Indian Journal of Clinical Practice May 2016

Indexed with IndMED

ISSN 0971-0876

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Volume 26, Number 12

May 2016, Pages 1101–1200

Peer Reviewed Journal

yy American Family Physician yy Cardiology yy Community Medicine yy Drugs yy ENT yy Gastroenterology yy Internal Medicine yy Obstetrics and Gynecology

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Volume 26, Number 12, May 2016 FROM THE DESK OF THE GROUP EDITOR-IN-CHIEF

1105 ACP Calls Upon Physicians to Combat Health Problems Associated with Climate Change

KK Aggarwal

AMERICAN FAMILY PHYSICIAN

1106 Evaluation of the Solitary Pulmonary Nodule

George E. Kikano, Andre Fabien, Robert Schilz

1112 Practice Guidelines 1113 Photo Quiz CARDIOLOGY

1117 A Case of Brucellosis Presented as Pericarditis: Rare Presentation

Sneha Vadhvana, Manish N Mehta, Aniket Bhardwaj

COMMUNITY MEDICINE

1119 Filling and Refilling: The Melancholy of Malaria Since Independence in India

Amitabha Sarkar, Sandip Ghosh

DRUGS

1126 Amitriptyline-induced Edema: A Case Report

Bhaghya Prasad, K Harikrishnan, Anjaly S, Maria C Kuriakose, Naresh Kumar V

ENT

1128 Clinicopathologic Study of Goiters in Warri, Nigeria

Afeyodion Akhator, CP Oside, E Ijomone

GASTROENTEROLOGY

1132 To Study the Correlation Between SAAG and Platelet Count/Spleen Size Ratio for Prediction of Esophageal Varices in CLD Patients

Javed Sayyed, Deepti Sharma, SR Meena, Sanket Singh, Pallavi Vij, Mukesh Verma

INTERNAL MEDICINE

1138 Prevalence of Microalbuminuria in Patients of HIV/AIDS and Its Correlation with CD4 Cell Count and the Duration of Ιllness

S Santheev, Lubna Zafar, Anjum Parvez, HS Khan

1143 Erythema Nodosum in Tuberculosis: Contemporaries or Causation

Shyamala G, Sunil Kumar N, Swathi BS, Mahesh Menon, Hemantha Kumar

OBSTETRICS AND GYNECOLOGY

1146 Prophylactic Preoperative Use of Rectal Misoprostol versus Intravenous Oxytocin Infusion During Cesarean Section to Reduce Intraoperative and Postoperative Blood Loss

Rekha Rani, Shikha Singh, Saroj Singh, Urvashi Verma, Ruchika Garg, Rachana Agrawal, Latica

OBSTETRICS AND GYNECOLOGY

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

1153 Intraperitoneal Bladder Injury During Tubectomy: A Conservative Approach

Shaveta Jain, Roopa Malik, Smiti Nanda, Nitin Jain

1156 Pelvic Hematoma Mimicking Ovarian Malignancy

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

Shreyasi Bid, Sambhu Nath Bandyopadhyay, Chandan Sasmal

1159 Programmed Labor and Its Effect on Labor Outcome

Copyright 2016 IJCP Publications Ltd. All rights reserved.

Ruchika Garg, Urvashi Verma, Soniya Dhiman, Mohita Agrawal, Meenal Jain

PSYCHIATRY

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.

1163 Mental Health in Children: An Overview

Krishan Kumar, Rajeev Dogra, Brij Lata Kotia

VENEREOLOGY

1176 Oral Tertiary Syphilis: A Case Report

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Deepa MS, Anita Balan, S Sunil, Bifi Joy

MEDILAW

1179 Not Practising Accepted Protocols While Examining a Patient CONFERENCE PROCEEDINGS 1182 60th Annual Conference of the Indian Orthopaedic Association (IOACON 2015) 1185 62nd Annual Conference of Cardiological Society of India (CSI 2016) 1188 India Live 2016 AROUND THE GLOBE

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Prof. Dr KK Aggarwal

Group Editor-in-Chief IJCP Group, eMedinewS and eMediNexus

ACP Calls Upon Physicians to Combat Health Problems Associated with Climate Change

T

he changing climate is one of the most important environmental concerns today.

Climate change directly affects five components of the environment: Water, air, weather, oceans and ecosystems. And, through changes in the environment such as heat waves, droughts, storms, worsening air quality, floods, etc. it also adversely affects human health.

With rise in temperatures, vector-borne diseases such as dengue are increasing in number making them more difficult and challenging to control. What is more, climate change may potentially spread the disease to areas that are currently not endemic for the disease.

The relationship between climate and human health has for long been a much studied topic. A report published in April 2010 by National Institute of Environmental Health Science, USA “A Human Health Perspective on Climate Change: A Report Outlining the Research Needs on the Human Health Effects of Climate Change” categorized health consequences of climate change into: ÂÂ

Asthma, respiratory allergies and airway diseases

ÂÂ

Cancer

ÂÂ

Cardiovascular disease and stroke

ÂÂ

Foodborne diseases and nutrition

ÂÂ

Heat-related morbidity and mortality

ÂÂ

Human developmental effects

ÂÂ

Mental health and stress-related disorders

ÂÂ

Neurological diseases and disorders

ÂÂ

Vector-borne and zoonotic diseases

ÂÂ

Water-borne diseases

ÂÂ

Weather-related morbidity and mortality.

In a position paper published online April 19 in the Annals of Internal Medicine, the American College of Physicians (ACP) has focused on the consequences of climate change on human health including more respiratory and heat-related illness, vector-borne diseases, water-borne diseases, food and water insecurity, malnutrition, behavioral health problems.

ACP has called for urgent "aggressive, concerted" action to fight climate change to counter the “devastating” health consequences.

The position paper emphasizes the crucial role that physicians can play in tackling them by educating themselves, their patients, community, policy makers about the adverse health effects of climate change and also support efforts to alleviate them.

The ACP also recommends that medical schools and continuing medical education (CME) providers include climate change-related coursework in their syllabus.

■■■■

Indian Journal of Clinical Practice, Vol. 26, No. 12, May 2016

1105

AMERICAN FAMILY PHYSICIAN

Evaluation of the Solitary Pulmonary Nodule GEORGE E. KIKANO, ANDRE FABIEN, ROBERT SCHILZ

ABSTRACT A solitary pulmonary nodule is a common radiologic finding that is often discovered incidentally and may require significant workup to establish a definitive diagnosis. A solitary pulmonary nodule is a well-circumscribed round lesion measuring up to 3 cm in diameter and surrounded by aerated lung. Once a nodule is discovered, clinical and radiologic features and quantitative models can be used to determine the likelihood of malignancy. Evaluation is guided by nodule size and assessment of probability of malignancy. Surgical resection or nonsurgical biopsy should be performed in patients with solid or subsolid solitary pulmonary nodules that show clear growth on serial imaging. Solid solitary pulmonary nodules that have been stable for at least two years typically do not need further evaluation. The workup for patients with solid solitary pulmonary nodules measuring 8 mm or greater in diameter, nodules measuring less than 8 mm in diameter, and subsolid nodules should be guided by the probability of malignancy, imaging results, and the risks and benefits of different management strategies. Management should be individual­ized according to patient values and preferences. Medicare now covers lung cancer screening with low-dose computed tomography for high-risk patients 55 to 77 years of age at institutions that can provide a comprehensive approach to the management of solitary pulmonary nodules.

Keywords: Solitary pulmonary nodule, malignancy, surgical resection, nonsurgical biopsy, low-dose computed tomography

T

he identification of solitary pul­monary nodules has become more common in the United States because of the increased use of computed tomography (CT). The incidence of cancer in patients with solitary pulmo­ nary nodules ranges from 10% to 70%.1 Recent U.S. Preventive Services Task Force recommendations for lung cancer screen­ing with CT will likely further increase the detection of solitary pulmonary nodules.2 Therefore, it is important that clinicians become familiar with evaluating and managing these nodules.

DEFINITIONS A solitary pulmonary nodule is defined as a single, well-circumscribed, radiologic opac­ity that measures up to 3 cm in diameter and is surrounded completely by aerated lung.1,3 Focal pulmonary lesions that are greater than 3 cm in diameter are called lung masses

GEORGE E. KIKANO, MD, is dean of the Central Michigan University College of Medicine in Mount Pleasant.

ANDRE FABIEN, MD, is chief fellow in the Division of Pul­monary, Critical Care, and Sleep Medicine at Case Western Reserve University School of Medicine in Cleveland, Ohio.

ROBERT SCHILZ, DO, PhD, is an associate professor in the Division of Pulmonary, Critical Care, and Sleep Medicine at Case Western Reserve University School of Medicine.

Source: Adapted from Am Fam Physician. 2015;92(12):1084-1091.

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Indian Journal of Clinical Practice, Vol. 26, No. 12, May 2016

and should be considered malignant until proven otherwise. In cancer screening trials of smokers at increased risk of malignancy, the prevalence of solitary pulmonary nodules ranged from 8% to 51%.4,5 The increased use of CT can also lead to the discovery of multiple or diffuse nodules. This is arbitrarily defined in the 2013 Ameri­ can College of Chest Physicians (ACCP) guidelines as patients with more than 10 nodules.6 Although diffuse nodules are more likely to cause symptoms, they rarely repre­sent a primary lung malignancy.

Characterization of Nodules The risk of malignancy rises with increasing nodule size (maximum diameter). Approxi­mately 80% of nodules greater than 20 mm are malignant, whereas only 1% of nodules between 2 and 5 mm are malignant.7,8 Malignant solid nodules typically have a doubling time within 400 days; therefore, experts agree that solid solitary pulmonary nodules that remain the same size over a two-year period are likely to be benign.6,9-11 Longer duration follow-up is advisable for groundglass nodules, which generally have a longer doubling time.

The risk of malignancy is also higher in spiculated lesions, in lesions with asym­metric calcification, and in lesions located in an upper lobe.8 In contrast, nodules

AMERICAN FAMILY PHYSICIAN with smooth borders and a central or concentric pattern of calcification are more likely to be benign (Figure 1).

Nodules can be clas­sified as solid or subsolid. Solid nodules are more common, but subsolid nodules have a higher likelihood of malignancy.12 Subsolid nodules can be further characterized into pure ground-glass or part-solid in nature. Part-solid nodules include a combination of ground-glass and solid components, the lat­ter obscuring lung architecture.13 DIFFERENTIAL DIAGNOSIS Causes of solitary pulmonary nodules can be categorized as benign or malig­ nant (Table 11,6). The estimated prevalence of each etiology varies among different populations. Even among screening stud­ies of smokers who are at increased risk of malignancy, the number of malignant nod­ules is small. Among 12,029 Table 1. Etiologies of Solitary Pulmonary Nodules Benign

Malignant

Infectious granuloma (80%)

Adenocarcinoma (60%) Squamous cell carcinoma (20%)

Atypical mycobacteria Coccidioidomycosis

Solitary metastasis (10%)

Histoplasmosis

Breast

Tuberculosis

Colon

Hamartoma (10%)

Kidney

Arteriovenous malformation (rare)

Small cell carcinoma (4%) Carcinoid tumor (rare)

Intrapulmonary lymph node (rare)

Extranodal lymphoma (rare)

Sarcoidosis (rare) Information from references 1 and 6.

nodules found in a large Canadian study, only 144 (1%) were malignant.8 INITIAL EVALUATION The 2013 ACCP guidelines for the evaluation of the solitary pulmonary nodule recom­ mend basing the assessment on nodule size and probability lines also address risk of malignancy.6 The guide­ stratification, choice of imaging modality, and frequency of imag­ing follow-up. Guidelines from the American College of Radiology address imaging modalities but not frequency of follow-up.14 This review focuses primarily on the ACCP guidelines.

Risk Assessment The probability of malignancy can be assessed clinically or by quantitative predic­ tive models as falling into one of three risk categories: very low probability (less than 5%), low/moderate probability (5% to 65%), or high probability (greater than 65%). Many experienced physicians use clini­ cal judgment to estimate the probability of malignancy. Studies report modest to excel­lent agreement between quantitative predic­tion models and clinical judgment.15,16 Quantitative predictive models combine clinical and radiologic features to estimate malignancy potential.

The most commonly used model from the Mayo Clinic (eTable A) estimates the probability of malignancy using six independent predictors: smoking history, older age, history of extrathoracic cancer more than five years before nodule detec­tion, nodule diameter, spiculation presence, and upper lobe location.17 An online calcula­tor is available at http://reference.medscape. com/calculator/solitary-pulmonary-nodule-risk.

eTable A. Calculating the Malignancy Probability of a Pulmonary Nodule Predictor

Value

Age

Patient’s age in years

Cancer history

1 if patient has a history of extrathoracic cancer diagnosed more than five years before nodule detection (otherwise = 0)

Diameter

Diameter of the solitary pulmonary nodule in mm

Location

1 if nodule is located in the upper lobe (otherwise = 0)

Smoking history

1 if patient is a current or former smoker (otherwise = 0)

Spiculation

1 if spiculation is present (otherwise = 0)

Note: Probability of malignancy* = e /(1 + e ), where x = –6.8272 + (0.0391 × age) + (0.7917 × smoking history) + (1.3388 × cancer history) + (0.1274 × diameter) + (1.0407 × spicula­tion) + (0.7838 × location). An online calculator is available at http://reference.medscape.com/calculator/solitarypulmonary-nodule-risk. *e is the base of natural logarithms.

Information from Swensen SJ, Silverstein MD, Ilstrup DM, Schleck CD, Edell ES. The probability of malignancy in solitary pulmonary nodules.

Application to small radiologically indeterminate nodules. Arch Intern Med. 1997;157(8):849-855. x

x

Indian Journal of Clinical Practice, Vol. 26, No. 12, May 2016

1107

AMERICAN FAMILY PHYSICIAN Newer models validated for use in high-risk populations are based on data from the Pan-Canadian Early Detection of Lung Cancer screening study and the Veterans Affairs Cooperative study.8,18 Odds ratios for malignancy of solitary pulmonary nodules based on risk factors from the Mayo Clinic and Veterans Affairs models are provided in Table 2.17,18

Imaging Most solitary pulmonary nodules are inci­ dental findings on imaging studies of the chest, abdomen, and upper extremities. One study found that solitary pulmonary nodules were noted in 0.09% to 0.2% of radiographs.19 In a study on whole-body CT screening, solitary pulmonary nodules were found in almost 15% of asymptomatic participants.20 Occasionally, nodules as small as 5 to 6 mm can be visualized on chest radiography. Soli­tary pulmonary nodules can be followed with chest radiography, CT, or fluorodeoxyglucose positron emission tomography (FDG-PET). When a nodule is identified on imaging, it is important to secure old films for compari­son to evaluate whether a nodule is new, old, stable, or growing over time.

The imaging tools used to evaluate soli­tary pulmonary nodules include chest CT and functional imaging (usually FDG-PET). Chest CT, preferably with thin sec­tions, should be obtained in all patients with unclearly characterized solitary pulmonary nodules visible on chest radiography.6 Chest CT has a higher specificity and sensitivity than chest radiography and can provide spe­cific information about location, size, and attenuation characteristics of nodules.6 Con­trast enhancement is not typically required when imaging a solitary nodule. Chest CT is the imaging modality of choice for reevalu­ation of pulmonary nodules visible on chest radiography and for continued surveillance of nodules for change in size.6 Radiologic features such as size, border, density, calci­fication, and growth can be used to predict malignancy (Table 3).5,6 Functional imaging with FDG-PET can further distinguish between benign and malignant nodules because of the increased metabolic activity typically found in cancers. FDG avidity is measured by the standard­ized uptake value. The optimal cutoff for malignant nodules under all circumstances is unknown.

In most studies, a standardized uptake value greater than 2.5 is used to iden­tify nodules that have a high probability of malignancy.21

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Indian Journal of Clinical Practice, Vol. 26, No. 12, May 2016

Table 2. Odds Ratios for Malignancy of Solitary Pulmonary Nodules from Clinical Prediction Models Risk factor

Odds ratio

Veterans Affairs model (for nodules > 7 mm in diameter) Current or past smoking

7.9

Patient age (per 10-year increment)

2.2

Nodule diameter (per mm)

1.1

Time since quitting smoking (per 10-year increment)

0.6

Mayo Clinic model (for nodules > 4 mm in diameter) History of extrathoracic cancer

3.8

Spiculated morphology

2.8

Current or past smoking

2.2

Upper lung location

2.2

Nodule diameter (per mm)

1.1

Patient age (years)

1.0

Information from references 17 and 18.

Table 3. Radiologic Features Suggestive of Benign or Malignant Solitary Pulmonary Nodules Radiologic feature

Suggests benign nodule

Suggests malignant nodule

Border

Smooth

Irregular or spiculated

Calcification

Concentric, central, Typically noncalcified or or popcorn pattern eccentric calcification

Density

Solid

Nonsolid, ground-glass

Doubling time

Less than one month or more than one year

One month to one year

Size

< 5 mm

> 10 mm

Information from references 5 and 6.

FDG-PET is most cost-effective when the clinical pretest probability of malignancy and the results of the CT are discordant (e.g., low pretest probability with chest CT character­istics that are clearly not benign).22 The 2013 ACCP guidelines recommend FDG-PET in persons with solid indeterminate nodules 8 mm or greater in diameter, and a low to inter­mediate pretest probability of malignancy.6 FOLLOW-UP EVALUATIONS Management approaches to solitary pul­monary nodules vary and are often incon­sistent with guidelines.23 Options include surgical diagnosis, nonsurgical biopsy (e.g., transthoracic or endoscopic needle biopsy), and surveillance with serial CT. Treatment should

AMERICAN FAMILY PHYSICIAN be tailored to the patient and take into account the probability of malignancy and nodule characteristics.

Nodules in patients with adequate prior imaging should be assessed for growth or stability. A solid or subsolid nodule that has shown clear growth on serial imaging has a high likelihood of malignancy and should be further evalu­ated with resection or biopsy unless there are specific contraindications, such as severe pulmonary dysfunction or other risks for surgery or general anesthesia.6 Figure 2 illustrates a suggested approach for patients with a solid nodule 8 mm or greater in diameter in whom previous imaging is insufficient to document growth or stability.6 Very-low-probability nodules (less than 5%) can be followed by serial CT. Low/moderateprobability nodules (5% to 65%) should be evaluated with FDG-PET scans. Nodules that demonstrate moderate or intense uptake on FDG-PET should be biopsied or resected.

The optimal management of solid nodules measuring less than 8 mm remains uncer­tain. Small nodules are difficult to biopsy and not reliably characterized on FDG-PET scan. Given the relatively low prevalence of malignancy, the risks of surgical diagnosis usually outweigh the benefits; therefore, solid nodules that are less than 8 mm are usually followed with serial CT at intervals deter­mined by expert consensus24 (Figure 36).

Figure 4 illustrates suggested management strategies for pure ground-glass, part-solid, and multiple nodules.6,13 In general, a purely subsolid nodule greater than 5 mm should be reevaluated with a single CT scan at three months, and further management should be

determined by size or emergence of a solid component if the nodule persists at three months. Subsolid nodules have a greater like­lihood of being malignant, and management should be based on size of the nodule.13 It is important to align the intensity of diagnostic and therapeutic interventions for pulmonary nodules with the patient’s elic­ited values and preferences. For example, the preferences of a 75-year-old patient with life-limiting chronic obstructive pulmonary disease would likely be different from those of an otherwise healthy 35-year-old patient with a nodule.

The choice of sampling procedure varies according to the size and location of the nod­ule, the availability of the procedure, and local expertise. Endoscopic techniques are generally preferred for large, centrally located lesions, and transthoracic biopsy techniques are pre­ferred for more peripheral lesions. Surgical resection is the diagnostic standard for malig­ nant solitary pulmonary nodules and the pre­ferred procedure for nodules at high risk of malignancy (greater than 65% probability).6 SOLITARY PULMONARY NODULES DISCOVERED DURING LUNG CANCER SCREENING Based on the results of the National Lung Screening Trial,25 the U.S. Preventive Services Task Force currently recommends—and Medicare reimburses for—a shared decision-making visit and annual screening for lung cancer with low-dose CT in adults 55 to 77 years of age who have at least a 30-pack-year smoking history and currently smoke or have quit within the past

Management of Subsolid Pulmonary Nodules Subsolid pulmonary nodule

Solitary pure ground-glass nodule

≤ 5 mm No CT followup required

> 5 mm Initial follow-up at 3 months to confirm persistence; annual surveillance with chest CT for at least 3 years

Solitary part-solid nodule Initial follow-up CT at 3 months to confirm persistence

Multiple nodules Each nodule assessed individually for probability of malignancy; CT surveillance vs. biopsy accordingly

If persistent and solid component < 5 mm, then annual surveillance for three years; if persistent and solid component ≥ 5 mm, then referral for biopsy/surgical resection

Figure 4. Algorithm for the management of subsolid pulmonary nodules.

CT = Computed tomography.

Information from references 5, 6, and 13.

Indian Journal of Clinical Practice, Vol. 26, No. 12, May 2016

1109

AMERICAN FAMILY PHYSICIAN Recommendations for Reporting and Managing Lung Cancer Screening CT Screening low-dose chest CT

Negative

Benign appearance

No nodules and definitely benign nodules

Very low likelihood of malignant growth

No lung nodules or nodules with specific calcifications: complete, central, or popcorn

Solid: < 6 mm or new < 4 mm Part-solid: < 6 mm total diameter at baseline Ground-glass: < 20 mm or ≥ 20 mm and unchanged/slowly growing

Annual screening with low-dose CT in 12 months

Probably benign

Suspicious

Low likelihood of malignant growth Solid: ≥ 6 to < 8 mm at baseline or new 4 to < 6 mm Part-solid: ≥ 6 mm total diameter/solid component < 6 mm or < 6 mm total diameter Ground-glass: ≥ 20 mm on baseline CT or new

Findings prompt additional testing/tissue sampling

Solid: ≥ 8 to < 15 mm at baseline or growing < 8 mm or new 6 to < 8 mm Part-solid: ≥ 6 mm with solid component ≥ 6 mm to < 8 mm or with a new or growing < 4 mm solid component Endobronchial nodule

6-month low-dose CT

*Depending on probability of malignancy and patient comorbidities.

Solid: ≥ 15 mm or new or growing, and ≥ 8 mm Part-solid: < 6 mm total diameter at baseline Chest CT with or without contrast FDG-PET with or without biopsy*

3-month low-dose CT; FDG-PET when ≥ 8 mm solid component

Figure 5. Recommendations for reporting and managing lung cancer screening CT. CT = Computed tomography; FDG-PET = Fluorodeoxyglucose positron emission tomography.

Information from reference 27.

15 years.2,26 It is recommended that lung cancer screening be performed at institutions that can provide a comprehensive approach to the management of solitary pulmonary nodules.26

REFERENCES

In 2014, the American College of Radiol­ogy Lung Imaging Reporting and Data Sys­tem was released to standardize lung cancer screening CT reporting and management recommendations (Figure 5).27 Although the requirements for lung cancer screening differ slightly from previous recommendations on management of solitary pulmonary nodules, it is likely that the evaluation and follow-up recommendations will become the same.

2. Moyer VA. Screening for lung cancer: U.S. Preventive Services Task Force recommendation statement. Ann Intern Med. 2014;160(5):330-338.

INDICATIONS FOR REFERRAL Patients may be referred to a pulmonologist if they have lesions that may be biopsied by bronchoscopy or if the best management approach is unclear. Interventional radiologists and surgeons can biopsy lesions by fineneedle aspiration or video-assisted tho­ racoscopic surgery, among other techniques, depending on nodule characteristics, patient preferences, and patient comorbidities.

Note: For complete article visit: www.aafp.org/afp.

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1. Ost D, Fein AM, Feinsilver SH. Clinical practice. The solitary pulmonary nodule. N Engl J Med. 2003;348 (25):2535-2542.

3. Tuddenham WJ. Glossary of terms for thoracic radiol­ogy: recommendations of the Nomenclature Committee of the Fleischner Society. AJR Am J Roentgenol. 1984;143(3):509-517.

4. Gohagan J, Marcus P, Fagerstrom R, Pinsky P, Kramer B, Prorok P. Baseline findings of a randomized feasibility trial of lung cancer screening with spiral CT scan vs chest radiograph: the Lung Screening Study of the National Cancer Institute. Chest. 2004;126(1):114-121.

5. Swensen SJ, Jett JR, Hartman TE, et al. Lung cancer screening with CT: Mayo Clinic experience. Radiology.

2003;226(3):756-761.

6. Gould MK, Donington J, Lynch WR, et al. Evaluation of individuals with pulmonary nodules: when is it lung cancer? Diagnosis and management of lung cancer, 3rd ed: American College of Chest Physicians evidence-based clinical practice guidelines. Chest. 2013;143(5 suppl): e93S-e120S. 7. Gould MK, Fletcher J, Iannettoni MD, et al. Evaluation of patients with pulmonary nodules: when is it lung can­cer?

AMERICAN FAMILY PHYSICIAN ACCP evidence-based clinical practice guidelines (2nd edition). Chest. 2007;132(3 suppl):108S-130S. 8. McWilliams A, Tammemagi MC, Mayo JR, et al.

Probability of cancer in pulmonary nodules detected on first screening CT. N Engl J Med. 2013;369(10):910-919.

9. Wahidi MM, Govert JA, Goudar RK, et al. Evidence for the treatment of patients with pulmonary nodules: when is it lung cancer? ACCP evidence-based clini­cal practice guidelines (2nd edition). Chest. 2007;132 (3 suppl): 94S-107S. 10. Weiss W. Tumor doubling time and survival of men with bronchogenic carcinoma. Chest. 1974;65(1):3-8.

11. Nathan MH, Collins VP, Adams RA. Differentiation of benign and malignant pulmonary nodules by growth rate. Radiology. 1962;79:221-232.

12. Henschke CI, Yankelevitz DF, Mirtcheva R, McGuinness G, McCauley D, Miettinen OS; ELCAP Group. CT screening for lung cancer: frequency and significance of partsolid and nonsolid nodules. AJR Am J Roentgenol.

2002;178(5):1053-1057.

13. Naidich DP, Bankier AA, MacMahon H, et al.

Recommendations for the management of subsolid pulmonary nodules detected at CT: a statement from the Fleischner Society. Radiology. 2013;266(1):304-317.

14. American College of Radiology ACR Appropriateness Cri­teria. Solitary pulmonary nodule. http://www.acr. org/~/media/ACR/Documents/AppCriteria/Diagnostic/ Solitary PulmonaryNodule.pdf. Accessed September 13, 2015.

15. Swensen SJ, Silverstein MD, Edell ES, et al. Solitary pulmonary nodules: clinical prediction model versus physicians. Mayo Clin Proc. 1999;74(4):319-329.

16. Balekian AA, Silvestri GA, Simkovich SM, et al. Accuracy of clinicians and models for estimating the probability that a pulmonary nodule is malignant. Ann Am Thorac Soc. 2013;10(6):629-635.

18. Gould MK, Ananth L, Barnett PG; Veterans Affairs SNAP Cooperative Study Group. A clinical model to estimate the pretest probability of lung cancer in patients with sol­ itary pulmonary nodules. Chest. 2007;131(2):383-388.

19. Holin SM, Dwork RE, Glaser S, Rikli AE, Stocklen JB. Solitary pulmonary nodules found in a community-wide chest roentgenographic survey: a five-year follow-up study. Am Rev Tuberc. 1959;79(4):427-439.

20. Furtado CD, Aguirre DA, Sirlin CB, et al. Whole-body CT screening: spectrum of findings and recommendations in 1192 patients. Radiology. 2005;237(2):385-394.

21. Grgic A, Yüksel Y, Gröschel A, et al. Risk stratification of solitary pulmonary nodules by means of PET using (18) F-fluorodeoxyglucose and SUV quantification. Eur J Nucl Med Mol Imaging. 2010;37(6):1087-1094.

22. Gould MK, Sanders GD, Barnett PG, et al. Costeffectiveness of alternative management strategies for patients with solitary pulmonary nodules. Ann Intern Med. 2003;138(9):724-735.

23. Wiener RS, Gould MK, Slatore CG, Fincke BG, Schwartz LM, Woloshin S. Resource use and guideline concor­dance in evaluation of pulmonary nodules for cancer: too much and too little care. JAMA Intern Med. 2014; 174(6):871-880.

24. MacMahon H, Austin JH, Gamsu G, et al. Guidelines for management of small pulmonary nodules detected on CT scans: a statement from the Fleischner Society. Radiology.

2005;237(2):395-400.

25. Church TR, Black WC, Aberle DR, et al.; National Lung Screening Trial Research Team. Results of initial low-dose computed tomographic screening for lung cancer. N Engl J Med. 2013;368(21):1980-1991.

26. Centers for Medicare and Medicaid Services. National Coverage Determination (NCD) for Screening for Lung Cancer with Low Dose Computed Tomography (LDCT).

February 2015. https://www.cms.gov/Newsroom/Media Release Database/Press-releases/2015-Press-releasesitems/2015-02-05.html. Accessed May 15, 2015.

17. Swensen SJ, Silverstein MD, Ilstrup DM, Schleck CD, 27.

Edell ES. The probability of malignancy in solitary pulmonary nodules. Application to small radiologically indeterminate nodules. Arch Intern Med. 1997;157(8): 849-855.

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American College of Radiology. Lung-RADS version 1.0 assessment categories release date: April 28, 2014. http:// www.acr.org/~/media/ACr/Documents/PDF/Quality Safety/Resources/LungRADS/AssessmentCategories.pdf.

Accessed May 15, 2015.

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AMERICAN FAMILY PHYSICIAN

Practice Guidelines ACP RELEASES BEST PRACTICE ADVICE ON SCREENING FOR CERVICAL CANCER Screening for cervical cancer has likely con­tributed to decreased incidence and mor­tality rates of the disease over the past several decades. However, the medical cost of screening is substantial. New evidence-based guidelines aim to minimize the harms of overscreening while maximizing benefit. Based on the best available evidence, the American College of Physicians (ACP) has released best practice advice on cervical can­ cer screening in average-risk, asymptomatic women 21 years or older. This advice is targeted to all clinicians, and refers to screen­ing for cervical precancerous and cancerous lesions detected on cytology and other tests for high-risk types of human papilloma­virus (HPV).

This advice is supported by the American Congress of Obstetricians and Gynecologists and endorsed by the American Society for Clinical Pathology.

Best Practice Advice ACP’s best practice advice focuses on increas­ ing the age at which to begin screening, increasing the screening interval, and discon­tinuing screening in lowrisk women.

(1) Clinicians should not screen average-risk women younger than 21 years. This applies regardless of sexual history. Cytologic abnor­malities are common in this age group, but clinically important cervical lesions are rare. If screened, many women younger than 21 years will have colposcopy and biopsy, with some treated for lesions with a high likeli­hood of regression.

(2) Clinicians should begin screening average-risk women at 21 years of age once every three years with cytology (cytologic test­ing without HPV tests). HPV testing is not recommended in this age group because of the high prevalence of HPV infection.

(3) Clinicians should not screen average-risk women with cytology more often than once every three years.

Annual screening is no longer recommended because of increased rates of false-positive results with minimal effect on subsequent cancer. The

Source: Adapted from Am Fam Physician. 2015;92(12):1107-1110.

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average time for a high-grade precancerous lesion to progress to cancer is 10 years. The three-year interval allows sufficient time for identifica­tion and treatment.

(4) Clinicians may screen using a combina­tion of cytologic and HPV testing once every five years in average-risk women 30 years or older who prefer longer screening intervals. This strategy, known as cotesting, is an alternative to cytology alone. The rationale for this approach is that women with normal cytologic results and no evidence of high-risk HPV are at low risk of cervical cancer; therefore, the screening interval may be safely extended to five years.

(5) Clinicians should not test for HPV in average-risk women younger than 30 years. HPV testing alone or in combination with cytology is not recommended for primary screening in this population. The U.S. Pre­ventive Services Task Force qualifies this as a grade D recommendation, because there are likely no net benefits or the harms outweigh them.

(6) Clinicians should discontinue screening average-risk women older than 65 years after three consecutive negative cytology results, or two consecutive negative cytology plus HPV test results within 10 years, if the last one was performed within the previous five years.

Cer­ vical cancer is uncommon in older women who have had normal previous screening results, although the chance of false-positive results with consequent invasive interven­tions continues.

(7) Clinicians should not screen average-risk women of any age after hysterectomy with removal of the cervix. After surgical removal of the cervix, the risk of cervical cancer is zero, making screening in these patients extremely low-value.

Talking Points with Patients When discussing cervical cancer screening with patients, clinicians should explain that beginning screening too early can lead to testing and treating lesions that may resolve on their own. Screening more often than every three years increases the chance of false-positive test results and invasive pro­cedures while offering little benefit. In low-risk women older than 65 years, continuing cervical cancer screening provides little to no benefit with the potential for invasive procedures.

After hysterectomy with removal of the cervix, patients can be reassured that there is no risk of cervical cancer.

AMERICAN FAMILY PHYSICIAN

Photo Quiz DIFFUSE, ERYTHEMATOUS, SCALY ERUPTION A 52-year-old male smoker presented with a mildly pruritic rash that began three months earlier on his back and spread to his scalp, trunk, and extremities, including the palms and soles. He had a history of alcoholic cir­rhosis. He had no recent new exposures, including medications.

Physical examination revealed numerous wellcircumscribed, erythematous, non­blanching plaques with adherent white scale involving approximately 70% of his body (Figures 1 and 2). His palms and soles dis­played thick scale with fissures, and he had oil spots and onycholysis affecting several fingernails.

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

Figure 1.

A. Cutaneous sarcoidosis.

B. Nummular eczema.

C. Plaque psoriasis.

D. Subacute cutaneous lupus erythematosus.

E. Tinea corporis.

Figure 2.

SEE THE FOLLOWING PAGE FOR DISCUSSION.

Source: Adapted from Am Fam Physician. 2015;92(12):1105-1106.

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AMERICAN FAMILY PHYSICIAN DISCUSSION

Summary Table

The answer is C: plaque psoriasis. Psoriasis is a common autoimmune condition with a strong genetic compo­nent that affects 2% to 5% of the population.1 There is a bimodal distribution for onset of disease, with about 75% of cases occurring between 15 and 20 years of age; there is a second peak from 50 to 60 years of age.2 Behavioral factors associated with psoriasis include smoking, alcohol abuse, and obesity.2 After controlling for these factors, patients with psoriasis have an increased risk of cardiovas­cular disease and metabolic syndrome.3

Condition

Characteristics

Cutaneous sarcoidosis

Round, flat-topped, erythematous plaques that may be scaly; other findings of sarcoidosis; symmetric distribution on the face, extremities, or trunk

Nummular eczema

Highly pruritic, coin-shaped, erythematous, vesicular, crusted plaques; often occurs after trauma or allergic exposure; typically begins on the extremities

Plaque psoriasis

Scaly, erythematous macules that coalesce to form plaques; symmetric, spreads peripherally

Psoriasis is a clinical diagnosis that encompasses a wide spectrum of presentations often categorized by morphol­ogy.4 Plaque psoriasis is the most common pattern, char­acterizing 90% of cases.3,4 As demonstrated in this case, it is generally symmetric, and begins as scaly, erythematous macules that spread peripherally and coalesce to form plaques that may become confluent. Fissuring can occur when lesions extend to palms, soles, or joint lines. One-half of patients with psoriasis display nail involvement, including oil spots, onycholysis, subungual hyperkeratosis, or pitting.3 About 30% of patients also develop arthritis.1

Subacute cutaneous lupus erythematosus

Small, scaly, erythematous papules or plaques that expand to form an annular lesion or a larger plaque; one-half of patients meet criteria for systemic lupus erythematosus; occurs primarily on sun-exposed skin

Tinea corporis

Well-circumscribed, circular patches with central clearing; scaly, raised, advancing edge; begins on the trunk, but may spread to extremities

Treatment of psoriasis depends on comorbidities and extent of disease. Topical treatments include tar, corticosteroids, and retinoids. Phototherapy is also effective.3,5 Systemic treatments include methotrexate, cyclosporine, acitretin, and biologics such as T-cell and tumor necrosis factor inhibitors.3 Systemic corticosteroids should be avoided because they can significantly worsen disease when withdrawn.3,4 Patients should also be counseled about smoking and alcohol cessation, as well as weight loss.3 Approximately 25% of patients with sarcoid­osis have skin involvement, which can have different manifestations. One form is plaque sarcoidosis, which appears as round, flat-topped, erythematous plaques that may be scaly. The plaques usually occur in a symmetric distribution on the face, extremities, or trunk.5,6 Nummular eczema typically begins on the extremi­ties, often after trauma or allergic exposure, as a highly pruritic, coin-shaped, erythematous, vesicular, and crusted plaque.5 Small papulovesicular satellite lesions form around the primary lesion and coalesce into a larger plaque.5 Subacute cutaneous lupus erythematosus occurs primarily on sun-exposed skin, beginning with small, scaly, erythematous papules or plaques that expand into one of two forms: an annular lesion or a larger

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plaque in the psoriasiform/papulosquamous variant.

One-half of these patients meet criteria for systemic lupus erythematosus.5,6 Tinea corporis is a superficial dermatophyte infection characterized by well-circumscribed, circular patches with central clearing and a scaly, raised, advancing edge.

It begins on the trunk but may spread to the extremities.

The diagnosis can be confirmed by demonstration of fungi on a potassium hydroxide examination of a skin scraping.5,6 REFERENCES 1. Raychaudhuri SK, Maverakis E, Raychaudhuri SP. Diagnosis and clas­sification of psoriasis. Autoimmune Rev. 2014;13(4-5):490-495.

2. Langley RG, Krueger GG, Griffiths CE. Psoriasis: epidemiology, clinical features, and quality of life. Ann Rheum Dis. 2005;64(suppl 2):ii18-ii23.

3. Menter A, Gottlieb A, Feldman SR, et al. Guidelines for the manage­ment of psoriasis and psoriatic arthritis: section 1.

J Am Acad Dermatol. 2008;58:826-850.

4. Weigle N, McBane S. Psoriasis. Am Fam Physician.

2013;87(9):626-633.

5. James WD, Elston DM, Berger TG, Andrews GC, eds.

Andrews’ Diseases of the Skin: Clinical Dermatology.

London, UK: Saunders/Elsevier; 2011.

6. Hsu S, Le EH, Khoshevis MR. Differential diagnosis of annular lesions. Am Fam Physician. 2001;64(2):289-296.

CARDIOLOGY

A Case of Brucellosis Presented as Pericarditis: Rare Presentation SNEHA VADHVANA*, MANISH N MEHTA†, ANIKET BHARDWAJ‡

ABSTRACT Brucella pericarditis is a rare condition with only a few reported cases. We review the literature, and describe a 24-year-old Indian male patient who was referred to our institute as a case of pyrexia of unknown origin. Patient was admitted with complaints of chest pain, sudden onset of breathlessness and severe joint pain. Electrocardiogram showed ST-segment elevation with concavity upward and 2D echocardiography of patient was suggestive of pericarditis with pericardial effusion. On history, he was found to be a farmer by occupation. We sent his blood for brucella IgM titer, which was found to be positive. We treated the patient with antibiotics and steroid therapy. Patient responded well and was discharged with oral antibiotics.

Keywords: Brucellosis, pyrexia of unknown origin, pericarditis, positive brucella IgM

B

rucellosis is a bacterial zoonosis transmitted directly or indirectly to humans from infected animals, predominantly domesticated ruminants and swine. The disease is known colloquially as undulant fever because of its remittent character.

Its distribution is worldwide apart from the few countries where it has been eradicated from the animal reservoir.

Although brucellosis commonly presents as an acute febrile illness, its clinical manifestations vary widely and definitive signs indicative of the diagnosis may be lacking. Thus, the clinical diagnosis usually must be supported by the results of bacteriologic and/or serologic tests.1

CASE REPORT A 24-year-old Hindu Indian patient, by occupation a farmer, came to our institute with chief complaints of high-grade fever with chills and rigor. Fever was intermittent and relieved after taking some drug. He was having fever since 15 days. Fever was associated with

*Assistant Professor †Professor and Head ‡2nd Year Resident Dept. of Medicine, GG Hospital, Jamnagar, Gujarat Address for correspondence Dr Manish N Mehta Shripati Apt.,Valkeshwari Nagri, Jamnagar, Gujarat E-mail: mnmehta1968@yahoo.com

severe multiple joint pain, which led to severe disability.

Patient was mainly having knee joint pain, which was swollen and tender. Patient gave history of ingestion of raw milk. With all above mentioned complains, patient was referred to us as a case of pyrexia of unknown origin with all basic reports done, which are given in Table 1.

We suspected brucellosis. For that brucella IgM (immunoglobulin M) antibody testing was done, which was found to be positive. At same time, the patient was complaining of chest pain with breathlessness at rest.

On examination, there was tachypnea and tachycardia.

We had ECG of the patient done which showed STsegment elevation with concavity upward in all chest leads. 2D echocardiography of patient revealed mild pericardial effusion with pericarditis, which responded to injectable furosemide with injectable hydrocortisone given for 5 days. Patient was given capsule doxycycline 200 mg b.i.d. for 6 weeks and injection streptomycin o.d. for 2 weeks. Patient’s fever subsided completely but the joint pain was still so severe that he could not move.

For that, we started injectable methylprednisolone for 5 days. Patient improved completely and was discharged.

DISCUSSION Human brucellosis is caused by strains of Brucella, a bacterial genus that was previously suggested, on genetic grounds, to comprise a single species, Brucella melitensis, with a number of biologic variants exhibiting particular host preferences. All brucellae are small,

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CARDIOLOGY Gram-negative, unencapsulated, nonsporulating, nonmotile rods or coccobacilli. They grow aerobically on peptone-based medium incubated at 37°C; the growth of some types is improved by supplementary CO2. In vivo, brucellae behave as facultative intracellular parasites.

Table 1. Results of the Investigation Done Investigation Hb

13.5 g/dL

TC

23,500 cells/mm3

DC

84/8

Platelet

5,03,000 cells/mm3

MP

Negative

Creatinine

0.6 mg/dL

Urea

20 mg%

Bilirubin (T/D/I)

1.8/0.8/1 mg/dL

SGPT

48 U/L

Blood C/S

Acinetobacter

ESR

48 mm/hour

S. widal

Negative

ASO titer

Negative

HBsAg

Negative

RVD

Negative

RA factor

Negative

CONCLUSION

Brucella IgMab

Pos (1.12) (29/1/16)

Electrocardiogram

S. tachycardia with PRsegment depression and ST-segment elevation

Brucella is rare cause of pericarditis but should be considered as one of the cause of bacterial pericarditis.

USG abdomen

Mild splenomegaly

USG left knee

Minimal effusion

Chest X-ray

WNL

2D echocardiogram

Thin rim of pericardial effusion with mild TR and mildly enlarged RA and RV

Urine C/S

Negative

The organisms are sensitive to sunlight, ionizing radiation and moderate heat; they are killed by boiling and pasteurization but are resistant to freezing and drying. Their resistance to drying renders brucellae stable in aerosol form, facilitating airborne transmission.1 Brucellosis can involve almost any organ of the body and can lead to multiorgan dysfunction.2 Our patient was a case of brucella pericarditis.

Cardiac complications from brucellosis are unusual, occurring in 0-2% of patients and usually manifest as endocarditis.2-4 Here patient was referred to us as a case of pyrexia of unknown origin as patient has went on all investigations except brucella titer before presenting to our institute.5

REFERENCES 1. White NJ, Bremen JG. Malaria (Chapter 157). In: Fauci AS, Kasper DL, Hauser SL, Longo DL, Jameson JL, Loscalzo et al (Eds.). Harrison’s Principles of Internal Medicine. 18th Edition, New York: McGraw-Hill; 2012.

2. Khorvash F, Keshteli AH, Behjati M, Salehi M, Emami Naeini A. An unusual presentation of brucellosis, involving multiple organ systems, with low agglutinating titers: a case report. J Med Case Rep. 2007;1:53.

Hb = Hemoglobin; TC = Total count; DC = Differential count; MP = Malarial parasites; T/D/I = Total/Direct/Indirect; SGPT = Serum glutamic pyruvic transaminase; C/S = Culture/Sensitivity; ESR = Erythrocyte sedimentation rate; S. = Serum; ASO = Antistreptolysin O; HBsAg = Hepatitis B surface antigen; RVD = Right ventricular dysfunction; RA = Rheumatoid arthritis; IgMab = Immunoglobulin M antibodies; USG = Ultrasonography; WNL = Within normal limits; TR = Tricuspid regurgitation; RV = Right ventricle; RA = Right atrium.

3. Jubber AS, Gunawardana DR, Lulu AR. Acute pulmonary edema in Brucella myocarditis and interstitial pneumonitis. Chest. 1990;97(4):1008-9.

4. García de Lucas MD, Castillo Domínguez JC, Martínez González MS. Brucella myopericarditis. Rev Esp Cardiol.

2004;57(7):709.

5. Hadda V, Khilnani G, Kedia S. Brucellosis presenting as pyrexia of unknown origin in an international traveller: a case report. Cases J. 2009;2:7969.

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Treat TIA Aggressively Findings of a study published April 21, 2016 in the New England Journal of Medicine suggest benefits of sending someone to a hospital even if muscle weakness or slurred speech has only lasted for a few seconds. Mini-strokes, also known as transient ischemic attacks or TIAs, are often the harbinger of a potentially-deadly stroke that can come within a matter of hours or days. Quick action can reduce the risk of a much more serious problem by about 50%.

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COMMUNITY MEDICINE

Filling and Refilling: The Melancholy of Malaria Since Independence in India AMITABHA SARKAR*, SANDIP GHOSH†

ABSTRACT This project aims to study the timeline of national programs in India that have been formulated over the years to deal with malaria. Malaria is India’s most chronic vector-borne disease and has plagued our nation for decades. It was the landmark Bhore Committee that first stated that malaria had to be dealt with by employing a dedicated national program. Thus, the first national program to curb the menace of malaria, the National Malaria Control Program (NMCP) was launched in 1953.

This was followed by the overambitious National Malaria Eradication Program (NMEP), which was met with relative failure.

The Urban Malaria Scheme was then launched to deal with this disease, followed by the Modified Plan of Operation (MPO).

A slew of similar programs were launched, all of which met with only slight success. After much deliberation and coming to terms with the reality that malaria may not be completely eradicable in a country like India, the government launched the National Anti-Malaria Program in the late 90s, finally integrating it into the National Vector-Borne Disease Control Program (NVBDCP). Malaria as a disease cannot be ignored and a holistic approach needs to be adopted to be able to decrease the mortality rate of this disease. This study, titled, “Filling and Refilling: The Melancholy of Malaria Since Independence in India” aims at understanding the timeline of strategies involved in dealing with malaria and a critical analysis of reasons for failure of each attempt. The study also wishes to highlight the manner in which it’s necessary to get to the root cause of this disease, which is the study of the vector itself, to really be able to become a country free of the malady, that is, malaria.

Keywords: Vector-borne diseases, NMCP, NMEP, host (human), causative agent (plasmodium), environment (breeding places, rainfall, humidity, etc.), vector (mosquito)

INTRODUCTION “They spread and spread till their eyes got sore; then they refilled their machines and sprayed some more”—the famous rhymes of ”Ode to Mosquito Men” was made for the malaria workers but also ironically representing the histories of malaria control efforts in India.

Malaria is the most chronic vector-borne disease in India and also a great hindrance to the progress of the nation. The disease has been prevailing for more than

*PhD Researcher Centre for Social Medicine and Community Health Jawaharlal Nehru University (JNU), New Delhi †Professor Dept. of Health Care and Hospital Administration Indian Institute of Social Welfare and Business Management, Kolkata, West Bengal Address for correspondence Dr Sandip Ghosh Professor Dept. of Health Care and Hospital Administration Indian Institute of Social Welfare and Business Management, Kolkata, West Bengal E-mail: sandip91@yahoo.com

centuries and thus has always been a cause of concern not only for the general population but also for the policy makers. In 1935, it was estimated by the then first director of the Malaria Institute of India (Brigadier JA Sinton) that at least 100 million people suffered and one million deaths took place in endemic areas from malaria, along with the toll of almost equal number of deaths where the disease acted as an underline cause of death.1 Since then, malaria control activities have been going on with utmost priority and experiencing different programmatic interventions from control mechanism to eradication envision. Malaria control activity is a very complex public health job. Analyzing malaria control activities in post independence India is not only limited to technical competence of the programs but also requires the understanding of epidemiology, entomology, changing social context, political economy of national and international affairs.

Malaria occurs when the epidemiological triad (hostagent-environment) gets formed. Identically, the entire malaria control activity comprises of host (human), causative agent (plasmodium) and environment (breeding places, rainfall, humidity, etc.). Vector

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COMMUNITY MEDICINE (mosquito) is an indispensable part in malaria control as it carries the malaria parasite (plasmodium, which causes the infection) which enters and multiplies inside the human body who then develops sign and symptom of malaria. Humans also act as a reservoir for plasmodium because the gametocyte (sexual form) takes place inside the human body, thus the mosquitoes bite humans to develop and lay eggs. This is the complexity of malaria where humans act both as a host and reservoir for the causative agent of the disease, hence, any anti-malaria activity cannot just destroy the reservoir (human) to stop the mode of transmission from agent to host. Concomitantly, the vector has significant role in malaria infection. Out of 45 species of Anopheline mosquito, majorly Anopheles culicifacies (exist in rural areas) and Anopheles stephensi (exist in urban areas) are vectors of primary importance in Indian context. Anopheles breeds usually in clean water and is even capable to breed in small quantum of water. They also have many behavioral preferences though not exclusive, like some mosquitoes bite usually human, some usually animal, some are indoor, whereas some are outdoor mosquitoes. Further, Anopheles mosquito usually bites during dusk and dawn but can also bite during day time or evening. So, the larval habitats (ecological factor) and host biting preference (behavioral factor) varies at large. This mosquito bionomics is unpredictable and multifarious thus posing huge challenge in vector control activity.

Also, environment component are supportive for rapid breeding of mosquitoes because of rainfall, humidity, unhygienic living condition, lack of self-consciousness, nutritional deficiencies and so on. This is the ambit of malaria control activity which public health can only combat with the vector control strategies to stop or reduce transmission of malaria infection.

In the first-half of the 20th century, malaria control activity was limited to military cantonments, plantation areas and ports, and Paris green was used as only available insecticide. The strategy was to use the Paris green in the located drainages and other possible breeding centers to stop growing mosquitoes. National Malaria Control Program (NMCP) was the first antimalaria activity in post independence India. Though, the root of this program had embedded into the recommendation of â&#x20AC;&#x2DC;â&#x20AC;&#x2DC;Health Survey and Development Committeeâ&#x20AC;?, 1946 (Bhore Committee report). It was the recommendation of that committee which convinced the Planning Commission in 1951 to endorse malaria as a top priority program. Notably, India registered 75 million cases of malaria and 0.8 million deaths at the time of its independence.1

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The Malaria Milestones Sir Bhore Committee Report

1946

National Malaria Control Program

1953

National Malaria Eradication Program (NMEP)

1958

Urban Malaria Scheme (UMS)

1971

Modified Plan of Operation (MPO)

1977

Malaria Action Program

1995

Enhanced Malaria Control Project (EMCP)

1997

National Anti-Malaria Program

1999

National Health Policy

2002

National Vector-Borne Disease Control Program (NVBDCP)

2004

NATIONAL MALARIA CONTROL PROGRAM The first malaria control program started in the year of 1953 with the objective of bringing down the malaria transmission level up to the extent from where it could be possible to cease as a major public health problem and afterward the states were required to curb the transmission level as low as possible.2 The program initially catered 200 million of population from the endemic areas and operationalized based on the areawise demarcated unit approach. Till 1957, a total of 175.5 units were made under the NMCP.1 The program was carried out under the financial assistance of United States Technical Cooperation Mission (USTCM), WHO, UNICEF and Rockefeller foundation.1 The successful experience of using dichlorodiphenyltrichloroethane (DDT) in other countries had motivated the control program to cover the human dwellings and cattle sheds with residual insecticide spray (DDT). Also, malaria control teams were made under state anti-malaria control organization to conduct survey and observe the malaria incidence in the program areas. Further, stress was given on the availability of anti-malarial drugs in the institutions, so that patient could access and report to the institution.2 The NMCP was active from 1953 to 1957 and recorded high success (more than 50% decline in malaria prone areas in 1957).1 It can be noted that the highly intensified DDT intervention had paved the way for huge success of the program. The indoor residual spray of DDT was used for the first time in most of the new program areas, which were so far not intervened by any measures of anti-malaria activities.

The major boost in funding came with international support, which could be contextualized in different political and economical aspects. The funding in

COMMUNITY MEDICINE malaria rooted in the politics of increasing economic productivity in South America. During and after World War I, United States Public Health Service (and also supported by Rockefeller foundation) promoted hookworm and anti-malaria campaign to safeguard the interest of military posted in South America and also ensure the productivity of civilians as the market was dominated by the US businessman and landlords. The same tactic was adopted by the European colonial government to ensure the resource drainage from third world (like, India) to first world.

Post independence situation in India, public health (along with medical care and education) was viewed as the resource generating investment as India was considered as cheap source of labor.3 Also, the decade of 1950 was the time of cold war in international affairs between the US and Union of Soviet Socialist Republics (USSR). Both the countries were in effort to expand their influence in various decision-making platforms (like, United Nation), and involved in successive situation driven strategies to confirm the allegiance from others. The international funding for first Indian anti-malaria program came at the backdrop of this puzzling international politics. India was not economically developed and technically sound, hence for the both of the need India had to depend on foreign assistance.

NATIONAL MALARIA ERADICATION PROGRAM The two factors worked behind the shifting from control to eradication program-continuous spray of DDT brought the malaria rate to zero in many countries; and development of the resistance of the vector to the DDT was feared to occur if the spraying continued even after zero reporting of transmission for several years. The phenomenon of resistance was rated as serious threat to the sustainability of the program in the long run. The push for control to eradication was first discussed in the IV International Congress of Tropical Medicine and Malaria in Washington, DC in 1955. In the same year, the Eighth World Health Assembly also supported the same perception. Finally in the year 1956, eradication of malaria as a goal had been accepted for all the SouthEast Asian countries under Ninth Regional Committee Session of South-East Region of WHO, Delhi.1 The control program became eradication with an objective to eradicate in next 7 to 9 years. Initially, the program was highly successful (malaria cases reduced to 0.1 million from the estimated 75 million in 1947) and even zero number of death was reported in 1965.

The elimination concept had been derived from the

military operational strategies; military style operation in Indian public health structure was very common as doctors usually came from military service to Indian Medical Service (IMS) till 1946. The NMEP had been designed in phased approach i.e., preparatory, attack, consolidation and maintenance. Though, NMEP started the program with attack phase because of the perception that sufficient experience and information had already been gathered during the NMCP era (1953-1957). The major eradication activities were spraying DDT twice in a year according to the appropriate season (like, monsoon and post monsoon), fortnightly surveillance and the proper treatment for all confirmed cases. For vector control activities, mainly chemical control (spraying DDT) and environment management (through source reduction by filling up the breeding places, covering of stored water, etc.) had given high priority. NMEP was a fully central sponsored program, which was unparallel to any public health program around that time. The same unit-wise operation of NMCP continued in NMEP. It was thought that 3 years would be adequate under attack phase to continue the activity (mainly spray) in hypoendemic areas, while 3 to 4 years for mesoendemic and hyperendemic areas.1 The success was achieved in the attack and consolidation phase of the program where termination of transmission of infection through vector control was the main agenda. These two phases were under the central commitment but the program experienced a setback majorly in maintenance phase where states were the responsible entities to ensure continuous monitoring.

There were technical and administrative criteria to enter into maintenance phase from the attack phase. The technical criterion was epidemiological (competence of laboratory services, sufficient case detection machinery, etc.) and administrative criteria was the capability of general health service under state patronage to take up the vigilance immediately after the abolition of special organization for NMEP. Government appointed special committee (for assessing these technical and administrative criterions) in 1963 recommended to set up vigilance units under the general health service that would be a part of comprehensive rural health service using primary health center as the base of the services. However, lack of political commitment, financial insufficiency, administrative snags, logistic challenges resulted in the failure of the program.

Malaria resurgence occurred by 70s in Madhya Pradesh, Gujarat, parts of Rajasthan and Uttar Pradesh, and by 1976 the overall number of malaria positive

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COMMUNITY MEDICINE cases in India rose to 6.4 million.1 Government formed many committees (Hinman Committee-1960, Chadha Committee-1967, Madhok Committee-1967, First Indepth Evaluation Committee-1970) to investigate the failure of much dreamt eradication program. The major findings of these committees were scarcity of external resources, shortage and inappropriate supply of materials including insecticides and scarcity of manpower recognized as administrative challenges.

Development of resistance by the vector and drug resistance to Plasmodium falciparum in few parts of the country had been identified as two most threatening technical challenges. Apart from the administrative and technical shortcomings, host of operational factors were also instrumental for the setback. It was the period of 1960s and 1970s when India was undergoing industrialization, rapid migration followed by urbanization which introduced many environmental and sanitation problems, thus operationally it was difficult for the program to cope with the changed situation in urban areas. Also, the tendency of mudplastering or lime-washing of house just immediately after the spray due to religious beliefs reduced the effectivity of the spray. These factors also multiplied by the frequent heavy rain falls, flood which made the situation more challenging in remote and hilly areas.1 The NMEP failed not only because of administrative, technical or operational limitations, the cause of these failure had been also influenced by the international activities happening at that time and also the perspective possessed by the Govt. of India. The boost for NMEP had started when US president Eisenhower expressed the desire of US financial support to WHO’s worldwide malaria eradication campaign (started in 1955) under the context of cold war politics to vie with USSR in the year 1956. The ‘‘politics of secret report” (as scrutinized by Cleaver in ‘‘The Official Report” of the International Development Advisory Board prepared for US president) narrated that the US Govt. recognized their own politics of malaria control effort in India, where malaria control activity pursued to combat with communist infiltration. American corporates were also close to WHO, as they offered fund to WHO, which was ultimately channelized to countries like India for malaria eradication program.1 India shifted from control program to eradication program because of the overachievement in NMCP and the recommendation made in World Health Assembly for eradication before the vector could grow resistance against the DDT. That was in brief the fund mobilization process for NMEP. One of the major reasons of failure was fund

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availability in malaria program in 1970s, which is partly attributed to the international situation. Apart from the international conflicts (cold war, domino effect), the US had encountered a long ignored internal indignation in the form of ‘black movement’, ‘feminist movement’ at the last phase of cold war (late 1960s to early-1970s), also the worldwide economic depression in early 1970s and over enthusiasm on neo-Malthusianism (population control) resulted in the fund cut. Also, WHO understood the problem of vertical program and the complexity of malaria program, which probably prompted it to conduct ‘‘WHO Interregional Conference on Malaria Control in Countries Where Time-Limited Malaria Eradication is Impractical at Present” in 1972.1 The complexity of malaria program can further be reviewed under the notion of technological dependency.

The successful eradication of small pox influenced the WHO and USTCM experts to overestimate the DDT intervention in malaria program and envisaged for eradication goal. That was the international context regarding malaria funding. On the other side, Govt. of India had also started shifting its main focus on population control (family planning programs) from malaria program. It seems that funding decision of the Govt. of India was made abruptly during that phase.

For example, the fund for malaria program had rose from $13 million (1968) to $22 million (1971), but again it was reduced to $14 million in 1973 in spite of the dire need of speeding up. Further, the fund has again increased in 1974-1975 to some $23-29 million despite the strong recommendation for minimum need of $81 million demand from Dr Gopalan (Head, ICMR).

Hence, it can be contemplated that the continuous fund cuts weakened the eradication program in both operational expansion and intensification. Hence, the malaria program came under the fund crunch situation.

Another major flaw in decision-making was merging malaria program with general health service. In attack (and also consolidation) phase of the eradication, the program worked too successfully but the failure started once it moved to the maintenance phase, which was under state’s responsibility. In late 1960s and 1970s, the general health service was not well-equipped and further accretion of malaria program had again pushed the overall eradication program towards future.

URBAN MALARIA SCHEME Failure of eradication program was partly because of lack of concentration in urban areas, and keeping that assumption in mind UMS was launched in 1971.

It was also thought that improper attention to urban

COMMUNITY MEDICINE areas might lead the malarial transmission from urban to rural in a larger scale. In spite of the focused effort to urban areas, the malaria cases recoded were much higher and which prompted for more stringent course of action.2 MODIFIED PLAN OF OPERATION In the year of 1977, the goal of malaria eradication had been withdrawn and MPO had been taken to decrease malaria morbidity, eliminate malarial deaths and sustain the success achieved so far through continuous reduction of malaria transmission. The major strategic changes had been done in operational aspects. The areas were demarcated based on the Annual Parasitic Index (API) indicator and accordingly intervention strategies were drawn.2 The MPO was conceptualized during the Consultative Committee of Experts (Rao Committee) and Second In-depth Committee in 1974 where government decided to go for a revised strategy (eradication to control).1 MPO was influenced by the rapid form of urbanization and green revolution, which collectively created more stagnant water and favorable environment for breeding of mosquitoes. To address these challenges, MPO was comprised with funding booster from government (75% of total budge made for communicable disease was spent on malaria), people’s participation by forming 2,00,000 drug distribution centers (DDC) and fever treatment depots (FTD) had been planned to initiate so that people could access malaria treatment, and strengthen the research in malariology.1 The research had given more importance in MPO as it had been found that lack of operational research during NMEP was the cause to unable to understand the field reality (like, amalgamation of malaria with general health service).

Strategy-wise, MPO had introduced API indicator-wise demarcation area. It had given the scope to distribute the available resources (finance, manpower, technological equipments, etc.) rationally and also effectively as per the epidemiological need. From community aspect also the treatment facility got wider after the establishment of DDC and FTD. MALARIA ACTION PROGRAM An expert committee was formed after 1994 malaria resurgence at Rajasthan, Manipur and Nagaland, in 1995 at Assam, Maharashtra and West Bengal, and again in 1996 at Rajasthan and Haryana. The committee recommended the guidelines which were formulated as Malaria Action Program in 1995. Hundred percent

central funding was back to malaria program. Again the areas were demarcated based on the advanced epidemiological parameters: hardcore areas (tribal areas), epidemic prone areas, project areas, triple insecticide resistant areas and urban areas.2 One major surveillance program (National Surveillance Program for Communicable Disease [NSPCD]) also had been initiated in 1996 to combat with various disease outbreaks across the country. It was an additional help for malaria program as it conducted outbreak investigation, epidemic control analysis, laboratory strengthening, training on human resource, etc.

ENHANCED MALARIA CONTROL PROJECT On the request of India, World Bank financed the EMCP to intensify the anti-malaria activity particularly in the 6 core tribal population representing 100 districts and 19 urban areas of 8 states. Also, other infrastructural upgradation took place as the Management Information System (MIS), training were carried out along with advocacy activities using IEC materials. Main objectives were to bring down the malaria morbidity, reduce malaria mortality and sustain the success made so far.2 Operation-wise EMCP bought many innovations to the program. Under the component of early case detection and prompt treatment, appointment of link workers, introduction of Dipstick test (on spot test) and involvement of private sectors in case detection and treatment were important. EMCP also designed and administered new ways of vector control.

Bioenvironmental methods (introduction of larvivorous fishes, environmental management methods), legislative measures (changes in structural design of buildings to reduce mosquito breeding place), personal protective measures (like, Bednet Program) were some of the new initiatives.

NATIONAL ANTI-MALARIA PROGRAM Government finally dropped the term ‘’National Malaria Eradication Program” in 1999 and renamed it as ‘’National Anti-Malaria Program’’. Though, the program has been included shortly within the ambit of NVBDCP.2 NATIONAL VECTOR-BORNE DISEASE CONTROL PROGRAM To address the need of convergence and on the background of series of epidemics of vector-borne diseases in the decades of 90s, the NVBDCP was formed in 2004 to control the five diseases (malaria, kala-azar,

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COMMUNITY MEDICINE filariasis, Japanese encephalitis and dengue). Since then, the malaria program is a part of NVBDCP. Finally, the entire NVBDCP was included under National Rural Health Mission (NRHM) to ensure increased and appropriate public health focus in rural areas for improved prevention and control of communicable diseases.2 In 2004, the Integrated Disease Surveillance Project (IDSP) had been launched. It was the newer form of NSPCD which reported, analyzed the various disease occurrences and operations across the country.

Malaria was back to international agenda after WHO started a new initiative in 1998, the Roll Back Malaria (RBM) effort. RBM was the global partnership between WHO, UNDP, UNICEF and World Bank. RBM was the effort for partnership between national government with NGOs, civil societies, research institutions, private sector, media, development banks and professional associations. Globally also, the Millennium Development Goal (2000) had also acknowledged the problem and set the goal no. 6 (combating human immunodeficiency virus/acquired immune deficiency syndrome [HIV/AIDS], malaria and other disease) and target no. 8 (halt and reverse the incidence of malaria and other major diseases).2 The 2002 National Health Policy had made the anti-malaria activity as priority by setting the goal of reduction in mortality from malaria and other vector-borne diseases by 50% within 2010 and efficient morbidity control.2 Also, Intensified Malaria Control Project had been started from 2005 under the aegis of Global Fund against Tuberculosis, AIDS and Malaria (GFATM). It came under the Health Sector Reform strategy which additionally supplemented the nationwide malaria control program with funding, infrastructure and manpower support. All these initiatives also programmatically, politically and strategically influenced the malaria control program in India.

CONCLUSION Malaria control is one of oldest and toughest public health problems in India. The complexity of this program makes it more difficult for the planners to strategize an effective control mechanism. The bionomics of the vector is very complicated and because of that also the vector control activity is also difficult. The history of malaria programs started with planning of malaria control then shifted to eradication and then again shifted to control strategy is adducing the same complexity. The malaria program

mostly implemented in vertical approach which gave very little scope for intersectoral collaboration. The transmission of malaria can be reduced through vector control, which is related to larger socioeconomic factors in India. Even in 2013, there are areas like Garhi (an urban village in New Delhi) which resembles 19th century England where the pipeline made for drinking water is laid alongside with the drainage route and having umpteen numbers of breeding places. The area alone houses thousands of migrants where the sanitary condition cannot be comparable at all with any model of civilized society. The malaria control unit has been set up by the Delhi Municipality for surveillance of the Garhi and adjacent areas, but the problem lies in many layers. Can these breeding places of Garhi only be combated by the surveillance of the Domestic Breeding Checkers (DBCs)? Is there any roles for public health engineering? What are the roles of Delhi Municipality for ensuring proper urbanization? Garhi along with many other malaria prone areas of India are waiting for these answers.4 In (the National Center for Disease Control [NCDC], the apex body of disease control), currently 14 Entomologists are in place and 12 positions are vacant. Entomology is the discipline which deals with the bionomics and without knowing the bionomics vector control strategy is not possible.

According to the head of the Entomology department in NCDC, the entomologists are becoming less important in public health field in India.5 The activity of malaria control cannot be limited to spraying or fogging or surveillance but also there is a need to actively engage the disciplines of epidemiology, entomology, public health engineering and relevant sectors to work collectively. Malaria eradication is a distant dream but not the effective control.

REFERENCES 1. Dutta PK. Study of NMEP: A System Approach. Prachi Prakashan, New Delhi; 1993.

2. Kishore J. National Anti Malaria Program. National Health Programs of India, 5th Edition, 2005. pp. 138-54.

3. Cleaver H. Political economy of malaria de-control.

Economic and Political Weekly. 1976;11(36):1463-73.

4. Garhi village, New Delhi was visited for the PhD Semester-I field work curriculum under the Centre for Social Medicine & Community Health, JNU on November 12, 2013.

5. NCDC, New Delhi was visited for the PhD Semester-I field work curriculum under the Centre for Social Medicine & Community Health, JNU on November 11, 2013.

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DRUGS

Amitriptyline-induced Edema: A Case Report BHAGHYA PRASAD*, K HARIKRISHNAN*, ANJALY S*, MARIA C KURIAKOSE*, NARESH KUMAR Vâ&#x20AC;

ABSTRACT Amitriptyline is a tricyclic antidepressant drug widely prescribed for treating depression and painful syndromes. The major aim of our study was to make physicians and patients aware about the fact that amitriptyline has the potential to cause edema.

As this side effect of amitriptyline is not much reported, we hope our study could provide some valuable information to the field of pharmacovigilance.

Keywords: Amitriptyline, drug-induced edema, tricyclic antidepressants, 5-HT2 blockade

E

dema is a condition characterized by abnormal accumulation of fluid in the interstitium, located beneath the skin and in the cavities of the body.

Edema or swelling occurs as a normal response to inflammation or injury.1 But, it can occur as druginduced also. It seems to be a common side effect of drugs which cause hypernatremia, antihypertensives, antineoplastics, nonsteroidal anti-inflammatory drugs (NSAIDs), calcium antagonists, insulin, etc. In this study, we report a case of amitriptyline-induced edema in a 50-year-old female patient.

CASE REPORT A 50-year-old female patient was admitted to the Dept. of Orthopedics in a tertiary care teaching hospital with complaints of severe neck pain radiating to the right upper limb and lower back ache radiating to right lower limb. The patient came for consultation to our hospital and was admitted to the Orthopedics department. Her laboratory vitals were checked and were found to be in the normal range with a blood pressure of 130/80 mmHg and pulse rate of 80 beats/minute. Her blood counts, liver function tests and renal function tests were also found to be within normal limits. She was diagnosed as a case of intervertebral disc prolapse from

*Dept.

of Pharmacy Practice National College of Pharmacy, Manassery, Calicut, Kerala â&#x20AC; Orthopedic Consultant KMCT Medical College Hospital, Manassery, Calicut, Kerala Address for correspondence Dr K Harikrishnan Dept. of Pharmacy Practice National College of Pharmacy, Manassery, Calicut, Kerala E-mail: hari8778krishna@gmail.com

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the magnetic resonance imaging (MRI) scan results.

She was given flupirtine and amitriptyline tablets for pain relief. Soon after administration, she developed swelling over face, hands and ankles. She was not able to move her hands and legs due to excessive heaviness.

But, when the patient medical history interview was conducted, she reported that she had developed edema earlier also when administered with amytriptyline 10 mg tablets. The clinician discontinued amitriptyline and the swelling subsided by the next day. After withdrawing amitriptyline from therapy, she was given gabapentin along with flupirtine. She had satisfactory relief from pain and was discharged.

DISCUSSION Amitriptyline is a tertiary amine tricyclic antidepressant drug used orally and parenterally. It closely resembles phenothiazines chemically and to a lesser extent pharmacologically. The drug FDA (Food and Drug Administration) approved it in 1961. The major clinical uses are in the treatment of depression, attention-deficit hyperactivity disorder, neuropathic pain, functional enuresis in children, phobic and panic disorders.

Amitriptyline is a mixed norepinephrine and serotonin reuptake inhibitor as it blocks norepinephrine transporter and serotonin transporter. These transporters terminate amine neurotransmission and this inhibition permits the neurotransmitter a longer stay in the intrasynaptic space at receptor site.2,3 Amitriptyline-induced edema is a very uncommon side effect. The mechanism by which amitriptyline causes swelling of face and limbs is not clearly known.

It depends on the pharmacokinetic variability among individuals. It can also occur at any dose depending

DRUGS on individual pharmacokinetic variations. The possible mechanisms for water retention in the body are: sodium overload, renal dysfunction and hyperpermeability of blood vessels.4,5 There are not many reported cases of amitriptyline-induced edema and no specific management is indicated. The condition can be resolved by withdrawal of the drug. The normal dose of amitriptyline is 50-200 mg daily.3

REFERENCES

In this case, there were no abnormalities in the laboratory investigations of the patient and the exact mechanism for amitriptyline-induced swelling remains unclear. The 5-HT2 (serotonin receptor) blockade due to amitriptyline can potentially increase the levels of cyclic adenosine monophosphate, which causes the relaxation of vascular smooth muscles through phosphorylation of myosin light chain kinase, which increases the vascular permeability. This could be a possible reason for development of edema due to amitriptyline administration.6-9

3. Potter WZ, Hollister LE. Antidepressant agents (Chap 30).

In: Katzung BG (Ed.). Basic and Clinical Pharmacology.

8th Edition, McGraw-Hill; 2007. pp. 498-508.

CONCLUSION In this case, we have shown that amitriptyline has the potential to cause swelling on the face, limbs and ankles. By reporting this rare adverse drug reaction, we hope our report would be an enlightenment to the field of pharmacovigilance and also make the physicians cautious about this rare side effect of amitriptyline.

1. Robbins SL, Cotran R (Eds.). Pathologic Basis of Disease.

Elsevier Saunders; 2004. pp. 120-2.

2. Baldessarini RJ. Drugs and the treatment of psychiatric disorders (Chap 19). In: Hardman JG, Limbird LE, Gilman AG (Eds.). Goodman & Gilman’s The Pharmacologic Basis of Therapeutics. 10th Edition, McGraw-Hill Publication; 2001. pp. 447-76.

4. Kaizu K, Abe M. Drug-induced edema. Nihon Rinsho.

2005;63(1):102-6.

5. Ravi PB, Ravishankar GM, Andrade C. Bilateral peripheral edema as a rare adverse effect of escitalopram. Indian J Psychiatry. 2014;56(1):97.

6. Franco K, Tamburrino M, Campbell N, Pentz J, Evans C. Dopaminergic activity and idiopathic edema.

Hosp Commun Psychiatry. 1991;42(3):309-10.

7. Hosseini SH, Ahmadi A. Peripheral edema occurring during treatment with risperidone combined with citalopram. Case Rep Med. 2012;2012:540732.

8. Kuchel O, Hamet P, Cuche JL, Tolis G, Fraysse J, Genest J. Urinary and plasma cyclic adenosine 3’,5’-monophosphate in patients with idiopathic edema. J Clin Endocrinol Metab. 1975;41(2):282-9.

9. Ng B, Postlethwaite A, Rollnik J. Peripheral oedema in patients taking olanzapine. Int Clin Psychopharmacol.

2003;18(1):57-9.

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FDA Approves Photrexa for Progressive Keratoconus Treatment FDA has approved a riboflavin ophthalmic solution (Photrexa, Avedro) that treats a corneal disease called progressive keratoconus with corneal collagen cross linking.

New Drug Against Skin Tutor Preliminary study suggests that an intravenous drug, marketed as Keytruda, is effective against skin tumor called Merkel cell carcinoma (MCC). The drug is already used to treat some advanced cases of melanoma, another dangerous form of skin cancer. (Source: American Association for Cancer Research Annual Meeting April 19, 2016)

Ketamine may Help Sustain Antidepressant Effect A study published in American Journal of Psychiatry has shown that repeated administration of ketamine may help sustain antidepressant effect in patients with treatment-resistant depression beyond the initial dose.

FDA approves Cannabidiol for Treatment of Tuberous Sclerosis Complex GW pharmaceuticals has received Orphan Drug Designation from FDA for cannabidiol (CBD) for the treatment of Tuberous Sclerosis Complex (TSC). TSC is a rare genetic disorder, the most common symptom of which is epilepsy.

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ENT

Clinicopathologic Study of Goiters in Warri, Nigeria AFEYODION AKHATOR*, CP OSIDE†, E IJOMONE‡

ABSTRACT Introduction: There is a 15% reported worldwide prevalence of goiter. The cause of goiters in endemic areas is iodine deficiency and in iodine replete areas are autoimmune diseases. The presentation is usually with simple diffuse goiter. There is a global shift of prevalence of thyroid cancer to papillary cancer with institution of iodine supplementation. Material and methods: This was a 2-year retrospective study conducted in Warri, Nigeria from January 2008 to December 2009. The Central Hospital, Warri runs an endocrine clinic that caters for breast and thyroid diseases. The case notes of patients with goiters were retrieved and analyzed. Results: There were 112 patients in the study, with a female-to-male ratio of 6.5:1. The commonest presentation was simple diffuse goiter accounting for 48.21%. Cosmesis accounted for 48% of the indications for surgery; the commonest surgery done was subtotal thyroidectomy. Colloid goiter was the most frequent histological type, and there was no follicular carcinoma in this study. Conclusion: Goiters in Warri, Nigeria have a similar presentation as in other parts of the country. The institution of supplementary iodized salt has made papillary carcinoma more common.

Keywords: Goiters, presentation, histological type, Warri, Nigeria

G

oiter is defined as enlargement of the thyroid gland from any cause.1 The prevalence of goiter worldwide is 15% and about 50% of people in the community have microscopic nodules.2 Seventy-five percent of patients with goiter live in the underdeveloped areas of the world where healthcare facilities are limited.3 In areas with severe iodine deficiency, the prevalence of goiter can be as high as 80%; the populations at risk are those living in remote mountainous areas in Central Africa, SouthEast Asia and Latin America.4 The commonest cause of goiter worldwide is iodine deficiency,5 and iodine deficiency may be potentiated by the intake of goitrogens such as cassava.1 In iodinereplete areas, the common cause of goiter is autoimmune diseases, ranging from Hashimoto thyroiditis to Graves disease.4,6

*Dept. of Surgery Faculty of Clinical Medicine College of Health Sciences, Delta State University, Abraka, Nigeria †Dept. of Surgery Delta State University Teaching Hospital, Oghara, Nigeria ‡Dept. of Pathology Central Hospital, Warri, Nigeria Address for correspondence Dr Afeyodion Akhator Dept. of Surgery Faculty of Clinical Medicine College of Health Sciences, Delta State University, PMB1, Abraka, Nigeria E-mail: doc_akhator@yahoo.com

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The most common presentation of goiter in the community is simple diffuse goiter;4 the highest prevalence is in the premenopausal woman with a female/male ratio of 4:1.7 Thyroid cancer is the most common endocrine cancer but constitutes only 1% of all cancers.8 Follicular carcinoma is reported to be commonest malignancy in endemic areas and papillary carcinoma in iodinereplete areas.9,10 The presentation and management of goiters has been reported from other parts of the country,11 and none from Warri, Nigeria. This study examines the presentation and pathology of goiters in Warri, Nigeria.

MATERIAL AND METHODS This is a 2-year retrospective study of goiters in Warri, Nigeria from January 2008 to December 2009.

The Central Hospital, Warri runs an Endocrine Clinic every Wednesday, that attends to both breast and thyroid patients. After clinical evaluation, patients with goiter were requested to go for thyroid function tests, thyroid scan and fine-needle aspiration for cytology (if there is clinical suspicion of malignancy; these enables them to be assessed as euthyroid, toxic, hypothyroid or malignant goiters. Euthyroid goiters were offered subtotal thyroidectomy, toxic goiters were made euthyroid with carbimazole and offered near-total or subtotal thyroidectomy and malignant goiters offered total thyroidectomy and referred for

ENT radioiodine therapy as appropriate. The names and hospital number of all the patients with goiter were extracted from the attendance register of the Endocrine Clinic, their case notes were retrieved from the records department and reviewed. Data extracted included the biodata, presentation; whether toxic, euthyroid or hypothyroid, treatment and histology of the goiters.

The data were entered into Microsoft excel spreadsheet and analyzed using simple percentages. Ethical approval was obtained from the Central Hospital, Warri Ethical Committee.

RESULTS There were a total of 112 patients in the period of study; there were 97 females and 15 males making a femaleto-male ratio of 6.5:1. The age range was 14-80 years with a mean of 41.67 years standard deviation (SD) 14.70. Table 1 shows the age distribution of the patients.

Simple diffuse goiter was the most common presentation accounting for 48.21% of cases and only one patient presented with clinical features of hypothyroid goiter (Table 2).

Table 1. Age Distribution Age range

Male

Female

Total

10-19

0

2

2

20-29

3

21

24

30-39

3

26

29

40-49

6

17

23

50-59

1

18

19

60-69

1

8

9

70-79

1

4

5

80-89

0

1

1

Total

15

97

112

Table 2. Clinical Assessment Clinical assessment

Female

Male

Total

Simple diffuse

47

7

54 (48.21%)

Simple multinodular

10

0

10 (8.93%)

Malignant

2

5

7 (6.25%)

Toxic

28

5

33 (29.46)

Cyst

2

0

2 (1.79%)

Solitary

2

1

3 (2.68%)

Hypothyroid

1

0

1 (0.89%)

Recurrent

2

0

2 (1.79%)

Total

94

18

112 (100%)

Table 3. Histology of Thyroidectomy Specimen Histology

Female

Male

Total

Colloid goiter

16

0

16 (64%)

Medullar carcinoma

0

1

1 (4%)

Papillary carcinoma

0

1

1 (4%)

Follicular variant of papillary carcinoma

3

0

3 (12%)

Follicular hyperplasia

1

0

1 (4%)

Follicular adenoma

3

0

3 (12%)

Total

23

2

25 (100%)

Twenty-five thyroidectomy were done over the 2-year period, 22 subtotal thyroidectomy and 3 total thyroidectomy. The indications for surgery were cosmesis in 12 (48%), toxic goiter in 5 (20%), obstructive symptoms in 3 (12%) and malignancy in 3 (12%). Colloid goiter was the most common histology subtype; there were five cases of thyroid cancer and of these, two of them were in male patients. The histology results of the specimens is shown in Table 3. The commonest postoperative complication was transient voice changes in 3 patients (12%); there was a case each of transient hypocalcemia and keloidal scar. There was no mortality.

DISCUSSION The female-to-male ratio in this study was 6.5:1, which is more than the world ratio of 4:1 but is similar to the 6:1 from the study done in Maiduguri, North Eastern Nigeria11 and less than that from neighboring Irrua of 15:1.12 The mean age of patients in this study of 41.67 years and SD of 14.70 is similar to that of the study from Ghana13 with 41.89 years and SD of 12.90 but slightly higher than that of the studies from Maiduguri and Irrua11,12 with 38.86 years and SD of 12.74 and 37.70 years and SD of 14.39, respectively.

Only 25 patients had surgery in the 2 years of study; while this can be attributed to the limited operating space in the hospital but may be more likely due to the sociocultural beliefs and financial limitations faced by the patients as explained by Musa et al.14 Cosmesis was the commonest indication for surgery in this study; as was also reported by other workers,11 the commonest surgery done was subtotal thyroidectomy.

Most surgeons in the country avoid total thyroidectomy for benign conditions because of the requirement of lifelong thyroxine replacement. The fear of availability of the drug and patientâ&#x20AC;&#x2122;s compliance are two major reasons why total thyroidectomy is avoided for benign

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ENT diseases. The complications of thyroidectomy in this study were few and minor, mostly transient voice changes; this corroborates other studies reporting the safety of thyroidectomy in resource limited countries.12,15 There were 5 cases of thyroid cancer in the study, 4 were papillary carcinoma and 1 was medullary carcinoma.

There was no follicular carcinoma in this study. This result corroborates the findings of Ijomone et al;16 they reported that 55% of their cases were papillary carcinoma and 30% follicular carcinoma but different from earlier report from Nigeria that had a higher incidence of follicular carcinoma.17 This high incidence in the frequency of papillary carcinoma is likely due to the iodized salt supplementary therapy that has been instituted in the country; similar increase in the incidence of papillary carcinoma has been reported from Argentina18 when iodine supplementation was instituted in the population.

CONCLUSION The age and sex incidence of goiters in Warri are similar to other parts of the country, subtotal thyroidectomy is the commonest surgery done for them. There is a change to predominantly papillary carcinoma in the area.

REFERENCES 1. Koutras DA. Endemic goiter - an update. Hormones (Athens). 2002;1(3):157-64.

2. Wang C, Crapo LM. The epidemiology of thyroid disease and implications for screening. Endocrinol Metab Clin North Am. 1997;26(1):189-218.

3. Gaitan E, Nelson NC, Poole GV. Endemic goiter and endemic thyroid disorders. World J Surg. 1991;15(2): 205-15.

4. Vanderpump MP. The epidemiology of thyroid disease.

Br Med Bull. 2011;99:39-51.

5. Zimmermann MB. Iodine deficiency. Endocr Rev. 2009;30(4):376-408.

7. Tunbridge WM, Evered DC, Hall R, Appleton D, Brewis M, Clark F, et al. The spectrum of thyroid disease in a community: the Whickham survey. Clin Endocrinol (Oxf). 1977;7(6):481-93.

8. Nix P, Nicolaides A, Coatesworth AP. Thyroid cancer review 1: presentation and investigation of thyroid cancer.

Int J Clin Pract. 2005;59(11):1340-4.

9. Löhrs U, Permanetter W, Spelsberg F, Beitinger M. Investigation of frequency and spreading of the different histological types of thyroid cancer in an endemic goiter region (author’s transl). Verh Dtsch Ges Pathol.

1977;61:268-74.

10. Figge JJ. Epidemiology of thyroid cancer. In: Wartofsky I, Van Nostrand D (Eds.). Thyroid Cancer: A Comprehensive Guide to Clinical Management. 2nd Edition, Humana Press; 2006. pp. 9-11.

11. Aliyu S, Ibrahim AG, Tahir MB, Babayo UD. Goiters: A ten-year experience in developing country. Int J Sci Res Pub. 2015;5(4):1-3.

12. Kpolugbo J, Uhumwangho O, Obasikene G, Alili U. Blood transfusion, antibiotics use, and surgery outcome in thyroid surgery: experience from a suburban center in Nigeria. Niger J Clin Pract. 2012;15(4):458-61.

13. Dakubo JC, Naaeder SB, Tettey Y, Gyasi RK. Pathology and the surgical management of goitre in an endemic area initiating supplementary iodine nutrition. West Afr J Med. 2013;32(1):45-51.

14. Musa ASA, Musa MT, Baba I. Cultural beliefs and attitudes: The psychosocial and economic problems associated with goiter and thyroidectomy in an African population. Thyroid Res Pract. 2014;11:22-5.

15. Elusoji SO, Iribhogbe PE, Osime OC. Thyroidectomy under ketamine anaesthesia in a semi urban hospital in Nigeria. Pak J Med Sci. 2009;25(4):695-7.

16. Ijomone EA, Dudeyemi BM, Udoye E, Nwosu SO. Histopathological review of thyroid diseases in Southern Nigeria - a ten year retrospective study. J Med Med Sci. 2014;5(6):127-32.

17. Adeneji KA, Anjorin AS, Ogunsulire IA. Histological pattern of thyroid diseases in a Nigerian population. Nig Qt J Hosp Med. 1998;8(4):241-4.

18.

6. Canaris GJ, Manowitz NR, Mayor G, Ridgway EC. The Colorado thyroid disease prevalence study. Arch Intern Med. 2000;160(4):526-34.

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Harach HR, Williams ED. Thyroid cancer and thyroiditis in the goitrous region of Salta, Argentina, before and after iodine prophylaxis. Clin Endocrinol (Oxf). 1995;43(6): 701-6.

GASTROENTEROLOGY

To Study the Correlation Between SAAG and Platelet Count/Spleen Size Ratio for Prediction of Esophageal Varices in CLD Patients JAVED SAYYED*, DEEPTI SHARMA†, SR MEENA‡, SANKET SINGH#, PALLAVI VIJ¥, MUKESH VERMA¥

ABSTRACT Aims and objectives: To study the correlation of esophageal varices with serum ascites albumin gradient (SAAG) and platelet count/spleen size ratio in patient’s of chronic liver disease (CLD). Material and methods: A study of CLD patient’s with ascites evidenced by abdominal USG and liver profile, aged between 18 and 65 years with no previous diagnosis of esophageal varices was carried out. Platelet count, spleen size, SAAG and platelet count/spleen size ratio was determined and endoscopy was done. Results: In our study, out of 100 CLD patients 78 patients had esophageal varices. The results showed that SAAG cut-off of ≥1.45 had 79.4% of sensitivity and 59.1% specificity and 87.3% of positive predictive value (PPV). A platelet count/ spleen size ratio cut-off value of ≤929 had sensitivity of 76.9%, specificity of 54.4% and a PPV of 85.7%. When both the SAAG and platelet count/spleen ratio is used simultaneously, the net sensitivity becomes 96.1% and PPV becomes 84.3%. Conclusion: Combined high SAAG and low platelet count/spleen size ratio are noninvasive parameters with very high-sensitivity (96%) and high PPV (84%) for esophageal varices in CLD patients and thus helpful in identifying the patients for early referral for endoscopy from periphery.

Keywords: Esophageal varices, serum ascites albumin gradient, platelet count/spleen size ratio, chronic liver disease, abdominal USG, liver profile

C

irrhosis is a condition that is defined histopathologically and has a variety of clinical manifestations and complications, some of which can be life-threatening. The clinical course of patients with advanced cirrhosis is often complicated by a number of important sequelae that can occur regardless of the underlying cause of the liver disease.

These include portal hypertension (PHTN) and its consequences of gastroesophageal variceal hemorrhage, splenomegaly, ascites, etc.1

PHTN is defined as the elevation of the hepatic venous pressure gradient >5 mmHg. PHTN is directly responsible for the two major complications of cirrhosis: variceal hemorrhage and ascites. Variceal hemorrhage

*Resident (3rd Year) †Professor ‡Senior Professor and Head #Ex-Resident ¥Resident (2nd year) Dept. of Medicine, Government Medical College, Kota, Rajasthan Address for correspondence Dr Javed Sayyed Ward No. 3, Near Madina Masjid, Fatehpur Shekhawati, Sikar - 332 301, Rajasthan

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Indian Journal of Clinical Practice, Vol. 26, No. 12, May 2016

is an immediate life-threatening problem with a 20-30% mortality rate associated with each episode of bleeding varices.1 The serum ascites albumin gradient (SAAG) is minimally invasive method that is highly precise and allows for classification of ascitic fluid according to the absence and presence of PHTN.2,3 In several studies on cirrhosis due to alcohol, the correlation between SAAG and esophageal varices was emphasized and additionally, SAAG was proposed to be a factor determining the degree of PHTN and the prognosis of patients with cirrhosis due to alcohol.4,5 Hypersplenism with the development of thrombocytopenia is a common feature of patients with cirrhosis and is usually the first indication of PHTN. However, in patients with chronic liver disease (CLD), the presence of decreased platelet count may depend on several factors other than PHTN such as shortened platelet mean lifetime, decreased thrombopoietin production or myelotoxic effects of alcohol or hepatitis virus.6 Splenomegaly in cirrhotic patients is likely to be due to vascular disturbances due to PHTN. In order to eliminate other causes for decreased platelet count in cirrhotics, platelet count/spleen diameter ratio

GASTROENTEROLOGY has been used as a parameter linking thrombocytopenia to spleen size in order to introduce a variable that takes into consideration, the decrease in platelet count, which most likely depends on hypersplenism caused

by PHTN.7 Routine endoscopic screening of all cirrhotic patients with or without varices has health service cost implications. Therefore, it might be cost-effective to identify those patients who would benefit most from routine noninvasive screening.3,8 In developing countries like India where the burden on health institutions is more, the screening of esophageal varices by endoscopy has high cost and secondarily, it is an invasive procedure that leads to more patient’s discomfort. Previous studies have been done on SAAG as well as on platelet count/spleen size (diameter) ratio for the prediction of esophageal varices. These are noninvasive and more cost-effective procedures.

But very few studies covered both the SAAG and platelet count/spleen size ratio for the prediction of esophageal varices. So, we planned a study undertaken to determine the correlation and association between the level of SAAG and platelet count/spleen size ratio for the prediction of esophageal varices found on upper gastrointestinal endoscopy.

fully automated cell counter as well as manual method.

Abdominal ultrasonography was carried out with Siemens Sonoline G60S using transducer 3-5 mHz to determine spleen size as bipolar diameter in millimeter.

Endoscopy was performed by expert endoscopist by using PENTAX video-endoscope to evaluate the presence of esophageal varices. Results were tabulated and conclusion was made on the basis of results of study after applying Chi-square test, Pearson’s correlation coefficient and receiver-operating-characteristic (ROC) curve.

RESULTS

MATERIAL AND METHODS

Most of our patients were in 31-45 years (47%) of age group. Mean age was 44.6 ± 12.7. Seventy-four percent patients out of 100 patients were males and only 26% were females. Cause of CLD in 49 patients out of 100 patients was alcohol. Forty-four patients out of 100 CLD patients had total serum bilirubin level in between 1 and 3 mg/dL. In our study, nearly half of the patients had serum glutamic oxaloacetic transaminase (SGOT) and serum glutamic pyruvic transaminase (SGPT) level in the range of 41-100 IU/L. Mean SGOT level was 88.6 ± 59.3 IU/L and mean SGPT level was 75.9 ± 59.8 IU/L. Nearly 80% patients in our study had total proteins in the range between 5.1 and 7 g/dL with mean value of 6.0 ± 0.78 g/dL. Nearly all the patients were hypoalbuminemic with mean albumin level of 2.6 ± 0.49 g/dL and mean serum globulin level was 3.3 ± 0.69 g/dL. In our study, 47% patients had PT-INR level in the range of 1.5 to 2 and 27% patients had in the range between 2.1 to 3.0. The mean alkaline phosphatase (ALP) level was 139 ± 95.8 IU/L.

This study has been carried out on patients of CLD admitted at our institute from January 2015 to November 2015. We included 100 patients in the age group of 18-65 years having CLD with ascites as evidenced by: abdominal ultrasound and liver profile derangement.

We excluded patients with other causes of ascites, patients operated for PHTN, patients on treatment with β-blockers, nitrates and diuretics, patients who had received platelet transfusion within the last 1 month, patients with known causes of thrombocytopenia other than cirrhosis and patients with known causes of splenomegaly other than cirrhosis.

Seventy-eight percent patients were found to have esophageal varices. We classified all our patients on the basis of Child-Pugh’s class and found that 3 patients were in Class A, 49 patients were in Class B and 48 patients were in Class C. Out of total patients, 38% had Grade 3 esophageal varices, 28% had Grade 2, 11% had Grade 1 and 1% had Grade 4 varices and according to Child-Pugh’s class, in Class B 73% had varices and in Class C 85% had varices. Ninety-one out of 100 CLD patients had high SAAG value of which 43 patients had in the range of 1.0-1.5 g/dL and 48 patients had in the range of 1.5-2.0 g/dL.

Purpose of this study was explained to the study subject and their relatives. The concentration of albumin in serum and ascitic fluid was determined by using Bromcresol Green method, simultaneously with these results SAAG was calculated. Platelet count (No. of platelets/µL) was performed by 6 part differential

Mean SAAG value was 1.58 ± 0.29 g/dL. Eighty patients out of 100 CLD patients had platelet counts below 1.5 lakhs/mm3 of which 48% patients were in the range of 75,000-1,50,000, 21% in the range of 50,000-75,000 and 11% had platelets below 50,000. Sixty patients had splenomegaly in the range of 100-150 mm and

AIMS OF STUDY To study the correlation of esophageal varices with SAAG and platelet count/spleen size ratio in patients of CLD.

Indian Journal of Clinical Practice, Vol. 26, No. 12, May 2016

1133

GASTROENTEROLOGY Table 1. Association of Lab Parameters with Esophageal Varices Lab parameter

Varices

N

Mean ± SD

T-test

P value

Serum bilirubin

Present

78

3.45 ± 4.25

0.441

0.66

Absent

22

3.03 ± 2.54

Serum total proteins

Present

78

6.06 ± 0.78

0.799

0.42

Absent

22

5.91 ± 0.77

Present

78

101688.46 ± 54362.07

-3.329

0.001

Absent

22

155500.0 ± 100459.30

Spleen size

Present

78

148.01 ± 30.22

1.336

0.18

Absent

22

138.4 ± 28.15

SGOT

Present

78

89.0 ± 58.53

0.126

0.90

Absent

22

87.18 ± 63.69

SGPT

Present

78

78.94 ± 63.28

0.010

0.99

Absent

22

65.18 ± 45.37

Present

78

1.63 ± 0.26

4.003

0.001

Absent

22

1.37 ± 0.30

Present

78

725.67 ± 433.77

3.460

0.001

Absent

22

1214.18 ± 952.20

Platelet count

SAAG PLT count/spleen size

34 patients had splenomegaly in the range of 150-200 mm. Mean spleen size was 145.9 ± 29.91 mm.

By applying Chi-square test (Table 1), we found that there was statistically significant difference between the mean platelet count of those who had the varices from those who did not. Statistically significant difference was found between the mean SAAG values of those who had the varices from those who did not (p = 0.001) and statistically significant difference was also found between the means of platelet count/spleen size of those who had varices as compared to those who did not (p = 0.001). No statistically significant association was found between grades of varices and platelet count/spleen size ratio (p = 0.056). Statistically significant association was found between grades of varices and SAAG (p = 0.01).

DISCUSSION Esophageal varices may cause life-threatening bleeding with attendant high hospital cost. Since effective preventive modalities for variceal hemorrhage have been established, early detection of esophageal varices is critical for prevention of bleeding. Currently, endoscopic screening is widely recommended to patients who have the diagnosis of CLD. However, the diagnosis of cirrhosis relies on histological evaluation which is costly and invasive and endoscopic screening also burdens medical resources. In our study, all patients underwent endoscopy and 78% patients had esophageal varices and 22% had no esophageal varices. Our study had

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Indian Journal of Clinical Practice, Vol. 26, No. 12, May 2016

similar results as studies done by Abu El Makarem9 et al, Baig10 et al, Sarangapani11 et al and González-Ojeda12 et al. According to these studies, there was nearly two-third of patients who were suffering from esophageal varices. Patients with CLD eventually progress to cirrhosis of liver and its associated problems like PHTN. Development of varices is one of the major problem of PHTN. Esophageal varices is the direct consequence of spontaneous formation of collateral vessels between the portal vein and esophageal veins via the left gastric or short gastric veins.

In our study, 38% had Grade 3 esophageal varices, 28% had Grade 2, 11% had Grade 1 and 1% had Grade 4 varices. Our study was similar to studies of Baig10 et al, Demirel13 et al, Kumar14 et al, Allam15 et al and El-Sharqawy16 et al; who showed that nearly 60-70% patients had large varices. Large varices shows the severity of PHTN in CLD. Larger the varix, the chances of bleeding is more. Our study was similar to studies of El-Sharqawy16 et al, Demirel13 et al, Allam15 et al, Abu El Makarem9 et al and González-Ojeda12 et al who also reported most of their patients in Child-Pugh’s Class B and C. Giannini7 et al, Baig10 et al and Hong17 et al reported more patients of Class A. This was because ascites and encephalopathy were present in less number of their patients indicating lesser severity.

We also studied the relation between Child-Pugh’s classification and presence or absence of varices in our patients.

GASTROENTEROLOGY In Class B, 73% had varices and in Class C, 85% had varices. But after applying Chi-square test no statistically significant correlation was found between them. This explains that esophageal varices are present mostly in Class B and C, which denotes decompensated liver disease. As patients progress to decompensated liver disease it is noted that presence of esophageal varices increases which was also supported by the studies done

by Torres5 et al, Zaman18 et al and Madhotra19 et al.

We compared the different lab parameters (Table 1) of 78 patients who had esophageal varices and 22 patients who did not have esophageal varices and found statistically significant difference between the mean platelet count, mean SAAG value and mean platelet count/spleen size ratio of those who had esophageal varices from those who did not have. This was similar to studies of Abu El Makarem9 et al who showed statistically significant difference between the mean platelet count, mean SAAG value and mean platelet count/spleen size ratio of those who had esophageal varices from those who did not have. To interpret the cut-off value of SAAG in our study, we used ROC curve (Fig. 1).

Area-under-the-curve (AUC) is 0.758. If the SAAG cut-off value is kept at 1.45 g/dL it will give (Table 2) 79.5% sensitivity and 59.1% specificity for predicting esophageal varices. With a cut-off value of 1.45 g/dL for SAAG, we found out the association of it with esophageal varices by applying Chi-square (Table 3) test which was statistically significant which was also observed by Torres5 et al, El-Sharqawy16 et al, Das20 et al, Jaffri21 et al,

Allam15 et al, Sukhiranwat22 et al and Kumar14 et al.

So, it is concluded that high SAAG is a noninvasive marker which helps in predicting esophageal varices.

A statistically significant association was found between SAAG and grades of varices in our study by applying Chi-square test. This was similar to studies of Kajani23 et al, El-Sharqawy16 et al, Masroor24 et al and Kumar14 et al; Torres5 et al, Demirel13 et al and Gurubacharya3 et al found that ascites and high SAAG in patients were directly related to presence of esophageal varices but were not related to the size of esophageal varices. According to their study, there was poor correlation between high SAAG and grades of varices. We also used the ROC curve (Fig. 2) Table 2. Sensitivity and Specificity of SAAG Against Endoscopy SAAG

Varices present (Endoscopy)

Varices absent (Endoscopy)

Total

â&#x2030;Ľ1.45 (varices present)

62

9

71

<1.45 (varices absent)

16

13

29

Total

78

22

100

Table 3. Association Between SAAG and Esophageal Varices SAAG Varices present Varices absent

Chi-square test

â&#x2030;Ľ1.45

62

9

10.601

<1.45

16

13

p = 0.001

ROC Curve

1.0

ROC Curve

1.0

0.8

Sensitivity

Sensitivity

0.8 0.6

0.4

0.6

0.4

0.2 0.2 0.0

0.0

0.2

0.4

0.6

Specificity

Figure 1. ROC of SAAG.

0.8

1.0

0.0

0.0

0.2

0.4

0.6

0.8

10

Specificity

Figure 2. ROC of platelet count/spleen size ratio.

Indian Journal of Clinical Practice, Vol. 26, No. 12, May 2016

1135

GASTROENTEROLOGY to interpret the cut-off value for platelet count/spleen size ratio in our study. AUC was 0.697. If cut-off value is taken as 929 then sensitivity (Table 4) will be 76.9% and specificity will be 59.1% for predicting esophageal varices. By using a cut-off value of platelet count/spleen size ratio as ≤929 and applying Chi-square (Table 5) test, we found a statistically significant association between platelet count/spleen size ratio and esophageal varices which was similar to González-Ojeda12 et al, Abu El Makarem9 et al, Sarangapani11 et al, Biag10 et al, Kaji25 et al and Table 4. Sensitivity and Specificity of Platelet Count/ Spleen Size Ratio Against Endoscopy Platelet count/ spleen size

Varices present Varices absent (Endoscopy) (Endoscopy)

Total

≤929

60

10

70

>929

18

12

30

Total

78

22

100

Sensitivity = 60/78 × 100 = 76.9%, Specificity = 12/22 × 100 = 54.5%, PPV = 60/70 × 100 = 85.7%.

Table 5. Association Between Platelet Count/Spleen Size with Esophageal Varices Platelet count/ spleen size

Varices present

Varices absent

Chi-square test

≤929

60

10

6.663

>929

18

12

p = 0.01

Table 6. Sensitivity and PPV of Simultaneous Testing of SAAG and Platelet Count/Spleen Size Ratio Against Endoscopic Findings Platelet count/spleen size + SAAG

Varices present

Varices absent

Total

Varices present

75

14

89

Varices absent

3

8

11

Total

78

22

100

Net sensitivity = 75/78 × 100 = 96.1%, PPV = 75/89 × 100 = 84.3%.

Table 7. Comparison of Sensitivity of SAAG, Platelet Count/Spleen Size, SAAG + Platelet Count/Spleen Size Parameters

Sensitivity

SAAG

79.4%

Platelet count/spleen size

76.9%

SAAG + Platelet count/spleen size

96.1%

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Indian Journal of Clinical Practice, Vol. 26, No. 12, May 2016

Giannini26 et al. In our study, we found that if cut-off value for platelet count/spleen size is ≤929 then it is a good predictor for esophageal varices in CLD patients.

There was no statistically significant association between grades of varices and platelet count/spleen size ratio found in our study.

Our study was similar to studies done by Giannini26 et al and González-Ojeda12 et al; they also reported that there is no correlation between the grades of varices and platelet count/spleen size ratio. In our study, when simultaneous testing was done with SAAG and platelet count/spleen size ratio against endoscopic findings (Table 6) then net sensitivity was 96.1% and PPV was 84.3% and while comparing the sensitivity (Table 7) of SAAG, platelet count/spleen size ratio and SAAG plus platelet count/spleen size ratio for predicting esophageal varices in CLD patients then SAAG had 79.4%, platelet count/spleen size ratio had 76.9% and when SAAG and platelet count/spleen size ratio were included together then sensitivity increased to 96.1% for prediction of esophageal varices.

So, combining these two noninvasive parameters in subgroup with ascites increases the reliability of predicting esophageal varices. Thus, simultaneous use of these parameters helps in identifying patients with a high probability of having esophageal varices without performing endoscopy. This may also help reduce costs and discomfort for these patients and the burden on endoscopy units.

CONCLUSION Combined high SAAG and low platelet count/spleen size ratio are noninvasive parameters with very high sensitivity (96%) and high PPV (84%) for esophageal varices in CLD patients and thus helpful in identifying the patients for early referral for endoscopy from periphery.

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In: Longo DL, Fauci AS, Kasper DL, Hauser SL, Jameson JL, Loscalzo J (Eds.). Harrison’s Principles of Internal Medicine, 18th Edition, New York: McGraw-Hill Medical; 2011. pp. 2592-7.

2. Runyon BA, Montano AA, Akriviadis EA, Antillon MR, Irving MA, McHutchison JG. The serum-ascites albumin gradient is superior to the exudate-transudate concept in the differential diagnosis of ascites. Ann Intern Med. 1992;117(3):215-20.

3. Gurubacharya DL, Mathura KC, Karki DB. Correlation between serum-ascites albumin concentration gradient

GASTROENTEROLOGY and endoscopic parameters of portal hypertension.

Kathmandu Univ Med J (KUMJ). 2005;3(4):327-33.

ascites albumin gradient. J Liaquat Uni Med Health Sci. 2013;12(3):167-71.

4. Paré P, Talbot J, Hoefs JC. Serum-ascites albumin concentration gradient: a physiologic approach to the differential diagnosis of ascites. Gastroenterology.

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15. Allam E, Ghoraba D, Abdelhakam S, Ibrahim WA. Correlation between serum-ascites albumin gradient and esophageal varices in patients with portal hypertension.

SciencePub. 2011;3(8):39-49.

5. Torres E, Barros P, Calmet F. Correlation between serumascites albumin concentration gradient and endoscopic parameters of portal hypertension. Am J Gastroenterol.

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16. El-Sharqawy EH, El-Badawy R, Fathy EM, El-Attar I, Amin H. Assessment of the relation between serumascites albumin concentration gradient with esophageal varices and its complication. Available at: www.bu.edu. eg/.../Entesar%20%20Husien%20Morsy%20EL%20 Sharqawy_PAPER.

6. de Franchis R; Baveno V Faculty. Revising consensus in portal hypertension: report of the Baveno V consensus workshop on methodology of diagnosis and therapy in portal hypertension. J Hepatol. 2010;53(4):762-8 7. Giannini E, Botta F, Borro P, Risso D, Romagnoli P, Fasoli A, et al. Platelet count/spleen diameter ratio: proposal and validation of a non-invasive parameter to predict the presence of oesophageal varices in patients with liver cirrhosis. Gut. 2003;52(8):1200-5.

8. Hoefs JC. Serum protein concentration and portal pressure determine the ascitic fluid protein concentration in patients with chronic liver disease. J Lab Clin Med. 1983;102(2):260-73.

9. Abu El Makarem MA, Shatat ME, Shaker Y, Abdel Aleem AA, El Sherif AM, Moaty MA, et al. Platelet count/bipolar spleen diameter ratio for the prediction of esophageal varices: The special Egyptian situation: Noninvasive prediction of esophageal varices. Hepat Mon. 2011;11(4):278-84.

10. Baig WW, Nagaraja MV, Varma M, Prabhu R. Platelet count to spleen diameter ratio for the diagnosis of esophageal varices: Is it feasible? Can J Gastroenterol.

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11. Sarangapani A, Shanmugam C, Kalyanasundaram M, Rangachari B, Thangavelu P, Subbarayan JK. Noninvasive prediction of large esophageal varices in chronic liver disease patients. Saudi J Gastroenterol. 2010;16(1):38-42.

12. González-Ojeda A, Cervantes-Guevara G, ChávezSánchez M, Dávalos-Cobián C, Ornelas-Cázares S, MacíasAmezcua MD, et al. Platelet count/spleen diameter ratio to predict esophageal varices in Mexican patients with hepatic cirrhosis. World J Gastroenterol. 2014;20(8): 2079-84.

13. Demirel U, Karincaoğlu M, Harputluoğlu M, Ateş M, Seçkin Y, Yildirim B, et al. Two findings of portal hypertension: evaluation of correlation between serumascites albumin gradient and esophageal varices in non-alcoholic cirrhosis. Turk J Gastroenterol. 2003;14(4): 219-22.

17. Hong WD, Dong LM, Jiang ZC, Zhu QH, Jin SQ. Prediction of large esophageal varices in cirrhotic patients using classification and regression tree analysis. Clinics (Sao Paulo). 2011;66(1):119-24.

18. Zaman A, Hapke R, Flora K, Rosen HR, Benner K. Factors predicting the presence of esophageal or gastric varices in patients with advanced liver disease. Am J Gastroenterol. 1999;94(11):3292-6.

19. Madhotra R, Mulcahy HE, Willner I, Reuben A. Prediction of esophageal varices in patients with cirrhosis. J Clin Gastroenterol. 2002;34(1):81-5.

20. Das BB, Purohit A, Acharya U, Treskova E. Serum-ascites albumin gradient: a predictor of esophageal varices with ascites. Indian J Pediatr. 2001;68(6):511-4.

21. Jaffri MSA, Shaikh AA, Jaffri MH, Munir SM. Diagnostic sensitivity and specificity of serum-ascites albumin gradient in patients with ascites. J Liaquat Uni Med Health Sci. 2009;8(3):196-200.

22. Sukhiranwat S, Pisespongsa P, Prisontarangkul O, Thongsawat S, Chitapanarux T, Leerapan A. Primary prevention of variceal bleeding in patients with serum ascites albumin gradient ≥ 1.5 g/dL. Thai J Gastroenterol.

2011;12(1):47-51.

23. Kajani MA, Yoo YK, Alexander JA, Gavaler JS, Stauber RE, Dindzans VJ, et al. Serum-ascites albumin gradients in nonalcoholic liver disease. Dig Dis Sci. 1990;35(1):33-7.

24. Masroor M, Qamar R, Ahmed I, et al. Do we always need endoscopy to predict varices. Med Channel. 2007;13(1): 55-8.

25. Kaji BC, Bhavsar YR, Patel P, Garg A, Kevadiya H, Mansuri Z. A study of clinical profile of 50 patients with portal hypertension and to evaluate role of noninvasive predictor of esophageal varices. Indian J Clin Pract. 2012;22(9):454-7.

26. Giannini EG, Zaman A, Kreil A, Floreani A, Dulbecco P, Testa E, et al. Platelet count/spleen diameter ratio for the noninvasive diagnosis of esophageal varices: results 14. Kumar S, Memon IA, Kaleem M, Alamani SA. Prediction of a multicenter, prospective, validation study. Am J of esophageal varices in cirrhotic patients with serum Gastroenterol. 2006;101(11):2511-9.

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INTERNAL MEDICINE

Prevalence of Microalbuminuria in Patients of HIV/ AIDS and Its Correlation with CD4 Cell Count and the Duration of Ιllness S SANTHEEV*, LUBNA ZAFAR†, ANJUM PARVEZ‡, HS KHAN#

ABSTRACT Nephropathy in the form of microalbuminuria and macroalbuminuria is an important cause of morbidity and mortality in human immunodeficiency virus/acquired immune deficiency syndrome (HIV/AIDS) and is a harbinger of many cardiovascular problems. Present study was conducted over a period of 2 years with the objective to evaluate the prevalence of microalbuminuria in HIV/AIDS patients and its correlation with CD4 cell count and the duration of illness. A total of 100 HIV/AIDS patients, attending the ART Center of JNMCH, were enrolled. Out of 100 patients, 58 (58%) were males and 42 (42%) were females.

Microalbuminuria was observed in 39 (39%) patients and significant correlation was found between CD4 cell count (<200/mm3) and prevalence of microalbuminuria (p < 0.001). Similarly, statistically significant correlation was observed between the duration of disease and nephropathy (p < 0.001). Use of microalbuminuria in HIV/AIDS as a screening test may benefit the patient by early recognition and appropriate intervention.

Keywords: Microalbuminuria, HIV/AIDS, CD4 cell count

H

uman immunodeficiency virus or HIV is a member of the genus Lentivirus, part of the family of Retroviridae. These are transmitted as single-stranded, positive sense, enveloped RNA viruses.

Upon entry into the target cell, the viral RNA genome is converted (reverse transcribed) into double-stranded DNA by a virally encoded reverse transcriptase that is transported along with the viral genome in the virus particle. The resulting viral DNA is then imported into the cell nucleus and integrated into the cellular DNA by a virally encoded integrase and host cofactors. Once integrated, the virus may become latent, allowing the virus and its host cell to avoid detection by the immune system. Alternatively, the virus may be transcribed, producing new RNA genomes and viral

*Junior Resident (3rd Year) †Assistant Professor ‡Associate Professor #Professor Dept. of Medicine JN Medical College, Aligarh Muslim University, Aligarh, Uttar Pradesh Address for correspondence Dr Anjum Parvez Flat No. 2, 2nd Floor Royal Apartment, Kela Nagar, Civil Lines, Aligarh, Uttar Pradesh E-mail: anjumparvez66@yahoo.com

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protein that are packaged and released from the cell as new virus particles that begin the replication cycle.

Two types of HIV have been characterized: HIV-1 and HIV-2. HIV-1 is the virus that was initially discovered and termed both lymphadenopathy-associated virus (LAV) and human T-lymphotropic virus type III (HTLV-III). It is more virulent, more infective and is the cause of the majority of HIV infections globally. The lower infectivity of HIV-2 compared to HIV-1 implies that fewer of those exposed to HIV-2 will be infected per exposure. Due to its relatively poor capacity for transmission, HIV-2 is largely confined to West Africa.1 Presently in India more than 5 million people are infected with HIV and have the second largest pool of HIV in the world.2 Infection with HIV-1 is associated with a progressive decline in CD4 cell count and an increase in the level of HIV in the blood. The stage of infection can be determined by measuring the patients CD4 cell count and viral load. The stages of HIV infection are acute infection (also known as primary infection), stage of latency and acquired immune deficiency syndrome (AIDS).

Acute Infection It lasts for several weeks and may include symptoms such as fever, lymphadenopathy, pharyngitis, rash, myalgia, malaise, oral and esophageal sores.

INTERNAL MEDICINE Stage of Latency

Inclusion Criteria

It involves few or no symptoms and can last from 2 weeks to 20 years or more depending on the individual.

HIV patients confirmed by rapid kit enzyme-linked immunosorbent assay (ELISA) and enrolled in ART Center, JNMCH, AMU, Aligarh.

AIDS

Exclusion Criteria

The final stage of HIV infection, is defined by low CD4 cell count (<200/µL), various opportunistic infections, cancers and other conditions.3

Patients with fever in past 2 weeks, previous renal disease, acute/chronic urinary tract infection (UTI), diabetes mellitus/hypertension, any history of cardiac ailment and pregnant females were excluded from the study. Patients with more than 1+ protein in dipstick test were also excluded from the study.

Broad-spectrum of renal diseases have been reported in patients with HIV/AIDS ranging from acid-base disorders to acute renal failure, to glomerular diseases such as immunoglobulin A (IgA) nephropathy, membranous nephropathy, membranoproliferative, mesangioproliferative, diffuse proliferative or crescentic glomerulonephritis. Apart from these, a distinctive form of sclerosing glomerulopathy called HIVAN (HIV-associated nephropathy) is seen in 5-10% of HIV patients. It may be the most common cause of end-stage renal disease (ESRD) in HIV patients. It is associated with proteinuria, which may be the first manifestation of this condition.4 Among HIV-infected patients the presence of proteinuria has been linked to chronic kidney disease (CKD), ESRD and new AIDS defining illness and mortality.5 Use of microalbuminuria as a routine screening test is recommended in HIV patients, its use in the screening phase itself can help detection of renal involvement in HIV in early stages and thus reduce patient morbidity and prolong patient survival in a better way. There is scarcity of Indian studies as far as renal spectrum of HIV is concerned and very little data is available on microalbuminuria and proteinuria in HIV patients.

AIMS AND OBJECTIVES ÂÂ

To study the prevalence of microalbuminuria in HIV/AIDS.

ÂÂ

To evaluate the correlation microalbuminuria and CD4 cell count.

ÂÂ

To evaluate the correlation between microalbuminuria and the duration of disease.

between

MATERIAL AND METHODS The study was an observational, single center, crosssectional study. It was conducted in 100 HIV/AIDS patients attending the Medicine OPD and ART Center, Jawaharlal Nehru Medical College and Hospital (JNMCH), AMU, Aligarh. The sampling method used in our study was simple random sampling and the patients entered the study after an informed consent.

Apart from the routine laboratory investigations like hemogram, blood urea, serum creatinine, liver function tests, serum lipid profile, CD4 cell counts, all patients were first screened for proteinuria using urine dipstick method and only those with either nil or trace proteins were selected for further quantification using spot urine albumin-to-creatinine ratio (ACR) test (Modified Jaffe’s reaction). On the basis of spot urine ACR test, patients with 30-300 mg/g were categorized under microalbuminuria and those with >300 mg/g were labeled as having macroalbuminuria. Study subjects were also categorized on the bases of CD4 cell count into three groups (<200, 200-500 and >500 cells/mm3) as well as on the basis of the duration of illness (<1, 1-5 and >5 years).

Statistical Analysis The data of all the 100 patients enrolled in the study was entered into the SPSS software. Categorical variables in the study were compared using Pearson’s Chi-squared test (χ2). P value of <0.05 was considered to be significant.

RESULTS Out of total 100 patients, 58 (58%) were males and 42 (42%) females (Table 1 and Fig. 1). Male-to-female ratio was 1.4:1. The most common route of transmission was sexual, seen in 56 (56%) patients followed by blood transfusion (24%), maternal-fetal transmission (8%) and intravenous drug abuse (2%) (Table 2 and Fig. 2).

All 100 patients were subjected to urinalysis by spot urine ACR method for quantification of albuminuria.

Thirty-nine (39%) patients had urine albumin in the range of 30-300 mg/g (microalbuminuria) and rest 61 (61%) had urine albumin >300 mg/g (macroalbuminuria) (Table 3 and Fig. 3). Therefore, the prevalence of microalbuminuria in our study was 39%. Microalbuminuria was present in all three groups

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INTERNAL MEDICINE Table 1. Gender-wise Distribution of Patients in Study Group Sex

No. of patients (n = 100)

Percentage (%)

Male

58

58

Female

42

42

Total

100

100

Male

Female Sex distribution

of CD4 cell count but with varying proportions. It was observed in 4 (10.3%), 27 (69.7%) and 8 (20.5%) patients with CD4 count <200, 200-500 and >500, respectively.

Out of 14 (14%) patients of those having CD4 cell counts >500, only 6 (42.8%) had macroalbuminuria, while 8 (57.1%) had microalbuminuria. Similarly, out of total 32 patients (32%) who had CD4 cell count <200, only 4 (12.5%) patients had microalbuminuria and 28 (87.5%) had macroalbuminuria (Table 4 and Fig. 4).

Macroalbuminuria indicating more severe degree of renal impairment was seen more in the group with CD4 Table 3. Prevalence of Microalbuminuria and Macroalbuminuria in Study Group

42

ACR (mg/g)

No. of patients (n = 100)

Percentage (%)

30-300 (microalbuminuria)

39

39

>300 (macroalbuminuria)

61

61

Total

100

100

58

Figure 1. Gender-wise distribution of patients in study group.

Table 2. Route of Transmission of HIV in Study Group Route of transmission

No. of patients (n = 100)

Percentage (%)

Sexual

56

56

Blood transfusion

24

24

Mother-to-child

8

8

IV drug abuse

2

2

Others

10

10

Total

100

100

60

50 40

20 10 0 Microalbuminuria

40

24

20 10

8 2

0 Sexual

Macroalbuminuria

Figure 3. Prevalence of microalbuminuria and macroalbuminuria in study group.

CD4 count

10

39

Table 4. Correlation of Microalbuminuria and Macroalbuminuria with CD4 Cell Count

56

30

61

60

30

50

Mother-toBlood transfusion child

IV drug abuse

Others

Figure 2. Route of transmission of HIV in study group.

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Indian Journal of Clinical Practice, Vol. 26, No. 12, May 2016

CD4 correlation

Total

30-300 >300 Microalbuminuria Macroalbuminuria

<200

4 (10.3%)

28 (45.9%)

32 (32.0%)

200-500

27 (69.7%)

27 (44.3%)

54 (54.0%)

>500

8 (20.5%)

6 (9.8%)

14 (14.0%)

Total

39 (100%)

61 (100%)

100 (100%)

Ď&#x2021;2 = 14.13; df = 2; p = 0.001.

INTERNAL MEDICINE cell count <200/mm3 i.e., more advanced stage of HIV/ AIDS and the correlation was found to be statistically significant (p < 0.05). Out of 7 patients with duration of illness less than 1 year, all (100%) had microalbuminuria and none had macroalbuminuria. Whereas out of 11 patients who were having disease duration more than 5 years, only 2 (18.1%) had microalbuminuria, whereas rest 9 (81.8%) had macroalbuminuria, indicating more severe degree of nephropathy in this group (Table 5, Fig. 5). This implies that with increase in the Microalbuminuria

Macroalbuminuria

35 28

30

27 27

25 20 15 8

10 5

6

4

0 200-500

<200

>500

Figure 4. Correlation of microalbuminuria and macroalbuminuria with CD 4 cell count.

Table 5. Correlation of Microalbuminuria with Duration of Illness Duration of illness (years)

ACR group 30-300

Total

>300

<1

7 (17.9%)

0 (0.0%)

7 (7.0%)

1-5

30 (76.9%)

52 (85.2%)

82 (82.0%)

>5

2 (5.1%)

9 (14.8%)

11 (11.0%)

39 (100%)

61 (100%)

100 (100%)

Total

Ď&#x2021;2 = 13.154; df = 2; p = 0.001.

Microalbuminuria

60

Macroalbuminuria 52

50 40 30

30 20 10

9

7 2

0

0 <1

1-5

>5

Figure 5. Correlation of microalbuminuria and macroalbuminuria with duration of illness.

duration of disease, severity of nephropathy increases and this correlation was found to be statistically significant (p â&#x2030;¤ 0.05).

DISCUSSION The study population comprised of 100 patients, 58 (58%) were males and 42 (42%) were females.

Male-to-female ratio was 1.4:1. In a study done by Janakiraman et al6 in Chennai, there were more males than females and male-to-female ratio was 1.8:1, which is comparable to our study. The routes of transmission in our study population was sexual (56%), followed by blood transfusion (24%). Eight percent got infected by maternal-fetal route, 2% via intravenous (IV) drug abuse and rest 10% got infected through supposedly miscellaneous routes (like tattooing, trauma and surgery). Janakiraman et al also reported heterosexual route to be the commonest mode of transmission.

The patients in our study were evaluated for albuminuria by spot urinary ACR (UACR) method. Out of total 100 patients, 39 patients, had ACR in the range of 30-300 mg/g; hence, the prevalence of microalbuminuria in our study was 39%. There were wide variations observed in the prevalence of microalbuminuria in other studies, ranging from 10% to 33% reported from Port Harcourt (Eke et al),7 Nigeria, Africa and India (Shah et al).8 Luke et al9 in a study conducted on 72 HIV-positive patients found microalbuminuria in 19.4%. Busch et al10 found a prevalence of 13% among 90 HIV-positive patients. Monje et al11 found 19% prevalence of microalbuminuria in 48 HIV-seropositive patients in different clinical stages. However, Han et al12 found a prevalence of 36% in a cross-sectional study conducted on HIV-positive patients in South Africa. This is comparable to our study, the reason may be the similar patient profile in their study like older population, lower CD4 counts, advanced HIV disease and patients not been on any antiretroviral therapy.

The reason for wide variation in the prevalence data might be because of varying sample sizes, differing cut-off values for the definition of microalbuminuria, differing assay techniques, widely varying study population and selection criteria specifically related to diabetes mellitus and hypertension. The higher prevalence observed in our study group may be attributed to lower CD4 cell counts in majority of patients in our study, thereby reflecting advanced HIV disease, like in the study by Han et al. The patients in our study were divided into three groups according to the CD4 cell counts (<200, 200-500 and >500/mm3), with the purpose of correlating the CD4 status with the presence of microalbuminuria.

Out of the 39 patients who had microalbuminuria in

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INTERNAL MEDICINE our study, 4 (10.3%), 27 (69.2%) and 8 (20.5%) were in <200, 200-500 and >500 CD4 count groups, respectively.

So, it is evident that majority of patients (89.7%) with microalbuminuria belonged to moderate-to-severe immunosuppression group (CD4 count <500/mm3).

Out of total 32 patients with CD4 cell count <200, 28 (87.5%) had macroalbuminuria and only 4 (12.5%) had microalbuminuria. Macroalbuminuria indicating more severe degree of renal impairment, was observed more, in <200 CD4 count group i.e., more advanced stage of disease. Thus, nephropathy was seen more at lower CD4 cell counts and late clinical stage of HIV/AIDS and this association was found to be statistically significant.

Similar observations were made by Szczech et al13 and Janakiraman et al in their respective studies.

In our study, patients were divided into three groups on the basis of duration of illness: less than 1 year, 1-5 years and more than 5 years. Out of 7 (7%) patients with duration of illness less than 1 year, all had microalbuminuria and none had macroalbuminuria.

There were 11 (11%) patients with duration of symptoms for more than 5 years, among them only 2 (18.2%) had microalbuminuria, whereas 9 (81.8%) had macroalbuminuria, indicating more severe degree of nephropathy in this group. This indicates that with increasing duration of illness, severity of nephropathy increases and the correlation was found to be statistically significant. Similar observations were made in studies conducted in Port Harcourt, Nigeria by Eke et al and in Tanzania by Fredrick et al.14 CONCLUSION Nephropathy is an important cause of morbidity and mortality in HIV/AIDS patients. We observed that nephropathy in the form of microalbuminuria and macroalbuminuria was associated with lower CD4 cell count, more advanced stage of HIV/AIDS and increased duration of illness. Use of microalbuminuria as a routine screening test in those who are HIV/AIDS positive will help in uncovering those cases, which are heading towards advanced renal impairment. This may help in instituting intensive management strategies to decrease the progression of disease. Further studies need to be done to see for the benefit of angiotensinconverting enzyme inhibitors and steroids on the progression of microalbuminuria in HIV/AIDS patients.

Further studies defining the prognostic significance of microalbuminuria among HIV/AIDS infected patients are also required.

REFERENCES 1. Gilbert PB, McKeague IW, Eisen G, Mullins C, GuĂŠyeNDiaye A, Mboup S, et al. Comparison of HIV-1 and HIV-

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2 infectivity from a prospective cohort study in Senegal.

Stat Med. 2003;22(4):573-93.

2. Selik RM, Byers RH Jr, Dworkin MS. Trends in diseases reported on U.S. death certificates that mentioned HIV infection, 1987-1999. J Acquir Immune Defic Syndr.

2002;29(4):378-87.

3. Centre for Disease Control and Prevention. HIV/AIDS Surveillance Report 2005, Vol. 17, Atlanta, US. Department of Health and Human Services, Centre for Disease Control and Prevention 2007. Available at: http://www.cdc.gov/ hiv/topics/surveillance/reports.

4. Seney FD Jr, Burns DK, Silva FG. Acquired immunodeficiency syndrome and the kidney. Am J Kidney Dis. 1990;16(1):1-13.

5. Szczech LA, Gupta SK, Habash R, Guasch A, Kalayjian R, Appel R, et al. The clinical epidemiology and course of the spectrum of renal diseases associated with HIV infection.

Kidney Int. 2004;66(3):1145-52.

6. Janakiraman H, Abraham G, Matthew M, Kuruvilla S, Panikar V, Solomon S, et al. Correlation of CD4 counts with renal disease in HIV positive patients. Saudi J Kidney Dis Transpl. 2008;19(4):603-7.

7. Eke FU, Anochie IC, Okpere AN, Eneh AU, Ugwu RO, Ejilemele AA, et al. Microalbuminuria in children with human immunodeficiency virus (HIV) infection in Port Harcourt, Nigeria. Niger J Med. 2010;19(3):298-301.

8. Shah I, Gupta S, Shah DM, Dhabe H, Lala M. Renal manifestations of HIV infected highly active antiretroviral therapy naive children in India. World J Pediatr.

2012;8(3):252-5.

9. Luke DR, Sarnoski TP, Dennis S. Incidence of microalbuminuria in ambulatory patients with acquired immunodeficiency syndrome. Clin Nephrol.

1992;38(2):69-74.

10. Busch HW, Riechmann S, Heyen P, Heidenreich S, Kaufmann CC, Rahn KH, et al. Albuminuria in HIVinfected patients. AIDS Res Hum Retroviruses.

1994;10(6):717-20.

11. Monje AL, Bortolozzi R, Sosa V, et al. Microalbuminuria in patients of HIV (positive) and its relationship with immunologic and viral markers. Int Conf AIDS. 1996;11:305.

12. Han TM, Naicker S, Ramdial PK, Assounga AG. A crosssectional study of HIV-seropositive patients with varying degrees of proteinuria in South Africa. Kidney Int. 2006;69(12):2243-50.

13. Szczech LA, Grunfeld C, Scherzer R, Canchola JA, van der Horst C, Sidney S, et al. Microalbuminuria in HIV infection. AIDS. 2007;21(8):1003-9.

14. Fredrick F, Ruggajo P, Maro EE, Iversen BM, Basu G. Renal manifestations and associated factors among HIV infected children at Muhimbili National Hospital, Dar es Salaam, Tanzania. BMC Infect Dis. 2012;12(Suppl 1):O11.

INTERNAL MEDICINE

Erythema Nodosum in Tuberculosis: Contemporaries or Causation SHYAMALA G*, SUNIL KUMAR N†, SWATHI BS†, MAHESH MENON†, HEMANTHA KUMAR†

ABSTRACT Erythema nodosum is a delayed hypersensitivity reaction that results from a variety of infectious, inflammatory, connective tissue disorders and certain drugs. Tuberculosis (TB) is one of the infectious causes of erythema nodosum, but erythema

nodosum as a sole presentation of TB. We report a case of a 15-year-old female who presented to casualty with intermittent fever with evening rise of temperature since 4 weeks and painful red asymmetrical skin lesions increasing in size over the shins bilaterally since 2 weeks. Since she had a positive tuberculin test and a positive response to anti-TB therapy.

She was diagnosed to a case of erythema nodosum due to TB.

Keywords: Erythema nodosum, tuberculosis, delayed hypersensitivity reaction, antitubercular drugs

T

uberculosis (TB) is one of the oldest diseases known to affect humans and about one-third of the world’s population, is infected with TB bacteria. In 2013, an estimated 9.0 million people developed TB.1 Cutaneous hypersensitivity reactions (tuberculids) to tuberculoprotein can be the first and only presentation of TB in a patient with/without evidence of active disease with an incidence of less than 0.1%.

CASE REPORT A 15-year-old female presented to casualty with intermittent fever with evening rise of temperature since 4 weeks and painful red asymmetrical skin lesions increasing in size over the shins bilaterally since 2 weeks (Figs. 1 and 2).

Erythema nodosum - most common form of tuberculids, is a rash that is characterized by pretibial erythematous, tender nodules found in the deep dermis and subcutaneous tissue. It is a delayed hypersensitivity reaction that results from a variety of infectious, inflammatory, connective tissue disorders and certain drugs.2 TB is one of the infectious causes of erythema nodosum, but erythema nodosum as a sole presentation of TB is very rare.3 We report a case of erythema nodosum as the only manifestation secondary to TB.

*Professor †Postgraduate Student Dept. of Medicine Vijayanagara Institute of Medical Sciences, Bellary, Karnataka Address for correspondence Dr Sunil Kumar N Postgraduate Student Dept. of Medicine Vijayanagara Institute of Medical Sciences, Bellary, Karnataka E-mail: sunil.kumar.n6@gmail.com

Figure 1. Asymmetrical skin lesions over shins.

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INTERNAL MEDICINE

Figure 2. Asymmetrical skin lesions over shins increasing in size.

Similar history of skin lesions was present thrice, symptoms lasting for mean duration of 2 weeks in the past 6 months. During the present episode, the patient consulted a general physician after 3 days of fever and was put on a 1 week course of antibiotics with no benefit. There was no history of sore throat, cough, joint pains, loss of appetite, weight loss and any gynecological problem. There was no alterations in bowel and bladder habits. Patient’s past, family and drug history was unremarkable.

Examination showed stable vitals, pulse - 87/minute, temperature - 98°F, respiratory rate - 19/minute and blood pressure (BP) - 110/70 mmHg. Local examination revealed multiple erythematous nodules, measuring about 3 × 5 cm, tender to touch, distributed symmetrically over both the legs. Joint examination was normal and there was no lymphadenopathy. Examination of respiratory system and cardiovascular system was also normal. The diagnosis of erythema nodosum was made clinically and underlying cause was evaluated.

The relevant investigations revealed hemoglobin 10.8 g/dL, total leukocyte count (TLC) - 11,000/mm3 (polys 36%, lymphocytes 55% and monocytes 7%), erythrocyte sedimentation rate (ESR) was 115 mm in 1st hour, antistreptolysin O (ASO) titer was <200 IU. Serum angiotensin-converting enzyme (ACE) and antinuclear antibody (ANA) was negative and the chest radiograph was normal (Fig. 3).

Mantoux test was performed and was found to be 18 mm after 72 hours. Abdominal ultrasonography was normal without any evidence of visceromegaly or lymphadenopathy.

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Indian Journal of Clinical Practice, Vol. 26, No. 12, May 2016

Figure 3. Normal chest radiograph.

Patient was empirically started on Category 1 antitubercular drugs (ATT) under directly observed treatment strategy (DOTS) regimen. Fever subsided and the skin lesion healed without a scar within 3 weeks. Finally patient was discharged with reference letter to continue ATT under DOTS regimen from nearby primary health center. Follow-up after 1 month showed ESR of 19 mm in 1st hour, normal hemogram, with subsidence of all symptoms. No recurrence of skin lesions was seen until completion of ATT. DISCUSSION Erythema nodosum is a panniculitis that produces painful nodules on the shins, and less commonly on thigh and forearm. It is a reaction pattern to infection and sometimes to drugs. Adult females are principally affected. Malaise, fever and arthralgia are common. Histological features suggest that this is an immunological reaction. Immune complex deposition within dermal vessels is an important component in the production of the symptom complex.

Erythema nodosum is classified as idiopathic or secondary to other diseases. Some causes of erythema nodosum are listed below. ÂÂ

Infections: Bacterial: Streptococcal infections, TB, Yersinia enterocolitica infection, Mycoplasma

INTERNAL MEDICINE pneumoniae infection, Lymphogranuloma venereum, Salmonella infection Campylobacter infection, Leptospirosis; Fungal: Histoplasmosis, blastomycosis, coccidioidomycosis; Parasitic: Toxoplasmosis; Viral: Hepatitis B virus infection. ÂÂ

Drugs: Sulfonamides, bromides, iodides, sulfonylureas, oral contraceptive pills and penicillin.

ÂÂ

Malignancies: Hodgkin’s disease, non-Hodgkin’s lymphoma and acute myelogenous leukemia.

ÂÂ

Granulomatous diseases: Sarcoidosis and Behcet disease.

ÂÂ

Inflammatory bowel diseases: Ulcerative colitis and Crohn’s disease.

The causes of erythema nodosum are different according to the disease pattern of the region.4 Davies and Ormerod described two cases of erythema nodosum and tuberculosis.5 ÂÂ

One case of a 16-year-old girl who lived in UK and had history of travel to Hong Kong at the age of 14. She was asymptomatic except for erythema nodosum on both shins for 2 years. Chest radiograph showed minimal lung shadowing around the left hilum. A tuberculin test was strongly positive. Bronchoscopy was normal, but washings were positive for acid-fast bacilli (AFB) on direct smear. There was resolution of X-ray shadowing and regression of erythema nodosum after anti-TB therapy.

ÂÂ

The other case was that of a 33-year-old woman who worked in Home for the aged. She was also asymptomatic except for erythema nodosum on both shins. Chest X-ray showed some hilar enlargement, mainly on the left, with some upper zone infiltration. The tuberculin test was strongly positive. Bronchoscopy showed no lesion but washings taken from the left upper lobe were culture positive for TB.

Our case shows pyrexia of unknown origin linked to waxing and waning skin lesions indentified clinically as erythema nodosum. The main features of erythema nodosum which led us to the diagnosis of tubercular etiology in our case was a positive tuberculin test and a positive response to anti-TB therapy. Bronchoscopy and culture of bronchoalveolar lavage could not be done due to financial constraints of the patient.

When erythema nodosum is diagnosed, it is important to find out the underlying cause. We need to take a detailed history, including drug and oral contraceptive use, do a careful physical examination and take a chest X-ray. However, in India, primary TB constitutes one of the important causes of erythema nodosum and may be the first sign of TB. Patients may be asymptomatic apart from the painful lumps on the legs. The erythema nodosum from TB usually settles rapidly with antiTB treatment as in our case. Simple analgesia or a nonsteroidal anti-inflammatory drug may be needed to relieve symptoms. Corticosteroids are rarely required.

CONCLUSION Skin manifestations provide a unique opportunity for physicians to suspect, investigate and diagnose systemic diseases early in their course. Erythema nodosum may be considered as a reaction pattern of the body to multifarious antigenic stimuli. The condition may be idiopathic or secondary to various internal diseases or treatments. If there is a treatable or removable (e.g., medication) cause to the erythema nodosum then this should be addressed, as rapid resolution is anticipated in such cases. In India, primary TB constitutes one of the important causes of erythema nodosum which responds rapidly to antitubercular drugs and hence highlighting the importance of considering TB in cases of erythema nodosum especially in India.

REFERENCES 1. World Health Organization. Global Tuberculosis Report.

2014.

2. Miller ML. Evaluation of suspected rheumatic disease. In: Kliegman RM, Behrman RE, Jenson HB, Stanton BF (Eds.).

Nelson Textbook of Pediatrics. 18th Edition, Philadelphia: WB Saunders; 2007. pp. 995-7.

3. Whig J, Mahajan V, Kashyap A, Gupta S. Erythema nodosum: Atypical presentation of common disease.

Lung India. 2010;27(3):181-2.

4. Wong SK, Yeung SD. Erythema nodosum as the first presenting complaint of asymptomatic pulmonary tuberculosis. Hong Kong J Emerg Med. 2001;8:166-8.

5. Davies PDO, Ormerod LP. Case Presentations in Clinical Tuberculosis. London: Arnold; 1999.

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OBSTETRICS AND GYNECOLOGY

Prophylactic Preoperative Use of Rectal Misoprostol versus Intravenous Oxytocin Infusion During Cesarean Section to Reduce Intraoperative and Postoperative Blood Loss REKHA RANI*, SHIKHA SINGH†, SAROJ SINGH‡, URVASHI VERMA*, RUCHIKA GARG*, RACHANA AGRAWAL*, LATICA#

ABSTRACT Objective: To compare the effectiveness of per-rectal misoprostol administered immediately after spinal anesthesia, before giving skin incision, with intravenous oxytocin infusion, just after delivery of neonate, in prevention of uterine atony and thereby reducing blood loss at cesarean section. Material and methods: Four hundred women with singleton term pregnancy undergoing elective lower segment cesarean section under spinal anesthesia were included in this study. They were randomly allocated to receive either misoprostol 400 μg per-rectally or intravenous infusion of 10 units of oxytocin soon after delivery of the neonate. The main outcome measures were blood loss at cesarean section, change in hemoglobin levels, need for additional oxytocics and drug-related side effects. Results: The mean blood loss estimated was almost equal in misoprostol group and oxytocin group (578 mL vs. 620 mL; p = 0.67). The incidence of side effects such as pyrexia, shivering and was significantly higher in misoprostol group compared to oxytocin group. Conclusion: Per-rectal misoprostol appears to be as effective as intravenous infusion of oxytocin in reducing blood loss at cesarean section. However, occurrence of transient side effects such as shivering, pyrexia and nausea were noted more frequently with the use of misoprostol.

Keywords: Misoprostol, oxytocin, blood loss, cesarean section

P

ostpartum hemorrhage (PPH) is defined as loss of blood >500 mL from the genital tract in the first 24 hours following delivery (World Health Organization [WHO], 2003) and this compares with 1,000 mL of blood loss for cesarean section. We can also define PPH as hemoglobin difference of more than 10% between before and 24 hours after cesarean delivery.

About 57,000 women died in childbirth every year in India (2010). The Millennium Development Goal (MDG) related to maternal health as one maternal death is being reported every 10 minutes in the country now.

The current maternal mortality rate (MMR) of India is 200 per one lakh live births (2010), whereas the country`s MDG in this respect is 109 per one lakh live births by 2015. Uterine atony is the commonest cause of severe PPH. Consequently, the administration of uterotonic drugs during cesarean section has become essential to diminish the risk of PPH and improve maternal safety.

The aim of our study was to evaluate and compare the effect of preoperative rectal administration of misoprostol and intravenous oxytocin on blood loss in selected cases of cesarean delivery.

MATERIAL AND METHODS

*Lecturer †Associate Professor ‡Professor and Head #3rd Year Junior Resident Dept. of Obstetrics and Gynecology SN Medical College, Agra, Uttar Pradesh Address for correspondence Dr Rekha Rani Lecturer Dept. of Obstetrics and Gynecology SN Medical College, Agra - 282 002, Uttar Pradesh E-mail: drrekha.gynae@gmail.com

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Indian Journal of Clinical Practice, Vol. 26, No. 12, May 2016

The study was conducted in SN Medical College, Agra from December 2011 to August 2013 on 400 patients. An informed consent was taken from all women included in the study. Thorough history taking and physical examination was done in all patients.

Inclusion Criteria ÂÂ Reproductive age group (21-35 years). ÂÂ Parity (≤4).

OBSTETRICS AND GYNECOLOGY ÂÂ

Elective cesarean cases.

ÂÂ

Patients booked in antenatal period.

ÂÂ

Hemoglobin ≥11 gm%.

Exclusion Criteria ÂÂ

Age more than 35 years.

ÂÂ

Grand multipara (more than 4 children).

ÂÂ

Previous history of PPH or retained placenta.

ÂÂ

Any risk factor associated with PPH (including abnormal placentation, multiple gestation, uterine fibroids, history of PPH or uterine atony and previous classical uterine incision).

ÂÂ

Patients undergoing emergency cesarean section.

ÂÂ

Patients with previous history of scar rupture or dehiscence in which repair of uterus or hysterotomy done.

ÂÂ

Malpresentation, medical and coagulation disorders (diabetes, epilepsy, heart diseases), history of bronchial asthma.

On the basis of above mentioned criteria, 400 patients were selected. They were divided into two groups.

In the study group (n = 200) 600 µg misoprostol was administered per-rectally just before the start of cesarean section after giving required anesthesia. In the control group (n = 200) 10 units IV oxytocin was started just after delivery of baby. ÂÂ

The main outcome measures were intraoperative and postoperative blood loss within 24 hours and the difference between preoperative and postoperative hemoglobin, hematocrit values, mean arterial pressure and heart rate.

The amount of blood loss was measured in the kidney tray applied after drainage of liquor, which was decanted into measuring cylinder. Blood soaked mops and linen were weighed, the known “dry weight”

25 mL

was subtracted and the calculated volume added to that cylinder/kidney tray (Each gm ↑ in linen and mops weight was equivalent to 1 mL of blood loss).

Postoperative blood loss was measured on standardsized pad applied locally. The blood loss estimation was done as shown in Figure 1.

Investigations ÂÂ Blood grouping, hemogram, urine-routine and microscopy, random blood sugar, blood urea, human immunodeficiency virus (HIV), hepatitis B surface antigen (HBsAg), clotting factors done before cesarean section. ÂÂ Hemoglobin was repeated 24 hours after cesarean section. ÂÂ Obstetric ultrasonography (USG).

Statistical Analysis ÂÂ Mean and standard deviation was calculated for numerical value i.e., age and parity. ÂÂ Frequency and percentage were presented for amount of blood loss and postoperative hemoglobin. ÂÂ Chi-square test was used to compare blood loss and postoperative hemoglobin in both groups. ÂÂ P < 0.05 was considered significant.

Following are the outcome measures: ÂÂ

Postoperative hemoglobin deficit in 24 hours.

ÂÂ

Intraoperative and postoperative (8 hours) blood loss estimation.

ÂÂ

Frequency of primary PPH.

ÂÂ

Side effects of misoprostol.

ÂÂ

Side effects of oxytocin.

ÂÂ

Acceptability of drug (misoprostol) by per-rectal route.

50 mL

100 mL

Figure 1. Estimation of blood loss.

Indian Journal of Clinical Practice, Vol. 26, No. 12, May 2016

1147

OBSTETRICS AND GYNECOLOGY RESULTS There was no significant difference between the groups in age, duration and number of pregnancy and surgery (Table 1). There were no differences in preoperative and postoperative hemoglobin concentration. The amount of intraoperative blood loss was less in the misoprostol group but the difference between the two groups was not statistically significant (Table 2).

The heart rate of patients in oxytocin group significantly increased from 104 ± 17 beats/min to 122 ± 21 beats/min

(p = 0.005). There was no change in the heart rate in the patients who received rectal misoprostol (96 ± 21 bpm vs. 99 ± 18 bpm; p = 0.48) (Table 3). The incidence of shivering was statistically higher in the misoprostol group, while the incidence of chest pain was statistically higher in the oxytocin group. Other side effects were not statistically different between the two groups.

Oxytocin reduces mean arterial blood pressure and peripheral vascular resistance, increases heart rate and creates ST-segment changes and consequently will lead to chest pain (Table 4).

Table 1. Mean ± SD of Age, No. of Pregnancies, Weeks of Pregnancy and Duration of Operation in Two Groups Variables

Study group (misoprostol group)

Control group (oxytocin group)

P value

Age (years)

26.6 ± 5.4

27.1 ± 5.3

0.64

No. of pregnancies

1.85 ± 0.92

1.91 ± 0.85

0.73

Duration of pregnancy (weeks)

38.65 ± 0.58

38.66 ± 0.85

0.94

38.5 ± 5.8

40.42 ± 6.1

0.11

Duration of operation (min)

Table 2. Mean ± SD of Amount of Intraoperative Bleeding and Mean Pre- and Postoperative Hemoglobin Level in the Two Groups Variables

Study group (misoprostol group)

Control group (oxytocin group)

P value

Hb% (g/dL) Preoperative

11.45 ± 1.02

11.29 ± 0.62

0.72

Postoperative

10.32 ± 0.83

10.19 ± 0.58

0.36

Mean Hb deficit

01.13 ± 0.19

1.10 ± 0.03

0.52

Intraoperative

578 ± 234

620 ± 375

0.39

Postoperative

185 ± 95

224 ± 167

Amount of bleeding (mL)

Table 3. Mean ± SD of Mean Arterial Pressure and Heart Rate in the Two Groups Variables Mean arterial pressure (mmHg)

Study group (misoprostol group) Before

After

82.4 ± 15.5

78.3 ± 14.8

96 ± 21

99 ± 18

Heart rate (beats/min)

P value

Control group (oxytocin group)

P value

Before

After

0.24

83.3 ± 13.3

75.1 ± 11.5

0.003

0.48

104 ± 17

122 ± 21

0.005

Table 4. The Comparison of Side Effects During and After Operation in the Two Groups Variables

Study group (misoprostol group)

Control group (oxytocin group)

P value

N = 200

%

N = 200

%

Chest pain

2

1.0

14

7.0

0.03

Nausea

10

5.0

14

7.0

NS

Vomiting

4

2.0

8

4.0

NS

Shivering

20

10.0

2

1.0

0.03

Hyperpyrexia >40°C

8

4.0

2

1.0

NS

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Indian Journal of Clinical Practice, Vol. 26, No. 12, May 2016

Every citizen of India should have the right to accessible, affordable, quality and safe heart care irrespective of his/her economical background

Sameer Malik Heart Care Foundation Fund An Initiative of Heart Care Foundation of India

E-219, Greater Kailash, Part I, New Delhi - 110048 E-mail: heartcarefoundationfund@gmail.com Helpline Number: +91 - 9958771177

“No one should die of heart disease just because he/she cannot afford it” About Sameer Malik Heart Care Foundation Fund

Who is Eligible?

“Sameer Malik Heart Care Foundation Fund” it is an initiative of the Heart Care Foundation of India created with an objective to cater to the heart care needs of people.

Objectives Assist heart patients belonging to economically weaker sections of the society in getting affordable and quality treatment.

Raise awareness about the fundamental right of individuals to medical treatment irrespective of their religion or economical background.

Sensitize the central and state government about the need for a National Cardiovascular Disease Control Program.

Encourage and involve key stakeholders such as other NGOs, private institutions and individual to help reduce the number of deaths due to heart disease in the country.

To promote heart care research in India.

All heart patients who need pacemakers, valve replacement, bypass surgery, surgery for congenital heart diseases, etc. are eligible to apply for assistance from the Fund. The Application form can be downloaded from the website of the Fund. http://heartcarefoundationfund.heartcarefoundation. org and submitted in the HCFI Fund office.

Important Notes The patient must be a citizen of India with valid Voter ID Card/ Aadhaar Card/Driving License.

The patient must be needy and underprivileged, to be assessed

by Fund Committee.

The HCFI Fund reserves the right to accept/reject any application for financial assistance without assigning any reasons thereof.

The review of applications may take 4-6 weeks.

All applications are judged on merit by a Medical Advisory Board who meet every Tuesday and decide on the acceptance/rejection of applications.

The HCFI Fund is not responsible for failure of treatment/death of patient during or after the treatment has been rendered to the patient at designated hospitals.

To promote and train hands-only CPR.

Activities of the Fund Financial Assistance

The HCFI Fund reserves the right to advise/direct the beneficiary to the designated hospital for the treatment.

Financial assistance is given to eligible non emergent heart patients.

Apart from its own resources, the fund raises money through donations, aid from individuals, organizations, professional bodies, associations and other philanthropic organizations, etc.

The financial assistance granted will be given directly to the treating hospital/medical center.

After the sanction of grant, the fund members facilitate the patient in getting his/her heart intervention done at state of art heart hospitals in Delhi NCR like Medanta – The Medicity, National Heart Institute, All India Institute of Medical Sciences (AIIMS), RML Hospital, GB Pant Hospital, Jaipur Golden Hospital, etc. The money is transferred directly to the concerned hospital where surgery is to be done.

Drug Subsidy

The HCFI Fund has the right to print/publish/webcast/web post details of the patient including photos, and other details. (Under taking needs to be given to the HCFI Fund to publish the medical details so that more people can be benefitted).

The HCFI Fund does not provide assistance for any emergent heart interventions.

Check List of Documents to be Submitted with Application Form Passport size photo of the patient and the family A copy of medical records Identity proof with proof of residence Income proof (preferably given by SDM)

The HCFI Fund has tied up with Helpline Pharmacy in Delhi to facilitate

BPL Card (If Card holder)

patients with medicines at highly discounted rates (up to 50%) post surgery.

Details of financial assistance taken/applied from other sources (Prime Minister’s Relief Fund, National Illness Assistance Fund Ministry of Health Govt of India, Rotary Relief Fund, Delhi Arogya Kosh, Delhi Arogya Nidhi), etc., if anyone.

The HCFI Fund has also tied up for providing up to 50% discount on imaging (CT, MR, CT angiography, etc.)

Free Diagnostic Facility

Free Education and Employment Facility

The Fund has installed the latest State-of-the-Art 3 D Color Doppler EPIQ 7C Philips at E – 219, Greater Kailash, Part 1, New Delhi.

HCFI has tied up with a leading educational institution and an export house in Delhi NCR to adopt and to provide free education and employment opportunities to needy heart patients post surgery. Girls and women will be preferred.

This machine is used to screen children and adult patients for any heart disease.

Laboratory Subsidy HCFI has also tied up with leading laboratories in Delhi to give up to 50% discounts on all pathological lab tests.

About Heart Care Foundation of India

Help Us to Save Lives The Foundation seeks support, donations and contributions from individuals, organizations and establishments both private and governmental in its endeavor to reduce the number of deaths due to heart disease in the country. All donations made towards the Heart Care Foundation Fund are exempted from tax under Section 80 G of the IT Act (1961) within India. The Fund is also eligible for overseas donations under FCRA Registration (Reg. No 231650979). The objectives and activities of the trust are charitable within the meaning of 2 (15) of the IT Act 1961.

Heart Care Foundation of India was founded in 1986 as a National Charitable Trust with the basic objective of creating awareness about all aspects of health for people from all walks of life incorporating all pathies using low-cost infotainment modules under one roof.

HCFI is the only NGO in the country on whose community-based health awareness events, the Government of India has released two commemorative national stamps (Rs 1 in 1991 on Run For The Heart and Rs 6.50 in 1993 on Heart Care Festival- First Perfect Health Mela). In February 2012, Government of Rajasthan also released one Cancellation stamp for organizing the first mega health camp at Ajmer.

Objectives Preventive Health Care Education Perfect Health Mela Providing Financial Support for Heart Care Interventions Reversal of Sudden Cardiac Death Through CPR-10 Training Workshops Research in Heart Care

Donate Now...

Heart Care Foundation Blood Donation Camps The Heart Care Foundation organizes regular blood donation camps. The blood collected is used for patients undergoing heart surgeries in various institutions across Delhi.

Committee Members

Chief Patron

President

Raghu Kataria

Dr KK Aggarwal

Entrepreneur

Padma Shri, Dr BC Roy National & DST National Science Communication Awardee

Governing Council Members Sumi Malik Vivek Kumar Karna Chopra Dr Veena Aggarwal Veena Jaju Naina Aggarwal Nilesh Aggarwal H M Bangur

Advisors Mukul Rohtagi Ashok Chakradhar

Executive Council Members Deep Malik Geeta Anand Dr Uday Kakroo Harish Malik Aarti Upadhyay Raj Kumar Daga Shalin Kataria Anisha Kataria Vishnu Sureka

This Fund is dedicated to the memory of Sameer Malik who was an unfortunate victim of sudden cardiac death at a young age.

Rishab Soni

HCFI has associated with Shree Cement Ltd. for newspaper and outdoor publicity campaign HCFI also provides Free ambulance services for adopted heart patients HCFI has also tied up with Manav Ashray to provide free/highly subsidized accommodation to heart patients & their families visiting Delhi for treatment.

http://heartcarefoundationfund.heartcarefoundation.org

OBSTETRICS AND GYNECOLOGY DISCUSSION

CONCLUSIONS

In this study, there were no differences in preoperative and postoperative hemoglobin concentration as well as the amount of intraoperative blood loss between the two groups (Table 2). Vimala et al in their study on comparison of 400 µg sublingual misoprostol with oxytocin found that intraoperative bleeding was more significant in oxytocin group, although postoperative hemoglobin level was not different. In Chaudhuri et al study with 800 µg rectal misoprostol, although postoperative hemoglobin level was not different in the two groups, the intraoperative bleeding was significantly lesser in misoprostol group.

Leading cause of PPH is uterine atony, which can be successfully treated with misoprostol. Misoprostol is a potent uterotonic drug. Its per-rectal use is much better in controlling PPH, has lesser side effects, better tolerability, cheaper and does not require refrigeration.

Its route of administration is noninvasive than other uterotonic drugs. It has long half-life. The features discussed above makes misoprostol a much better option in developing countries. Misoprostol is a synthetic analog of prostaglandin E1, which is easier to use, there is no need for intramuscular or intravenous administration and can be kept at room temperature and so is easily transportable. Misoprostol can be administered by rectal, vaginal, oral and sublingual routes and there is no need for ringer’s solution or injection. Misoprostol may therefore be considered as an alternative agent when oxytocin is relatively contraindicated in patients with pre-eclampsia, prolonged labor or cardiac disease.

Although in different studies, intraoperative blood loss was equal in both groups but intraoperative blood loss with the use of misoprostol has a varied widely from 500 mL to 1,000 mL. This wide range of blood loss may be due to differences in the dose, route and timing of administration of misoprostol. Chaudhuri used 800 µg rectal misoprostol before making incision on the uterus followed by infusion of 6 units of oxytocin in half an hour but Vimala used 400 µg of oxytocin in half an hour. In measuring hemoglobin level, the changes are almost similar in different studies e.g., in spite of 500 cc difference in amount for intraoperative blood loss in Chaudhuri and Vimala studies, the difference in hemoglobin changes is only 0.3 mg/dL (0.411 vs.

0.1 mg/dL, respectively). The rate of bleeding and the hemoglobin changes found in our study was similar to most other studies. The differences between our study and that of Chaudhuri may be due to the lower dose of rectal misoprostol (400 µg vs. 800 µg) and higher dose of oxytocin in our study.

Changes in blood pressure and heart rate are side effects of oxytocin. In our study, decrease in mean arterial blood pressure and increase in heart rate were significantly more common in patients receiving oxytocin. Vimala has reported shivering in 26% of patients with 400 µg of sublingual misoprostol and 4% in oxytocin group. In Lapaire study with 800 µg of misoprostol; the incidence of shivering was 36% in comparison with 8% in oxytocin group. Chaudhuri reported 8.3% and 1.1% in misoprostol and oxytocin group, respectively. Shivering was seen in 16% of our patients in misoprostol group and 2% in oxytocin group.

These findings are compatible to previous studies.

The difference of nausea and vomiting in the two groups was not significant. Similar findings were reported in previous studies. Hyperpyrexia was seen in 8% of patients who received misoprostol and 2% with oxytocin. The difference was not significant. Previous studies have reported similar findings.

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Indian Journal of Clinical Practice, Vol. 26, No. 12, May 2016

SUGGESTED READING 1. Khan FA, Khan M, Ali A, Chohan U. Estimation of blood loss during caesarean section: an audit. J Pak Med Assoc.

2006;56(12):572-5.

2. Magann EF, Evans S, Hutchinson M, Collins R, Lanneau G, Morrison JC. Postpartum hemorrhage after cesarean delivery: an analysis of risk factors. South Med J. 2005;98(7):681-5.

3. Acharya G, Al-Sammarai MT, Patel N, Al-Habib A, Kiserud T. A randomized, controlled trial comparing effect of oral misoprostol and intravenous syntocinon on intra-operative blood loss during cesarean section. Acta Obstet Gynecol Scand. 2001;80(3):245-50.

4. Vimala N, Mittal S, Kumar S. Sublingual misoprostol versus oxytocin infusion to reduce blood loss at cesarean section. Int J Gynaecol Obstet. 2006;92(2):106-10.

5. Eftekhari N, Doroodian M, Lashkarizadeh R. The effect of sublingual misoprostol versus intravenous oxytocin in reducing bleeding after caesarean section. J Obstet Gynaecol. 2009;29(7):633-6.

6. Chaudhuri P, Banerjee GB, Mandal A. Rectally administered misoprostol versus intravenous oxytocin infusion during cesarean delivery to reduce intraoperative and postoperative blood loss. Int J Gynaecol Obstet.

2010;109(1):25-9.

7. Combs CA, Murphy EL, Laros RK Jr. Factors associated with hemorrhage in cesarean deliveries. Obstet Gynecol.

1991;77(1):77-82.

8. Prendivellie W, Elbourne D. Care during the third stage of labour. In: Chalmers I, Enkin M, Keirse MJNC (Eds.).

Effective Care in Pregnancy and Childbirth. Oxford: Oxford University Press; 1989. pp. 1145-69.

9. Collins R. Antiplatelet agents for IUGR and pre-eclampsia.

Enkin MW, Keirse MJNC, Renfrew MJ, Neilson JP, Crowther C (Eds.). Pregnancy and Childbirth Module. In: Cochrane Collaboration: Cochrane Pregnancy and Childbirth Database. Issue 2, Oxford: Update Software; 1995.

OBSTETRICS AND GYNECOLOGY

Intraperitoneal Bladder Injury During Tubectomy: A Conservative Approach SHAVETA JAIN*, ROOPA MALIK†, SMITI NANDA‡, NITIN JAIN#

ABSTRACT Iatrogenic bladder injury is a recognized rare complication of gynecological surgery and may result in significant morbidity when associated with intraperitoneal perforation. We present a case of iatrogenic bladder injury following tubectomy (minilap).

We have also discussed conservative management of small intra-abdominal bladder injury, which could prevent unnecessary laparotomy. A 27-year-old, female presented to gynecological emergency with complaints of not being able to pass urine and abdominal distension for 3 days. She had history of undergoing tubectomy (minilap) at primary health center 3 days back.

On CT scan, contrast could be seen in between bowel loops suggesting intraperitoneal bladder injury. Patient was managed conservatively. Simple step of evacuating bladder before any gynecological procedure may prevent devastating occurrence of bladder injury, which may go undiagnosed while doing minilap.

Keywords: Tubectomy, bladder injury, intraperitoneal perforation, minilap, conservative management

I

atrogenic bladder injury is a recognized complication of gynecological surgery and may result in significant morbidity when associated with intraperitoneal perforation. Most commonly it is seen during total laparoscopic hysterectomy (3%),1 transabdominal hysterectomy (0.4%),2 vaginal hysterectomy or during transvaginal tape (TVT) procedure. We present a case of iatrogenic bladder injury following tubectomy (minilap) and managed by conservative management.

CASE REPORT A 27-year-old, P5L5, female presented to gynecological emergency with complaints of not being able to pass urine and abdominal distension for 3 days. She had history of undergoing tubectomy (minilap) at primary health center 3 days back. Following tubectomy, she was discharged same day but she returned with complaints of not being able to pass urine next day.

*Assistant Professor †Associate Professor ‡Professor and Head Dept. of Obstetrics and Gynecology #Senior Resident Dept. of Radiology Pt BD Sharma, PGIMS, Rohtak, Haryana Address for correspondence Dr Nitin Jain House No. 629, Sector 14, Rohtak - 124 001, Haryana E-mail: logindrnitin@gmail.com

Abdominal distension was noticed and she was kept nil per oral and put on intravenous fluids. In view of increasing abdominal distension, she was referred to our hospital. She was pale, dyspneic and having fever.

Her pulse rate was 100/min and blood pressure was 110/70 mmHg. On systemic examination, chest and cardiovascular system was normal. On per abdominal examination, there was generalized distension. Shifting dullness was present suggesting of free fluid and bowel sounds were absent. There were no signs of muscular guarding or rigidity. Foley’s catheterization was done and 200 cc of clear urine collected in urobag.

On investigations, all biochemical investigations like complete hemogram (Hb - 10 g/dL, TLC - 9,500/cc, DLC - 66N,30L,M2,E2), blood sugar (96 mg%), blood urea (36 mg%), serum electrolytes (serum Na+ 138 mEq/mL, serum K+ - 4.1 mEq/mL), serum creatinine (0.8 mg%) were within normal limits. Abdominal drain kit (ADK) was put in abdominal cavity under local anesthesia, which drained 900 cc of pale-colored fluid with ammonia like odor. Specific gravity of fluid was 1.013 and urea levels were 36 mg% and creatinine levels of 480 μmol/mL. A diagnosis of urinary ascitis was made.

On ultrasound examination, uterus was normal, bilateral adnexae were normal and free fluid was +++. On retrograde cystogram, there was a rent of

Indian Journal of Clinical Practice, Vol. 26, No. 12, May 2016

1153

OBSTETRICS AND GYNECOLOGY

Figure 1. CECT abdomen axial section showing extravasation of contrast in between bowel loops.

5 mm on left side of dome of urinary bladder from which dye could be seen leaking into peritoneal cavity suggesting intraperitoneal bladder injury. On computed tomography (CT) scan, same findings were confirmed and contrast could be seen in between bowel loops (Fig. 1). Laparoscopic suturing of bladder was not done in view of late presentation and small leak. Patient was kept on intake output charting and was counseled for mobilization. Foleyâ&#x20AC;&#x2122;s catheter was removed after 3 weeks and abdominal drain was removed after 2 days of Foleyâ&#x20AC;&#x2122;s removal. Patient was followed up after 2 months and retrograde cystogram was done, which was found to be normal.

DISCUSSION There are various immediate and delayed complications of tubectomy like low abdominal pain, dyspareunia and menstrual pattern changes which constitutes what is known as post-ligation syndrome, and technical failure (0.1-0.12/100 women years).3 Visceral injuries including gut and bladder are known to occur during laparoscopic tubectomy but rare with minilap tubectomy.4 Injury might have occurred due to small abdominal incision of minilap, less visibility and less expertise of the operating surgeon. Most of the bladder injuries described in the literature in gynecology are during dissection of bladder from cervix during vaginal or abdominal hysterectomy. Recently bladder injuries are also described during TVT procedure.

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Indian Journal of Clinical Practice, Vol. 26, No. 12, May 2016

The anatomic proximity of the reproductive tract and lower urinary tract predisposes them to iatrogenic trauma during obstetric and gynecological surgeries.

Bladder and distal ureters are most commonly involved organs.5 Risk factors for bladder injuries include previous surgical interventions, pelvic inflammatory disease, endometriosis, anatomic anomalies and pelvic adhesions.6 Pandyan et al reviewed retrospectively iatrogenic bladder injuries during obstetrics and gynecology procedures, they found 90% of injuries during obstetrics procedures and only 15% during gynecological procedures.5 Thus, though iatrogenic ureteric and bladder injuries are globally rare in gynecological procedures, they are liable to occur due to inherent anatomic and pathological factors in the pelvis. Ninety percent of urological injuries were recognized intraoperatively and managed.5 Our case of bladder injury was diagnosed after 4 days of tubectomy.7 The probability of injury varies according to degree of bladder distension, therefore, a full bladder is more likely to become injured than an empty one.

When in doubt regarding iatrogenic bladder injury, methylene blue test should be done and if indicated surgical opinion should be taken regarding cystoscopy.

Repair of the bladder injury at the time of primary surgery is easier, more successful and less morbid for the patient and medicolegally advantageous for the surgeon. Delayed diagnosis is suspected when postoperatively there is oliguria, hematuria, elevated urea/creatinine ratio, lower abdominal pain, distension, paralytic ileus or urinary ascites as was seen in the present case.8 Thus, unexplained ascites and decreased renal function in a previously healthy person with a recent history of pelvic surgery should raise the suspicion of intraperitoneal bladder leak. A very high creatinine level in ascitic fluid is diagnostic of urinary ascites. An ascitic fluid creatinine: serum creatinine ratio >1 is highly suggestive of intraperitoneal urine leak.9 The management of bladder perforations has been a controversial issue. Usually, extraperitoneal perforations are managed by conservative management with temporary bladder drainage and intraperitoneal ruptures on the other hand, are usually managed primarily by open repair, mostly because of concern about communication between the environment and peritoneal cavity. Our case illustrates that even a conservative approach in the treatment of small intraperitoneal ruptures may be considered if a number of conditions are maintained: urinary antibiotic prophylaxis and continued urinary drainage

OBSTETRICS AND GYNECOLOGY through an indwelling catheter for a minimum of 2 weeks until closure of the perforation is evident on CT cystogram. Patients should be warned, however, that an unsuccessful result with persistent communication to the peritoneal cavity is possible.

CONCLUSION Urinary bladder injury should be considered in the differential diagnosis of ascites in patients who have had recent pelvic surgery. Serum and ascites biochemistry in conjunction with CT cystography are key to diagnosis. Our case illustrates that a conservative approach is possible, even in cases with intraperitoneal rupture. Simple step of evacuating bladder before any gynecological procedure may prevent devastating occurrence of bladder injury, which may go undiagnosed while doing minilap. As part of tubectomy training more emphasis should be laid on how to suspect and diagnose bladder injuries during minilap tubectomy to avoid morbidity.

REFERENCES

2. Meikle SF, Nugent EW, Orleans M. Complications and recovery from laparoscopy-assisted vaginal hysterectomy compared with abdominal and vaginal hysterectomy.

Obstet Gynecol. 1997;89(2):304-11.

3. Huggins GR, Sondheimer SJ. Complications of female sterilization: immediate and delayed. Fertil Steril.

1984;41(3):337-55.

4. Singhal RS, Sangwan K, Malhotra N. Gut injury: a rare complication of mini-laparotomy tubal sterilization.

J Obstet Gynecol Ind. 2004;54(6):594.

5. Pandyan GV, Zahrani AB, Awon AR, Al-Rashid M, Al-Assiri M, Dahnoun M. Iatrogenic bladder injuries during obstetric and gynecological procedures. Saudi Med J. 2007;28(1):73-6.

6. Mteta KA, Mbwambo J, Mvungi M. Iatrogenic ureteric and bladder injuries in obstetric and gynaecologic surgeries.

East Afr Med J. 2006;83(2):79-85.

7. Rapp DE, Corman JM. Conservative management of iatrogenic bladder injury with foreign body. Int Urogynecol J Pelvic Floor Dysfunct. 2008;19(9):1319-21.

8. Gomez RG, Ceballos L, Coburn M, Corriere JN Jr, Dixon CM, Lobel B, et al. Consensus statement on bladder injuries. BJU Int. 2004;94(1):27-32.

9. Heyns CF, Rimington PD. Intraperitoneal rupture of the 1. Schindlbeck C, Klauser K, Dian D, Janni W, Friese K. bladder causing the biochemical features of renal failure.

Comparison of total laparoscopic, vaginal and abdominal hysterectomy. Arch Gynecol Obstet. 2008;277(4):331-7.

Br J Urol. 1987;60(3):217-22.

■■■■

Women with BRCA1 Mutation have Reduced Ovarian Reserves Women with a germ line mutation in BRCA1 have reduced ovarian reserves as measured by anti-Müllerian hormone (AMH). Circulating AMH is a biomarker of ovarian reserve and hence reproductive lifespan. (Source: Hum Reprod. 19 April 2016)

Women’s Health: Cranberry Supplements not Very Effective in Preventing UTIs Taking cranberry supplements has long been recommended to prevent urinary tract infections (UTI), but tests of seven popular cranberry-pill brands in the U.S. showed that most contained too little of the key bacteria-fighting ingredient to have any effect. (Source: Am J Obstet Gynecol. 2016)

Migraine Related to Increased Birth Complications A study suggests that women who seek treatment for acute migraine during pregnancy go on to have rates of preeclampsia, preterm delivery, and low-birthweight babies that far exceed national averages. (Source: Am Acad Neurol. April 2016)

Indian Journal of Clinical Practice, Vol. 26, No. 12, May 2016

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OBSTETRICS AND GYNECOLOGY

Pelvic Hematoma Mimicking Ovarian Malignancy SHREYASI BID*, SAMBHU NATH BANDYOPADHYAY†, CHANDAN SASMAL‡

ABSTRACT Warfarin is a very useful drug for thrombotic disorders, but sometimes its use is associated with over anticoagulation. We present herein an interesting case of a patient who was getting warfarin for cortical sinus thrombosis came with abdominal distension.

Radiological findings showed adnexal mass but on laparotomy a huge hematoma detected on anterolateral wall of pelvis.

Keywords: Warfarin, hematoma, thrombotic disorders

H

ematoma is a collection of blood, usually clotted, outside of a blood vessel that may occur because of an injury to the wall of a blood vessel allowing blood to leak out into the tissues where it does not belong. Warfarin is an anticoagulant, used for treatment and prevention of thromboembolism.

Although effective, warfarin use is potentially complicated by supratherapeutic anticoagulation (over anticoagulation) causing hemorrhage. Common sites of bleeding are the oropharynx, soft tissue, gastrointestinal tract and urinary tract. Pelvic hematoma is a rare complication and clinical consequences depend upon the rate of blood loss and the total amount of blood in hematoma pseudocyst.

CASE REPORT Bula Singha, a 38-year-old Hindu female was alright till 13/09/2013. To start with she developed acute onset headache with loss of consciousness and convulsions.

She was admitted in a private hospital, where she was diagnosed to have cortical sinus thrombosis.

Signal changes were present in bilateral basal ganglia, thalamus and cerebral hemisphere on magnetic resonance imaging (MRI) (Fig. 1). She was treated with warfarin 5 mg o.d. dose. Subsequently, she developed

*RMO cum Clinical Tutor †Assistant Professor ‡Junior Resident Dept. of Obstetrics and Gynecology Institute of Post Graduate Medical Education & Research (IPGMER) Kolkata, West Bengal Address for correspondence Dr Shreyasi Bid Dakshi Apartment, 75 James Long Sarani, Joka - 700 104, Kolkata, West Bengal E-mail: drshreyasibid@gmail.com

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Indian Journal of Clinical Practice, Vol. 26, No. 12, May 2016

abdominal distension and right-sided hemiplegia. Then she was referred to Bangur Institute of Neurology. Here ultrasonography (USG) of whole abdomen showed focal large cystic and heterogeneous space occupying lesion (SOL) in right lower abdomen, uterus - normal size and ovaries were not visualized (Fig. 2). Further evaluation by computed tomography (CT) scan showed a large hypodense cystic SOL measuring 12.07 × 8.8 cm containing dependent, nonenhancing hyperdensity in right lower abdomen, no ascitis, large bowel loops appeared distended ? due to subacute obstruction.

MRI pelvis revealed a pelvic mass (Fig. 3). She was referred to the Dept. of Obstetrics and Gynecology on 02/11/2013, where she developed diarrhea. She is P1+0, LUCS done 13 years back. She had attained menopause 1 year ago. She was hypothyroid and taking tablet levothyroxine 100 µg o.d. She had never used any oral

Figure 1. MRI of brain showing cortical sinus thrombosis.

OBSTETRICS AND GYNECOLOGY contraceptive pill (OCP) in her life. On examination, her abdomen was tense with absence of shifting dullness.

Per vaginal examination revealed small and atrophic uterus, fullness in right fornix, which may be due to ovarian SOL. We further evaluated the patient by doing USG, which revealed a large complex cystic mass with few solid component and internal vascularity having multiple septations and septal calcification in pelvis

arising from right adnexa. None of the ovaries were visualized. The impression was suspected malignant ovarian mass. The other investigation reports were as follows: Hemoglobin (Hb) - 14 g/dL, total count (TC) 8,200/mm3, platelet - 1,80,000/mm3, urea - 12 mg/dL, creatinine - 0.8 mg/dL, international normalized ratio (INR) - 2.5, CA-125 - 48.3.

With suspicion of malignancy the patient was taken for laparotomy on 07/11/2013. After opening the abdomen by right paramedian incision, small and large intestine, both were founded to be hugely distended (Fig. 4). The uterus was small and both ovaries were atrophic due to menopause. A large deep seated mass was palpated in anterolateral wall of pelvis adjacent to bladder on right side (Fig. 5). Retrograde decompression of intestine was

Figure 2. USG abdomen showing large cystic and heterogeneous SOL.

Figure 4. Hugely distended gut loops.

Figure 3. MRI showing pelvic mass.

Figure 5. Pelvic hematoma appearing as a solid mass.

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OBSTETRICS AND GYNECOLOGY pelvic hematoma located below the iliacus muscle and adhering to bone in posterior acetabulum. The condition was complicated by ulceration and focal osteolysis of the adjacent bone.5 Andrade et al reported a case of abdominal compartment syndrome due to warfarin related retroperitoneal hematoma in 2007, which led to a straight forward decision for laparotomy.6

Figure 6. Blood clot coming out from the hematoma.

done. A huge amount of old blood clot was evacuated from the mass (Fig. 6).

We started injection enoxaparin 40 mg o.d. from first postoperative day. The abdominal drain was removed on third postoperative day. She recovered gradually from diarrhea, abdominal distension and hemiplegia.

DISCUSSION Oral anticoagulants have an expanding role in cardiovascular and thrombotic disorders. Major indications for warfarin use are nonvalvular atrial fibrillation, venous thrombosis, rheumatic heart disease, mechanical heart valve prosthesis, pulmonary, cerebral and systemic embolism.1-3 Warfarin therapy is associated with various hemorrhagic complications that are usually caused by inadequate control of anticoagulation. A similar case was reported by Donald H Marks, R Phillip Dellinger in 1984. A 41-year-old anticoagulated lady presented with increasing pelvic pain following sexual intercourse.

An USG and CT scan confirmed the diagnosis of pelvic hematoma. The hematoma resolved spontaneously with normalization of clotting studies.4 Kinkor et al reported a case in 2007 of a 50-year-old woman who underwent total hip arthroplasty due to developmental dysplasia, warfarin therapy was started due to inherited disorder blood coagulation. One year later, she developed a large

Our case is unique in that none of the imaging reports could diagnose the case as a hematoma, moreover the ultrasound report further misled us by suspecting the mass to be a malignant one. As laparotomy is indicated in both ovarian malignancy and hematoma, so patient received the correct treatment whatever may be the preoperative diagnosis. Another interesting point is that, though this patient was normotensive and not using any hormone replacement therapy, still she developed venous thrombosis. Whether premature menopause itself is a risk factor for thrombotic manifestation is still unknown.

REFERENCES 1. Chan TY, Miu KY. Hemorrhagic complications of anticoagulant therapy in Chinese patients. J Chin Med Assoc. 2004;67(2):55-62.

2. Fanikos J, Grasso-Correnti N, Shah R, Kucher N, Goldhaber SZ. Major bleeding complications in a specialized anticoagulation service. Am J Cardiol.

2005;96(4):595-8.

3. Fihn SD, McDonell M, Martin D, Henikoff J, Vermes D, Kent D, et al. Risk factors for complications of chronic anticoagulation. A multicenter study. Warfarin Optimized Outpatient Follow-up Study Group. Ann Intern Med. 1993;118(7):511-20.

4. Marks DH, Dellinger RP, Orrison WW. Pelvic hematoma after intercourse while on chronic anticoagulation. Ann Emerg Med. 1984;13(7):554-6.

5. Kinkor Z, Koudela K Jr, Koudela K, Havlícek F, Koudelová J. Warfarin-induced hemorrhagic pseudocyst in the pelvis of a woman with an inherited disorder of blood coagulation, complicated by pelvic bone pseudoxanthoma mimicking Erdheim-Chester disease. Acta Chir Orthop Traumatol Cech. 2007;74(2):114-7.

6. Andrade MM, Pimenta MB, Belezia Bde F, Xavier RL, Neiva AM. Abdominal compartment syndrome due to warfarin-related retroperitoneal hematoma. Clinics (Sao Paulo). 2007;62(6):781-4.

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OBSTETRICS AND GYNECOLOGY

Programmed Labor and Its Effect on Labor Outcome RUCHIKA GARG*, URVASHI VERMA*, SONIYA DHIMAN†, MOHITA AGRAWAL*, MEENAL JAIN*

ABSTRACT Programmed labor is a protocol based on the incorporation of the three principles of “Active management of labor”, synergistic application of analgesic and antispasmodic during active phase of labor and plotting of the patient’s partogram to monitor events during labor, so as to detect early any dysfunctional labor and adopt timely corrective measures to optimize labor outcome.

A prospective study of programmed labor had been undertaken in the Dept. of Obstetrics and Gynecology, SN Medical College, Agra, Uttar Pradesh. To determine the influence of the programmed labor protocol on the events of labor and obstetric outcome.

Keywords: Programmed labor, partogram, active management of labor, labor outcome

P

rogrammed labor is a protocol developed by the researchers over a period of a decade. It is based on the incorporation of the three principles of “Active management of labor”, synergistic application of analgesic and antispasmodic during active phase of labor and plotting of the patient’s partogram to monitor events during labor, so as to detect early any dysfunctional labor and adopt timely corrective measures to optimize labor outcome. The use of alert and action lines on the partogram in the management of labor is a major advancement in the obstetrical field and has helped immensely to decide how long to passively wait and watch for the progress of labor and when to interfere. Thus, it has helped to control the duration of labor and the complications associated with prolonged labor. Viewed in this context, this present piece of prospective study of programmed labor had been taken up to determine the influence of the programmed labor protocol on the events of labor and obstetric outcome.

The American College of Obstetricians and Gynecologists (ACOG) (2003) has concluded that active management may shorten labor although it has not consistently been shown to reduce rates of cesarean delivery.

The term “active management of labor” was coined by an obstetrician, Kieran O’Driscoll, to describe a process, which was aimed at preventing prolonged labor (O’Driscoll et al, 1969).

ÂÂ

Normal primigravida/multigravida (Confirmed by Date/USG).

ÂÂ

High risk pregnancies are avoided.

ÂÂ

Anesthesiologist and Neonatologist should be present to evaluate the mother and baby, respectively.

ÂÂ

Consent obtained from the patient after proper counseling about the procedure.

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The patient enters the study when she is in the “Active phase of labor”. When cervical dilation is >3 cm and effacement >50%, show is present and CPD has been excluded.

*Assistant Professor †Senior Resident Dept. of Obstetrics and Gynecology SN Medical College, Agra, Uttar Pradesh Address for correspondence Dr Ruchika Garg Assistant Professor Dept. of Obstetrics and Gynecology SN Medical College, Agra, Uttar Pradesh E-mail: ruchikagargagra@gmail.com

AIM OF THE STUDY The aim of the study was to determine the influence of the programmed labor protocol on the events of labor and obstetric outcome.

MATERIAL AND METHODS

Place of the Study This study has been undertaken in the Dept. of Obstetrics and Gynecology, SN Medical College, Agra, Uttar Pradesh.

Selection Criteria at

term

Two hundred fifty patients who satisfied the above criteria formed the subject of our study. A detailed

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OBSTETRICS AND GYNECOLOGY history of each case was taken as described in the proforma with special reference to labor i.e., duration since labor pain had started and time of rupture of membrane. A detailed personal profile regarding socioeconomic status, literacy rural/urban, booked/ unbooked, referred/direct were recorded her past obstetric history about type, duration and place of delivery were inquired.

Table 1. Distribution of Cases According to Gestational Age Primigravida No. (%)

Multigravida No. (%)

Total

37-38

29 (11.6)

11 (4.4)

40 (16)

38-39

33 (13.2)

20 (8)

53 (21.2)

39-40

66 (26.4)

58 (23.2)

124 (49.6)

History of current pregnancy, whether she had regular antenatal check-up, about immunization and type of care she had received. A thorough clinical examination of each case was carried out along with thorough obstetric examination.

>40 to <42

21 (8.4)

12 (4.8)

33 (13.2)

149 (59.6)

101 (40.4)

250 (100)

Analgesics and antispasmodics were given 2 mg IV bolus diazepam was given at the initiation of active phase. Pentazocine 6 mg IV bolus single dose and 50-100 mg of tramadol deep intramuscular was given.

Ketamine 0.25-0.5 mg/kg was given; in these doses, it does not cause respiratory depression. Antispasmodics anafortin and drotaverine were given for cervical dilatation. Early ARM was done. Partograph was maintained.

Gravida

OBSERVATIONS AND RESULTS In the study, 11.6% primigravida came in labor at 37-38 weeks of gestational age (GA), 13.2% primigravida at 38-39 weeks GA, 26.4% primigravida at 39-40 weeks GA and 8.4% primigravida at >40 to <42 weeks GA. Whereas out of 101 cases, in multigravida 4.4% were admitted at 37-38 weeks of GA, 8% cases at 38-39 weeks GA, 23.2% cases at 39-40 weeks and 4.8% cases of multigravida at >40 to <42 weeks of GA (Table 1).

Table 2 shows that in primigravida, cervical dilatation with oxytocin was 1.75 cm/hr and whereas in multigravida, cervical dilatation was 2.15 cm/hr with oxytocin.

GA (weeks)

Total

Table 2. Rate of Cervical Dilatation Mean rate of cervical dilation

Primigravida

1.75 cm/hr

Multigravida

2.15 cm/hr

Table 3. Duration of Labor Mean duration

Primigravida

Multigravida

1st stage

4.5 hr

2.5 hr

2nd stage

2 hr

1 hr

3rd stage

2.6 min

3 min

Table 4. Pain Score at Initiation of Labor Pain score

No. of cases

Percentage (%)

‘0’

No appreciation of pain

00

00

‘1’

Appreciation of pain which is bearable

9

3.6

‘2’

Presence of severe pain, desire for pain relief

42

16.8

‘3’

Presence of severe pain, demand for pain relief

199

79.6

250

100

Mean duration of labor in primigravida was 6.5 hours, whereas in multigravida it was 3.5 hours (Table 3).

Total

Majority cases had pain score ‘3’, 16.8% cases with pain score ‘2’ and 3.6% cases had bearable pain (Table 4).

It was observed that ketamine-induced substantial or complete relief of pain in majority of the cases (Table 5).

Table 5. Pain Relief Score with Ketamine Analgesia

Out of 250 cases undergoing programmed labor in our study, 87.2% cases delivered vaginally. In 6% cases cesarean section was done (Table 6).

In majority of lower segment cesarean section (LSCS) was done because of fetal distress in 1st stage of labor (Table 7). Majority of the babies were between the birth

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Pain score

No. of cases

‘0’

No relief of pain

00

‘1’

Some relief of pain

7

‘2’

Substantial relief of pain

41

‘3’

Complete relief of pain

197

Analgesia not given Total

5 250

OBSTETRICS AND GYNECOLOGY Table 6. Mode of Delivery Mode of delivery

No. of cases

Percentage (%)

218

87.2

Normal delivery Ventouse application

9

3.6

Forcep application

8

3.2

LSCS

15

6

Total

250

100

In our present study, 40.42% cases were delivered within 8 hours and 47.65% cases delivered between 8 and 12 hours. Only 11.2% cases delivered after 12 hours.

Table 7. Indication for LSCS Indication

No. of cases

Fetal distress

07

Deep transverse arrest: failed ventouse

05

Persistent occipito-posterior presentation

03

Total

15

Table 8. Birth Weight of Babies Delivered Vaginally Weight (kg)

No. of cases

Percentage (%)

<2.5

17

7.23

2.5-3.5

187

79.58

>3.5

31

13.19

Total

235

100

Table 9. Neonatal Outcome Outcome

Mode of delivery VD

54 minutes in the controls. The mean duration of 2nd stage was 17.46 minutes in subjects and 31 minutes in controls. The mean duration of 3rd stage was 4.94 minutes in subjects and 7.66 minutes in controls.

LSCS

Total

Live birth

234

15

249

Deeply asphyxiated baby

01

00

01

VD = Vaginal delivery.

weight 2.5 and 3.5 kg (Table 8). Only a single deeply asphyxiated baby, who had only heart beat at the time of delivery but could not be revived and died after 5 minutes of birth was born. This baby had three rounds of cord around the neck and did not show any sign of distress until the end of 2nd stage of labor (Table 9).

DISCUSSION In the study by SN Daftary and SV Desai (2003), out of 200 cases subjected for programmed labor, all patients except 2 cases of persistent occipito-posterior position were delivered within 8 hours. The mean duration of active phase of labor was 3.5 hours. Second and third stage was 32 minutes. In a study by Meena et al (2006), mean duration of 1st stage of labor was 2 hours 45 minutes in the subjects compared to 3 hours

SN Daftary and associates concluded that 72% of patients had complete and satisfactory pain relief. It was also found to be safe, as all the babies had Apgar score >8 at the end of 5 minutes. Only 54% of the patients experienced some degree of hallucination, which were easily well-controlled with diazepam, 98% of patients delivered within 5 hours. Meena et al (2006) stated that the mean time of onset of analgesia was 17 minutes.

Fifty-four percent of the subjects achieved good pain relief and 32% moderate pain relief.

SN Daftary and associate had shown that out of 200 low risk primigravida 97% cases delivered vaginally, instrumental assisted in 6.5% of the cases and LSCS rate was 3%. Meena et al (2006) stated that 98% of subjects and 94% of the controls delivered normally vaginally.

Two percent of the subjects and 2% of the controls needed forceps application and 4% of the controls have ventouse extraction.

Meena et al (2006) concluded that the mean Apgar score was above 7 in both the groups at 1 and 5 minutes. In our study, 79.58% of the newborn babies weighted between 2.5 and 3.5 kg. There was only one case of neonatal death. The baby had three rounds of cord around the neck. Following vaginal delivery, there was fetal heart sound but no respiratory movement, resuscitation was done but we were unable to revive the baby.

In SN Daftary study group, administration of analgesic and antispasmodic drugs were shown to cause nausea, vomiting, tachycardia and alteration of blood pressure.

In this study, morbidity like tachycardia (82%) cases, rise of blood pressure (13% cases), fall of blood pressure (2%), nausea and vomiting (5%), pyrexia (3.5%), vaginal tear (14%), hallucination (6.5%) and anemia (12%).

However, postpartum hemorrhage and postpartum psychosis were not seen in this study.

Meena et al (2006) observed tachycardia >100/min in 4% cases, nausea (4%), vomiting (6%), diarrhea (6%), drowsiness (4%), cervical/vaginal tears (10%).

CONCLUSION Active management of labor has been gaining acceptance ever since K â&#x20AC;&#x2DC;Oâ&#x20AC;&#x2122; Driscoll introduced it in 1969.

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OBSTETRICS AND GYNECOLOGY The essence of the programmed labor for active management of labor was: ÂÂ

Maintaining of partograms for the events of labor in each patients, so as to intervene as and when necessary

ÂÂ

Judicious and synergistic administration analgesics and antispasmodics

ÂÂ

Acceleration of labor with IV oxytocin whenever uterine contractions were less effective.

of

Most of the patients were satisfied with the protocol at the end of the deliveries. The ease of administration, the need for minimal patient monitoring with systemic analgesia has made programmed labor protocol highly acceptable. The optimizing labor protocol shortens the duration of labor and the duration of 3rd stage. It improves the maternal and neonatal outcome and need for obstetric interventions. Analgesia is quite effective and side effects of drugs are minimal and safe for the fetus as well.

“Motherhood”, a women’s most cherished moment remains as natural as normal labor without any bad feelings. Therefore, this protocol should be tried in each and every laboring patient, so that childbirth becomes an event of joy and satisfaction. Programmed labor protocol seems to be a logical answer to improving our management practices.

SUGGESTED READING 1. Arias F. Abnormal labour and delivery (Chapter 19). In: High Risk Pregnancy and Delivery. 2nd Edition, Missouri: Mosby.

2. Friedman E. The graphic analysis of labor. Am J Obstet Gynecol. 1954;68(6):1568-75.

3. Cunningham FG, Leveno KJ, Bloom SL, Hauth JC, Gilstrap LC III, Wenstrom KD (Eds.). Dystocia; abnormal labour (Chapter 20). In: Williams Obstetrics. 22nd Edition, USA: McGraw-Hill; 2005. p. 504.

4. Sheiner E, Levy A, Feinstein U, Hallak M, Mazor M. Risk factors and outcome of failure to progress during the first stage of labor: a population-based study. Acta Obstet Gynecol Scand. 2002;81(3):222-6.

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8. Oláh KS, Neilson JP. Failure to progress in the management of labour. Br J Obstet Gynaecol. 1994;101(1):1-3.

9. Bhaskar Rao K. Prolonged and obstructed labour (Chapter 22). In: Arulkumaran S (Ed.). The Management of Labour.

2nd Edition, Orient Longman; 2005. p. 343.

10. Kappy KA, Cetrulo CL, Knuppel RA, Ingardia CJ, Sbarra AJ, Scerbo JC, et al. Premature rupture of the membranes: a conservative approach. Am J Obstet Gynecol.

1979;134(6):655-61.

11. American College of Obstetricians and Gynaecologists: Fetal heart rate patterns: Monitoring, interpretation and management. Technical Bulletin No. 207, July 1999b.

12. American Academy of Pediatrics (AAP) and the American College of Obstetricians and Gynaecologists (ACOG). In: Guidelines for Perinatal Care. 5th Edition, Washington, DC: AAP and ACOG; 2002.

13. O’Driscoll K, Jackson RJ, Gallagher JT. Prevention of prolonged labour. Br Med J. 1969;2(5655):477-80.

14. O’Driscoll K, Foley M, MacDonald D. Active management of labor as an alternative to cesarean section for dystocia.

Obstet Gynecol. 1984;63(4):485-90.

15. Thornton JG, Lilford RJ. Active management of labour: current knowledge and research issues. BMJ. 1994;309(6951):366-9.

16. López-Zeno JA, Peaceman AM, Adashek JA, Socol ML. A controlled trial of a program for the active management of labor. N Engl J Med. 1992;326(7):450-4.

17. Fraser WD, Marcoux S, Moutquin JM, Christen A. Effect of early amniotomy on the risk of dystocia in nulliparous women. The Canadian Early Amniotomy Study Group. N Engl J Med. 1993;328(16):1145-9.

18. Frigoletto FD Jr, Lieberman E, Lang JM, Cohen A, Barss V, Ringer S, et al. A clinical trial of active management of labor. [Erratum in: N Engl J Med 1995;333(17):1163.] N Engl J Med. 1995;333(12):745-50.

19. Rogers R, Gilson GJ, Miller AC, Izquierdo LE, Curet LB, Qualls CR. Active management of labor: does it make a difference? Am J Obstet Gynecol. 1997;177(3):599-605.

20. Sadler LC, Davison T, McCowan LM. A randomised controlled trial and meta-analysis of active management of labour. BJOG. 2000;107(7):909-15.

21. Impey L, Hobson J, O’herlihy C. Graphic analysis of actively managed labor: prospective computation of labor progress in 500 consecutive nulliparous women in spontaneous labor at term. Am J Obstet Gynecol.

2000;183(2):438-43.

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5. Cammu H, Martens G, Ruyssinck G, Amy JJ. Outcome after elective labor induction in nulliparous women: a matched cohort study. Am J Obstet Gynecol. 2002;186(2):240-4.

6. Forouzan I. Dystocia. eMedicine. Com, Inc, 2005.

7. American College of Obstetricians and Gynaecologists: Induction of labour. Practice Bulletin No. 10, November 1999a.

PSYCHIATRY

Mental Health in Children: An Overview KRISHAN KUMAR*, RAJEEV DOGRA†, BRIJ LATA KOTIA‡

ABSTRACT Traditionally, psychiatry has always assumed that mental health could be defined as the synonym of mental disorder. However, mental health is “not the absence of negatives but the presence of positives”. In modern psychiatry, there are different empirical approaches to the concept of mental health, but definitions and concepts of mental health/disorder in adults cannot be always generalized to childhood population. The child is continually changing and growing and because mental processes and behaviors change as a child develops, it is also not clear whether same diagnosis can be applied across the age range. In this overview, an attempt has been made to throw light on the epidemiology, diagnosis, clinical assessment and pharmacological and psychosocial management of mental health disorders in children.

Keywords: Child psychiatry, mental health, developmental psychopathology, cognitive development, ICD-10, DSM-IV

T

raditionally, psychiatry has always assumed that mental health could be defined as the synonym of mental disorder. In other words, mental health was thought to be the absence of psychopathology.

Because, mental illness was easier to define, the concept of positive health was ignored. But, mental health is "not the absence of negatives but the presence of positives" (Vaillant, 2005). In modern psychiatry, there are different empirical approaches to the concept of mental health: ÂÂ Mental health as above normal or above average mental state that is objectively desirable ÂÂ Mental health as positive psychology - as epitomized by presence of multiple human strengths ÂÂ Mental health as developmental maturity ÂÂ Mental health as socioemotional intelligence ÂÂ Mental health as subjective well-being, a mental state subjectively experienced as happy, contented and desired

*Clinical Psychologist (Computational Neuroscience) National Brain Research Centre, Manesar, Haryana †Associate Professor Dept. of Psychiatry Postgraduate Institute of Medical Sciences, Rohtak, Haryana ‡Professor and Head Dept. of Psychology University of Rajasthan, Jaipur, Rajasthan Address for correspondence Dr Krishan Kumar Clinical Psychologist (Computational Neuroscience) Flat No. 104-B, National Brain Research Centre, NH-8 Near NSG Campus, Manesar, Haryana E-mail: keshusony@rediffmail.com

ÂÂ

Mental health as resilience, as the capacity for successful adaptation and homeostasis in the face of adversity.

Every model has advantages and limitations. Thus, mental health was described by Freud as "an ideal fiction" and described by Aubrey Lewis as "an invincibly obscure concept."

Characteristics of mentally healthy people (Jahoda, 1958): ÂÂ

They are in touch with own identity and feelings

ÂÂ

They are oriented towards the future and over time, they should remain fruitfully invested in life

ÂÂ

They should develop resistance to stress

ÂÂ

They should possess autonomy and should recognize what suits their needs

ÂÂ

They should perceive reality without distortion and yet possess empathy

ÂÂ

They should be masters of their environment able to work/play/love and be efficient in problem solving.

However, definitions and concepts of mental health/ disorder in adults cannot be always generalized to childhood population. Following factors should be considered before diagnosing mental disorder in children: ÂÂ

The child is continually changing and growing.

Sound knowledge is therefore required of normal development and its limits. Because mental processes and behaviors change as a child develops, it is also not clear whether same diagnosis can be

Indian Journal of Clinical Practice, Vol. 26, No. 12, May 2016

1163

PSYCHIATRY

ÂÂ

applied across the age range e.g., repetitive rituals may be normal in 5 years old, but abnormal in 8 years old. Once identified as abnormal, it is again helpful to decide if abnormalities are due to delay or due to deviance from usual pattern of development.

A subsequent study using similar design found rates of all types of disorders as twice than Isle of Wight, in an inner London borough. (Rutter, 1975) 1 year follow-up of Isle of Wight study (Rutter et al, 1976) revealed 1 year prevalence of 20% in adolescents.

Secondly, majority of childhood cases arise from an excess of behavior exhibited by normal young people e.g., aggression. They are seldom due to qualitatively distinct phenomena more often seen in adult conditions e.g., hearing voices. Consequently, choosing a cut-off point to make a diagnosis is inevitably an arbitrary process.

Selected Correlates

ÂÂ

Thirdly, children's difficulty often arises in the context of relationships within the family. Some or all of the problems may be in structure and functioning of the family, rather than in the individual child.

ÂÂ

Fourthly, information is gathered typically from multiple informants - child/parents/teachers, etc.

This may be non-corroborative leading to diagnostic bias and confusion, since the weight given to a particular informant may vary according to clinical condition e.g., if parent says that child has conduct disorder features but child denies this, parent is more likely to be right. However, if the parent says that child is not depressed but examination of child reveals otherwise, it is the parent who may be ignorant of the child's true state.

ÂÂ

Fifthly, comorbidity is rule rather the exception in childhood disorders, further confusing clinical diagnosis. True comorbidity may arise by:

Shared risk factors (e.g., early deprivation may lead to both ODD and attachment disorder).

Overlap between risk factors (e.g., depressed mother may genetically contribute to depression in child and provide inconstant discipline predisposing to CD).

One disorder creating increased risk for the other (CD leading to addiction).

Comorbid pattern itself constitutes a meaningful syndrome (e.g., depressive CD).

EPIDEMIOLOGY The classic Isle of Wight study by Rutter (1976) was a landmark 2 phase survey for determining prevalence of mental disorder in a sample of total 2,193 school attending children, using multiple informants (parents/ teachers) (screening followed by in depth assessment of selected subsample). The 1 year prevalence rate of psychiatric disorder was 7% and M:F ratio was 2:1.

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Indian Journal of Clinical Practice, Vol. 26, No. 12, May 2016

In a recent review of 52 separate communities-based studies, mean prevalence was noted as 15.8% (Roberts et al, 1998). ÂÂ

Age: Prevalence increases with age e.g., Prevalence of - 10% for preschoolers and 16.5 for adolescents (Roberts et al, 1998)

ÂÂ

Sex: In pre-adolescents, mental illness is more prevalent in boys due to higher occurrence of behavior problems. In adolescence, girls have higher rates than boys because of higher rates of emotional problems, especially depression.

Higher rates were also correlated with:

Chronic health problems and disability (Cadman et al, 1987)

Organic brain disorders like epilepsy (Rutter, 1985)

Low IQ and learning disorders (Hinshaw, 1992)

Difficult temperament (Hirschfield et al, 1992).

In a review of 55 Indian epidemiological studies in community and school settings, Bhola and Kapur (2003) found persistently lower rates of prevalence in Indian children (range - 0.48-17.2%), which may be due to methodological limitations or true crosscultural differences. Higher rates of conversion disorders and mild MR have been reported in India (Srinath and Girimaji, 1999).

Interesting epidemiological trends over time has been reported in both positive and negative directions. Performance in IQ tests has risen substantially around the world at all ages, a phenomenon known as the Flynn effect (Flynn, 1987). Average increase of 3 IQ points per decade has been found from 1952 to 1992 (Flynn, 1999).

Obviously, such massive shifts can not be explained by hereditary changes within one generation.

Environmental factors implicated are:

Improved nutrition

Increased urbanization

Better quality primary education

Exposure to media, especially television

More cognitively demanding jobs.

PSYCHIATRY

On the other hand, Ryan et al (1992), reported secular increase in childhood affective disorder, especially depression over time. Achenbach and Howell (1993), using Child Behavior Check List (CBCL) (Parent's version) over a 13-year-old period, found significantly increased scores in problem items in 1989 compared to 1976. Eighteen percent of 1,989 subjects were in clinical range versus 10% of 1976 subjects. While this may reflect true environmental influences, as above, methodological artefacts can also be responsible More refined diagnostic criteria/techniques Recall bias.

HISTORICAL PERSPECTIVE Historically, children were viewed merely as underdeveloped adults on the fringe of society.

However, by the 19th century, children were viewed as having unique psychological, physical and educational needs. Charles Darwin did much to generate interest in evolution and development of all sorts including that of children. Sigmund Freud startled the entire world when he theorized that adult abnormalities are rooted in early childhood experiences. John Watson propagated the concept of behaviorism, which emphasized the role of environment in shaping childhood behavior. Other influential theorists in this field were Maudsley, Emminghaus, Kanner, Bowlby and Piaget while pioneers in clinical research include Cantwell and Rutter.

The Diagnostic and Statistical Manual of Mental Disorders (DSM) I did not have separate category for childhood disorders which first appeared in DSM II as "behavior disorders of childhood and adolescence" with 6 diagnostic categories while DSM III first introduced multiaxial framework and operationalized diagnostic criteria.

In India, the earliest record of child development is found in the Ayurveda. It was considered that feeding practices, especially breastfeeding, formed the major influence on personality development (Kapur, 1995).

As a result of rapid advances cited above, the field of developmental psychology came into forefront. It is the study of how human behavior changes throughout the life span and especially during the childhood years.

development. It forms a liaison between abnormal psychology and developmental psychology and focuses on psychopathology as developmental deviations. This discipline was defined by Sroufe and Rutter (1984) as "The study of origins and cause of individual pattern of behavioral maladaptation, whatever the age of onset, whatever the causes, whatever the transformations in behavioral manifestations and however complex the developmental pattern may be": Various developmental theorists have given models explaining developmental underpinning of childhood mental health and disorders.

Psychodynamic Developmental Theories ÂÂ Freud's psychosexual theory: Over the course of childhood (birth to adolescence), sexual impulses shift their focus from oral to anal to genital regions of the body. He emphasized that how parents manage their child's sexual and aggressive drives in the first few years of life is crucial for healthy personality development. Too much or too little gratification of the child’s drives can cause his/her psychic energies to be fixated or arrested at a particular stage. ÂÂ Erikson’s psychosocial theory: Erikson expanded Freud’s theory emphasizing the psychosocial outcomes of development. A basic psychosocial conflict, which resolved along a continuum from positive to negative, determines healthy or maladaptive outcomes at each stage. Also, he did not regard important developmental tasks as limited to early childhood but to occur throughout the life span, thereby three adult stages to Freud’s model.

Behavioral/Learning Theories ÂÂ

Traditional behaviorism: Pioneers like Watson or Skinner rejected psychoanalytic perspectives of inner drives and concluded that environment is the supreme force in child development. Adults, thus, could mold future behavior of child by carefully controlling reinforcements and punishments.

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Social learning theory: Expanding behavioral theories, Bandura and colleagues demonstrated that modeling, also known as imitation or observational learning, is the basis for wide variety of childhood behaviors. Children acquire many favorable and unfavorable responses in the absence of direct rewards and punishments, simply by watching or listening to others around them.

DEVELOPMENTAL PSYCHOPATHOLOGY Developmental psychopathology is an emerging discipline, which studies how abnormal behavior can be understood in terms of processes underpinning human

Theories of Cognitive Development ÂÂ

Jean Piagets' cognitive developmental theory: According to Piaget, children actively construct

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PSYCHIATRY knowledge as they manipulate and explore their world. Children move through 4 broad stages of development, each of which is characterized by qualitatively distinct ways of thinking. In the sensori motor stage, cognitive development begins with the use of senses and movements to explore the world. These action patterns evolve into the symbolic but illogical thinking of the preschooler in the preoperational stage. Then cognition is transformed into more organized reasoning of the school age child in the concrete operational stage.

Finally, in the formal operational stage, thought becomes the complex, abstract reasoning system of the adolescent and the adult. ÂÂ

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Vygotsky's sociocultural theory: Lev Vygotsky focused on how culture- the values, belief customs and skills of a social group is transmitted to the next generation; social interaction, especially cooperative dialogues between children and more knowledgeable members of the society, is necessary for acquisition of knowledge. As adults and more expert peers help children master culturally meaningful activities, the communication between them becomes part of children's thinking.

Information processing theories: In these theories, human mind is perceived as a complex, system, through which information flows. Like Piaget, this model regards children as active beings who modify their own thinking in response to environmental demands. But unlike Piaget, there are no discrete stages. Rather, the thought processes (e.g., perception, attention, planning) are assumed to be similar in all ages but present to a lesser extent in children. Thus, development occurs by continuous increase rather than abrupt, stage-wise changes.

Theories of Socioemotional Development Attachment Theories John Bowlby in his ethological theory of attachment took a view of that how infants build emotional bonding with caregiver. This begins with a set of innate signals by the infant that call the adult to the baby's side. Attachment develops in 4 stages: ÂÂ

Pre-attachment phase (Birth to 6 weeks)

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Attachment in the making phase (6 weeks to 6 months)

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Phase of clear-cut attachment (6 months to 2 years)

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Formation of a reciprocal relationship (2 years onward).

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Temperament Theories Temperament consists of stable individual differences in quality and intensity of emotional reaction. Chess and Thomas studied different dimensions of temperament: activity level, rhythm city, distractibility, persistence, intensity of reaction, threshold of responsiveness and quality of mood; they found that temperament is a major factor in increasing the risk that a child will develop psychological problems or alternatively be protected from stress. Three types of children were noted: ÂÂ

Easy child: Quickly establishes regular routines, is generally cheerful, adapts readily to new experiences

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Difficult child: Irregular daily routines, tends to react negatively and intensely to new experiences

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Slow to warm up child: Inactive, shows mild, low key reactions to environmental stimuli, adjusts slowly to new experience.

Theories of Language Development This involves development of both semantics and pragmatics: ÂÂ

Semantics: Component of language concerned with understanding the meaning of word and word combinations

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Pragmatics: Component of language concerned with how to engage in socially effective and appropriate communication with others.

Learning Theories According to Skinner, language, just like any other behavior, is learned as adults apply the principles of operant conditioning to their children's verbalizations.

As the baby makes sounds, parents reinforce those that are most like words with rewards like hugs or smiles.

Classical conditioning also proposed to be involved in children's ability to respond appropriately to the language they hear. Imitation also explains partly how children rapidly pick up complex verbal behaviors, such as whole phrases and sentences.

Nativist Theories According to linguist Noam Chomsky, rather than being influenced fully by environment, language is a biologically based, innate, uniquely human accomplishment. Human are born with a language acquisition device which is an inborn system for picking up language that needs only to be triggered by verbal inputs from the environment.

PSYCHIATRY Theories of Moral Development

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Piaget's Theory

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Identified 2 broad stages of moral understanding: ÂÂ

Heteronomous morality or moral realism: (5-10 years) - children view rules as handed down by authorities (e.g., God/parents, teachers), as having a permanent existence, as unchangeable and requiring strict obedience.

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Axis II: Specific disorders of development Axis III: Intellectual level Axis IV: Associated medical conditions Axis V: Associated abnormal psychosocial condition Axis VI: Global social functioning.

DSM IV: Uses a similar multiaxial (5 axis) format for both adult/childhood disorders.

Kohlberg's Theory

Rutter (1975) has also developed a multiaxial framework from the developmental perspective: ÂÂ Diagnostic category ÂÂ Developmental delays ÂÂ Level of intellectual functioning ÂÂ Medical condition likely to have influenced the symptoms ÂÂ Psychosocial stressors (coded into 16 categories).

He organized his 6 stages of moral development into 3 general levels. He regarded the stages as invariant and universal - a sequence through which all people everywhere pass in a fixed order, albeit not in same pace or extent.

A new diagnostic framework: "Diagnostic Classification of Mental Health and Developmental Disorders of Infancy and Early Childhood" has been introduced for 0 to 3 years old (DC: 0-3) taking into account of unique developmental issues of very young children.

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Autonomous morality or morality of cooperation (10 years or above) through cognitive development, children become aware that people can have different perspectives about moral action and that intentions, not objective consequences, should serve as the basis for judging behavior.

The preconventional level: Morality is externally controlled, children blindly accept rules of authority figures, and actions are judged by their consequences.

Conventional level: Individuals continue to confirm to social rules, but not for reasons of selfinterest. They believe that actively maintaining the current social system is important for ensuring positive human relationships and societal order.

Post conventional/principled level: Individuals move beyond unquestioning support for own societal rules, they define morality in terms of abstract principles and values that apply to all situations and societies.

CLASSIFICATION

i. Primary diagnosis ii. Relationship disorder iii. Medical and developmental diagnosis iv. Psychosocial stressors v. Functional - Emotional developmental (Greenspan and Wieder, 2003).

level

In contrast to the above categorical systems, Achenbach and Edelbrock (1978) has given a dimensional system based on scores obtained on CBCL. The 2 major dimensions factorially derived were: ÂÂ

Internalizing disorders: Includes emotional disorders (anxiety/depression summarization).

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Externalizing disorders: Includes conduct and hyperkinetic disorders.

Classification systems may be categorical or dimensional.

They may follow uniaxial or multiaxial frameworks.

FACTORS INFLUENCING MENTAL HEALTH IN CHILDREN

A simple diagnostic classification:

These factors may be risk factors or protective factors.

Again, risk factors may be predisposing, precipitating and perpetuating/maintaining. ÂÂ Predisposing factor: Increases vulnerability of children to developing psychological problems. ÂÂ Precipitating factor: Triggers the onset or exacerbation of psychological problems. ÂÂ Perpetuating factor: Maintains psychological problems and prevent their resolution, once they have developed.

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Emotional disorders depression).

(e.g.,

anxiety/phobia/

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Disruptive disorders (e.g., CD/ADHD).

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Developmental disorders (e.g., spectrum, language disorders).

MR,

autism

ICD-10 has special multiaxial framework for psychiatric disorders in childhood and adolescence: ÂÂ

Axis I: Clinical psychiatric syndromes

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PSYCHIATRY Protective Factor Prevents further deterioration and have implications for prognosis and response to treatment. Any causally related factors may again be: ÂÂ

Personal: Referring to individual biological or psychological characteristics of the child e.g., family history and temperament.

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Contextual: Referring to features of child’s psychosocial environments (e.g., school/peer group influences).

Risk Factors Biological ÂÂ Genetic factors: Recent population based twin and adoption studies demonstrate that development of various discrete disorders as well as predisposition/ vulnerability characteristics like intelligence or temperament is greatly influenced by genetic factors. Size of this genetic influence has been estimated to account for 30-60% of overall variation within a population (Rutter, 1991).

Mechanism is usually nonmendelian and polygenic. Direct or strong genetic influences have been identified for limited disorders like Tourrette disorder/autism/juvenile bipolar disorder while otherwise genetic influences are mediated indirectly via broader characteristics like temperament (Plomin, 1991). ÂÂ Prenatal/Perinatal complications: Intrauterine environment may entail hazards which compromise healthy development of fetus (Rutter, 1991). This is influenced by antenatal factors like: Advanced maternal age Blood group incompatibility Maternal malnutrition Smoking Alcohol and drug use Maternal infections like rubella/syphilis/ AIDS (acquired immune deficiency syndrome) Prematurity and intrauterine growth restriction (IUGR) leading to low birth weight «2,000 g).

Perinatal/birth complications are commonly associated with forceps delivery, breech delivery and prolonged or obstructed labor, leading to fetal distress/injury during birth canal passage.

Premature infants are particularly susceptible to brain injury during birth due to poorly formed skull vault.

Perinatal damage is most commonly associated with developmental delays/ hyperactivity (Hinshaw, 1993).

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Physical injuries/diseases: Organic brain disorders especially head trauma/epilepsy are one of the strongest predictors of later psychological problems (Rutter, 1976).

Childhood injury may result in cognitive impairment, disinhibition and behavioral problems. Extent of sequelae is related to severity of damage but not closely to the site/location. Progress is also related to the social context in which recovery occurs (Hawkins et al, 1998).

Head trauma sequelae in children differ from adult in following ways: Capacity to compensate: Immature brain is more able than adult brain to compensate for localized damage e.g., hemispherectomy in early childhood may be followed by normal language development.

Delayed effects: Early damage may not become manifest as a disorder until late stage of development.

Often, subtle damage insufficient to cause definite neurological signs or structural changes can cause behavioral problem later on - this concept known as "Minimal brain dysfunction."

Childhood epilepsy especially temporal lobe epilepsy, often contributes to psychiatric disorder in following ways: yy The brain lesion causing epilepsy may cause psychiatric disorder yy Psychosocial consequences of seizures may be contributory yy Antiepileptic drugs may contribute through side effects (e.g., phenobarbitone and hyperactivity).

Other disorders associated with increased risk: yy Meningitis/encephalitis yy Hypoxia resulting from near drowning/ electrocution yy Childhood human immunodeficiency virus (HIV) infection yy Chronic lead poisoning (-low IQ and hyperactivity) (Taylor, 1991) yy Chronic medical illness, not involving CNS, like asthma/diabetes/renal failure/cancer (Eiser, 1990).

Psychological Individual psychological characteristics of child may be contributory: ÂÂ

Temperament: In a 26-year-old longitudinal follow-up study, Chess and Thomas (1984) studied

PSYCHIATRY outcome of 3 types of temperament. Initially, an easy temperament was found in 40%, difficult temperament in 10% and slow to warm up temperament in 15% of children. Easy temperament was a protective factor, while difficult temperament predicted future psychological difficulties,- these children experienced more conflict and negative reactions from care-givers/peers/teachers. Prognosis for "slow to-warm up" children was intermediate. ÂÂ

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Intelligence: Low IQ and mental retardation are associated with increased psychiatric disorder up to 2-3 times (Hinshaw, 1992). This dual diagnosis entails major additional handicap and impairment of adaptive behavior.

Immature/neurotic defense mechanisms: When excessively used, allow child to regulate anxiety in short-term but entail long-term difficulties (Conte and Plutchik, 1995).

Coping strategies: These may be problem focused or emotion focused and is used consciously in crises. Use of dysfunctional coping strategies like avoidance of a problem/alcohol or drug use, maintain or exacerbate long-term difficulties (Zeidner and Endler, 1996).

Other cognitive distortions in children that contribute to future risk: External locus of control (Rotter, 1966) Low self-esteem (Rolf, 1990) Deficient self-regulatory beliefs e.g., depressive attribution style and school-based learned helplessness.

in males is particularly high (Kranzler et al, 1990). However, bereaved children may show resilience in presence of various protective factors. Risk factors in children are: yy Young age (especially before 11 years) yy Female sex yy No preparation for death yy Sudden or catastrophic death yy Witnessing the death yy Death of mother yy Prior ambivalent relationship yy Previous psychiatric disorder yy Previous and subsequent losses yy Poor social support yy Inability to mourn, no involvement in death rituals yy Lack of bereavement counseling.

yy Parental depression is associated with three-fold increased risk of depression in offspring, as well as increased rates of phobias/panic disorder/alcohol dependence and conduct disorder (Weissman et al, 1997). yy Parental substance use and personality disorders contribute to conduct disorders and substance abuse (Merikangas et al, 1998).

Socioenvironmental ÂÂ

Parental and familial factors Attachment/bonding: Ainsworth et al (1978) first described patterns of mother infant interaction following brief episode of experimentally contrived separation denoted as "strange situation".

Three types of attachment were: yy Secure attachment yy Anxious attachment yy Resistant attachment.

Lack of secure attachment predicts future psychological problem (Fonagy et al, 1994).

Parental separation and loss: Psychiatric morbidity has been found to be persistently higher in bereaved children than controls, at both short-term and long-term followup, depression and anxiety disorders occur most commonly but alcohol and drug use

Parental psychiatric/medical illness: Besides contributing to genetic transmission, parental illness also adversely affects children via environmental mechanisms like insecure attachment, chaotic family environment, marital disharmony and economic difficulties.

yy Parental chronic physical illness like cancer/ AIDS/heart disease cause increased risk for anxiety/low self-esteem and poor social skills (Grant and Compas, 1995).

Parenting style: Four types of parenting styles have been described with different developmental outcomes of the child: yy Authoritative style: It is a protective factor with maximum benefit to child (Darling and Steinberg, 1993) yy Authoritarian style: Results in shy/anxious child yy Permissive style: Results in poor impulse control yy Neglecting problem.

style:

Results

in

conduct

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PSYCHIATRY

Parental marital status/relationship:

However, ultimate risk is tempered by effects of both quality of family environment and nature of subsequent life events...

Neglect: (Physical, emotional, medical care and educational) results in failure to thrive (Psychosocial dwarfism), developmental delays, attachment disorders and conduct problems.

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Peer-related factors: Beyond family, relationships with peers provide unique and essential contribution to social, emotional and cognitive development. Increased risk may be caused by (Hawkins, 1992): Rejection/isolation by peers: Results in low self- esteem and poor social skills.

Affiliation with behaviorally deviant peers: Predispose to conduct problems.

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School-related factors: School life brings its own particular demands and challenges. Adverse influences include (Rutter, 1985): Frequent change of school Chaotic school environment Absence of consistent discipline/rules Corporal punishment Bullying in school.

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Community-related factors: Poverty and social disadvantage: Lower socioeconomic class and persistent financial difficulties are strongly associated with difficulties in cognitive skills and educational achievements (Carlson et al, 2000).

Urban inner city residential area: Risk of disorders were doubled in some studies (Rutter, 1975).

Increased community violence, criminality and unemployment.

Lack of supportive community and social network.

Increased prevalence of alcohol and substance use.

yy Parental divorce is associated with psychological/behavioral problems, specially in short-term with boys, with particular risk for conduct problems and academic failure (Cherlin et al, 1991). yy More than the divorce itself, marital discord/ conflict preceding divorce especially increase risk of conduct problems. Single parent and step-parent/reconstituted families show higher mean levels of emotional problems and educational underachievement (Dunn et al, 1998).

Dysfunctional/disorganized family environment: Apart from above family related factors, increased risk for both externalizing/ internalizing disorders in children are associated with: yy Inconsistent/unclear rules yy yy yy yy yy

Ineffective monitoring and supervision Lack of intellectual stimulation Over punitive/harsh discipline Excessive use of corporal punishment Younger maternal ages (especially teenage mothers) yy Large family size. yy Abnormal parent child interactions like hostility/lacking of warmth/disengagement overprotection/inadvertent reinforcement of undesirable behaviors.

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Child abuse and maltreatment: yy Child abuse includes physical abuse/sexual abuse/emotional abuse and neglect. yy Physical abuse (nonaccidental physical injury) results in "battered child syndrome" and results in physical sequelae as well as behavioral problems like poor social skills, chronic oppositional and aggressive behavior and academic failure (Cicchetti and Toth, 1995). yy Sexual abuse: This can lead to wide range of psychological sequelae (Kendall-Tackett et al, 1993). yy Affective symptoms: Phobia/PTSD/ depression. yy Behavior problems: Conduct disorder, hyperactivity, sexualized behavior, selfdestructiveness. yy Cognitive functioning: Educational/ language difficulties.

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Protective Factors ÂÂ Biological factors: (Rutter, 1995) Good physical health Absence of genetic vulnerabilities No history of serious illness or injuries Uncomplicated birth Adequate nutrition Female gender before puberty and male gender thereafter.

PSYCHIATRY ÂÂ

Psychological factors (Carlson, 2000) Easy temperament High level of intellectual ability High self-esteem Use of mature defenses and functional coping.

Familial factors (Darling and Steinberg, 1993) Secure attachment Authoritative parenting style Parental marital harmony Involvement of father in child-rearing Explicit/consistent family rules Clear and direct communication.

Educational factors (Rutter, 1985) High quality day-care Preschool early intervention educational program Favorable school environment with firm authoritative leadership Involvement with peer group.

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Psychiatric examination of child: Establishing rapport is of crucial importance. The examiner should not only focus on presenting symptom but also use a judicious mixture of appropriate techniques of play, drawing, painting, storytelling, etc.

Verbal, nonverbal gestures and behaviors should be picked up by examiner. ÂÂ

General appearance: Stature, nutrition, congenital defects, injury suggestive of abuse, attitude towards examiner.

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Motor function: Activity compulsions.

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Speech: Articulation, vocabulary, fluency, abnormal speech, stammering, receptive or expressive language deficits.

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Content of talk and thought: Logical stream, abnormal use of words, delusions, obsessions, suicidal ideas.

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Perception: Illusions, hallucinations

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Intellectual function: Attention, general information, abstraction (age and background appropriate).

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Emotional state: Affective display, attitude to family and school, separation responses.

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Inquiry about fantasy life: Three wishes, worse or best things, dreams, ambitions.

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Indicators of social adjustment; peer relationship, hobbies, interests, games, (follower/leader, bully/ bullied).

Assessment Dramatic advance has occurred in concept of psychiatric assessment of children in recent years, as follows: ÂÂ

The identification of child as key informant

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The re-emergence of descriptive psychopathology instead of psychodynamic formulations

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The emergence of more highly specified diagnostic criteria for child and adolescent disorders

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The development of structured diagnostic interviews for children, parents and teachers

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Increasing awareness that diagnostic comorbidity is the norm

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Importance of identifying both strengths and weaknesses in a particular child.

Assessment will include: ÂÂ Detailed history ÂÂ Physical examination of child ÂÂ Psychiatric examination of child ÂÂ Examination of family and environment ÂÂ Psychological testing and assessment.

History should cover: ÂÂ

Presenting complaints

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Obstetric history

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Developmental history

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Family and past history

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School and play history.

level,

coordination,

Physical examination of child: Including detailed neurological exam, and search for signs of abuse and neglect.

Examination of family ÂÂ Family structure Parents: Age, occupation, current physical/ emotional states, history of psychiatric disorders Siblings: Ages, presence of problems Home circumstances, sleeping arrangements. ÂÂ Family function Quality of parental relationship: Mutual affection, capacity to communicate, sharing of attitudes.

Quality of parent child relationship: Positive interaction, mutual enjoyment, criticism, hostility, rejection.

Sibling relationship.

Overall pattern of family dynamics: Alliance, communication, exclusion, scapegoating, inter generational confusion.

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PSYCHIATRY Psychological assessment should focus on the following areas: ÂÂ Cognition (Intelligence, language and number skills, achievement, aptitude) ÂÂ Personality (temperament, adjustment) ÂÂ Perception of environment (attitude toward parents, peers) ÂÂ Self concept ÂÂ Social behavior ÂÂ Sensory motor skills/brain damage ÂÂ Physical attributes ÂÂ Environment

Treatment Issues Important differences between management issues between children and adolescents.

Referral Issue Child is usually brought to clinic because someone else (parent, teacher) is concerned or annoyed by child’s behavior. Thus patient may be passive, if not reluctant, participant in treatment.

Ethical Issues ÂÂ

Of prescription drugs marketed, 80% are not approved by Food and Drug Administration (FDA) for pediatric use. Thus, psychiatrists face the dilemma of either depriving children of potentially beneficial medical treatment or prescribing such medication "off-label" (Jensen et al, 1999).

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Confidentiality is a key issue with the dilemma being how much disclosure to be made to parents, especially in case of adolescents.

Prevention Prevention aims to reduce quantity and burden of psychiatric disorder in a population and may act on primary, secondary and tertiary levels. Primary prevention may involve 2 approaches (Kellam, 1993) ÂÂ

Targeted interventions: Aimed at selected highrisk group of children and families (e.g., child care training for single mothers in lower social classes).

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Universal interventions: Aimed at benefit for entire populations (e.g., primary education for everyone).

To be effective, intervention measures should have following features: ÂÂ

Must be active and persistent

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Must start at an early age

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Must be rooted in developmental processes

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Must address the needs of child's individual environment.

Health promotion may be done in school, home and community settings, setting up any preventive program includes the following steps: ÂÂ

Identification of a problem/disorder

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Identification of risk and protective factors

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Carrying out pilot efficacy studies

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Launching and evaluating large scale effectiveness trails

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Dissemination of the program in variety of community settings.

Prevention approaches to conduct disorder has been most established and successful. Evidence in support was found for the following interventions in high risk children (Hill, 2000): ÂÂ

Home visits by nurses

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Compensatory preschool education

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Social skills and problem solving training.

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Pharmacokinetic Issues There are a number of pharmacokinetic differences which frequently lead to need for higher doses in children on milligram per kilogram basis to achieve similar drug concentration as in adults on the usually effective adult doses (Leeder and Kearns, 1997). ÂÂ

Activity of most drug metabolizing enzymes (CYP/ glucorunidation) is absent in fetus but rapidly increase after birth and greatly exceed adult levels over first year of life; usual adult levels are achieved only after puberty.

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Renal clearance is more rapid in children than in adults (Thus higher dose of lithium is required in children).

Effectiveness Issues Many drugs proved effective in adults are not wellestablished in pediatric patients.

Tricyclic antidepressants with proved efficacy in adults were mostly found to be equally effective to placebo in children and adolescents in controlled trials. Only 2 trials have proven modest benefit over placebo (Preskorn et al, 1987), while typically high placebo response rates (up to 68%) have been reported (PuigAntich et al, 1987). This lower efficacy and higher placebo response has been attributed to following factors (Birmaher et al, 1996). ÂÂ Greater importance of psychosocial variables in childhood depression (e.g., more hospitalization/

PSYCHIATRY

ÂÂ

ÂÂ ÂÂ ÂÂ

ÂÂ ÂÂ

removal from home environment resulting in response even to placebo).

Depression in children being heterogeneous entity with high comorbidity, predicting poorer drug response.

Inclusion of mild/moderate depression, lower prevalence of melancholic depression in children.

Insufficient dosage/duration in pediatric drug trials.

Mostly tertiary amine tricyclic antidepressants (TCA) used in trials (e.g., imipramine) having major effect on noradrenergic system, which is fully developed only after puberty.

More efficient hepatic deamination in children resulting in decreased TCA efficacy.

Pubertal hormonal changes (e.g., increased gonadal steroids) inhibiting neurotransmitter function.

adult counterparts (Rutter, 1995). Individual disorders have been shown to have significant continuity into adulthood either in a diagnosis-specific manner or in terms of nonspecific psychosocial impairments.

Important questions addressed in outcome studies in children are (Rutter, 1995): ÂÂ

What happens to the children diagnosed to have psychiatric disorders?

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What is natural course of the disorder?

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Do these children continue to suffer from the same or some other psychiatric disorder?

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Does any specific intervention alter the course of the disorders favorably and to what extent?

Individual disorder specific findings are: ÂÂ

Depressive disorders are resistant, chronic and recurrent, with higher risk of bipolarity, than adults (Birmaher et al, 2002)

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Bipolar disorders show increased frequency of mixed episodes and rapid cycling with poorer rate of recovery (Carlson et al, 2000)

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About 50% of ADHD patients will have persistent symptoms in adulthood with higher risk of antisocial behavior, substance abuse and sociooccupational dysfunction (Mannuzza and Klein, 2000)

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Twenty-five percent of children with ODD develop conduct disorder while 10% progress to ASPD, while 40% of children with conduct disorder will ultimately develop ASPD in future (Steiner et al, 1990)

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OCD has a chronic and relapsing course, with poorer response to medications (Leonard, 1993).

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In childhood autism, only up to 15% had good outcome while up to 75% had poor! Very poor outcome.

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In almost all disorders, any comorbidity predicted poorer outcome (Mannuzza et al, 1991).

Tolerability Issues Side effects may be particularly deleterious in children with possible long-term effects on growth and development, due to prolonged cumulative exposure. Of particular concern in this population are (Janicak et al, 2001): ÂÂ

Stimulants and growth retardation

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Selective serotonin reuptake inhibitors and suicidal intentions

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TCAs and cardiotoxicity

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Neuroleptics and tardive dyskinesia.

Psychotherapeutic Issues Nonsomatic treatments may be more acceptable in child populations due to lesser risk of iatrogenic side effects. However, psychotherapy has to be flexibly and intelligently adjusted to be effective, including the following factors: ÂÂ Therapist has to deal not only with child but also with environmental and familial dynamics. ÂÂ Close collaboration is needed with child and parents as well as school, legal officers, social welfare agencies and community leaders at times. ÂÂ Therapist must be aware of the individual child's physical, emotional and cognitive development to understand symptoms and set treatment goals. ÂÂ The child is less proficient~ in abstract language use and therapist has to involve nonverbal indirect techniques like play, art, writing and fantasy.

Course and Outcome in Child Psychiatry Childhood psychiatric disorders are generally associated with poorer outcome and graver prognosis than their

CONCLUSION It is evident that mere extrapolation of research data from adults to childhood populations is undesirable and untenable. Childhood mental health and disorder appears to be different in many aspects of diagnosis, management and outcome, from their adult counterparts. There is an unfortunate dearth of research in fields of pediatric epidemiology, clinical assessment, pharmacological and psychosocial management, which needs to be addressed systematically in future.

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18. Hill P. Prevention of mental disorder in childhood. In: Gelder M, Lopez-Ibor J, Andreasen NC (Eds.). New Oxford Textbook of Psychiatry. Oxford: Oxford University Press; 2000. pp.1705-11.

19. Hinshaw SP, Lahey BB, Hart EL. Issues of taxonomy and comorbidity in the development of conduct disorder.

Development and Psychopathology Special Issue: Toward a Developmental Perspective on Conduct Disorder. Develop Psychol. 1993;5: 310-49.

20. Hinshaw SP. Externalizing behavior problems and academic underachievement in childhood and adolescence: causal relationships and underlying mechanisms. Psychol Bull. 1992;111(1):127-55.

21. Hirshfeld DR, Rosenbaum JF, Biederman J, Bolduc EA, Faraone SV, Snidman N, et al. Stable behavioral inhibition and its association with anxiety disorder. J Am Acad Child Adolesc Psychiatry. 1992;31(1):103-11.

22. Jahoda M. Current concepts of positive mental health.

Basic Books: New York; 1958.

23. Janicak PG, Davis JM, Preskorn SH, et al. Principles and Practice of Psychopharmacotherapy. 3rd Edition, Philadelphia: Lippincott Williams & Wilkins; 2001.

24. Jensen PS, Bhatara VS, Vitiello B, Hoagwood K, Feil M, Burke LB. Psychoactive medication prescribing practices for U.S. children: gaps between research and clinical practice. J Am Acad Child Adolesc Psychiatry.

1999;38(5):557-65.

25. Kellam SG. Concluding remarks at the 5th IndoUS symposium on Child Mental Health. Bangalore: NIMHANS; 1989.

26. Kendall-Tackett KA, Williams LM, Finkelhor D. Impact of sexual abuse on children: a review and synthesis of recent empirical studies. Psychol Bull. 1993;113(1):164-80.

27. Kranzler EM, Shaffer D, Wasserman G, Davies M. Early childhood bereavement. J Am Acad Child Adolesc Psychiatry. 1990;29(4):513-20.

28. Leeder JS, Kearns GL. Pharmacogenetics in pediatrics.

Implications for practice. Pediatr Clin North Am. 1997;44(1):55-77.

29. Leonard HL, Swedo SE, Lenane MC, Rettew DC, Hamburger SD, et al. A 2- to 7-year follow-up study of 54 obsessive-compulsive children and adolescents. Arch Gen Psychiatry. 1993;50(6):429-39.

30. Loeber R. The prevention of serious delinquency and violence. In: Howell JC, Krisberg B, Hawkins JD, et al (Eds.). Sourcebook on Serious, Violent and Chronic Juvenile Offenders. Thousand Oaks, CA: SAGE; 1995. pp.

213-37.

31. Mannuzza S, Klein RG. Long-term prognosis in attentiondeficit/hyperactivity disorder. Child Adolesc Psychiatr Clin N Am. 2000;9(3):711-26.

32. Mannuzza S, Klein RG, Bonagura N, Malloy P, Giampino TL, Addalli KA. Hyperactive boys almost grown up. V. Replication of psychiatric status. Arch Gen Psychiatry.

1991;48(1):77-83.

PSYCHIATRY 33. Merikangas KR, Dierker LC, Szatmari P. Psychopathology among offspring of parents with substance abuse and/ or anxiety disorders: a high-risk study. J Child Psychol Psychiatry. 1998;39(5):711-20.

34. Plomin R. Genetic risk and psychosocial disorders.

In: Rutter M, Caeser D (Eds.). Biological Risk Factors for Psychosocial Disorders. Cambridge: Cambridge University Press; 1991. pp. 101-38.

47. Scott S. Developmental psychopathology and classification in childhood and adolescence. In: Gelder M, Lopez-Ibor J, Andreasen NC (Eds.). New Oxford Textbook of Psychiatry. Oxford: Oxford University Press; 2000. pp.

1705-11. pp 1685-90.

48. Shaffer D, Fisher P, Dulcan MK, Davies M, Piacentini J, Schwab-Stone ME, et al. The NIMH Diagnostic Interview Schedule for Children Version 2.3 (DISC2.3): description, acceptability, prevalence rates, and performance in the MECA Study. Methods for the Epidemiology of Child and Adolescent Mental Disorders Study. J Am Acad Child Adolesc Psychiatry. 1996;35(7): 865-77.

35. Preskorn SH, Weller EB, Hughes CW, Weller RA, Bolte K. Depression in prepubertal children: dexamethasone nonsuppression predicts differential response to imipramine vs. placebo. Psychopharmacol Bull.

1987;23(1):128-33.

36. Puig-Antich J, Perel JM, Lupatkin W, Chambers WJ, 49.

Tabrizi MA, King J, et al. Imipramine in prepubertal major depressive disorders. Arch Gen Psychiatry. 1987;44(1): 81-9.

50.

37. Roberts RE, Attkisson CC, Rosenblatt A. Prevalence of psychopathology among children and adolescents. Am J Psychiatry. 1998;155(6):715-25.

38. Rolf J, Masten A, Cichetti D, et al. Risk and protective 51. factors in the development of psychopathology. New York: Cambridge University Press; 1990.

52.

39. Rotter JB. Generalized expectancies for internal versus external control of reinforcement. Psychol Monogr.

1966;80(1):1-28.

53.

40. Rutter M. A children's behaviour questionnaire for completion by teachers: preliminary findings. J Child 54.

Psychol Psychiatry. 1967;8(1):1-11.

41. Rutter M. Brain damage syndrome in childhood: concepts and findings. J Child Psychol Psychiatry. 1975;18(1):1-21.

42. Rutter M. Family and school influences on behavioural 55. development. J Child Psychol Psychiatry. 1985;26(3): 349-68.

43. Rutter M. Nature, nurture, and psychopathology: A new 56. look at an old topic. Develop Psychopathol. 1991;3(2): 125-36.

44. Rutter M. Relationships between mental disorders 57. in childhood and adulthood. Acta Psychiatr Scand.

1995;91(2):73-85.

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Med. 1976;6(2):313-32.

46. Ryan ND, Williamson DE, Iyengar S, Orvaschel H, Reich T, et al. A secular increase in child and adolescent onset 59. affective disorder. J Am Acad Child Adolesc Psychiatry.

1992;31(4):600-5.

■■■■

Srinath S, Girimaji S. Epidemiology of child and adolescent mental health problems and mental retardation.

NIMHANS J. 1999;17:355-66.

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Sroufe LA, Rutter M. The domain of developmental psychopathology. Child Dev. 1984;55(1):17-29.

Taylor DC. The concept of mental health in children. Eur Child Adolesc Psychiatry. 2003;12(3):107-13.

Taylor E. Developmental neuropsychiatry. J Child Psychol Psychiatry. 1991;32(1):3-47.

Vaillant GE, Vaillant CO. Normality and mental health.

In: Sadock BJ, Sadock VA (Eds.). Comprehensive Textbook of Psychiatry. 8th Edition, Vol. 1, Philadelphia: Lippincott Williams & Wilkins; 2000.

Vogel JM, Vemberg EM. Part 1: Children's psychological responses to disasters. J Clin Child Psychol. 1993;22: 464-84.

Wallerstein JS, Kelly JB. Surviving the Breakup: How children and their parents cope with divorce. New York: Basic Books; 1980.

Wallerstein JS, Carbin SB. The child and vicissitudes of divorce. In: Lewis M (Ed.). Child and Adolescent Psychiatry. Philadelphia: Lippincott Williams & Wilkins; 2004. pp. 1275-84.

Weissman MM, Warner V, Wickramaratne P, Moreau D, Olfson M. Offspring of depressed parents. 10 years later.

Arch Gen Psychiatry. 1997;54(10):932-40.

Zeidner M, Endler N. Handbook of Coping: Theory, Research, Applications. New York: Wiley; 1996.

Patients at High-risk of Depression After a Stay in ICU Study suggests that majority of people who survived life-threatening illness with a stay in ICU are at high-risk for persistent depression, anxiety and post-traumatic stress disorder, especially if they are female, young or unemployed. (Source: Johns Hopkins Medicine. 20 April 2016)

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VENEREOLOGY

Oral Tertiary Syphilis: A Case Report DEEPA MS*, ANITA BALAN†, S SUNIL‡, BIFI JOY#

ABSTRACT A case of benign tertiary syphilis presenting as a solitary hypertrophic lesion on the dorsum of the tongue is described. The oral aspects of tertiary syphilis and the need for dentists to be aware of changing trends in relevant infectious diseases are highlighted. Currently, tertiary syphilis is very rarely seen, however, this case emphasizes that it still exists and must be considered in the differential diagnosis of oral lesions.

Keywords: Spirochete, tertiary syphilis, infection, oral lesions

S

yphilis is a complex systemic illness, because of defects in cell caused by the spirochete Treponema pallidum. The term “Syphilis” came from a poem written in 1530 by the Italian poet Hiero Fracastor.

Transmission of syphilis occurs via close contact with an infected lesion; which usually occurs on the genitals or through blood.

presentation nor did she have a history of any skin lesions in the past. She had no systemic complaints at the time of presentation. Her husband had died 17 years back. She had 4 healthy children. She had no history of recurrent abortions or early neonatal deaths.

She didn’t have any significant illness in the past or any habituation.

Following contact, T. pallidum penetrates the genital or oral mucosa, multiplies at the site of entry and systematically spreads through the lymphatic and blood. The oral mucosa is commonly affected as a consequence of orogenital contact.1,2

On examination, she had a solitary painless 2 × 2 cm well-defined ulcer in the middle of dorsum of tongue (Fig. 1). Pale granulation tissue formed the base.

There was no fluid exudation on pressure. Cervical and generalized lymphadenopathy was not present.

Systemic examination revealed no abnormality.

CASE REPORT A 65-year-old lady was referred to the Dept. of Oral Medicine and Radiology for the evaluation of a solitary painless ulcer on the dorsum of tongue from the Dept. of Venereology, Medical College, Trivandrum, Kerala.

She had increased salivation for the past 5 years. There were no active skin or genital lesion at the time of

*Professor and HOD Dept. of Oral Medicine Azeezia College of Dental Sciences and Research, Kollam, Kerala †Professor and Head Dept. of Oral Medicine and Radiology, Govt. Dental College, Calicut, Kerala ‡Professor Dept. of Oral and Maxillofacial Pathology Azeezia College of Dental Sciences and Research, Kollam, Kerala #Former PG Student Dept. of Dermatology, Medical College, Trivandrum, Kerala Address for correspondence Dr Deepa MS “Nandhanam” TC 1/955 (3), TLRA-59/A, Thoppil Lane, Medical College Trivandrum - 695 011, Kerala E-mail: docdeepams@yahoo.co.in

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Subsequent hematological, serological and histopathological investigations were carried out. Hematological examinations were within normal limits. Blood serologic tests for syphilis (STS) showed positivity in 1 in 32 dilutions. Blood T. pallidum hemagglutination assay (TPHA) was positive, hepatitis B surface antigen

Figure 1. Clinical photograph showing ulcer on the dorsum of tongue.

VENEREOLOGY with general manifestations is uncommon.6 The various orofacial manifestations of the different stages of syphilis are shown in Table 1.7

Figure 2. Photomicrograph showing nonspecific inflammation of the connective tissue (H&E section, 10X).­­

Gummas tend to arise on the hard palate and tongue, although very rarely they may occur on the soft palate, lower alveolus and parotid gland. The signs and symptoms of primary and secondary syphilis resolve spontaneously and patients then enter the latent stage of infection.8,9 Manifestations of tertiary syphilis may appear after several years of nontreatment with cardiovascular and neurologic involvement including severe manifestation of general paresis and aneurysm of aorta. Benign tertiary syphilis is characterized by the tissue immunological reaction that leads to a specific lesion designed as gumma. These lesions are destructive granulomatous inflammation that may develop in any organ.10 In the present case, the lesion observed in the dorsum surface of the tongue was of “gummatous inflammation” of tertiary syphilis. Patients with tertiary syphilis may have not remembrance of lesions during earlier stages of the disease.11 Conclusive diagnosis Table 1. The Orofacial Manifestations of Different Stages of Syphilis

Figure 3. Photomicrograph showing dense collection of inflammatory cells in the area of ulceration (H&E section, 10X).

Stage of disease

Orofacial manifestations

Primary

Chancre Nontender cervical lymphadenopathy

(HbsAg) and enzyme-linked immunosorbent assay (ELISA) for human immunodeficiency virus (HIV) were negative. Histopathological examination revealed only a chronic nonspecific inflammation (Figs. 2 and 3).

Based on the results of serological examination patient was diagnosed as having a gummatous ulcer on the tongue and was put on injection-PP12 lakh units deep IM daily for 12 consecutive days. There was resolution of the lesion 2 weeks after the initiation of penicillin therapy and blood STS become nonreactive after 3 months.

Secondary

‘Rubbery’ cervical lymphadenopathy Maculopapular eruptions, moth-eaten alopecia Leukoderma patches of hypopigmentation Condylomata lata, ulceronodular disease (lues maligna) Nodular disease Tertiary

Gumma (palate and tongue) Osteomyelitis, atrophic and interstitial glossitis Syphilitic leukoplakia, syphilitic sialadenitis Trigeminal neuropathy (Hitzig’s syndrome)

DISCUSSION Infective syphilis is caused by the spirochete T. pallidum.

Transmission occurs via close contact with an infected lesion, which usually occurs on the genitals. Following contact, T. pallidum penetrates the genital or oral mucosa, multiplies at this site of entry and systemically spreads via the lymphatics and blood. Syphilis gives rise to a wide-spectrum of orofacial manifestations.3-5 However, the exclusive oral localization not associated

Mucous patch

Argyll-Robertson pupil Congenital syphilis

Moon’s/Mulberry molars Hutchinson’s incisors Facial deformity - High-arched or gothic palate, maxillary hypoplasia ‘Bulldog’ jaw, saddleshaped deformity of nose, frontal bossing Mucous patches Rhagades, cranial neuropathies

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VENEREOLOGY of syphilis infection is based on confirmation of the clinical signs and symptoms with laboratory test.9 T. pallidum can be identified in lesions by dark field microscopy or direct immunofluorescence, but usually serological confirmation is necessary. The diagnostic STS include those detecting antibodies to nonspecific treponemal antigens - the Rapid Plasma Reagin (RPR) and Venereal Disease Research Laboratory (VDRL) and those detecting antibodies specific to T. pallidum - the TPHA and fluorescent treponema antibodies absorbed assay (FTA-Abs). The nonspecific antibody tests are inexpensive, rapid screening tools and markers of disease activity. The specific tests are more sensitive than the nonspecific assay. FTA-Abs detects antibodies to T. pallidum in the early stages of infection.12,13 In the secondary stage, microorganisms may be detected by special silver impregnation techniques and direct fluorescent antibody testing.

Meyer and Shklar reported the features of 1° and 2° syphilis to be essentially nonspecific and the 3° lesion to be the most obviously granulomatous and populated with Langhans-type giant cells.14 The histopathologic features in the primary lesions consist of an ulcerated epithelium. The underlying connective tissue may show moderate vascularity with intense chronic inflammatory cell infiltration, predominantly lymphocytes and plasma cells with perivascular pattern. In secondary syphilis, the features include hyperplastic epithelium and the connective tissue shows perivascular infiltration with chronic inflammatory cells. In tertiary lesions, ulcerated epithelium with inflammation of connective tissue and foci of granulomatous inflammation with histiocytes and giant cells are noticed.14-16 This is in general agreement with the findings reported

by Barrett et al17 who reviewed the histopathology of five oral lesions in patients with serologically proven syphilis, whereas contradictory to the findings reported

by Jefferies et al.18 Features of c/c granulomatous inflammation without significant necrosis are typical of early nodular lesions of 3° syphilis and the sparse numbers of plasma cells can mask the diagnosis.19 Tertiary lesions are only sparsely populated with spirochetes.20 Easy, consistent and reliable identification of T. pallidum, however remains problematic.

CONCLUSION The importance of this case report is to stress the importance of keeping alive the dentist’s knowledge of syphilis, as its tertiary stages could easily be the cause of embarrassing misdiagnosis, leading to the patient being treated for the wrong disease, sometimes for decades.

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REFERENCES 1. Laskaris G. Oral manifestations of infectious diseases.

Dent Clin North Am. 1996;40(2):395-423.

2. Edwards S, Carne C. Oral sex and transmission of nonviral STIs. Sex Transm Infect. 1998;74(2):95-100.

3. Aloi F. Lip syphilitic chancre in a child. Pediatr Dermatol.

1987;4(1):63.

4. Bhatt AP. Case of the mouth. Primary Chancre of the lower lip. Indian Dent Assoc. 1986;58:1.

5. Hart G. Syphilis tests in diagnostic and therapeutic decision making. Ann Intern Med. 1986;104(3):368-76.

6. Aquilina C, Viraben R, Denis P. Secondary syphilis simulating oral hairy leukoplakia. J Am Acad Dermatol.

2003;49(4):749-51.

7. Carlesimo M, Palese E, Mari E, Feliziani G, La Pietra M, De Marco G, et al. Isolated oral erosions: an unusual manifestation of secondary syphilis. Dermatol Online J. 2008;14(2):23.

8. Anderson J, Mindel A, Tovey SJ, Williams P. Primary and secondary syphilis, 20 years’ experience. 3: Diagnosis, treatment, and follow up. Genitourin Med. 1989;65(4):239-43.

9. Hutchinson CM, Hook EW 3rd. Syphilis in adults. Med Clin North Am. 1990;74(6):1389-416.

10. Hook EW 3rd, Marra CM. Acquired syphilis in adults.

N Engl J Med. 1992;326(16):1060-9.

11. Aarestrup FM, Vieira BJ. Oral manifestation of tertiary syphilis: case report. Braz Dent J. 1999;10(2):117-21.

12. Alam F, Argiriadou AS, Hodgson TA, Kumar N, Porter SR. Primary syphilis remains a cause of oral ulceration.

Br Dent J. 2000;189(7):352-4.

13. Young H. Syphilis.

1998;16(4):691-8.

Serology.

Dermatol

Clin.

14. Meyer I, Shklar G. The oral manifestations of acquired syphilis. A study of eighty-one cases. Oral Surg Oral Med Oral Pathol. 1967;23(1):45-57.

15. Little JW. Syphilis: an update. Oral Surg Oral Med Oral Pathol Oral Radiol Endod. 2005;100(1):3-9.

16. Montone KT. Infectious diseases of the head and neck: a review. Am J Clin Pathol. 2007;128(1):35-67.

17. Barrett AW, Villarroel Dorrego M, Hodgson TA, Porter SR, Hopper C, Argiriadou AS, et al. The histopathology of syphilis of the oral mucosa. J Oral Pathol Med. 2004;33(5):286-91.

18. Jefferies SD, Ord RA. An unusual presentation of oral syphilis. Br J Oral Maxillofac Surg. 1985;23(5):376-80.

19. Mckee P. Infectious diseases in skin pathology. Edinburgh: Churchill Livingstone; 1997. pp. 549-54.

20. Siegel MA. Syphilis and gonorrhea. Dent Clin North Am. 1996;40(2):369-83.

MEDILAW

Not Practising Accepted Protocols While Examining a Patient A man approached the Medical Council and filed a complaint against the treating doctor stating that his wife died because the treating doctor did not properly examine her well at the first visit and simply prescribed treatment for upper respiratory infection. As a result, his wife developed serious complication during the course of treatment. She eventually succumbed to her illness despite treatment.

This doctor did not properly examine my patient and simply dictated the treatment.

We issue a warning to you with a direction to adopt accepted protocols while examining patients in future.

Proceed

Lesson: In an order DMC/DC/F14/246/2007, the Council highlighted the importance of right protocols being followed while examining a patient.

CASE SUMMARY

ÂÂ

A complaint was submitted to the Delhi Medical Council by Mr X (Complainant) against Respondents 1 to 4 alleging medical negligence and professional misconduct. The council examined the complaint, written statements of Respondents 1, 2 and 4, medical records of Hospital Y and other documents on record.

Respondent No. 3 did not participate in proceedings in spite of notice.

25.8.2003: The patient was still unrelieved and her condition worsened. Dr B examined her and advised immediate hospitalization in Hospital Y. A diagnosis of Pneumonia L with viral fever was made; necessary treatment started.

ÂÂ

28.8.2003: Despite treatment, the patient could not recover and died. An autopsy was not done, because the patient clinically had fulminant type of pneumonia, which is associated with high mortality rates even with treatment.

Course of Events

Complainant Allegation

ÂÂ

21.8.2003: Respondent No. 1 first saw the patient in his clinic. The diagnosis was upper respiratory tract infection (URTI); treatment started accordingly.

ÂÂ

24.8.2003: Respondent No. 1 was called for a home visit as the patient continued to have symptoms.

Further necessary treatment was started after examination.

The main complaint was that Respondent No. 1 missed the diagnosis on the two occasions he saw the patient because he did not examine the patient properly.

Council Observations According to Respondent No. 1, he had examined the patient and had also done a chest examination.

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MEDILAW However, the court observed that as the patient had already died it was not possible to verify this statement.

Moreover, fulminant type of pneumonia was not easy to diagnose in its early stages and it also takes a rapidly progressive course. The treatment prescribed

by Respondent No. 1 encompassed the entire spectrum of the existing clinical situation. Respondent No. 1 did not have access to the daily progress of the patient.

Dr B was contacted only when the patient developed difficulty in breathing, subsequent to which the patient was hospitalized in Hospital Y.

The hospital authorities also failed to provide the patient records to the complainant despite repeated requests.

Council Opinion ÂÂ The treatment administered to the patient at Hospital Y was in line with the accepted professional practise for such clinical situations. And, the patient died due to the disease, which takes a natural fulminant clinical course. The patient unfortunately developed the complication of fulminant type of pneumonia from a simple viral URTI. ÂÂ The approach taken in the initial treatment provided to the patient is disturbing because a doctor is expected to examine a patient properly or to at least follow the scientific assessment protocol, which may enable him to arrive at a probable diagnosis.

ÂÂ

Respondent No. 1 stated in a written statement that the presenting complaints on the first visit on 21.8.2003 were fever, blocked nose, slight cough and loss of appetite. On examination, vital signs were normal; there was mild congestion in the throat, patient was febrile and the chest was clear on examination.

When he saw the patient the second time on 24.8.2003, the vitals were stable, throat was congested; there were few crepts on auscultation; so, he diagnosed the patient as having lower respiratory tract infection (LRTI) with URTI for which he prescribed ofloxacin, cough expectorant, analgesics and gargles.

Though the prescription notes of Respondent No. 1 contain the treatment prescribed, they do not mention the diagnosis, which he stated in his written statement.

Council Judgement The Council issued a warning to Respondent No. 1 with a direction to adopt accepted protocol whilst examining patients in future. The complaint was disposed as no medical negligence could be attributed in the treatment of the patient.

Reference 1. DMC/DC/14/2/Comp.246/2007/dated 29th May, 2007.

FIVE PRINCIPLES TO IMPROVE DOCTOR-PATIENT RELATIONSHIP: AIDET Most doctor-patient disputes today are because of a communication gap or miscommunication. To ensure a better doctor-patient relationship, there are etiquettes that doctors should observe, whenever a patient comes for a consultation.

Remember the acronym AIDET; it represents the principles that doctors should follow to communicate better with their patients and build a doctor-patient relationship based on mutual trust and respect. These principles are: 1. Acknowledge: Whenever a patient comes to you, greet the patient and call them by his/her name.

2. Introduce: Introduce yourself or any other member of your staff to the patient and explain what you would be doing for the patient.

3. Duration: Keep your patient informed about the expected duration of treatment; how long would treatment continue or, any waiting time.

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4. Explanation: Always describe to your patients the diagnosis, the tests or procedures in a language they are able to understand. This is the concept of informed consent.

5. Thank you: Say thank you to the patient for their communication and cooperation. Doing this will develop trust and respect in the patient for you as his/ her physician.

Adapted from: www.studergroup.com/hardwired-results/ hardwired-results-03/hardwire-the-five-fundamentals-of-service

The Three Components of Medical Negligence Negligence is the breach of a duty caused by the omission to do something which a reasonable man, guided by those considerations which ordinarily regulate the conduct of human affairs would do, or doing something which a prudent and reasonable man would not do.1

MEDILAW The essential components of negligence, as recognised, are three: “duty”, “breach” and “resulting damage”, that is to say:2 1. The existence of a duty to take care, which is owed by the defendant to the complainant; 2. The failure to attain that standard of care, prescribed by the law, thereby committing a breach of such duty; and 3. Damage, which is both causally connected with such breach and recognised by the law, has been suffered by the complainant (Para 1.23). If the claimant satisfies the court on the evidence that these three ingredients

are made out, the defendant should be held liable in negligence (Para 1.24).

The standard of care has to be judged in the light of knowledge or equipment available at the time (of the incident) and not at the date of the trial.

References 2. Yadav M, Singh H, Sharma G, et al. Recent scenario of criminal negligence in India doctor, community & apex court. JIAFM 2005;27(4):252-7.

3. 334/2005/SCI/144-145 of 2004: Jacob Mathew vs State of Punjab and Anr: 5th day of August 2005: R C Lahoti, CJI: Hon’ble Mr. Justice G P Mathur, Hon’ble Mr. Justice P K Balasubramanyan.

WHAT IS NOT MEDICAL NEGLIGENCE?

evidence of negligence. To establish liability on that basis, it must be shown:

A “Medical Accident” is not Negligence

1. That there is a usual and normal practise

In Jacob Mathew v. State of Punjab SC/0457/2005: (2005) 6 SCC 1, the Supreme Court of India has observed: “… a mere accident is not evidence of negligence.”

2. That the defendant has not adopted it and

“Not Getting Cured” is not Negligence

3. That the course in fact adopted is one no professional man of ordinary skill would have taken had he been acting with ordinary care.”

In its judgement in Jacob Mathew v. State of Punjab SC/0457/2005: (2005) 6 SCC 1, the Supreme Court of India has observed: “Simply because a patient has not favourably responded to a treatment given by a physician or a surgery has failed, the doctor cannot be held liable per se by applying the doctrine of res ipsa loquitur.”

Errors can be Made in an Emergency Even by Experts and may not Amount to Negligence

“Error of Judgement” is not Negligence

Difference of Opinion is not Negligence

In Jacob Mathew v. State of Punjab SC/0457/2005: (2005) 6 SCC 1, the Supreme Court of India has observed: “… an error of judgement on the part of a professional is not negligence per se.”

Deviation from Medical Practise does not Always Mean Medical Negligence The Supreme Court of India has observed in Jacob Mathew v. State of Punjab SC/0457/2005: (2005) 6 SCC 1: “Deviation from normal practise is not necessarily

In SCI: 3541 of 2002, dated 17.02.2009, Martin F. D’Souza vs Mohd. Ishfaq, the Supreme Court of India has observed: “The higher the acuteness in an emergency and the higher the complication, the more are the chances of error of judgement.”

The Supreme Court of India has observed in Jacob Mathew v. State of Punjab SC/0457/2005: (2005) 6 SCC 1: “In the realm of diagnosis and treatment there is ample scope for genuine difference of opinion and one man clearly is not negligent merely because his conclusion differs from that of other professional men. The true test for establishing negligence in diagnosis or treatment on the part of a doctor is whether he has been proved to be guilty of such failure as no doctor of ordinary skill would be guilty of if acting with ordinary care.”

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CONFERENCE PROCEEDINGS

60th Annual Conference of the Indian Orthopaedic Association (IOACON 2015) SCAPHOID FRACTURE: TIPS & TRICKS Dr PP Kotwal, New Delhi ÂÂ

Most surgical techniques involve the insertion of headless screws/K wires.

ÂÂ

Open techniques: Nonunions and fractures with unacceptable and irreducible displacement.

ÂÂ

Percutaneous techniques: Acute fractures with no/ minimal displacement.

ÂÂ

Approach - Volar and dorsal Depends upon fracture location Proximal pole: Dorsal (Antegrade) Distal pole: Volar (Retrograde) Waist fracture: Either approach.

ÂÂ

Associated injuries

ÂÂ

Key Points ÂÂ Prognosis depends upon associated injuries. ÂÂ 2D/3D CT an important tool. ÂÂ Patient positioning and surgical approach decided by combination of injuries. ÂÂ Radiographic parameters are very helpful in patient selection.

TECHNICAL TIPS OF PROXIMAL HUMERUS LOCKING PLATE Dr M Shantharam Shetty, Mangalore ÂÂ

Proximal humeral locking plate has improved outcomes as compared to traditional methods of treatment. However, it is not a magic wand.

ÂÂ

Medial support and bone quality are the two important factors that predict the outcome.

ÂÂ

Filling screws in empty space does not provide support.

ÂÂ

Cement augmentation in osteoporotic bone.

ÂÂ

Cannot predict AVN.

Associated instability: Dorsal intercalated

segment instability, secondary osteoarthritis

High incidence of scapholunate ligament injury.

INTRA-ARTICULAR GLENOID FRACTURE: TIPS & TRICKS Dr Rajesh Malhotra, New Delhi ÂÂ

Scapula fracture is high energy by definition.

ÂÂ

1st Rule: Search for other injuries; associated injuries are seen in 80-90%. Fracture of rib, ipsilateral clavicle, spine, brachial plexus injury, etc.

ÂÂ

Examination of patient involves ATLS protocol, complete neurologic examination of the ipsilateral upper extremity, symmetricity of pulses, abrasions.

ÂÂ

2nd Rule: Excellent and detailed imaging is a prerequisite

TECHNICAL TIPS OF PERCUTANEOUS FIXATION: PROXIMAL HUMERUS FRACTURE Dr Parvinder Singh Sandhu, Amritsar ÂÂ

Proximal humerus fractures are the third most common fracture group after hip and distal radial fractures among osteoporotic patients with advanced age.

ÂÂ

Most proximal humeral fractures are minimally displaced and so can be satisfactorily treated by conservative methods. Some displaced and comminuted fractures may require internal fixation either by closed or open methods.

ÂÂ

Percutaneous fixation methods: Interfragmentary screw fixation, multiple percutaneous threaded pins or K-wire fixation, rush nail and screw fixation.

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During placement, care should be taken about the orientation of pins and screws to avoid injury to

Standard chest X-ray (to r/o pneumothorax,

other chest injuries), lateral cervical spine X-ray, AP shoulder, axillary and scapular Y views

2D/3D CT: Must if planning for surgery. ÂÂ

Scapular neck fracture: Operate if scapular neck angulated >40° or displaced ≥1-2 cm or a displaced double disruption of the superior shoulder suspensory complex.

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Surgical dangers: Suprascapular nerve, ascending branch of circumflex scapular artery.

CONFERENCE PROCEEDINGS the axillary nerve, the radial nerve and the anterior circumflex humeral vessels lying medially. ÂÂ

Advantages Minimally invasive procedure, minimal tissue

dissection, preserves vascularity to the humeral head.

Implants are cheap, cost-effective and readily

available.

Decreased perioperative blood loss vs. other

more extensive surgical procedures.

FRACTURE DISLOCATION ELBOW: TIPS & TRICKS Dr Ravi Mittal ÂÂ

Important to identify mechanism and fracture patterns.

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Convert fracture dislocation to simple dislocations ORIF.

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Do not excise radial head - ORIF/replace.

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LCL repair usually required.

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Coronoid fracture: Type 2 - Always fix

Technical expertise easy to learn; can be done

Type 1 - Fix the big fragment, small fragments

in peripheral centers and by surgeons with less expertise.

option open

Type 3 - Always fix.

→ Length of hospitalization → early mobilization

and post-op recovery.

The surgical scar formed is small. ÂÂ

Disadvantages

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ISOLATED DEPRESSED TIBIAL CONDYLE FRACTURES: TIPS & TRICKS

Reduction is improper/difficult in 4 part

fractures.

Subacromial impingement sometimes due to

implant → limited range of abduction during early follow-up; after implant is removed, range of movement improves.

FIXATION OF MALLEOLAR FRACTURES-ANKLE Dr Navin Thakkar, Ahmedabad ÂÂ

Fixation sequence for restoration of fibular length: Medial exploration/fixation, post malleolar fixation, assessment of mortise stability, syndesmotic fixation. But this is not hard & fast! Achieving fibular length and syndesmotic stability are the most important!!

ÂÂ

If fibula is comminuted, then medial side may be reduced first.

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Ankle fracture injury is bad soft tissue injury with a fracture.

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Soft tissue gives you more trouble. Timing is important. Poor timing → poor outcome

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Ask the radiologist for soft tissue window in CT scan; understand soft tissue interposition.

MCL repair rarely required.

Dr Vasudevan PN, Palakkad ÂÂ

Local compression fracture (Type III): central or peripheral depression.

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Flexion angle of the knee at the time of injury determines depth of depression: In extension it is limited to 6 mm, in flexion up to 30 mm.

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Central depressions are usually stable due to intact peripheral ligament.

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CT a ‘must’ to find out the depth and location of depressed fragment. Get a 3D in your mind. Look for any peripheral splits that may be used as a window for elevation.

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Aims of treatment: To get a painless, stable & mobile joint. The key is good articular reconstruction & axial alignment.

ÂÂ

There is no universal agreement on what is acceptable depression. Up to 5 mm may be Ok. A depressed fragment cannot be elevated by traction. It requires surgery.

ÂÂ

Avoid axial malalignment to prevent secondary OA. Ring fixator is the best for this.

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Problems: Redepression, valgus instability, AVN of fragments, delay weight-bearing till healing in buttress plating and not in Ilizarov; can span the knee SOS.

zz

Pitfall: We see only fracture on static X-rays and miss instability.

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zz

Pearl: Think - Dynamic stability - Unseen plane -Third plane.

Indications of surgery: valgus instability, >8 mm depression.

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zz

Tip: Always check for instability.

A compromised soft tissue is a contraindication for early ORIF. It’s not a contraindication for Closed Reduction and Ring Fixation.

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CONFERENCE PROCEEDINGS ÂÂ

Do not hesitate to open if not happy with closed reduction.

ÂÂ

If it can be well fixed by a single plate go for ORIF.

ÂÂ

3 Tips to achieve success: Proper height, proper retroversion and proper position of tuberosities.

ÂÂ

A superolateral approach facilitates mobilization and location of greater tuberosity but requires axillary nerve isolation if there is distal extension of the fracture.

ÂÂ

Surgical tips: Locate tuberosities, humeral head, bicipital groove and long head of biceps.

ÂÂ

If tuberosities together: Don’t separate them.

ÂÂ

Mobilizing tuberosities in old cases may take some time.

ÂÂ

Pass suture in tuberosities through cuff tissue rather than bone.

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Check soft tissue tension: One should be able to move the prosthesis by 50% distance along the glenoid surface.

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Implanting of prosthesis: While cement setting, keep on moving sutures, so that they do not fix with cement.

“I prefer Ring fixation to double plating and make them walk earlier by Closed/Open reduction & Ring Fixation. Span knee SOS.” PINNING OF NECK RADIUS FRACTURES IN CHILDREN: TIPS & TRICKS Dr PN Gupta, Chandigarh ÂÂ

ÂÂ

IM pinning using Metaizeau’s technique is gold standard for radial neck fractures. Achieve reduction of greatly displaced/angulated fractures before IM pinning. Use the bend of the elastic nail to fine tune the reduction.

Joy stick, leverage techniques of reduction are useful modifications to the technique.

Joystick technique: Reduce the fracture with

joy-sticking the head fragment

Leverage technique: Lever radial head on top

of shaft.

ÂÂ

Pitfalls of elastic nail: Minimum diameter of titanium elastic nail (TEN) is 2 mm, use a thinner K-wire if diameter less.

ÂÂ

Closed reduction and percutaneous pinning: Results inferior to CR and IM pinning, higher complications (J Orthop Traumatol. 2013;14(4):291-7).

ÂÂ

Intramedullary and percutaneous pinning can be combined in unstable situations.

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Tips of IM Pinning with K wire: Modified closed intramedullary pin reduction for radial neck fractures allows stable anatomic reconstruction and avoids complications of classical Metaizeau technique (Eur J Orthop Surg Traumatol.

2015;25(1):99-103).

SHOULDER ARTHROPLASTY: TIPS & TRICKS

ÂÂ

Dr Alok Aggarwal ÂÂ

Olecranon fractures are common fractures.

ÂÂ

Some people call it the beginner’s fractures as it is considered simple.

ÂÂ

TBW principles is not viable in olecranon fractures.

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One should have the whole range of implant and instruments to mold the olecranon LCP to bone.

BENNETT FRACTURE - PERCUTANEOUS AND OPEN: TIPS & TRICKS Dr Binu Thomas

Pearls on K-wire Fixation

Dr Ravi Gupta, Chandigarh ÂÂ

OLECRANON TBW AND PLATING: TIPS & TRICKS

Contraindications include: Active or recent shoulder joint infection, paralysis with complete loss of rotator cuff and deltoid function, neuropathic arthropathy, irreparable rotator cuff tear.

Timing of surgery: Elective and not emergency; mobilization and fixation of tuberosity is difficult after 20 days due to bone consolidation and resorption.

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Blind K-wire introduction is not advisable as painful neuromas may result.

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Fluoroscopy is inadequate to assess reduction.

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X-rays may be necessary after fixation.

ÂÂ

If closed reduction is not adequate, proceed to open reduction

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Open fractures best treated by K-wire fixation after thorough debridement.

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CONFERENCE PROCEEDINGS

62nd Annual Conference of Cardiological Society of India (CSI 2016) ADVANCED IMAGING IN THE CATH LAB: NEW IDEAS AND CONCEPTS Dr Y Chandrashekhar, USA ÂÂ

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Advanced imaging is showing a lot of promise and thus generates a lot of interest for improved outcomes in practice.

We can now see things that were unthinkable just a few years ago. Some technologies like OCT are reaching resolution nearer to that seen with microscopy.

Methods like NIR allow us to detect lipid laden plaques and these seem to cause ACS and suboptimal stenting.

Imaging is thus likely to help us choose which patients need intervention better than conventional methods. In addition, we can better predict outcome of invasive therapies.

The future seems to be trending towards high speed acquisition and fusion imaging (OCT + NIR, IVUS + OCT, etc.), which combine the best of both methods and reduce limitations of each.

Ultimately, all these methods need to show that using them improved outcomes otherwise they may just remain interesting modalities with limited use in daily practice.

BENEFITS OF YOGA IN HEART DISEASE: DO WE HAVE EVIDENCE?

ÂÂ

However, there are limitations of the studies, larger studies are needed.

ÂÂ

But, yoga being a cost-effective and a safe technique, should be recommended for prevention of heart disease.

STATUS OF NONSTATIN ANTILIPIDEMIC THERAPY Dr Ramesh Babu, Hyderabad ÂÂ

Lower the LDL, the better, irrespective of how it is achieved.

ÂÂ

PCSK9 usage may increase in the coming years.

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Knocking down the gene that makes PCSK9 may be the ultimate answer. Need to wait for another 5 years to know the answer.

ÂÂ

RNA interference is the next genetics revolution in science; may become a reality sooner than later.

AMBULATORY BP MONITORING: PAST, PRESENT AND FUTURE Dr A George Koshy, Trivandrum ÂÂ

LVH, microalbuminuria and other evidence of TOD better correlate with ambulatory BP than office BP.

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ABP is a more sensitive predictor of cardiovascular events.

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Nocturnal BP, dipping status and morning surge are particularly important in risk prediction.

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ABPM has a definite role whenever there is discordance between office BP values and target organ involvement.

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Normal ABPM values: Mean BP during 24 hours <130/80 mmHg, mean daytime BP <135/85 mmHg, mean night-time BP <120/70 mmHg.

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Diurnal index is the difference in systolic BP between awake and sleep period expressed as a percentage. Normal dipping is 10-20%. A 0-10% fall is considered as nondippers. In those with reverse dipping, nocturnal BP is higher than daytime BP. Diurnal index >20% is considered extreme dipping.

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In “white coat HT”, office BP is high but ABP is normal and there should be no TOD.

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“Masked HT” is reverse of “white-coat HT”. Office BP is normal but ABP is higher and often associated with TOD.

Prof Dr SC Manchanda, New Delhi ÂÂ

Cardiovascular diseases are rapidly increasing, especially in the developing countries mainly because of unhealthy lifestyles like mental stress, unhealthy diet, lack of exercise and smoking.

ÂÂ

Yoga is a holistic lifestyle, which has the potential to control these risk factors.

ÂÂ

Several scientific randomized trials have shown that yoga can control HT, DM, dyslipidemia, obesity, mental stress and smoking. Recently American Heart Association (AHA) has also accepted that meditation can be used for controlling high BP.

ÂÂ

Yoga has also been shown to reverse blockages in coronary arteries, control arrhythmias and HF.

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CONFERENCE PROCEEDINGS ÂÂ

ABPM is useful in the evaluation of “resistant HT”. One-third cases may prove to be pseudoresistant HT.

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Increasing emphasis is given for ABPM in the new ESH/ESC and NICE guidelines.

TECHNIQUES AND COMPLICATIONS OF BMV

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Each time the patient presents with any feature of rheumatic fever, rheumatic activity, rheumatic carditis, sore throat he/she must be given a repeat course of tablet azithromycin 500 mg 1 o.d. for 5 days for prophylaxis followed by tablet azithromycin 500 mg 1 tab once a week for 1 year only.

ÂÂ

Azithromycin is the most safe, effective, easily available efficacious drug for treatment of Group A β-hemolytic streptococcus and hence the best drug for RF/RHD.

ÂÂ

We have been using azithromycin regime for RF/RHD in the PG Institute of Medicine GSVM Medical College, Kanpur IPD and OPD and all patient sources in and around Kanpur for past 10 years or more.

Dr BC Srinivas, Bengaluru ÂÂ

BMV is safe and effective procedure in patients with mitral stenosis.

ÂÂ

Echo facilitates BMV procedure in technically challenging situations.

ÂÂ

Transseptal puncture is challenging in technically difficult cases. Pulmonary angio with Levophase opacification of LA facilitates better understanding of the septal profile and septal puncture.

POST-MI PATIENTS WHO CANNOT AFFORD AN ICD

Knowing different methods of crossing the mitral valve is essential in technically challenging cases.

Over the wire technique is useful in patients with challenging anatomy and LA clot.

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BMV in complex anatomy should be undertaken by experienced operators.

Documented VT/VF (Scar-related): Amiodarone + β-blockers, catheter ablation + β-blockers (Success 50%).

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Primary prevention: Revascularize, β-blockers.

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Complications do occur in early learning curve period and while treating technically challenging cases of mitral stenosis.

ÂÂ

In All: Optimize other medical therapies - ACEI/ ARBs, MRA, statins, antiplatelets.

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Cardiac tamponade and acute severe MR during BMV are the dreaded complications, which can be life-threatening.

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Awareness and swift management are key in cardiac tamponade. Pericardiocentesis with autoperfusion bails out majority of cases. Minority of cases need surgical intervention.

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Acute severe MR should be operated early preferably within 24 hours as perioperative mortality is the least during that period.

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Device-related complications are seen with reuse of the equipments.

RHEUMATIC FEVER/RHEUMATIC HEART DISEASE

Dr KK Sethi, New Delhi

CARDIOMYOPATHY: A SPECTRUM ON MRI Dr Mona Bhatia, New Delhi ÂÂ

The role of cardiac MRI in cardiomyopathy is to confirm the diagnosis, establish the etiology, assess the severity, guide management, prognosticate and follow-up patients.

ÂÂ

Cardiac MRI (CMR) with its high spatial and temporal resolution is excellent for ventricular morphology and functional assessment and is currently the gold standard for both right and left ventricular volumetric analysis and myocardial mass quantification.

ÂÂ

The hallmark of CMR is myocardial tissue characterization and Gadolinium-enhanced images assist in characterization of myocardial pathology and help differentiate ischemic from nonischemic cardiomyopathy. It has a growing role in myocarditis and other infective and inflammatory cardiomyopathies.

ÂÂ

In ischemic myocardial involvement, CMR has amongst the highest sensitivity and specificity to answer the 3 critical questions of cardiac function, perfusion and viability for risk stratification, management and prognostication of these patients.

Dr Prof Arati Lalchandani, Kanpur ÂÂ

Azithromycin for treatment and prophylaxis of rheumatic fever.

ÂÂ

Benzathine penicillin must not be used in RF/RHD.

ÂÂ

Azithromycin is the best drug for RF/RHD.

ÂÂ

Regime: Tablet azithromycin 500 mg 1 o.d. for 5 days. For prophylaxis followed by tablet azithromycin 500 mg 1 tablet once a week for 1 year only.

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CONFERENCE PROCEEDINGS ÂÂ

ÂÂ

ÂÂ

In hypertrophic cardiomyopathy, CMR enables accurate LV mass assessment, and detailed characterization of HCM phenotype including atypical forms. Myocardial fibrosis detected on CMR has a clinical significance and may reclassify the risk prediction and management of patients.

The superior myocardial tissue characterization of CMR makes it extremely sensitive in the detection of amyloidosis, noncompaction, arrythmogenic RV cardiomyopathy and other cardiomyopathies.

Pre-ablation CMR assessment is extremely useful in localization and characterization of myocardial scars, prediction of successful ablation sites and reduction of procedure and fluoroscopy times.

NSR or in AF Frequent ventricular ectopic beats Assess LV capture Fusion and pseudofusion beats ÂÂ

Step 3. Check the device (Device interrogation)

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Step 4. Check the lead position

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Step 5. Check the mechanical resynchronization effect by Echo

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Step 6. Check the medication and comorbidities.

RESISTANT HT: CAUSES, CONSEQUENCES AND CARE Dr Ajay K Sinha, Patna

STEP BY STEP GUIDE TO PROGRAMMING A CRT

ÂÂ

Rule out measurement error and white-coat effect; consider associated comorbidities; reconsider secondary causes; address volume overload and interfering substances; intensify therapy; consult HT specialist.

ÂÂ

Ask about adherence to the treatment plan.

ÂÂ

Ensure that adherence to medications is as simple as possible (e.g., once-daily dosing regimens, generics, fixed-dose combination pills).

ÂÂ

Repeat office measurement of BP making sure that the cuff size is correct (too small a cuff will overestimate BP) and proper technique is followed; consider out-of office monitoring

ÂÂ

Address CKD, if present; emphasize weight loss, if patient is overweight; assess adherence to therapy in older patients; test for primary aldosteronism; consider testing for OSA. Consider rarer causes such as Cushing’s syndrome, coarctation of aorta, pheochromocytoma and hyperparathyroidism.

ÂÂ

Emphasize reducing dietary sodium; consider consulting nutrition specialist; discontinue or reduce medications, supplements and other agents (e.g., alcohol) that interfere with BP control; consider options for intensifying pharmacologic therapy.

ÂÂ

Newer intervention such as renal denervation may be considered in future.

Dr Viveka Kumar, New Delhi ÂÂ

ÂÂ

CRT is an effective therapy in selected patients with advanced drug-refractory HF. Nevertheless, about 20-30% of patients in randomized trials do not respond clinically.

This may be due to a variety of reasons, such as patient selection (? utility of echo), absence of dyssynchronous basal LV contraction, inappropriate lead positioning and pacing site selection, suboptimal device programming.

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Optimal follow-up of patients with CRT is important to ensure that patients will derive maximum benefit from this treatment.

ÂÂ

In addition to ensuring adequate therapy delivery by evaluating standard parameters such as pacing thresholds and percentage of ventricular stimulation, AV and VV delays may be optimized.

ÂÂ

Clinical benefit of AV and VV interval optimization still has to be demonstrated in prospective randomized studies.

A Multidisciplinary Approach ÂÂ

Step 1. CRT patients clinical examination

ÂÂ

Step 2. Check the ECG with and without pacing The more the QRS width is reduced by CRT,

the more beneficial CRT therapy is

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CONFERENCE PROCEEDINGS

India Live 2016 OCT: CORE CONCEPTS

ÂÂ

Moreover, there is no issue in HEAT with bivalirudin dosing or observed ACT values. The study used the correct dose regimes, producing the expected antithrombotic effect.

ÂÂ

It is time for the “ACT disinformation issue” to be buried once and for all.

ÂÂ

The antiplatelet therapy is not central to the avoidance of very early stent thrombosis. The key is an adequate antithrombotic effect that is sustained for some hours after the index procedure.

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Overall, heparin at a dose of 60-70 U/kg “will be hard to beat,” it was concluded. Use of bivalirudin infusions pre- and post-PPCI will increase drug and nursing cost. There are signals that the use of infusions may abolish the stent thrombosis hazard, but the overall safety and efficacy of the approach remain in doubt.

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It is difficult to directly compare drugs in a registry study because of the possibility of hidden confounders. Bivalirudin, for example, has been used especially for frail patients with high bleeding risk. Of note, bleeding complications could not be evaluated using the SCAAR data.

Dr G Sengottuvelu, Chennai OCT started as a research tool, but now is graduating to become an important clinical tool particularly to view the endoluminal structure of the blood vessels.

The basic principles of OCT consists of a single mode optic fiber that transmits and receives infrared light waves at a bandwidth of 1250-1350 nm, which is the ideal spectral range for imaging biological tissue. The received signals depending on the tissue characters (that determines the back scatter and attenuation) is reconstructed and displayed in cross-section. The back scattered optical echoes are processed based on the frequency change (frequency domain) or time change (time domain). As the speed of light is extremely high a reference mirror is used in the time domain OCT to calculate the relative rather than the absolute change.

Processing of frequency domain OCT signals has better spatial and temporal resolution. The present generation OCT machines use only FD-OCT. Optical resolution is the measure of the smallest physical feature that can be detected using an imaging system and it is dependent on the wave length and bandwidth of light. The high speed of light waves produces an axial resolution of 10-20 µm that is 10 times higher than IVUS. As blood is opaque to light it has to be replaced with a transparent medium like the contrast-medium or removed by proximal balloon occlusion during image acquisition.

SCAAR: STENT THROMBOSIS RISK AFTER PRIMARY PCI NO HIGHER WITH BIVALIRUDIN THAN OTHER ANTITHROMBOTICS Dr Bhanu Duggal, Mumbai ÂÂ

In a large, real-world population of STEMI patients, early stent thrombosis is equally rare regardless of whether bivalirudin, heparin, or a glycoprotein IIb/ IIIa inhibitor is used during primary PCI.

ÂÂ

The reason why acute stent thrombosis was “so high” with bivalirudin in the trial was because patients were treated with bivalirudin in accordance with the labeled dosing at the time.

ÂÂ

They did not receive any additional heparin or continued infusion of bivalirudin.

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TAP TECHNIQUE: BEST STRATEGY FOR PROVISIONAL STENTING FOR BIFURCATION LESIONS Dr Harminder Singh, Mumbai Strategies for stenting in bifurcation lesions are broadly divided into two-stent techniques and provisional stenting techniques where the main branch is stented but the side branch is stented only if necessary. TAP Technique (T-stent with protrusion),1 also called Carina Modification Technique is a technique where the side branch stent is deployed in such a way that the stent in side branch protrudes inside the main branch stent (one example is shown in the pictures). It has following advantages: ÂÂ

Operator is committed to only one stent strategy at the onset of the procedure. If result after main branch stent and kissing balloon is considered good, the procedure can be stopped without SB stent.

Second stent in side branch is only needed in case of

CONFERENCE PROCEEDINGS Whether non-IRA lesions should be treated directly during the index admission, by a staged procedure 4 to 6 weeks later, or with optimal medical therapy (as suggested by the COURAGE trial) remains controversial.

Complete revascularization at index admission in India will be of economic value. Type of lesion in IRA should always be considered for complete revascularization.

Complex non-IRA lesion should be treated by a staged procedure 4 to 6 weeks later. dissection in SB, TIMI-2 flow or less and/or angina/ ECG changes due to SB compromise. ÂÂ

It ensures coverage of the side branch ostium.

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Nearly 100% success in re-crossing/stent delivery to the side branch.

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No need for any dedicated bifurcation stents thus simplifying the procedure and reducing cost.

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Avoids large area of 2 or 3 layers of stent struts as in crush technique.

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It has become the preferred technique in most cath labs.

Reference 1. Burzotta F, et al. Catheter Cardiovasc Interv. 2007;70(1): 75-82.

DO WE HAVE ENOUGH DATA TO RECOMMEND TREATMENT OF NON-IRA? Dr Deepak Gupta, Ranchi In India, about 50 to 70% of patients presenting with STsegment elevation myocardial infarction (STEMI) have multivessel coronary artery disease (CAD). Obstructive CAD in a non-infarct artery is associated with increased mortality in a meta-analysis of patients with STEMI, but the optimal therapeutic strategy remains unclear. There is uncertainty about how to manage non-IRA disease in STEMI patients because no large trial has definitively addressed the question. Smaller studies comparing aggressive vs more conservative approaches to non-IRA disease have yielded mixed results, although the recent PRAMI and CvLPRIT trials have provided support for more complete revascularization. Even PRAMI and CvLPRIT probably do not provide enough evidence to recommend intervening on non-IRA lesions, but they might be enough to at least remove the Class III recommendation against complete revascularization in primary PCI.

TRANSCATHETER CLOSURE OF LARGE PDA USING CUSTOM MADE DEVICES Dr Rohit Manoj, Chandigarh There has been a paradigm shift in the transcatheter closure of PDA over the last 45 years. With the availability of various coils, plugs and occluders, PDA of almost all shapes and sizes are amenable to transcatheter closure. However, very large PDA diagnosed late in life are being referred for surgical closure in the absence of availability of large size devices, especially in developing countries. Patients with large PDA diagnosed late in life are commonly seen in developing countries. Dedicated custom made transcatheter devices can be used successfully for transcatheter closure of these PDA without significant complications, instead of using expensive muscular VSD occluders or subjecting the patients to surgery.

DRUG-COATED BALLOON THERAPY IN CORONARY AND PERIPHERAL ARTERY DISEASE Dr Jayesh Prajapati, Ahmedabad Nonstent-based local drug delivery during PCI offers potential for sustained antirestenotic efficacy without the limitations of permanent vascular implants.

Preclinical studies have shown that effective local tissue concentrations of drugs can be achieved using drug-coated balloon (DCB) catheters. Matrix coatings consisting of a mixture of lipophilic paclitaxel and hydrophilic spacer (excipient) are most effective.

Clinical applications most suited to DCB therapy are those for which stent implantation is not desirable or less effective, such as in-stent restenosis, bifurcation lesions or peripheral artery stenoses.

Randomized trials have shown superiority of DCBs over plain-balloon angioplasty for both bare-metal and drug-eluting coronary in-stent restenosis, and similar efficacy as repeat stenting with a drug-eluting stent (DES). In contrast, randomized trials of DCBs in

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CONFERENCE PROCEEDINGS de novo coronary stenosis have, to date, not shown similar efficacy to standard-of-care DES therapy. In peripheral artery disease, DCB therapy has proven superior to plain-balloon angioplasty for treatment of de novo femoropopliteal and below-the-knee disease, and shown promising results for in-stent restenosis.

NOVEL STENTING TECHNIQUE SHOWS PROMISE FOR “TRUE” BIFURCATION LESIONS Dr Tarun Dave, Ahmedabad For patients with bifurcation lesions, the new dualstent modified “flower petal” technique offers several advantages over available stenting options, including complete coverage of the side branch ostium, according to a small single-center study published in the May 2013 issue of JACC: Cardiovascular Interventions. The novel strategy has also shown good procedural and early clinical outcomes. Thirty patients were selected with “true” bifurcation lesions (Medina type 1.1.1, or >50% stenosis of the proximal and distal main branch as well as the side branch) for implantation with drug-eluting stents using the modified flower petal technique.

Study Details The mean age of patients was 65 years, and just over one-half (66.7%) were male. The most common PCI indication was stable angina (80.8%), and 14 (46.6%) patients had diabetes. All procedures were performed by using ZES (Endeavor, Medtronic, Minneapolis, MN), PES (Coraxel, Alvi Medica, Istanbul, Turkey) and SES (Coracto, Alvi Medica). All patients were pretreated with aspirin 300 mg and clopidogrel 300 mg followed by clopidogrel 75 mg daily.

The modified flower petal technique starts with wiring both branches and predilating all significantly stenosed branches. The plastic stent cover is pulled back slightly to expose the final proximal stent strut and the stent delivery system balloon is inflated and then deflated to expand the final proximal stent strut. The main vessel

wire is then passed through the now expanded, final proximal stent strut. The stent cover is removed and another, compliant balloon is loaded on the main vessel wire and centered on the last proximal stent strut.

The prepared side branch stent-main vessel balloon system is advanced through the guiding catheter to the lesion location until the main vessel balloon stops the advancement of the side branch stent. The first kissing balloon inflation is then performed by simultaneously inflating the side branch and the main vessel balloons.

Both balloons and the side branch wire are withdrawn and another stent is positioned in the main vessel. The main vessel was predilated in 17 patients (56.7%) and the side branch was predilated in 21 patients (70%).

Final kissing balloon inflation could be performed in all patients; procedural success (defined as successful implantation of 2 stents in the main vessel and side branch, yielding a final residual stenosis of 30% or less) was also seen in all patients. There were no in-hospital instances of MACE (cardiac death, acute MI or TLR), but in 4 patients (13.4%) the balloon system could not be advanced to the lesion location because the wires were twisted together.

At 9 months, there were no cases of death, MI or subacute or late stent thrombosis. However, 1 patient reported in-stent restenosis at the side branch ostium requiring reintervention as well as exertional angina.

The new technique holds several advantages over available techniques for bifurcation lesions in that it: Is easier; offers complete coverage of the side branch ostium; lowers metallic burden at carina; has a high success rate of the final kissing balloon inflation; shows excellent immediate and mid-term clinical outcome.

The modified flower petal technique appears to be a feasible and safe novel technique in treating Medina type 1.1.1 bifurcation lesions they write. However, multicenter prospective randomized studies comparing our technique with other techniques would be necessary to confirm the initial very promising results obtained in this single-center study.

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2016

Delays Insulin Therapy

AROUND THE GLOBE

News and Views Understanding Metastasis and How it can be Checked A special issue ‘Fatal Migrations’ of the journal Science published on April 8 contains many review and perspective articles that outline the latest advances in understanding the process of metastasis, and also how it could be stopped. Some of articles included are “A collective route to metastasis: Seeding by tumor clusters”, “Metastasis as an evolutionary process”, “Hypoxic control of metastasis”.

Ondansetron should not be First Choice for Nausea in Pregnancy Use of ondansetron to relieve nausea and vomiting of pregnancy should be reserved for those women whose symptoms have not been adequately controlled by other methods, says a new study published online April 4 in Obstetrics & Gynecology. According to a systematic review by Shaun D. Carstairs, MD, from the Division of Medical Toxicology, Dept. of Emergency Medicine, University of California, San Diego, there is an overall low risk of birth defects associated with ondansetron exposure. There may be a small increase in the incidence of cardiac abnormalities in ondansetron-exposed neonates.

Study Suggests a Link Between Vitamin D Deficiency and AMD According to a new systematic review and meta-analysis published online April 2 in the journal Maturitas, adults with circulating 25-hydroxyvitamin D [25(OH)D] below 50 nmol/L had the highest risk for age-related macular degeneration (AMD). Cedric Annweiler, MD, PhD, from Angers University Hospital in France, and colleagues suggest that high 25(OH)D concentrations may be protective against AMD and correction of vitamin D deficiency may improve the prognosis.

Guidance-based Program Significantly Lowers Cardiometabolic Risk in PAD In an online first publication April 6, 2016 in JAMA Surgery, Mohamad A Hussain, MD, Division of Vascular Surgery, St Michael’s Hospital, Toronto, Ontario, Canada and colleagues say that a guideline-recommended riskreduction program targeted at patients with peripheral artery disease (PAD) was associated with fewer

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cardiovascular and limb outcomes over the long-term.

Patients with symptomatic PAD who were enrolled in the Systematic Assessment of Vascular Risk (SAVR) program at a single tertiary vascular center in Ontario between July 2004 and April 2007 had significantly lower rates of death, acute myocardial infarction or ischemic stroke. They were also less likely to undergo major or minor amputation, bypass surgery or hospitalized for heart failure.

Long-acting Recombinant Coagulation Factor IX Albumin Fusion Protein in Hemophilia B A global phase 3 trial evaluating recombinant fusion protein linking coagulation factor IX with albumin (rIX-FP) in previously treated male patients with severe hemophilia B (factor IX [FIX] activity ≤2 concluded that rIX-FP is safe and effective for preventing and treating bleeding episodes in patients with hemophilia B at dosing regimens of 40 IU/kg weekly and 75 IU/kg every 2 weeks while maintaining FIX trough levels above the target of 1 IU/dL commonly recommended for prophylaxis. The study by Elena Santagostino, Istituto di Ricovero e Cura a Carattere Scientifico Ca’ Granda Foundation, Maggiore Hospital Policlinico, Milan, Italy and colleagues is published April 7, 2016 in the journal Blood.

Utility of Decision Rules for Transcutaneous Bilirubin Measurements Although all of the decision rules can be used effectively to screen newborns for jaundice, each will “miss” some infants with a total serum bilirubin (TSB) level at/ above the phototherapy threshold, according to a study reported online April 6, 2016 in the journal Pediatrics.

The three decision rules tested were: Transcutaneous bilirubin (TcB) levels at least 75th percentile on the Bhutani TSB nomogram, TcB levels above 70% of the TSB phototherapy threshold based on the AAP practice guideline and TcB levels greater than or equal to the AAP phototherapy threshold minus 3.0 mg/dL. TcB, a less invasive measure than TSB, aims to identify newborns with significant hyperbilirubinemia during their birth hospitalization.

Graded Oral Provocation Challenge to Diagnose Amoxicillin Allergy According to a study published online April 4, 2016, JAMA Pediatric, graded oral provocation challenge

AROUND THE GLOBE provides an accurate and safe confirmatory test for skin-related reactions to amoxicillin. Among all participants, 94.1% tolerated the provocation challenge, 2.1% developed mild immediate reactions, while 3.8% developed nonimmediate reactions. The graded provocation challenge had a specificity of 100.0%, a negative predictive value of 89.1% and a positive predictive value of 100.0%. Dr Moshe Ben-Shoshan, from McGill University Health Center, Montreal, Quebec, Canada, said, “A graded PC with an appropriate followup is a safe and cost-effective strategy to diagnose non-life-threatening reactions to amoxicillin. Current existent tests such as PrePen and penicillin G are not sensitive methods to diagnose immediate reactions to amoxicillin.”

Women may Prefer Intrauterine Levonorgestrel Over Subdermal Etonogestrel

Global Mass-participation Mobile-health Intervention has Favorable Impact on Heart Health

Peripheral Edema, CVP Linked to Risk of Acute Kidney Injury in the Critically Ιll Patient

Results of the Stepathlon Cardiovascular Health Study conclude that distributed mHealth implementation of a low-cost lifestyle intervention is associated with shortterm reproducible large-scale improvements in physical activity, sitting and weight. Stepathlon is an international low-cost mass-participation mHealth intervention and the study analyzed prospectively collected cohort data from participants completing Stepathlon, an annual 100-day global event in 2012, 2013 and 2014. There was an improvement in step count, exercise days, sitting duration and weight. Improvements occurred in women and men, in all geographic regions and in both high and lower-middle income countries, and reproduced in the three cohorts. The findings were presented at the annual scientific session of the American College of Cardiology and also published April 2016 in the Journal of American College of Cardiology.

Venous congestion, as manifested as either peripheral edema or increased central venous pressure (CVP) is directly associated with acute kidney injury (AKI) in critically ill patient. In a study reported April 7, 2016 in the Clinical Journal of the American Society of Nephrology, peripheral edema was associated with a 30% higher risk of AKI than pulmonary edema. Compared to patients who did not have edema, levels of trace, 1+, 2+ and 3+ edema were associated with 34%, 17%, 47% and 57% higher adjusted risk of AKI, respectively.

And, each 1 cm H2O higher CVP was associated with a 2% higher adjusted risk of AKI.

Risk of Mortality Higher in RA Patients Following Joint Surgery Following an episode of joint surgery, patients with rheumatoid arthritis (RA) are at a significantly increased risk of death at 6 weeks including increased risk of myocardial infarction (MI) and death at 1 year, compared to the general population, says a new study from Australia published in the journal Arthritis Research & Therapy. The risks are elevated not just for surgeries like hip joint replacement, but also for relatively minor procedures such as shoulder surgery.

Sharon Van Doornum, MD, and colleagues from the Royal Melbourne Hospital and University of Melbourne, Australia suggest that RA patients should be considered at higher risk in the perioperative period.

Women are more likely to keep using an intrauterine levonorgestrel system (LNG-IUS 8) for contraception than they are a subdermal etonogestrel (ENG) implant.

According to a 12-month multicenter, randomized study reported online March 23 in Fertility and Sterility, the LNG-IUS 8 was associated with a significantly lower 12-month discontinuation rate versus ENG implant; mainly because ENG implant users frequently discontinued due to increased bleeding. And, more LNG-IUS 8 users than ENG users reported being “very/ somewhat satisfied” with their bleeding pattern, and reported a preference to continue using their study treatment after the study.

Adding Mitral-valve Repair to CABG Offers no Significant Advantage in Moderate Ischemic MR In patients with moderate ischemic mitral regurgitation undergoing CABG, the addition of mitral-valve repair did not lead to significant differences in left ventricular reverse remodeling at 2 years compared to CABG alone, according to a study published April 3, 2016 in the New England Journal of Medicine. Mitral-valve repair provided a more durable correction of mitral regurgitation but did not significantly improve survival or reduce overall adverse events or readmissions and was associated with an early hazard of increased neurologic and supraventricular arrhythmias.

Autism Awareness Day: No Change in Autism rate According to CDC reports, autism rate was 1 in 68 children in 2012 and 2010. Research published in the Journal of American Academy of Child and Adolescent Psychiatry, showed that technology helped identify children with autism from children without autism but

Indian Journal of Clinical Practice, Vol. 26, No. 12, May 2016

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AROUND THE GLOBE with other developmental issues like ADHD, anxiety and intellectual disabilities. The CDC recommends that parents should track their child’s development, act quickly, and get their child screened if they have a concern. (Source: CDC)

Medtronic’s Micra TPS Miniature Pacemaker Gets FDA Approval Medtronic’s Micra TPS - the world’s smallest pacemaker - is the first ever product with miniaturized pacing technology to be awarded an FDA approval. This MRIcompatible device is useful for patients who need a single-chamber pacemaker. Physicians can collect and send data of patients remotely via Medtronic CareLink Network. (Source: Nasdaq)

FDA Approves Impella Left-ventricular Heart Pumps for Cardiogenic Shock FDA has approved a line of percutaneous ventricularassist devices for treatment of cardiogenic shock patients. Four Impella heart pumps have been approved for ongoing cardiogenic shock that occurs within 48 hours of MI or open-heart surgery as a result of left ventricular failure unresponsive to medical therapy and conventional treatment. The devices are approved for use in patients with or without an intra-aortic balloon pump. (Source: Abiomed)

CDC’s Promotion of Prediabetes as a Health Condition Criticized by Experts Recent reports by WHO state that global diabetes cases have quadrupled over 34 years. However, the launch of a prediabetes web site by CDC is being criticized as unnecessary as experts consider the condition prediabetes, as non-existent. Experts say that CDC, would be making millions of Americans who took the survey in the portal believe they do have the ailment and make 86 million Americans sick.

(Source: International Business Times/American Council on Science and Health)

Health officials confirm sexual transmission of Zika virus New research shows high concentrations of Zika virus in male testes, suggesting that the virus can be transmitted sexually. Researchers working on Zika virus vaccines and treatments have developed a mouse model for testing Zika therapies. The testicles seem to harbor higher concentrations of the virus than spinal cord and brain.

(Source: Inquisitr/Daily Mail)

Is it possible to make new Esophagus?

American doctors at the Medical College of Wisconsin have made a new esophagus for a young man, using donated skin tissue and metal stents. The case report provides proof of concept that regrowth of lost oesophagus is possible without complex tissue engineering, but the new approach requires validation in animal studies before proceeding to clinical trials.

(Source: Lancet)

No Alternatives for imported medicines in Pakistan Most of the imported medicines, including anesthetic gases, gonadotropins, biological and various vaccines, are not manufactured in Pakistan. According to Pakistan Chemists and Druggists Association (PCDA) members their import must not be discouraged as patients have no other alternatives available (Source: The Express Tribune, Pakistan).

Affordable generation of Pan-specific Antiserum against Elapid Snakes of Asia Snakebite envenomation is considered as a neglected tropical disease by WHO. Antivenom (AV) treatment is unaffordable and/or unavailable in many affected countries and is specific to only few snake venoms.

Scientists at Chulabhorn Research Institute, Thailand have produced affordable pan-specific antiserum effective against major medically important elapids snakes in Asia. Due to economies of scale, the antivenom could be produced inexpensively and save many lives (Source: PLoS Negl Trop Dis)

■■■■

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Indian Journal of Clinical Practice, Vol. 26, No. 12, May 2016

LIGHTER READING

PEACE OF MIND Once, Buddha was walking from one town to another town with a few of his followers. This was in the initial days. While they were traveling, they happened to pass a lake. They stopped there and Buddha told one of his disciples, “I am thirsty. Do get me some water from that lake there.”

The disciple walked up to the lake. When he reached it, he noticed that some people were washing clothes in the water and, right at that moment, a bullock cart started crossing through the lake.

As a result, the water became very muddy, very turbid. The disciple thought, “How can I give this muddy water to Buddha to drink!”

So he came back and told Buddha, “The water in there is very muddy. I don’t think it is fit to drink.”

After about half an hour, again Buddha asked the same disciple to go back to the lake and get him some water to drink. The disciple obediently went back to the lake. This time he found that the lake had absolutely clear water in it.

The mud had settled down and the water above it looked fit to be had. So he collected some water in a pot and brought it to Buddha.

HUMOR

Buddha looked at the water, and then he looked up at the disciple and said, “See what you did to make the water clean. You let it be… and the mud settled down on its own – and you got clear water… Your mind is also like that. When it is disturbed, just let it be. Give it a little time. It will settle down on its own. You don’t have to put in any effort to calm it down. It will happen. It is effortless.”

“I’m sorry,” the clerk said. “This man just ordered our last bunch.”

The desperate customer turned to me and begged, “May I please have those roses?”

“What happened?” I asked. “Did you forget your wedding anniversary?”

“It’s even worse than that,” he confided. “I crashed my wife’s hard drive!”

I KNOW, DOC A man swallowed a mouse while sleeping on the couch one day. His wife quickly called the doctor and said, “Doctor, please come quickly. My husband just swallowed a mouse and he’s gagging and thrashing about.”

“I’ll be right over,” the doctor said. “In the meantime, keep waving a piece of cheese over his mouth to try to attract the mouse up and out of there.”

When the doctor arrived, he saw the wife waving a piece of fish over her husband’s mouth. “Uhh, I told you to use cheese, not fish, to lure the mouse.”

“I know, doc,” she replied, “but first I’ve got to get the darn cat out of him.”

Dr. Good and Dr. Bad SITUATION: A patient with positive malaria came with severe thrombocytopenia.

This is classical malaria

Also look for dengue

21ST CENTURY MARRIAGE I stopped at a florist shop after work to pick up roses for my wife. As the clerk was putting the finishing touches on the bouquet, a young man burst through the door, breathlessly requesting a dozen red roses.

© IJCP Academy

INSPIRATIONAL STORY

Lighter Side of Medicine

LESSON: Malaria and dengue may co-exist in the same patient.

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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,

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Indian Journal of Clinical Practice, Vol. 26, No. 12, May 2016

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.

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.

–

The legend must include enough information to permit interpretation of the figure without reference to the text.

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. 26, No. 12, May 2016

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In This Issue —

Asian Journal of Diabetology

Emerging role of Cardiac MRI in Ischemic and Non-ischemic Cardiomyopathy

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Acute Renal Failure and Silent Myocardial Infarction Following Multiple Honey Bee Stings

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Superficial Brachial Artery: Its Embryological and Clinical Significance

—

Glucose Tolerance in Nondiabetic Patients after First Attack of Acute Myocardial Infarction and its Outcome

—

A Case of Left Atrial Myxoma Presenting as Severe Pulmonary Hypertension

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Double-Chambered Right Ventricle with Transient 2:1 Atrioventricular Block: A Rare Presentation

—

Cornary Artery Air Embolism

Volume 17, Number 5

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January-March 2015

Volume 1, Number 1

Asian Journal of OBS & Gynae Practice Asian Journal of Paediatric Practice

Volume 18, Number 3

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