Indian journal of clinical practice march 2014 by IJCP

Indexed with IndMED

ISSN 0971-0876

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Volume 24, Number 10

March 2014, Pages 901-1000

Peer Reviewed Journal

zz American Family Physician zz Anesthesiology zz

Cardiology zz Community Medicine zz Diabetology zz Hematology zz Infections zz Internal Medicine zz Neurology zz Neurosurgery zz Obstetrics and Gynecology zz Ophthalmology zz Pediatrics zz Surgery zz Medilaw

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IJCP Group of Publications Dr Sanjiv Chopra Prof. of Medicine & Faculty Dean Harvard Medical School Group Consultant Editor Dr Deepak Chopra Chief Editorial Advisor Padma Shri, Dr BC Roy National & DST National Science Communication Awardee

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 10, March 2014 from the desk of THE group editor-in-chief

905 The Future of Healthcare: A Collective Vision-Conference Highlights

KK Aggarwal

American Family Physician

909 Diagnosis and Management of Physical Abuse in Children

Charles Kodner, Angela Wetherton

916 Practice Guidelines 919 Photo Quiz Anesthesiology

921 Conscious Sedation: An Observation

Jayashree Sen, Bitan Sen

CARDIOLOGY

925 Superficial Brachial Artery: Its Embryological and Clinical Significance

Meenakshi Khullar

Community Medicine

929 Study of Vitamin B12, Folic Acid and Related Hematological Indices in Tobacco Users

Tarachand Saini, Subhash Saini, Maniram Kumhar

Diabetology

932 Association Between Indexes of Insulin Sensitivity/Resistance

and Serum Magnesium Levels in Overweight Diabetic Subjects

Neetesh Kumar Gupta, Sonali Sharma, GG Kaushik, Bhavana Gupta

Hematology

938 Leukemia Cutis with PML-RAR-a Translocation

Leena Dennis Joseph, K Krishnarathnam, Suresh Masilamani, Rajendiran Swaminathan

941 Coomb’s Negative Hemolytic Anemia in Wilson’s Disease

V Padma, Halleys Kumar

Infections

944 Bacteriological Study of Infective Endocarditis from a Rural Area of Maharashtra

Sabiha S Tamboli, SL Nilekar

Internal Medicine

948 Atypical Presentation of Multiorgan Failure Leptospirosis (Weil’s Disease) without Fever

Swamikannu Murugan, Muhammed Zohaib Ghatala, Anand Sankar S, Jothi Krishnan

952 A Clinical Study of Febrile Thrombocytopenia: A Hospital-based Retrospective Study

Praveen Kumar, Kalpana Chandra

Neurology

958 An Experience of Chronic Inflammatory Demyelinating Polyradiculoneuropathy with Pregnancy

Debasmita Mandal, Chaitalli Dattaray, Mousumi Datta, Alok Pandit, Saroj Mandal, Shyamal Das

Neurosurgery

962 Pneumocephalus after Ventriculoperitoneal Shunt: Diagnostic

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

Dilemma and its Endoscopic Management

Hanish Bansal, Rakesh Kaushal, Manish Munjal

Obstetrics and Gynecology

968 Vaginal Leiomyoma: Unusual Case Presentation

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

Kavyashree G, Manohar R, Kala B

970 Imaging Diagnostic Dilemma of Large Subchorionic Hematoma

PS Baldawa

974 Assessment of Cesarean Section Scar Strength: Still A Challenge?

The copyright for all the editorial material contained in this journal, in the form of layout, content including images and design, is held by IJCP Publications Ltd. No part of this publication may be published in any form whatsoever without the prior written permission of the publisher.

Urvashi Verma, Mukesh Chandra, Arun Nagrath, Saroj Singh, Rachana Agrawal

978 Exceptional Case of Omphalocele (Exomphalos Major)

Editorial Policies

K Tabassum, Mohd Zulkifle, Mohd Nasir, Yasmeen K

Ophthalmology

The purpose of IJCP Academy of CME is to serve the medical profession and provide print continuing medical education as a part of their social commitment. The information and opinions presented in IJCP group publications reflect the views of the authors, not those of the journal, unless so stated. Advertising is accepted only if judged to be in harmony with the purpose of the journal; however, IJCP group reserves the right to reject any advertising at its sole discretion. Neither acceptance nor rejection constitutes an endorsement by IJCP group of a particular policy, product or procedure. We believe that readers need to be aware of any affiliation or financial relationship (employment, consultancies, stock ownership, honoraria, etc.) between an author and any organization or entity that has a direct financial interest in the subject matter or materials the author is writing about. We inform the reader of any pertinent relationships disclosed. A disclosure statement, where appropriate, is published at the end of the relevant article.

980 Management of a Complicated Case of Symblepharon with Amniotic Membrane Transplantation

P Jain, JP Chugh

PEDIATRICS

983 Cord Blood Nucleated RBC as a Predictor of Perinatal Asphyxia, Severity and Outcome

Anil Kumar Mohanty, Leena Das, Subal Pradhan, Bijay Meher, Siba Shankar Beriha

Surgery

987 Omental Torsion: A Review of Literature and Case Report

Y Ghosh, R Arora

MEDILAW

989 Acid Throwing: A Cause of Concern in India

DS Bhullar

eMEDINEWS INSPIRATION

992 An Inspirational Story about Faith

Note: Indian Journal of Clinical Practice does not guarantee, directly or indirectly, the quality or efficacy of any product or service described in the advertisements or other material which is commercial in nature in this issue.

eMEDI QUIZ

994 Quiz Time LIGHTER READING

996 Lighter Side of Medicine

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from the desk of THE group editor-in-chief Dr KK Aggarwal Padma Shri, Dr BC Roy National & DST National Science Communication Awardee Sr. Physician and Cardiologist, Moolchand Medcity President, Heart Care Foundation of India Group Editor-in-Chief, IJCP Group and eMedinewS National Senior Vice President, 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)

The Future of Healthcare: A Collective Vision-Conference Highlights

he Future of Healthcare: A Collective Vision”, a firstof-its kind global healthcare conference was held in New Delhi on March 3-4, 2014 with an objective to provide a powerful platform to industry stakeholders to brainstorm unique solutions and innovative strategies to help lead humanity towards a healthier future. With participation from over 15 countries and the presence of more than 500 delegates, the two-day event hosted by the Healthcare Alliance, was a grand success with a large number of thought leaders, policy makers, senior Government officials and business and health leaders from India and across the globe in attendance. The first day of the Conference, hosted by The Healthcare Alliance, saw a splendid turnout of thought leaders, policy makers, senior Government officials and business and health leaders from India and across the globe. The inaugural session witnessed the presence of personalities like Montek Singh Ahluwalia, Deputy Chairman, Planning Commission of India; Lov Verma, Health Secretary, Ministry of Health & Welfare, Government of India; Prof K Srinath Reddy, President, Public Health Foundation of India; Lord Nigel Crisp, Crossbench member, House of Lords and Dr Prathap C Reddy, Chair of The Healthcare Alliance and Chairman of Apollo Hospitals Group, all of whom delivered a special address to the audiences. The second and the concluding day of the Conference began with special addresses by health ministers from Botswana, Maldives, Mongolia, Mozambique and Sri Lanka who shared their vision of the future of healthcare with the audiences. This was followed by a special address by Krishna Udayakumar, Head, Global Innovation, Duke Medicine. With participation from over 15 countries and the presence of more than 500 delegates, the powerpacked, morning-to-evening agenda focused on three critical issues facing the healthcare industry worldwide: ÂÂ The rising incidence of noncommunicable diseases (NCDs) and how to curb it through primary and preventive

healthcare

ÂÂ Setting up successful Public-Private-People (PPP) Partnerships ÂÂ Meeting the manpower needs of the future by up-skilling and up-scaling talent.

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from the desk of THE group editor-in-chief Dr Prathap C Reddy, Chair of The Healthcare Alliance & Chairman of Apollo Hospitals Group addressed the audience at the formal inauguration of the conference. He said, “Amazing progress has been made in healthcare over the last 30 years, yet barriers of accessibility, quality and cost persist. New challenges have risen, such as the worrying ascent of NCDs, which claim 36 million lives every year in the world, with nearly 80% of these deaths occurring in low- and middle-income countries. The need of the hour is four-fold: Preventive healthcare, making people partners in PPP, up-scaling and up-skilling the manpower, and accelerating the pace of innovation. This Conference provides a common platform for collective thinking for stakeholders of the nation and global thought leaders to come up with an agenda for the future. We have to work towards the dream of a disease-free world. This is the big challenge for the future of healthcare.” He further said, “The current healthcare systems of countries would become unsustainable soon if they continue to function as they do currently. While healthcare is primarily organized within national boundaries the issues and challenges involved are truly global. At the broadest level, sustainability and convergence are the two major issues to be dealt with across the global. I am sure the solutions and the action agenda that have arisen from this two-day Conference would not only favorably impact healthcare in India, but also serve as a unique model for addressing health challenges globally.” The Conference began with opening remarks by Sangita Reddy, Executive Director, Apollo Hospitals Group, who warmly welcomed the guests. She expressed hope that the deliberations and sessions over 2 days of the event would result in concrete recommendations to shape the future of healthcare not only in India but also in other countries facing similar demographic and economic challenges. Highlights of the Conference The main highlights of the entire Conference were its power-packed sessions focusing on the immediate and urgent challenges in healthcare that are needed to be addressed to ensure a healthier tomorrow and the launch of four white papers by knowledge partners of The Healthcare Alliance formulated by KPMG, Brain & Company, PwC, and McKinsey & Company. The white papers, each focusing on a specific area of the conference highlighted by the sessions, are a result of over 3 months of collaboration between members of The Healthcare Alliance and thought leaders from around the world to arrive at global solutions that are systemic, sustainable and impactful. Each paper looks into a definitive way forward and an action plan to impact the future of healthcare in the 21st century. Plenary Session 1: Control of NCDs through Primary and Preventive Healthcare Shobana Kamineni, Executive Director (New Initiatives), Apollo Hospitals Group, set the context for the plenary session on “Control of NCDs through Primary and Preventive Healthcare” which was followed by the keynote address by Prof K Srinath Reddy, President, Public Health Foundation of India. The insightful panel discussion saw several significant stakeholders as participants, including Anshu Prakash, Principal Secretary (Health & Family Welfare), Government of India; Planning Commission Member Syeda Hameed; John Brooks, President & CEO, Joslin Diabetes Center; Dr V Mohan, Chairman & Chief of Diabetology, Dr Mohan's Diabetes Specialty Centre, and Shailesh Ayyangar, MD & President, Sanofi India. The session was moderated by Karan Singh, Bain & Company’s Asia-Pacific Healthcare practice head. The main take-away from the discussion: With NCDs snatching away precious lives, a population equal to the size of a nation like Canada, each year across the world, this is a threat that can no longer be ignored. The solution lies in strengthening primary care for early detection and popularizing preventive care to bring down the incidence. Panelists recommended high-impact interventions and large-scale outreach throughout the country, articulation of a national vision for combating NCDs, and partnering with community service organizations for creating better awareness. They also called upon the health service providers to expand their reach, deliver high quality but affordable care, and address the demand for information and specially trained professionals. Pharmaceutical and medical technology companies need to develop and deploy an integrated approach to providing cost-effective medical products and work with policy makers to make affordable medicines available, the panelists recommended. Plenary Session 2: Public-Private-People Partnerships The panelists at the session on Public-Private-People Partnerships (PPPP) were unanimous about the importance of including people as partners in the existing PPP model to make it more effective and inclusive. They noted

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from the desk of THE group editor-in-chief that global healthcare systems are increasingly coming under stress due to rising costs. India too needs huge investments to bring its healthcare infrastructure to international levels of penetration. Even as PPPs are becoming popular for service delivery, it is essential to consider people as a critical part of the health ecosystem, the participants concluded in a free-wheeling discussion moderated by Rana Mehta, Leader - Healthcare, PwC India. Chandrajit Banerjee, Director General, Confederation of Indian Industry (CII), set the context for the discussions that revolved around the ingredients required to deliver successful healthcare PPPs. Dr Paul Da Rita, Head, Global Health PPP Advisory, International Finance Corporation, delivered the keynote address. Panelists recommended that the Government develop a health PPP policy framework, create an institutional mechanism to support health PPPs, ensure contractual flexibility and continued sharing of risks and rewards, devise an appropriate pricing and incentive mechanism to improve quality, affordability and viability, and benchmark best practices. Other action points from the panelists included the need for providers to evolve business models with fair margin and high volumes, collaborate with the Government in developing a policy framework, benchmark their own performance and develop strategies for human resource augmentation. The participants also came up with specific recommendations for the community and citizens at large. Plenary Session 3: Talent Fast-forward: Upskill, Upscale The keynote address by Lord Nigel Crisp, Crossbench member, House of Lords, kick-started the session titled “Talent fast-forward: Upskill, Upscale,” with the context being set by Rajendra Pawar, Chairman, NIIT. The acute dearth of adequately educated or trained healthcare professionals was deeply felt by the panelists, who pointed out that this issue is limiting access and quality of healthcare services in India. They deliberated upon the challenge of ensuring sufficient supply of manpower for expansion of healthcare to all corners of the country and came up with many interesting ideas that showed the most practical way forward. The Government being the strongest influencer among all the stakeholders, the panelists recommended that it should ensure standardization across key elements of talent development, put together a policy framework to minimize entry barriers, and lay down regulations for up-skilling. They were of the view that healthcare trainers also need to redesign training structure and introduce innovations in training, while healthcare providers should restructure HR processes to comply with accreditation guidelines and collaborate with other stakeholders to achieve workforce outcomes. Plenary Session 4: Role of Innovation in Achieving Universal Access to Healthcare Dr. Didar Singh, Secretary General, FICCI, set the context for the debate at the plenary session on the “Role of Innovation in Achieving Universal Access to Healthcare” while Dr. Victor Dzau, Chancellor, Health Affairs, Duke, University and soon to be President of Institute of Medicine, USA delivered the keynote address. Thomas Kibasi, Associate Partner, McKinsey & Company, proficiently moderate the discussion that included panelists from Sequoia Capital, One Family, Medical, Swasth India, EI Camino Hospital, and Labour Welfare Department, Government of India. Panelists called upon the Government to set up an institute for innovative healthcare service delivery and an innovation incubator to fund innovators. They also suggested it should set up cells to exclusively deal with PPPs and innovative pilots, draft a PPP policy that is aligned with public policy goals, and offer tax rebates to healthcare products designed and made in India. The Participants advised the healthcare industry to conduct 'innovation expos' to showcase healthcare innovations, create a formal innovation alliance among multiple stakeholders to encourage innovations in the industry, and set up an in-house venture-capital arm to acquire innovative firms. Other recommendation included launching incubators for healthcare research at educational institutes and incentivizing faculty to conduct joint research with starts-ups, industry and students. The session also saw the launch of White Paper by McKinsey & Company titled “Role of Innovation in Achieving Universal Access to Healthcare.”

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from the desk of THE group editor-in-chief Plenary Session 5: Future Perfect At the final session, heads of Apollo Hospitals, Fortis Healthcare, Medicity, Narayana Health and Stanford Hospital and Clinic along with the World Health Organization outlined their vision of the future of healthcare for India and the world. Luminaries who spoke on the occasion included Suneeta Reddy, Dr Devi Shetty, Dr Naresh Trehan, Shivinder Singh, Amir Dan Rubin and Dr Seif Seleman Rashidi (Minister of Health, Tanzania). The Conference also included a lively conversation on the theme "The Where, What and How - for the Future of Healthcare” facilitated by Dr Anupam Sibal, Group Medical Director, Apollo Hospitals, along with Dr. John Adler, Inventor CyberKnife and Chief of new Clinical Applications, Varian, Dr Rajiv Doshi, Executive Director, StanfordIndia Biodesign and Dr Euan Thomson, Operating Partner, Khosla Ventures. Recommendations arising from the deliberations at the conference as four White Papers were presented to Shri Pranab Mukherjee, The Hon’ble President of India and Shri Ghulam Nabi Azad, Minister of Health & Family Welfare, Government of India, at a private event at the Rashtrapati Bhawan Auditorium on March 4, 2014, the second and final day of the event. The delegation from The Healthcare Alliance was led by its Chair Dr Prathap C Reddy, Founder Chairman, Apollo Hospitals Group along with Prof K Srinath Reddy, President, Health of Foundation of India and Dr Jaishreeben Mehta, President, Medical Council of India. The action agenda submitted to the Government by The Healthcare Alliance includes recommendations such as: ÂÂ Setting up an institute for innovative healthcare service delivery ÂÂ Establishing an innovation incubator for healthcare ÂÂ Creating cells to exclusively deal with PPPs and innovative pilots ÂÂ Developing the policy framework and institutional mechanism for health PPPs ÂÂ Offering tax rebates to indigenously designed and manufactured healthcare products ÂÂ Standardizing across key elements of health manpower development ÂÂ Creating a policy framework to minimize entry barriers for medical education ÂÂ Driving high-impact interventions and forging partnership for large-scale outreach in healthcare ÂÂ Allowing private players to manage primary healthcare centers in under-served areas ÂÂ Partnering with community service organizations to build awareness about health challenges ÂÂ Allowing health insurers to introduce products that meet community requirements ÂÂ Facilitating scaling up of successful experiments in healthcare service delivery. ■■■■

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American Family Physician

Diagnosis and Management of Physical Abuse in Children CHARLES KODNER, ANGELA WETHERTON

Abstract Child abuse is the third leading cause of death in children between one and four years of age, and almost 20% of child homicide victims have contact with a health care professional within a month of their death. Therefore, family physicians are in an ideal position to detect and intervene in cases of suspected child maltreatment. There is currently insufficient evidence that screening parents or guardians for child abuse reduces disability or premature death. Assessment for physical abuse involves evaluation of historical information and physical examination findings, as well as radiographic and laboratory studies, if indicated. The history should be obtained in a non-accusatory manner and should include details of any injuries or incidents, the patient’s medical and social history, and information from witnesses. The physical examination should focus on bruising patterns, injuries or findings concerning for abuse, and palpation for tenderness or other evidence of occult injury. Skeletal survey imaging is indicated for suspected abuse in children younger than two years. Imaging may be indicated for children two to five years of age if abuse is strongly suspected. Detailed documentation is crucial, and includes photographing physical examination findings. Physicians are mandated by law to report child abuse to the local child protective services or law enforcement agency. After a report is made, the child protection process is initiated, which involves a multidisciplinary team approach.

Keywords: Child abuse, radiographic, laboratory, imaging, documentation, child protection

hild abuse is a significant problem that often goes unrecognized until severe injury or death has occurred.1 In 2008, the number of child abuse fatalities was six times that of influenza A (H1N1) fatalities in children.2 In 2009, child abuse was the third leading cause of death in children between one and four years of age.3 As many as 50% of abused children are abused multiple times.4 According to one study, almost 20% of child homicide victims had contact with a health care professional within one month of their death.1

Although the devastating and sometimes deadly consequences of child abuse are undeniable, studies providing data on optimal means of prevention, intervention, and management are lacking. A system atic review for the US Preventive Services Task Force found insufficient evidence that screening and behavioral interventions for parents or guardians for physical abuse or neglect of children reduced disability or premature death.5

CHARLES KODNER, MD, is an associate professor in the Department of Family and Geriatric Medicine at the University of Louisville (Ky.) School of Medicine. ANGELA WETHERTON, MD, is an associate professor in the Department of Family and Geriatric Medicine at the University of Louisville School of Medicine. Source: Adapted from Am Fam Physician. 2013;88(10):669-675.

Child protective services agencies received approximately 3.4 million referrals involving the alleged maltreatment of approximately 6.2 million children during the 2011 federal fiscal year.6 Teachers, law enforcement, legal personnel, and social services were the most common sources of reports that year, whereas medical personnel accounted for 8.4% of referrals.6 Child abuse is a diagnosis physicians cannot afford to miss. Family physicians can play a key role in protecting children by considering abuse as part of the differential and reporting it if suspected. Definition The Child Abuse Prevention and Treatment Act, as amended by the Keeping Children and Families Safe Act of 2003, defines abuse as “any recent act or failure to act on the part of a parent or caretaker which results in death, serious physical or emotional harm, sexual abuse or exploitation” or “an act or failure to act which presents an imminent risk of serious harm.”7 Each state has its own definition of child abuse based on this standard, although there is significant variation in intolerance of corporal punishment and in what constitutes abuse.8 Most states recognize four major types of maltreatment: neglect, physical abuse, psy chological maltreatment, and sexual abuse. Because of the broad nature of this topic, this article focuses on physical abuse.

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American Family Physician

The American Academy of Family Physi cians acknowledges that the diagnosis and treatment of child abuse are complex, and require a multidisciplinary approach to caring for the child involved, as well as the child’s family.9 There is insufficient evidence that any specific screening strategy or behavioral intervention produces better health outcomes than clinician awareness and evaluation of potential signs of abuse.5 Table 1 summarizes key steps that physicians can take to counsel families and prevent abuse.10

abuse may present with difficulty breathing or unre sponsiveness.1 Children who are evaluated for an apparent life-threatening event may also be victims of abuse. In a prospective series of 243 infants admitted to a tertiary care medical center for evaluation of an appar ent life-threatening event, 2.5% were diagnosed with abusive head injuries.12 Epistaxis in children is common, but may be a sign of physical abuse during the first two years of life.13 In a retrospective series of infants who were evaluated for symptoms that were not initially recognized as the result of abusive head trauma, 65% were described as irritable and 56% were vomiting.14

History

Physical Examination

In addition to asking parents, caregivers, or other witnesses for a detailed description of the circumstances surrounding a suspicious injury, assessing the child’s general medical, social, and developmental history is critical.8 A complete, well-documented history that occurs early in the course of evaluation can serve crucial legal and medical roles. The history should be obtained in a thorough but non-accusatory manner.8 Features of the history that should be elicited, as well as features that are concerning for intentional trauma, are listed in Table 2.8,11 Physicians must evaluate the consistency of a caregiver’s history with other findings from the history or physical examination.

Table 3 lists physical examination steps to perform in an evaluation for child abuse, with possible causes or findings that are suggestive of abuse.8 In general, injuries to multiple areas, injuries in various stages of healing, and specific patterns of injuries are suspicious for physical abuse.11 Although accidental injuries often occur on bony prominences, inflicted injuries tend to occur in protected areas, such as the neck, buttocks, trunk, and upper arms.8 The TEN-4 bruising clinical decision rule may be useful to identify children and infants who should be evaluated for physical abuse.15 This rule was developed from a case-control study of 95 children younger than 48 months who were admitted to a pediatric intensive care unit because of trauma.15 The TEN-4 rule states that bruising on the torso, ear, or neck (TEN) in a child four years or younger, or bruising

Recognition, Screening, and Prevention

Physically abused children may present with nonspecific symptoms. Children with severe injuries resulting from

Table 1. Steps Primary Care Physicians Can Take to Prevent Child Abuse Step

Comment

Obtain and periodically update a child’s social history.

Screen for risk factors or problems, and reinforce or correct parenting skills; see the parent assessment form at http://brightfutures.aap.org/pdfs/Other%203/PSQ_screen.pdf and other resources at http://brightfutures.aap.org.

Acknowledge difficulties and frustrations with parenting.

Provide anticipatory guidance for situations or developmental stages that may be triggers for child maltreatment.

Talk with parents about their infant’s crying and how they cope with it.

Discuss normal infant behavior and methods to respond to crying.

Recognize the increased risk of abuse in children with disabilities.

Discuss options for respite care; talk with parents about who else has contact with their child.

Assess parents for intimate partner violence and postpartum depression.

Refer parents to appropriate community services if intimate partner violence is identified, and provide or refer for appropriate care for depression.

Guide parents in providing effective discipline.

See American Academy of Pediatrics’ guidance at http://pediatrics.aappublications.org/ content/101/4/723.full.

Information from reference 10.

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American Family Physician Table 2. Medical History in Children with Suspected Intentional Trauma Comprehensive history components Medical history, including prior injuries, trauma, hospitalizations, medical illnesses, or congenital conditions Family history, particularly of bleeding disorders, bone disorders, or metabolic/genetic conditions Pregnancy history, including whether the pregnancy was planned or unplanned Description of familial disciplinary patterns or practices Description of the child’s temperament, especially whether he or she is typically active, fussy, easygoing, etc. History of abuse toward the child, siblings, or parents Developmental history, including milestones, language, gross motor skills, and fine motor skills History of substance abuse by parents, caregivers, or others in the home Recent social or financial stressors History of violent interactions among other family members

Table 3. Physical Examination for Suspected Child Abuse Examination component

Possible abnormal findings or cause

General assessment of alertness, eye opening, and responsiveness

Intracranial hemorrhage, head injury

Height, weight, head circumference (compared with past measurements, if possible)

Failure to thrive, neglect, or growth failure with concurrent physical abuse

Mouth and teeth examination

Dental caries suggestive of neglect

Scalp examination

Patchy hair loss caused by traumatic alopecia or severe malnutrition

Funduscopic examination of the eyes

Retinal hemorrhages

Skin examination for bruising or burns

Multiple patterns of bruising suggestive of abuse: bruise in child younger than four months; bruise in torso, ear, and neck areas; ear bruising (suggests “boxing ears”); buttocks bruising; patterned bruises (hand, cord, belt, object); bruises at different stages of resolution; burn injuries

Palpation for tenderness, especially of the neck, torso, and extremities

Occult fracture

Deep tendon reflexes, muscle tone, or responsiveness to tactile stimuli

Spinal cord injury

Historical components that suggest intentional trauma No explanation or vague explanation for a significant injury Significant delay in seeking medical attention An important detail of the history changes dramatically over time Explanation is inconsistent with the pattern, age, or severity of the injury History does not explain the injuries identified Explanation is inconsistent with the child’s physical or developmental capabilities Different witnesses provide markedly different explanations for the injury Information from references 8 and 11.

Information from reference 8.

of any region in a child younger than four months, requires further evaluation for abuse. The initial study reported a sensitivity and specificity of 97% and 84%, respectively.

Coagulopathies (e.g., leukemia, cystic fibrosis with vitamin K deficiency, hemophilia, von Willebrand disease) may cause easy bruising, retinal hemorrhages, subdural hematomas, and other findings suggestive of abuse.17

A cross-sectional survey of 973 children presenting for well-child visits found bruises in 203 children (21%).16 Consistent with previous studies, this study found bruising to be rare in children younger than six months; however, children between six and nine months of age who were beginning to ambu late (“cruise”) started to show bruises in predictable locations, such as the leg, knee, or forehead, as well as in less common areas, such as the back and chest. Unusual events or accidents, in addition to uncommon medical problems, may also explain an observed clinical pattern.

Radiographic Imaging Physical abuse often results in skeletal injury. Radiographic imaging of children with suspected physical abuse may consist of evaluation of localizing symptoms or physi cal examination signs, as well as screening skeletal surveys. Although skeletal injuries (other than skull fractures) are not always the life-threatening injuries most associated with abuse, identification of occult fractures may provide the clearest evidence of abuse as the cause of other identified injuries.

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American Family Physician Skeletal survey imaging is typically recommended for all cases of suspected abuse in children younger than two years. Children older than five years can usually give a sufficient history of pain, and screening imaging is not recommended. Instead, imaging should be based on clinical findings. Screening imaging in children between two and five years of age should be guided by other findings or indicators of possible abuse, and performed in cases where abuse is strongly suspected.18 The content of the skeletal survey imaging series is outlined in Table 4.19 In general, each anatomic region should be imaged separately so that optimal exposure and image quality are ensured for each area; singleimage studies (“babygrams”) are not considered suffi cient for diagnosis and should be avoided.20 Obtaining both oblique projections to the anteroposterior view of

Table 4. Complete Skeletal Survey Appendicular skeleton Humeri (AP) Forearms (AP) Hands (PA) Femurs (AP) Lower legs (AP) Feet (AP)

the rib cage may increase the yield of rib fractures.19 Other imaging studies, such as computed tomography of the head, nuclear medicine imag ing, or positron emission tomography, may be indicated depending on patient circumstances. Concerning findings on radiographic imaging include injury patterns that are highly or moderately specific for the diagnosis of child abuse20,21 (Table 522). Findings with relatively high specificity include metaphyseal lesions, posteromedial rib fractures, scapular or spinous process fractures, and sternal fractures.20,21 Laboratory Studies Laboratory studies are useful to identify dis orders that might explain observed findings (particularly coagulopathies), or occult or more severe injury not

Table 5. Injuries Detected on Radiographic Imaging That Are Specific for Child Abuse Highly specific injuries* Classic metaphyseal lesions Rib fractures, especially posteromedial Sternal, scapular, and spinous process fractures Moderately specific injuries* Multiple fractures

Axial skeleton

Fractures in different stages of healing

Thorax (AP, lateral, right and left obliques), to include ribs, thoracic and upper lumbar spine

Epiphyseal separations Vertebral body fractures and subluxations

Pelvis (AP), to include the mid lumbar spine

Digital fractures

Lumbosacral spine (lateral)

Complex skull fractures

Cervical spine (lateral)

Common but low specificity

Skull (frontal and lateral) AP = Anteroposterior; PA = Posteroanterior.

Clavicular fractures *Quantitative information for high or moderate specificity is unavailable.

Table 6. Potentially Helpful Laboratory Tests in Children with Suspected Abuse Test

Possible abnormal findings or cause

Complete blood count, including platelet count, coagulation times (e.g., prothrombin time, activated partial thromboplastin time)

Coagulopathy causing unexplained bruising or bleeding

Fibrinogen, von Willebrand factor, platelet aggregation studies, clotting factor assays

Coagulopathy causing unexplained bruising or bleeding

Hepatic transaminase, amylase, lipase levels

Occult abdominal injury

Toxicology screen

Overdose or poisoning

Urinalysis, renal and electrolyte panel

Occult back or kidney injury

Calcium, alkaline phosphatase, phosphorus, albumin, parathyroid hormone levels

Malnutrition, bone mineralization disorders (e.g., rickets)

Information from reference 17.

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American Family Physician evident on examination. Table 6 lists useful laboratory studies and their possible findings.17 Testing for sexually transmitted infection may be necessary if sexual abuse is suspected. Hepatic transaminase levels have a modest sensitivity and specificity (77% and 82%, respectively) for occult abdominal injuries at a cutoff level of 80 U per L (1.34 μkat per L). Although universal screening of injured children is not indicated, it may be useful to measure transaminase levels in children with suspected abuse (particularly suspected abdominal injuries) in whom abdominal computed tomography is not already planned.23

of the technology. Table 7 lists simple principles to follow to ensure that photographs will be of suitable quality and provide the best evidence should investigation of child abuse proceed to legal action.24 Reporting

Documentation

Physicians and other health care profes sionals are mandated by law to report child maltreatment in 48 states. The remaining two states mandate that all persons report child abuse.25 If a physician suspects or has reason to believe that a child has been abused or neglected, he or she must notify the local child protective services office or law enforcement agency. An additional resource is the Childhelp National Child Abuse Hotline at 800-4-A-CHILD (800-422-4453).

Documentation of the history, physical examination, diagnostic study results, clini cal impression, and diagnostic reasoning is vital not only for medical care, but also for legal purposes. This includes photography of physical examination findings that raise concern for abuse. Although digital photography has largely replaced traditional film, a few principles should be followed to provide the best documentation, regardless

After a report of suspected child maltreatment has been made, the child pro tection process is initiated. Details of this process are beyond the scope of this article, but include intake (determine whether the report meets statutory and agency guide lines for investigation), initial assessment and investigation (determine whether mal treatment occurred), family assessment, case planning (specify goals to eliminate

Table 7. Steps for Photographing Findings Suspicious for Child Abuse Utilize a system to keep track of the patient’s name and date of the photographs. Take a picture of the child’s/adolescent’s face with the name card to identify him/her. Take full-body photographs for identification purposes. When photographing the patient’s back, have the child/adolescent turn his/her face toward the camera for identification purposes. Take photographs head-on so that the surface to be photographed is parallel to the camera and at the same level. Compose the picture the way you normally look at the area. Use an uncluttered, neutral-colored background. Skin is best photographed against a blue background. Lighting is crucial to accurate color reproduction. In the absence of proper lighting, it is very important to document in writing in the medical chart the color and description of the lesion. Document a finding with several shots taken from different distances and angles. Take some photographs of a lesion that include landmarks such as an elbow or a knee so that the lesion is seen in its proper location. Use the rule of three. Take at least two shots of three orientations: full body, medium range of the finding, and close up. Document the size of the injury by using an inch scale. Be sure that there is at least one other close-up of the injury without the scale to demonstrate that the scale was not covering evidence. Document pattern or circumferential injuries, such as burns and bite marks, using photographs showing anteroposterior and lateral views. Use close-ups to document pattern injuries and marks of restraint or bondage so that these injuries might later be compared with the rope or object that made the marks. Take close-up photographs of hands and fingernails to show damage to the nails; missing nails; or traces of blood, skin, or hair. Photograph transfer evidence that may be present on the patient’s body or clothing, such as dirt, gravel, or vegetation. Ultraviolet light may be helpful for photographing bite wounds months later, even when the overlying skin appears totally normal. It may be useful to take serial photographs of injuries over a period of time to show progression of healing.

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American Family Physician Table 8. Guidelines to Enhance Communication with the Parent, Family, or Nonoffending Caregiver Develop an initial rapport with the family as well as the child/ adolescent patient. Clearly state your role as an advocate for the child/adolescent. Remain neutral in tone, and avoid confrontational or accusatory statements. Invite parents to step out of the room so you can interview the child/adolescent alone. Explain that abuse can exist in the absence of physical examination findings. Explain that you need help assessing the child/adolescent for safety or possible abuse, and introduce the need for other agencies. Inform parents if you need to contact police and/or child protective services; however, it is not necessary to tell parents if you are concerned that notifying them would increase the risk to the child/adolescent. Explain your duty to report concerns, and explain your concerns to family members. Remind the family that you will be present and available throughout the process. Information from reference 27.

the risk of maltreatment), service provision (pro vide in-home services), evaluation of family progress, and case closure (determine if the family can protect the child without further child protective services intervention). The child protection process varies from state to state, but ideally involves the legal system and a multidisciplinary team approach.26 Communicating with Family Members Parents are understandably frightened and concerned when physicians raise the issue of child abuse. There are no clear guidelines for effective communication strategies, although development of an initial rapport with the child and the family is important and ben eficial during further discussions. Table 8 summarizes additional recommendations for communicating with the patient and the family, particularly a nonoffending caregiver.27 REFERENCES 1. King WK, Kiesel EL, Simon HK. Child abuse fatalities: are we missing opportunities for intervention? Pediatr Emerg Care. 2006;22(4):211-214. 2. Every Child Matters Education Fund. We can do bet ter: child abuse and neglect deaths in America. 2nd ed. Washington, DC: Every Child Matters Education Fund; September 2010.

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3. Kochanek KD, Xu J, Murphy SL, Miniño AM, Kung HC. Deaths: preliminary data for 2009. Natl Vital Stat Rep. 2011;59(4):1-68. 4. Saade DN, Simon HK, Greenwald M. Abused children: missed opportunities for recognition in the ED. Acad Emerg Med. 2002;9(5):524. 5. Selph SS, Bougatsos C, Blazina I, Nelson HD. Behavioral interventions and counseling to prevent child abuse and neglect: a systematic review to update the U.S. Preven tive Services Task Force recommendation. Ann Intern Med. 2013;158(3):179-190. 6. U.S. Department of Health and Human Services, Administration for Children and Families, Administra tion on Children, Youth and Families, Children’s Bureau. Child maltreatment. 2011. http://www.acf.hhs.gov/ programs/cb/stats_research/index.htm#can. Accessed October 20, 2013. 7. Child Welfare Information Gateway. Definitions of child abuse and neglect in federal law. http://www. childwelfare.gov/can/defining/federal.cfm. Accessed October 20, 2013. 8. Kellogg ND; American Academy of Pediatrics Commit tee on Child Abuse and Neglect. Evaluation of suspected child physical abuse. Pediatrics. 2007;119(6):1232-1241. 9. American Academy of Family Physicians. AAFP policies: Child abuse. 2008. http://www.aafp.org/about/policies/ all/child-abuse.html. Accessed October 20, 2013. 10. Flaherty EG, Stirling J Jr; American Academy of Pediat rics. Committee on Child Abuse and Neglect. Clinical report—the pediatrician’s role in child maltreatment prevention. Pediatrics. 2010;126(4):833-841. 11. McDonald KC. Child abuse: approach and management. Am Fam Physician. 2007;75(2):221-228. 12. Altman RL, et al. Abusive head injury as a cause of apparent life-threatening events in infancy. Arch Pediatr Adolesc Med. 2003;157(10):1011-1015. 13. McIntosh N, Mok JY, Margerison A. Epidemiology of oro nasal hemorrhage in the first 2 years of life: implications for child protection. Pediatrics. 2007;120(5):1074-1078. 14. Jenny C, Hymel KP, Ritzen A, Reinert SE, Hay TC. Analy sis of missed cases of abusive head trauma [published correction appears in JAMA. 1999;282(1):29]. JAMA. 1999;281(7):621-626. 15. Pierce MC, Kaczor K, Aldridge S, O’Flynn J, Lorenz DJ. Bruising characteristics discriminating physical child abuse from accidental trauma [published correction appears in Pediatrics. 2010;124(4):861]. Pediatrics. 2010;125(1):67-74. 16. Sugar NF, Taylor JA, Feldman KW. Bruises in infants and toddlers: those who don’t cruise rarely bruise. Puget Sound Pediatric Research Network. Arch Pediatr Adolesc Med. 1999;153(4):399-403. 17. Laposata ME, Laposata M. Children with signs of abuse: when is it not child abuse? Am J Clin Pathol. 2005;123(suppl):S119-S124.

American Family Physician 18. Botash AS. Child abuse evaluation & treatment for medi cal providers. Radiology: injuries associated with abuse. Syracuse, NY: SUNY Upstate Medical University; 20052013. http://childabusemd.com/radiology/injuries.shtml. Accessed October 20, 2013. 19. Faerber EN. ACR–SPR practice guideline for skeletal surveys in children. Revised 2011. (Resolution 54). http://www. acr.org/~ media/9BDCDBEE99B84E87BAAC2B1695BC07B6. pdf Accessed October 20, 2013. 20. Dwek JR. The radiographic approach to child abuse. Clin Orthop Relat Res. 2011;469(3):776-789. 21. Hattingh L. Non-accidental injury. Curr Orthop. 2007;21(4):301-309. 22. Kleinman PK. Skeletal trauma: general considerations. In: Kleinman PK. Diagnostic Imaging of Child Abuse. St. Louis, Mo.: Mosby; 1998:8-25. 23. Lindberg D, Makoroff K, Harper N, et al.; ULTRA Inves tigators. Utility of hepatic transaminases to recognize abuse in children. Pediatrics. 2009;124(2):509-516. 24. Botash AS. Child abuse evaluation & treatment for medical providers. Documentation: photographic documentation.

Syracuse, NY: SUNY Upstate Medical University; 2005-2013. http://childabusemd.com/documentation/documentingphotographic.shtml. Accessed October 20, 2013. 25. Child Welfare Information Gateway. Mandatory report ers of child abuse and neglect. http://www.childwelfare. gov/systemwide/laws_policies/statutes/manda.pdf. Accessed October 20, 2013. 26. Goldman J, Salus MK, Wolcott D, Kennedy KY. A Coordi nated Response to Child Abuse and Neglect: The Foun dation for Practice. Washington, DC: U.S. Department of Health and Human Services, Administration for Children and Families, Administration on Children, Youth and Families, Children’s Bureau, Office on Child Abuse and Neglect; 2003. 27. Botash AS. Child abuse evaluation & treatment for med ical providers. Treatment and follow-up: responding to families. Syracuse, NY: SUNY Upstate Medical Univer sity; 2005-2013. http://childabusemd.com/treatment/ treatment-responding-families.shtml. Accessed October 20, 2013.

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Practice Guidelines AAP Releases Guideline on Managing Type 2 Diabetes Mellitus in Patients 10 to 18 Years of Age Childhood obesity has dramatically increased in North America over the past 30 years, leading to earlier onset of type 2 diabetes mellitus, which previously did not normally occur until later in life. Childhood type 2 diabetes poses a challenge to many physicians who are not used to treating this disease in such young patients. The American Academy of Pediatrics (AAP) has released a guideline of evidence-based recommendations for treating type 2 diabetes in patients 10 to 18 years of age. The guideline focuses on treatments that have been shown to affect clinical outcomes in these patients. Definitions Childhood type 2 diabetes is disease in a child who typically: ÂÂ Is overweight (body mass index in the 85th to 94th

percentile) or obese (body mass index in the 95th percentile or greater)

ÂÂ Has a strong family history of type 2 diabetes ÂÂ Has substantial residual insulin secretory capacity at

diagnosis (reflected by normal or elevated insulin and C-peptide concentrations)

ÂÂ Has insidious onset of disease ÂÂ Demonstrates insulin resistance (includ ing clinical

evidence of polycystic ovary syndrome or acanthosis nigricans)

ÂÂ Lacks evidence for diabetic autoimmunity (negative

for autoantibodies typically associated with type 1 diabetes); these patients are more likely to have hypertension and dyslipidemia than are those with type 1 diabetes

Diabetes is defined as one of the following: ÂÂ A1C level of 6.5% or greater (test performed in an

appropriately certified laboratory)

ÂÂ Fasting (no caloric intake for at least eight hours)

Source: Adapted from Am Fam Physician. 2013;88(10):710-716.

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plasma glucose level of 126 mg per dL (7.0 mmol per L) or greater ÂÂ Two-hour plasma glucose level of 200 mg per dL

(11.1 mmol per L) or greater during an oral glucose tolerance test (using a glucose load containing the equivalent of 75 g anhydrous glucose dissolved in water)

ÂÂ A random plasma glucose level of 200 mg per dL or

greater with symptoms of hyperglycemia

Action Statements Clinicians must ensure that insulin therapy is initiated in children and adolescents with ketosis or diabetic ketoacidosis, in whom the distinction between type 1 and 2 diabetes is unclear. Usually, insulin therapy should be initiated in patients with a random venous or plasma blood glucose concentration of 250 mg per dL (13.9 mmol per L) or greater, or an A1C level greater than 9%. Type 2 diabetes in children and ado lescents may present differently depending on disease stage. In early disease, before diagnostic criteria are met, blood glucose concentrations may be normal much of the time and patients may be asymptomatic. At this stage, the disease may be detected only with abnormal blood glucose measurements during screening. As insulin secretions decline, patients will likely begin to have symptoms of hyperglycemia, sometimes with ketosis or frank ketoacidosis. Diabetic ketoacidosis is treated with insulin and fluid, as well as electrolyte replacement to prevent the disease from worsening. These patients need immediate inpa tient therapy under the care of a physician experienced in treating diabetic ketoacidosis. Children and adolescents who have type 2 diabetes and poor glycemic control, but no evidence of ketosis or ketoacidosis, may also benefit from insulin therapy, at least short term. Initially, it may be difficult to differentiate type 1 and type 2 diabetes. Insulin therapy should be administered while appropriate testing is performed. Clinicians should initiate a lifestyle modification program, including nutrition and physical activity, and start metformin

American Family Physician (Glucophage) as first-line therapy at the time of type 2 diabetes diagnosis, unless insulin is needed to reverse glucose toxicity in the case of significant hyperglycemia or ketoacidosis.

medications with a risk of hypoglycemia; are starting or changing a diabetes treatment regimen; have not met treatment goals; or have comorbid illnesses.

Because the combination of diet and exercise alone has not been highly successful in children and adolescents with type 2 diabetes, lifestyle modifications should be initiated with metformin. Gastrointestinal adverse effects are common at the beginning of metformin therapy; therefore, it should be started at a low dosage of 500 mg daily, and increased by 500 mg every one to two weeks to a maximum of 2,000 mg daily in divided doses. Extended-release metformin may be considered, although data regarding adverse effects are lacking.

Although the benefit of frequent blood glucose monitoring has not been evaluated in children and adolescents with type 2 diabetes, a fasting blood glucose concentration of 70 to 130 mg per dL (3.9 to 7.2 mmol per L) is a reasonable goal in most adolescents.

In children and adolescents, a multidisciplinary approach to lifestyle modifications with the involvement of the whole family is most successful. Expert consensus is that less than 10% of children and adolescents will maintain lifestyle changes long term. Patients are more likely to succeed if they are treated simultaneously with medications, possibly because they will have a greater degree of concern for their health than if medication is not needed. In patients with more modest hyperglycemia (e.g., random blood glucose level of 200 to 249 mg per dL [11.1 to 13.8 mmol per L]) or asymptomatic type 2 dia betes, metformin alone, insulin alone, or metformin and insulin are reasonable options for initial pharmacologic management. A1C concentrations should be monitored every three months and treatment intensified if results do not meet the goals for finger-stick blood glucose and A1C concentrations. The A1C target ideally should be less than 7%. If this seems unattainable for a patient, an individualized goal should be set, with the intention of ultimately meeting the guideline target of less than 7%. In the absence of hypoglycemia, a lower goal can be considered. If goals are not reached, therapy should be intensified if possible. This may include increasing clinic visits, monitoring blood glucose levels more often, adding one or more antidiabetic agents, consulting a registered dietitian or diabetes educator, and increasing attention to diet and exercise regimens. If A1C concentrations remain relatively stable, testing may be extended to every six months. Clinicians may advise patients to monitor finger-stick blood glucose concentrations if they are taking insulin or other

Current American Diabetes Association recommen dations for finger-stick monitoring may be applied to most children and adolescents with type 2 diabetes: (1) monitoring should be performed at least three times daily for patients using multiple insulin injections or insulin pump therapy; (2) for patients using less frequent insulin injections, noninsulin therapies, or medi cal nutrition therapy alone, monitoring may be useful as a guide to the success of therapy; and (3) to achieve postprandial glucose targets, postprandial finger-stick monitoring may be appropriate. All patients with a new diagnosis should perform fingerstick blood glucose testing before meals (including the morning fasting concentration) and at bedtime, regardless of treatment plan. The frequency of testing can be decreased in some patients after the target level is met. Patients and families should receive a written action plan. In patients using a regimen consisting of a single bedtime insulin injection (basal insulin only), the best way to determine the appropriate dose is by using the morning fasting blood glucose concentration. Therefore, a daily fasting blood glucose measurement is recommended. Although more labor intensive, basal bolus insulin regimens may be appropriate for children and adolescents with type 2 diabetes. The bolus dose is calculated using a correction algorithm for the premeal blood glucose concentration and a “carb ratio,” in which 1 U of insulin is given for a certain amount of carbohydrates consumed. In addition, more insulin is given when the blood glucose concentration is above the target level. For example, if an adolescent has a blood glucose con centration of 250 mg per dL, will eat a meal containing 60 g of carbohydrates, with a carb ratio of 1:10 (1 U of insulin for every 10 g of carbohydrates) and an assigned correction dose of 1:25 > 125 (1 U of insulin for every 25 mg per dL that the glucose level is above the target of 125 mg per dL), the mealtime bolus dose of insulin would be as follows:

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60 g/10 carb ratio = 6 U rapid-acting insulin for the meal

plus (250 – 125)/25 = 125/25 = 5 U rapid-acting insulin for correction Thus, the total bolus insulin coverage at mealtime would be: 11 U (6 + 5) of rapid-acting insulin. Clinicians may incorporate the Academy of Nutrition and Dietetics’ Pediatric Weight Management Evidence-Based Nutrition Practice Guidelines in their counseling of patients with type 2 diabetes, at the time of diagnosis and as part of ongoing management. Patients should be referred to a registered dietitian with expertise in the nutritional needs of children and adolescents with type 2 diabetes and advised to follow guidelines from the Academy of Nutrition and Dietetics.

These recommendations include a balanced macronutri ent diet with lifestyle modifications, nutritional coun seling, and caregiver participation. Clinicians may encourage patients to participate in adequate exercise and limit screen time. Children and adolescents with type 2 diabetes should participate in moderate to vigorous exercise for at least 60 minutes daily. This may be completed in several, shorter increments (e.g., 10 to 15 minutes) throughout the day. A written exercise prescription that takes into account the patient’s physical abilities, preferences, and circumstances may increase adherence. Medication dos ages may need to be adjusted when initiating an aggres sive physical activity program. Nonacademic screen time should be limited to less than two hours a day.

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American Family Physician

Photo Quiz Mottled Skin Changes A 62-year-old woman presented with a four-week history of edema in both of her upper extremities, as well as changes in skin pigmentation. She had alopecia involving the frontal area of the scalp. She had dyspnea on exertion, which had worsened over several weeks. Physical examination showed firm skin with nonpitting edema in the forearms, hands, and fingers. She also had pigmenta tion changes on her face, neck, and upper back (Figures 1 through 3). Laboratory results included the following: white blood cell count, 10,000 per mm3 (10.0 × 109 per L); hemoglobin, 8.5 g per dL (85 g per L); erythrocyte sedimentation rate, 115 mm per hour (normal, 0 to 30 mm per hour); sodium, 137 mEq per L (137 mmol per L); potassium, 4.4 mEq per L (4.4 mmol per L); blood urea nitrogen, 23 mg per dL (8.2 mmol per L); creatinine, 1.4 mg per dL (124 μmol per L); urinalysis, normal; antinuclear antibody, positive (1:640) with a nucleolar pattern; and rheumatoid factor, 24.6 IU per mL (normal, 0 to 13.9 IU per mL). Chest radiography showed cardiomegaly with evidence of vascular congestion.

Figure 1.

Figure 2.

Question Based on the patient’s history, physical examination, and laboratory findings, which one of the following is the most likely diagnosis? A. Dermatomyositis. B. Rheumatoid arthritis. C. Scleroderma. D. Systemic lupus erythematosus. E. Vitiligo with repigmentation.

Figure 3.

SEE THE FOLLOWING PAGE FOR DISCUSSION.

Source: Adapted from Am Fam Physician. 2013;88(10):707-708.

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American Family Physician Summary Table Condition

Clinical course

Skin changes

Dermatomyositis

Proximal muscle weakness causing difficulty climbing stairs, rising from a seat, or combing hair; skin changes may precede, follow, or present simultaneously with muscle involvement

A pathognomonic heliotrope erythema around the eyelids; Gottron papules on the knuckles and sides of the fingers, and dusky-red to violet skin changes over sun-exposed areas; periungual erythema and telangiectasis may develop

Rheumatoid arthritis

Chronic symmetrical polyarthritis beginning with fatigue, weakness, morning stiffness, synovial thickening, and vague musculoskeletal symptoms; rheumatoid nodules may occur; rheumatoid vasculitis can affect nearly any organ system

Cutaneous vasculitis may present as crops of small brown spots in the nail beds, nail folds, and digital pulp; larger ischemic ulcers may develop, often in the lower extremity

Scleroderma

Systemic condition often affecting the upper extremities, initially with edema, later with skin thickening and fibrosis

“Salt-and-pepper” skin may occur in some patients with dark skin; taut, shiny skin with slow-healing ulcerations develops later

Systemic lupus erythematosus

Nonpruritic, erythematous to violaceous plaques; telangiectasias, alopecia, urticaria, and Raynaud phenomenon are also common

Plaques on sun-exposed areas, with butterfly-shaped facial distribution; erythema and telangiectasis tend to spare the knuckles

Vitiligo with repigmentation

Progressive disease caused by autoimmune destruction of melanocytes; loss of pigmentation may be localized or generalized

Tends to occur on the face, hands, in body folds, and around body openings (e.g., eyes, nose, mouth); repigmentation begins around hair follicles

Discussion The correct answer is C: scleroderma. Nonpitting edema may appear months or years before the characteristic changes of scleroderma develop.1 These changes may include tightly bound skin, with ulcer formation, tightness of the facial skin with fine perioral wrinkling, and an inability to fully open the mouth. The skin changes tend to affect fingers and hands initially, with gradual proximal spread to the forearms.1 The lower extremities tend to be relatively spared.1 “Salt-and-pepper” pigmentation changes are characteristic of scleroderma with peri follicular sparing of pigment. This pattern is most common on the scalp, upper back, and chest.2 Dermal sclerosis may obliterate hair follicles, resulting in hair loss. Pulmonary involvement may include interstitial lung disease and pulmonary artery hyper tension.2 Nucleolar pattern antinuclear antibodies are associated with antiribonucleoprotein, which is characteristic of sclero derma and rare in other immune disorders.3 Dermatomyositis often presents as proximal muscle weakness and a heliotrope rash, commonly involving the eyelids.4 Rheumatoid arthritis is typically associated with symmetrical joint involvement, morning stiffness,

synovial thickening, and a family history of the disease.2 Systemic lupus erythematosus can man ifest in a variety of ways. Dermatologic manifestations include nonpruritic, erythematous to violaceous plaques, often on sun-exposed areas. Telangiectasias, alopecia, urticaria, and Raynaud phenomenon are also common.4 Vitiligo with repigmentation can appear similarly to this patient’s presentation, with areas of repigmentation beginning in the perifollicular area. Although vitiligo has been associated with several other conditions (e.g., hypothyroidism, Graves disease, Addison disease, pernicious anemia, diabetes mellitus), most patients with vitiligo have no other associated findings.4 REFERENCES 1. Harrison TR, Fauci AS, eds. Harrison’s Principles of Inter nal Medicine. 14th ed. New York, NY: McGraw-Hill; 1998. 2. Harrison TR, ed. Harrison’s Principles of Internal Medicine. 17th ed. New York, NY: McGraw Hill; 2008. 3. Wallach JB. Interpretation of Diagnostic Tests. 6th ed. Boston, Mass.: Little Brown; 1996. 4. Habif TP. Clinical Dermatology. 5th ed. Edinburgh, Scot land: Mosby; 2009.

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Anesthesiology

Conscious Sedation: An Observation JAYASHREE SEN*, BITAN SEN†

Abstract Conscious sedation is a drug-induced depression of consciousness while the patient remains awake to respond to the verbal commands. Certain diagnostic and therapeutic procedures can be carried out under local anesthesia with sedation and analgesia without any requirement for intervention of maintenance of cardiorespiratory function. The hemodynamic status and the level of consciousness needed for the procedures remain continuously under the vigilance and control of a qualified anesthesiologist. An essential component of conscious sedation or monitored anesthesia care, which is a planned procedure, is the assessment and management of a patient’s actual or anticipated physiological derangements or medical problems that may occur during the diagnostic or therapeutic procedure carried out under sedation.

Keywords: Sedatives, consciousness, procedures, monitoring

onscious sedation, as defined by the American Society of Anesthesiologists (ASA), is a specific anesthesia service for a diagnostic or therapeutic procedure done under local anesthesia along with sedation and analgesia. This ‘conscious’ sedation or monitored anesthetic care (MAC), is a drug-induced depression of consciousness. The process makes the patient calm while he remains awake and responsive to follow commands, either alone or accompanied by light tactile stimulation. No intervention is required for maintaining normal respiratory and cardiovascular function. Conscious sedation, as per the ASA, includes the nature of the procedure, clinical condition of the patient and/or the potential need to convert sedation to a general or regional anesthesia. Monitoring of the patient is done continuously by an anesthesiologist, of the anesthetic procedure, the vital signs and level of consciousness as required for the surgical technique. It incorporates varying levels of sedation, analgesia and anxiolytics as necessary. After the procedure is over, the anesthesiologist will discharge the patient fully awake and almost pain free.

*Associate Professor Dept. of Anesthesiology Goldfield Institute of Medical Sciences and Research, Chhainsa, Faridabad, Haryana †Junior Resident Emergency Medicine, Apollo Hospital, New Delhi Address for correspondence Dr Jayashree Sen Associate Professor Dept. of Anesthesiology Goldfield Institute of Medical Sciences and Research, Chhainsa, Faridabad, Haryana E-mail: jayashree_sen@rediffmail.com

Purpose The purpose of conscious sedation or MAC is to provide the patient with relief of discomfort and anxiety associated with the proposed surgical or investigative procedure so that the patient remains motionless and can co-operate actively following verbal commands throughout the procedure. Indication Conscious sedation may be appropriate for: a) Diagnostic purposes such as gastrointestinal endoscopy or bronchoscopy; b) interventional pain procedures; c) ENT surgeries such as myringoplasty, ear-lobe reconstruction; d) ophthalmological procedures such as intraocular lens application, blepharoplasty; e) cardiothoracic procedures such as angiography, transvenous cardiac pacemaker surgery; f) neurological procedure such as stereotactic surgeries; g) gynecological procedures such as tubectomy or medical termination of pregnancy; h) urological surgeries such as stent application or stent removal; i) orthopedic procedures like removal of external fixators; j) radiological procedures like computerized tomography (CT) or magnetic resonance imaging (MRI) and k) some minor surgeries or liposuction for which the patient needs to lie still for more than a few minutes. Pre-requisites Conscious sedation includes a pre-procedure visit (preanesthetic check-up), intra-procedure care and postprocedure anesthesia management along with certain specific services:

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Anesthesiology ÂÂ ÂÂ

ÂÂ ÂÂ ÂÂ ÂÂ ÂÂ

Explanation of the procedure and request to the patient for active co-operation. Administration of drugs such as sedatives, analgesics, hypnotics, anesthetic agents or other medications as necessary for patient safety. Maintenance of hemodynamics. Support of psychological aspects. Care of physical comfort. Diagnosis and management of clinical problems that might occur during the procedure.

infusion dose along with local anesthetic injection. Sedation can be deepened by more bolus dose at stimulating moments. Infusion dose titrated at the end of the procedure to make the patient awake to follow commands.

Provision of emergency management.

Ketamine

Technique The procedure begins once oxygen is given via nasal cannulae, the intravenous (IV) access established, skin sensitivity test for local anesthetic done, cardiopulmonary and other required monitors connected. Drugs Chosen Conscious sedation includes the use of drugs whose clinical effects can be modified according to the surgical requirements and which can induce amnesia so that the patient will not remember the procedure after it took place. Moderate sedation can be achieved using pharmacologic agents for sedation, anxiolysis and analgesia. The procedure can also be achieved using patient controlled sedation, target controlled infusion or continuous IV infusion.

Midazolam A short-acting, water-soluble benzodiazepine, an ideal agent for its amnestic and anxiolytic properties. Midazolam, with a half-life of 2 hours, has limited cardiovascular effects, allows for quick recovery and has no postoperative sequelae such as nausea and vomiting.

Slow administration maintains hemodynamics. Does not cause postoperative nausea or vomiting but may cause postoperative shivering. Dose: Bolus - 0.5-1 mg/kg; infusion - 25 µg/kg/min.

Agent of choice as an analgesic in conscious sedation. Produces dissociated anesthesia. Psychotic reactions such as hallucination, serious cardiovascular adverse effects, seizures and postoperative shivering have been reported. Dose: 2 mg/kg IV or 6-10 mg/kg IM.

Dexmedetomidine Has both sedative and analgesic properties, does not cause respiratory depression, though hemodynamic parameters need to be closely monitored. Has a high incidence of postoperative dry mouth. Dose: 1 μg/kg-1 IV.

Local Anesthetic Agent One percent lidocaine can be used either plain or with epinephrine (EPI) 1:2,00,000 or 1:1,00,000 for direct injection into the incisional site. Xylocaine, an amide, has a rapid-onset of the anesthetic effect while bupivacaine, another amide has a longer duration of action. Dose: Lidocaine 7.0 mg/kg with EPI; 4.5 mg/kg without EPI; duration: 30-60 minutes.

Dose: 0.05 mg/kg bolus IV.

Bupivacaine (0.5% or 0.75% or 0.25%), 225 mg/dose with EPI; 175 mg/dose without EPI; duration: 30-90 minutes.

Fentanyl

Complication

A rapidly-acting narcotic analgesic, with little sedative effect. May cause depression of respiratory function. The patient may experience postoperative nausea and vomiting. Dose: Boluses of 25-50 µg increments for analgesia.

Propofol A rapidly-acting sedative and hypnotic agent having a quick recovery property. Can be used in bolus and

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Complications due to use of sedatives include hypoxia, hypercarbia and cerebral hypoperfusion. Complications due to local anesthetic toxicity can manifest as local or systemic adverse effects. Localized reactions with local anesthetics present as urticaria, rash and/or allergic reactions including anaphylaxis. Prolonged or permanent paresthesia, anesthesia and motor weakness, local vasoconstriction effect resulting in necrosis may also occur.

Anesthesiology entropy monitoring, auditory8 evoked potentials, SNAP monitor and the Narcotrend monitor. But these are unreliable: 1) At extremes of age; 2) certain N-methyl-d-aspartate (NMDA) receptor antagonist agents such as nitrous oxide, ketamine or Xenon suppress the cortical EEG activity less and 3) affected by the interference from other biological potentials as electromagnetic (EMG) or external electrical signals as electrosurgery.

Systemic adverse effects can result in breathlessness, hypotension, angina pectoris, dysrhythmias and even cardiovascular collapse. The possible effects of central nervous system (CNS) toxicity with local anesthetics are disorientation, decreased responsiveness, auditory and visual hallucinations, respiratory and cardiovascular collapse including seizures and coma. Other less severe complications, not related to drugs, may be discomfort due to uncomfortable position or a member of the surgical team leaning on the patient, IV site extravasation, pruritus, hypothermia, hyperthermia, bladder distention, prolonged tourniquet inflation. Monitoring during Conscious sedation ÂÂ

Pulse oximetry: For O2 saturation.7 The predisposing factors for hypoxia other than sedatives include obesity, extremes of age, lithotomy position, pre-existing upper airway obstruction and respiratory disease. The respiratory events constitute the single largest source of adverse outcome as analyzed by the ASA Committee on Professional Liability.

ÂÂ

Capnography: For end-tidal carbon dioxide (EtCo2) measuring side stream capnograph using face masks, nasal airways or nasal cannulae is the procedure of choice.

ÂÂ

ECG and noninvasive blood pressure (NIBP) for cardiovascular system: The ECG lead II continuously should be displayed and NIBP measured and recorded at least every 5 minutes. The pulse should be monitored by palpation or oximetry. Use of precordial stethoscope is an inexpensive, effective, risk-free way of monitoring.

ÂÂ

Temperature: External and core body temperature for detecting inadvertent hypothermia, particularly in the elderlies during regional and conscious sedation techniques and also hyperthermia, which may be due to use of too much drapings during the procedure in a hot climate or malignant neuroleptic syndrome. Response to communication: For titration of sedation, continuous evaluation for response to verbal commands and tactile stimulation should be carried out. Other clinical findings as shivering, pallor, cyanosis or acute changes in neurological or cardiorespiratory status are to be observed. Depth of sedation: Monitoring can be done through bispectral index (BIS), electroencephalogram (EEG)

Conscious sedation in pregnancy This can be considered medically necessary for certain procedures. Due to physiological changes in pregnancy, the doses of anesthetic or sedative agents also require alteration. Propofol however is taken as a safe agent. The American College of Obstetricians and Gynecologists (ACOG) has recommended that intermittent or continuous fetal monitoring during conscious sedation is a more sensitive and important indicator of placental perfusion and fetal oxygenation than observations of maternal hemodynamic stability.

Disadvantage The disadvantages of conscious sedation mainly are the lack of airway control and the risk of airway obstruction or aspiration. Thus to minimize the disadvantage, the medication should be selected and titrated under the hawk eyes of an anesthesiologist to maintain a spontaneous respiration and an anesthetic depth so that the desired and optimal intraoperative sedative effect and postoperative outcome obtained. Risk factors ÂÂ ÂÂ ÂÂ ÂÂ ÂÂ ÂÂ ÂÂ

ÂÂ

Unco-operative or acutely agitated individual with delirium, senile dementia, organic brain disease. Cognitive dysfunction, psychological impairment, or intoxication (unable to follow simple commands). Severe comorbidity (ASA III physical status or greater). Morbid obesity (body mass index [BMI] >40). Patients of extreme age. Documented sleep apnea. History or anticipated intolerance to standard sedatives, e.g., chronic opioid use/chronic benzodiazepine use/alcohol abuse. Patients with risk for airway obstruction due to: zz

Spasticity or movement disorder

Dysmorphic facial features, such as PierreRobin syndrome or trisomy-21

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ÂÂ

Jaw abnormality (e.g., micrognathia)

Oral abnormalities (e.g., macroglossia)

Neck abnormalities (e.g., neck mass)

Stridor.

Patients who are pregnant.

Observation Fifty cases were observed in a teaching institute, in a period of time between January to December 2012, following a body weight (per kg) depended standard dose protocol of different drugs. Midazolam, fentanyl, propofol or ketamine was used either as a single agent (e.g., propofol) or in combination (e.g., midazolam + ketamine/midazolam + fentanyl) for conscious sedation in different patients. Drugs were administered in bolus with additional doses given when required for adequate sedation for the procedure concerned. ASA I and II groups within an age range of 18-60 years of either sex and BMI within 20-25 were accepted. The average procedural time was 90 minutes. Any complication was noted. Result The primary outcome recorded was respiratory depression of 7 (14%) patients requiring airway modification such as chin lift or mask ventilation for some minutes to those requiring no modification. No patient but required endotracheal intubation. Some cases had to be treated for nausea and postoperative pain. The patients received sedation, remained responsive to commands throughout the procedures and were monitored by a qualified anesthesiologist and thus the procedures met the definition of conscious sedation or monitored anesthesia care. Conclusion The use of conscious sedation has been increasing rapidly over the last decade, is the first choice in 10-30% of all diagnostic and therapeutic procedures and has been applied to patients with lower anesthetic

risk. A shared decision-making to weigh the risks and benefits of a patient is the recommendation by Liu and colleagues who studied the utilization of anesthesia services among low-risk patients (ASA I and II). The success of conscious sedation lies in the provider’s (anesthesiologist) ability to intervene to rescue a patient’s airway from any sedation-induced compromise and also management of post-procedure responsibilities such as relief of pain, side effects of medication used, adverse physiological responses as well as diagnosis and treatment of complications. Suggested reading 1. American Society of Anesthesiologists. Statement on nonoperating room anesthetizing locations. Amended October 22,2008. Available online at: http://www.asahq. org/For-Members/Standards-Guidelines-and-Statements. aspx. Last accessed March 6, 2013. 2. American Society of Anesthesiologists. Guidelines for ambulatory anesthesia and surgery. Amended October 15, 2008. Available online at: http://www.asahq.org/ForMembers/Standards-Guidelines-and-Statements.aspx. Last accessed March 6, 2013. 3. American Society of Anesthesiologists 2009. Distinguishing monitored anesthesia care (“MAC”) from Moderate sedation/analgesia (conscious sedation). Retrieved 3/8/13 from http://www.asahq.org/publicationsAndService/ standards/35.pdf. 4. Sarmento KM Jr, Tomita S. Retroauricular tympanoplasty and tympanomastoidectomy under local anesthesia and sedation. Acta Otolaryngol 2009;129(7):726-8. 5. Gan TJ. Pharmacokinetic and pharmacodynamic characteristics of medications used for moderate sedation. Clin Pharmacokinet 2006;45(9):855-69. 6. Bailey PL, Pace NL, Ashburn MA, Moll JW, East KA, Stanley TH. Frequent hypoxemia and apnea after sedation with midazolam and fentanyl. Anesthesiology 1990;73(5):826-30. 7. Alhashemi JA. Dexmedetomidine vs midazolam for monitored anaesthesia care during cataract surgery. Br J Anaesth 2006;96(6):722-6. 8. Myles PS, Leslie K, McNeil J, Forbes A, Chan MT. Bispectral index monitoring to prevent awareness during anaesthesia: the B-Aware randomised controlled trial. Lancet 2004;363(9423):1757-63.

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In a new study, 5-year overall survival was significantly better in patients with gastric cancer who did not experience any perioperative complications than in those who did (43% vs 27%; p < 0.001). Preoperative characteristics associated with complications included older age, elevated American Society of Anesthesiologists class, previous gastrectomy and upper gastrointestinal bleed.

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CARDIOLOGY

Superficial Brachial Artery: Its Embryological and Clinical Significance Meenakshi Khullar

Abstract The principal arteries of the upper limb show a wide range of variations that are of considerable interest to orthopedic surgeons, plastic surgeons, radiologists and anatomists. We present here a case of bilateral superficial brachial artery found during the routine dissection of the upper limbs of a 50-year-old female cadaver. In both the limbs, the third part of the axillary artery divided into superficial brachial and deep brachial arteries; denominated according to their relation to the median nerve. The superficial brachial artery continued in the arm without giving any branches and ended in the cubital fossa dividing into radial and ulnar arteries. The deep brachial artery gave rise to anterior circumflex humeral, posterior circumflex humeral and profunda brachii arteries. Earlier superficial brachial artery has been reported with a prevalence rate varying from 0.2% to 25% but bilateral variation is extremely rare. The great variability of this arterial pattern may be attributed to the failure of regression of some paths of the embryonic arterial trunks.1 The embryological and clinical significance of this variant are also discussed in detail.

Keywords: Axillary artery, superficial brachial artery, deep brachial artery

xillary artery (AA) is a continuation of the subclavian artery from the outer border of the first rib. It ends at the inferior border of the teres major and continues in the arm as brachial artery. According to textbooks, an AA penetrates the dorsoventral divisions of the brachial plexus by passing between the lateral and medial roots of the median nerve. Rarely, an aberrant AA is unable to penetrate the brachial plexus. In this case, the AA is positioned superficial to the brachial plexus and then, this is known the superficial brachial artery (SBA).

The SBA has been reported by many authors because of its relatively high frequency in comparison with other vascular variations.2,3 It is necessary, however, to pay attention to the branches originating from the aberrant AAs, in addition to the various courses of the AA, in order to understand their morphogenesis. Case report During the routine undergraduate dissections on the upper limbs of a 50-year-old female cadaver, it was

Assistant Professor Dept. of Anatomy Guru Gobind Singh Medical College Faridkot, Punjab Address for correspondence Dr Meenakshi Khullar 43, Vikas Vihar (Phase-1), Ferozepur City - 152 002, Punjab E-mail: meenakshikhullar8@gmail.com

observed that on both the sides, the third part of the AA after giving the subscapular artery bifurcated into a SBA and a deep brachial artery. The SBA descended superficial to the lateral root of the median nerve; did not give any branch in the arm and continued as the brachial artery proper. Finally, on reaching the cubital fossa it terminated by dividing into radial and ulnar arteries. The deep brachial artery passed deep to the medial root of the median nerve and gave anterior and posterior circumflex humeral branches of AA and profunda brachii branch of brachial artery. Then it terminated by giving twigs to the muscles of arm (Fig. 1). Discussion Variations in the arterial pattern of the upper limb are common and have been reported by several investigators.1 The presence of a SBA and the usual pattern of its branching in the upper arm or forearm have also been reported.4-6 The definition of the SBA was set for the first time by Adachi in 1928 and runs as follows: â&#x20AC;&#x153;The SBA is the one that runs superficial to the median nerve.â&#x20AC;?7 It may replace the main trunk or may be accompanied by an equally important, less important or more important trunk running deep to median nerve. Table 1 shows the prevalence of SBA as observed by different authors from time-to-time.

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SBA

(I)

(II)

SPA (III)

AIA

UA MA

MA MA

AIA

SPA (IV)

AIA MA

UA UA

SPA (V)

Figure 2. Stages of development of arteries of upper arm. Figure 1. Photograph showing the third part of the axillary artery (AA) dividing into the superficial brachial artery (SBA) and the deep brachial artery [BA(p)]; MN(lr) - (lateral root of median nerve) , MN(mr) - (medial root of the median nerve), MN (median nerve).

SC = Subclavian artery; MA = Median artery; AIA = Anterior interosseous artery; SBA = Superficial brachial artery; UA = Ulnar artery; SPA = Superficial palmar arch; RA = Radial artery.

ÂÂ

The disappearance of vessels which are normally retained

ÂÂ

An incomplete development

Table 1. Showing the Incidence of the SBA in Various Studies

ÂÂ

The fusion and absorption of parts which are normally distinct

Name of Author

Year

% of cases with SBA

ÂÂ

Quain12

1844

0.2

A combination of factors leading to an atypical pattern normally encountered.

Gruber13

1848

0.4

Muller14

1903

Adachi7

1928

3.1

1939

Miller15 al6

1953

0.12

Skopakoff4

1959

19.7

al5

McCormack et

1985

Rao and Chaudhary16

2001

4.2

Rodriguez-Niedenführ et al17

2001

4.9

Patnaik et al18

2002

al19

2010

Fuss et

Kachlik et

Ontogeny The embryological background of these variations in the vasculature of the upper limb may be explained as abnormal deviations in the normal vascular patterns. Arey and Jurjus mentioned six explanations for the variations observed:8,9 ÂÂ

The choice of unusual paths in the primitive vascular plexus

ÂÂ

The persistence of vessels which are normally obliterated

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Ontogenic basis of the present case can be easily made out if we look at Singer’s five stages of development of the brachial artery (Fig. 2):10 ÂÂ Stage I: Originally, the subclavian artery extends to the wrist, where it terminates by dividing into terminal branches for the fingers. The distal portion of the artery becomes the interosseous artery of the adult. ÂÂ Stage II: The median artery arises from the interosseous artery and becomes larger while interosseous artery subsequently undergoes retrogression. During this process, the median artery fuses with the lower portion of interosseous artery and ultimately forms the main channel for the digital branches becoming the principle artery of the forearm. ÂÂ Stage III: In embryos of 18 mm, the ulnar artery arises from brachial artery and unites distally with the median artery to form superficial palmar arch. Digital branches arise from this arch. ÂÂ Stage IV: In embryo of 21 mm length, the SBA develops in the axillary region and traverses the medial surface of the arm and runs diagonally from the ulnar to the radial side of the forearm to the posterior surface of the wrist. There it divides over the carpus into branches for the dorsum of the thumb and index finger.

CARDIOLOGY Clinical Significance

SBA

C UA

AIA

SBA

SPA "A"

SPA "B"

Figure 3. Showing the normal development of the brachial artery in “A” and that in the present case in “B”. SBA = Superficial brachial artery; RA = Radial artery; UA = Ulnar artery; MA = Median artery; AIA = Anterior interosseous artery; SPA = Superficial palmar arch.

ÂÂ

Stage V: Finally three changes occur. When the embryo reaches the length of 23 mm the median artery undergoes retrogression becoming a small slender structure, now known as 'arteria nervi mediani'. The SBA gives off a distal branch, which anastomoses with the superficial palmar arch already present. At the elbow an anastomotic branch between brachial artery and SBA becomes enlarged sufficiently to form with the distal portion of the latter, the radial artery, as a major artery of the forearm; the proximal portion of the SBA atrophies correspondingly.10

In the present case, it seems that in Stage III of Singer, ulnar artery came from brachial artery as usual.10 SBA continued as radial artery and anastomosis between SBA and brachial artery developed normally (See Fig. 3). However, brachial artery between origin of SBA and ulnar artery (‘A' in Fig. 3) retrogressed and lost its communication with common interosseous artery. The SBA failed to retrogress and continued to supply radial artery. The anastomosis between SBA and brachial artery (‘B’ in Fig. 3), which usually forms proximal part of radial artery now formed proximal part of ulnar artery, thus giving appearance that ulnar artery and radial artery are terminal branches of SBA and common interosseous artery (‘C’ in Fig. 3) came as a branch of ulnar artery.

Gonzalez-Compta highlighted the diagnostic, interventional and surgical significance of such a vascular variation.11 Diagnostically, it may disturb the evaluation of angiographic images. Interventionally, accidental puncture of superficially placed arteries may occur while attempting venipuncture. Surgically, it is vulnerable in both orthopedic and plastic surgery operations. Hence, the anatomic knowledge of the vascular patterns of upper limb is of crucial importance not only for neurosurgeons, but for all those involved in radiodiagnostics, particularly in cases involving traumatic injuries, as improved knowledge would allow more accurate diagnostic interpretation and surgical treatment. References 1. Rodríguez-Baeza A, Nebot J, Ferreira B, Reina F, Pérez J, Sañudo JR, et al. An anatomical study and ontogenetic explanation of 23 cases with variations in the main pattern of the human brachio-antebrachial arteries. J Anat 1995;187(Pt 2):473-9. 2. Aharinejad S, Nourani F, Hollensteiner H. Rare case of high origin of the ulnar artery from the brachial artery. Clin Anat 1997;10(4):253-8. 3. Jurjus A, Sfeir R, Bezirdjian R. Unusual variation of the arterial pattern of the human upper limb. Anat Rec 1986;215(1):82-3. 4. Skopakoff C. Variability of branches and distribution of the superficial brachial artery. Anat Anz 1959;106 (17-20):356-68. 5. Fuss FK, Matula CW, Tschabitscher M. The superficial brachial artery. Anat Anz 1985;160(4):285-94. 6. McCormack LJ, Cauldwell EW, Anson BJ. Brachial and antebrachial arterial patterns; a study of 750 extremities. Surg Gynecol Obstet 1953;96(1):43-54. 7. Adachi B. Arterensystem des japaner. Kyoto 1928; 1:205-10. 8. Arey LB. Development anatomy. In: Development of Arteries. 6th edition, WB Saunders Company: Philadelphia 1957:p.375-7. 9. Jurjus AR, Correa-De-Aruaujo R, Bohn RC. Bilateral double axillary artery: embryological basis and clinical implications. Clin Anat 1999;12(2):135-40. 10. Singer E. Embryological pattern persisting in the arteries of the arm. Anat Rec 1933;55(4):403-9. 11. Gonzalez-Compta X. Origin of the radial artery from the axillary artery and associated hand vascular anomalies. J Hand Surg Am 1991;16(2):293-6. 12. Quain R. Anatomy of the arteries of the human body. Taylor & Walton: London 1844:p.326-37.

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14. Muller E. Beitrage zur Morphologie des Gefässytstems. I. Die Armarterien des Menschen. Anat Hefte 1903;22: 377-575.

17. Rodríguez-Niedenführ M, Vázquez T, Nearn L, Ferreira B, Parkin I, Sañudo JR. Variations of the arterial pattern in the upper limb revisited: a morphological and statistical study, with a review of the literature. J Anat 2001;199(Pt 5):547-66.

15. Miller RA. Observations upon the arrangement of the axillary artery and brachial plexus. Am J Anat 1939;64(1):143-63.

18. Patnaik VVG, Kalsey G, Singla RK. Branching pattern of brachial artery: a morphological study. J Anat Soc Ind 2002;51(2):176-86.

16. Rao PV, Chaudhary SC. Superficial brachial artery terminating as radial and superficial ulnar arteries: a case report. Centr Afr J Med 2001;47(3):78-80

19. Kachlik D, Konarik M, Baca V. Vascular patterns of upper limb: an anatomical study with accent on superficial brachial artery. Bosn J Basic Med Sci 2011;11(1):4-10.

13. Gruber W. Zur Anatomie der Arteria radialis. Arch Anat Physiol Wissen Med 1864:p.434-55.

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ÂÂ

Highly electronegative low-density lipoprotein (LDL) from patients with ST-elevation myocardial infarction (STEMI) triggers platelet activation and aggregation according to data reported in the journal Blood. L5, the most highly electronegative fraction of LDL, is markedly elevated in patients with STEMI. Utilizing in vitro studies, investigators demonstrate that L5 increased adenosine diphosphate (ADP)-induced platelet aggregation, platelet P-selectin expression, GPIIb/IIIa activation and platelet-endothelial cell adhesion. When injected into mice, L5 also activated platelets. These findings suggest that elevated L5 may promote coronary artery thrombosis leading to STEMI, offer further insight into the role of platelets in coronary artery occlusion, and provide a potential entry point for future therapies.

ÂÂ

According to a meta-analysis, as a whole, the new oral anticoagulants improve outcomes versus warfarin in patients with nonvalvular atrial fibrillation, at the expense of more gastrointestinal bleeding. Pooled results of the pivotal trials of dabigatran, apixaban, rivaroxaban and edoxaban showed a significant reduction in stroke or systemic embolism, primarily due to a reduction in hemorrhagic stroke. The newer drugs also reduced all-cause mortality relative to warfarin during follow-up (RR 0.90, 95% CI 0.85-0.95), but did not affect ischemic stroke or MI. The findings are reported online in The Lancet.

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Community Medicine

Study of Vitamin B12, Folic Acid and Related Hematological Indices in Tobacco Users TARACHAND SAINI*, SUBHASH SAINI†, MANIRAM KUMHAR‡

Abstract Tobacco use among youth is a major public health problem around the world. It kills millions of people worldwide, causes immense suffering, and also has enormous economic and social cost. A study was conducted to find out the effect of tobacco use on serum vitamin B12 and folic acid levels and related hematological indices and to find the correlation between duration of tobacco use, socioeconomic and education status with serum vitamin B12 and folic acid levels. It was seen that levels of vitamin B12, folic acid were significantly lower in tobacco users. Further, this level was lowest in subjects who consumed both chewable and smoked tobacco and lower in smokers in comparison to chewers.

Keywords: Tobacco use, vitamin B12, folic acid, hematological indices

obacco use among youth is a major public health problem around the world. Every day, some 80,000-1,00,000 young people around the world become addicted to tobacco.1 The number of smokers in the population of the Third World will increase from 4.5-7.1 billion by 2025.2,3 Tobacco use kills millions of people worldwide, causes immense suffering and also has enormous economic and social cost.4 Although, there is wide documentation of the adverse effects of tobacco smoking on a variety of diseases and disturbances, but effects of other form of tobacco use and on nutrient concentration is very less studied as well as contradictory results of the previous studies about serum vitamin B12 and folic acid level in tobacco users inspired us for further study and evaluate the effect of tobacco use on serum vitamin B12 and folic acid and related hematological indices. AIMS AND OBJECTIVES ÂÂ

To find out the effect of tobacco use on serum vitamin B12 and folic acid levels and related hematological indices.

*Senior

Resident Year Resident Professor Dept. of Medicine Jawaharlal Nehru Medical College, Ajmer, Rajasthan Address for correspondence Dr Tarachand Saini C/o: Dr Maniram Kumhar 20-Jeevan Jadav, Gaurav Enclave, Near City Palace Civil Lines, Ajmer, Rajasthan - 305 001 E-mail: drtcsaini20@gmail.com

†3rd

‡Associate

ÂÂ

To find the correlation between duration of tobacco use, socioeconomic and education status with serum vitamin B12 and folic acid levels.

MATERIAL AND METHODs This study was conducted at Dept. of Medicine, Jawaharlal Nehru Medical College, Ajmer, Rajasthan. A total of 100 apparently healthy subjects of age 20-60 years were included in the study. Persons who had been using tobacco (chewable or smoking or both) for >2 years were included in the case group (tobacco users, n = 70) and person who never used tobacco in any form were included in the control group (nontobacco users, n = 30). Tobacco users were further divided in smokers, chewers and mixed groups depending on form of tobacco used. Each case and control individual was subjected to detailed clinical examination for signs and symptoms of vitamin B12 and folic acid deficiency and detailed history, particularly about duration, amount and form of tobacco used, diet, drugs and present and past medical and surgical illness, socioeconomic and education status. Any other cause of vitamin B12 and folic acid deficiency was excluded. RESULTS This study emphasized the effect of tobacco use on vitamin B12, folic acid and related hematological indices. Study concluded that levels of vitamin B12, folic acid were significantly lower in tobacco users. Further, this level was lowest in subjects who consumed both chewable and smoked tobacco and lower in smokers

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Community Medicine in comparison to chewers. Vitamin B12 and folic acid were significantly lower in subjects belonging to low socioeconomic and education status, who used tobacco for longer duration and used more amount of tobacco. Vitamin B12 was significantly lower in vegetarians and folic acid was lower in nonvegetarians. Hematological indices like hemoglobin, hematocrit and platelets were significantly lower and mean corpuscular volume (MCV) was significantly higher in tobacco users in comparison to nontobacco users. Mean serum vitamin B12 levels, which was significantly lower in chewers, smokers and mixed groups were 285.60 ± 93.11, 256.58 ± 68.34, 249.89 ± 86.89 pg/mL, respectively, which as compared to 351.71 ± 131.82 pg/mL in control group. Mean folate level was significantly lower in chewer, smoker, mixed groups 6.78 ± 3.13, 6.28 ± 1.83 and 5.94 ± 1.80 ng/mL, respectively as compared to 8.83 ± 3.99 ng/mL in control group. Mean Hb level was significantly lower in case group 11.47 ± 1.36 and in control group it was 12.29 ± 0.87 g/dL. Mean hematocrit levels in case group was 38.89 ± 3.27 and in control group it was 40.35 ± 1.77. Mean platelet counts in case group were 1.78 ± 0.79 lac/µL and in control group they were 2.06 ± 0.81. MCV level in case group was 95.74 ± 9.04 as compared to 89.48 ± 6.20 in control group. DISCUSSION Smokers have increased blood levels of cyanide due to its presence in the tobacco smoke. Cyanide readily combines with hydroxycobalamin, a form of vitamin B12 to cyanocobalamin, which is devoid of coenzyme function. In addition, hydrogen sulfide, which is also present in the cigarette smoke, has greater affinity for the cobalt atom of vitamin B12 than the carbon-nitrogen group of cyanides. The resulting sulfocobalamin is not a biological active vitamin B12 coenzyme. Furthermore, nitrous oxide present in cigarette smoke is known to inactivate methylcobalamin through oxidation of the cobalt atom.5 Smoking also affects nutritional intake, assimilation and excretion of vitamin B12 from the body. Vitamin B12 is metabolized in the body in a similar way to cyanide. Body excretes vitamin B12 along with the poisonous substance. Studies show that smokers have reduced serum levels and increased urinary output of vitamin B12. Smokers possess a relative depletion of tetrahydrofolate and 5,10-methylenetetrahydrofolate and a relative accumulation of pteroylmonoglutamate and formyltetrahydrofolate in buccal cells. Concomitant

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with this altered folate profile, smokers exhibited lower concentrations of both plasma vitamin B6 and B12 than nonsmokers. This change in the folate coenzyme profile may be a secondary consequence of reduced activity of vitamin B6- and B12-dependent enzymes.6 RBC folate status may be influenced through several smoking-related mechanisms: 1) The intermediates in the folate-dependent homocysteine metabolic pathway are extremely labile and sensitive to the redox balance in the cell; 2) cigarette smoking is a significant source of oxidative stress and may alter the ability of the cell to metabolize and store folate and7 3) people who smoke may eat less folate-rich foods or be less likely to take supplements. Via chemical inactivation, exposure to cigarette smoke may result in folic acid deficiency that principally affects the bronchial epithelium, rendering it more susceptible to neoplastic transformation by the carcinogenic hydrocarbons of tobacco smoke. Several of the hundreds of chemical components of cigarette smoke, primarily organic nitrites, nitrous oxide, cyanates and isocyanates, have been shown to interact with folic acid and vitamin B12 coenzymes, transforming them into biologically inactive compounds.8 Tungtrongchir et al (2003)8 observed that there were low serum folate levels in tobacco users compared with nontobacco users. In our study, serum levels of folate were also significantly lower in case group (6.39 ± 2.43 ng/mL) as compared to control group (8.83 ± 3.99 ng/mL). Erdemir et al9 studied relationship between smoking and folic acid, vitamin B12 and some hematological variables in patients with chronic periodontal disease. They reported results similar to our study of lower serum folic acid concentration in smokers as compared to nonsmokers (p < 0.05). Gabriel et al6 studied association of chronic cigarette smoking with diminished folate status, altered folate form distribution and increased genetic damage in the buccal mucosa of healthy adults. They observed that after correction for dietary intake, the smokers displayed lower plasma, erythrocyte and buccal mucosal cell (BMC) folate (20%, 32% and 50% lower, respectively; p < 0.05) and lower plasma vitamin B12 and pyridoxal 5-phosphate (p < 0.05) than did nonsmokers. Similar to this study, our study also found similar results of low vitamin. B12 and folate in tobacco users. Dastur et al10 found serum vitamin B12 in vegetarians was significantly lower than in nonvegetarians regardless of their smoking habits. On the other hand, folate was significantly higher in vegetarians (mean 6.60 ng/mL) than in nonvegetarian

Community Medicine (mean 4.79 ng/mL) reflecting the greater content of folate in vegetarian diet. The significantly lower serum vitamin B12 values in vegetarians than in nonvegetarians are probably a reflection of the lower intake of the vitamin in their diet particularly meat products. Vegetarians who take adequate amounts of milk and nuts, which are also rich in B12, can maintain adequate serum levels. Results of our study are similar in regards of vegetarians and nonvegetarians to this study. Herrmann et al (2003)11 also reported low vitamin B12 in vegetarian compared to nonvegetarian similar to our study. REFERENCES 1. Warren CW, Jones NR, Peruga A, Chauvin J, Baptiste JP, de Silva VC, et al. Global Youth Tobacco Surveillance, 2000-2007. CDC Morbidity and Mortality Weekly Report. 2008:57(SS-1): 2. United Nations. World Population Prospects 1990. New York: United Nations 1991:p.226-31. 3. United Nations. Sex and Age Distributions of Population. 1990 Revision. New York: United Nations, 1991;4. 4. Health facts. J Indian Med Assoc 1999;97(9):375. 5. Piyathilake CJ, Macaluso M, Hine RJ, Richards EW, Krumdieck CL. Local and systemic effects of cigarette smoking on folate and vitamin B-12. Am J Clin Nutr 1994;60(4):559-66.

6. Gabriel HE, Crott JW, Ghandour H, Dallal GE, Choi SW, Keyes MK, et al. Chronic cigarette smoking is associated with diminished folate status, altered folate form distribution, and increased genetic damage in the buccal mucosa of healthy adults. Am J Clin Nutr 2006;83(4):835-41. Erratum in: Am J Clin Nutr 2006;84(1):263. 7. Northrop-Clewes CA, Thurnham DI. Monitoring micronutrients in cigarette smokers. Clin Chim Acta 2007;377(1-2):14-38. 8. Tungtrongchitr R, Pongpaew P, Soonthornruengyot M, Viroonudomphol D, Vudhivai N, Tungtrongchitr A, et al. Relationship of tobacco smoking with serum vitamin B12, folic acid and haematological indices in healthy adults. Public Health Nutr 2003;6(7):675-81. 9. Erdemir EO, Bergstrom J. Relationship between smoking and folic acid, vitamin B12 and some haematological variables in patients with chronic periodontal disease. J Clin Periodontol 2006;33(12):878-84. 10. Dastur DK, Quadros EV, Wadia NH, Desai MM, Bharucha EP. Effect of vegetarianism and smoking on vitamin B12, thiocyanate, and folate levels in the blood of normal subjects. Br Med J 1972;3(5821): 260-3. 11. Herrmann W, Schorr H, Obeid R, Geisel J. Vitamin B-12 status, particularly holotranscobalamin II and methylmalonic acid concentrations, and hyperhomocysteinemia in vegetarians. Am J Clin Nutr 2003;78(1):131-6.

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Eating High Fiber Diet ÂÂ

There are two types of fibers. One is soluble and the other is insoluble.

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Soluble fiber includes those that are made up of carbohydrates and absorb in water. Examples are oats, barley and legumes.

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Insoluble fiber comes from plant cells and does not dissolve in water. Examples are wheat, ragi and other grains.

ÂÂ

Traditionally, fiber is insoluble fiber.

ÂÂ

Dietary fiber is a combination of soluble and insoluble fiber.

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The recommended amount of dietary fiber is 20-35 g in a day.

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Eating a high-fiber diet both can prevent constipation, reduce cholesterol and help in reversing obesity and heart diseases in children and adults.

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A high–fiber diet should be a balanced diet with food from all food groups.

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The common sources of fiber are whole grain produce and cereals, legumes, fruits and vegetables.

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One should eat fruits with significance, such as prunes and peas, which are natural laxatives.

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Salads with dark green lettuce provide high fiber content.

ÂÂ

Eating whole wheat bread or with added fiber is a rich source of fiber.

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You can eat whole wheat carbohydrates, bran muffins, bran cereals or oat meals.

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Avoid eating refined white flour, cereals and other starches.

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Fruits are better than juices

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Diabetology

Association Between Indexes of Insulin Sensitivity/ Resistance and Serum Magnesium Levels in Overweight Diabetic Subjects Neetesh Kumar Gupta*, Sonali Sharma†, GG Kaushik‡, Bhavana Gupta#

Abstract Objective: To study the association of serum magnesium level and indexes of insulin sensitivity/resistance in overweight diabetic subjects and evaluate the relationship of serum magnesium level with body mass index (BMI) in overweight diabetic subjects. Study design: This case-control study was conducted on 50 overweight type 2 diabetic patients. The overweight diabetic subjects were defined as (BMI ≥ 25.0-30.0 kg/m2) according to the criteria of World Health Organization (WHO), 2004. Diagnosis of type 2 diabetes mellitus was made according to the criteria recommended by the American Diabetes Association standards - 2012. Material and methods: The study was conducted on 50 overweight type 2 diabetic patients of either gender attending/admitted in OPD/wards of the Dept. of General Medicine, Jawaharlal Nehru Medical College and Associated Group of Hospitals, Ajmer, Rajasthan over a period of 12 months. Results: In overweight diabetic subjects, serum magnesium level were found to be low, HOMA-IR was high and QUICKI values was found to be low in comparison to normal weight nondiabetics. Serum magnesium significantly inversely correlated with BMI, plasma glucose, HbA1C, serum insulin, HOMA-IR and a positive correlation of serum magnesium with QUICKI (overweight subjects) was found in our study. Conclusion: Poor glycemic control in hypomagnesemia patients has been observed in the present study when compared with normomagnesemia patients. Hypomagnesemia may aggravate insulin resistance state in overweight subjects. This can predispose them to metabolic complication of diabetes mellitus.

Keywords: Diabetes mellitus, hypomagnesemia, insulin

ver the last decades, there has been a rapid increase in the prevalence of type 2 diabetes in parallel with the obesity epidemic. Diabetes mellitus is a leading cause of morbidity and mortality worldwide, with an estimated 346 million adults being affected in the year 2011-2012.1 Type 2 diabetes is characterized by peripheral insulin resistance, impaired regulation of hepatic glucose production, hyperinsulinemia, β-cell dysfunction and subsequent β-cell failure.2 Direct associations of trace microelements with diabetes mellitus have been observed in many research studies.3

*Postgraduate †Associate Professor ‡Professor Dept. of Biochemistry #Postgraduate Dept. of Microbiology Jawaharlal Nehru Medical College, Ajmer, Rajasthan Address for correspondence Dr Sonali Sharma SONANK, 2-K-12, Shastri Nagar, Ajmer, Rajasthan E-mail: sonalisharma14@gmail.com

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Magnesium plays an important role in carbohydrate metabolism. It may influence the release and activity of insulin, the hormone that helps control blood glucose levels. Low blood levels of magnesium (hypomagnesemia) are frequently seen in individuals with type 2 diabetes.4 Study of role of magnesium in obese diabetic subjects has been a matter of interest of researchers in the past years. However, studies on association of trace microelement magnesium with indexes of insulin sensitivity/resistance in overweight type 2 diabetics are scarce. The present study was undertaken to study indexes of insulin sensitivity/ resistance and their association with serum magnesium levels in overweight diabetic subjects. Material and methods This case-control study has been conducted on 50 type 2 diabetic overweight patients of either gender attending/admitted in OPD/wards of the Dept. of General Medicine, Jawaharlal Nehru Medical College and Associated Group of Hospitals, Ajmer, Rajasthan. The results were compared with age- and gendermatched 100 normal weight nondiabetic healthy

Diabetology subjects acting as controls. Consent from all the subjects was obtained for the study.

Inclusion Criteria Overweight adults in the age group of 35-55 years were screened for eligibility and majority of patients of either gender selected for the study were in the age group of 35-45 years. All participants were asked to maintain their usual diet and not make any significant changes in diet or physical activity. Dietary intake of magnesium in all subjects was adequate. The overweight diabetic subjects were defined as (BMI ≥ 25.0-30.0 kg/m2) according to the criteria of World Health Organization (WHO), 2004.5 Diagnosis of type 2 diabetes mellitus was made according to the criteria recommended by the American Diabetes Association standards 2012.6

Exclusion Criteria Patients with positive clinical history of malignancy, chronic alcoholism, pregnancy, insulin therapy, medical conditions predisposing to hypomagnesemia (gastroenteritis, chronic kidney disease, chronic liver disease), subjects receiving magnesium supplementation or treated with drugs known to modify magnesium metabolism e.g., diuretics, thyroxine, lithium or calcium antagonists were excluded from the study. The subjects selected for the study were grouped as follows: ÂÂ

Group I: Type 2 overweight diabetic subjects (n = 50).

ÂÂ

Group II: Nondiabetic normal weight control subjects (n = 100).

Anthropometric Measurements Weight was measured in light clothes and without shoes using a calibrated digital weighing scale with an accuracy of 0.1 kg and height was measured without shoes using a calibrated wall mounted stadiometer to the nearest 0.5 cm. Body mass index (BMI) was calculated by using the formula: mass (in kg)/height2 (in meters).7

Biochemical Parameters An overnight, 12 hours fasting blood sample was aseptically collected from anticubital vein of all subjects, serum/plasma was separated and fasting plasma glucose, glycosylated hemoglobin (HBA1C) and serum magnesium were estimated on fully automated analyzer (Randox Daytona). Fasting serum insulin

was estimated using enzyme-linked immunosorbent assay (ELISA) technique. Following indexes derived from fasting blood samples for assessment of insulin sensitivity/resistance were calculated: ÂÂ

Homeostasis Model Assessment for Insulin Resistance (HOMA-IR) was calculated using the formula of Matthews et al, 1985.8

ÂÂ

Quantitative Insulin Sensitivity Check Index (QUICKI) was calculated using the formula of Katz et al, 2000.9

Statistical Analysis Data were recorded in a predesigned proforma and managed in an excel spread sheet. Data were reported as mean ± SD (standard deviation) median (range). Comparison of physical and biochemical parameters between overweight diabetics and nondiabetics normal weight healthy control subjects was performed using equal or unequal variance unpaired student t-test for continuous variables (as applicable). The relation between continuous variables was examined using Pearson’s correlation coefficient (r). A multiple linear regression analysis was performed in order to explore the variables independently related to serum magnesium. The variables included were plasma glucose, HbA1C, serum insulin and BMI. All p values were based on Table 1. Age and Sex Distribution of Overweight Diabetics Age (years) 35-45

Male 23 (46%)

Sex

Female 11 (22%)

Total 34 (68%)

46-55

9 (18%)

7 (14%)

16 (32%)

Total

32 (64%)

18 (36%)

50 (100%)

Table 2. Anthropometric Parameters of Overweight Diabetics and Normal Weight Nondiabetic Subjects (Controls) Parameters

Age (years) Weight (kg) Height (cm) BMI (kg/m2)

Group I Overweight diabetics mean ± SD (n = 50) 40.18 ± 2.8 70.34 ± 4.5 159.42 ± 0.05 27.72 ± 1.9

Group II Normal weight nondiabetics mean ± SD (n = 100) 40.35 ± 2.9 51.58 ± 4.9 155.52 ± 4.4 21.34 ± 1.5

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Diabetology Table 3. Comparison of Biochemical Parameters of Overweight Diabetics and Normal Weight nondiabetics Subjects (Controls) Parameters

Group I Overweight diabetics mean ± SD (n = 50) 230.82 ± 21.73

Group II Normal weight nondiabetics mean ± SD (n = 100) 87.12 ± 10.6

‘t’ value

‘P’ value*

44.21

< 0.0001 (HS)

8.2 ± 0.45

4.90 ± 0.5

40.77

< 0.0001 (HS)

Serum insulin (µIU/mL)

9.8 ± 1.4

3.5 ± 0.8

29.50

< 0.0001 (HS)

Serum magnesium (mg/dL)

1.2 ± 0.14

2.0 ± 0.2

28.43

< 0.0001 (HS)

Plasma glucose (mg/dL) HbA1C (%)

*p value <0.0001, highly significant (HS); p value <0.01, significant (S); p value >0.05, nonsignificant (NS).

a two-sided test of statistical significance. Significance was accepted at the level of p < 0.05.

Majority of the patients satisfying the inclusion criteria were in the age group of 35-45 years (68%). Out of 50 patients of this study group, 32 were males (64%) and 18 were females (36%) (Table 1). Table 2 depicts the anthropometric parameters of overweight diabetics and normal weight nondiabetic, subjects. The biochemical parameters viz., plasma glucose (mg/dL), HbA1c (%), serum insulin (µIU/mL) and serum magnesium (mg/dL) levels in overweight diabetics and normal weight nondiabetics are summarized in Table 3. The mean plasma glucose level and mean HbA1C level in mean ± SD were found to be significantly high in Group I as compared to Group II. A similar trend was observed in mean serum insulin and magnesium levels in Group I, when statistically compared with Group II (Table 3 and Fig. 1). Table 4 shows statistically insignificant age difference between Group I and II. A highly significant increase in BMI has been observed in Group I when compared with Group II. In overweight diabetic subjects, serum magnesium levels were found to be low in comparison to normal weight nondiabetics. The difference was highly significant in Group I and II, respectively (Table 4 and Fig. 2).

Normal weight nondiabetics

250 230.82

Values of parameters

Results

Overweight diabetics

200 150 87.12

100 50 0

Glucose (mg/dL)

8.2 4.9

9.8

HbA1C (%)

Insulin (µIU/mL)

3.5

1.2 2.0 Magnesium (mg/dL)

Parameters

Figure 1. Comparison of biochemical parameters of overweight diabetics and normal weight nondiabetics subjects (controls).

HOMA-IR and QUICKI, indexes of insulin resistance/ sensitivity showed highly significant difference between Group I and Group II. The overweight diabetics had increased value of HOMA-IR and decreased value of QUICKI (Table 5 and 6, Fig. 3). Pearson correlation coefficient (r) analysis was used to determine the correlation of serum magnesium levels with BMI in overweight subjects. Magnesium significantly inversely correlated with BMI (in overweight subjects) (r= -0.50; p < 0.0001) (Fig. 4). Magnesium significantly negatively correlated with

Table 4. Comparison of BMI and Serum Magnesium in Overweight Diabetics and Normal Weight Nondiabetic Subjects (Controls) Parameters Age (years) BMI (kg/m2) Serum magnesium (mg/dL)

Group I Overweight diabetics mean ± SD (n = 50) 40.18 ± 2.8

Group II Normal weight nondiabetics mean ± SD (n = 100) 40.35 ± 2.9

‘t’ value -0.34

0.7290 (NS)

27.72 ± 1.9 1.2 ± 0.14

21.34 ± 1.5 2.0 ± 0.2

18.78 28.43

< 0.0001 (HS) < 0.0001 (HS)

*p value <0.0001, highly significant (HS); p value <0.01, significant (S); p value >0.05, non significant (NS).

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Indian Journal of Clinical Practice, Vol. 24, No. 10, March 2014

‘P’ value*

Diabetology Overweight diabetics

25 20

26.81 21.34

10 5

1.2 2.0 BMI

5 4 3 2 0.75

1 0

Magnesium

HOMA-IR

Parameters

Figure 2. Comparison of BMI and serum magnesium in overweight diabetics and normal weight nondiabetics subjects (controls).

QUICKI

Indexes

QUICKI

Group I Overweight diabetics mean ± SD (n = 50)

Group II Normal weight nondiabetics mean ± SD (n = 100)

5.7 ± 1.2

0.75 ± 0.20

0.30 ± 0.009

0.40 ± 0.020

plasma glucose (r = -0.62; p < 0.0001) (Fig. 5), HbA1C (r= -0.29; p < 0.0001) (Fig. 6), serum insulin (r = -0.62; p < 0.0001), HOMA-IR (r= -0.63; p < 0.0001) and a positive correlation of serum magnesium with QUICKI (r = 0.65; p < 0.0001) was found in our study. Multiple linear regression analysis showed that serum insulin and BMI were independently related to serum magnesium levels in overweight diabetic subjects and explained 49.75% of the magnesium variation. Discussion Among the endocrine and metabolic disorders associated with magnesium deficiency,

Serum magnesium

HOMA-IR

0.3 0.4

Figure 3. Comparison between HOMA-IR and QUICKI in overweight diabetics and normal weight nondiabetics (controls)

Table 5. Indexes Derived from Fasting Blood Samples for Assessment of Insulin Sensitivity/ Resistance in Overweight Diabetics and Normal Weight Nondiabetic Subjects (Controls) Indexes

Normal weight nondiabetics

5.7

Overweight diabetics

Values of indexes

Values of parameters

Normal weight nondiabetics

1.6 1.2 0.8 0.4 0

BMI

Figure 4. Linear correlation between BMI and serum magnesium level in overweight diabetic subjects.

diabetes mellitus is the most common. The present study was undertaken in two groups viz. Group I and Group II i.e., overweight diabetics and normal weight nondiabetics, respectively. We have reported significantly lower serum magnesium levels in overweight subjects in comparison to normal weight nondiabetics. The results, thus confirm that magnesium is negatively regulated in overweight subjects. Previous reports have shown that serum magnesium level was found lower in overweight subjects.10

Table 6. Comparison of Indexes for Assessment of Insulin Sensitivity/Resistance in Overweight Diabetic and Normal Weight Nondiabetic Subjects (Controls) Indexes HOMA-IR QUICKI

Group I Overweight diabetics mean ± SD (n = 50) 5.7 ± 1.2

Group II Normal weight nondiabetics mean ± SD (n = 100) 0.75 ± 0.20

‘t’ value

‘P’ value*

28.96

< 0.0001 (HS)

0.30 ± 0.009

0.40 ± 0.020

46.40

< 0.0001 (HS)

*p value <0.0001, highly significant (HS); p value <0.01, significant (S); p value >0.05, nonsignificant (NS)

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935

Serum magnesium (mg/dL)

Diabetology require greater amounts of insulin to maintain blood glucose within normal levels. Kidneys possibly lose their ability to retain magnesium during periods of severe hyperglycemia.

1.8 1.6 1.4 1.2 1

The increased loss of magnesium in urine may then result in lower blood levels of magnesium in older adults, and correcting magnesium depletion may improve insulin response and action.12

0.8 0.6 0.4 0.2 0

100

150 200 250 Plasma glucose (mg/dL)

300

Serum magnesium (mg/dL)

Figure 5. Linear correlation between plasma glucose and serum magnesium level in overweight diabetic subjects.

Large scale prospective studies are needed to establish that magnesium plays an important role in improving insulin sensitivity and preventing diabetes mellitus in overweight subjects.

1.7

Conclusion

1.5

In overweight diabetic subjects, serum magnesium level were found to be low, HOMA-IR was high and QUICKI values was found to be low in comparison to normal weight nondiabetics. Serum magnesium significantly inversely correlated with BMI, plasma glucose, HbA1C, serum insulin, HOMA-IR and a positive correlation of serum magnesium with QUICKI was found in our study (overweight subjects). Type 2 diabetes mellitus is the main factor accounting for low serum magnesium levels in overweight diabetics. Hypomagnesemia may aggravate insulin resistance state in overweight subjects. This can predispose them to metabolic complications of diabetes mellitus.

1.3 1.1 0.9 0.7 0.5

6 7 8 HbA1C (%)

Figure 6. Linear correlation between (HbA1C) and serum magnesium level in overweight diabetic subjects.

Magnesium deficiency may play an important role in both insulin sensitivity and insulin secretion processes. The release of insulin caused by a glucose challenge is partly dependent on adequate magnesium. Magnesium is essential for insulin secretion, insulin receptor interaction, postreceptor events (involving tyrosine kinase-mediated phosphorylation) and normal carbohydrate utilization (by magnesiumdependent enzymes).11 The mechanism by which magnesium deficiency may lead to insulin resistance has not yet been fully elucidated. Magnesium is a cofactor for multiple enzymes involved in carbohydrate metabolism. It may influence the release and activity of the hormones that helps control blood glucose levels. Hypomagnesemia may worsen insulin resistance, a condition that often precedes diabetes, or may be a consequence of insulin resistance. Individuals with insulin resistance cannot use insulin efficiently and

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Limitations

Indian Journal of Clinical Practice, Vol. 24, No. 10, March 2014

It can be stated that lower levels of magnesium reported in moderately obese subjects are related to the presence of diabetes and glycemic control. Thus in conclusion, it can be stated that poor glycemic control and hypomagnesemia has been observed in overweight diabetic patients in the present study when compared with normomagnesemia patients. Glycemic control is one of the most important therapeutic challenges in present day. Magnesium level should be monitored in all overweight diabetic patients. References 1. World Health Organization. Diabetes. Fact sheet N째312. October 2013. Available at: http://www.who.int/ mediacentre/factsheets/fs312/en/index. html. 2. Stumvoll M, Goldstein BJ, van Haeften TW. Type 2 diabetes: principles of pathogenesis and therapy. Lancet 2005;365(9467):1333-46. 3. Nourmohammadi I, Shalmani IK, Shabbani M, Gohari L. Zinc, copper, chromium, manganese and

Diabetology magnesium levels in serum and hair of insulin dependent Diabetics. Arch Iranian Med 2000;2:88-100.

plasma glucose and insulin concentrations in man. Diabetologia 1985;28(7):412-9.

4. Ma B, Lawson AB, Liese AD, Bell RA, Mayer-Davis EJ. Dairy, magnesium, and calcium intake in relation to insulin sensitivity: approaches to modeling a dose-dependent association. Am J Epidemiol 2006;164(5):449-58.

9. Katz A, Nambi SS, Mather K, Baron AD, Follmann DA, Sullivan G, et al. Quantitative insulin sensitivity check index: a simple, accurate method for assessing insulin sensitivity in humans. J Clin Endocrinol Metab 2000;85(7):2402-10.

5. World Health Organization. Classification for overweight and obesity in relation to BMI. WHO, 2004. 6. American Diabetes Association. Clinical recommendations. Diabetes Care 2012;6:1-16.

practice

7. Murray RK, Granner DK, Mayes PA, Rodwell VW, et al. Harpers Illustrated Biochemistry. 26th edition, McGraw Hill 2003;Chapter-44:478. 8. Matthews DR, Hosker JP, Rudenski AS, Naylor BA, Treacher DF, Turner RC. Homeostasis model assessment: insulin resistance and beta-cell function from fasting

10. Lecube AL, Baena-Fustegueras JA, Fort JM, et al. Diabetes is the main factor accounting for hypomagnesemia in obese subjects. Plos One 2012;7. 11. Pham PC, Pham PM, Pham SV, Miller JM, Pham PT. Hypomagnesemia in patients with type 2 diabetes. Clin J Am Soc Nephrol 2007;2(2):366-73. 12. Paolisso G, Sgambato S, Gambardella A, Pizza G, Tesauro P, Varricchio M, et al. Daily magnesium supplements improve glucose handling in elderly subjects. Am J Clin Nutr 1992;55(6):1161-7.

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SMBG Helps Achieve Individualized HbA1C Targets Current glycemic targets advised for diabetes patients don’t align with recommended HbA1C levels, a new analysis of continuous glucose monitoring data suggests. The findings, from the A1C-Derived Average Glucose (ADAG) study, were published online February 10 in Diabetes Care by Nancy Wei, MD, from the Diabetes Center at Massachusetts General Hospital, Harvard Medical School, Boston, and colleagues. Professional societies’ recommendations for diabetes management advise HbA1C goals of 6.5% or less, or less than 7%, with individualization based on a variety of factors. But HbA1C is measured only once every 3 months, and day–to– day self-management of diabetes to achieve and maintain the individualized target HbA1C is facilitated by selfmonitored blood glucose (SMBG) values, especially in patients treated with insulin.

It is Fruit Juice which Increases the Risk of Diabetes and Not the Fruits A research published in the British Medical Journal has shown that eating blueberries, apples and grapes may be linked to a reduced risk and type 2 diabetes. However, increased consumption of fruit juice was linked to a higher risk. It is a typical Ayurvedic teaching that one should eat fruits and not take fruit juice unless one is sick when digestion is weak. It is a myth that eating grapes can cause diabetes. The well–known saying that eating an apple a day keeps the doctor away is true from this study especially green apples, which are known to be more health-friendly then the red apples. The answer is simple… anything which is natural cannot be harmful. Fruits are natural but juices are not. Eating brown rice instead of white rice may help prevent and control diabetes in rice-eating populations. In the first randomized controlled trial to compare the two in India, substituting brown rice for white rice in a population of overweight/obese individuals helped significantly reduce glucose levels and lower serum insulin. The findings were presented at the International Diabetes Federation World Diabetes Conference 2013 last month.

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937

Hematology

Leukemia Cutis with PML-RAR-a Translocation Leena Dennis Joseph*, K Krishnarathnam, Suresh Masilamani, Rajendiran Swaminathan

Abstract Leukemia cutis is the infiltration by neoplastic leukocytes or their precursors into the epidermis, dermis or the subcutis resulting in clinically identifiable cutaneous lesions. The diagnosis is of great value in cases where leukemia cutis aids in the diagnosis of leukemia. This has a poor prognosis and strongly correlates with additional signs of extramedullary involvement. A 27-year-old male patient, known case of AML-M3, presented with cutaneous nodules on both lower limb, which on biopsy proved to be leukemic deposits. Immunohistochemistry confirmed the diagnosis and the patient was discharged with advice to continue chemotherapy.

Keywords: Cutaneous nodules, AML, IHC, PML-RAR

chloroma is an extramedullary manifestation of acute myeloid leukemia (AML) in which there is a solid collection of leukemic cells occurring outside the bone marrow. It is also known as granulocytic sarcoma and the most common manifestation of chloroma is in the form of leukemia cutis. This infiltration of the dermis by the leukemic cells is also known as cutaneous granulocytic sarcoma. This case is reported for its rarity and to highlight the molecular study done for the same.

Case report A 27-year-old Iraqi patient, presented with a history of fever and bleeding gums. He had similar complaints in Iraq for which he was investigated and diagnosed as AML-M3. He was referred to our institution for further management. Baseline blood investigations were within normal limits. Coagulation profile, renal function tests, liver function tests, lactate dehydrogenase, thyroid profile and ultrasound were within normal limits. The bone marrow aspiration was done, but was inadequate for a definite opinion. The bone marrow was negative for PML-RAR translocation. The patient also presented with cutaneous nodules over both the lower limbs (Fig. 1). A skin biopsy was taken, which showed evidence of leukemia cutis on light microscopy. There

*Professor Dept. of Pathology and Hemato Oncology Sri Ramachandra Medical College and Research Institute, Porur, Chennai Address for correspondence Dr Leena Dennis Joseph Professor, Dept. of Pathology Sri Ramachandra Medical College and Research Institute, Porur, Chennai E-mail: leenadj@rediffmail.com

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Indian Journal of Clinical Practice, Vol. 24, No. 10, March 2014

Figure 1. Cutaneous nodule as pointed with an adjacent biopsy scar.

Figure 2. Skin nodule showing monotonous leukemic infiltrate in the dermis (H&E Ă&#x2014; 40)

Hematology

Figure 3. Skin nodule showing monotonous leukemic infiltrate in the dermis (H&E × 100).

Figure 6. PCR gel showing the PML-RAR-α fusion band as marked.

Figure 4. IHC showing CD45 positivity in the tumor cells (IHC × 100).

was a perivascular and periadnexal infiltrate of atypical mononuclear cells (Figs. 2 and 3). The exact nature of these atypical cells were studied by immunohistochemistry (IHC). There was positivity for CD45 (Fig. 4), CD68 and S100. These cells were focally positive for CD34. They were negative for CD3, CD20, CD15, myeloperoxidase and CD117. The skin biopsy specimen was also sent for fluorescent in situ hybridization (FISH) for t 15:17 (Fig. 5) and PML-RAR-α fusion gene by reverse transcriptase polymerase chain reaction (RT-PCR) (Fig. 6) and both confirmed the diagnosis of APML. The patient was discharged with in structions to continue with chemotherapeutic agents. Discussion

Figure 5. Positive FISH signal for PML-RAR-α as marked.

Leukemia cutis is the infiltration of neoplastic leukocytes or their precursors into the epidermis, dermis or the subcutis resulting in clinically identifiable cutaneous lesions. The accurate diagnosis has a tremendous prognostic significance and may establish a diagnosis in cases in which leukemia cutis is the harbinger of a systemic leukemic process. A diagnosis of leukemia cutis has a poor prognosis and strongly correlates with additional sites of extramedullary involvement.1 Like all leukemias, leukemia cutis is thought to result from a local proliferation of the leukemic cells within the skin. Cutaneous infiltration

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Hematology by neoplastic lymphocytes may be seen in AML, acute lymphocytic leukemia, chronic myeloid leukemia (CML), chronic lymphocytic leukemia, prolymphocytic leukemia and myelodysplastic syndromes. The specific migration of leukemic cells to the skin is due to a chemokine, integrin and other adhesion molecules, which play a specific role in skin specific homing of T and B leukemic cells. Because leukemia cutis is a relatively rare condition and it may manifest in a variety of leukemia subtypes. In USA, the highest incidence is of Adult T cell leukemia in patients seropositive for human T-lymphotropic virus 1 (HTLV-1). The next highest rates of leukemia cutis is for AML, especially AML-M4 and M5 types, which have an incidence of 30%. The incidence of leukemia cutis is high among children. In most cases, systemic disease precedes the development of skin lesions, however in 7% of patients with leukemia cutis localized disease occurs prior to bone marrow infiltration and other systemic manifestation. The prevalence of leukemia cutis in Vienna was studied by Agis et al and found to be 2.9-3.7% for AML.2 The incidence of AML deposits in skin is 2.5 cases/1,00,000 population in the USA as studied by Baer et al.3 More specific cutaneous lesions are papules and nodules, indurated plaques, hemorrhagic plaques, perifollicular acneiform papules, macules, ulcers, bullae and palpable purpura. Genetic and environmental factors are found to be involved in many leukemias. Patients with genetic syndromes like Down’s syndrome, Bloom syndrome, Klinefelter’s syndrome, etc. have shown an increased incidence of leukemia. Cytogenetic studies have demonstrated that as many as 50% of the patients with AML-M4 or M5 develop leukemia cutis. Karyotypic studies of leukemic cells have demonstrated the translocation of chromosome 8 and 21 in these subtypes of AML. Skin biopsy with appropriate immunohistochemical staining is the key to the diagnosis of aleukemic leukemia or identifying leukemia cutis, a sign of extramedullary extension of the leukemia and a poor prognosis. On histology of the skin lesions, there is a dermal infiltrate of leukemic cells, which is often perivascular

and periadnexal. The prognosis is poor with many patients having other extramedullary disease and poor survival rates. Most patients die within months of diagnosis. In a study of 26 patients with cutaneous infiltrates, Kaddu et al reported a median survival of 7.6 months of AML and in CML, 9.4 months.4 In a smaller case series by Shaikh et al with only five patients with AML all the patients died within 6 months of their diagnosis of leukemia.5 Skin infiltration is associated with advanced stage and poor prognosis.6 The importance of a skin biopsy in cases of aleukemic leukemia cutis, rests on the fact that if the biopsy is not performed promptly, a delay in the treatment results. If appropriate immunostaining is not performed and an incorrect diagnosis is made, again the treatment will be delayed. Another important aspect is that skin biopsy should be performed even in an established case of leukemia because a concurrent different leukemia could be present or transformation of the original leukemia may have occurred. If biopsy is delayed appropriate treatment will also be delayed. References 1. Cho-Vega JH, Medeiros LJ, Prieto VG, Vega F. Leukemia cutis. Am J Clin Pathol 2008;129(1):130-42. 2. Agis H, Weltermann A, Fonatsch C, Haas O, Metterbauer G, Mullauer L, et al. A comparative study of demographic, hematological, and cytogenetic findings and prognosis in acute myeloid leukemia with and without leukemia cutis. Ann Hematol 2002;81(2):90-5. 3. Baer MR, Barcos M, Farell H, Raza A, Preisler HD. Acute myelogenous leukemia with leukemia cutis. Eighteen cases seen between 1969 and 1986. Cancer 1989;63(11):2192-200. 4. Kaddu S, Smolle J, Cerroni L, Kerl H. Prognostic evaluation of specific cutaneous infiltrates in B-chronic lymphocytic leukemia. J Cutan Pathol 1996;23(4):487-94. 5. Shaikh BS, Frantz E, Lookingbill DP. Histologically proven leukemia cutis carries a poor prognosis in acute nonlymphocytic leukemia. Cutis 1987;39(1):57-60. 6. Cerroni L, Hofler G, Bäck B, Wolf P, Maier G, Kerl H. Specific cutaneous infiltrates of B cell chronic lymphocytic leukemia (B-CLL) at sites typical for Borrelia burgdorferi infection. J Cutan pathol 2002;29(3):142-7.

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The common antifungal drug itraconazole may be useful in treating basal cell carcinoma (BCC), according a phase 2 study published online last week in the Journal of Clinical Oncology. Itraconazole showed anti-BCC activity in a 29-patient study: 24% of the 19 patients treated for a month with common doses of the drug had a reduced tumor area. Also, itraconazole reduced cell proliferation by 45%.

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Hematology

Coomb’s Negative Hemolytic Anemia in Wilson’s Disease V Padma*, Halleys Kumar†

Abstract Wilson’s disease is a rare inherited disorder of copper metabolism. Liver and brain are the main organs affected. Hemolytic anemia is a rare clinical manifestation of Wilson’s disease. We present a case of Wilson’s disease who presented with hemolytic anemia.

Keywords: Wilson’s disease, hemolytic anemia

ilson’s disease is an autosomal recessive disorder of copper metabolism characterized by excessive amount of copper in liver, brain, eye and other body tissues. The main clinical symptoms are hepatic (42%) and neurological (34%).1 Hemolytic anemia is rare.2 We present this case for its rarity. CASE REPORT A 37-year-old female patient, a known case of Wilson's disease came to the OPD with complaints of ecchymotic patches over right hand and purpuric spots over both lower limbs for 2 weeks. There was no history of trauma, gum bleeding, fever, weight loss and loss of appetite. Patient did not have any other medical illness. General examination showed anemia. Her blood pressure was 120/80 mmHg, pulse rate was 82/min. There were nonpalpable purpuric spots seen in both upper limbs and lower limbs echymosis, Kayser-Flescher ring was present in both the eyes (Figs. 1 a and b). Patient had dysarthria. There was no cardiac and renal involvement. Abdominal examination showed moderate splenomegaly, mild hepatomegaly. INVESTIGATIONS Hemoglobin was 6.8 g/dL, total leukocytes were 3,550, platelet count was 52,000. The differential *Professor

†Postgraduate

Dept. of Medicine Sree Balaji Medical College, Chrompet, Chennai Address for correspondence Dr V Padma Professor Dept. of Medicine Sree Balaji Medical College, Chrompet, Chennai

Figure 1 (a and b). Kayser-Flescher ring present in boh the eyes.

count was N69%L26%E4%M1%. Peripheral smear showed normocytic normochromic anemia, with pancytopenia. Serum bilirubin was 4 mg/dL, direct bilirubin 0.4 and indirect bilirubin was 3.6 mg/dL, serum albumin 3.8 g/dL, alkaline phosphatase 192 IU/L, reticulocyte count was 9%, urine for hemoglobin was absent. Hepatitis B surface antigen (HBsAg) and anti-hepatitis C virus were negative. Coomb’s test performed twice showed negative results. Ultrasound abdomen showed moderate splenomegaly. Bone marrow aspiration: Out of 500 cells studied 2 were megakaryocytes, 156 myeloid series cells, 14

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Hematology erythroid series cells noted, indicating normoerythroid hyperplasia with lesser myeloid megakaryocytic cells. D-pencillamine was stopped to confirm drug-induced hemolytic anemia but there was no improvement. During follow-up patient had one episode of hemolysis and 2 units of blood transfusion was given. DISCUSSION Wilson’s disease is a rare inherited disease presenting between 5-35 years of age.3 The disease does not manifest clinically before 4-5 years of age as it takes time for copper to accumulate in liver. Hepatic manifestations are common early and neurological symptoms are common in adolescents.4 Hemolysis in Wilson’s disease (10-15%) is uncommon. Hemolysis is due to deficiency of ceruloplasmin, a copper transport protein, which results in excessive inorganic copper in blood circulation, much of it which accumulates in red blood cells. The exact mechanism of hemolysis is not known. The diagnosis of Wilson’s disease is based on Kayser-Flescher rings, low serum ceruloplasmin levels and elevated basal urinary copper excretion. Hemolytic anemia often remits and may occasionally recur.

CONCLUSION Hemolytic anemia is rare in Wilson’s disease and can be a cause of anemia. Hemolytic anemia may also be a presenting episode in Wilson’s disease. This is a case of Coomb's negative hemolytic anemia in Wilson’s disease patient not precipitated by D-pencillamine, which is a rare presentation. Hemolytic anemia with liver failure should make a doctor suspect Wilson’s disease as a cause. REFERENCES 1. Grudeva-Popova JG, Spasova MI, Chepileva KG, Zaprianov ZH. Acute haemolytic anemia as an initial clinical manifestation of Wilson’s disease. Folia Med (Plovdiv) 2000;42(2):42-6. 2. McIntyre H, Clink HM, Levi AJ, Cumings JN, Sherlock S. Hemolytic anemia in Wilson’s disease. N Engl J Med 1967;276:439-44. 3. Roberts EA, Schilsky ML; Division of Gastroenterology and Nutrition, Hospital for Sick Children, Toronto, Ontario, Canada. A practice guidelines on Wilson’s disease. Hepatology 2003;37(6):1475-92. 4. Kalra V, Khurana D, Mittal R. Wilson’s disease - early onset and lessens from a pediatric cohort in India. Indian Pediatr 2000;37(6):595-601.

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Risk for stroke shows a graded association with rising levels of HbA1C in women with type 2 diabetes, new findings from a large prospective study show. Notably, poor control of blood sugar was found to have the strongest effect on stroke in diabetic women over 55 years of age. The Louisiana State University Hospital-Based Longitudinal Study (LSUHLS) aimed to better understand the relationship between glycemic control and stroke and is published online February 24 in Diabetologia. As per FDA, the targeted drug ibrutinib (Imbruvica) can be used as second-line therapy for patients with relapsed or refractory chronic lymphocytic leukemia (CLL). Ibrutinib was first approved last November as a treatment for mantle cell lymphoma in patients who failed at least one prior therapy. It inhibits Bruton’s tyrosine kinase, a key component of the intracellular signalling cascade that drives malignant cell proliferation.

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Infections

Bacteriological Study of Infective Endocarditis from a Rural Area of Maharashtra Sabiha S Tamboli*, SL Nilekar†

Abstract Background: To evaluate the role of blood culture in infective endocarditis patients attending a rural hospital of Maharashtra, India. Material and methods: One hundred thirty-eight blood samples from 46 patients with clinical diagnosis of infective endocarditis were investigated. Blood culture was done. After growth, Gram-staining, biochemicals and antibiotic sensitivity testing was performed. Results: Blood culture yielded a positive result in 24 cases. All the organisms isolated were gram-positive cocci. Staphylococcus aureus was the predominant organism isolated followed by Streptococcus viridans. Most of the organisms were sensitive to cephalexin and ciprofloxacin. Conclusion: The initial therapy in our hospital may be aimed at gram-positive organisms and cephalexin and ciprofloxacin can be used as first-line drugs. This shows the role of microbiology is important in diagnosis of causative organisms responsible for infective endocarditis and their antibiotic susceptibility testing, which will be helpful in early and specific treatment.

Keywords: Blood culture, infective endocarditis, Staphylococcus aureus

ndocarditis is an endogenous infection acquired when organisms entering the blood stream establish on the heart valves, therefore, any bacteremia can potentially result in endocarditis. Infective endocarditis is an uncommon disease that often presents as pyrexia of unknown origin. The mortality rate in endocarditis was very high before the antibiotic era, even now a day, the mortality rate is around 20%.1

The present study was undertaken to know the prevalence rate of different bacteria and their antibiotic sensitivity pattern, isolated from blood cultures of infective endocarditis patients admitted in a rural hospital. MATERIAL and METHODS

The primary causes of infective endocarditis are streptococci, enterococci, Staphylococcus aureus and coagulase-negative Staphylococcus.2 In recent reviews, S. aureus has accounted for a larger portion of cases of bacterial endocarditis, with a prevalence of about 30%.3 A definite diagnosis of infective endocarditis is desirable to guide management protocol. Durack and coworkers modified earlier criteria of Von Reyn et al, which is more versatile and practical.4 Blood culture is the most important investigation for diagnosing infective endocarditis.

A total of 138 blood cultures were received from 46 clinically diagnosed cases of bacterial endocarditis (31 males and 15 females with a median age of 39 years) admitted in SRTR Medical College, Ambajogai, Maharashtra during 2-year period. Blood sample was collected under all aseptic precautions from antecubital vein; 5 mL of blood was withdrawn from the patients. Blood sample was collected before starting antimicrobial therapy. In patients already on antibiotic therapy, blood sample was taken just before the next dose of antimicrobial agents. In all cases, three blood samples were collected (drawn more than 12 hours apart).4 Informed consent was obtained from each patient.

*Assistant Professor Dept. of Microbiology, MIMSR Medical College, Latur, Maharashtra †Associate Professor and Head Dept. of Microbiology, SRTR Medical College, Ambajogai, Maharashtra Address for correspondence Dr Mrs. Sabiha S Tamboli Assistant Professor, Dept. of Microbiology MIMSR Medical College, Latur, Maharashtra E-mail: microbiopharma@yahoo.com

Five milliliter of blood was collected using aseptic precautions and inoculated into Brain Heart Infusion Broth-Brain Heart Infusion Agar (BHIB-BHIA) medium. The cultures were incubated at 37°C and processed as per the recommended procedures.5 Bottles were examined daily for any evidence of growth for a period of 3 weeks before being

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Indian Journal of Clinical Practice, Vol. 24, No. 10, March 2014

Infections discarded. The isolated organisms were identified as per the standard recommended procedures.6 Blood cultures were declared as sterile if there was no growth of any organism after 3 weeks of incubation. In case of no growth, blind subcultures were done on blood agar and MacConkey agar. Organisms were identified by Gram`s stain and standard biochemical tests.7 Antimicrobial sensitivity was done on MullerHinton agar or blood agar, depending on nature of isolate, by using Kirby- Bauer disc diffusion method.8 RESULTS One hundred thirty-eight blood samples were cultured over 2 yearâ&#x20AC;&#x2122;s period from 46 patients. Out of 46 patients, 24 showed bacterial growth, while 22 were sterile. Table 1 shows the organisms isolated. All the isolates were gram-positive. S. aureus was the most common isolate (14) followed by Streptococcus viridans (6) coagulase-negative staphylococcus (2) and enterococci (2) in the descending order of frequency. Table 2 shows the antibiotic sensitivity pattern of all the isolates. Cephalexin was the most effective agent active against 79.10% of the isolates followed by

Table 1. Organisms Isolated from Blood Culture Organisms

Number

Percentage (%)

S. aureus

58.33

S. viridans

Coagulase-negative staphylococci

8.3

Enterococci

8.3

ciprofloxacin (62.5%). Ampicillin and penicillin were moderately sensitive. Majority of the isolates were resistant to gentamicin, amikacin, cotrimoxazole, norfloxacin and erythromycin. DISCUSSION Infective endocarditis is a challenging disease to diagnose. The organisms isolated from infective endocarditis reflect to some degree the patient population particularly age, underlying disease, etc. It is a life-threatening infection which presents with highly variable and nonspecific manifestations. The Duke criteria for the diagnosis of infective endocarditis includes echocardiographic findings, which have proved to be substantially more sensitive than earlier criteria that did not includes echo data.9 Blood culture is the essential investigation for the management of infective endocarditis. In the present study, out of 46 patients, blood culture was positive in 24 (52.17%). Other studies have reported a much lower incidence of positive blood cultures. Lupis et al and Dhawan et al reported a 41% and 43% incidence of positive blood cultures, respectively10,11 Dudkiewicz et al found a 33% incidence of positive blood cultures in 120 patients with endocarditis.12 On the contrary, the culture positivity rate in our study is low when compared to published data. In the US culture positive endocarditis constitutes 70-97.5% of all clinically diagnosed cases while in the Netherlands this figure is even as high as 99%.13,14 Our study suggests that in patients suspected of having bacterial endocarditis (who have not received any antimicrobial agents prior to blood collection), three

Table 2. Antibiotic Sensitivity Pattern of Gram-positive Isolates Isolates antibiotics

S. aureus (n = 14)

Coagulase-negative staphylococci (n = 2)

S. viridans (n = 6)

Enterococci (n = 2)

Total (n = 24)

Ampicillin

8 (57.14)

1 (50)

4 (66.66)

1 (50)

14 (58.33)

Gentamicin

1 (7.14)

1 (50)

1 (16.66)

3 (12.5)

Cotrimoxazole

2 (14.28)

1 (16.66)

3 (12.5)

Ciprofloxacin

10 (71.42)

1 (50)

3 (50)

1 (50)

15 (62.5)

Cephalexin

11 (78.57)

2 (100)

5 (83.3)

1 (50)

19 (79.10)

Norfloxacin

1 (7.14)

1 (16.66)

2 (8.33)

Amikacin

1 (7.4)

1 (50)

1 (16.66)

1 (50)

4 (16.66)

7 (50)

2 (100)

4 (66.66)

1 (50)

14 (58.33)

5 (35.71)

1 (50)

4 (66.66)

10 (41.66)

Penicillin Erythromycin

(Figures in the bracket represent percentage).

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Infections blood cultures obtained within a 24 hours period should be adequate to establish the diagnosis in the great majority of patients. If a microorganism is not isolated from one of the first three blood cultures, it is unlikely that it will be isolated from additional cultures. The present study shows that all the isolates were gram-positive cocci. Most common isolate was S. aureus (58.33%). Bannur et al and Bayer et al15,16 reported similar findings in their studies, whereas Staphylococcus epidermidis was the most frequently isolated organism in other studies.11,17 The high incidence of S. aureus may be due to affinity for establishing infection in endothelium, increased use of intravascular devices and use of injecting drugs. When S. aureus is the causative organism, the disease is usually not subtle and is associated with complications. This stresses on immediate empiric antimicrobials to be started, since culture and sensitivity reports are not available before 48 hours. Antibiotic sensitivity pattern of the isolates were studied. Cephalexin was the most effective agent active against 79.10% of the isolates followed by ciprofloxacin (62.5%). Ampicillin and penicillin were moderately sensitive. This finding is to be emphasized because based on the above observations; therapy can be started immediately after collection of blood for culture. This may be particularly useful for seriously ill patients where antibiotic treatment can be started with any of the above agents. Treatment may be altered after getting the preliminary Gram-stain report or subsequent to the antimicrobial sensitivity report. Literature shows that the incidence of anaerobic microorganisms in bacterial endocarditis is less than 1%.18 and in our institute anaerobic set up is not available therefore we have not studied role of anaerobes in bacterial endocarditis. Thus, the initial therapy in our hospital may be aimed at grampositive organisms and cephalexin and ciprofloxacin can be used as first-line drugs. This shows the role of microbiology is important in diagnosis of causative agent responsible for infective endocarditis and their antibiotic susceptibility testing, which will be helpful in early and specific treatment. Acknowledgment The author thanks Dr BS Nagoba, Assistant Dean, MIMSR Medical College, Latur and Dr SB Tamboli, Associate Professor and Head, Dept. of Pharmacology, Dr SC Govt. Medical College, Nanded for their kind support.

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REFERENCES 1. Mims, Playfair, Roitt, Wakelin, Wiliams. Diagnosis of infection and assessment of host defense mechanisms. In: Medical Microbiology. 2nd edition, Mosby: London 2000:p.163-77. 2. Forbes BA, Sahm DF, Weissfeld. Bloodstream infection. In: Bail and Scott’s Diagnostic Microbiology. 11th edition, Mosby: USA 2002:p.865-83. 3. Weems JJ. The many faces of Staphylococcus aureus infection. In: Staphylococcal Infections Part 1, McGraw-Hill Publications: USA 2004:p.5-13. 4. Durack DT, Lukes AS, Bright DK. New criteria for diagnosis of infective endocarditis: utilization of specific echocardiographic findings. Duke Endocarditis Service. Am J Med 1994;96(3):200-9. 5. Sonnenwirth AC, Jarett L. Collection and culture of specimens and guides. In: Gradwohl’s Clinical Laboratory Methods and Diagnosis. Volume II. 11th edition, The CV. Mosby Company: London 1980:p. 1560-8. 6. Collee JG, Miles RS, Watt B. Tests for the identification of bacteria. In: Mackie & McCartney Practical Medical Microbiology. 14th edition, Collee JG, Marmion BP, Fraser AG, Simmons A (Eds.), Churchill Livingstone: Philadelphia 1996:p.131-49. 7. Cheesbrough M. Microbiological tests-culturing blood. In: District Laboratory Practice in Tropical Countries. Part 2. 1st edition, Cambridge University Press: Cambridge 2000:p.124-30. 8. Barry AL, Coyle MB, Thornsberry C, Gerlach EH, Hawkinson RW. Methods of measuring zones of inhibition with the Bauer-Kirby disk susceptibility test. J Clin Microbiol 1979;10(6):885-9. 9. Hoen B, Béguinot I, Rabaud C, Jaussaud R, Selton-Suty C, May T, et al. The Duke criteria for diagnosing infective endocarditis are specific: analysis of 100 patients with acute fever or fever of unknown origin. Clin Infect Dis 1996;23(2):298-302. 10. Lupis F, Giordano S, Pampinella D, Scarlata F, RomanoA. Infective endocarditis: review of 36 cases. Infez Med 2009;17(3):159-63. 11. Dhawan A, Grover A, Marwaha RK, Khattri HN, Anand IS, Kumar L, et al. Infective endocarditis in children: profile in a developing country. Ann Trop Paediatr 1993;13(2):189-94. 12. Dudkiewicz B, Mikucki J, Ostrowski S. Infective endocarditis - changes in the microbiological profile. Mater Med Pol 1996;28(2):49-56. 13. Mylonakis E, Calderwood SB. Infective endocarditis in adults. N Engl J Med 2001;345(18):1318-30. 14. Koegelenberg CF, Doubell AF, Orth H, Reuter H. Infective endocarditis in the Western Cape Province

Infections of South Africa: a three-year prospective study. QJM 2003;96(3):217-25.

with and without endocarditis. Arch Intern Med 1987;147(3):457-62.

15. Bannur M, Fule RP, Saoji AM, Jahagirdar VL. Study of bacteraemia using conventional and biphasic culture methods. Indian J Pathol Microbiol 1995;38(2):147-51.

17. Etienne J, Brun Y, el Solh N, Delorme V, Mouren C, Bes M, et al. Characterization of clinically significant isolates of Staphylococcus epidermidis from patients with endocarditis. J Clin Microbiol 1988;26(4):613-7.

16. Bayer AS, Lam K, Ginzton L, Norman DC, Chiu CY, Ward JI. Staphylococcus aureus bacteremia. Clinical, serologic, and echocardiographic findings in patients

18. Kerr A Jr. Subacute Bacterial Endocarditis. Springfield III; Charles Thomas, Publisher, 1955:p.72-3.

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The FDA has announced that the antibacterial doripenem will now carry a warning of mortality risk and poorer clinical cure rate when used to treat pneumonia that develops on mechanical ventilation. Doripenem is however not approved to treat any type of pneumonia.

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A 6–week treatment regimen appeared to be as effective as the more standard 12 weeks of therapy for patients with hepatitis C virus infection, researchers reported at the annual Conference on Retroviruses and Opportunistic Infections. In a pilot study that treated 20 patients in each of three arms, all patients treated with the combination of sofosbuvir (Sovaldi, nucleotide NS5B inhibitor) 400 mg with ledipasvir (NS5A inhibitor) 90 mg once daily for 12 weeks achieved a sustained virologic response at 12 weeks’ posttreatment (SVR12).

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The Hindu dated March 3, 2014 reports that since March 1, administration of oral polio vaccine (OPV) six weeks before departure has become mandatory for all India-bound travellers from seven countries where polio cases are still being reported: Afghanistan, Ethiopia, Syria, Kenya, Somalia, Nigeria and Pakistan. Indians headed for these countries will also be administered the vaccine. This new preventive measure has been initiated as per the recommendations of the national and international expert bodies and the guidelines of the World Health Organisation, according to Anuradha Gupta, Additional Secretary, Health Ministry.

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A histoplasmosis case cluster in Arkansas in October 2011 suggests that exposure to a bamboo bonfire may be a new risk factor clinicians should ask about when a patient presents with characteristic symptoms, according to a report published in the February 28 issue of the Morbidity and Mortality Weekly Report. The investigators point out that heating of spores may potentially increase transmission efficiency and could create a local outbreak among persons exposed to burning bamboo containing bird feces.

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Researchers report that in 2012, only 20.0% of adults were current on their recommended pneumococcal vaccinations, and only 64.2% were up-to-date with their tetanus shots. Coverage with the vaccine against hepatitis A was especially low, at only 12.2% of adults aged 19-49 years, and just a tad more than a third of adults aged 19-49 years (35.3%) were fully protected against hepatitis B. The findings are reported in the Feb 7 issue of Morbidity and Mortality Weekly Report.

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947

Internal medicine

Atypical Presentation of Multiorgan Failure Leptospirosis (Weil’s Disease) without Fever Swamikannu Murugan*, Muhammed Zohaib Ghatala†, Anand Sankar S†, Jothi Krishnan‡

Abstract Leptospirosis is a zoonotic disease of sporadic occurrence caused by bacteria that belongs to the genus Leptospira. Here we report a case of rare form of leptospirosis with multiorgan failure called Weil’s disease. This patient did not have a fever which is the most common presentation of leptospirosis.

Keywords: Leptospirosis, zoonotic disease, multiorgan failure, Weil’s disease

eptospirosis is a zoonotic disease caused by the bacteria that belongs to the genus Leptospira. Leptospira interrogans is pathogenic for humans. The genus can be separated into more than 200 serovars belonging to 23 serogroups. The median global incidence of endemic human leptospirosis, excluding cases due to outbreaks, was five cases/1,00,000 population, but in some areas the incidence was as high as 975 cases/ 1,00,000. The mean annual global incidence of epidemic leptospirosis, as reported in outbreak reports, was 14 cases/1,00,000 population. Some concern was expressed at the significant lack of data, especially from Africa and the Eastern Mediterranean region, and at the substantial heterogeneity in the data.

He was taken to a nearby hospital where his chest X-ray (Fig. 1) showed right upper zone patch. During his stay there, he was treated with bronchodilators and

Case Report A 68-year-old male was brought to our hospital with chief complaints of decreased level of consciousness, breathing difficulty and decreased urine output. The patient had a past medical history of asthma and hypertension. He was a nonsmoker and nonalcoholic. Two weeks prior to presentation at our hospital, he had an episode of vomiting while running his daily errands and subsequently developed breathing difficulty.

*Consultant Physician †Senior House Officer ‡Senior Registrar Dept. of Internal Medicine Sundaram Medical Foundation, Anna Nagar, Chennai Address for correspondence Dr Muhammed Zohaib Ghatala #67, AJ Block, 3rd Street, Anna Nagar, Chennai - 600 040, Tamil Nadu E-mail: zghatala@gmail.com

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Indian Journal of Clinical Practice, Vol. 24, No. 10, March 2014

Figure 1. Patient’s initial X-ray showing right upper lobe patch.

Figure 2. CT chest showing patchy-diffuse bilateral ground glass attenuation.

Internal medicine antibiotics (cefaperazone/sulbactum and azithromycin). He progressively became drowsy and his urine output decreased and further evaluation showed deranged liver and renal functions. He was then referred to our hospital for higher level of care. Vitals in the emergency room at our hospital were notable for a normal temperature, pulse rate of 93/min and a blood pressure of 150/100 mmHg. The patient was drowsy but obeying commands with a Glasgow comma scale (GCS) of 10/15 (E4 V2 M4). He did not have neck stiffness. He did not have a history of fever, headache, body pain, abdominal pain, hematuria or melena. Ocular examination was notable for scleral icterus. The chest on auscultation revealed crepitation, which were greater on the right side and the abdomen was soft and nontender. Initial laboratory study revealed a white blood count of 23,000/uL, which was polymorphonuclear predominant (poly 78.4%), hemoglobin of 11.3 g/dL, platelet of

17,000/uL, creatinine of 8.2 mg/dL, blood urea nitrogen (BUN) of 194 mg/dL, total bilirubin of 8.4 mg/dL, direct bilirubin of 5.7 mg/dL, aspartate aminotransferase (AST) of 60 U/L, alanine aminotransferase (ALT) of 84 U/L, alkaline phosphatase of 67 U/L, serum cortisol level was 39.88 Âľg/dL and lactate dehydrogenase (LDH) was 1,053 U/L. Computed tomography (CT) scan of his chest showed patchy-diffuse bilateral ground glass attenuation with minimal right side pleural effusion (Fig. 2). Ultrasound of his abdomen showed bulky and hypoechoic kidneys. The patient was admitted to intensive care unit (ICU) because of multiorgan dysfunction. The possibility of sepsis was considered for which the patient was started meropenem and fluid resuscitation. As the patient was afebrile, leptospirosis was an unlikely diagnosis but given his clinical presentation, doxycycline was also added to the treatment regimen. The following day, the patientâ&#x20AC;&#x2122;s urine output and level of consciousness decreased further and he was in uremic

Creatinine

Bilirubin Levels

8 6

Direct bilirubin

Total bilirubin

10 8.2

9.2

8 6.4

4 2

3.1

4.3 4.7 4.2 3.8 3.6 4.1

0 1

8.4 5.7

6 4.8

3.1 2.7 2.5 2.2

9 10 11 12 13 14 15

Day Figure 3a. The arrows indicate the point at which dialysis was done. X-axis indicates days from admission; Y-axis indicates serum creatinine.

Platelet count

150000 100000 50000

2 0

1.2 1.4

2.2 1

1.2

Figure 3b. X-axis indicates days from admission; Y-axis indicates serum bilirubin.

12 10 8

Day Figure 3c. X-axis indicates the days from admission; Y-axis indicates the platelet count.

11.3 9.4

7.1 6.9

8.5

7.5 7.2

2 0

2.6

1.6 2

Hemoglobin

181000 157000 129000 105000 74000 41000 25000 17000

3.6

2.8 2.2

2.7

Platelet 200000

Indirect bilirubin

Day

Figure 3d. Arrow indicates hemoglobin value after transfusion of 1 unit of PRBC.

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Internal medicine animals. Rats are the most common reservoir in India. Human infections can occur either by direct contact with infected urine of the infected animal.

Figure 4. Patient’s X-ray at discharge.

encephalopathy with a serum creatinine of 9.2 mg/dL and a BUN of 229 mg/dL. CT-brain showed diffuse agerelated cerebral and cerebellar atrophy and small vessel ischemic disease. The patient was started on dialysis considering his poor renal function. By then his leptospirosis serology test returned positive, dengue serology was negative, blood culture and urine culture were sterile. The patient was dialyzed thrice during this period and there was gradual improvement in his urine output along with improvement in his renal function, liver function and platelet counts (Figs. 3 a-d). Patient was also transfused 2 units of packed red blood cells (PRBC). Repeat chest X-ray was taken which showed good resolution. Patient was transferred to the wards on the 7th day with improving urine output, a progressively improving renal function and a GCS of 15/15. In wards, the same line of management was continued with no further need of dialysis. At discharge patient was symptomatically better with a hemoglobin of 8.0 g/dL, platelet count of 1,81,000/uL, serum creatinine of 2.2 mg/dL, AST of 41 U/L, ALT of 56 U/L, total bilirubin of 2.2 mg/dL, indirect bilirubin of 1.0 mg/dL, direct bilirubin of 1.2 mg/dL and normal chest X-ray (Fig. 4). One week after discharge from the hospital, the patient’s serum creatinine was 1.8 mg/dL and hemoglobin was 9.3 g/dL on follow-up visit. Discussion Leptospirosis is the most widespread zoonosis in the world. Tropical countries and low socioeconomic conditions with poor sanitation have particularly been identified as favorable for disease transmission. Human leptospiral infections result primarily from direct or indirect exposure to the urine of infected

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A retrospective study reported that in patients with leptospirosis, the common clinical features included fever (100%), headache (75%), myalgia (55%), arthralgia (45%) and vomiting (39%). Leptospirosis is usually biphasic. The first phase is the septicemic phase that usually lasts a week. The patient presents with fever, headache, conjunctival congestion, nausea, vomiting, joint pain and myopathy. This phase is followed by a brief afebrile period of variable duration that, in turn, is followed by the immune phase of illness. During this phase, the patient has multiorgan involvement. This severe form of leptospirosis is called Weil’s disease. The common organs involved during this phase are the liver, kidneys and lungs. Liver involvement leads to elevated liver enzymes and a high total bilirubin. Kidney involvement can give rise to azotemia, hematuria, uremia and pyuria. The patients with lung involvement can present with cough, hemoptysis, chest pain and shortness of breath, pulmonary hemorrhage or acute respiratory distress. Leptospirosis can present atypically with predominant pulmonary manifestation, which normally results in misdiagnosis and hence delayed appropriate treatment. Some of the common differential diagnosis of leptospirosis include dengue, malaria, encephalitis and scrub typhus. Diagnosis of leptospirosis is based on clinical suspicion and laboratory investigations. The commonly ordered laboratory investigation in a suspected case of leptospirosis at our hospital is detection of leptospirosis immunoglobulin M (IgM) antibody by enzyme-linked immunosorbent assay (ELISA) test. A confirmatory test is microscopic agglutination test (MAT), although this is not commonly done when there is high suspicion of leptospirosis based on clinical presentation and a positive leptospirosis IgM by ELISA. Leptospirosis can be treated with antibiotics like penicillin, doxycycline and ceftriaxone. A JarischHerxheimer reaction can occur during the treatment but it is usually mild. It is important to start the treatment early to shorten the hospital stay. A retrospective case-control study identified predictors of mortality as - age >40 years, development of oliguria, platelet count <70,000/μL, creatinine >3 mg/dL and pulmonary involvement. Mortality rate of Weil’s disease is 5-15%.

Internal medicine retrospective study of 201 patients in a metropolitan city of Brazil. Braz J Infect Dis 2010;14(1):3-10.

Conclusion Our patient did not present with fever and he did not have the classic symptoms of the septicemic phase of leptospirosis either, but because of pulmonary, hepatic and renal involvement, we had leptospirosis as one of our main differential diagnosis. We wish to emphasize that leptospirosis should be considered as a differential diagnosis in tropical countries when a patient presents with multiorgan failure or fever of >3 days duration without an obvious cause.

4. Hicham S, Ihsane M, Abderahim el B, Brahim B, Labib S, Mustapha H, et al. Multivisceral organ failure related to leptospirosis in pregnant patient. Indian J Crit Care Med 2013;17(1):43-5. 5. Bal AM. Unusual clinical manifestations of leptospirosis. J Postgrad Med 2005;51(3):179-83.

Suggested reading

6. Maroun E, Kushawaha A, El-Charabaty E, Mobarakai N, El-Sayegh S. Fulminant Leptospirosis (Weil’s disease) in an urban setting as an overlooked cause of multiorgan failure: a case report. J Med Case Rep 2011;5:7.

1. Davidson’s Principles and Practice of Medicine. 20th edition, Page no. 321.

7. Gulati S, Gulati A. Pulmonary manifestations of leptospirosis. Lung India 2012;29(4):347-53.

2. World Health Organization. Report of the Second Meeting of the Leptospirosis Burden Epidemiology Reference group. 2011:p12.

8. Marotto PC, Nascimento CM, Eluf-Neto J, Marotto MS, Andrade L, Sztajnbok J, et al. Acute lung injury in leptospirosis: clinical and laboratory features, outcome, and factors associated with mortality. Clin Infect Dis 1999;29(6):1561-3.

3. Daher EF, Lima RSA, Silva GB Jr, Silva EC, Karbage NNN, Kataoka RS, et al. Clinical presentation of leptospirosis: a

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According to Marlijne Ikink, MD, from the University Medical Center Utrecht in the Netherlands, magneticresonance-guided high-intensity focused ultrasound might still be the best option for many patients with symptomatic fibroids, mostly those with single dominant fibroids that are not too big and have very low signal intensity. The findings were presented at the European Congress of Radiology 2014.

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Using gene editing to mimic a mutation that prevents HIV from entering CD4 T cells appears to be safe in a small group of patients, according to a study published online March 5 in the New England Journal of Medicine. CCR5 (chemokine (C-C motif) receptor 5) is the major transmembrane protein that serves as coreceptor, with CD4, for HIV. Individuals who are homozygous for a 32-base deletion in the CCR5 gene are naturally resistant to infection by the virus. The “Berlin patient,” Timothy Brown, made the CCR5 effect famous when he was apparently cured of HIV infection after receiving bone marrow from a homozygous mutant donor to treat leukemia.

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According to a meta-analysis in Annals of Internal Medicine, metabolically healthy obese people are at a long-term greater risk for death and cardiovascular events compared with their normal-weight counterparts, suggesting there is no such thing as benign obesity. When studies with follow-ups of a decade or more were considered, obese people with no metabolic abnormalities had a 24% increased risk for these events vs metabolically healthy, normal-weight people.

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Internal Medicine

A Clinical Study of Febrile Thrombocytopenia: A Hospital-based Retrospective Study Praveen Kumar*, Kalpana Chandra†

Abstract Introduction: Febrile thrombocytopenia is a usually condition commonly caused by infections. The present study is intended to know the underlying etiology of febrile thrombocytopenia in our community, the various presentations and relationship between platelet count and severity of disease and prognosis. Material and methods: The study was conducted on 190 patients who presented with fever and thrombocytopenia and were admitted in Sri Ram Murti Smarak Institute of Medical Sciences (SRMS-IMS), Bhojipura, Bareilly, Uttar Pradesh from January 2011 to December 2011. Results and observations: Febrile thrombocytopenia affected all age group ranging from 18 to 88 years of age but was common in 18-40 years age group (52%) with male-to-female ratio 66.3:38.9%. It was common during the months of July to September. Fifty percent patients were having platelet > 50,001/mm3. Malaria was the commonest cause constituting 32.6%, which was closely followed by septicemia forming 31.2%. About 76.8% patients had good recovery. In 18 mortality cases, 83.33% were due to septicemia with multiorgan dysfunction and 16.67% were due to complicated malaria. Conclusion: Febrile thrombocytopenia is an important clinical condition commonly caused by malaria and septicemia.

Keywords: Febrile thrombocytopenia, malaria, septicemia, multiorgan dysfunction

hrombocytopenia may be defined as a subnormal number of platelets in the circulating blood. A normal human platelet count ranges from 1,50,000 to 4,50,000 platelets/µL of blood. Often patients with thrombocytopenia are asymptomatic and are diagnosed by routine complete blood count. Occasionally, there may be bruising, purpura, petechiae, nose bleeding and gum bleeding. Rarely, platelet count may be as low as 5,000/mm3 predisposing the patients to life-threatening bleeding in the central nervous system (CNS) or from the gastrointestinal and genitourinary tracts.1 Thrombocytopenia occurs due to decreased platelet production, which occurs in condtions such as vitamin B12 and folate deficiency, leukemia, sepsis (bacterial or viral infection) and hereditary disease. Thrombocytopenia may also occur due to increased

*Associate

Professor Dept. of General Medicine †Associate Professor Dept. of Pathology Sri Ram Murti Smarak Institute of Medical Sciences, Bhojipura Bareilly, Uttar Pradesh Address for correspondence Dr Praveen Kumar Associate Professor Dept. of General Medicine Sri Ram Murti Smarak Institute of Medical Sciences, Bhojipura Bareilly, Uttar Pradesh

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destruction such as idiopathic thrombocytopenic purpura (ITP), thrombotic thrombocytopenic purpura (TTP), hemolytic uremic syndrome (HUS), disseminated intravascular coagulation (DIC), paroxysmal nocturnal hemoglobinuria (PNH), systemic lupus erythematosus (SLE), antiphospholipid syndrome, post-transfusion purpura and hypersplenism. Drugs, which can cause thrombocytopenia are quinine, valproic acid, methotrexate, carboplatin, interferon, isotretinoin and heparin.1-6 Febrile thrombocytopenia is the thrombocytopenia associated with fever. Diseases which commonly present with fever and thrombocytopenia are malaria, leptospirosis, rickettsial infections, septicemia, typhoid, borreliosis, arbovirus such as dengue or yellow fever, rodent-borne viruses such as Hanta and Lassa fever, human immunodeficiency virus (HIV), visceral leishmaniasis and TTP-HUS.1,7 The study was intended to know the underlying etiology of febrile thrombocytopenia in our community, the various presentations and relationship between platelet level and severity of disease and prognosis. OBJECTIVE The aim of the study was to know the underlying etiology of febrile thrombocytopenia in our community, the various presentations and relationship between platelet level and severity of disease and prognosis.

Internal Medicine MATERIAL and METHODS

Table 1. Preliminary Data of the Study

The study was conducted on 190 patients admitted in Sri Ram Murti Smarak Institute of Medical Sciences (SRMS-IMS), Bhojipura, Bareilly, Uttar Pradesh from January 2011 to December 2011. The patients were selected as per protocol based on inclusion and exclusion criteria.

Total number of cases Male:Female Age range Age-wise prevalence 18- 40 41-65 >66 Month-wise prevalence January to March April to June July to Sep October to December Platelet count distribution < 20,000/mm3 20,001-50,000/mm3 >50,001/mm3 Outcome Discharged Expired LAMA Referral to higher center Etiological diagnosis Malaria Septicemia Dengue Viral infection Enteric fever Pulmonary tuberculosis Kala-azar Acute leukemia Clinical feature Fever Headache Body ache Joint pain Petechial rashes Abdominal pain Vomiting Loose motion GI bleed Cough and dyspnea CNS Hematuria Abnormal RFT Abnormal LFT Hypotension Tachycardia

Inclusion Criteria ÂÂ

All new patients above 18 years with fever (temperature >99.9°F).

ÂÂ

Thrombocytopenia (platelet count <1,00,000 cells/mm3).

Exclusion Criteria ÂÂ

Patient presenting with thrombocytopenia without fever.

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Diagnosed case of immune thrombocytopenic purpura.

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Patient with thrombocytopenia already diagnosed to have hematological disorder/malignancy or on treatment with chemotherapy and other immunosuppressive agent.

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Diagnosed cases dysfunction.

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Patients on treatment with antiplatelet drugs and other drugs causing thrombocytopenia.

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Patients with cirrhosis and chronic liver disease.

platelet

disorder

and

Outcome Variables ÂÂ

Primary outcome variable

ÂÂ

Platelet count

ÂÂ

Secondary outcome variable

ÂÂ

Mortality

This was a retrospective analysis of charts of patients admitted to a tertiary care hospital, between January 2011 to December 2011. Patients for this study were selected from hospital records based on inclusion and exclusion criteria. Data of the selected patients were collected from medical record from record room. Complete history and clinical findings and investigations as noted in the medical record were noted down. RESULTS AND OBSERVATIONS A total of 190 patients admitted over a period of 1 year in our hospital were studied. The study subjects were in the age group of 18-88 years. Out of 190 patients suffering from fever with thrombocytopenia, 126 were male and 74 were females.

190 126:74 18-88 115 (60.52%) 58 (30.52%) 17 (8.94%) 27 (14.21%) 23 (12.10%) 84 (44.21%) 56 (29.47%) 20 (10.52%) 75 (39.47%) 95 (50.00%) 146 (76.84%) 18 (9.47%) 10 (5.26%) 16 (8.42%) 62 (32.63%) 60 (31.57%) 30 (15.78%) 12 (6.31%) 7 (3.68%) 2 (1.05%) 1 (00.52%) 16 (8.42%) 190 (100%) 16 (8.42%) 8 (4.21%) 5 (2.63%) 7 (3.68%) 31 (16.31%) 36 (18.94%) 9 (4.73%) 10 (5.26%) 15 (7.89%) 13 (6.84%) 4 (2.10%) 62 (32.63%) 47 (24.73%) 24 (12.63%) 66 (34.73%)

LAMA = Left against medical advice; GI = Gastrointestinal; CNS = Central nervous system; RFT = Renal function test; LFT = Liver function test.

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Internal Medicine Table 2. Data of Expired Patients Total death

18 (9.47%)

Causes of death Septicemia

15 (83.33%)

Malaria

3 (16.66%)

Male:Female

Female (33.7%) Male (66.3%)

14:4

Clinical and Lab features Fever

18 (100%)

Abdominal pain

3 (16.60%)

Vomiting

4 (22.22%)

GI bleed

1 (5.55%)

Respiratory symptoms

3 (16.66%)

H/O DM

1 (5.55%)

H/O CRF

1 (5.55%)

Tachycardia

8 (44.44%)

Hypotension

7 (38.88%)

Anemia

3 (16.60%)

Leukopenia

1 (5.55%)

Leukocytosis

17 (94.44%)

2 (11.11%)

Platelet count

â&#x2030;¤20,000/mm3

Platelet count 20,001-50,000/mm3 Platelet count >

50,000/mm3

5 (27.11%) 11 (61.11%)

Abnormal RFT

14 (77.77%)

Abnormal LFT

7 (38.88%)

Pneumonia

1 (5.55%)

H/O DM = History of diabetes mellitus; H/O CRF = History of chronic renal failure; RFT = Renal function test; LFT = Liver function test.

Febrile thrombocytopenia was common in young to middle age group affecting 115 patients below 40 years. Fifty-eight patients were in the age group of 41-65 years and 17 patients were above 66 years of age. Febrile thrombocytopenia was common in between July to September affecting 84 patients. Fifty-six patients were affected between October to December, 27 from January to March and 23 from April to June. Out of 190 patients under study, 62 patients had definite diagnosis of malaria, which turned out to be the commonest cause of febrile thrombocytopenia in our institution in study year, which was closely followed by septicemia in 60 patients, dengue in 30, viral infection in 12, enteric fever in 7, pulmonary tuberculosis in 2 and one case of Kala-azar. The number of newly diagnosed cases of acute leukemia was significant, which constituted 16 patients. Commonest symptom after fever was vomiting (36) followed by abdominal pain (31), loose motion (9), gastrointestinal bleed (10) and respiratory symptoms like cough and dyspnea

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Figure 1. Sex-wise prevalence in %.

Indian Journal of Clinical Practice, Vol. 24, No. 10, March 2014

60.52

30.52

8.94 18-40

41-65

>66

Figure 2. Age-wise prevalence %.

50 45 40 35 30 25 20 15 10 5 0

44.21

29.47

14.21

12.10

Jan-Mar April-June

July-Sep

Oct-Dec

Figure 3. Month-wise prevalence in %.

60 50

50 39.47

40 30 20 10 0

10.52

<20,000

20,001-50,000

Figure 4. Platelet count in %.

>50,001

Internal Medicine 90 80 70 60 50 40 30 20 10 0

76.84

9.47 Discharge

Expired

5.26

8.42

LAMA

Referral to higher center

Figure 5. Outcome in %.

35 30

DISCUSSION

32.63 31.57

Febrile thrombocytopenia is a common clinical condition and is caused by infectious and noninfectious etiology.

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Out of 190 patients, 146 of them had good recovery, 18 patients expired, 10 left against medical advice and 16 cases of hematological malignancies were referred to higher centers (Table 1 and Figs. 1-6). Out of 18 cases of mortality, 15 were due to septicemia with multiorgan dysfunctions and three were due to complicated malaria. The expired patients were having hypotension in seven cases, abnormal renal function in 14 cases and abnormal liver function test in 7. Eleven patients were having platelet count >50,001/mm3, five had platelet count between 20,00150,000/mm3 and two had < 20,000/mm3 (Table 2 and Fig. 7).

Figure 6. Etiology in %.

Malaria (16.66%)

Septicemia (83.33%)

Figure 7. Etiology of death in %.

in 15. Abnormal renal function was in 62 patients and abnormal liver function test in 47. In our study, 20 patients had platelet count <20,000/µL, followed by 75 patients in the range of 20,001-50,000/µL and 95 patients had > 50,001/µL. Clinical manifestations of thrombocytopenia were noted in 21 patients. Out of 21, GI bleed was found in 10 patients, seven presented with petechial rash and four had hematuria.

A total of 190 patients admitted over a period of 1 year in our hospital were studied. The affected populations were in the age group of 18-88 years with prevalence common in males (66.31%) and in age group of <40 years (61.15%). The disease was most commonly prevalent in the month of July to September (44.21%). This high incidence in July to September was due to large number of cases of malaria and dengue in this region during that period. Malaria was the commonest cause accounting 32.63%, which was followed by septicemia (31.57%), dengue (15.78%), acute leukemia (8.42%), viral infection (6.31%), enteric fever (3.6%), pulmonary tuberculosis (1.055%) and Kala-azar (0.52%). In a study by Lohitashwa et al on 100 patients from March 2004 to September had similar observation (i.e., malaria being the commonest cause).8 Another prospective study, which was conducted on 228 patients with fever and thrombocytopenia in medical unit of Hayat Abad Medical Complex during 2008-2010 was showing malaria as a commonest cause (53%) out of which 68% were having falciparum malaria.9 Malaria is commonly accompanied by mild-tomoderate thrombocytopenia in 40.53-85% (78.4% by Jadhav et al, 80.6% by Medical Unit 3, JPMC, Karachi, 85.5% by Shaikh et al).10-12 In an observational study conducted by Malik et al at Karachi on endemicity of malaria and hematological finding in Gadap region on 392 patients observed malarial prevalence in 11.72%, out of which thrombocytopenia was observed in 70% cases.13 Thrombocytopenia in malaria is probably due to increased splenic sequestration, immune-mediated destruction, and a shortened platelet survival and

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Internal Medicine consumption by DIC. Along with quantitative defects, qualitative defects have also been documented, which are platelet hyperactivity, due to aggregating agent like immune complexes and damage of endothelial cells followed by platelet hypoactivity, which returns to normal in 1-2 weeks. Thrombocytopenia along with acute febrile syndrome is having 100% sensitivity, 70% specificity, 100% negative predictive value and 86% positive predictive value in malarial diagnosis.14 Another study had reported 60% sensitivity and 88% specificity of thrombocytopenia for malaria diagnosis in acute febrile patients.15 Thrombocytopenia is the very common finding in septicemia and is an independent prognostic marker. In a study conducted by Lee et al on 53 patients with septicemia thrombocytopenia was observed in 57% patients and DIC in 35% patients.16 The etiology of thrombocytopenia in sepsis is multifactorial. It is commonly associated with DIC and is caused by splenic destruction of immune complex coated platelets, platelet adherence to damaged vascular surfaces and by direct platelet toxicity caused by microorganisms.7 It is also probably related to impaired production of platelets from within the bone marrow, active phagocytosis of megakaryocytes and other hematopoietic cells by monocytes and macrophages hypothetically due to stimulation with high levels of macrophage colony-stimulating factor (M-CSF) in sepsis and platelet consumption due to ongoing generation of thrombin. Dengue is the most common arbovirus disease worldwide and occurs in tropical countries. Thrombocytopenia is an important finding and has got predictive as well recovery parameter of dengue fever/dengue hemorrhagic fever/dengue shock syndrome (DF/DHF/DSS). Thrombocytopenia in DF is caused by bone marrow suppression (i.e., decreased platelet synthesis and increased immune-mediated destruction of platelets).17 Commonest symptom after fever was vomiting in 18.94%, abdominal pain in 16.31%, loose motion in 4.73% cases, GI bleed in 5.26% cases and respiratory symptom like cough and dyspnea in 7.89%. Abnormal renal function was detected in 32.63% and abnormal liver function test in 24.73%. So, GI symptoms were the most common symptoms associated with febrile thrombocytopenia. In our study, platelet count was commonly > 50,001/ mm3 (50%) followed by 20,001/- 50,000/mm3 (39.47%) and <20,000/mm3 in 10.52% cases. So, we observed in the study, thrombocytopenia is commonly mild

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in febrile thrombocytopenia. Clinical manifestations of thrombocytopenia were noted in 11.05% patients (GI bleed - 5.26% patients, petechial rashes - 3.67% and hematuria - 2.10%). But, the study conducted by Lohitashwa et al observed bleeding manifestation in 49% cases and petechiae was the commonest bleeding manifestation.8 Out of 190 patients 76.84% of them had good recovery, 9.47% patients expired, 5.26% left against medical advice and 8.42% were referred to higher centers. Study conducted by Lohitashwa et al observed similar outcome of recovery in 82% cases and mortality in 18% cases.8 Out of 18 cases of mortality, 83.33% were due to septicemia with multiorgan dysfunction and 16.67% were due to complicated malaria. The expired patients were having hypotension (38.88%), abnormal renal function (77.77%) and abnormal liver function test (48.88%). About 61.11% patients were having platelet >50,000/mm3. This indicates deaths were not related to degree of thrombocytopenia but were related to underlying etiology and concomitant involvement of other organs leading to multiorgan dysfunction. Renal failure was the commonest organ dysfunction, which was related to compromised systemic perfusion and direct effect of underlying etiology. Study conducted by Lohitashwa et al observed that septicemia was the most cause of death (78%) followed by dengue.8 CONCLUSION Febrile thrombocytopenia is an important clinical condition commonly caused by infections, particularly malaria and septicemia. It commonly manifests as symptom/signs of underlying condition and sometime with bleeding manifestation. Treatment of underlying condition will lead to rapid improvement in platelet count with complete clinical recovery. Mortality in febrile thrombocytopenia is not directly associated with degree of thrombocytopenia but with concomitant involvement of other organs leading to multiorgan dysfunction.

Acknowledgment I take this opportunity to extend my gratitude and sincere thanks to all those who helped me to complete this study. I am highly thankful to Dept. of Medicine, Surgery, Pulmonology, gynecology, Pathology, Microbiology and Critical Care department for providing me adequate facility, which helped me to carry out this study. I owe great sense of indebtedness to dean SRMS-IMS, Bhojipura, Bareilly, Uttar Pradesh for permitting me to carry out this study.

Internal Medicine REFERENCES 1. Konkle BA. Disorders of platelets and vessel wall. In: Harrison’s Principles of Internal Medicine. Vol. 1, 17th edition, Fauci AS, Braunwald E, Kasper DL, et al. (Eds.), McGraw-Hill: New York, NY 2008:p.718-23. 2. Craig JIO, McClelland DBL, Watson HG. Thrombocytopenia. In: Davidson’s Principles and Practice of Medicine. 21st edition, College NR, Walker BR, Ralston SH (Eds.), Churchill Livingstone Elsevier: Edinburgh 2010:p.1003-4. 3. Bichile SK. Platelet disorder. In: API Textbook of Medicine. Vol. 1, 9th edition, Munjal YP (Ed.), Jaypee Brothers: New Delhi 2012:p.987-8. 4. Firkin F, Penington D, Chesterman C, Rush B. The hemorrhagic disorders. In: deGruchy’s Clinical Hematology in Medical Practice. 5th edition, Oxford University Press: Bombay 1989:p.375-92. 5. Lee GR, Foerster J, Lukens J, Paraskevas F, Greer JP, Rodgers GM. Shirley Parker Levine - Thrombocytopenia: Pathophysiology and Classification. In: Wintrobe’s Clinical Haematology. Vol. 2, 10th edition, Lipincott Wlliams & Wilkins: Philadelphia 1999:p.1579-82. 6. Diz-Kucukkaya R, Chen J, Geddis A, Lopez JA. Thrombocytopenia. In: William’s Hematolgy. 8th edition, Kaushansky K, Lichtman MA, Beutler E, Kipps TJ, Selisohn U, Prchal JT, (Eds.) New York 2011:p.1891-918. 7. Lee GR, Foerster J, Lukens J, Paraskevas F, Greer JP, Rodgers GM. Shirley Parker Levine - Miscellaneous causes of thrombocytopenia. In: Wintrobe’s Clinical Haematology. Vol. 2, 10th edition, Lipincott Williams: Philadelphia 1999:p.1623-9.

8. Lohitashwa SB, Vishwanath BM, Srinivas G. Clinical and Lab Profile of Fever with Thrombocytopenia. Abstract Free Paper Oral Presentation - APICON, 2008. Available at: http://www.japi.org/march_2009/oral_presentation 9. Khan SJ, Abbass Y, Marwat MA. Thrombocytopenia as an indicator of malaria in adult population. Malar Res Treat 2012;2012:405981. 10. Jadhav UM, Patkar VS, Kadam NN. Thrombocytopenia in malaria - correlation with type and severity of malaria. J Assoc Physicians India 2004;52:615-8. 11. Shaikh QH, Ahmad SM, Abbasi A, Malik SA, Sahito AA, Munir SM. Thrombocytopenia in malaria. J Coll Physicians Surg Pak 2009;19(11):708-10. 12. Shaikh MA, Ahmed S, Diju IU, Dur-E-Yakta. Platelet count in malaria patients. J Ayub Med Coll Abbottabad 2011;23(1):143-5. 13. Malik AM, Zaffar N, Ali N, Malik AM, Khan R. Haematological findings and endemicity of malaria in Gadap region. J Coll Physicians Surg Pak 2010;20(2):112-6. 14. Patel U, Gandhi G, Friedman S, Niranjan S. Thrombocytopenia in malaria. J Natl Med Assoc 2004;96(9):1212-4. 15. Lathia TB, Joshi R. Can hematological parameters discriminate malaria from nonmalarious acute febrile illness in the tropics? Indian J Med Sci 2004;58(6):239-44. 16. Lee KH, Hui KP, Tan WC. Thrombocytopenia in sepsis: a predictor of mortality in the intensive care unit. Singapore Med J 1993;34(3):245-6. 17. Jayashree K, Manasa GC, Pallavi P, Manjunath GV. Evaluation of platelets as predictive parameters in dengue Fever. Indian J Hematol Blood Transfus 2011;27(3):127-30.

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In its latest report, the US Preventive Services Task Force (USPSTF) has concluded that there is insufficient evidence to determine whether vitamins help prevent either cancer or cardiovascular disease. However, the USPSTF does recommend against supplementing with either beta-carotene or vitamin E (Grade D recommendation). The evidence shows that there is no benefit to taking vitamin E, and that beta-carotene can increase the risk for lung cancer in some populations. The report, published in the February 25 issue of the Annals of Internal Medicine, is an update of the 2003 recommendations.

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The US FDA has approved Amylin Pharmaceuticals’ Myalept (metreleptin for injection) as replacement therapy to treat the complications of leptin deficiency, in addition to diet, in patients with congenital generalized or acquired generalized lipodystrophy. This is the first approved therapy for treating the complications associated with congenital or acquired generalized lipodystrophy and follows an 11 to 1 vote in favor of the use of metreleptin in pediatric and adult patients with this condition by an FDA advisory committee in December 2013.

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Episodes of binge drinking are risky for anyone, but they are particularly so for aging adults who are moderate drinkers. In a study published online March 3 in Alcoholism: Clinical and Experimental Research, compared with moderate-drinking older adults who do not binge, those that do have a 2-fold increased risk of dying during a 20–year period. According to the authors, these findings demonstrate that among older adults, drinking patterns need to be addressed along with overall consumption in order to understand alcohol’s health effects. Even among those with apparently modest average consumption, a number of these folks may be drinking in risky ways.

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Neurology

An Experience of Chronic Inflammatory Demyelinating Polyradiculoneuropathy with Pregnancy Debasmita Mandal*, Chaitalli Dattaray†, Mousumi Datta‡, Alok Pandit#, Saroj Mandal||, Shyamal Das¶

Abstract Pregnancy with chronic inflammatory demyelinating polyradiculoneuropathy (CIDP) is a very rare association. Although pregnancy influences the clinical outcome of CIDP, whether the opposite also occurs is yet to be proved. We have described here successful outcome of a pregnancy experienced with CIDP and tried to emphasize on important management options during gestation.

Keywords: Pregnancy, chronic inflammatory demyelinating polyradiculoneuropathy, outcome

hronic inflammatory demyelinating polyradiculoneuropathy (CIDP) was first described by Dyck et al in 1975.1 It is a chronic polyradiculoneuropathy, autoimmune in nature of at least 2-month duration, which affects motor and sensory nerves by destroying the myeline sheath surrounding the nerves. CIDP is usually associated with albuminocytological dissociation and where adult males are affected commonly. This disease is mainly characterized by slowly progressive, symmetrical limb weakness, widespread areflexia and loss of large fiber sensibility, while sensory symptoms are paresthesia numbness; resultant respiratory weakness may require mechanical ventilation. Thorough Medline search revealed instances of women with CIDP experiencing pregnancy. Hence, we have discussed our experience of this disease during the course of a pregnancy, as awareness regarding the disease and its required management is necessary because of its debilitating consequences.

*Assistant

Professor Professor cum Clinical Tutor Dept. of Obstetrics and Gynecology #Assistant Professor Dept. of Neurology ||Dept. of Cardiology ¶Professor Dept. of Neurology IPGME & R, SSKM Hospital, Kolkata, West Bengal Address for correspondence Dr Debasmita Mandal C/11, SSKM Hospital Campus 242, AJC Bose Road, Kolkata - 700 020, West Bengal E-mail: drdebasmitamondal@yahoo.com; debasmita_mandal@rediffmail.com †Associate ‡RMO

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Case Report A 28-year-old G2P1L1 (post-cesarean) with 5 months gestation attended Obstetrics and Gynecology OPD with chief complaints of tingling sensation and tenderness over both plantar regions. These symptoms were progressive in nature, starting from left foot, involving the left leg and thereafter affecting the right leg within a span of 1 month. On examination, she was 156 cm tall, 43 kg in weight with an average nutritional status. The woman was normotensive with normal respiratory and cardiovascular parameters. Uterine height corresponded to 22 weeks gestation. Ultrasonography conducted at 10 and 24 weeks gestation confirmed the gestational age and excluded any gross congenital anomaly. Her Hb% was 11.3 gm% with 34% packed cell volume. Liver function tests, renal function tests and coagulation profile were within normal range. Central nervous system examination showed a normal level of higher function, speech, spine, cranium and cranial nerves with no evidence of motor atrophy and fasciculation. On the other hand, motor system examination showed both distal and proximal weakness around Grade IV/V without any atrophy, but deep tendon reflexes (DTR) were absent. Motor nerve study diagnosed a grossly reduced compound motor action potential (CMAP) amplitude in bilateral median, ulnar, tibial and peroneal nerves, with grossly reduced conduction velocity (CV) and delayed distal latencies. These led to a suspicion of acquired demyelinating (with secondary axonal) type of sensorimotor polyradiculoneuropathy involving all four limbs. Nerve conduction velocity (NCV)

Neurology and cerebrospinal fluid (CSF) study confirmed the diagnosis of CIDP. Sural nerve biopsy suggested the etiopathogenesis to be of vasculitis origin. Simultaneously antinuclear factor was in higher titer (> 1:320) and autoantibodies i.e., SS-A, Ro-52 were strongly positive and proliferating cell nuclear antigen (PCNA) was of borderline significance. These investigations excluded the secondary cause of CIDP as systemic lupus erythematosus (SLE). Considering the risk of sudden respiratory failure in such patients, she was shifted to a respiratory care unit. Regular monitoring and supplementation of antenatal iron, protein and calcium were continued. Physiotherapy and low-dose prednisolone (40 mg) constituted the neurological management. Fetal growth restriction became evident from 32 weeks onwards along with oligohydramnios, which failed to improve. Intravenous (IV) immunoglobulin was unaffordable by the patient. At the onset of 32 weeks gestation she had intrauterine growth restriction (IUGR) and oligohydramnios. Consequently pregnancy was electively terminated at 33 weeks 4 days gestation by lower-segment cesarean section under general anesthesia. A female baby weighing 2.14 kg was delivered with Apgar score of 9/10 and 10/10 in 1 and 5 minutes. Postpartum routine investigations were within normal limit except a raised serum glutamic oxaloacetic transaminase (SGOT) (450 IU) and serum glutamic pyruvic transaminase SGPT (290 IU), probably as a result of amytriptyline therapy. Typically, her existing neurological symptoms aggravated from third postpartum day and examination revealed motor quadriparesis (UL-3/5, LL-2/5) with grossly reduced DTR in all four limbs. Prednisolone dose was increased to 60 mg. Patient was taken over by neurology team after removal of stitches. Systemic examinations and investigations of baby revealed no abnormality. Neurological status appeared to have improved during her follow-up visits at sixth and 12 weeks. Discussion Recent data shows CIDP to be relatively uncommon with an estimated prevalence in populations from UK, Australia, Italy, Norway and Japan of 0.8-7.7 per 1,00,000.2 We found limited literature showing coincidental pregnancy with CIDP. The disease mostly starts insidiously and evolves slowly either in a progressive (>60%) or relapsing manner (one-third of all CIDP patients) with partial or complete recovery between recurrences.2 Physical examination usually

reveals proximal symmetric muscle weakness with or without distal sensory loss and deep tendon reflexes are generally reduced or absent without any central nervous system (CNS) manifestations. The present case typically presented with similar findings. She had worsened LL weakness from late second trimester onwards to few weeks of puerperal period. Many authors have suggested that in CIDP, there is an increased frequency of relapse during the last trimester and puerperium compared to nonpregnant state.3 McCombe et al studied nine women with CIDP who had 30 pregnancies and observed five of the eight relapses (62.5%) were during third trimester of pregnancy or 3 months postpartum.4 Oral contraceptives can also worsen the symptoms of CIDP.3 From these data it can be concluded that probably, conditions, which cause hormonal alteration, whether pregnancy itself or drugs like oral contraceptives can precipitate the aggravation of symptoms of CIDP. So, a nonhormonal contraception is desirable if required. Although etiopathogenesis of relapses of CIDP in pregnancy is uncertain immunological studies of pregnancy have implicated the mechanism of protection of fetus from maternal rejection.5 McCombe et al enumerated probable existence of crossreactivity between fetal and maternal neural antigens or an immune response in pregnancy that provokes an anamnestic response to neural antigen.4 Treatment of CIDP includes IV immunoglobulin, plasmapheresis and steroids.3 As safety and efficacy of plasmapheresis is still not well-proven during pregnancy and lactation, in the present case titrated low-dose of oral steroid was preferred as the main stay of treatment. Long-term immunosuppressive therapy is common in CIDP, so patients in reproductive age group must be counseled regarding teratogenecity. No literature has stressed on the effect of CIDP on pregnancy outcome. The present case had IUGR and oligohydramnious, which might be coincidental. Thus, while dealing with CIDP in pregnancy vigilant antenatal care is also necessary to avoid associated fetal morbidity. In this case, during the LSCS, general anesthesia was administered in order to avoid any respiratory catastrophe. Regional anesthesia administration to patients with neurological dysfunction can be of concern because of their impaired respiratory function. High sensory levels required for adequate anesthesia during cesarean delivery might paralyze the intercostals muscles and

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Neurology trigger respiratory distress in patients dependent on intercostals function for adequate respiration.6

April, 2010). Available at URL:http://eMedicine.medscape. com/article/1172965-overview.

An adequate counseling of the patient and her family is important so that the progressive nature and probable chance of respiratory failure are well-understood. In a country like ours, where regular antenatal supervision is commonly regarded as superfluous this ensures a timely follow-up and may prevent the patient from presenting at a stage when the process has already exacerbated.

3. Shamer DM, Bradley WG, Daroff RB, Fenichel GM, Jankovic J. Neurological Problems of Pregnancy. Neurology in Clinical Practice. 4th edition, Elsevier Inc.: Philadelphia. 2004:p.2535.

References 1. Dyck PJ, Lais AC, Ohta M, Bastron JA, Okazaki H, Groover RV. Chronic inflammatory polyradiculoneuropathy. Mayo Clin Proc 1975;50(11):621-37. 2. Lewis RA. Chronic inflammatory demyelinating polyradiculoneuropathy. eMedicine article (Cited on 26th

4. McCombe PA, McManis PG, Firth JA, Pollard JD, McLeod JG. Chronic inflammatory demyelinating polyradiculoneuropathy associated with pregnancy. Ann Neurol 1987;21(1):102-4. 5. Jacoby DR, Olding LB, Oldstone MB. Immunologic regulation of fetal-maternal balance. Adv Immunol 1984; 35:157-208. 6. Harrop-Griffiths AW, Ravalia A, Browne DA, Robinson PN. Regional anaesthesia and cough effectiveness. A study on patients undergoing cesarean section. Anaesthesia 1991;46(1):11-3.

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Cognitive Therapy as a Stand-alone Therapy for Schizophrenia A research reported at the International Stroke Conference observed that exposure to five common viruses viz. Helicobacter pylori, cytomegalovirus, Chlamydia pneumoniae and herpes simplex 1 and 2 was associated with poorer executive function and language skills among adults 55 and older (p = 0.002 and p = 0.04, respectively). Cognitive therapy may be a viable alternative to antipsychotic drugs in patients with schizophrenia who cannot or will not take an antipsychotic, new research suggests. In the first randomized trial of cognitive therapy as a stand-alone therapy for schizophrenia, researchers found that it significantly reduced the severity of psychiatric symptoms and improved personal and social functioning and some dimensions of delusional beliefs and voice hearing. The study was published online February 6 in the Lancet.

Smell Check, Scratch and Sniff, a New Test for Parkinson’s Disease Olfactory dysfunction presenting as odor detection, discrimination and identification is a common finding in patients with early nonvascular Parkinson’s disease. As per a study of 2,267 men published in the Annals of Neurology, an impaired sense of smell could be an early indicator of Parkinson’s disease, occurring up to four years before motor skill problems appear. In the study, decreased odor identification was associated with older age, smoking, more coffee consumption, less frequent bowel movements, lower cognitive function and excessive daytime sleepiness, but even after adjusting for these factors, those with the lowest odor identification scores had a five time greater risk of developing Parkinson’s disease than those with the highest scores. Nerve loss and the formation of Lewy bodies - abnormal clumps of proteins inside nerve cells that are thought to be a marker of the disease - are known to take place in the olfactory structures of patients with the disease. An impaired sense of smell could also be caused by impaired sniffing, which may be another motor symptom of Parkinson’s. Early indicators of Parkinson’s disease are olfactory abnormality, constipation and sleep disturbances. Besides Parkinson’s disease, obesity, diabetes, hypertension, malnutrition, Alzheimer’s disease, multiple sclerosis and Korsakoff’s psychosis are all accompanied or signaled by smell disorders.

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Neurosurgery

Pneumocephalus after Ventriculoperitoneal Shunt: Diagnostic Dilemma and its Endoscopic Management Hanish Bansal*, Rakesh Kaushal†, Manish Munjal‡

Abstract Pneumocephalus, a common entity in neurosurgical practice is a very rare phenomenon after ventriculoperitoneal shunt insertion and generally is result of long-standing hydrocephalus causing bony erosion. Defect may remain completely plugged by gliotic brain tissue and meningeal scarring but lowering of intracranial pressure following shunt placement causes opening up of fistula and pneumocephalus. We report a case of a 55-year-old male with pineal region tumor with hydrocephalus who presented to us with severe headache after ventriculoperitoneal shunt insertion for hydrocephalus. Computed tomography (CT) head revealed tension pneumocephalus and pneumoventricle. Thin cut coronal CT images localized the air leak to left basifrontal region and patient underwent successful endoscopic transnasal skull base repair using fat and fascia lata graft. Pneumocephalus, a well-known condition in neurosurgery practice is extremely rare after shunt operations. Air can gain access to the intracranial cavity only when there is a break in basal structures in connection with the paranasal sinus, and when the nasal air pressure exceeds the intracranial pressure. Most cases resolve spontaneously but recurrent cases require definite repair. Thin axial CT cuts are used to localize the defect in the skull base. We add a new dimension to the treatment of this rare complication via endoscopic transnasal skull base repair technique.

Keywords: Pneumocephalus, ventriculoperitoneal shunt, hydrocephalus

neumocephalus, a common entity in neurosurgical practice is a very rare phenomenon after ventriculoperitoneal shunt insertion and less than 50 cases have been described in the literature. Pneumocephalus after ventriculoperitoneal shunt generally is result of long-standing hydrocephalus causing bony erosion. Defect may remain completely plugged by gliotic brain tissue and meningeal scarring but lowering of intracranial pressure following shunt placement causes opening up of fistula and pneumocephalus. Management involves prompt diagnosis and closure of the defect if conservative treatment fails. We report this case so as to add to the existing scanty literature and also add a new dimension

*Resident †Professor and Head Dept. of Neurosurgery ‡Professor Dept. of ENT Dayanand Medical College and Hospital, Ludhiana, Punjab Address for correspondence Dr Hanish Bansal Dept. of Neurosurgery 10-B, Udham Singh Nagar, Civil Lines Ludhiana -141 001 Punjab E-mail: y2khanish@rediffmail.com

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to the treatment of this rare complication via endoscopic transnasal skull base repair technique. CASE REPORT We report a case of a 55-year-old male who presented to us with gait ataxia and who after complete diagnostic work-up was later diagnosed as a case of pineal region tumor ?? pineocytoma with obstructive hydrocephalus. Patient underwent ventriculoperitoneal shunt and was discharged in satisfactory condition. The patient was later readmitted 2 days after discharge with complaint of severe headache. Computed tomography (CT) head revealed extensive pneumocephalus with pneumoventricle (Fig. 1). Patient was initially managed conservatively with supplementary O2 and was kept on strict bed rest in supine position. CT head done after 1 week revealed resolution of air. Patient symptoms reappeared once patient was ambulated. Repeat CT head revealed increase in pneumocephalus. The shunt tube was ligated and the repeat CT head revealed hydrocephalus with resolution of pneumocephalus with focal air collection in left basifrontal region. Thin axial cuts of CT head localized left basifrontal region as suspected site of air leak

Neurosurgery

Figure 1. CT head showing extensive pneumocephalus and pneumoventricle.

Figure 2. CT head showing hydrocephalus with focal air collection in left basifrontal region.

(Fig. 2). The patient was then taken up for endoscopic transnasal skull base exploration, which revealed yellowish smooth tissue prolapsing from the roof of posterior ethmoidal sinus. The mass was fulgrated and an endoscopic transnasal skull base repair was done

using fat and fascia lata graft. Postoperative course was uneventful and the shunt was restored few days later. Repeat CT head showed complete resolution of pneumocephalus and patient was discharged in satisfactory condition.

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Neurosurgery In our case, the mechanism of development of pneumocephalus was mainly based on two factors: A reduction in the intracranial pressure and the presence of a defect in the dura and skull that was caused by long-standing elevation in intracranial pressure, due to hydrocephalus secondary to pineal region tumor. Probably because of the ball-valve action of a dural leaflet, there was no cerebrospinal fluid (CSF) leakage. His neurosurgical history could indicate neoplastic fistula, but the primary site of the tumor was far from the identified pneumocephalus. DISCUSSION Pneumocephalus, also known as intracerebral aerocele or pneumatocele is defined as the presence of gas within any of the intracranial compartments (intraventricular, intraparenchymal, subarachnoid, subdural and epidural) of the cranial vault.1 Pneumocephalus is a well-known condition in neurosurgery practice and the common causes of pneumocephalus are trauma, surgery, tumors and infections.2 Pneumocephalus is a common finding after intracranial surgery and generally resolves spontaneously. It is extremely rare after shunt operations and less than 50 cases have been described in the literature. CSF shunting has been associated with a significant number of complications. Infections, shunt malfunction, slit ventricle, subdural hematomas are among the most common. Although, pneumoventricle is common immediately after the shunting procedure, tension pneumocephalus or pneumoventricle following CSF diversion is an extremely rare complication.3 Air can gain access to the intracranial cavity only when there is a break in basal structures in connection with the paranasal sinus, and when the nasal air pressure exceeds the intracranial pressure.4 The bone defect may be congenital but more often occurs as a result of bony erosion by long-standing raised intracranial pressure by hydrocephalus. The common sites of congenital skull base defects are anterior fossa, followed by the middle fossa and tegmen tympani in temporal bone.5 Osteomas, epidermoid and pituitary tumors are examples of neoplasms that can cause erosion through the skull base or skull. Infection with gas-producing organisms or a ventriculoperitoneal shunt catheter perforating the colon remain unlikely possibilities of post-shunt pneumocephalus.6 The possible mechanism of pneumocephalus development is based mainly on two factors: 1) The presence of a defect in the dura and skull causing air

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inflow with a 'one-way ball valve mechanism'; and 2) a decrease in intracranial pressure causing a pressure imbalance. The pressure gradient between the outside and inside of the skull, which increases in the sitting or standing position, causes inflow of air into the subdural and subarachnoid spaces, although no defect could be found radiologically. Probably because of the ballvalve action of a dural leaflet, there may be no CSF leakage. Gliotic brain tissue and cicatrized meninx may possibly invaginate into this defect and the defect may then not allow entry of air to the intracranial cavity during the long-lasting intracranial hypertension. Significant lowering of intracranial pressure, following shunt placement, causes unplugging of the defect that results in the opening up of the fistula.7 Clinical presentation includes headaches, nausea and vomiting, seizures, dizziness and depressed neurological status. Management of pneumocephalus is based on the treatment of elevated intracranial pressure, treatment of meningitis, shunt management and finally closure of the main source of air inflow. The etiology of pneumocephalus has to be verified clearly in most cases with careful clinical evaluation and the air entrance site may be searched by thin slice CT, which is sensitive for detecting intracerebral/ intracranial air as small as 0.5 cc. Furthermore, 3D CT may show the defect of basis cranii as a possible site of air entry. Smaller and multiple fistulous tracts at the skull base are difficult to diagnose and are frequently associated with recurrent pneumocephalus or meningitis. When a porencephalic cyst is present, the identification of fistulous defect is relatively easier because of its close proximity with the cyst.8 Most cases of small pneumocephalus do not require any surgical management. Intracranial air also often resolves spontaneously. Supplemental oxygen increases the rate of absorption of pneumocephalus. The treatment must be focused on direct surgical closure of the main site of air entry. If the site of fistula cannot be established, dural repair in the most likely site of the fistula is recommended. Temporary closure of the shunt may stop the vicious circle established between displaced volume of CSF, intracranial negative pressure and pneumocephalus.9 CONCLUSION We report a very rare case of pneumocephalus secondary to ventriculoperitoneal shunt insertion and its endoscopic transnasal skull base repair. Due to rarity of the condition there is scanty data related to its

Neurosurgery diagnosis and management. We also bring about a new dimension to the treatment of this rare complication via endoscopic transnasal skull base repair technique. REFERENCES 1. Schirmer CM, Heilman CB, Bhardwaj A. Pneumocephalus: case illustrations and review. Neurocrit Care 2010;13(1):152-8. 2. Sunada S, Yamaura A, Hosaka Y, Uozumi A, Makino H. Tension pneumocephalus as a complication of a ventriculoperitoneal shunt. Case report. Neurol Med Chir (Tokyo) 1984;24(1):42-5. 3. Tuğcu B, Tanriverdi O, Günaldi O, Baydin S, Postalci LS, Akdemir H. Delayed intraventricular tension pneumocephalus due to scalp-ventricle fistula: a very rare complication of shunt surgery. Turk Neurosurg 2009;19(3):276-80. 4. Ikeda K, Nakano M, Tani E. Tension pneumocephalus complicating ventriculoperitoneal shunt for cerebrospinal

fluid rhinorrhoea: case report. J Neurol Neurosurg Psychiatry 1978;41(4):319-22. 5. Kim YH, Lee WI, Park MN, Choi HS, Kim NH, Han SJ. Otogenic pneumocephalus associated with a ventriculoperitoneal shunt. Clin Exp Otorhinolaryngol 2009;2(4):203-6. 6. Shetty PG, Fatterpekar GM, Sahani DV, Shroff MM. Pneumocephalus secondary to colonic perforation by ventriculoperitoneal shunt catheter. Br J Radiol 1999;72(859):704-5. 7. Lee WY, Kim SH, Kim OL, Choi BY. Delayed tension pneumocephalus caused by ventriculoperitoneal shunt. J Korean Neurosurg Soc 2007;41:47-9. 8. Sankhla S, Khan GM, Khan MA. Delayed tension pneumocephalus: a rare complication of shunt surgery. Neurol India 2004;52(3):401-2. 9. Pieri F, Anania CD, Perrini P, Puglioli M, Parenti GF. Delayed otogenic pneumocephalus complicating ventriculoperitoneal shunt. Neurol India 2011;59(4):616-9.

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Low temperatures, large changes in temperature within a day, and a higher average dew point are all associated with increased stroke hospitalizations, according to a new study presented at the American Stroke Association International Stroke Conference (ISC) 2014.

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The National Institute of Mental Health and Neurosciences (NIMHANS) will conduct a national mental health survey this year and a pilot study will begin this month, Union minister of health and family welfare Ghulam Nabi Azad said, reported the Express News Service on February 6, 2014. The survey will be conducted across states and union territories. NIMHANS director Satish Chandra said the pilot phase of the National Mental Health Survey would begin this month, while the survey will be completed by the end of the financial year.

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Guidelines have been drawn up for the first time to operate on patients with major depression and obsessive compulsive disorders (OCD). The World Society for Stereotactic & Functional Neurosurgery last month published guidelines to ensure that surgery is not misused against patients with psychiatric illnesses as reported in TOI Feb 15, 2014, 03.24 am IST. The guidelines were published in the Journal of Neurology, Neurosurgery & Psychiatry.

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Obstetrics and Gynecology

Vaginal Leiomyoma: Unusual Case Presentation Kavyashree G*, Manohar R†, Kala B‡

Abstract Vaginal leiomyomas are rare to exist as a primary tumor of vagina. Approximately 300 cases have been reported in world literature. They usually arise from anterior vaginal wall and are firm to hard in consistency with varied clinical presentations. Here, we report a case of vaginal leiomyoma presenting as mass per vagina, diagnosed postoperatively with the help of histopathological and immunohistochemical studies.

Keywords: Vaginal leiomyomas, anterior vaginal wall, mass per vagina

aginal leiomyomas are rare benign solid tumors of the vagina. They are usually located in the anterior wall and rarely in the lateral wall and vulvar region. Its etiology is unknown, though some authors have speculated that it could be due to residual embryonic blood vessel tissues and smooth muscle fibers.1

Figure 1. Mass situated in the anterior vaginal wall.

CASE REPORT Smt. XX, 45-year-old lady was referred from surgery OPD as a case of prolapse uterus. She gave history of mass per vagina since 2 years, which was not associated with white discharge per vagina, menstrual disturbances and urinary symptoms. Her medical and surgical history were unremarkable. On examination, a mass about 5 × 4 cm, cystic-firm in consistency was situated in the anterior vaginal wall, about 1 cm below the external urethral meatus and up to the cervicovaginal junction and was nontender on palpation (Fig. 1). Under spinal anesthesia, patient was put in lithotomy position, bladder was catheterized. A semi-circular incision was made at the anterior vaginal wall and mass was enucleated and removed easily. Anterior vaginal wall closure was done using 2-0 vicryl and hemostasis

*Associate

Professor †Assistant Professor Dept. of Obstetrics and Gynecology ‡Assistant Professor Dept. of Pathology Mandya Institute of Medical Sciences, Mandya, Karnataka Address for correspondence Dr Manohar R Assistant Professor, Dept. of Obstetrics and Gynecology Mandya Institute of Medical Sciences, Mandya, Karnataka E-mail: manoharrangaswamy@gmail.com

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Figure 2. Oval grey-white firm soft tissue mass, measuring 5 × 3 cm.

secured. Specimen was sent for histopathological examination. Gross morphology: Oval grey-white firm soft tissue mass, measuring 5 × 3 cm (Fig. 2). Cut section showed well-circumscribed homogenous grey-white having whorling (Fig. 3). Microscopy: Spindle cells showing nuclear palisading mimicking neurofibroma (Fig. 4). Initial histopathological report was in favor of neurofibroma of the anterior vaginal wall, which is a rare entity (H&E, 40X). Further, immunohistochemistry studies and result of smooth muscle markers were in favor of leiomyoma of the anterior vaginal wall.

Obstetrics and Gynecology

Figure 3. Cut section showing well-circumscribed mass having whorling.

Figure 4. Spindle cells showing nuclear palisading mimicking neurofibroma.

Figure 5. Spindle cells in fascicles with elongated nuclei and eosinophilic cytoplasm (H&E, 40X).

Figure 6. Strong cytoplasmic membrane positivity for SMA (40X).

DISCUSSION

vaginal wall. Thus histopathological and immunohistochemical studies play a major role in diagnosing the leiomyomas.

Vaginal leiomyomas are very rare with approximately 300 cases reported in the world literature. In the vagina, they commonly present along the anterior wall and next along the lateral wall. They may arise from the posterior wall and may present even after hysterectomy and also in the form of ischiorectal abscess. Very often diagnosis it is difficult to diagnose them preoperatively.2 Vaginal leiomyomas vary from 0.5 to 15 cm in diameter. They may occur anywhere within the vagina and usually arise in the smooth muscle layer of the midline anterior vaginal wall. Vaginal leiomyomas can be asymptomatic or present with symptoms, such as dyspareunia, pain or dysuria. Usually, the tumor is single and most are small and slow growing. Vaginal leiomyomas are estrogendependent tumors. These tumors can grow rapidly during pregnancy and regress after menopause.3 The tumors are usually moderately firm, but since they may undergo degenerative changes as that occur in the uterus, they may vary in consistency from firm to soft.4 Surgery through the vaginal approach has generally been recommended as the treatment of choice for these tumors.5 In this case, the diagnosis of anterior vaginal wall cyst was made preoperatively as the mass was cystic-firm in consistency and situated in the anterior

CONCLUSION Vaginal leiomyomas can rarely present as mass per vagina and it should be kept in mind as a differential diagnosis. The preoperative diagnosis of vaginal leiomyomas is difficult and can be diagnosed postoperatively with the help of histopathological examination and immunohistochemical studies. REFERENCES 1. Dane C, Rustemoglu Y, Kiray M, Ozkuvanci U, Tatar Z, Dane B. Vaginal leiomyoma in pregnancy presenting as a prolapsed vaginal mass. Hong Kong Med J 2012;18(6):533-5. 2. Shrivastava D, Bhute S, Kakani A, Patil V, Jajoo S, Joshi S. A rare case of vaginal leiomyoma diagnosed postoperatively. J South Asian Fed Obstet Gynaecol 2011;3(3):143-4. 3. Bae JH, Choi SK, Kim JW. Vaginal leiomyoma: a case report and review of the literature. J Womenâ&#x20AC;&#x2122;s Med 2008;1(2): 92-4. 4. OruĂ§ S, Karaer O, Kurtul O. Coexistence of a prolapsed, pedunculated cervical myoma and pregnancy complications: a case report. J Reprod Med 2004;49(7):575-7. 5. Hameed N. Leiomyoma of the vagina. J Ayub Med Coll Abbottabad 2003;15(2):63-4.

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Obstetrics and Gynecology

Imaging Diagnostic Dilemma of Large Subchorionic Hematoma PS Baldawa

Abstract Vaginal bleeding in first-half of pregnancy occurs in one-fourth of all pregnant women. This case report mainly highlights the occurrence of large subchorionic hematoma (SH) (area >13.7 cm2/, stripping of >50% of chorionic circumference) in first trimester. Usually, large SHs occur in second trimester, are associated with pregnancy loss but are relatively uncommon in first trimester. This case describes a 32-year-old G2P1L1â&#x20AC;&#x2122; who presented with complaints of vaginal spotting, was misdiagnosed to have threatened abortion with twin gestation. Later, the diagnosis was confirmed to be a large SH. Patients with large SH are at greater risk for eventual fetal death, hence the need for serial scanning to determine final outcome of their gestation.

Keywords: Hypoechoic mass lesion, subchorionic hematoma, twin gestational sac

ubchorionic hematoma (SH) may be detected sonographically in the first trimester by the presence of a crescent-shaped echo-free area outlining the intact gestational sac.1 But at times, this sonographic appearance may not be echo-free, which is why it needs to be differentiated from other differential diagnoses. This case report identifies such a diagnostic dilemma. CASE report A 32-year-old lady presented to Gynecology OPD with complaints of spotting per vaginum. Her obstetric history was P1L1. She had a full-term normal vaginal delivery 1 year ago. She was still lactating and had amenorrhea since last year. On clinical examination, she was afebrile; the vital parameters were stable with pulse rate of 88/minute and blood pressure of 120/80 mmHg. On examination, abdomen was nontender, nondistended, with normal bowel sounds. The uterus was not palpable. There was no rebound tenderness or guarding or rigidity. On pelvic exam, the cervical os was closed and scant altered dark blood was noted in the vaginal vault. No active bleeding was Assistant Professor Dept. of Obstetrics and Gynecology Shree Uthrodham Thirunal Medical College Vattappara, Trivandrum, Kerala Address for correspondence Dr PS Baldawa Baldawa Hospital, Budhwar Peth, Near Kasturba Market Solapur - 413 002, Maharashtra E-mail: guptapj@yahoo.com

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present. The patient had a positive Chadwickâ&#x20AC;&#x2122;s sign. Bimanual exam revealed neither masses nor cervical motion tenderness. The remainder of the physical exam was unremarkable. Her laboratory tests revealed hemoglobin of 10.2 g/dL, total white blood cell (WBC) count of 5,600/mm3; urine pregnancy card test was weakly positive. She was sent for ultrasound imaging (Figs. 1-4). A diagnosis of threatened abortion with twin gestation was made and the patient was managed conservatively with bed rest and progesterone injections. But 2 days later, the patient had profuse bleeding and repeat scanning revealed the image as shown in Figure 5. Due to the excessive bleeding, conservative management was aborted and emergency dilation and curettage (D&C) was done. During curettage, the products of conception were removed but still no grating sensation

Figure 1. Transabdominal scan showing two hypoechoic intrauterine areas appearing as ? twin gestational sacs.

Obstetrics and Gynecology

Figure 2. Transvaginal scan showing one gestational sac with yolk sac within it but no fetal pole and the other ? gestational sac with some hyperechoic areas within it ? fetal parts.

Figure 5. Transabdominal scan showing that the upper hypoechoic area had become more isoechoic suggesting it was a large SH which had now become organized and the patient had developed a second SH at the lower pole of the gestational sac.

and sent for histopathology. The histopathology report confirmed it to be just a hematoma with no traces of any vanishing or reduced twin gestational sac or chorionic tissue. REVIEW OF LITERATURE

Figure 3. The gestational sac with the yolk sac had mean diameter of 13.7 mm corresponding to 5 weeks 2 days and the other hypoechoic area measured 4.2 x 3.5 cm = 14.7 cm2 and was surrounding 50-60% of the gestational sac (as seen on transabdominal scan - Fig. 1).

Figure 4. Color Doppler revealed no vascularity in the hypoechoic mass and very poor vascularity of gestational sac.

could be felt. Hence, an intraoperative ultrasound was performed that revealed the disrupted hematoma still within the uterine cavity. An old organized clot (darkbrown colored) of ~4 × 4 cm was removed piecemeal

Bleeding per vaginum in the first-half of pregnancy occurs in approximately one-fourth (25%) of women and about half of these pregnancies terminate in abortion.2 The main reasons for vaginal bleeding in early gestation are SH and rupture of a marginal placental sinus.3 Its etiology is largely unknown, although uterine malformations, history of repeated abortions and infection4 have been suggested as possible predisposing factors. The size of the hematoma is graded according to the percentage of chorionic sac circumference elevated by the hematoma as follows.5,6 ÂÂ

Small indicates less than one-third of the chorionic sac circumference elevated by hematoma.

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Moderate indicates one-third to one-half of the chorionic sac circumference elevated by hematoma.

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Large indicates one-half to two-thirds or greater of the chorionic sac circumference elevated by hematoma.

Bennett et al showed that there was little difference in the rates of spontaneous abortion between pregnancies with small and moderate-size separations (7.7% and 9.2%, respectively), but the rate nearly doubled when the separation was large (18.8%).5 Kahn et al have described a similar case report of a 24-year-old G3P1A1 Hispanic woman who presented to the Emergency Department (ED) at 6½ weeks POG by date with vaginal bleeding of 1-day duration. She underwent

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Obstetrics and Gynecology

Figure 6. Line diagram for classification of hematomas in and around placenta. P: Placenta, Orange color: Hematoma, Grey line: Amnion, Black line: Chorion A: Retroplacental bleeding is found behind placenta. B: Subchorionic bleeding dissects chorion and endometrium. When such bleeding involves the margin of placenta, it is called marginal SH. C: Subamniotic hemorrhage is contained within the amnion and chorion and thus extends anteriorly to placenta but is limited by reflection of amnion on placental insertion site of umbilical cord. Subamniotic bleeding is rare.

a bedside endovaginal ultrasound in the ED.7 The emergency physician identified a live intrauterine pregnancy (IUP) with another structure that appeared to be a second gestational sac. The patient subsequently had an endovaginal ultrasound in the radiology department, 46 minutes later. The attending radiologist described one live IUP and a SH. Comparison of the ED and radiology ultrasound showed that the second structure, identified as SH, had significantly decreased in size. Endovaginal ultrasound in the evaluation of possible ectopic pregnancy is a useful bedside tool in the ED. They have discussed a pitfall that can occur with endocavitary ultrasound when a twin gestation is presumed.7 Hence, it is worthwhile knowing the differential diagnosis of SH, which include a twin gestational sac, uterine leiomyoma (fibroid), focal myometrial contraction, chorioamniotic separation, prominent retroplacental veins.8 SHs should also be distinguished from retroplacental hematoma and subamniotic hematoma (Fig. 6).9 SHs are usually described as crescentic anechoic collections lifting the chorionic membrane. But as described by Trop et al9 and Nyberg et al10 in their articles, depending on the time elapsed since the bleeding, the collection will have variable echotexture; it will be hyperechoic initially, with decreasing echotexture over time.9,10 Twin sac has an echogenic rim of chorionic tissue, which distinguishes it from a SH.11 A SH may be present in conjunction with multiple pregnancy and it is important not to confuse it with

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a vanishing or spontaneously reduced twin. Unlike a gestational sac, the size and shape may be variable and may contain low level internal echoes. Although, they occur frequently in multiple pregnancies, till date only a single case series reports on SH in multiple pregnancy.6,11 Dickey and colleagues retrospectively analyzed the incidence of SH and embryonic death in both singleton and twin pregnancy. Interestingly in their report 50% of twin pregnancies had a SH.11 The detection of a large SH on ultrasound increases the risk for miscarriage, stillbirth, placental abruption and preterm labor.12 Patients with SH are at greater risk for eventual fetal death even if signs of fetal life are present initially on sonography.5 We recommend that these patients be scanned serially to determine the final outcome of their gestation. REFERENCES 1. Jouppila P. Clinical consequences after ultrasonic diagnosis of intrauterine hematoma in threatened abortion. J Clin Ultrasound 1985;13(2):107-11. 2. Abu-Yousef MM, Bleicher JJ, Williamson RA, Weiner CP. Subchorionic hemorrhage: sonographic diagnosis and clinical significance. AJR Am J Roentgenol 1987;149(4):737-40. 3. Saurbrei EE, Pham DH. Placental abruption and subchorionic hemorrhage in the first half of pregnancy: US appearance and clinical outcome. Radiology 1986;160(1):109-12. 4. Queck M, Berle P. Spontaneous abortion after vaginal hemorrhage in intact early pregnancy - an etiologic analysis. Geburtshilfe Frauenheilkd 1992;52(9):553-6.

Obstetrics and Gynecology 5. Bennett GL, Bromley B, Lieberman E, Benacerraf BR. Subchorionic hemorrhage in first-trimester pregnancies: prediction of pregnancy outcome with sonography. Radiology 1996;200(3):803-6. 6. Dickey RP, Olar TT, Curole DN, Taylor SN, Matulich EM. Relationship of first trimester subchorionic bleeding detected by color Doppler ultrasound to subchorionic fluid, clinical bleeding, and pregnancy outcome. Obstet Gynecol 1992;80(3 Pt 1):415-20. 7. Kahn A, Kahn AL, Fox JC, Langdorf MI. Subchorionic hemorrhage appearing as twin gestation on endovaginal ultrasound. West J Emerg Med 2008;9(2):115-7. 8. Avneesh Chhabra (Author), Eugene C Lin (Chief Editor). Subchorionic haemorrhage: Overview. Available at: http://emedicine.medscape.com/article/404971- overview.

9. Trop I, Levine D. Hemorrhage during pregnancy: sonography and MR imaging. AJR Am J Roentgenol 2001;176(3):607-15. 10. Nyberg DA, Cyr DR, Mack LA, Wilson DA, Shuman wp. Sonographic spectrum of placental abruption. AJR Am J Roentgenol 1987;148(1):161-4. 11. Monteagudo A, Timor-Tritsch IE. Transvaginal sonography of first trimester multifetal pregnancy. In: Ultrasound and Multifetal Pregnancy. Monteagudo A, Timor-Tritsch IE (Eds.), Parthenon Publishing Group: New York 1998:p.31-60. 12. Ball RH, Ade CM, Schoenborn JA, Crane JP. The clinical significance of ultrasonographically detected subchorionic hemorrhages. Am J Obstet Gynecol 1996;174(3):996-1002.

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5 Things Obstetrician/Gynecologist Shouldn’t Do The Society for Maternal-Fetal Medicine (SMFM) released a list this month of 5 procedures that ob/gyns should question. The list is part of the American Board of Internal Medicine Foundation’s Choosing Wisely® campaign, an initiative launched in 2012 that is meant to encourage physicians to question the benefit of some commonly used tests and procedures. Inherited Thrombophilia Evaluation: The Recommendation: Don’t do an inherited thrombophilia evaluation for women with histories of pregnancy loss, intrauterine growth restriction (IUGR), preeclampsia, and abruption. The Rationale: There isn’t enough evidence to show an association between the inherited thrombophilias and adverse pregnancy outcomes. Testing for antiphospholipid antibodies should be limited to lupus anticoagulant, anticardiolipin antibodies, and beta-2 glycoprotein antibodies. Cerclage Placement: The Recommendation: Don’t place a cerclage in women with a short cervix who are pregnant with twins. The Rationale: These women are at high risk for delivering preterm, but data, including a meta–analysis published on this issue, shows that a cerclage is not only ineffective, but also may be associated with an increase in preterm births. Noninvasive Prenatal Testing: The Recommendation: Don’t offer noninvasive prenatal testing (NIPT) to low– risk patients or make irreversible decisions on the basis of the results of this screening test. The Rationale: NIPT has only been adequately evaluated in high–risk pregnancies, defined as maternal age older than 35 years; positive screening; sonographic findings suggestive of aneuploidy; translocation carrier at increased risk for trisomy 13, 18 or 21; or prior pregnancy with a trisomy 13, 18, or 21. In addition, pretest counseling must be provided, and a positive NIPT result should be confirmed with invasive diagnostic testing. Screening for IUGR: The Recommendation: Don’t screen for IUGR with Doppler blood flow studies. The Rationale: Studies have shown inconsistent results regarding the benefit of Doppler blood flow studies for IUGR screening. Once the diagnosis is suspected, however, umbilical artery Doppler flow studies are beneficial Progestogens for Preterm Birth: The Recommendation: Don’t use progestogens for preterm birth prevention in uncomplicated multifetal gestations. The Rationale: Progestogens haven’t proven to reduce the incidence of preterm birth in women with uncomplicated multifetal gestations.

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Obstetrics and Gynecology

Assessment of Cesarean Section Scar Strength: Still A Challenge? Urvashi Verma*, Mukesh Chandra†, Arun Nagrath‡, Saroj Singh#, Rachana Agrawal*

Abstract Objective: To assess the integrity (strength) of cesarean scar of uterus during interval period (nonpregnant state) by ultrasonography (USG), hysterography and hysteroscopy and their correlation. Material and methods: The study was conducted in the Dept. of Obstetrics and Gynecology and Dept. of Radiology, SN Medical College, Agra. Three hundred nonpregnant women with cesarean section in past were recruited to undergo USG, hysterography and hysteroscopy along with proper history and other routine examination. The thickness and appearance of anterior uterine wall especially at scar area was noted down during investigations. Results: The mean scar thickness was more (11.59 ± 1.33 mm) in women with only one cesarean section in comparison of women having more than one cesarean section (9.08 ± 9.2 mm). Healthy abdominal scar healed with primary intention correlated with good uterine strength. More breaking on hysterography was associated with thin scar on USG. When scar area was found irregular and wide on hysteroscopy the thickness of scar was less on USG also. Conclusion: A prospective idea of uterine scar strength can be obtained by careful history taking, local examination of abdominal scar as well as p/v findings along with USG, hysterography and hysteroscopy in nonpregnant women. If findings are suggestive of weak scar, a lady can be counsel for planned cesarean section in her future pregnancy in spite of trial for vaginal birth after cesarean. Accordingly, if she can afford further risk and cesarean section, she should become pregnant otherwise should avoid further confinement in future.

Keywords: Cesarean scar integrity, ultrasonography, hysterography, hysteroscopy, interval period

esarean section is the most commonly performed surgical procedure involving the uterus in fertile women, with low transverse incision being the most common type of uterine hysterotomy.1 Every woman who has undergone cesarean delivery aborts the chances of normal vaginal delivery in future pregnancies. Almost all of us are very frequently asked by most of the women who have undergone cesarean section recently or in past, “Doctor, will I have a normal vaginal delivery (NVD) in future or not.” It will be better, if we have some method, which

*Lecturer †Professor Dept. of Obstetrics and Gynecology SN Medical College, Agra, Uttar Pradesh ‡Professor and Head Dept. of Obstetrics and Gynecology UP Rural Institute of Medical Sciences and Research, Saifai, Ethawah, Uttar Pradesh #Professor and Head Dept. of Obstetrics and Gynecology SN Medical College, Agra, Uttar Pradesh Address for correspondence Dr Urvashi Verma Lecturer Dept. of Obstetrics and Gynecology SN Medical College, Agra, Uttar Pradesh E-mail - rajushikamal@rediffmail.com

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could assess strength of uterine (cesarean) scar before a lady plans for her subsequent pregnancy/delivery. To seek an answer for this important and frequently asked question by almost every woman, this study was contemplated. In women, who have undergone a cesarean section, a previous cesarean section casts a shadow over any future pregnancy (Jackson 1961), though under favorable circumstances, a repeat cesarean section may not be necessary. Today, a more uptodate version of the old saying ‘once a cesarean always a cesarean’ would be ‘once a cesarean always a hospital delivery’. Effort to encourage vaginal birth after cesarean (VBAC) appears to be the most productive approach to lowering the cesarean rate. Since, a fair number of cesarean sections are done for nonrecurring indications, the question of allowing them a vaginal delivery in the future becomes a pressing problem in the mind of the obstetrician especially in developing countries like India. Poidevin (1959) found that, on opening all uteri, which had previously been subjected to lower-segment cesarean section (LSCS) a larger or smaller depressed scar would always be seen. If the depression is not >5 mm deep, the scar can be relied upon not to

Obstetrics and Gynecology

Figure 2. Hysteroscopic view of dehiscent scar (white arrow). Figure 1. Anterior wall thickness at scar area (white marker) on USG.

give way. A defect within the lower uterine cavity in patients with a history of cesarean section has been described by Simpson et al on hysterosalpingography.2 Ash et al described that patients who had a cesarean section will exhibit anatomic abnormality in lower uterine segment on ultrasonography (USG).3 Material and Methods This was a prospective study done on 300 women out of which 160 women had one cesarean section and 140 women had two cesarean sections attending the OPD in Dept. of Obstetrics and Gynecology, SN Medical College, Agra. Range of age group varied from 15 to 45 years. Detailed obstetric history along with general, systemic and local examination was done along with urine pregnancy test. Women having recent pelvic infection and/or allergy to dye were excluded from the study. Under local examination, any healing defect, scarring, pain, tenderness and any discharge from stitch line were noted. Genital tract examination was done to see the condition (mobility) of cervix, uterus and adnexal pathology. Every woman was subjected to USG, hysteroscopy and hysterography along with other routine investigations. On ultrasound, scanning was done in serial longitudinal and transverse planes across the whole length of scar in postmenstrual phase with full bladder (Fig. 1). Scar was identified as a hyperechoic small line or dots (equal sign) in lower part of uterus and its thickness was measured at various points by moving probe from side-to-side. Hysteroscopy (direct visualization of scar) was performed on 9th postmenstrual day or

Figure 3. Hysterography after cesarean section reveal a wide and deep scar at the level of subisthemic incision (white arrow).

when bleeding stopped completely and whole of the anterior uterine wall scanned upto internal os. Scar identified as whitish and fibrotic area or line horizontally (Fig. 2). The findings of scar area were compared with the findings by means of other methods. Hysterography (hysterosalpingography) was also performed on 9th postmenstrual day or when bleeding stopped completely and films in lateral view were taken (Fig. 3). The depth of breaking/notching or filling defect was identified, measured and categorized in three groups (< 1 mm, 1 mm and >1 mm). These findings were also compared with findings by means of other methods. Results As shown in Table 1, in women having only one cesarean section, the mean scar thickness was

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Obstetrics and Gynecology Table 1. Distribution of Cases and their Ultrasonography and Hysterography Findings According to Number of Cesarean Section No of cesarean section

Depth of scar area on hysterography

Scar thickness by USG (mean ± SD) in mm

No. of women

< 1 mm

1 mm

> 1 mm

110 (68.75%)

30 (18.75%)

20 (12.75%)

11.59 ± 1.33

160

60 (42.85%)

40 (28.57%)

9.08 ± 0.92

140

170

10.37 ± 1.2

300

Total ‘t’ = 2.181; p < 0.05

Table 2. Distribution of Cases According to Hysterographic (Isthmographic) Findings and its Correlation with USG Findings

Table 3. Distribution of Cases According to the Abdominal Wall Scar Status and its Relation to the Uterine Scar Thickness on USG

Depth of beak on hysterographic (mm)

No. of cases

Scar thickness by USG (mean ± SD min)

Abdominal scar on par abdomen examination

> 1 mm = 1 mm < 1 mm Total > 1 vs 1 < 1 vs >1 1 vs >1

70 70 160 300 ‘t’ 0.272 3.531 2.567

8.86 ± 1.36 10.00 ± 0.00 10.75 ± 1.25 10.37 ± 1.20 p > 0.05 < 0.05 < 0.05

No. of cases

Uterine scar thickness on USG (mean ± SD min)

Fine/Linear (FL) Wide/Puckeled (WP)

230 40

1024 ± 0.9 9.50 ± 1.12

Hypertrophic/Keloid (K)

8.67 ± 1.2

300 ‘t’ 2.463 3.610 0.926

p < 0.05 < 0.05 > 0.05

Total FL vs WP FL vs K WP vs K

Table 4. Distribution of Cases and their Mean Scar Thickness by USG According to Hysteroscopic Findings Uterine outline on hysteroscopy

No. of cases

Scar thickness on USG (mean ± SD)

‘t’ test

p value

Regular

250

10.68 ± 0.93

3.965

< 0.05

Irregular

8.80 ± 1.17 3.262

< 0.05

Wide

9.44 ± 1.17

Linear

210

10.76 ± 0.97

11.59 ± 1.33 mm and in women having two cesarean sections, the mean scar thickness was 9.08 ± 9.2 mm; this is statistically significant. It was concluded that, in women having more number of cesarean sections the scar becomes more thin, which can also be proved by hysterography as shown in the same table, the deformities shift to the larger type as the number of cesarean sections increase. According to Tables 1 and 2, on hysterography it was evident that 70 patients had depth of beak >1 mm and mean scar thickness of 8.86 ± 1.36 mm, and equal number of patient had a beak of 1 mm and mean scar thickness of 10.00 mm. There were 160 women who had

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<1 mm deep beak and mean scar thickness of 10.75 ± 1.35 mm. On comparing the two groups <1 mm and >1 mm deep beak, scar thickness was found to be statistically significant (p < 0.05). It was concluded that if scar was found to be thin on USG, there will be more beaking in anterior uterine wall (scar area) on hysterography. On hysteroscopy, interior of uterine cavity was seen and classified into two groups according to the regularity and irregularity of scar area and again, whether it was wide or linear. If uterine outline, anteriorly at scar area, was found irregular or wide, both conditions indicate a weak scar. It was further confirmed by USG as well by hysterography (Table 3).

Obstetrics and Gynecology As seen in Table 4, 230 cases had fine linear abdominal scars and mean scar thickness of uterus by USG was 10.74 mm while 40 cases had wide puckered scar over abdomen and mean scar thickness of uterine scar was 9.50 mm. There were only 30 cases having keloid/ hypertrophid scar formation over abdomen and mean uterine scar thickness of 8.67 mm on USG. The values are statistically significant (p < 0.05). Discussion Although not many studies are available regarding uterine scar status especially in nonpregnant condition, Alfred Warionch in his study in 1967, using hysterography concluded that as the number of cesarean sections increase, the scars become thinner. Osser et al also found that myometrial thickness at the level of isthmus uteri decreases as the number of cesarean sections increase; the frequency of the large scar defect increases.4 This was also found in our study (Table 1). Now many surgeons have started practicing excision of scar area after identifying it as fibrosed, nonvascular thinned portion during cesarean section in a hope to get a healthy and good strength scar in future. During hysterocervicography, a steep oblique or lateral view may be helpful in better defining this particular cesarean section scar because certain defects can be obscured on a frontal view.5 Though, in the interpretation of hysterosalpingography, awareness of the appearance of cesarean scar defect is important in avoiding misdiagnosis of the scar for underlying pathology or normal variant such as prominent cervical glands, post-myomectomy diverticulum, synechiae and focal adenomyosis.2,6 On hysterosalpingography, the defects were categorized by location (lower uterine segment, uterine isthmus, upper endocervical canal), side (right, left, bilateral, small midline) and size by Surapaneni and Silberzweig.5 In comparison with hysterosalpingographic diagnosis of cesarean scar defect, Regnard et al detected a similar rate of cesarean section scar (57.5%) via saline contrast sonohysterography.7 Fabres et al suggested that the defect may be related to the suture material used, the suturing technique it self or a combination of both.8 It is presumed that the most ischemic technique and slowest reabsorbable suture would be the worst combination and thus most likely to produce a cesarean scar defect.7 In the study by Surapaneni and Silberzweig, out of 148 women with history of cesarean section and technically adequate hysterosalpingography, 89 (60%) were found to have anatomic defect.5 In a study by Ofili-Yebovi on USG lower-segment, uterine scars were detected in 321/324 women with a history of previous cesarean section, 63 women had evidence of deficient cesarean scar.9

Conclusion If we want to avoid more and more encounters impending dehiscence, dehiscence and uterine rupture following cesarean section we have to be alert since beginning of the story. We have to correct anemia before a lady gets pregnant and during her pregnancy. During labor we should be alert for warning signs and should shift the patient in time. Nonabsorbable or slow absorbing sutures and very tight stitching (ischemic technique) should be avoided. Postoperative anemia and infections must be avoided. The integrity of scar is affected by various factors like general condition of woman at the time of cesarean section, technique of stitching, type of suture material, preoperative, peroperative or postoperative infections as well. If the thickness of scar area is <10 mm on USG or depth of beak on hysterography is >1 mm or if it looks wide and irregular on hysteroscopy all are indicative of a weaker uterine scar. This procedure can be done during the interval period and the patients accordingly counseled with regard to their chances of achieving their subsequent reproductive goals. Repeat elective cesarean section, then is chiefly indicated in case of established weak/deficient scar found by above mentioned method and investigations as in disproportion and after a classical operation. References 1. Ecker JL, Frigoletto FD Jr. Cesarean delivery and the riskbenefit calculus. N Engl J Med 2007;356(9):885-8. 2. Simpson WL Jr, Beitia LG, Mester J. Hysterosalpingography:are-emerging study Radiographics 2006;26(2):419-31. 3. Ash A, Smith A, Maxwell D. Cesarean scar pregnancy. BJOG 2007;114(3):253-63. 4. Osser OV, Jokubkiene L, Valentin L. High prevalence of defects in cesarean section scars at transvaginal ultrasound examination. Ultrasound Obstet Gynecol 2009;34(1):90-7. 5. Surapaneni K, Silberzweig JE. Cesarean section scar diverticulum: appearance on hysterosalpingography. AJR Am J Roentgenol 2008;190(4):870-4. 6. Ubeda B, Paraira M, Alert E, Abuin RA. Hysterosalpingography: spectrum of normal variants and nonpathologic findings. AJR Am J Roentgenol 2001;177(1):131-5. 7. Regnard C, Nosbusch M, Fellemans C, Benali N, van Rysselberghe M, Barlow P, et al. Cesarean section scar evaluation by saline contrast sonohysterography. Ultrasound Obstet Gynecol 2004;23(3):289-92. 8. Fabres C, Aviles G, De La Jara C, Escalona J, Mu単oz JF, et al. The cesarean delivery scar pouch: clinical implications and diagnostic correlation between transvaginal sonography and hysteroscopy. J Ultrasound Med 2003;22(7):695-700; quiz 701-2. 9. Ofili-Yebovi D, Ben-Nagi J, Sawyer E, Yazbek J, Lee C, Gonzalez J, et al. Deficient lower-segment cesarean section scars: prevalence and risk factors. Ultrasound Obstet Gynecol 2008;31(1):72-7.

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Obstetrics and Gynecology

Exceptional Case of Omphalocele (Exomphalos Major) K Tabassum*, Mohd Zulkifle†, Mohd Nasir‡, Yasmeen K#

Abstract An unregistered case of a 27-year-old multipara with 8 years married life was admitted on 3/11/09 at 10.30 pm with complaints of tightness of abdomen, backache and draining per vagina and delivered a fetus of 19 weeks in cephalic presentation with omphalocele (i.e., stomach, liver, bowel and bladder protruding into the proximal part of umbilical cord) on 5/11/09 at 9.00 pm at Sameena Maternity and Nursing Home, Hyderabad, Andhra Pradesh.

Keywords: Omphalocele, herniation of abdominal viscera, exomphalos, TIFFA scan diagnosis and termination of pregnancy

mbilical hernia can be discussed under three headings: Umbilical hernia of new born (omphalocele or exomphalos); umbilical hernia of infants and children and umbilical hernia of adults.

The incidence of umbilical hernia is one in 6,000 live births. It is due to failure of midgut as a whole or a part to enter coelomic cavity during embryonic life resulting in exomphalos. It is also associated with weak abdominal musculature. The anomaly is more common in males. It is estimated that 26-54% cases are due to chromosomal abnormalities and the average is 39%.1 Two types of umbilical hernia have been recognized: Exomphalos minor and major. In exomphalos minor, umbilical cord is attached to the summit of the sac. Sac is small. It is treated by twisting the cord and ligating the sac. Care should be taken to avoid damage to the intestines. In exomphalos major, the umbilical cord is attached to the inferior aspect of the sac, containing intestines, abdominal viscera. Many children are stillbirth. This type of hernia is associated with absent abdominal musculature. Operation should be done before the rupture of the sac. During the operation, skin flaps are raised on both sides to cover the defect. True repair is necessary, which is done at a later life.2,3

*Reader Dept. of Obstetrics and Gynecology †Reader Dept. of Preventive Medicine, National Institute of Unani Medicine, Bangalore ‡Lecturer Dr Abdul Haq Unani Medical College and Hospital, Kurnool, Andhra Pradesh #DMO, Sameena Maternity and Nursing Home, Talab Katta, Hyderabad

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Case Report A 27-year-old G5P2L2A2 with 8 years married life, an unregistered case with 19-20 weeks pregnancy was admitted on 3/11/09 at 10.30 pm in the maternity ward of our hospital. She had complaints of tightness of abdomen, backache and draining per vagina since 2 hours. No history of consanguinity. Patient had two live births and two abortions. First and second abortions were of 3 and 2 months, respectively. Third (male) and forth (female) were spontaneous vaginal deliveries at Sameena Maternity Hospital, Hyderabad, Andhra Pradesh. Both were alive and healthy. There was no history of any types of congenital anomalies. Her last child birth was 3 years back. Ultrasonography report on 3/11/09 showed single live fetus of 19 weeks in cephalic presentation with omphalocele (i.e., stomach, liver, bowel and bladder protruding into the proximal part of umbilical cord). Posterior wall fibroid in the body of uterus was also observed. The fetal heart pulsation was 133 beats/min, fetal tone and movements were normal and her scan expected date of delivery was 14/4/2010. With these ultrasonographic findings, she was provisionally diagnosed as a case of congenital omphalocele. Trageted imaging for Fetal anomalies (TIFFA) report on 3/11/09 showed: ÂÂ Fetal head: Occipital horn was 8.3 mm in Posterior fossa was shallow. ÂÂ Fetal spine: Kyphoscoliosis in thorax meningocele at lower end. ÂÂ Fetal face: Visualized normal. ÂÂ Fetal heart appeared normal, 4 chambers visualized. ÂÂ Evidence of narrow thoracic cavity.

scan size. with

view

Obstetrics and Gynecology

(a)

(b)

Figure a and b. Herniation of abdominal viscera (exomphalos major).

ÂÂ ÂÂ

Evidence of herniation of stomach, liver, bowel and bladder outside the abdominal cavity. Evidence of posterior wall fibroid of 59 × 58 mm in the body of the uterus.

On physical examination, she was afebrile and hemodynamically stable. Human immunodeficiency virus (HIV) and hepatitis B surface antigen (HBsAg) were negative. Urine albumin and sugar were nil. The vitals were recorded hourly and first readings on admission were recorded as blood pressure 120/80 mmHg, pulse was 98/min. On systemic examination, no abnormality was detected. As per abdominal examination height of uterus was 19-20 weeks and fetal heart sounds were clear. On 4/11/09 at 10.00 pm emecredil was injected. On 5/11/09, fetal movements and fetal heart sounds disappeared. Patient delivered a grossly abnormal dead male baby on 5/11/09 at 9.00 pm. Patient was stable after delivery. Discussion Congenital omphalocele is a herniation of abdominal contents into the proximal part of the umbilical cord. Embryological defect responsible for this condition is a failure of return of intestine into the abdominal cavity during 7th week of intrauterine life. Herniation

of intestines into the cord occurs in about one of 5,000 births and herniation of liver and intestine in one of about 10,000 births.2 The size of hernia depends upon its contents. In the present case along with liver and intestines, stomach and urinary bladder were also in the hernial contents. So, the case was diagnosed as exomphalos major. The abdominal cavity was proportionately small because the normal contents were absent. The covering of hernial sac was the epithelium of the umbilical cord, a derivative of the amnion externally and mesothelium internally. Though stomach was present in hernial sac, but it was not a case of gastroschisis, because the split was not related to umbilicus. The exact cause for exomphalos is not known, but probably it may be due to teratogenic or nutritional or environmental interference. References 1. Braunwald E, Fauci AS, Kasper DL, Hauser S L, Lingo DL, Jameson L. Harrison’s Principles of Internal Medicine. 15th edition, McGraw-Hill Medical Publishing Division. 2005:p.846. 2. Bailey & Love’s, Short Practice of Surgery. 23rd edition, Arnold Publications p.1156-57. 3. Rajgopal Shenoy K. Manipal Manual of Surgery. 2nd edition, CBS Publications, 2005:p.566-7.

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Oophorectomy prior to menopause was associated with a greater risk for carotid artery thickening and bone loss more than a decade postmenopause. Sara J Mucowski, MD, of the University of Southern California Keck Medical Center in Los Angeles, and colleagues report in Feb. 14 in Fertility and Sterility that after excluding women who used estrogen or bisphosphonates, women without their ovaries showed a larger rate of bone mineral density decline in the lumbar spine compared with women with intact ovaries, both 5-10 years after menopause (–11.2, 95% CI –19.8–minus 2.53, p = 0.02) and more than 10 years after menopause (–6.45, 95% CI –14.1-1.24, p = 0.08).

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Ophthalmology

Management of a Complicated Case of Symblepharon with Amniotic Membrane Transplantation P Jain*, JP Chughâ&#x20AC;

Abstract Amniotic membrane transplantation (AMT) has gained widespread acceptance in various ocular diseases. Its anti-inflammatory activity and close resemblance to conjunctival epithelium has propagated it as an ideal substitute for ocular surface reconstruction. Here is a case report of a complicated case of recurrent symblepharon and ankyloblepharon after fire cracker injury that was managed successfully with AMT with excellent cosmetic results.

Keywords: Amniotic membrane transplantation, symblepharon, ankyloblepharon Case History A 12-year-old boy presented to us with cosmetic disfigurement and difficulty in opening right eye associated with watering since the past 2 years after fire cracker injury in the same eye. Before presenting to us, he had already undergone symblephrectomy once somewhere else followed by recurrence 1 month after surgery. On examination, recorded Snellen acuity was 20/20 in both eyes. Medial ankyloblepharon was present involving upper and lower lacrimal puncta along with symblepharon involving nasal side of the bulbar conjunctiva in the right eye (Fig. 1 a and b). There was restricted abduction and elevation of the same eye. Rest of the ocular examination was within normal limits. Lid and ocular surface reconstruction after symblepharectomy along with medial canthoplasty was done using fresh amniotic membrane under general anesthesia (Fig. 2 a-g). Lacrimal puncta could not be identified after excision of fibrous tissue. Hence, lacrimal drainage apparatus was not reconstructed in the same sitting. The patient was prescribed topical steroids, antibiotics and lubricating eye drops postoperatively. Follow-up was done for 6 months postoperatively. There was no evidence of recurrence

â&#x20AC; Senior

Professor Regional Institute of Ophthalmology Postgraduate Institute of Medical Sciences, Rohtak, Haryana Address for correspondence Dr Prachi Jain Post Graduate Institute of Medical Sciences, Rohtak, Haryana

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Indian Journal of Clinical Practice, Vol. 24, No. 10, March 2014

b Figure 1. Preoperative image showing medial (a) ankyloblepharon and (b) symblepharon.

Ophthalmology

Figure 2. Surgical steps. (a) Laterally rotated eyeball showing thickened conjunctival fold along with medial ankyloblepharon and symblepharon. (b) Thickened conjunctival fold excised. (c) Ankyloblepharon and symblepharon released. (d) Lid margin reconstruction. (e) Raw area covered with amniotic membrane. (f) End of surgery. (g) Conformer in situ.

Figure 3. Six months postoperative image showing excellent cosmetic restoration and no evidence of recurrence.

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Ophthalmology after 6 months of surgery with good cosmetic results (Fig. 3). Discussion Amniotic membrane is the innermost layer of placenta with various beneficial properties. It is now widely used in the treatment of nonhealing corneal ulcers, persistent epithelial defects and ocular surface reconstruction. Histologically, it closely resembles the basement membrane of conjunctiva.1 It has inhibitory effect on various inflammatory cytokines like interleukin (IL)-1a, IL-2, IL-8, IFN-γ, TNF-β and platelet-derived growth factor that imparts antiinflammatory properties to it.2 It prevents epithelial scarring by inhibiting TGF-β signaling thereby preventing myofibroblastic differentiation of corneal and conjunctival fibroblasts.3 These properties make it an ideal substitute for ocular surface reconstruction following chemical injuries, cicatricial ocular surface disorders, pterygium and ocular surface growth

excisions. It promotes epithelization of raw surfaces and therefore prevents recurrence of symblepharon. All these properties helped in preventing recurrence of the complicated symblepharon and ankyloblepharon along with good ocular surface restoration in our case. References 1. Fukuda K, Chikama T, Nakamura M, Nishida T. Differential distribution of subchains of the basement membrane components type IV collagen and laminin among the amniotic membrane, cornea, and conjunctiva. Cornea 1999;18(1):73-9. 2. Solomon A, Rosenblatt M, Monroy D, Ji Z, Pflugfelder SC, Tseng SC. Suppression of interleukin 1alpha and interleukin 1beta in human limbal epithelial cells cultured on the amniotic membrane stromal matrix. Br J Ophthalmol 2001;85(4):444-9. 3. Lee SB, Li DQ, Tan DT, Meller DC, Tseng SC. Suppression of TGF-beta signaling in both normal conjunctival fibroblasts and pteryigial body fibroblasts by amniotic membrane. Curr Eye Res 2000;20(4):325-34.

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ÂÂ

Computer-based vision training may improve vision for patients with glaucoma, possibly because of plasticity in the retina and vision-related areas of the brain, according to an article published online February 6 in JAMA Ophthalmology.

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Surgeons are fine-tuning their approach to Descemet membrane endothelial keratoplasty (DMEK) to improve corneal transplant outcomes and allay concerns ophthalmologists have about performing the challenging procedure. Friedrich Kruse, MD, from the University of Erlangen, in Germany, a leader in the DMEK field, presented new ideas at the American Academy of Ophthalmology 2013 Annual Meeting.

ÂÂ

The American Academy of Ophthalmology (AAO) is launching the country’s first comprehensive eye disease registry. Intelligent Research in Sight (IRIS) will open in April 2014. According to William Rich III, MD, medical director of health policy for the AAO, IRIS is expected to have a groundbreaking effect on improving quality and outcomes for physicians, group ophthalmology practices, and the entire profession.

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Taking a multivitamin supplement daily may stave off development of cataracts in middle–aged and older men, according to an article published online November 21 in Ophthalmology. However, there appeared to be no association between daily vitamins and visually significant age-related macular degeneration (AMD).

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PEDIATRICS

Cord Blood Nucleated RBC as a Predictor of Perinatal Asphyxia, Severity and Outcome Anil Kumar Mohanty*, Leena Das†, Subal Pradhan‡, Bijay Meher‡, Siba Shankar Beriha‡

Abstract Objective: To study the correlation of cord blood nucleated red blood cell (NRBC)/100 white blood cell (WBC) count with perinatal asphyxia in terms of severity and short-term outcome. Material and methods: A prospective, comparative case-control study was undertaken in a tertiary care hospital from January 2011 to December 2012, which included a total of 200 neonates with 100 asphyxiated babies (case group) and 100 normal babies (control group). The cord blood was collected immediately after delivery for measurement of NRBC/100 WBC, and pH. Early neonatal outcome of both groups was also evaluated in relation to the NRBC/100 WBC count. Statistical analysis was performed with chi-square and student t-test. Results: The mean NRBC/100 WBC count was 50.82 ± 23.85 (range from 5 to 106) in case group and 1.67 ± 1.005 (range from 0 to 13) in control group (p < 0.001). Also a statistically significant correlation existed between severity of asphyxia (stage of hypoxic-ischemic encephalopathy [HIE]), poor outcome and higher number of NRBC/100 WBC count (p < 0.001). Conclusion: It is an inexpensive and easily available procedure to evaluate perinatal asphyxia, specially in a resource poor country like ours, where blood gas analysis facilities are not available in majority of places. Also, it is a good predictor of short-term outcome of asphyxiated babies.

Keywords: Cord blood, nucleated red blood cells, perinatal, asphyxia

erinatal asphyxia is a major cause of acute mortality and chronic neurologic disability amongst survivors, and is a complication that occurs between 2-10% of deliveries.1 No single parameter can define perinatal asphyxia, rather a combination of parameters like fetal distress, meconium-stained liquor, low Apgar score, umbilical cord blood pH and clinical features of hypoxicischemic encephalopathy (HIE) can predict it. The 1996 guideline from the American Academy of Pediatrics (AAP) and American College of Obstetricians and Gynecologists (ACOG)2 for HIE indicate that all of the following must be present for designation of perinatal asphyxia severe enough to result in acute neurological injury: ÂÂ

Profound metabolic or mixed academia (pH <7) in an umbilical blood sample and persistence of an Apgar score of 0-3 for longer than 5 minutes

*Professor †Associate Professor ‡Assistant Professor Dept. of Pediatrics SCB Medical College, Cuttack, Odisha Address for correspondence Dr Anil Kumar Mohanty Professor, Dept. of Pediatrics Duplex-31, Bhawani Construction, Sector-6, CDA Cuttack - 753 014, Odisha E-mail: ctcanil55@gmail.com

ÂÂ

Neonatal neurologic sequelae (e.g., seizure, coma, hypotonia)

ÂÂ

Multiple organ involvement (e.g., kidney, lungs, liver, heart and intestines).

But, as per Cloherty et al 3 perinatal asphyxia is defined as a condition of fetal hypoxia and hypercarbia, identified by fetal acidosis as umbilical artery pH <7. The condition can be diagnosed by fetal distress, meconium aspiration, low Apgar score <6 by 5 minutes, umbilical cord blood pH <7. Recent studies on hematological variations in asphyxiated neonates as a predictor of neonatal asphyxia have suggested that number of nucleated red blood cells (NRBCs) in cord blood of asphyxiated neonates help in identifying birth asphyxia. The number of NRBC/100 white blood cells (WBC) is quite variable but is rarely >10.4-7 The instances, where number of NRBCs exceed 10/100 WBC are asphyxia, prematurity, Rh-sensitization, maternal diabetes mellitus and intrauterine growth retardation. Considering the hematopoietic response to hypoxia in utero the elevated NRBC/100 WBC count is being hailed as the marker for not only perinatal asphyxia but also the chances of the neonates to develop neurological sequelae.4,7-10 The present study was undertaken to evaluate the cord blood NRBC/100 WBC count as a marker of perinatal

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PEDIATRICS asphyxia in conjunction with other clinical markers and its ability as a predictor of perinatal asphyxia, its severity and short-term outcome. Material and methods A prospective, case-control study was conducted in the Dept. of Pediatrics, SCB Medical College and Hospital, Cuttack, Odisha from January 2011 to December 2012. In this study, hematological profile of a total number of 200 neonates were evaluated (100 asphyxiated/case group and 100 nonasphyxiated/control group). The case group included the mothers in labor between 38-42 weeks of gestation with singleton pregnancies. They were observed during labor for development of signs of fetal distress, thick meconium-staining of liquor, Apgar at 1 minute and 5 minutes <6 and umbilical arterial pH <7.0. Control group included nonasphyxiated newborns with appropriate gestational age (neonates from 38 to 42 weeks gestation), birth weight >2,500 g, Apgar score >7 at both 1 and 5 minutes, normal intrapartum fetal heart rate (FHR) pattern, clear amniotic fluid, normal neurologic evaluation during the 1st week. Neonates born to mothers with pre-eclamptic toxemia (PET), diabetes mellitus, Rh-sensitization, multiple pregnancies, born by breech presentation, born before 37 weeks gestation and birth weight <2.5 kg were excluded from the study. Immediately after birth of baby, 1 mL of blood was collected in heparinized syringe from doubly clamped segment of umbilical cord for pH estimation and another 2 mL blood collected in ethylenediaminetetraacetic acid (EDTA) vial from which hemoglobin (HB), total leukocyte count (TLC) were estimated. Along with it a thin blood film was prepared on a glass slide, which was dried and stained with Leishman’s stain. The slide was first examined with low power objective to screen the whole slide to assess the adequacy of cell distribution quality of staining: Subsequently, the slide was examined with oil immersion lens (90 or 100 x 10 = 900 or 1,000 magnification) to examine the red cells for deviation from normal. These NRBCs/100 WBC was counted. Asphyxiated babies were shifted to neonate intensive care unit (NICU) after resuscitation and normal babies to Obstetrics ward. Detailed clinical examination including anthropometric measurement and gestational age was recorded in all cases. Daily evaluation for detection of abnormal symptoms and signs and neurological examination were done

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at birth, 24 hours after birth and every day thereafter till discharge/death. Grading of neonates was done according to Sarnat and Sarnat staging for HIE. Correlation of cord blood NRBC/100 WBC count with clinical condition at different stages of HIE during hospital management was observed until discharge or death. Adverse, or poor short-term outcome was diagnosed as the presence of at least one of the following condition death, hemiplegia, hypertonicity or significant hypotonia, unreliable sucking, seizures resistant to phenobarbital and sensorineural hearing loss. Controls were followed up in the same manner. Statistical analysis was done with Chi-square (χ2) analysis (for quantitative analysis), student t-test (comparing mean NRBC in different stages) by SPSS version 20 software for biostatistics. Results Both the case group and control group were similar in terms of gestational age, birth weight, sex of baby, maternal parity and maternal age. However, there was a statistically significant difference in both 1 minute and 5 minutes Apgar score and cord blood pH leading to HIE (p < 0.001) (Table 1). The NRBC/100 WBC count for case group was 50.82 ± 23.85 with a range from 5 to 106, whereas, it was 1.67 ± 1.05 with range from 0 to 13 in normal babies (control, group). T value was 20.32 and p value was <0.001, which was statistically significant (Table 2). The NRBC/100 WBC count correlated with degree of asphyxia and staging of HIE. The NRBC count was found to be 15.88 (range 5-28) in Stage Ι HIE, 46.5 (range 6-89) in Stage ΙΙ HIE and 77.12 (range 8-106) in Stage ΙΙΙ HIE. There was a significant

Table 1. Various Parameters of Study Population Parameters Sex (M/F) Maternal age

Asphyxia

Control

56/44

58/42

>0.05

p value

24.3 ± 6

23.6 ± 5

>0.05

Parity (p/m)

47/53

38/62

>0.05

Mode of delivery (ND/CS)

46/54

81/19

>0.05

Birth weight (gr) Gestational age (weeks)

2,865 ± 404 2,776 ± 405 >0.05 38.4 ± 1.4

37.6 ± 1.3

>0.05

Apgar score 1 minutes

4 ± 1.2

8.6 ± 0.5

<0.001

Apgar score 5 minutes

5.4 ± 1.4

9.0 ± 0.4

<0.001

Cord pH

7.0 ± 1.4

7.34 ± 0.1

<0.001

Data presented as mean ± SD; ND = Normal delivery, CS = Cesarean section.

PEDIATRICS Table 2. Distribution of NRBCs in Both Groups NRBC/100 WBC

Asphyxiated group n (%)

Control n (%)

0-10

4 (4%)

98 (98%)

11-50

55 (55%)

2 (2%)

51-100

38 (38%)

nil

101-150

3 (3%)

nil

100

50.82 ± 23.85

1.67 ± 1.05

5-106

0-13

Total Mean ± SD Range

p value

Cord blood NRBC count was found to be a good predictor of perinatal asphyxia with sensitivity of 96%, specificity of 98%, positive predictive value of 97.9% and negative predictive value of 96%. Discussion <0.001

Values expressed as mean ± SD, NRBC = Nucleated red blood cell; WBC = White blood cell. T = 20.32, p value <0.001

Table 3. NRBC in Different Stages of HIE Stage of HIE

NRBC range

Mean

Stage Ι

5-28

15.88

Stage ΙΙ

6-89

46.5

Stage ΙΙΙ

8-106

77.125

NRBC = Nucleated red blood cell; HIE = Hypoxic-ischemic encephalopathy. P value <0.001.

Table 4. HIE Staging and Outcome Clinical staging

The NRBC/100 WBC count was significantly higher in babies with adverse outcome, than the babies with good outcome, 65.44 (range 32-106) versus 42.14 (range 5-104) (p < 0.001) (Table 5).

Cases

Death/Disability n (%)

Stage Ι

3 (12%)

Stage ΙΙ

16 (32%)

Stage ΙΙΙ

18 (72%)

Total

100

37 (37%)

Table 5. Relation of NRBC/100 WBC Count with Outcome. Mean NRBC/100 WBC with range

Outcome

65.44 (32-106)

Death/Disability

42.14 (5-104)

Survived with normal neurodevelopment

P value <0.001

relationship between NRBC/100 WBC and HIE staging (p < 0.001) (Table 3). Among asphyxiated group 63 (63%) had good outcome (survived with normal neurologic development), whereas remaining 37 (37%) had poor outcome (either death or disability like neurological sequelae) (Table 4).

In the present study, attempt has been made to evaluate the relation of cord blood NRBC/100 WBC in predicting perinatal asphyxia and its immediate outcome. In our study, the NRBC/100 WBC count for normal newborn was 1.67 ± 1.05, and in the case group it was 50.82 ± 23.85. Several studies have reported an increased NRBC in neonatal cord blood following perinatal asphyxia.5,6,9,11-13 Gupta et al14 in their study had found out NRBC/100 WBC count of 5.7 ± 2.33212 in control group and 10.34 ± 3.87883 in asphyxiated group. Previous studies suggested that erythropoietin increases erythroid production and release of erythrocytes into the peripheral circulation in response to hypoxia.5,10 NRBC/100 WBC count was also related to Sarnat and Sarnat’s grading of HIE. We found out the higher value of NRBC/100 WBC count, in higher degree of severity of HIE; 15.88 in Stage Ι, 46.5 in Stage ΙΙ and 77.12 in Stage ΙΙΙ of HIE. This is statistically significant, as p value is <0.001. Hermansen et al,9 Phelan et al12 and Hanlon-Lundberg et al15 had found higher number of cord blood NRBC in severe asphyxia cases. Boskabadi et al16 in their study had found NRBC as follows, 11.94 in Grade Ι HIE, 21.08 in Grade ΙΙ HIE and 29.18 in Grade ΙΙΙ HIE cases. In our study, among the asphyxiated babies, 37% had poor outcome (either death or survived with sequelae) and in these babies NRBC count was higher, 65.44 (range 32-106), whereas in babies with good outcome the count was less, 42.14 (range 5-104), which is statistically significant (p value <0.001). Other authors like Boskabadi et al16 and Ferns et al17 had found similar observations in their study and reported that rate of erythropoiesis was related to degree of asphyxia, which in term influenced the neurological impairment. Conclusion In our study, the cord blood NRBC count was shown to be a good predictor of perinatal asphyxia

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PEDIATRICS with sensitivity of 96%, specificity of 98%, positive predictive value of 97.9% and negative predictive value of 96%. Since, it is cost-effective and does not require any special expertise or any high-tech facilities, it may be a useful, reliable, inexpensive and easily available marker to evaluate perinatal asphyxia, specially in a resource poor country like ours, where blood gas analysis facilities are not available in majority of place. References 1. Low JA. The role of blood gas and acid-base assessment in the diagnosis of intrapartum fetal asphyxia. Am J Obstet Gynecol 1988;159(5):1235-40. 2. Use and abuse of the Apgar score. Committee on Fetus and Newborn, American Academy of Pediatrics, and Committee on Obstetric Practice, American College of Obstetricians and Gynecologists. Pediatrics 1996;98(1): 141-2. 3. Cloherty JP, Eichenwald EC, Hansen AR, Stark AR. Perinatal asphyxia and hypoxic-ischemic encephalopathy. (Chapter 55). In: Manual of Neonatal Care. 7th edition, Wolter Kluwer, Lippincott Williams & Wilkins: Philadelphia USA 2011:p.713-26. 4. Green DW, Mimouni F. Nucleated erythrocytes in healthy infants and in infants of diabetic mothers. J Pediatr 1990;116(1):129-31. 5. Phelan JP, Ahn MO, Korst LM, Martin GI. Nucleated red blood cells: a marker for fetal asphyxia? Am J Obstet Gynecol 1995;173(5):1380-4. 6. Philip AG, Tito AM. Increased nucleated red blood cell counts in small for gestational age infants with very low birth weight. Am J Dis Child 1989;143(2):164-9. 7. McCarthy JM, Capullari T, Thompson Z, Zhu Y, Spellacy WN. Umbilical cord nucleated red blood cell

counts: normal values and the effect of labor. J Perinatol 2006;26(2):89-92. 8. Ghosh B, Mittal S, Kumar S, Dadhwal V. Prediction of perinatal asphyxia with nucleated red blood cells in cord blood of newborns. Int J Gynaecol Obstet 2003;81(3):267-71. 9. Hermansen MC. Nucleated red blood cells in the fetus and newborn. Arch Dis Child Fetal Neonatal Ed 2001;84(3): F211-F215. 10. Saraçoglu F, Sahin I, Eser E, Göl K, Türkkani B. Nucleated red blood cells as a marker in acute and chronic fetal asphyxia. Int J Gynaecol Obstet 2000;71(2):113-8. 11. Naeye RL, Localio AR. Determining the time before birth when ischemia and hypoxemia initiated cerebral palsy. Obstet Gynecol 1995;86(5):713-9. 12. Phelan JP, Korst LM, Ahn MO, Martin GI. Neonatal nucleated red blood cell and lymphocyte counts in fetal brain injury. Obstet Gynecol 1998;91(4):485-9. 13. Thilaganathan B, Athanasiou S, Ozmen S, Creighton S, Watson NR, Nicolaides KH. Umbilical cord blood erythroblast count as an index of intrauterine hypoxia. Arch Dis Child Fetal Neonatal Ed 1994;70(3): F192-F194. 14. Sikarwar S, Gupta S. The correlation of clinical perinatal asphyxia with counts of NRBC/100 WBC in cord blood. Webmed Central Obstet Gynaecol 2011;2(1):WMC001511 15. Hanlon-Lundberg KM, Kirby RS. Nucleated red blood cells as a marker of acidemia in term neonates. Am J Obstet Gynecol 1999;181(1):196-201. 16. Boskabadi H, Maamouri G, Sadeghian MH, GhayourMobarhan M, Heidarzade M, Shakeri MT, et al. Early diagnosis of perinatal asphyxia by nucleated red blood cell count: a case-control study. Arch Iran Med 2010;13(4):275-81. 17. Ferns SJ, Bhat BV, Basu D. Value of nucleated red blood cells in predicting severity and outcome of perinatal asphyxia. Indian J Pathol Microbiol 2004;47(4):503-5.

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Flu in Children

The classical features of uncomplicated flu in children include abrupt onset of fever, headache, muscle pain and malaise affected by manifestation of respiratory tract illness – sore throat, sough and nasal discharge. All the above features may not be present in children. Flu sometimes may last for more than a week in children. Ear discharge, development into asthma and pneumonia are common complications in children. Complicated pneumonia may be severe and rapidly fatal, especially if the bacterium is Staph. During winter,flu should be considered in all children with fever; children with fever and acute onset of respiratory illness; children with fever and exhilaration of underlying chest condition; children with pneumonia and children with fever of more than 100, with severe cough or sore throat. Fever is present in over 95% of cases, often more than 39oC. Cough is present in over 77% patients. Nasal discharge is present in more than 78% patients. Headache is present in more than 26% patients. Muscle pain is present in more than 71 % patients. Incubation period is 1–4 days with high transmissibility. The treatment is often symptomatic. Cough hygiene should be practiced.

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Surgery

Omental Torsion: A Review of Literature and Case Report Y Ghosh, R Arora

Abstract Eitel first described omental torsion in 1899. Omental torsion is rarely diagnosed preoperatively, knowledge of this pathology is important to the surgeon as it mimics common acute surgical abdomen. For this reason in the absence of diagnosed preexisting abdominal pathology including cyst, tumors, foci of intra-abdominal inflammation, postsurgical wounds or scarring and hernia sacs, omental torsion can present a surprise. Exploratory laparotomy represents the diagnostic and definitive therapeutic procedure, presently laparoscopy is the first choice procedure.

Keywords: Omental torsion, exploratory laparotomy, acute surgical abdomen

mental torsion is a condition in which a pedicle of the omental apron twists on its longer axis to such an extent that its vascularity is comprised. Eitel in 1899, first reported a case of omental torsion unassociated with hernia.1 Since that time many reports have appeared in the literature notably by Morris in which 164 cases of torsion of the omentum were gathered from 1905 to 1930.2 Primary omental torsion occurs when a mobile, thickened segment of omentum rotates around a proximal fixed point in the absence of any associated or secondary intra-abdominal pathology. Morris reported that, though omental torsion can occur at any age, it is mainly seen in the age group of 30 and 50 years with males predominance.3 Secondary omental torsion occurs due to underlying pathology. Morris, Adams,3 Barcia and Nelson4 emphasized that hernias of the right inguinal variety were scrotal type, of long duration, easily reducible and that they almost invariably contained omentum. In this condition, patients suffering from recurring pain may have temporary twists of the omentum. The omental ball and the omental fibrotic thickenings occasionally found, result from these recurring attacks of incomplete omental torsion. A certain number of omental torsion are caused by inflammatory foci within the abdominal cavity, which produces an inflammation by contiguity in the neighboring omentum. This may be true in cases of mild or subsiding appendicitis or cholecystitis

Punjab Institute of Medical Sciences, Jalandhar, Punjab Address for correspondence Dr Y Ghosh Punjab Institute of Medical Sciences, Jalandhar, Punjab

in which the original focus subsides but the changes induced in the omentum remain. In conclusion, primary omental torsion is unipolar when the proximal omentum remains fixed and the rest is free. Secondary omental torsion is bipolar due to fixation of omentum both proximally to the colon and distally, subsequently to adhesions for pathological conditions. CASE REPORT A 37-year-old gentleman presented with pain in the right iliac region for the last 3 days with worsening of pain 2 hours prior to presentation. There was history of associated nausea and vomiting, with no history of obstipation or constipation. On examination, he was conscious, oriented to time, place and person with a pulse rate of 110/minute and blood pressure of 110/90 mmHg. On abdominal examination, he had tenderness in the right iliac fossa with guarding and rigidity and rebound tenderness. Rovsingâ&#x20AC;&#x2122;s sign and Blumberg sign were positive and a working diagnosis of appendicitis was made. During ultrasound, probe tenderness was present, appendix was not visualized but fat was seen to be extending to the abdominal wall. Routine investigations showed a normal hemogram with a total leukocyte count of 9,000 and polys 70%, rest of the investigations were within normal range. A differential diagnosis of acute appendicitis, Meckelâ&#x20AC;&#x2122;s diverticulitis was made and the patient was shifted to OT. Under general anesthesia, a laparoscopic examination was carried out which revealed a normal appendix; the small and the large bowels and the pelvic organs were healthy; the omentum was found to be twisted on its self and fixed to the posterior abdominal wall.

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Surgery The omental ball was suspended on its pedicle, which was twisted on its axis. The part of the omentum which was attached to the abdominal wall was separated and the twisted part of the omentum was resected. Our patient had uneventful recovery and was discharged on the 3rd post-op day. Histology showed omental pedicle of 10 × 10 × 6 cm with cyanotic look. Microscopy showed hemorrhagic infarction and fat necrosis. DISCUSSION Omental torsion is a rare pathological condition, which presents with generic symptoms and mimics acute abdominal conditions such as appendicitis, acute diverticulitis and Meckel’s diverticulum. The predisposing factors for this condition are recognized anatomical anomalies like presence of tongue like projections in the omentum, bifid and accessory omentum, anomalous vascular blood supply and other vascular anomalies that modify the weight of omentum, vascular kinking and irregular omental pad seen mostly in obese patients.5 Secondary omental torsion is more common as compared to primary omental torsion and is associated with pre-existing abdominal pathologies including cysts, tumors, foci of intra-abdominal inflammations6,7 and surgical wounds or scarring and hernial sacs.6 The omentum twists in a clockwise direction, with engorgement of the tortuous veins that are easily compressed. This compromises the venous return and the distal omentum becomes congested and edematous. Recovery may follow or the process may go on. Resultant hemorrhagic extravasation creates a characteristic serosanguineous fluid inside the great omentum and abdominal cavity. As the torsion progresses, arterial occlusion leads to acute hemorrhagic infarction and eventual necrosis of the omentum.8 Furthermore, omental infarction can occur without torsion due to hypercoaguable state or vascular abnormalities predisposing to thrombosis.8 The diagnosis of omental torsion is a difficult one and is seldom made before surgery. Ultrasound and CT scan are helpful in clinching the diagnosis; usual ultrasound findings are evaluated as normal. Sometimes,

ultrasound may show complex mass or a mixture of solid material and hypoechoic zones. CT scan is an effective procedure in diagnosis of acute abdominal torsion.7,8 Omental torsion is usually diagnosed on exploratory laparotomy that represents both diagnostic and therapeutic modality. Thus, laparoscopy is the first choice of procedure for diagnosis and treatment. CONCLUSION Omental torsion is a rare pathological condition, which mimics many acute abdominal conditions. The pathogenesis of omental torsion has not been established. The symptoms and laboratory findings are not specific and they mimic other pathological conditions. The differentiation helpful between primary torsion and secondary torsion is difficult to make and is seldom made before surgical operations. Both ultrasound and CT scan are. Laparoscopy, nowadays, is the first choice procedure for diagnosis and treatment of acute abdominal torsion. References 1. Eitel GG. Rare omental torsion. NY Med Rec 1899;55:715-6. 2. Moris JH. Torsion of the omentum: Its clinical importance. Arch Surg 1932;24(1):40-76. 3. Adams JT. Primary torsion of the omentum. Am J Surg 1973;126(1):102-5. 4. Barcia PJ, Nelson TG. Primary segmental infarction of the omentum with and without torsion. Am J Surg 1973;126(3):328-31. 5. Young TH, Lee HS, Tang HS. Primary torsion of the greater omentum. Int Surg 2004;89(2):72-5. 6. Maeda T, Mori H, Cyujo M, Kikuchi N, Hori Y, Takaki H. CT and MR findings of torsion of greater omentum: a case report. Abdom Imaging 1997;22(1):45-6. 7. Sasmal PK, Tantia O, Patle N, Khanna S. Omental torsion and infarction: a diagnostic dilemma and its laparoscopic management. J Laparoendosc Adv Surg Tech A 2010;20(3): 225-9. 8. Andreuccetti J, Ceribelli C, Manto O, Chiaretti M, Negro P, Tuscano D. Primary omental torsion (POT): a review of literature and case report. World J Emerg Surg 2011;6:6.

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mediLAW

Acid Throwing: A Cause of Concern in India DS Bhullar

cid throwing, date and gang rape, sexual violence at workplace, female feticide and forced abortion, honor killing, bride burning and dowry death are a few crimes against women attracting national and international attention and focus of the modern world.

impaired vision and physical handicap. This negatively impacts their economic viability, causing hardships on the families/spouses that care for them. Moreover, acid survivors who are single when attacked almost certainly become ostracized from society, effectively ruining marriage prospects.

Acid throwing, also called an acid attack or Vitriolage, is a form of violent assault defined as the act of throwing acid or a similarly corrosive substance onto the body of another “with the intention to disfigure, maim, torture or kill.” Perpetrators of these attacks throw acid at their victims, usually at their faces, burning them and damaging skin tissue, often exposing and sometimes dissolving the bones. The long-term consequences of the attacks may include blindness, as well as permanent scarring of the face and body along with far-reaching social, psychological and economic difficulties. According to researchers and activists, countries typically associated with acid assault include Bangladesh, India, Pakistan, Cambodia, Vietnam, Laos, Hong Kong China, the United Kingdom, Kenya, South Africa, Uganda and Ethiopia.

Women are at an increased risk of acid violence in certain countries, such as Bangladesh and India. Another factor that puts victims at increased risk for an acid assault is their socioeconomic status, as those living in poverty are more likely to be attacked. Additionally, all three nations with the most noted incidence of acid attacks; Bangladesh, India and Cambodia - are ranked 93rd, 114th and 104th, respectively, out of 134 countries on the Global Gender Gap Index, a scale that measures equality in opportunities between men and women in nations.

The most notable effect of an acid attack is the lifelong bodily disfigurement. Consequently, the victim is faced with physical challenges, which require long-term surgical treatment. Acid assault survivors also face many mental health issues upon recovery like anxiety, depression, lowered self-esteem and increased selfconsciousness, both in general and in the social sphere. Many social implications exist for acid survivors especially women, like such attacks usually leave victims handicapped in some way, rendering them dependent on either their spouse or family for everyday activities, such as eating and running errands. These dependencies are increased by the fact that many acid survivors are not able to find suitable work, due to

Editor-in-Chief, Journal of PAFMAT Dept. of Forensic Medicine and Toxicology Government Medical College, Punjab

Acid attacks are often referred to as a ‘crime of passion,’ fueled by jealousy and revenge. Actual cases though, show that they are usually the result of rage at a woman who dares to refuse the advances of a male. One study showed that refusal of marriage proposals accounted for 55% of acid assaults, with abuse from husband/ family member (18%), property disputes (11%) and refusal of sexual or romantic advances (2%) as other leading causes. Additionally, the use of acid attacks in dowry arguments has been reported in Bangladesh with 15% of cases studied by the Acid Survivors Foundation citing dowry disputes as the motive. The chemical agents most commonly used to commit these attacks are hydrochloric acid and sulfuric acid. India is the fourth most dangerous place in the world for women to live in as women belonging to any class, caste or creed and religion can be victims of this cruel form of violence and disfigurement, a premeditated crime intended to kill or maim her permanently and act as a lesson to “put her in her place”. In India, acid attacks on women who dared to refuse a man’s proposal of marriage or asked for a divorce are a form of revenge. The number of acid attacks has been rising in India. There are no official figures available but it

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mediLAW is estimated that here are, 1,000 acid attacks a year in India. India’s incidence rate of chemical assault has been increasing in the past decade, with a high 27 reported cases in 2010. Altogether, from January 2002 to October 2010, 153 cases of acid assault were reported in Indian print media, while 174 judicial cases were reported for the year of 2000. However, scholars think that this is an underestimation, given that not all attacks are reported in the news, nor do all victims report the crime to officials. Motivation for acid attacks in India mirrors those in Bangladesh. Thirty-four of the analyzed by print media in India cited rejection of marriage or refusal by women of sexual advances as the cause of the attack and dowry disagreements have been shown to spur acid attacks. Land, property and/or business disputes accounted for 20% of acid assaults in India from 2002 to 2010.

categorize acid as poison. ÂÂ The Court said anyone under the age of 18 will

not be able to purchase acids like hydrochloric, sulfuric and nitric.

ÂÂ Shops will have to keep details like the quantity

sold and the addresses of buyers, who will need to present photo identification to purchase acids.

ÂÂ ‘Over the counter’ sale of acid is completely

prohibited unless the seller maintains a log/ register recording the sale of acid, the Supreme Court said.

ÂÂ Retailers will have to declare the amount of acid

being stocked to the Police, the Court said. Failure to do so would lead to undeclared stock being confiscated and a fine of up to 50,000 rupees.

ÂÂ In its order, the Supreme Court said that acid

attacks become a non-bailable offence and said survivors should receive 3,00,000 rupees in compensation, a third of which must be given within 15 days of the attack.

Legislation in India India’s top court has ruled that authorities must regulate the sale of acid used by jilted boyfriends and others to attack women. The Supreme Court’s ruling on July 16, 2013 comes after a particularly notorious incident in which four sisters suffered severe burns after being attacked with acid by two men on a motorbike. ÂÂ The Supreme Court has directed the states and

union territories to issue licenses to retailers selling acid after the government said it will

Following the gang rape of a 23-year-old student on a bus in Delhi late last year, India’s Parliament approved a bill strengthening laws on assaults against women. Acid attacks were included in the bill and made a criminal offence with a minimum 10-year prison term. The doctors dealing with acid attack victims have a professional, ethical, legal and social obligation to treat and respect the physical, mental, social and psychological feelings of these patients.

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emedinews inspiration

An Inspirational Story about Faith

n the abyss between life and death resides only faith. Experts call this abyss ‘Motherhood.’

Lying on a cold, hard bed only 6 months along with my first child, I faced the frightening implications of this truth. My body shook uncontrollably as abject terror clutched at me. My only lifeline was my husband’s hand clutching mine over the abyss as love for life- mine and the tiny, still-unseen child’s-burned deep in our hearts. One after another after another the nurses piled the bloody sheets into the corner until the doctor pronounced those fateful words, “The baby’s coming.” Only then, with control slipping past me into a haze of drugs and fear, did I make that one, final leap - the leap from control to faith - the leap from childlessness into motherhood. My next recollection was my husband’s hand once again holding mine as he said the words that officially changed my life, “We have a little girl.” The images of the next 2 months blurred together as ups and downs alternated at break-neck speed. One minute spent holding my two-pound and yet weightless daughter in my arms versus the next 3 weeks spent holding only tiny fingers through the isolate windowwaiting for the next opportunity to take my baby out of the incubator again. The drugs, powerful enough to keep her safe from infection, again and again blew through her small veins while all I could do was watch, pray and hang onto the faith that somehow we would get through this. If we could just make it to the next horizon, through the next transfusion and the next round of drugs, then I could live again. Until then survival was my only goal. In the darkness of a soul in crisis, my prayers became much deeper. No longer were they for selfish requests. Now they were centered wholly on the tiny baby God had entrusted to my care. The Lord has said, “Cast your burden upon the Lord, and He shall sustain you” (Psalms 55:22), and during those long days, that was what kept me going. As good as that sounds, however, reality was that my only real positives at the time were formed by the negatives. “It’s not pneumonia.” “It’s not an infection.”

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“We won’t have to put the IV in her head-this time.” The struggle to live was being waged not only by the tiny baby lying helplessly in the incubator, but by her mother’s spirit as well. Fear laced every call to the hospital, every question, every conversation. But always the faith remained. Somehow we would make it. Somehow God sustained me somehow. Then in one faltered heartbeat the negatives became negatives again, and I faced a test of faith more terrifying than my own journey through the abyss - my baby’s journey to the edge of the River Jordan. All her veins had been blown, and a new IV would have to go in her head-all the other options had been exhausted. In utter desperation my husband and I left the hospital, and on a rain-soaked highway with the amber glow of the streetlights flashing above me, I reached a place that I never even knew existed-the place where faith no longer resides. “Why?” I asked the darkness around me. “Why?” But God has promised, “I will never leave you, nor forsake you” (Hebrews 13:5), and I am here to tell you, He does send messengers to help when you ask. Truth is, mine was sitting right by my side-exactly where he had been through the whole ordeal. Slowly my husband reached over, took my hand, and spoke the words that I would cling to not only for this one night but for the rest of eternity. “She’s going to be okay. You’ve just got to have faith.” Every day for the next 5 years that faith has been tested over and over again. Every time I let my baby-big girl, now-off at play school. Every time my second daughter lets go of my hand and walks off on her own. Every time one child or the other screams in pain or in fear at 2 o’clock in the morning-the words come back to me, “She’s going to be okay. You’ve just got to have faith.” In the days to come, the phrase will only become more powerful. During the long nights when the girls fail to call and on the days when they experience their own grieve, the words will be there to help me through. Time and again as I hold my children for one brief moment and then release them into the abyss, the words will be there. Through school, best friends, boyfriends, first dates, first heartbreaks, in partnership with God and my

emedinews inspiration husband, I will remain the rock on which these two girls can build their lives. Until someday in some beautiful sunlit church, I will watch from a front pew as they stand before God and pledge themselves to another forever. Then as they turn, kiss me and walk away into their own lives, the words will again be there. “She’s going to be okay. You’ve just got to have faith.”

In some darkened room on another cold, hard bed I will step toward the abyss to make my final journey home. However, this time I will have not one but three sets of hands to hold onto. Then, looking up into the eyes of the two beautiful women my daughters have become, the sadness at our imminent parting will be there, but a greater understanding will hold me also.

The day will come of course when the abyss will stretch before me again “when Christ, who is our life, shall appear, then shall you also appear with Him in glory” (Colossians 3:4).

Beyond a doubt, I know that as I slip from the darkness of this world into the light... beyond, I will hear that voice one more time: “They’re going to be okay. You’ve just got to have faith.”

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eMedi Quiz

Quiz Time 1.

The extent to which ionization of a drug takes place is dependent upon pKa of the drug and the pH of the solution in which the drug is dissolved. Which of the following statements is not correct:

pKa of a drug is the pH at which the drug is 50% ionized.

Lung cancer

B. Small changes of pH near the pKa of a weak acidic drug will not affect its degree of ionization.

Hodgkin’s lymphoma

Superior vena caval obstruction

A vitreous aspirate has been collected in an emergency at 9 pm what advice you like to give to the staff on duty regarding the overnight storage of the sample.

Knowledge of pKa of a drug is useful in predicting its behavior in various body fluids.

A 60-year-old male presented to the emergency with breathlessness, facial swelling and dilated veins on the chest wall. The most common cause is:

A. Thymoma

D. Phenobarbitone with a pKa of 7.2 is largely ionized at acid pH and will be about 40% nonionized in plasma.

A. The sample should be kept at 4°C.

High resolution computed tomography of the chest is the ideal modality for evaluating:

B.`

The sample should be incubated at 37°C.

Pleural effusion

The sample should be refrigerated deep freezer.

Interstitial lung disease

Lung mass

The sample should be refrigerated for the initial 3 hours and then incubated at 37°C.

Mediastinal adenopathy

Which one of the following is a recognized X-ray feature of rheumatoid arthritis?

A 20-year-old man complains of difficulty in reading the newspaper with his right eye. Three weeks after sustaining a gunshot injury to his left eye. The most likely diagnosis is:

A. Juxta-articular osteosclerosis

A. Macular edema

B. Sacroilitis

Sympathetic ophthalmia

Bone erosions

Optic nerve avulsion

Peri-articular calcification

Delayed vitreous hemorrhage

Answers to eMedi Quiz Published in February 2014 Issue Q1. D. Calcaneum Q2. C. Hemophilia Q3. D. Clostridium perfringens infection Q4. B. Bilateral cordectomy Q5. B. Oral rehydration therapy Q6. D. 0%

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.

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lighter reading

A Buddhist monk approaches a hot dog stand and says, “Make me one with everything.” The vendor has heard this one before, and without a word he simply makes the hot dog and hands it to the Buddhist monk, who pays with a $20 bill. The vendor puts the bill in the cash box and closes it. “Excuse me, but where’s my change?” asks the Buddhist monk. The vendor replies, “Change must come from within.” Communication Technician A communication technician drafted by the army was at a firing range. At the range, he was given some instructions, a rifle and 50 rounds. He fired several shots at the target. The report came from the target area that all attempts had completely missed the target. The technician looked at his weapon, and then at the target. He looked at the weapon again, and then at the target again. He then put his finger over the end of the rifle barrel and squeezed the trigger with his other hand. The end of his finger was blown off, whereupon he yelled toward the target area: “It’s leaving here just fine, the trouble must be at your end!”

“Take the attitude of a student, never be too big to ask questions, never know too much to learn something new.” −Og Mandino

Make Sure

During Medical Practice A patient on amlodipine developed severe gum hypertrophy.

Oh my God! Why was amlodipine not stopped?

©IJCP Academy

The Hot Dog Vendor

Quote

LAUGH-A-WHILE

Lighter Side of Medicine

Make sure that all patients on amlodipine are watched for gum hypertrophy as its side effect.

Dr. Good and Dr. Bad

KK Aggarwal

Situation: A patient with CKD wanted to know whether he can take calcium or not?

You can take

©IJCP Academy

you cannot take

ILLUSION

Lesson: In CKD, patient can have decreased calcium, increased phosphate or both. If the calcium is low, then this patient requires calcium supplementation.

KK Aggarwal

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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). –

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.

–

All pages should be numbered consecutively beginning with the title page.

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. – Ethical guidelines followed by the investigations should be described. 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). – Method of allocating the subjects into different groups. – 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.

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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.

Figures – Two complete sets of glossy prints of high quality should be submitted. The labelling must be clear and neat. – All photomicrographs should indicate the magnification of the print. – Special features should be indicated by arrows or letters which contrast with the background. – The back of each illustration should bear the first author’s last name, figure number and an arrow indicating the top. This should be written lightly in pencil only. Please do not use a hard pencil, ball point or felt pen. – Color illustrations will be accepted if they make a contribution to the understanding of the article. –

Do not use clips/staples on photographs and artwork.

–

Illustrations must be drawn neatly by an artist and photographs must be sent on glossy paper. No captions should be written directly on the photographs or illustration. Legends to all photographs and illustrations should be typed on a separate sheet of paper. All illustrations and figures must be referred to in the text and abbreviated as “Fig.”.

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

5. Special requests _____________________________

Stansfield AG. Lymph Node Biopsy Interpretation Churchill Livingstone, New York 1985.

6. Suggestions for reviewers (name and postal address)

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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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. 10, March 2014

Indian 1.____________Foreign 1.________________

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

Indian Journal of Clinical Practice, Vol. 24, No. 10, March 2014

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R.N.I. No. 50798/90 Date of Publication 13th of Same Month Date of Posting 13-14 Same Month

POSTAL REGISTRATION NO. DL (S)-01/3200/2012-2014 Posted in N.D. PSO New Delhi