blastocyst or not to blastocyst? That is the question. Hum Reprod 2001;16(4):617-9.

3. de los Santos MJ, Mercader A, Galán A, Albert C, Romero JL, Pellicer A. Implantation rates after two, three, or five days of embryo culture. Placenta 2003;24 Suppl B:S13-9.

4. Gardner DK, Surrey E, Minjarez D, Leitz A, Stevens J, Schoolcraft WB. Single blastocyst transfer: a prospective randomized trial. Fertil Steril 2004;81(3):551-5.

5. Kolibianakis EM, Zikopoulos K, Verpoest W, Camus M, Joris H, Van Steirteghem AC, et al. Should we advise patients undergoing IVF to start a cycle leading to a day 3 or a day 5 transfer? Hum Reprod 2004;19(11): 2550-4.

6. Papanikolaou EG, Camus M, Kolibianakis EM, Van Landuyt L, Van Steirteghem A, Devroey P. In vitro fertilization with single blastocyst-stage versus single cleavage-stage embryos. N Engl J Med 2006;354(11): 1139-46.

7. Van der Auwera I, Debrock S, Spiessens C, Afschrift H, Bakelants E, Meuleman C, et al. A prospective randomized study: day 2 versus day 5 embryo transfer. Hum Reprod 2002;17(6):1507-12.

8. Mangalraj AM, Muthukumar K, Aleyamma T, Kamath MS, George K. Blastocyst stage transfer vs cleavage stage embryo transfer. J Hum Reprod Sci 2009;2(1):23-6.

■■■■

What Precautions Should be Carried While Carrying a Multiple Pregnancy?

Monitoring a multiple pregnancy: Prenatal diagnosis by chorionic villus sampling can be done near the end of the first trimester to screen for Down syndrome and other genetic abnormalities. Amniocentesis is performed between 16 and 20 weeks. Many physicians perform cervical examinations every week or two beginning early in pregnancy to determine if the cervix is thinning or opening prematurely. If an exam or ultrasound shows that the cervix is thinning or beginning to dilate prematurely, a cerclage, or suture placed in the cervix, may prevent or delay premature dilatation. Tocolytic agents are medications that may slow or stop premature labor. These medications are given in hospital “emergency” settings in an attempt to stop premature labor.

Cesarean section: Vaginal delivery of twins may be safe in some circumstances. Many twins can be delivered vaginally if the presenting infant is in the head first position. Most triplets are delivered by Cesarean section.

Appropriate anesthesia and neonatal support are essential, whether delivery is performed vaginally or requires cesarean section.

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OBSTETRICS AND GYNECOLOGY

Randomized Control Study of Oral Versus Vaginal and Sublingual Misoprostol with Mifepristone for First-Trimester MTP SAHU RR*, SONI AA*, RAUT VS*

ABSTRACT Objective: To compare the outcome of two regimes of mifepristone and misoprostol (oral vs vaginal and sublingual administration of misoprostol) for medical termination of early pregnancy (within 49 days). Study design: A randomized controlled study was conducted. On 75 women undergoing medical termination of pregnancy (MTP) within 49 days of amenorrhea (7 weeks). These women were divided into two groups â&#x20AC;&#x201C; Group 1: received tablet mifepristone 200 mg orally followed by tablet misoprostol 600 mcg oral after 48 h. Group 2: received tablet Mifepristone 200 mg orally followed by misoprostol tablet 800 mcg, two tablets administered per vaginum and two tablets advised to be taken sublingually after 12 h. An ultrasonography pelvis was performed on all patients pre-MTP to confirm the location and age of gestation and post-MTP on day 15 to confirm no retained products of conception. Statistical analysis was done by two proportion tests for individual side effect with the null hypothesis.

Results: The complete abortion rates in Group 1 were 91.4% as compared to 90% in Group 2. Only 11.4% of women in Group 1 and 12.5% in Group 2 had bleeding for more than 15 days. The duration and amount of bleeding were statistically similar in both groups. Conclusion: We concluded that after 48 h of administration of mifepristone, oral 600 mcg of misoprostol is as efficient as 800 mcg of misoprostol (administered vaginally, 400 mcg and sublingually, 400 mcg) in inducing medical abortion of pregnancy within 49 days of amenorrhea.

Keywords: Mifepristone, misoprostol, medical termination of pregnancy

I

n India, 6.7 million induced abortions are performed per year, with a ratio of 60 induced abortions per 1,000 women of child-bearing age.1 In spite of legalization of medical termination of pregnancy (MTP) in India, the incidence of illegal abortion is at times more common than legal abortion. Unsafe abortions are a major cause of mortality among women in India accounting for 12% of all maternal deaths.

Medical abortion using combination of mifepristone and misoprostol offers a potentially simple and safe method than surgical abortion.

Mifepristone was approved for abortion in the United States by the Food and Drug Administration (FDA) in September 2000. In India, medical method of

*Consultant

Dr LH Hiranandani Hospital, Powai Mumbai, Maharashtra Address for correspondence Dr Rakhee R Sahu C-202, Blooming Heights, Pacific Enclave CHSL G.L. Compound, Powai - 400 076 Mumbai, Maharashtra E-mail: rakhee.sahu@hiranandanihospital.org

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termination was approved only in 2002, for pregnancies up to 49 days after the last menstrual period. Later, the Drug Controller in the year 2010 approved the use of MTP pill up to 63 days of pregnancy. Various regimes and combination of mifepristone and misoprostol have been experimented to achieve complete abortion rates with low doses and least side effects.

We conducted this study for medical abortion using two regimes of mifepristone with misoprostol in different doses and different routes of administration of misoprostol. This study was conducted to find an optimally effective regime for medical termination of early pregnancy. Mifepristone, a 19-nor-steroid, is a derivative of the synthetic progestin norethindrone.

Mifepristone acts as a competitive receptor antagonist and binds to the progesterone receptors with three to four times greater affinity resulting in necrosis of the endometrium and deciduas. It also causes softening of cervix and mild uterine contractions. Mifepristone also sensitizes the uterus to prostaglandins and increases the efficacy of prostaglandins. It also acts as a competitive antagonist at the glucocorticoid receptor.

OBSTETRICS AND GYNECOLOGY

The patients were clinically examined for pallor, systemic examination, and per vaginal examination to assess the size of uterus and exclude ectopic pregnancy.

Anti-D injections were administered if the pregnant women had Rh negative blood group. Ultrasonography pelvis was performed for all patients to confirm intrauterine pregnancy and weeks of gestation.

The basic characteristics of the patients are shown in Table 1 and Figure 1.

Patients of Group 1 received mifepristone tablet 200 mg orally on day 1. On day 3, that is, after 48 h of

Age (years)

20–38

21–42

Primigravida

18

19

Multigravida

17

21

4–6.6

5–6.3

04

06

Weeks of gestation (ultrasonography) Previous LSCS

Group 1 Group 2

25 20 15 10

S sL SC iou

ida rav ltig

Pr

ev

0

We ge eks sta of tio n.. .

5

Mu

The study was conducted at Dr LH Hiranandani Hospital, Mumbai, from November 2011 to August 2012. The study included women who requested for MTP within 49 days of amenorrhea, that is, seven weeks of pregnancy. Exclusion criteria were women with severe anemia, suspected ectopic pregnancy, known case of coagulopathy or on anticoagulant therapy, cardiovascular diseases such as uncontrolled hypertension, angina, valvular disease, and arrhythmia, severe renal, liver, or respiratory disease, uncontrolled seizure disorder, inherited porphyria, and allergic to mifepristone or misoprostol. Women who opted for MTP gave written informed consent and agreed for suction evacuation if there was heavy bleeding and incomplete abortion.

40

ida

MATERIAL AND METHODS

35

av

Women seeking MTP were given option of medical as well as surgical termination of pregnancy. Women who opted for medical termination using pills were further counseled regarding the procedure and visits for MTP and written valid consent was taken. All the patients were explained that in case of incomplete abortion or continuation of pregnancy, surgical uterine evacuation was advised.

Group 2 Group 1 (Mifepristone 200 mg (Mifepristone 200 + Oral Misoprostol mg + Misoprostol 800 mcg) 600 mcg)

Total patients

igr

This study was conducted to evaluate the efficacy of two regimes of MTP using different dosage and route of misoprostol administration.

Parameter

im

AIM

Table 1. Basic Characteristics of the Patients Included in the Study

Pr

Misoprostol is a synthetic analogue of prostaglandin E1 (PGE1). It was approved by the US FDA for the prevention of nonsteroidal anti-inflammatory drug (NSAID)-induced gastric ulcers. The action of misoprostol on the pregnant uterus was first described

by Rabe et al in 1987; they discovered that it binds to the EP-2/EP-3 prostanoid receptors and induces effective uterine contraction. Although misoprostol is licensed for oral administration, it is now often used vaginally and also sublingually.

Figure 1. Basic characteristics of the patients included in the study.

mifepristone, patients were advised to take misoprostol tablet 600 mg orally.

Patients of Group 2 received mifepristone tablet 200 mg orally on day 1. On day 3, patients were advised to insert misoprostol tablet 400 mcg per vaginum followed by misoprostol tablet 400 mcg sublingually (total 800 mcg misoprostol).

STATISTICAL ANALYSIS The data was managed in Microsoft Excel spreadsheet.

Demographics were described as average, standard deviation, minimum and maximum observation, and median (middle value). Demographics and general information for various parameters with all permutations and combinations were calculated in Microsoft Excel. Two proportion tests with null hypothesis of equal proportion was used to investigate and model impact of various parameters like result of

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OBSTETRICS AND GYNECOLOGY Table 2. Amount of Bleeding in Both Groups Amount of Bleeding

35

Group 1

Group 2

Heavy bleeding

03

03

25

Moderate bleeding

32

37

20

Comparison of amount of bleeding between Groups 1 and 2.

Incomplete abortion

15 10

Test and CI for Two Proportions Sample

X

N

Sample p

5

1

31

35

0.885714

0

2

37

40

0.925000

Difference = p (1) p (2); Estimate for difference: −0.0392857 95% CI for difference: (−0.172599, 0.0940279); Test for difference = 0(vs not = 0): Z = −0.58; p-value = 0.564.

Conducted two proportion tests with the null hypothesis: “Moderate bleeding (in amount of bleeding) in Group 1 is equal to Group 2.”

Conclusion: As the p value is >0.05, there is no significant difference in moderate bleeding for amount of bleeding between Groups 1 and 2.

outcome of MTP, duration of bleeding, and side effects between the two groups. A p value <0.05 was considered statistically significant (Table 2). All graphs were drawn and all statistical analysis was done using Minitab 16.

All patients were asked to note the onset of bleeding after medication, and the amount and duration of bleeding. Patients reported any of the side effects of medications like nausea, vomiting, giddiness, diarrhea, painful cramps in abdomen, rash, or allergic reaction.

All patients were advised to follow-up after 14 days of mifepristone tablets for clinical examination and ultrasound confirming no retained products of conception. Post-MTP ultrasonography was done for all patients in our study to look for complete expulsion of products of conception. On day 15 of follow-up, the amount and duration of bleeding and any of the side effects were noted. Few patients reported mild bleeding on day 2 after oral mifepristone, 8.5% in Group 1 and 8.8 % in Group 2. Most of the patients reported onset of bleeding usually 4–6 h after misoprostol tablets ingestion. All the parameters and abortion rates were statistically analyzed by the two proportion test with null hypothesis of equal proportion. A p value <0.05 was considered statistically significant. Successful outcome of medical termination was considered when there were no retained products of conception seen in post-MTP ultrasonography and when there was no need for surgical intervention of suction evacuation for heavy bleeding or retained products of conception.

The abortion rate in Group 1, which was treated with mifepristone tablet 200 mg followed by misoprostol

670

Complete abortion

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Indian Journal of Clinical Practice, Vol. 24, No. 7, December 2013

Group 1

Group 2

Figure 2. Comparison of outcome of MTP between Groups 1 and 2.

Table 3. Treatment Outcome of the Regimes Outcome of MTP

Group 1 (Total = 35)

Group 2 (Total = 40)

Complete abortion

32

36

Incomplete abortion

3

4

Dilation and curettage required

3

4

Test and CI for Two Proportions Sample

X

N

Sample p

1

3

35

0.085714

2

5

40

0.125000

Difference = p(1) p(2); Estimate for difference: −0.0392857; 95% CI for difference: (−0.177508, 0.0989361); Test for difference = 0 (vs not = 0): Z = −0.56; p value = 0.577 Conducted two proportion tests with the null hypothesis: “The percentage defective in outcome of MTP is equal for Groups 1 and 2.”

Conclusion: As the p value is >0.05, the null hypothesis is accepted at 95% CI. This means that there is a no significant difference in outcome of MTP between Groups 1 and 2.

tablet 600 mcg orally, was 91.4% (Table 3). The complete abortion rate in Group 2, which was treated with 200 mg of mifepristone followed by misoprostol tablet 400 mcg vaginally and 400 mcg sublingually, 12 h apart on day 3, was 90% (Table 3). The comparison of outcome of MTP between Group 1 and 2 is shown in Figure 2.

The p value was >0.05, the null hypothesis is accepted at 95% confidence interval (CI), and there is no statistical difference in outcome of MTP between Groups 1 and 2.

The duration and amount of bleeding were similar in both groups (Table 4). As the p value is >0.05 for all the parameters, there is no significant difference in duration of bleeding between Group 1 and Group 2. Oral misoprostol 600 mcg was tolerated well by patients and

OBSTETRICS AND GYNECOLOGY PHARMACOKINETICS OF MIFEPRISTONE

Table 4. Duration of Bleeding Duration of Bleeding

Group 1

Group 2

<7 days

1

2

7–10 days

30

33

>14 days

4

5

Comparison between Groups 1 and 2 for duration of bleeding.

Conducted two proportion tests for individual duration with the null hypothesis: “The duration of bleeding is equal between Groups 1 and 2.”

Conclusion: As the p value is >0.05 for all the parameters, there is no significant difference in duration of bleeding between Groups 1 and 2.

Table 5. Side Effects of Misoprostol Group 1

Group 2

Nausea

Side Effects of Misoprostol

2

4

Vomiting

2

2

Pain in lower abdomen requiring analgesic

3

4

Fainting

0

0

Rash and allergic reaction

0

0

Emergency services required

0

0

Comparison between Groups 1 and 2 for various side effects.

Conducted two proportion tests for individual side effect with the null hypothesis: “The proportion of side effect for Group 1 is equal to the proportion of Group 2.”

Conclusion: As the p value is >0.05 and t test of mean difference 0 is within the CI, the null hypothesis is accepted at 99% CI. This means there is a no significant difference in side effects between Groups 1 and 2.

6 5 4 3 2 1 0

Fa R in tin re ash ac a g tio n n da E lle re me rg qu rg ic ire en d cy se rv ic es

iti ng Pa ab in do in m lo en w ... er

Vo m

N

au s

ea

Group 1 Group 2

Figure 3. Comparison of outcome of MTP between Groups 1 and 2.

lowering the dose did not reduce the abortion rates and the amount or duration of bleeding when compared with total 800 mcg of misoprostol. The incidence of nausea and vomiting was lesser with vaginal and oral misoprostol as compared to sublingual route (Table 5, Fig. 3).

In the presence of progestins, mifepristone acts as a competitive receptor antagonist for progesterone receptors. When administered in early pregnancy, it causes decidual breakdown by blockade of uterine progesterone receptors, which leads to detachment of blastocyst resulting in decrease of human chorionic gonadotropin production. This, in turn, decreases the progesterone from the corpus luteum, softens the cervix, and enhances uterine contractions. The bioavailability of mifepristone is approximately 60% of the administered dose, with 85% of the drug being absorbed after oral administration and peak serum levels occurring 1–2 h later. Concentrations remain stable for 12 h and then start to decline with a half-life of approximately 24 h in pregnant or nonpregnant women. Mifepristone causes endometrial shedding by direct inhibition of the endometrial progesterone receptor, leading to decreased glandular secretion activity and accelerated degenerative changes that usually occur within 48–72 h of drug administration.

Pharmacodynamics and Pharmacokinetics of Misoprostol Misoprostol is a synthetic PGE1. PGE1 causes myometrial contractions by interacting with specific receptors on myometrial cells. This interaction results in a change in calcium concentration, thereby initiating muscle contractions. By interacting with prostaglandin receptors, misoprostol causes the cervix to soften and the uterus to contract, resulting in expulsion of uterine contents. Misoprostol is extensively absorbed and undergoes rapid de-esterification to its free acid, which is responsible for its clinical activity, and unlike the parent compound, is detectable in plasma. The alpha chain undergoes beta oxidation and the beta side chain undergoes omega oxidation followed by reduction of the ketones to give prostaglandin F analogs. The compound is a lipophilic methyl ester prodrug and is readily metabolized to the free acid, which is the biologically active form.

Following oral administration, the plasma concentration increased rapidly with a peak of 30 min, declined rapidly by 120 min, and remained low thereafter. In contrast, after vaginal administration, the plasma concentration gradually increased, reaching maximum levels after 70–80 min and slowly declined with detectable levels present after 6 h. Vaginal misoprostol was present in the circulation longer than oral misoprostol and hence its duration of stimulation of the uterus exceeds that of oral misoprostol.2 Vaginal application of misoprostol results in slower increase

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OBSTETRICS AND GYNECOLOGY and lower plasma concentrations of misoprostol acid than does oral administration, but overall exposure to drug is increased. Misoprostol inhibits gastric acid secretion in humans and there is also some evidence that it limits the extent of gastrointestinal damage induced by ulcerogenic agents in animals and healthy volunteers at doses lower than those required to inhibit acid secretion. NSAIDs inhibit prostaglandin synthesis and a deficiency of prostaglandin within the gastric mucosa may lead to diminishing bicarbonate and mucus secretion and may contribute to the mucosal damage caused by these agents. Misoprostol increases bicarbonate and mucus production, but in man it has been shown that at doses 200 mcg and above they are antisecretory. It is therefore not possible to tell whether the ability of misoprostol to reduce the risk of gastric ulcer is the result of its antisecretory effect or its mucosal effect, or both. The recommended adult dose for reducing the risk of NSAID-induced ulceration is 100–200 mcg four times a day with food. If the patient becomes pregnant on misoprostol therapy, she has to be appraised of potential harm to the fetus and should be advised abortion. The use of misoprostol in first trimester of pregnancy has been associated with a specific type of moebius sequence with or without limb deficiency.3,4 DISCUSSION Medical abortion offers great potential for improving abortion access and safety, as it requires less extensive infrastructure than surgical abortion. Also there is, no need for anesthesia and operation theater facilities, and maintains patient’s need for privacy. The disadvantages would be that the women requires at least three visits to the hospital, unpredictable outcome in few patients, longer duration of bleeding, and potential risk of fetal malformation if it fails to cause abortion. The factors that may prevent the women from accepting the medical method of termination of pregnancy is the abdominal cramps and heavy bleeding, duration of bleeding (average 7–10 days), and the need to follow-up after 2 weeks for clinical examination and sonography.

We conducted this study to find the efficacy of the regime of pretreatment with mifepristone followed by low-dose misoprostol administered orally along with vaginal and sublingual route. The abortion rate in Group 1 (600 mcg misoprostol orally) was 91.4% and in Group 2 (400 mcg vaginally and 400 mcg sublingually 12 h apart) was 90%.

Most of the patients would start bleeding within 6 h of misoprostol tablets. The incidence of minimal bleeding on day 2 after mifepristone was observed in 8.8% of

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Indian Journal of Clinical Practice, Vol. 24, No. 7, December 2013

patients in Group 1 and 8.5% in Group 2. There is evidence that it is beneficial to perform a routine ultrasonography at the time when a patient is seen for the first time for a termination of pregnancy.5 The scan allows the exact determination of the gestational age, especially in women with irregular cycles, which is important for advising the patient about the most appropriate method of termination. It also helps to diagnose multiple pregnancies, exclude/diagnose ectopic pregnancy, diagnose a molar pregnancy, and diagnose coincidental pelvic pathology like fibroid or ovarian cyst. Multicentric trails conducted by the World Health Organization demonstrated that the effectiveness of 600 mg of mifepristone can be compared with 200 mg dosage.6 Chuni and Chandrashekhar7 conducted a study on 112 women for MTP of 63 days duration with oral mifepristone 200 mg followed by oral misoprostol 400 mcg 48 h apart. The rates of complete abortion were 92.8%, 83%, and 80% in the <49 days group, 50–59 days group, and 57–63 days group, respectively. Mittal et al8 conducted a study comparing oral versus vaginal misoprostol and continued use of misoprostol after mifepristone for early medical abortion. Women within 9 weeks of pregnancy were included and all were given mifepristone 200 mg on day 1 followed by misoprostol after 48 h. In this study, patients were divided into three groups: Group 1 received 800 mcg misoprostol orally and placebo vaginally; Groups 2 and 3 received misoprostol 800 mcg vaginally and placebo orally. Those in Groups 1 and 2 received oral misoprostol 400 mcg twice a day from day 4 for 7 days, while Group 3 took placebo. The abortion rates were 100%, 98%, and 96% in Groups 1, 2, and 3, respectively. The addition of misoprostol for 7 days from day 4 did not help in decreasing the abortion rates nor the duration or the amount of bleeding. Since misoprostol also has protective action on the gastric mucosa, there was no increased incidence of nausea and vomiting in the oral group.

A study was conducted by the World Health Organization (WHO),9 Geneva, on 1589 pregnant women with menstrual delay of less than or equal to 35 days requesting for nonsurgical abortion. A double-blinded study assigned a single oral dose of mifepristone, either 200 mg or 600 mg, followed by oral misoprostol 400 mcg. The complete abortion rate with the lower dose of mifepristone was similar to that of higher dose (89.3% vs 88.1%). The efficacy of the mifepristone prostaglandin regime was not reduced by decreasing the dose of mifepristone from 600 to 200 mg. However, it was noted that this regime was not sufficiently efficient in inducing complete abortion

OBSTETRICS AND GYNECOLOGY when the length of pregnancy was more than seven weeks. A clinical study of medical termination on 263 women with up to nine weeks of pregnancy showed that vaginal administration of 800 mcg after pretreatment with mifepristone resulted in higher complete abortion rate (95%) than with oral route (87%). study10

The WHO multinational of mifepristone combined with three different misoprostol regimes – (a) 800 mcg vaginally on day 3 only; (b) 800 mcg vaginally on day 3 followed by 400 mcg orally twice a day daily for 7 days; or (c) 800 mcg orally on day 3 followed by 400 mcg orally twice a day orally daily for 7 days; n = 2,219. This study found that in women with gestation periods more than 59 days, the risk of failure was higher in group (c) compared to group (b) (RR 2.8, CI 1.3–5.8), but there were no significant differences in efficacy in women with gestation periods less than 59 days.

A study was conducted by el-Refaey et al11 on induction of abortion with mifepristone (600 mg) and oral or vaginal misoprostol (800 mcg) in 270 pregnant women within 63 days from onset of amenorrhea. The rate of complete abortion was 87% in the oral misoprostol group and 95% in the vaginal group (p = 0.03). Vomiting and diarrhea were reported more frequently by the women who received oral misoprostol than by those who received vaginal misoprostol. They concluded that vaginal administration of misoprostol is more effective and better tolerated than oral administration for induction of first-trimester abortion. A study by Ashok et al12 showed an efficacy of 98% in a series of 2,000 women up to 63 days from last menstrual period with 200 mg mifepristone orally, followed by 2 days later by 800 mcg misoprostol vaginally.

CONCLUSION The complete abortion rate with mifepristone followed by oral misoprostol (600 mcg) (91.4%) was comparable to that with mifepristone followed by vaginal and sublingual misoprostol (800 mcg) (90%). The amount and the duration of bleeding were comparable in both the groups. The patients were more comfortable with oral tablets of misoprostol rather than the vaginal insertion.

Access to safe abortion is limited in many developing countries because of legal restrictions, administrative and financial barriers, and lack of adequately trained providers. More trails are needed to find a method of medical termination that is efficient and acceptable with minimal side effects. There is a need to examine the different dosages, routes, and timings of administration of mifepristone and misoprostol to determine the most appropriate treatment protocol.

Acknowledgment The authors would like to thank Dr Sujit Chatterjee, CEO, Dr LH Hiranandani Hospital, Mumbai, for allowing to conduct and publish the study.

REFERENCES 1. Chhabra R, Nuna SC. Abortion in India: an overview.

Delhi: Ford Foundation; 1994.

2. Zeiman M, Fong SK, Benowitz NL, Banskter D, Darney PD. Absorption kinetics of misoprostol with oral or vaginal administration. Obstet Gynecol 1997;90(1):88-92.

3. Paustuszak AI, Schuler L, Speck-Martins CE. Use of misoprostol during pregnancy and Möbius syndrome in infants. N Engl J Med 1998;338:1881-5.

4. Gonealez CH, Vargas FR, Perez AB, et al. Limb deficiency with or without Möbius sequence in seven Brazilian children associated with misoprostol use in the first trimester of pregnancy. Am J Med Genet 1993;47:59.

5. McGalliard C, Gaudoin M. Routine ultrasound for pregnancy termination request increases women’s choice and reduces inappropriate treatments. Br J Obstet Gynecol 2004;111:79-82.

6. World Health Organisation Task Force on Post-ovulatory Methods of Fertility Regulation; Special Programme of Research, Development and Research Training; World Health Organisation. Comparison of two doses of mifepristone in combination with early medical abortion: a randomized trial. Br J Obstet Gynecol 2000;107:524-30.

7. Chuni N, Chandrashekhar TS. Early pregnancy termination with a simplified mifepristone: medical abortion outpatient regimen. Kathmandu Univ Med J 2009;7(27):209-12.

8. Mittal S, Agarwal S, et al. Comparison of oral versus vaginal misoprostol and continued use of misoprostol after mifepristone for early medical abortion. Indian J Med Res 2005;122:132-6.

9. World Health Organization Task Force on Post-ovulatory Methods of Fertility Regulation. Medical abortion at 57 to 63 days gestation with a lower dose of mifepristone and gemeprost. A randomized controlled trial. Acta Obstet Gynecol Scand 2001;80:447-51.

10. von Hertzen H, Honkanen H, Piaggio G, et al; WHO Research Group on Post-ovulatory Method for Fertility Regulation. WHO multinational study of three misoprostol regimen after mifepristone for early medical abortion. I: efficacy. Br J Obstet Gynecol 2003;110(9):808-18.

11. el-Refaey H, Rajasekar D, Abdalla M, Calder L, Templeton A. Induction of abortion with mifepristone and oral or vaginal misoprostol. N Engl J Med 1995;332(15):983-7.

12. Ashok PW, Penney GC, Flett GM, Templeton A. An effective regime for early medical abortion: a report of 2000 consecutive cases. Hum Reprod 1998;13:2962-5.

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ONCOLOGY

Immature Teratoma with Somatic Tumor-Type Sarcoma: A Case Report CHANDOKE RK*, VERMA AK*, KAUR O*, YADAV N*, AGARWAL S*, BHUSHAN B*, MEHRA P*

ABSTRACT Teratoma is a germ cell tumor seen mainly in neonates and young adults; it contains elements derived from all three germinal layers, with its usual site of occurrence being the ovary and testis and less common sites being several extragonadal locations.

This case is of a 10-year-old boy who presented with an asymptomatic mass, heterogenous on ultrasonography and showing enhanced solid areas along with nonenhancing cystic areas on contrast enhanced computed tomography. Cytological diagnosis of malignant mesenchymal tumor was made; however, exact categorization could not be done. After surgical excision, histological and immunohistochemical studies yielded the diagnosis of immature teratoma with somatic malignancy – sarcoma.

Teratomas with malignant transformation refer to a form of germ cell tumor in which a somatic teratomatous component becomes morphologically malignant and develops aggressively. These are associated with chromosomal abnormalities i (12p) reflecting germ cell tumor clonality. The occurrence of an identifiable sarcomatous component is a well recognized but distinctly uncommon phenomenon.

Keywords: Teratoma, contrast enhanced computed tomography, malignant mesenchymal tumor, malignant transformation, chromosomal abnormalities

T

eratoma is a germ cell tumor containing elements derived from three germinal layers, namely, ectoderm, mesoderm, and endoderm,1,2 which usually occurs not only in the ovary and testis but also in several extragonadal locations, such as the retroperitoneum, mediastinum, sacrococcegeal area, pineal gland, and the head and neck region.3,4 Primary retroperitoneal tumors account for 1%–11% of retroperitoneal neoplasms and are most commonly found in neonates and young adults.5 The histologic appearance of teratomas may differ significantly, depending upon the type of tissue present and their degree of maturity. Mature teratomatous elements resemble well-differentiated tissues while immature teratomas contain elements mimicking embryonal or fetal tissues, primarily neuroectodermal.

CASE REPORT A 10-year-old boy presented with a asymptomatic mass. Ultrasonography revealed a heterogenous mass

*Dept. of Pathology

ESI Hospital, Basaidarapur, New Delhi Address for correspondence Dr Onkar Kaur A-9, Defence Colony New Delhi -110 024 E-mail: kauronkar@ymail.com

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Indian Journal of Clinical Practice, Vol. 24, No. 7, December 2013

measuring 29 × 19 × 10 cm with extensive necrotic, calcified, and gross solid components, displacing liver and kidney (Fig. 1). Contrast enhanced computed tomography (CECT) was done that showed enhancing solid areas along with nonenhancing cystic areas with minimal stippled calcification. No definite fat attenuation was seen. All blood investigations were within normal limits. On fine needle aspiration cytology (FNAC), a diagnosis of malignant mesenchymal tumor was made (Fig. 2); however, exact categorization could not be done.

Ascitic fluid examination showed smears positive for malignant cells (Fig. 3). On gross examination, the mass was irregular and encapsulated. The cut surface was variegated, solid, fleshy, gray tan with few cystic areas along with hemorrhage and necrosis (Fig. 4), a finding consistent with the attenuation and signal intensity seen in CECT.5 One pole of the tumor showed welldemarcated hematoma. On microscopic examination, smears showed highly cellular tumor with necrotic areas. Cellular areas were composed of immature tissue mainly neuroectodermal arranged in sheets and focal rosetting. Mature cartilage and glandular structures were also seen (Figs. 5-7). The other component in the tumor was composed of plump to spindle-shaped cells arranged in sheets and interlacing fascicles, showing marked cellular and nuclear pleomorphism along with binucleation and abnormal mitosis (Fig. 8). Adrenal tissue showing extensive hemorrhage was identified.

ONCOLOGY

Figure 1. Abdominal CECT revealing a well-circumsribed heterogenous mass showing enhanced solid areas and nonenhanced cystic areas, displacing liver and kidney.

Figure 2. FNAC smear showing scattered singly lying malignant tumor cells with oval nuclei, coarse chromatin, and abundant gray–blue cytoplasm (aspiration cytology, Giemsa, 400×).

Figure 4. Cut section of the gross specimen showing variegated appearance composed of solid fleshy areas predominantly with few cystic areas, hemorrhage, and necrotic.

Figure 3. Ascitic fluid showing positivity for malignant cells (fluid cytology, Giemsa, 400×).

Figure 5. Tumor showing foci of mature cartilage tissue adjacent to undifferentiated tumor cells (H&E, 100×).

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Figure 6. Focal areas of glial tissue identified (H&E, 100×).

Figure 7. Photomicrograph showing epithelial component forming glandular structures (H&E, 100×).

Figure 8. Pleomorphic sarcomatous areas with tumor cells arranged in sheets; also seen is abnormal mitosis (H&E, 400×).

Figure 9. Tumor cells showing vimentin positivity in the sarcomatous component throughout on IHC (400×).

Figure 10. Immunohistochemistry showing focal NSE positivity (400×).

Figure 11. Immunohistochemistry showing focal S-100 positivity (400×).

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ONCOLOGY Immunohistochemistry (IHC) markers put for the case were vimentin (positive), neuron-specific enolase (NSE), S-100 (focal positivity), desmin, and smooth muscle actin (negative), thus giving a diagnosis as immature teratoma with somatic malignancy – sarcoma (Figs. 9-11).

of an identifiable sarcomatous component is a wellrecognized but distinctly uncommon phenomenon, contributing to about 4.34% of retroperitoneal teratomas with malignant components.8 REFERENCES 1. Rosai J. Ackerman’s Surgical Pathology. 8th edition, Vol. 1.

St. Louis, Missouri: Mosby 1995;8(1):1257-97.

DISCUSSION Retroperitoneal teratomas are rare entities, representing only 1%–11% of all primary retroperitoneal tumors.

Incidence is bimodal with peaks in the first six months of life and in early adulthood. Due to their location, they are usually identified only after they have grown to huge proportions.6 Teratomas (both mature and immature, sometimes referred to as grade 0 and grade 1 teratomas) have a risk of malignancy, the frequency being more in case of immature ones.1 Teratoma with malignant transformation refers to a form of germ cell tumor in which a somatic teratomatous component becomes morphologically malignant such as carcinoma, sarcoma, neuroendocrine, and leukemias, and develops aggressive growth.2 Sarcoma developing in a retroperitoneal teratoma tends to develop massive cystic degeneration, thus exhibiting central necrosis more commonly than other sarcomas, whereas fat and calcification are not typically present.7 These are associated with chromosomal abnormalities i(12p) reflecting germ cell tumor clonality. The occurrence

2. Young RH. New and unusual aspects of ovarian germ cell tumors. Am J Surg Pathol 1993;13:1210-4.

3. Ulbright TM. Germ cell neoplasms of the testis. Am J Surg Pathol 1993;17:1075-91.

4. Dehner LP. Gonadal and extragonadal germ cell neoplasia of childhood. Hum Pathol 1983;14:493-509.

5. Lane RH, Stephens DH, Reiman HM. Primary retroperitoneal neoplasms: CT findings in 90 cases with clinical and pathologic correlation. Am J Roentgenol 1989;152:83-9.

6. Gatcombe HG, Assikis V, Kooby D, Johnstone PAS. Primary retroperitoneal teratomas: a review of the literature. J Surg Oncol 2004;86(2):107-13.

7. Rosai J. Soft tissues. In: Ackerman’s Surgical Pathology.

8th edition, Rosai J (Ed.), Mosby: St Louis, Missouri 1996:p.2021-133.

8. Malagón HD, Valdez AM, Moran CA, Suster S. Germ cell tumors with sarcomatous components: a clinicopathological and immunohistochemical study of 46 cases. Am J Surg Pathol 2007;31(9):1356-62.

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Red Meat Consumption Linked to Increased Risk of Early Death A study from the Harvard School of Public Health and published in the Archives of Internal Medicine has linked red meat to a higher risk of early death. Eating red meat –– any amount and any type –– appears to significantly increase the risk of premature death, according to the study.

The researchers found that those who increased consumption of unprocessed red meat by one serving each day had an 18% higher risk of dying from heart disease and a 10% greater risk of dying from cancer, while those who ate one more daily serving of processed red meat had a 21% higher risk of dying from heart disease and a 16% increased risk of dying from cancer.

The increased risks linked to processed meat, like bacon, were even greater: 20% overall, 21% for cardiovascular disease, and 16% for cancer.

The researchers estimated that substituting one daily serving of red meat with fish, poultry, nuts, legumes, whole grains, or low-fat dairy products would reduce the risk of dying in this stage of life by 7%–19%.

If people ate less than half a serving of red meat a day, deaths during the 28 years of follow-up could have been reduced by 9.3% for men and 7.6% for women.

About 3 years ago, a study by the National Cancer Institute found that people who ate the equivalent of a quarterpound burger or small steak each day had about a 30% greater risk of dying over 10 years than people who only ate red meat occasionally.

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Marcus Gunn Jaw-Winking Phenomenon: Brief Communication JHAGTA HS

ABSTRACT Marcus Gunn jaw-winking phenomenon is the most common form of congenital synkinetic neurogenic ptosis.

The unilaterally ptotic eyelid elevates with jaw movements due to cross innervations between oculomotor nerve and mandibular branch of trigeminal nerve. We report a case of a 12-year-old female who presented with complaint of drooping of left upper lid since birth associated with elevation of left upper lid while chewing. She was diagnosed to have Marcus Gunn jaw-winking syndrome.

Keywords: Marcus Gunn jaw-winking phenomenon, blepharoptosis, congenital synkinetic neurogenic ptosis

A

pproximately 50% of blepharoptosis cases are congenital. Incidence of Marcus Gunn jawwinking syndrome among this population is approximately 4%–5%.1,2 Marcus Gunn jaw-winking phenomenon is the most common form of congenital synkinetic neurogenic ptosis. In this synkinetic phenomenon, the unilaterally ptotic eyelid elevates with jaw movements due to cross innervations between oculomotor nerve and mandibular branch of trigeminal nerve.

CASE DESCRIPTION A 12-year-old female presented with complaint of drooping of left upper lid since birth associated with elevation of left upper lid while chewing. Drooping was nonprogressive with time. The patient also complained of obstruction of vision in left eye, to overcome which she used to keep her mouth open.

On examination, best-corrected visual acuity was 6/6 with −1.25 DS in both eyes. Left eye vertical interpalpebral aperture was 4 mm in primary position of gaze and 6 mm in downgaze and the amount of ptosis calculated was 7 mm. Lid crease was absent and LPS action was 4 mm in left eye. Marcus Gunn jaw-winking phenomenon was present and Bell’s phenomenon was poor in the left eye. Lower eyelid was normal in position and ocular movements were full.

Dept. of Ophthalmology Sankara Eye Hospital, Ludhiana, Punjab

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No other ocular or systemic association was found.

After taking the history and taking into account the findings on examination, diagnosis of congenital synkinetic ptosis was made.

DISCUSSION Jaw-winking is an example of synkinesis due to aberrant connection between the third and the fifth cranial nerve that leads to simultaneous co-contraction of ipsilateral levator palpebrae superioris and lateral pterygoid muscle. It is usually first noticed by the mother when she is feeding or nursing the baby. It is usually unilateral but may be bilateral in rare cases.1,2 The characteristic feature of the phenomenon is that the raising and not winking of the affected eyelid is synchronous with and proportionate to the opening of the mouth. This response is followed by a rapid return to a lower position. The amplitude of the wink tends to be worse in downgaze. This rapid, abnormal motion of the eyelid can be the most disturbing aspect of the jaw-winking syndrome. The amount of jawwinking is the excursion of the upper eyelid with synkinetic mouth movement. It is measured with a millimeter ruler. Jaw-winking is assessed as: Mild < 2 mm; Moderate 2–5 mm; Severe ≥ 6 mm.1,3 The jaw-wink is considered cosmetically significant if it is 2 mm or more.3 Ocular associations are strabismus (50%–60%), anisometropia (5%–25%), and amblyopia (30%–60%).4 Systemic anomalies in association with Marcus Gunn phenomenon are rare.

OPHTHALMOLOGY Cleft lip/cleft palate, CHARGE syndrome, (reported in association with bilateral cases) and renal calculi have been seen.

TREATMENT

levator resection followed by frontalis suspension of the lid is indicated. Beard2 advocated performing more resection than normal to avoid undercorrection.

In severe ptosis, a super maximum (>30 mm) levator resection with frontalis suspension is necessary.7

Medical Care

REFERENCES

If amblyopia is encountered, treat aggressively with occlusion therapy and/or correction of anisometropia prior to any consideration of ptosis surgery. Taping of the ptotic eyelid can be adopted as a temporary measure to avoid visual obstruction.

1. Doucet TW, Crawford JS. The quantification, natural course and surgical results in 57 eyes with Marcus Gunn (jaw-winking) syndrome. Am J Ophthal 1981;92:702-7.

Surgical Care As with any patient who requires eyelid surgery, first address associated strabismus. Many techniques are described for the correction of jaw-winking ptosis, reflecting the ongoing controversy regarding the surgical management of this condition. If the jawwinking is cosmetically insignificant, it can be ignored in the treatment of the ptosis. If the ptosis is mild, the patient may elect not to proceed with surgery. If correction is desired, perform a Muller muscle and conjunctival resection, a Fasanella– Servat procedure, or a standard external levator resection.5,6 If the ptosis is moderate to severe, a

2. Beard C. Ptosis, 3rd edition. St. Louis: CV Mosby 1981: 76-143, 150-74, 184, 207.

3. Demirci H, Frueh BR, Nelson CC. Marcus Gunn jawwinking synkinesis: clinical features and management.

Ophthalmology 2010;117(7):1447-52.

4. Pratt SG, Beyer CK, Johnson CC. The Marcus Gunn phenomenon: a retrospective review of 71 cases.

Ophthalmology 1984;90:27-30.

5. Pratt SG, Beyer CK, Johnson CC. The Marcus Gunn phenomenon. A review of 71 cases. Ophthalmology 1984;91(1):27-30.

6. Bullock JD. Marcus-Gunn jaw-winking ptosis: classification and surgical management. J Pediatr Ophthalmol Strabismus 1980;17(6):3759.

7. Epstein GA, Putterman AM. Super-maximum levator resection for severe unilateral congenital ptosis.

Ophthalmic Surg 1984;15(12):971-9.

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Cipro Group of Drugs May Not be Safe The US Food and Drug Administration announced that fluoroquinolone antibiotics taken orally or by injection pose the risk for permanent peripheral neuropathy, a risk that will appear on updated labels for the drugs.

There are 6 FDA-approved fluoroquinolone drugs in the market: ciprofloxacin, gemifloxacin, levofloxacin, moxifloxacin, norfloxacin, and ofloxacin. The topical fluoroquinolones, applied to the eyes or ears, are not known to have the risk for peripheral neuropathy.

A recent review of cases with the outcome of disability in the FDA Adverse Event Reporting System from January 1, 2003 to August 1, 2012 showed that the onset of peripheral neuropathy after the start of fluoroquinolone therapy was rapid, often within a few days. Some patients who had stopped taking the drug continued to experience nerve damage symptoms for more than a year.

The agency advises clinicians to put patients receiving a fluoroquinolone drug on another class of antibiotics if they develop symptoms of peripheral neuropathy, unless the clinician believes the benefits of fluoroquinolone treatment outweigh the risks. (Medscape)

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A Case of Biotinidase Deficiency Presenting as Quadriparesis THAPAR R*, VENKATNARAYAN K†

ABSTRACT Biotinidase deficiency is a rare disorder with a wide-spectrum of neurological, dermatological, and immunological dysfunction.

Identification of this disorder is important as it is easily treatable and the patients show dramatic response to therapy, besides the fact that it can prove fatal if not diagnosed. We report a case of biotinidase deficiency who presented with quadriparesis, highlighting all these issues.

Keywords: Biotin, biotinidase

B

iotinidase deficiency is a rare metabolic disease with estimated incidence of approximately 1:60,089.1 This enzyme is required for the restoration of free biotin from biocytin after it has activated various carboxylases in the biotin cycle.2,3 Absence of biotinidase results in biotin deficiency, which results in a wide spectrum of neurological, dermatological, and immunological abnormalities.4 CASE REPORT A 3 year 10-month-old girl child was referred to our hospital with complaints of episodes of rapid breathing and progressive weakness of all four limbs. Her complaints had started about 3 months prior when she was admitted for a “lower respiratory tract infection” with predominant complaints of rapid breathing.

Subsequent to this, she continued to have episodes of rapid breathing, for which she received treatment on OPD basis.

Over a period of time, she developed weakness of all four limbs, predominatly of the proximal muscle group, manifesting as unsteady gait and inability to self-feed.

The weakness progressed and she was bedridden at the time of admission (Fig. 1). There was also history of one

*Professor and HOD †Assistant Professor Dept. of Pediatrics Command Hospital (Eastern Command), Alipore, Kolkata Address for correspondence Dr Rajeev Thapar Dept. of Pediatrics Command Hospital (Eastern Command), Kolkata 700 027 E-mail: rajeevrenuthapar@gmail.com

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episode of generalized clonic–tonic seizures 2 weeks prior. She was a product of a nonconsanguineous marriage, with no remarkable delay in attaining the target developmental milestones. Her elder brother had died following similar clinical manifestations of progressive weakness at 4 years of age. In fact, this heightened the parental anxiety to seek medical help.

Clinically, she was alert and had silent tachypnea. Skin manifestations in form of candidal lesions of the axilla (Fig. 2) and the toe clefts (Fig. 3) along with alopecia were present (Fig. 4). The bilateral plantars were extensor with gross hypotonia and the power in the proximal muscles of both limbs was Grade II (as per Medical Research Council Grading System of United Kingdom). Baseline investigations revealed partially compensated metabolic acidosis. Magnetic resonance imaging (MRI) studies showed mild cerebral atrophy with hypoplasia of cerebellar vermis. MRI of spine was suggestive of myelopathy (Fig. 5). Cerebrospinal fluid (CSF) study and ophthalmologic and audiological evaluations were normal.

In view of family history and the episodic nature of respiratory complaints suggestive of metabolic acidosis, along with the skin manifestations, possibility of neurometabolic syndrome was considered. Serum lactate was elevated (31 mg/dL [4.5–19.8 mg/dL]) and the biotinidase activity was 0 nmol/min/mL. The child was started on daily oral biotin 20 mg and made significant recovery. Hyperventilation subsided in 12 h; the child could sit without support in 2 days and started walking in the second week of treatment. Skin lesions healed in the third week and there was hair growth.

PEDIATRICS

Figure 1. Patient presenting with hypotonia and quadriparesis (left panel) and improvement following biotin replacement therapy (right panel).

Figure 2. Axillary candidal skin lesions before (left panel) and after treatment (right panel).

DISCUSSION Biotinidase is an essential enzyme required for recycling biotin by lysing lysine moiety from biocytin, as elucidated in the biotin cycle.2,3 Deficiency of biotinidase results in the deficiency of biotin, which is required as a catalyst for the carboxylase systems in the body. The four main carboxylase systems being: (1)

Pyruvate carboxylase (required for glucose production; inactivity lowers blood sugar resulting in hypoglycemia and lactic acidosis); (2) acetyl-CoA carboxylase (required for biosynthesis of fatty acids by liver and fat cells; inactivity results in reduced availability of stored fatty acids for exercise resulting in hypotonia); (3) propionyl-CoA carboxylase (required for breakdown of amino acids with an odd number of carbons; inactivity

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Figure 3. Candidiasis of toe clefts before (left panel) and after treatment (right panel).

Figure 4. Note the degree of alopecia in a 4-year-old girl child.

Figure 5. MRI cervical spine showing hyperintensities suggestive of myelopathy.

results in propionic academia and reduced activity of citric acid cycle resulting in reduced energy production in the brain, resulting in developmental delays); and (4) methylcrotonyl-CoA carboxylase (required for breakdown of leucine; inactivity results in lowered carnitine levels and methylcrotonylglycinuria).4

with skin lesions, and corroborating with laboratory features of lactic acidosis suggested the diagnosis of biotinidase deficiency in this case.

Although individual deficiencies of all four carboxylases have been reported, the clinical spectrum varies widely from a severe form presenting early (multiple carboxylase deficiency, holocarboxylase synthase deficiency) to milder varieties presenting late (biotinidase deficiency).5,6 The clinical presentation of repeated episodes of hyperventilation, progressive neurological deterioration

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The clinical spectrum of biotinidase deficiency depends on the severity of the defect. The clinical manifestations predominatly include neurological and skin and respiratory manifestations. The neurological spectrum includes seizures, hypotonia, and developmental delay in the early period. Some older children present with progressive spastic quadriparesis and hearing and visual impairment.7 The present case had muscle weakness. In view of the clinical presentation and previous case reports of recurrent myelopathy,7 MRI of spine was done, which was suggestive of myelopathy

PEDIATRICS (Fig. 5). Seborrheic dermatitis, alopecia, and candidal infections due to immunological dysfunction are the predominant skin manifestations and our patient had most of these features. Metabolic acidosis resulting in hyperventilation often masquerades as a primary respiratory illness, as in this patient.

Identification of this disorder is important as it can be treated with supplementation of biotin. Lifelong supplementation upto 40 mg/day is needed that results in both clinical and radiological improvement.

REFERENCES 1. Wolf B. Worldwide survey of neonatal screening for biotinidase deficiency. J Inherit Metab Dis 1991;14(6): 923-7.

2. Frank Y, Ashwal S. Neurologic disorders associated with gastrointestinal diseases, nutritional deficiencies and fluid-electrolyte disorders. In: Pediatric Neurology: Principles and Practice. 4th edition, Swaiman K,

Ashwal S, Ferriero D (Eds.), Elsevier: Philadelphia 2006:p.2317.

3. Enns G, Cowan T, Klein O, Packman S. Aminoacidemias and organic acidemias. In: Pediatric Neurology: Principles and Practice. 4th edition, Swaiman K, Ashwal S, Ferriero D (Eds.). Elsevier: Philadelphia 2006:p.590e1.

4. Wolf B. Disorders of biotin metabolism. In: The Metabolic and Molecular Basis of Inherited Disease. 8th edition, Scriver CR, Beaudet AL, Sly WS, Valle D (Eds.). McGrawHill: New York 2001:p.3935-62.

5. Burri BJ, Sweetman L, Nyhan WL. Mutant holocarboxylase synthetase. Evidence for the enzyme defect in early infantile biotin responsive multiple carboxylase deficiency.

J Clin Invest 1981;68(6):1491-5.

6. Dahiphale R, Jain S, Agarwal M. Biotindase deficiency.

Indian Pediatr 2008;45:777-9.

7. Raha S, Udani V. Biotinidase deficiency presenting as recurrent myelopathy in a 7-year-old boy and a review of the literature. Pediatr Neurol 2011;45(4):261-4.

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ÂÂ

According to a study presented at the annual meeting of the European Respiratory Society, third–hand smoke –– residue that remains on the skin, clothes, and furniture of smokers, even if they do their smoking out of the house –– still impacts children’s breathing. The risk of respiratory tract infections in children from infancy to 13 years of age more than doubled in households in which parents smoked cigarettes but claimed to smoke only outside. There was also a more than doubling of the incidence of recent wheezing in homes where third– hand smoke was reported.

ÂÂ

Two studies that were presented at the American Heart Association’s High Blood Pressure Research meeting in New Orleans have shown that even occasional high blood pressure (BP) readings –– as well as overweight and obesity –– in childhood predicted an increased likelihood of being diagnosed with hypertension in adulthood.

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Medicolegal Cases in Injury Patients and Indian Law AGGARWAL KK

SECTION 324 OF IPC IN MEDICAL PRACTICE

GRIEVOUS HURT AS PER IPC

ection 324: Voluntarily causing hurt by dangerous weapons or means: “Whoever, except in the case provided for by Section 334, voluntarily causes hurt by means of any instrument for shooting, stabbing or cutting, or any instrument which, used as weapon of offence, is likely to cause death, or by means of fire or any heated substance, or by means of any poison or any corrosive substance, or by means of any explosive substance or by means of any substance which it is deleterious to the human body to inhale, to swallow, or to receive into the blood, or by means of any animal, shall be punished with imprisonment of either description for a term which may extend to 3 years, or with fine, or with both”.

S 320 IPC defines grievous hurt and lists eight kinds of hurt which it lables as “grievous”. These clauses are not mutually exclusive for there can be injuries which may fall in more than one clause. However, the list is exhaustive in the sense that, the framers of the Code have used the term “only”, while listing the type of hurts which they designated as “grievous”.

This positively shows that the list is exhaustive and no hurt outside the list given in S. 320 can be termed as ‘grievous hurt’.

S

It is the duty of the attending doctor to record all injuries, their dimensions as much as possible, and the body parts where the injuries are located; the nature of injury, whether simple or grievous; whether caused by sharp/blunt object; age or duration of injury and vital parameters like blood pressure, pulse respiration along with the mental status of the patient.

When an investing officer comes to the hospital he needs some specific answers for his legal investigation and to book a case under the law of land. ÂÂ Are the injuries present, self-inflicted or fabricated?

If yes, please mention the forensic justification.

ÂÂ Are there any signs/symptoms or smell of alcohol

or any drug intoxication? If yes, please opine about the mental status due the influence of intoxication.

Also, preserve the sample of blood.

ÂÂ Please opine if the injured or intoxicated patient is

fit to give statement? If no, please give due reasons and an approximate time interval for medical reevaluation for his/her fitness for statement.

ÂÂ Is the condition of patient critical, severe or serious?

If so, the dying declaration must be recorded by attending doctor before one or two witnesses.

Senior Physician and Cardiologist Moolchand Medcity, New Delhi

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The following kinds of hurt only are designated as “grievous”: First: Emasculation; Secondly: Permanent privation of the sight of either eye; Thirdly: Permanent privation of the hearing of either ear; Fourthly: Privation of any member or joint; Fifthly: Destruction or permanent impairing of the powers of any member or joint; Sixthly: Permanent disfiguration of the head or face; Seventhly: Fracture or dislocation of a bone or tooth; Eighthly: Any hurt which endangers life or which causes the sufferer to be during the space of twenty days in severe bodily pain or unable to follow his ordinary pursuits.

Explanation: To make out the offence of causing grievous hurt, there must be a specific hurt, coming within any of the eight kinds enumerated in this section. A simple hurt cannot be designated as grievous simply because it was on a vital part of the body, unless the dimensions or the nature of the injury or its effects are such that (in the opinion of the doctor) it actually endangers life. For the courts to determine whether the hurt caused is grievous, the extent of the hurt and the intention of the offender have to be taken in to account. Further, it has to be proved that the offender intended to cause or had the knowledge that his act was likely to cause grievous hurt. Intention to cause grievous hurt is inferable from the circumstances of the case and the nature of the injury caused. The medical person, however, must confine himself to only opining whether a given hurt is grievous or otherwise, as per the 8 Clauses of S 320 IPC, and leave the “intention/ knowledge” part to the courts to decide. “Grievous bodily harm, which is defined in the book, is not

MEDILAW necessarily either permanent or dangerous, but harm that seriously interferes with health or comfort. That is sufficient”. An injury is not grievous per se unless the nature, extent and effects of the said injury are such as to endanger the life of the victim, as per the opinion of the doctor, formed in good faith.

MEDICAL TESTIMONY OF DOCTOR IN THE COURT OF LAW (Do not misrepresent documents/medical literature in the Court of Law) When evidence is read into the record of a trial, only that portion of the document, which validates the information being discussed needs to be read aloud.

One paragraph or even one part of a paragraph may be all that is necessary to substantiate the point you are making. Documents must be presented in the words of the author. When you paraphrase evidence, you argue in a circle. Reading the remainder of the document, even if it establishes a context for the evidence, is unnecessary and time–consuming. When a document is cut in a manner, which lends the quoted passage a meaning other than what would be derived from a more complete reading, you are misrepresenting the document. This does not mean, however, that you are responsible for drawing the same conclusions from information as the author of the document. Drawing a contrary conclusion from passages accurately interpreted does not constitute misrepresentation. The fact that the author of the document reached a different conclusion from the information argues perhaps persuasively against your conclusion. However, you have not misused the evidence.

MEDICOLEGAL CASES AND INJURY, ASSAULT AND HURT IN INDIAN LAW The words injury, assault and hurt are invariably used by doctors in hospital practice and are used as synonyms. But all three have a different meaning as per law. It is defined by the Indian Penal Code as below: ÂÂ Injury: Section 44 of IPC defines injury as any

harm whatever illegally caused to any person in body, mind, reputation or property.

ÂÂ Assault: Section 351 of IPC defines assault as an

offer or threat or attempt to apply force on body of another in a hostile manner. It may be a common/ simple assault or an intention to murder.

ÂÂ Hurt: Section 319 of IPC defines hurt as whoever

causes bodily pain, disease or infirmity to any person is said to cause hurt.

When we as doctors deal with cases of hurt/body injury, it means bodily pain, wound, disease or infirmity

voluntarily caused to any person in medicolegal cases.

These would include abrasions, contusions, lacerations, stab wounds, electric shock, firearm, or ligatures, etc. resulting in injury to the human body. The doctor who is certifying an injury report should keep in mind the Penal provisions (as below) required by police to book the case. ÂÂ Simple injury: IPC Section 323. ÂÂ Simple injury caused by dangerous weapons: IPC

Section 324.

ÂÂ Grievous injury: IPC Section 325. ÂÂ Grievous injury caused by dangerous weapons:

IPC Section 326.

ÂÂ Dangerous injury: IPC Section 307. ÂÂ Injury likely to cause death: IPC Section 304. ÂÂ Injury sufficient to cause death: IPC Section 302. ÂÂ Causing hurt by means of poison: IPC Section 328.

PREPARATION OF MLC IN INJURY CASES BY THE ATTENDING DOCTOR ÂÂ Injuries produced by a blunt weapon on tense

skin covering the bones, as on scalp, eyebrow, iliac crest, shin, perineum, knee or elbow look like incised wounds. During the preparation of medicolegal cases (MLC) report the doctors should keep in mind that he has to provide a clue about the weapon used, whether sharp-edged one or otherwise, the direction of the force, the duration of injury and the location of the wound, which may suggest mode of production i.e., suicide, accident, homicides along with whether the injury is fabricated or otherwise.

ÂÂ Wounds produced by a blunt weapon or by a fall

on the hard surface, object, on tense structures/skin covering the bones, such as the scalp, eyebrow, iliac crest, shin, perineum, knee or elbow when the limb is flexed look like incised wounds; but, they are lacerated wounds, also called split lacerations.

These wounds may mislead the doctor and the investigating authorities about a sharp weapon.

ÂÂ When incised-looking wounds are examined by

doctor under magnifying lens, the edges of such wounds are found to be irregular with bruising and wounds are produced by blunt weapon.

ÂÂ An incised wound, cut, slash and slice is a clean

cut through the skin, it may or may not involve underlying tissues and structures. It is caused by a sharp-edged instrument, which is longer than the depth of wound. It is produced by infliction of an object having a sharp-cutting edge such as knife, razor, blade, scalpel, sword over the body.

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MEDIFINANCE

FAQs in Income Tax Planning Q. 1. I am a Doctor in service, I plan to resign from the present job. I intend to setup my own clinic. On starting of own clinic do I have to get registered anywhere?

Ans. On setting-up of a new clinic, you have to first select the constitution and ownership of the said clinic.

It can be a proprietary concern, a partnership, a private limited company or an LLP. For a proprietary concern you do not require any registration. For a partnership concern you need to have a stamped partnership deed which is to be registered with the Registrar of firms. For a company and an LLP you have to get incorporation certificate after complying with the requisite formalities.

In case of proprietary concern your existing Permanent Account Number (PAN) shall hold good, however, in case of the other three entities you have to get a new PAN allotted.

Q. 2. What are the incentives available for Doctors under the Income Tax Act? Ans. There are no special incentives available under the Income Tax Act but on the contrary persons carrying on profession including medical are required to maintain books of account and other documents as may enable the assessing officer to compute the total taxable income in accordance with the provisions of Income Tax Act. However, if you are carrying on profession which includes X-ray, imaging or diagnostic center, etc. and where machinery is installed for manufacture or production of any article or thing an additional depreciation @20% of actual cost of machinery or plant is allowed as deduction. For example, machines used for a production of X-ray, magnetic resonance imaging (MRI), computed tomography (CT) scan, ultrasound images have been accepted as the plant and machinery used for production of article or thing. Similarly, ECG machine, automatic plants and other diagnostic machine, which produce reports are also covered under the said provisions.

Q. 3. For the purpose of setting-up of a diagnostic center-cum-clinic, I float a company and introduce capital of 8 lakhs as if received from 40 shareholders each contributing 20,000/- in cash. Is there anything wrong for which I may have to pay any additional tax?

Ans. Apparently, there is nothing wrong in the process adopted, but the income tax officer can question the

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genuineness of deposits. To satisfy the tax officer you should obtain share application form signed by each applicant giving full details about his address, description and PAN number. Secondly, if you also obtain proof of credit worthiness of the depositor, no addition can be made towards the said deposits. As far as cash payment is concerned, since the depositor is making payment for purchase of an asset, cash payment is also permitted.

Q. 4. I had inherited a house in which I am living with my family. During the year I have purchased another residential flat, for the purpose of investment which has been vacant during the whole year. What shall be the tax effect on the current year income?

Ans. During the year in which you have purchased the second flat, which has been vacant for the whole year, notional income as if earned from the second flat would be taxable at the rate at which the said flat is expected to be let-out in the open market.

Q. 5. I am carrying on the medical profession and have been regularly filing the Income Tax Returns. Taxes due are also paid from time-to-time. This year, if I pay a salary of 22,000/month to my sister-in-law who is living with our family and has no other income, will the expense so incurred be allowed as a deduction out of my taxable income?

Ans. You should be able to justify the payment in relation to the services rendered by your sister-in-law at the clinic. Whether, she looks after administration, maintenance, staff relations, insurance, accounts, finance, banking, clinic consumables, reception, house keeping, cleanliness or other fields; if you can reasonably justify any such services rendered the amount paid as salary shall be allowed as deduction, but since you are making a payment of taxable salary you have to deduct tax at source and to pay the same to the credit of Central Government within seven days from the end of the month of salary payment. For this purpose you are required to obtain a tax deduction account number (TAN) which is to be quoted on all payment challans and on all returns. You have to then file TDS returns quarterly giving details of taxes deducted at source and taxes paid. On all delayed payments of TDS, interest is payable @1% for each month or part of the month.

eMEDI QUIZ

Quiz Time 1.

All of the following are examples of traction epiphysis, except:

4.

A. Mastoid process.

B.

Tubercles of Humerus.

C.

Trochanters of femur.

Marco who was diagnosed with brain tumor was scheduled for craniotomy. In preventing the development of cerebral edema after surgery, the nurse should expect the use of:

A. Diuretics.

D. Condyles of tibia.

B.

Antihypertensive.

2. In all of the following conditions neuraxial blockade is absolutely contraindicated, except:

C.

Steroids.

A. Patient refusal.

B.

Coagulopathy.

C.

Severe hypovolemia.

D.

Pre–existing neurological deficits.

3.

The primary role of chaperones is to help in:

D. Anticonvulsants.

5.

What percentage of your diet should fat make up?

A. About 10% of your daily calories.

B.

About 20% of your daily calories.

A. Protein synthesis.

C.

About 30% of your daily calories.

B.

Protein degradation.

D. About 40% of your daily calories.

C.

Protein denaturation.

E. There is no recommended amount of fat; you should strive to eat as little of it as possible.

D. Protein folding.

Answers to eMedi Quiz Published in November 2013 Issue Q1. (D) Tamoxifen may be associated with an increased risk of ischemic cerebrovascular complications.

Q2. (B) Fluoxetine is the “selective serotonin reuptake inhibitors (SSRI)” of choice for the management of hot

flushes in women taking tamoxifen.

Q3. (D) Unusual geographic clustering of disease.

Q4. (B) Pre-oxygenation is mandatory.

Send your answers to the Editor-Indian Journal of Clinical Practice.

E-mail: editorial@ijcp.com The correct answers will be published in the next issue of IJCP.

Indian Journal of Clinical Practice, Vol. 24, No. 7, December 2013

687

eMEDINEWS INSPIRATION

Two Traveling Angels

T

wo traveling angels stopped to spend the night in the home of a wealthy family. The family was rude and refused to let the angels stay in the mansion’s guest room. Instead the angels were given a small space in the cold basement.

As they made their bed on the hard floor, the older angel saw a hole in the wall and repaired it. When the younger angel asked why, the older angel replied, “Things aren’t always what they seem.” The next night the pair came to rest at the house of a very poor, but very hospitable farmer and his wife.

After sharing what little food they had, the couple let the angels sleep in their bed where they could have a good night’s rest. When the sun came-up the next morning, the angels found the farmer and his wife in tears. Their only cow, whose milk had been their sole income, lay dead in the field.

The younger angel was infuriated and asked the older angel, “How could you have let this happen? The first man had everything, yet you helped him,” she accused.

“The second family had little but was willing to share everything, and you let the cow die.” “Things aren’t always what they seem,” the older angel replied.

“When we stayed in the basement of the mansion, I noticed there was gold stored in that hole in the wall.

Since the owner was so obsessed with greed and unwilling to share his good fortune, I sealed the wall so he wouldn’t find it. Then last night as we slept in the farmer’s bed, the angel of death came for his wife.

I gave him the cow instead. Things aren’t always what they seem.”

Sometimes that is exactly what happens when things don’t turn out the way they should. If you have faith, you just need to trust that every outcome is always to your advantage. You might not know it until sometime later.

Should you find it hard to get to sleep tonight, remember the homeless family who has no bed to lie in.

Should you find yourself stuck in traffic, don’t despair; there are people in this world for whom driving is an unheard of privilege.

Should you have a bad day at work, think of the man who has been out of work for many months struggling to feed his family.

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Indian Journal of Clinical Practice, Vol. 24, No. 7, December 2013

Should you notice a new gray hair in the mirror, think of the cancer patient in chemo who wishes she had hair to examine.

Should you find yourself at a loss and pondering what is life all about, asking, “What is my purpose?”, be thankful, there are those who didn’t live long enough to get the opportunity.

THE TATTOOED HOMELESS MAN He was scary. He sat on the grass with… his cardboard sign, his dog (actually his dog was adorable) and tattoos running up and down both arms and even on his neck.

His sign proclaimed him to be “stuck and hungry” and to please help.

I’m a sucker for anyone needing help. My husband both loves and hates this quality in me. It often makes him nervous, and I knew if he saw me right now, he’d be nervous. But he wasn’t with me right now.

I pulled the van over and in my rear-view mirror, contemplated this man, tattoos and all. He was youngish, may be forty. He wore one of those bandannas tied over his head, biker/pirate style. Anyone could see he was dirty and had a scraggly beard. But if you looked closer, you could see that he had neatly tucked in the black T-shirt, and his things were in a small, tidy bundle. Nobody was stopping for him. I could see the other drivers take one look and immediately focus on something else – anything else.

It was so hot out. I could see in the man’s very blue eyes how dejected and tired and worn-out he felt. The sweat was trickling down his face. As I sat with the airconditioning blowing, the scripture suddenly popped into my head. “Inasmuch as ye have done it unto one of the least of these, my brethren, so ye have done it unto me.”

I reached down into my purse and extracted a tendollar bill. My 12-year-old son, Nick knew right away what I was doing. “Can I take it to him, Mom?” “Be careful, honey.” I warned and handed him the money. I watched in the mirror as he rushed over to the man, and with a shy smile, handed it to him. I saw the man, startled, stand up and take the money, putting it into his back pocket. “Good,” I thought to myself,

eMEDINEWS INSPIRATION “now he will at least have a hot meal tonight.” I felt satisfied, proud of myself. I had made a sacrifice and now I could go on with my errands.

drove away, he was on his knees, arms around his dog, kissing his nose and smiling. I waved cheerfully and then fully broke down in tears.

When Nick got back into the car, he looked at me with sad, pleading eyes. “Mom, his dog looks so hot and the man is really nice.” I knew I had to do more.

I have so much. My worries seem so trivial and petty now. I have a home, a loving husband, four beautiful children. I have a bed. I wondered where he would sleep tonight. My step-daughter, Brandie turned to me and said in the sweetest little-girl voice, “I feel so good.”

“Go back and tell him to stay there, that we will be back in fifteen minutes,” I told Nick. He bounded out of the car and ran to tell the tattooed stranger. I could see the man was surprised, but nodded his agreement. From my car, my heart did a little flip-flop of excitement.

We then ran to the nearest store and bought our gifts carefully. “It can’t be too heavy,” I explained to the children. “He has to be able to carry it around with him.” We finally settled on our purchases. A bag of “Ol’ Roy” (I hoped it was good – it looked good enough for me to eat! How do they make dog food look that way?); a flavored chew-toy shaped like a bone; a water dish, bacon flavored snacks (for the dog); two bottles of water (one for the dog, one for Mr. Tattoos); and some people snacks for the man.

We rushed back to the spot where we had left him, and there he was, still waiting. And still nobody else was stopping for him. With hands shaking, I grabbed our bags and climbed out of the car, all four of my children following me, each carrying gifts. As we walked up to him, I had a fleeting moment of fear, hoping he wasn’t a serial killer.

I looked into his eyes and saw something that startled me and made me ashamed of my judgment. I saw tears.

He was fighting like a little boy to hold back his tears.

How long had it been since someone showed this man kindness? I told him I hoped it wasn’t too heavy for him to carry and showed him what we had brought. He stood there, like a child at Christmas, and I felt like my small contributions were so inadequate. When I took out the water dish, he snatched it out of my hands as if it were solid gold and told me he had no way to give his dog water. He gingerly set it down, filled it with the bottled water we brought, and stood up to look directly into my eyes. His were so blue, so intense and my own filled with tears as he said “Ma’am, I don’t know what to say.” He then put both hands on his bandanna-clad head and just started to cry. This man, this “scary” man, was so gentle, so sweet, so humble.

I smiled through my tears and said “Don’t say anything.” Then I noticed the tattoo on his neck. It said “Mama tried.” As we all piled into the van and

Although it seemed as if we had helped him, the man with the tattoos gave us a gift that I will never forget. He taught that no matter what the outside looks like, inside each of us is a human being deserving of kindness, of compassion, of acceptance. He opened my heart.

BURNED BISCUITS When I was a little child, my mom liked to make breakfast food for dinner every now and then. And I remember one night in particular when she had made breakfast after a long, hard day at work.

On that evening so long ago, my mom placed a plate of eggs, sausage and extremely burned biscuits in front of my dad. I remember waiting to see if anyone noticed!

Yet all my dad did was reach for his biscuit, smile at my mom and ask me how my day was at school. I don’t remember what I told him that night, but I do remember watching him smear butter and jelly on that biscuit and eat every bite!

When I got up from the table that evening, I remember hearing my mom apologize to my dad for burning the biscuits. And I’ll never forget what he said: “Baby, I love burned biscuits.”

Later that night, I went to kiss Daddy good night and I asked him if he really liked his biscuits burned. He wrapped me in his arms and said, “Your Momma put in a hard day at work today and she’s real tired. And besides – a little burned biscuit never hurt anyone!”

You know, life is full of imperfect things… and imperfect people. I’m not the best housekeeper or cook. What I’ve learned over the years is that learning to accept each other’s faults – and choosing to celebrate each other’s differences – is one of the most important keys to creating a healthy, growing, and lasting relationship.

And that’s my prayer for you today!

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Indian Journal of Clinical Practice, Vol. 24, No. 7, December 2013

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Indian Journal of Clinical Practice, Vol. 24, No. 7, December 2013

AROUND THE GLOBE

News and Views ÂÂ As per a new study presented at CHEST 2013, for

fellows in pulmonary and critical care medicine, training with a video laryngoscope, rather than a direct scope, improves first-pass success and decreases the complications of urgent endotracheal intubation. Although research has shown that video laryngoscopy improves glottic visualization during elective surgery in the operating room, direct laryngoscopy is routinely used to perform uncomplicated endotracheal intubation outside the operating room.

ÂÂ Pregnant women who enter the hospital for

reasons unrelated to their pregnancy face a sharply increased risk for thromboembolism during their stay and several weeks thereafter as reported in a study published online November 7 in BMJ. In a review of data on more than 200,000 women, hospital admission during pregnancy was associated with a 17.5-fold increase in the risk for venous thromboembolism (VTE) during the stay and a 6-fold increase in risk in the four weeks after discharge compared with pregnant women who did not require hospitalization.

ÂÂ Diabetes not only affects life of the patient, it has

an adverse impact on the life of immediate family members too as reported in TOI, November 14, 2013. The recently released diabetes attitude wishes and needs (DAWN2) study has captured the trend.

As per the survey, over 61% of the respondents said they faced high level of stress because of their relative with diabetes. Besides, 19% of the respondents perceived a notable diabetes related burden on the family.

ÂÂ Voided

midstream urine cultures frequently contained bacteria not found in paired urethral catheter specimens, questioning the value of midstream voided urine for diagnosis of acute bladder infection. The study reported in NEJM found that the presence of Escherichia coli in midstream specimens had 93% positive predictive value for acute cystitis. However, more than 10% of cultured specimens also grew enterococci and Group B streptococci, which had poor correlation with catheter urine cultures.

ÂÂ The relationships between clinicians and staff play

an important role in patients’ perception of quality care. A new scale, known as the work relationship

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Indian Journal of Clinical Practice, Vol. 24, No. 7, December 2013

scale (WRS), can be used to measure these relationships and may help optimize care delivery in the primary setting. Erin P. Finley, PhD, MPH, from South Texas Veterans Health Care System in San Antonio, Texas, and colleagues published the results of their study in the November/December issue of the Annals of Family Medicine. ÂÂ Healthy people do not require vitamin and/

or mineral supplements to prevent cancer or cardiovascular disease (CVD), according to an analysis of several studies that was published online November 11 in the Annals of Internal Medicine.

ÂÂ Clarithrom`ycin prescribed for patients already

taking antihypertensive calcium-channel blockers is associated with increases in hospitalization for acute kidney injury, hypotension and death, according to new research. The results, presented here at Kidney Week 2013, were also published online November 9 in JAMA.

ÂÂ Teens were more likely to actively respond to

aggressive cues than were children or adults. The study presented at the Society for Neuroscience meeting found that in a go/no–go task, where aggressive faces were a target for “no go,” teens showed a higher propensity than adults or children to react (pressing a button) when presented with an aggressive face. Teens who successfully avoided pressing the button during the no–go cue showed greater activation of the ventromedial prefrontal cortex-the part of the brain that monitors personality and impulse control-when showing restraint against reacting to the aggressive stimulus.

ÂÂ The

number of acquired moles, particularly atypical ones, on children who are at risk for familial melanoma may help predict who will develop the malignancy. According to the authors, physicians should take additional care of children from families at high risk of melanoma. Children with a high number of melanocytic nevi and children with atypical nevi should be included in a surveillance program with the parents. Buttocks should be checked for moles.

ÂÂ A new systematic review has identified nine

variables associated with whether athletes will return to sport after undergoing anterior cruciate ligament (ACL) repair. These include: higher

AROUND THE GLOBE a new analysis published online October 31, 2013 in Diabetes Care. Although younger women were less likely to develop CAD than men if they didn’t have diabetes, the presence of diabetes upped their risk to the point where it equaled their male counterparts, report investigators. Dr Rita Kaylani, Johns Hopkins University, Baltimore, MD, the lead researcher said that while women have a far lower risk of heart disease in the absence of diabetes than men, diabetes effectively equalizes the risk by gender.

postoperative quadriceps strength; less knee effusion; less pain; fewer episodes of instability; greater tibial rotation; lower kinesiophobia; higher athletic confidence; higher preoperative knee self– efficacy; and higher preoperative self–motivation. ÂÂ Testosterone therapy in veterans –– both those who

had coronary artery disease and those who didn’t –– was associated with increased risk of mortality, myocardial infarction, and ischemic stroke, a retrospective cohort study found. The absolute rate of events was 19.9% in a group that did not receive testosterone therapy compared with 25.7% in the group that did, with an absolute risk difference of 5.8% (95% CI, 1.4% to 13.1%) 3 years after the cohort underwent coronary angiography.

ÂÂ Treating obstructive sleep apnea (OSA) modestly

brought down some measures of resistant hypertension beyond what blood pressure medications could achieve alone. In a small randomized trial reported in the November issue of Chest, 6 months of continuous positive airway pressure (CPAP) treatment cut daytime ambulatory blood pressure by 6.5/4.5 mm Hg whereas it rose by 3.1/2.1 mm Hg among controls on medical therapy alone.

ÂÂ Sugar intake was not associated with nonalcoholic

fatty liver disease (NAFLD) in a population of overweight men who were otherwise healthy. In the study reported in the journal Gastroenterology, overweight men who consumed high–fructose or high–glucose diets did not see significant increases in insulin resistance (increase of 0.8 in a homeostasis model assessment versus 0.1), serum concentration of uric acid (22 µmol/L versus 23 µmol/L), concentration of hepatic triacylglycerol, or body weight.

ÂÂ Fine–tuning

the ketogenic diet can have a modest effect on seizure control in children with refractory epilepsy. The retrospective study found that adjusting diet and changing medications had similar benefits and were helpful in meeting seizure control expectations in about 1 in 5 children.

The study findings were presented at the Child Neurology Society (CNS) 2013 Annual Meeting.

ÂÂ Major depressive disorder (MDD) is the second

leading cause of disability worldwide and a major contributor to the burden of suicide and ischemic heart disease, according to new data published online in November 5 in PLoS Medicine. The findings stem from the latest Global Burden of Disease (GBD) study and highlight the importance of including depressive disorders as a global health priority.

ÂÂ According to a study presented at the annual

ÂÂ Total

deaths worldwide from cirrhosis and liver cancer rose by 50 million per year over 2 decades, according to the first–ever WHO study of liver disease mortality. The liver disease–specific findings from the WHO Global Burden of Disease Study were presented at the Liver Meeting 2013.

ÂÂ Young and middle–aged women with diabetes

have a significantly increased risk of coronary artery disease (CAD), according to the results of

meeting of the American Association for the Study of Liver Diseases, use of high–dose steroids as an adjuvant treatment after hepatoportoenterostomy for pediatric biliary atresia did not help prevent the need for liver transplantation. Of the 70 children assigned to receive corticosteroids following hepatoportoenterostomy, 58.6% achieved a total bilirubin of < 1.5 mg/dL at 6 months with his or her native liver vs 48.6% of the 70 children who were treated with placebo, for an adjusted relative risk of 1.14 in both the intention–to–treat analysis and in the per–protocol analysis. In the secondary endpoint, survival with the native liver at 24 months was 58.7% with steroids and 59.4% with placebo.

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Indian Journal of Clinical Practice, Vol. 24, No. 7, December 2013

693

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LIGHTER READING

Lighter Side of Medicine QUOTE

MAKE SURE

During Medical Practice An 18–year–old girl complained of purulent nasal discharge, nasal congestion, pain in the cheek and upper teeth for last 10 days. CT scan showed maxillary sinusitis.

“For success, attitude is equally as important as ability.”

–Harry F. Banks

MIND TRIVIA

Remember to give macrolides.

1.

Below are 3 pairs of words. Find the words that fit in the middle of each pair of words to create two new words, one front-ended and one backended.

Example: EVER - ______ - HORN ©IJCP Academy

Answer: EVER - GREEN - HORN

Make sure to remember that clarithromycin (macrolide) 500 mg twice-daily for 7 days is not only effective in maxillary sinusitis but also in other sinusitis.

Ans. (1) LENGTH - WISE - CRACK (2) WITH - HOLD - OVER (3) MAKE - SHIFT - LESS

ILLUSION

Dr. Good and Dr. Bad SITUATION: A patient came with back pain which was worse in the morning and improved with walking.

©IJCP Academy

It is inflammatory spinal arthritis

LESSON: Inflammatory spinal arthritis means (back pain of more than 3 months duration) of back discomfort before the age of 40 years, insidious onset, improvement with exercise, no improvement with rest and pain at night with improvement upon arising. Presence of 4 out of 5 features has 77% sensitivity and 92% specificity for inflammatory spinal joint disease.

KK Aggarwal

696

2. WITH - _______ - OVER 3. MAKE - _______- LESS

KK Aggarwal

It is osteoarthritis

1. LENGTH - _____- CRACK

Indian Journal of Clinical Practice, Vol. 24, No. 7, December 2013

Information for Authors Manuscripts should be prepared in accordance with the ‘Uniform requirements for manuscripts submitted to biomedical journals’ compiled by the International Committee of Medical Journal Editors (Ann. Intern. Med. 1992;96: 766-767).

Indian Journal of Clinical Practice strongly disapproves of the submission of the same articles simultaneously to different journals for consideration as well as duplicate publication and will decline to accept fresh manuscripts submitted by authors who have done so.

The boxed checklist will help authors in preparing their manuscript according to our requirements. Improperly prepared manuscripts may be returned to the author without review. The checklist should accompany each manuscript.

Authors may provide on the checklist, the names and addresses of experts from Asia and from other parts of the World who, in the authors’ opinion, are best qualified to review the paper.

Covering letter –

– –

The covering letter should explain if there is any deviation from the standard IMRAD format (Introduction, Methods, Results and Discussion) and should outline the importance of the paper.

Principal/Senior author must sign the covering letter indicating full responsibility for the paper submitted, preferably with signatures of all the authors.

Articles must be accompanied by a declaration by all authors stating that the article has not been published in any other Journal/Book. Authors should mentioned complete designation and departments, etc. on the manuscript.

Manuscript Three complete sets of the manuscript should be – submitted and preferably with a CD; typed double spaced throughout (including references, tables and legends to figures).

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The manuscript should be arranged as follow: Covering letter, Checklist, Title page, Abstract, Keywords (for indexing, if required), Introduction, Methods, Results, Discussion, References, Tables, Legends to Figures and Figures.

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Note: Please keep a copy of your manuscript as we are not responsible for its loss in the mail. Manuscripts will not be returned to authors.

Title page Should contain the title, short title, names of all the authors (without degrees or diplomas), names and full location of the departments and institutions where the work was performed,

name of the corresponding authors, acknowledgment of financial support and abbreviations used.

– The title should be of no more than 80 characters and should represent the major theme of the manuscript.

A subtitle can be added if necessary.

– A short title of not more than 50 characters (including inter-word spaces) for use as a running head should be included.

– The name, telephone and fax numbers, e-mail and postal addresses of the author to whom communications are to be sent should be typed in the lower right corner of the title page.

– A list of abbreviations used in the paper should be included. In general, the use of abbreviations is discouraged unless they are essential for improving the readability of the text.

Summary – The summary of not more than 200 words. It must convey the essential features of the paper.

– It should not contain abbreviations, footnotes or references.

Introduction – The introduction should state why the study was carried out and what were its specific aims/objectives.

Methods – These should be described in sufficient detail to permit evaluation and duplication of the work by others.

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Statistics The following information should be given: – The statistical universe i.e., the population from which the sample for the study is selected.

– Method of selecting the sample (cases, subjects, etc. from the statistical universe).

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– Statistical methods used for presentation and analysis of data i.e., in terms of mean and standard deviation values or percentages and statistical tests such as Student’s ‘t’ test, Chi-square test and analysis of variance or non-parametric tests and multivariate techniques.

–

Confidence intervals for the measurements should be provided wherever appropriate.

Results –

These should be concise and include only the tables and figures necessary to enhance the understanding of the text.

Indian Journal of Clinical Practice, Vol. 24, No. 7, December 2013

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Discussion –

This should consist of a review of the literature and relate the major findings of the article to other publications on the subject. The particular relevance of the results to healthcare in India should be stressed, e.g., practicality and cost.

References These should conform to the Vancouver style. References should be numbered in the order in which they appear in the texts and these numbers should be inserted above the lines on each occasion the author is cited (Sinha12 confirmed other reports13,14...). References cited only in tables or in legends to figures should be numbered in the text of the particular table or illustration. Include among the references papers accepted but not yet published; designate the journal and add ‘in press’ (in parentheses). Information from manuscripts submitted but not yet accepted should be cited in the text as ‘unpublished observations’ (in parentheses).

At the end of the article the full list of references should include the names of all authors if there are fewer than seven or if there are more, the first six followed by et al., the full title of the journal article or book chapters; the title of journals abbreviated according to the style of the Index Medicus and the first and final page numbers of the article or chapter. The authors should check that the references are accurate. If they are not this may result in the rejection of an otherwise adequate contribution.

Examples of common forms of references are: Articles Paintal AS. Impulses in vagal afferent fibres from specific pulmonary deflation receptors. The response of those receptors to phenylguanide, potato S-hydroxytryptamine and their role in respiratory and cardiovascular reflexes.

Q. J. Expt. Physiol. 1955;40:89-111.

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Please complete the following checklist and attach to the manuscript: 1. Classification (e.g. original article, review, selected summary, etc.)_______________________________ 2. Total number of pages ________________________ 3. Number of tables ____________________________ 4. Number of figures ___________________________

Books

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Stansfield AG. Lymph Node Biopsy Interpretation Churchill Livingstone, New York 1985.

Indian 1.____________Foreign 1._ _______________

Articles in Books

2.____________

2._ _______________

Strong MS. Recurrent respiratory papillomatosis. In: Scott Brown’s Otolaryngology. Paediatric Otolaryngology Evans JNG (Ed.), Butterworths, London 1987;6:466-470.

3.____________

3._ _______________

4.____________

4._ _______________

Tables –

These should be typed double spaced on separate sheets with the table number (in Roman Arabic numerals) and title above the table and explanatory notes below the table.

Legends – These should be typed double spaces on a separate sheet and figure numbers (in Arabic numerals) corresponding with the order in which the figures are presented in the text.

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698

The legend must include enough information to permit interpretation of the figure without reference to the text.

Indian Journal of Clinical Practice, Vol. 24, No. 7, December 2013

6. Suggestions for reviewers (name and postal address)

7. All authors’ signatures________________________ 8. Corresponding author’s name, current postal and e-mail address and telephone and fax numbers __________________________________________

Online Submission Also e- Issue @ www.ijcpgroup.com For Editorial Correspondence

Dr KK Aggarwal

Group Editor-in-Chief Indian Journal of Clinical Practice E-219, Greater Kailash, Part-1 New Delhi - 110 048. Tel: 40587513 E-mail: editorial@ijcp.com Website: www.ijcpgroup.com

R.N.I. No. 50798/90 Date of Publication 13th of Same Month Date of Posting 13-14 Same Month

DL (S)-01/3200/2012-2014 Posted in N.D. PSO New Delhi