Sangeeta Basu, C D Aundhakar, Jitendra Kumar, Amit Galgali, Rakesh Patil, Sharanabasav Kirdi
Abstract: Seizures are the most common pediatric neurologic disorder, with 4% to 10 % of children suffering at least one seizure in the first 16 years of life. 3 If the response of the first antiepileptic drug trial is a powerful marker of outcome, then the early identification of patients who are at risk to fail the initial antiepileptic drug trial should be a priority. The AED chosen for the initial therapy should be one that is for the highly effective for the particular seizure type or syndrome and that is safe and well tolerated. We conclude that presence of history of seizures in family members and the presence of microcephaly can have a significant role to play in the outcome of the trial with the first AED. Good seizure control can be achieved by using mono therapy with the standard first line AED drugs in moderate doses.
1. Friedeman, M.J and Shareiff, G.Q. Seizures in children. Pediatric Clinics of North America 2006, 53; 257-277.
2. Fact sheet: Epilepsy (internet ).WHO (2012 ). at
Sangeeta J. Sarkate, Sangita R. Phatale, P. S. Bhakare
Background and Objective: Meditation is described as condition of inner tranquility and attaining of higher state of consciousness. The present study was undertaken to find out the effect of meditation on BMI. Material and method: The study was conducted on 74 subjects in the age group of 45 to 55years of either sex. BMI was recorded before and after two months training of meditation. Results: BMI was decreased and was statistically highly significant. Conclusion: Meditation practice found to reduced the BMI.
1. Morgan, King and Robinson: introduction to Psychology, sixth edition: page 254-255. 2. Benson, Alexander and Feldman: decreased premature ventricular contractions through the use of relaxation responses in patient with stable CHD. The Lancet 1975:2:380-382. 3. Albert G. NON communicable diseases: tomorrow’s pandemics. Bulletin of World Health Organization 2001; 79(10):907. 4. Ornish D. Dr. Dean Ornish’s Programme for Reserving Heart Disease. New York: IVY Books Ballantine Publication. 1990. 5. Baride JP, Sancheti SS. Meditation: a boon for health? (Letter) World Health Forum 1994; 15 (1): 61-62. 6. Barnald R.J. Effect of life style modification on serum lipids. Arch intern Med 1991; 151: 1389 -1394. 7. Barnard RJ, Ugianskis EJ, Matins DA, Inkeles SB. Role of diet and exercise in the management of hyperinsulinemia and associated atherosclerotic risk factors. The American Journal of Cardiology 1992; 41(1):440-444. 8. Schwartz RS, William PS, Larson V et al. The effect of intensive endurance exercise training on body fat distribution in young and older men. Metabolism 1991; 40(5): 545-551. 9. Ornish D, Scherwitz L.W, Billings JH et al. Intensive Life style changes for reversal of coronary heart disease. Journal of American Medical Association 1998; 280 (23); 2001-2007 10. Ornish D, Sherwitz LW, Doody RS. et. Effect of stress management training and dietary changes in treating CHD. Journal of American Medical Association 1983; 249: 54-59. 11. Mahajan AS, Reddy KS, Sachdev U: Lipid profile of coronary risk subjects following meditation lifestyle intervention. Indian Heart Journal 199-51(1): 37-40. 12. Lance GK, Ornish D, Larry S, et al. Changes in myocardial perfusion abnormalities by position emission tomography after long term intense risk factor modification. Journal of American Medical Association 1995; 274(11): 894-901. 13. Anderson RE, Wadden TA, Bartlet ST. Zamel B, Verde TJ, Frankowiak SC. Effect of lifestyle activity vs structured aerobic exercise in obese women: A randomized trial. Journal of American Medical Association 1999; 281(4): 335-340.
Mohammad Hafiz Deshmukh, Ashish Deshmukh, Sunil Jadhav, Shivprasad Kasat, Sandeep Dandin
Abstract: We report a case history of a 43 yr old lady, who presented with acute abdominal pain and then went into respiratory failure. The patient was not a known case of myasthenia gravis. The Chest X-ray was normal, blood gas analysis showed respiratory acidosis, CT scan of abdomen showed pseudocyst of pancreas with necrosis in tail of pancreas. Myasthenia crisis can be triggered by a variety of factors, in this case by acute pancreatitis. In our case myasthenia gravis was diagnosed since we had difficulty in weaning her off from the ventilator. Myasthenia crisis with pseudocyst of pancreas and acute pancreatitis is rare. After putting her on ventilator, there was improvement in blood gas, but she could not be weaned off the ventilator even after repeated attempts because of poor respiratory muscle activity. Serum Acetylcholineesterase receptor auto antibodies were found to be high, and she was then diagnosed as having Myasthenia gravis. Myasthenia gravis should be suspected in a patient with unexplained respiratory failure.
1. Journal Article Richard S. Bedlack, Donald B. Sanders- how to handle myasthenic crisis. Vol. 107/no.4/april 2000/postgraduate medicine. 2. Journal Article Vaidya H et al. – case of the month: unusual presentation of myastuenia gravis with acute respiratory failure in emergency room. emerg med j. 2006 may ; 23(5) : 410 – 3 3. Journal article D’ angelo AJ JR et al. respiratory failure as initial presentation of myasthenia gravis. Ear nose throat j. 1989 jan; 68(6) : 472-473 4. Journal Article Rieder P, Loius M, Jolliet P, et al. The repeated measurement of vital capacity is a poor predictor of the need for mechanical ventilation in myasthenia gravis. intensive care med.1995,2118:663-8.
Kalpana U. Rakshit, Neelima Rajhans, Pankaj Kamble, Nilkanth Mhaske, Nikesh Moolya, Sudeep HM
Introduction: The periodontal tissues mount an immune inflammatory response to bacteria and their products and the systemic challenge with these agents also induce a major vascular response. Oral infection models have emerged as useful tools to study the hypothesis that infection is a cardiovascular disease (CVD) risk factor. Periodontal infections are a leading culprit, with studies reporting associations between periodontal disease and CVD. Material and Methods: The study was conducted on a group of 50 individuals aged 30 to 65 years, divided in five different groups depending on the type of cardiovascular disease diagnosed. These five groups were: Ischemic heart disease, bacterial endocarditis, Congestive cardiac failure, valvular heart disease and cardiomyopathies. The dental investigations comprised of Ramjford’s periodontal disease severity index and clinical attachment level Laboratory investigations were done for lipid profile analysis. Observations and Results: Ramjford’s disease severity index showed a significant difference (p<0.05) between Bacterial endocarditis and Valvular heart disease. This index also showed significant positive correlation with total cholesterol, triglycerides and VLDL and showed negative correlation with HDL. Attachment level was not significant between Valvular heart disease and Cardiomyopathies. However, it showed positive correlation with total cholesterol. Lipid profile showed dyslipidaemia with Ischemic Heart Disease. Conclusion: The study concludes that Bacterial endocarditis and Ischemic heart diseases have severe degree of periodontitis as compared to Valvular heart diseases, cardiomyopathies and congestive cardiac failure.
1. Kuller IJ, Fisher L, McClelland R et al. Differences in prevalence of and risk factors for subclinical vascular disease among black and white participants in the Cardiovascular Health Study. Arterioscler Thromb Vasc Biol. 1998; 18:283–293. 2. WHO. The World Health Report 2001. Annex Table 2 Deaths by cause, sex and mortality stratum in WHO Regions, estimates for 2000. 3. KeilU. Coronary artery disease: the role of lipids, hypertension and smoking. Basic Res Cardiol. 2000; 95:I52–I58. 4. WoodD. Established and emerging cardiovascular risk factors. Am Heart J. 2001; 141:49–57. 5. AdamE, Melnick JL, DeBakey ME. Cytomegalovirus infection and artherosclerosis. Eur J Publ Health. 1997; 5:99–106. 6. DaneshJ, Youngman L, Clark S et al. Helicobacter pylori infection and early onset myocardial infarction: case-control and sibling pairs study. Br Med J. 1999; 319:1157–1162. 7. ChengJW, Rivera NG. Infection and atherosclerosis — focus on cytomegalovirus and Chlamydia pneumoniae. Ann Pharmacother. 1998; 32:1310–1316. 8. CoombesBK, Mahony JB. Chlamydia pneumoniae infection of human endothelial cells induces proliferation of smooth muscle cells via an endothelial cell-derived soluble factor(s). Infect Immun. 1999; 67:2909–2915. 9. HerzbergMC, Meyer MW. Effects of oral flora on platelets: possible consequences in cardiovascular disease. J Periodontol. 1996; 67:1138–1142. 10. DalyCG, Mitchell DH, Highfield JE et al. Bacteremia due to periodontal probing: a clinical and microbiological investigation. J Periodontol. 2001; 72:210–214. 11. QuirynenM, Mongardini C, de Soete M et al. The role of chlorhexidine in the one-stage full-mouth disinfection treatment of patients with advanced adult periodontitis. Long-term clinical and microbiological observations.J ClinPeriodontol. 2000; 27:578–589. 12. DebelianGJ, Olsen I, Tronstad L. Bacteremia in conjunction with endodontic therapy. Dent Traumatol. 1995; 11:142–149. 13. Page RC, Offenbacher S, Schroeder HE, Seymour GJ, Kornman KS. Advances in the pathogenesis of periodontitis: summary of developments, clinical implications and future directions. Periodontol 2000.1997; 14: 216–248. 14. Pearson TA, Mensah GA, Alexander RW, Anderson JL, Cannon III RO. Criqui M, Fadl YY, Fortmann SP, Hong Y, Myers GL, Rifai N, Smith, Jr SC, Taubert K, Tracy RP, Vinicor F. Markers of inflammation and cardiovascular disease: application to clinical and public health practice: a statement for healthcare professionals from the Centers for Disease Control and Prevention and the Am Heart Association. Circulation.2003; 107: 499–511. 15. Glurich I, Grossi S, Albini B, Ho A, Shah R, Zeid M, Baumann H, Genco RJ, De Nardin E. Systemic inflammation in cardiovascular and periodontal disease: comparative study. ClinDiagn Lab Immunol.2002; 9: 425–432. 16. Slade GD, Ghezzi EM, Heiss G, Beck JD, Riche E, Offenbacher S. Relationship between periodontal disease and C-reactive protein among adults in the Atherosclerosis Risk in Communities Study. Arch Intern Med. 2003; 163: 1172–1181. 17. Buhlin K, Gustafsson A, Pockley AG, Frostegård J, Klinge B. Risk factors for cardiovascular disease in patients with periodontitis. Eur Heart J. 2003; 24: 2099–2107. 18. Chiu B. Multiple infections in carotid atherosclerotic plaques. Am Heart J. 1999; 138: S534–S536. 19. Haraszthy VI, Zambon JJ, Trevisan M, Zeid M, Genco RJ. Identification of periodontal pathogens in atheromatous plaques.J Periodontol.2000; 71: 1554–1560. 20. Deshpande RG, Khan MB, Genco CA. Invasion of aortic and heart endothelial cells by Porphyromonasgingivalis. Infect Immun. 1998; 66: 5337–5343. 21. Dorn BR, Dunn WA Jr., Progulske-Fox A. Invasion of human coronary artery cells by periodontal pathogens. Infect Immun. 1999; 67: 5792–5798. 22. Roivainen M, Viik-Kajander M, Palosuo T, Toivanen P, Leinonen M, Saikku P, Tenkanen L, Manninen V, Tapani H, Mänttäri M. Infections, inflammation and the risk of coronary heart disease. Circulation. 2000; 101: 252–257 23. Lee HM, Ciancio SG, Tuter G, Ryan ME, Komaroff E, Golub LM.Subantimicrobial dose doxycycline efficacy as a matrix metalloproteinase inhibitor in chronic periodontitis patients is enhanced when combined with a non-steroidal antiinflammatorydrug. J Periodontol 2004: 75: 453-463. 24. Montebugnoli L, Servidio D, Miaton RA, Prati C, Tricoci P, Melloni C. Poor oral health is associated with coronary heart disease and elevated systemic inflammatory and haemostatic factors. J ClinPeriodontol 2004; 31(1): 25-9. 25. Miyaki K, Masaki K, Naito M, Naito T, Hoshi K, Hara A et al. Periodontal disease and atherosclerosis from the viewpoint of the relationship between community periodontal index of treatment needs and brachial-ankle pulse wave velocity.BMC Public Health2006;6:131. 26. Lopez R, Oyarzun M, Naranjo C, Cumsille F, Ortiz M, Baelum V. Coronary heart disease and periodontitis - a case control study in Chilean adults.J ClinPeriodontol 2002; 29(5): 468-73. 27. Cueto A, Bravo M, Ocana-Riola R.Periodontitis as risk factor for acute myocardial infarction. A case control study of Spanish adults.J Periodont Res 2005; 40(1): 36-42. 28. Mattila KJ, Nieminen MS, Valtonen VV, Rasi VP, Kesaniemi YA, Syrjala SL et al. Association between dental health and acute myocardial infarction.BMJ 1989; 298(66): 779-81. 29. Persson GR, Ohlsson O, Pettersson T, Renvert S.Chronic periodontitis, a significant relationship with acute myocardial infarction.Eur Heart J 2003; 24(23): 2108-15. 30. Persson GR, Persson RE.Cardiovascular disease and periodontitis: an update on the associations and risk. J ClinPeriodontol 2008;35(Suppl 8):362-79. 31. Stein JM, Kuch B, Conrads G, Fickl S, Chrobot J, Schulz S.Clinical periodontal and microbiologic parameters in patients with acute myocardial infarction.J Periodontol 2009;80(10):1581-9. 32. Tuominen R, Reunanen A, Paunio M, Paunio I, Aromaa A. Oral health indicators poorly predicts coronary heart disease deaths. J Dent Res2003; 82: 713. 33. Dietrich T, Jimenez M, Elizabeth A, Kaye K, Vokonas PS, Garcia RI.Age dependent associations between chronic periodontitis/edentulism and risk of coronary heart disease.Circulation 2008;117:1668-1674.
Kedar Joshi, Deepak K. Bokankar, Hardas V. M.
Introduction: Thyroid hormones influence all the major metabolic pathways. Their most obvious and well known action is increase in basal energy expenditure obtained acting on protein, carbohydrate and lipid metabolism. With specific regards to lipids, thyroid hormone affects synthesis, mobilization and degradation of lipids, although degradation is influenced more than synthesis. Aims and objectives: To study changes in lipoprotein levels in overt and subclinical hypothyroidism patients and compare it with matched healthy controls in population. Material and method: The present study was conducted in Government Medical College and Hospital, Aurangabad from October 2005 to October 2007. Lipid profile of patients of hypothyroidism was compared with control group. Results: Thus among the patients with overt hypothyroidism, we found highly significant increase in TC, LDL and HDL values and no significant change in TG and VLDL when compared with controls. Among the patients with subclinical hypothyroidism, we found significant increase in TC and LDL while no change in TG, HDL and VLDL when compared with controls. Conclusion: that in overt and subclinical hypothyroidism patients, the lipid profile is clearly atherogenic.
1. N. Kochupallai, Clinical endocrinology in India, current Science. vol.79, no.8, 25 oct 2000. 2. CappolaA.R., Ladenson P.W. Hypothyroidism and atherosclerosis. J. Clin. Endo. Meta. 88;2438-2444. 3. Hak A.E. ,Pols H.A , Hofman A,. Subclinical hypothyroidism is an independent risk factor for atherosclerosis and myocardial infarction in elderly women, Rotterdam study. Ann. Int . Med.; 132;270-78 4. Klein I. Ojamma K. thyroid hormone and cardiovascular system. N Engl. J. Med. 344:501-509. 5. Caron P et al. Decreased HDL-C in subclinical hypothyroidism: The effect of L- thyroxine therapy. Clinical Endo. (oxf). 1990; 33:519-523. 6. Staub J J, et al. Spectrum of subclinical and overt hypothyroidism: Effect on thyrotropin, prolactin and thyroid reserve, and metabolic impact on peripheral target tissues. AMJ. 1992; 92: 631-642. 7. Kung A W et al. Elevated serum Lp(a) in subclinical hypothyroidism. Clinical Endo. (oxf).1995: 43: 445-449. 8. Tanis BC. Effect of thyroid substitution on hypercholesterolemiain patients with subclinical hypothyrodism : a reanalysis of intervention studies. Clin. Endo. (oxf) 1996.4: 643-649. 9. Erem C. et al. Plasma lipoprotein(a) concentration in hypothyroid, euthyroid and hyperthyroid subjects. J. Clin. Endo. Meta. 1999; 54(2):77-81. 10. Razirl A et al. The influence of thyroid function on serum lipid profile. Atherosclerosis. 1982; 41(2-3): 321-326. 11. Jeffrey Abrams et al. Metabolism of plasma triglycerides in hypothyroidism and hyperthyroidism in man. J. of Lipid Research. 1981; 22: 307-322. 12. F. Monzani, N. Caraccio, M. Kozakowa, A. Dardano, E. Ferannini. Effect of levothyroxine replacement on lipid profile and intima thickness in subclinical hypothyroidism: A double blind, placebo controlled study. Journal of Clinical Endocrinology. 2004: 89, 2099-2106.
Kiran B Bhaisare, Sunil S Holikar, L. S. Deshmukh
Introduction: As many as 2% of foetuses are infected in utero, and up to 10% of infants have infections in the 1st mo of life. Infections are a frequent and important cause of neonatal and infant morbidity and mortality. nosocomial infection rates are increasing with an incidence inversely proportional to the gestational ages of the infants populating the NICUs. Causative organisms, Group B Streptococci or Escherichia coli that are most likely acquired perinatally. The reported incidence of nosocomial sepsis in India ranges from 1.5-37%. Klebsiella emerging as an important cause of nosocomial sepsis. Outcome depends upon weight and marturity of neonate, type of etiologic agent, antibiotic sensitivity and adequacy of specific and supportive therapy. Material and Methods: All babies admitted in NICU showing clinical features of sepsis, in whom laboratory investigation support the diagnosis of sepsis. Study Period: January 2008 to October 2010.Study design: Observational study. Methods: Babies enrolled in the study were subjected to laboratory investigations Blood culture and Sensitivity was sent in all babies admitted and if sepsis was suspected. Conclusion: Total 1580 neonates were admitted during the study period. Out of these 223 were enrolled in study, Seven neonates were lost during follow up. Fifty neonates of neonatal infection died during the study period. Septic screen was positive in 91.92%, CRP (84.75%), blood culture ( 74.88%), meningitis(18.8%). Most common organism isolated was Klebsiella pneumoniae (28.7%) and least was streptococcus species (5.3%).Mortality due to neonatal sepsis was 24.4%.
1. Joan Newby. Nosocomial Infection in Neonates Inevitable or Preventable? J Perinat Neonat Nurs 2008: 22(3); 221–227. 2. David Kaufman and Karen D. Fairchild. Clinical Microbiology of Bacterial and Fungal Sepsis in Very-Low-Birth-Weight Infants. Clinical microbiology reviews, 2004:17( 3); 638–680. 3. A. Malik, S.E Hasani, M Shahid, HM Khan,AJ Ahmad. Nosocomial klebseilla infection in neonates in tertiary care hospital, protein profile by SDS-PAGE and KLEBOCIN typing as epideimological marker. Ind j Med Micro 2003 21(2):82:86. 4. Kliegman Nelson Textbook of Pediatrics, 18th ed. Barbara J. Stoll, Chapter 109 – Infections of the Neonatal Infant 2007. 5. Khalid N. Haque. Definitions of bloodstream infection in the newborn: Pediatr Crit Care Med 2005 (6):545-549. 6. M. Jeeva Sankar, Ramesh Agarwal, Ashok K Deorari, Vinod K Paul. Sepsis in the Newborn- AIIMS- NICU protocols Ind j ped 2008;75(3);261-266. 7. Reese Clark, Richard Powers, Robert White et al. Nosocomial Infection in the NICU: A Medical Complication or Unavoidable Problem?:J of Perinat 2004; 24:382–388. 8. Kurien Anil Kuruvilla, Swati Pillai, Mary Jesudason et al. Bacterial Profile of Sepsis in a Neonatal Unit in South India: Ind Ped 1998; 35:851-858. 9. Abed El Hakeem Noman El Jadba, Mansour Sobhi El Yazji. neonatal septicemia in gaza city hospitals: Pak J Med Sci 2009 : 25(2):226-231. 10. Shaw CK, Shaw P, Thapalial A. Neonatal sepsis bacterial isolates and antibiotic susceptibility patterns at a NICU in a tertiary care hospital in western Nepal: A retrospective analysis: Kathm Univ Med Jour (2007):5: (2) : 153-160. 11. Shubhra Singh, Gopa Banerjee, S.K. Agarwal. Prevalence of Mec A Gene positive coagulase negative Staphylo-cocci in NICU of a tertiary care hospital: Biomed Res 2009; 20 (2): 94-98. 12. Ludo M. Mahieu, Aime´ O. De Muynck, Jozef J. De Dooy ey al. Prediction of nosocomial sepsis in neonates by means of a computer-weighted bedside scoring system (NOSEP score): Crit Care Med 2000 : 28(6);2026-2033. 13. S Vergnano, M Sharland, P Kazembe et al, Neonatal sepsis: an international perspective: Arch. Dis. Child. Fetal Neonatal Ed. 2005;90;F220-f224. 14. Payman Salamati, Ali Akbar Rahbarimanesh, Masood Yunesian and Mohsen Naseri Neonatal Nosocomial Infections in Bahrami Children Hospital Ind J Pedia.2008;73(3):12-17. 15. Duha Sabeeh Jumah and Mea'ad Kadhum Hassan. Predictors Of Mortality Outcome In Neonatal Sepsis. The Medical Journal Of Basrah University. 2005 12(3):555-561 16. Kapoor L, Randhawa VS, Deb M.Microbiological profile of neonatal septicemia in a pediatric care hospital in Delhi: J Commun Dis. 2005 Sep;37(3):227-32.
Vikas N. Solunke, Milind B. Kamble, Amol R. Suryawanshi, Pallavi Saple, Manish M. Tiwari, Bhete S. B., Garad S. B.
Introduction: The increase in pediatric HIV infection has had a substantial impact on childhood mortality both in industrialized countries and developing countries. Pediatric HIV is a major world health problem which is progressing at an alarming rate. Aims and objectives: a) To study the prevalence of HIV infection in children. b) To study various presenting signs and symptoms in pediatric HIV patients. Methodology: The present study was carried out in the department of pediatrics from January 2008 to June 2009. All the patients attending the pediatric department i.e. OPD and IPD were enrolled in the study. Out of these patients suffering from HIV were diagnosed. The study population included was patients who were already HIV positive or diagnosed later on investigation on suspicion of the clinical features. Results: A sum of 24828 children attended pediatric department during study period. Amongst those 144 were found to be HIV reactive. Hence the prevalence of HIV infection during the study period was 0.58%. Vertical transmission was seen in 98.62% and infection via blood transfusion in 1.38%. Male to female ratio was 1.93:1. On first presentation fever was the most common symptom. On examination severe malnutrition (PEM Gr III and IV) was the most common finding (59.02%) followed by pallor (51.38%), respiratory signs (47.22%). Conclusion: prevalence of HIV in children attending pediatric department was 0.58%. Fever was the most common complaint reported by the study population and malnutrition was also most commonly associated finding in pediatric HIV patients.
1. Gottlieb MS, Schroff R, Schanker HM, et al. Pneumocystis carinii pneumonia and mucosal candidiasis in previously healthy homosexual men. Evidence of a new acquired cellular immunodeficiency. New Engl. J. Med 1981; 305:1425. 2. Merchant R.H, Oswal J,Karkare J et al. Clinical Profile of HIV infection. Indian Pediatrics 2001; vol.38, (3):239-246. 3. Chu SY, Buehler JW, et al. Impact of the human immunodeficiency virus epidemic on mortality in Children in United States. Pediatrics 1991;89:806-810. 4. Nicoll A, Timaeus I, et al. The Impact of HIV-1 Infection on mortality in children under 5 yrs of age in sub – Saharan Africa, A demographic and epidemiological analysis, AIDS, 1994;8: 995 – 1005. 5. Asnake Sehbat, Solomon Amsalu. Clinical manifestation of HIV/AIDS in children in northwest Ethiopia. Ethiop, J.Health Dev.2005:19(1):24-28 6. Lodha R, Singh T, Jain Y, Kabra S, Seth P, Seth V. Paediatric HIV infection in a Tertiary Care Center in North India: Early Impressions. Indian Pediatrics 2000 Vol 37(9); 982-986. 7. Friesen H. Pediatric HIV Infection. PNG Med. J. 1996; 39(3):183 -189. 8. Lahiri S, Shahab T, Malik Alam S. HIV seropositivity in hospitalized children with high likelihood of AIDS. Indian Pediatrics 2002; 39:372-375. 9. Diack Mbaye A, Signate Sy H, Diagne Gueye NR,Ba A, Sylla A, Diouf S, Diagne I, Sarr M, Sow HD. Epidemiological and clinical aspects of paediatric HIV infection in Albert-Royer paediatric Hospital (Dakar, Senegal). Arch Pediatr. 2005 Apr;12(4):404-9. 10. Madhivanan P, Mothi SN, Kumarswamy N, Yepthomi T, Venkatesan C, Lambert JS, Soloman S: Clinical manifestation of HIV infected children Indian Journal of Pediatrics 2003 Aug;70(8) :615-20 11. Abubaker Bedri, Sileshi Lulseged. Clinical description of children with HIV/AIDS admitted to a referral hospital in Addis Ababa. Ethiop Med J, 2001; 39(3):203-211s 12. Pol R R,Shepur TA,Ratgeri VH. Laboratory profile of pediatric HIV in Karnataka. Indian Journal of Pediatrics 2007; 74(12):1071-1075. 13. Sirisanthana V. Opportunistic Infections in HIV infected children at Chiang Mai University Hospital, Chaing Mai, Thailand. J Infect Dis Antimicrobial Agent 1995; 12:59-62 14. Lodha Rakesh, Amit Upadhyay, Vishal kapoor, et al. Clinical profile and natural history of children with HIV infection. Indian J Paediatrics 2006;73(3):201-204. 15. Madhivanan P, Mothi SN, Kumarswamy N, Yepthomi T, Venkatesan C, Lambert JS, Soloman S: Clinical manifestation of HIV infected children Indian Journal of Pediatrics 2003 Aug;70(8) :615-2 16. Shahab T. Zoha M.S, Malik A, et al. Prevalence of Human immunodeficiency virus in children with Tuberculosis. Indian Pediatrics 2004, Vol 41 (6): 595-599. 17. Pol R R,Shepur TA,Ratgeri VH. Laboratory profile of pediatric HIV in Karnataka.Indian Journal of Pediatrics 2007;74(12):1071-1075. 18. Verghese V P, Thomas cherion, et al. Clinical manifestations of HIV -1 infections. Indian paediatrics 2002,Vol 39,Jan 17,(57-63). 19. Dhurat R, Mangalani M et al. Clinical Spectrum of HIV infection. Indian Pediatrcs 2000, Vol 37(8): 8 20. Parthasarathy P. Mittal S,K. Sharma V.K. Prevalence of Pediatric HIV in New Delhi. Indian J Pediatrics 2006; 73(3) : 205-207 21. Emodi IJ, Okafor GO. Clinical manifestation of HIV infection in children at Enugu. Nigeria J Trop Pediatr 1998;44:73-75 22. Lodha R, Kabra S.K. Upadhyay A.,et al. Antiretroviral therapy in HIV-1 Infected children. Indian Pediatrics, Vol 42,(8),2005: 789-796. 23. Kaul D, Patel J. Clinical Manifestation of pediatric HIV infection. Indian Journal of Paediatrics 2001, Vol 68(7): 623 – 631.
Baby Abrarunnisa Begum, N. Devanna, Md. Sibgatullah, Asma
Abstract: Rapid industrialization has resulted in pollution of ground water recourses. Patencheru in Medak district is one such industrial hub near Hyderabad. The treated industrial waste in released into stream nakkavagu which joins river manjeera a tributary of river Godavari. Bachigudem village was selected for ground water assessment as it lies in the nakkavagu catchment area. Parameters from eight sources were analyzed for parameters such as color, turbidity, pH, total alkalinity, total dissolved solids, total hardness, chlorides, sulphates, nitrates, fluorides and electrical conductivity. The sampling was done in month of july which is a peak rainy season. The results showed gross contamination of the ground water in bachigudem village. Fresh water is one of the essentials for life on earth. The Indian subcontinent is one of the wettest places on the earth with annual precipitation of over 4000 km3 with a river flow of 1880 km3 and potential ground water resources of about 431 km 3 besides water glaciers, ponds and lakes. But still we have the demand for good quality water because of growing population and use and abuse of existing resources.
1. Subramaniam. V and ramanathan. A. 1999, saketh environmental handbook, “water pollution” school of environmental sciences, jntu, pg 245-262 2. MFR Sowers; MK Clark; Am J Epidemiol, 1991; 133: 649–60 3. Shaik, R., Srikant, V.N.V., Rao, D.M. & Ramakrishna, C. (2012), ‘‘Study of Ground Water Quality in Industrial Zone Of Visakhapatnam’’, Appl. Sci. Res., 2012, 3(4):2463-2467. 4. APHA (1998) Standard methods for the examination of water and wastewater. Amer. Pub. Health Assoc. 5. Fletcher GD (1986) Groundwater and wells,2nd ed., Johnson Division Publ., Sr. Paul Mimnesala. pp: 1089. 6. Raghunath HM (1987) Groundwater. Wiley-Eastern Ltd., New Delhi. 7. Feth JH, Nitrogen compounds in natural water –a review. 1966. Water REs. Res. 2(1), 41-48. 8. Hem JD, Study and interpretation of the chemical characteristics of natural water. 1991. Scientific Publ., Jodhpur.
Deepak Kishan Bokankar, Kedar Balwant Joshi, Patil V. P.
Introduction: Incidence of coronary heart disease (CHD) has shown an upward trend in Indian in the last decade. Estimation of serum lipids like Cholesterol and triglycerides were used to assess the risk of CHD. However, the correlation between serum Cholesterol and CHD is not ideal. Apoplipoprotein play an important role in many disorders of lipid metabolism. Indeed, it has become increasingly clear that while the lipids in lipoproteins are the transported moieties, the protein moieties of lipoproteins - the apoproteins - perform the crucial roles of transporting the lipids, and apoproteins can determine the levels of lipoprotein lipids. Therefore, attempts have been made to assess the relationships between plasma apoprotein concentrations and CHD. Aim and Objectives: To see the association of serum apolipoprotein A-I and B in patient with Coronary Heart Disease. Materials and Methods: The present study was conducted at Government Medical College and Hospital, Aurangabad. Levels of Apolipoprotein A-I and B in 60 Coronary Heart Disease patients admitted with first episode of coronary heart disease in ICCU were compared with 60 healthy apparently normal age, sex matched individuals. Results: it was observed that levels of apolipoprotein A-I and the ratio of apolipoprotein A-1 and B were decreased in CHD patients where as levels of apolipoprotein B was increased in CHD patients as compared to control group. And the difference was also statistically significant. Conclusion: concentration of apo A-I, apo B and its ratio can be a useful summary index of risk of CHD.
1. S.G. Sarvotham, J.N. Berry. Prevalence of Coronary Heart Disease in an Urban population in Northen India. Circulation 1968;37:939-953 2. Ramachandran S. Vasan, Emelia J. Benjamin, Lisa M. Sullivan, Ralph B. D’Agostino. The burden of increasing worldwide cardiovascular disease. Hurst’s The Heart, 11th ED;2004;vol I;ch.2:15-43 3. David J. Maron, Scott M. Grundy, Paul M. Ridker, Thomas A. Pearson Dyslipidemia, other risk factors and the prevention of coronary heart disease. Hurst’s The Heart,11th ED;2004;vol I;ch.43:1093 4. P. P. Jadhav, A. P. Taskar, R. D. Darne. Evaluation of Apolipoprotein A-I and B in survivors of Myocardial Infarction. JAPI 1994;42(9):703-705 5. William P. Castelli, Joseph T. Doyle, Tavia Gordon, Curtis G. Hames, Marthana C. Hjortland, Stephen B. Hulley, et al. HDL Cholesterol and other lipids in coronary heart disease. The co-operative lipoprotein phenotyping study. Circulation 1977;55:767-775 6. P. Avogaro, G. Bittolo Bon, G. Cazzolato, G. B. Quinci. Are Apolipoproteins better discriminators for Atherosclerosis? Lancet. 1979;28:901-903 7. Alaupovic P. Apolipoproteins and lipoproteins. Atherosclerosis 1971;13:141-153 8. Onitri A.C., Jover E. Comparative serum apolipoproetins studies in ischaemic heart disease and control subjects. Clin chem. Acta 1980; 108:25-30 9. Steven P. Sedlis, Kenneth B. Schechtman, Philip A. Ludbrook, Burton E. Sobel, Gustav Schonfeld. Plasma apoproteins and the severity of coronary artery disease. Circulation.1986; 73-5:978-986. 10. Goran Walldius, Ingmar Jungner. Rationale for using apolipoprotein B and apolipoprotein A-I as indicators of cardiac risk and as targets for lipid-lowering therapy. Eur Heart J 2004;26:210-212 11. Paul S. Roheim. Atherosclerosis and lipoprotein metabolism: Role of reverse cholesterol transport. Am J Cardiol 1986; 57:3C-10C. 12. Hitoshi Kukita, Mareomi Hamada, Kunio Hiwada, Tatsuo Kokubu. Clinical significance of measurements of serum Apolipoprotein A-I, A-II and B in Hypertriglyceridemic male patients with and without coronary artery disease. Atherosclerosis,55 (1985) 143-149 13. Wolfgang Schwartzkopff, Jan Schleicher, Ingrid Pottins, Shi-Bei Yu, Chai-Zhang Han, Dian-Yun Du. Lipids, lipoproteins, apolipoproteins and other risk factors on Chinese men and women with and without myocardial infarction. Atherosclerosis, 82 (1990) 253-259 14. Peter O. Kwiterovich, Josef Coresh, Hazel H.Smith, Paul S. Bachorik, Carol A. Derby, Thomas A. Pearson. Comparision of the plasma levels of apolipoproteins B and A-I, and other risk factors in men and women with premature cornary artery disease. Am J Cardiol 1992;69:1015-1021 15. Bahl VK, Vaswani M, Thatai D, Wasir HS Plasma levels of apolipoproteins A-I and B in Indian patients with angiographically defined coronary artery disease. Int J Cardiol.1994; 46(2):143-9 16. Maria Stella Graziani, Luisa Zanolla, Gabriella Righetti, Cristina Marchetti. Plasma apolipoproteins A-I and B in survivors of myocardial infarction and in control group. Clinical Chemistry.1998;44:134-140 17. Goran Walldius, Ingmar Jungner, Ingar Holme, Are H Aastveit, Werner Kolar, Eugen Steiner. High apolipoprotein B, low apolipoprotein A-I, and improvement in the prediction of fatal myocardial infarction (AMORIS study): a prospective study. Lancet 2001;358:2026-33 18. Gerald Luc, Jean-Marie Bard, Jean Ferrieres, Alun Evans, Philippe Amouyel. Value of HDL cholesterol, apolipoprotein A-I, lipoprotein A-I, and lipoprotein A-I/A-II in prediction of coronary heart disease. The PRIME study. Arteriosclerosis, Thrombosis, and Vascular Biology.2002;22:1155 19. Johan Franzen, Goran Fex. Low serum Apolipoprotein A-I in acute myocardial infarction survivors with normal HDL cholesterol. Atherosclerosis, 59 (1986) 37-42 20. Michael F.R eardon, Paul J. Nestel, Ian H. Craig, Richard W. Harper. Lipoprotein predictors of the severity of coronary artery disease in men and women. Circulation 71,No.5,881-888,1985 21. MJ Stampfer, FM Sacks, S Salvini, WC Willett, CH Hennekens. Aprospective study of cholesterol, apolipoproteins, and the risk of myocardial infarction. N. Engl. J. Med. 1991; 325:373-381 22. Benoit Lamarche, Sital Moorjani, Paul J. Lupien, Bernard Cantin, Paul-Marie Bernard. Apolipoprotein A-I and B levels and the risk of ischaemic heart disease during a five-year follow-up of men in the Quebec cardiovascular study. Circulation. 1996; 94:273-278 23. Christa Meisinger, Hannelore Loewel, Wilfried Marz, Wolfgang Koenig. Prognostic value of apolipoprotein B and A-I in the prediction of myocardial infarction in middle-aged men and women: result from the MONICA/KORA Augsburg cohort study. Eur Heart J. 2004; 26(3):271-278 24. M. Rosseneu, J. C. Fruchart, J. M. Bard, V. Nicaud, N. Vinaimont, F. Cambien, G. De Backer. Plasma apolipoprotein concentrations in young adults with a parental history of premature coronary heart disease and in control subjects. The EARS study. Circulation. 1994; 89:1967-1973 25. Francois Cambien, Jean-Michel Warnet, Alain Jacqueson, Pierre Ducimetiere, Jacques-Lucien Richard, Jean-Roger Claude. Relation of parental history of myocardial infarction to the level of apoprotein B in men. Circulation 76, No.2, 266-271, 1987 26. C.Snehalatha, A.Ramachandran, S Sivasankari, K Satyavani, V Viswanathan. Is increased apolipoprotein B- A major factor enhancing the risk of coronary artery disease in type 2 diabetes? J Assoc Physicians India 2002;50:1036-1038 27. G. De Backer, M. Rosseneu, J. P. Deslypere. Discriminative value of lipids and apoproteins in coronary heart disease. Atherosclerosis. 42 (1982):197-203 28. Sahi N, Pahlajani DB, Sainani GS. Apolipoproteins A-I and B as predictors of angiographically assesses coronary artery disease. J Assoc Physicians India.1993 Nov; 41(11):713-5 29. Philippa J. Talmud, Emma Hawe, George J. Miller, Steve E. Humphries. Nonfasting apolipoprotein B and triglycerides levels as a useful predictor of coronary heart disease risk in middle aged UK men. Arteriosclerosis, Thrombosis, and Vascular Biology.2002;22:1918-1923 30. Adnan I. Qureshi, Wayne H. Giles, Janet B. Croft, Lee R.Guterman, L. Nelson Hopkins. Apolipoproteins A-I and B and the likelihood of non-fatal stroke and myocardial infarction- data from third national health and nutrition examination survey. Med Sci Monit, 2002;8(5):CR311-316 31. Tobias Pischon, Cynthia J. Girman, Frank M. Sacks, Nader Rifai, Meir J. Stampfer. Non-high-density lipoprotein cholesterol and apolipoprotein B in the prediction of coronary heart disease in men. Circulation.2005;112:3375-3383.
Sandhya Panjeta Gulia, Swati Anil Wadhai, Lavanya M , Roshni Menon, Madhusudan Chaudhary, SP Arun Kumar
Aims: This study is conducted to study the prevalence of various skin lesions attending the outpatient department of dermatology over a period of one year dec2012-dec2013. Materials and Methods: A total of 125 cases of skin lesions for over a year were taken for the study. Diagnosis was confirmed by histopathological examination with Hand E stain. Special stains were done wherever required. Results : Out of 125 cases, 30(24%)were reported under the category of non-infectious erythematous papulosquamous diseases, 20(16%) cases of leucocytoclasticvasculitis, 6(4.8%) cases of vesiculobullous and vesiculopustular diseases, 15 (12%)cases were reported as connective tissue disorders amongst which morphea, 12(9.6%)was the commonest, granuloma annulare 1 case(0.8%), erythema nodosum 2 (1.6%), 5(4%) cases of cutaneous drug toxicities, infectious etiology was reported in 15(12%) cases, pigmentary disorders of the skin was reported in 5(4%), 2(1.6%) cases of tumors arising from epidermal appendages, 5(4.0%) cases of tumors and cysts of epidermis and miscellaneous category,15(12%) cases. Conclusion : Among skin infections papulosquamous lesions were more common in our region with psoriasis being the most common lesion.
1. Rook A, Savin JA, Wilkinson DS. The prevalence, incidence and ecology of diseases of skin, In: Rook A, Wilkinson DS, Ebling FJ, Champion RH, Burton JL, editors, Textbook of dermatology. Oxford University Press:Mumbai1987.p.39-53 2. SK Sarkar, AKMS Islam, KG Sen, ARS Ahmed. Pattern of Skin Diseases in Patients Attending OPD of Dermatology Department at Faridpur Medical College Hospital, Bangladesh. Faridpur Med Coll.J.2010;5(1):14-16 3. Symvoulakis E K, Krasagakis K, Komninos I D, Kastrinakis I, Lyronis I, Philaliyhis A, Tosea A D. Primary care and pattern of Skin diseases in a Mediteranean island. BMC Family Practice 2006;7:6[http:\\www.biomedcentral.com\1471-2296\7\6] 4. Das A, HalderS, DasJ, Mazumdar G, Biswas S, Sarkar JN. Dermatologic disease pattern in an urban institution in Kolkata. Indian J Dermatol 2005;50(1):22-4 5. Th. Bijayanti Devi, G Zamzachin. Pattern of skin diseases in Imphal. Aiandian J Dermatol 2006;51(2):149-50 6. N Asokan, PriyaPrathap, Ajithkumar K, Ambooken Betsy, Binesh V G, George S. Pattern of skin diseases among patients attending a tertiary care teaching hospital in Kerela. Indian J Dermatol Venerol Leprol 2009;75(5):517 7. Anand IS, Gupta S. A profile of skin disorders in children in Saurashtra. J Indian Med Assoc 1998;96:245-6 8. Sudip Das, Tapash Chatterjee. Pattern of Skin Diseases in a Peripheral Hospitals Skin OPD: A Study of 2550 Patients. Indian J Dermatol 2007;52(2):93-95 9. RGB Langley, GG Krueger, CEM Griffiths. Psoriasis: epidemiology, clinical features and quality of life. Ann Rheum Dis 2005;64(suppl II):18-23 10. Moorchung N, Khullar JS, Mani NS, Chatterjee M, Vasudevan B, Tripathi T. A study of various histopathological features and their relevance in pathogenesis of psoriasis. Indian J Dermatol 2013;58:294-8 11. Katta R. Lichen Planus. Am Fam Physician 2000;61(11):3319-28 12. Silverman S Jr, Gorsky M, Lozada-Nur F. A prospective follow-up study of 570 patients with oral lichen planus: persistence, remission and malignant association. Oral Surg Oral Med Oral Pathol.1985;60:30-4 13. Fernandez-Gonzalez F, Vazquez-Alvarez R, Reboiras-Lopez D, Gandara-Vila P, Garcia-Garcia A, Gandara-Rey JM. Histopathological findings in oral lichen planus and their correlation with the clinical manifestations. Med Oral Patol Oral Cir Bucal 2011;16(5):641-6 14. Ismail SB, Kumar SK, Zain RB. Oral lichen planus and lichenoidreactions:etiopathogenesis, diagnosis, management and malignant transformation. J Oral Sci 2007;49:89-106 15. Bagan-Sebastian JV, Milian-Masanet MA, Penorrocha-Diago M, Jimenez Y. A clinical study of 205 patients with oral lichen planus. J Oral MaxillofacSurg 1992;50:116-8 16. Eisen D, Carrozo M, Bagan Sebastian JV, Thongprasom K. Number V Oral Lichen Planus: clinical features and management. Oral Dis 2005;11:338-49 17. CemAygun, OrhanKocaman, YesimGurbuz, Altay Celebi, Omer Senturk, SadettinHulagu. Erythema AnnulareCentrifugum:A Rare Skin Finding of Autoimmune Hepatitis. Gastroenterology Research 2010;3(2):96-98 18. Von den Driesch P. Sweet syndrome: Acute febrile neutrophilicdermatosis. J Am AcadDermatol 1994;31:535-56 19. Nischal KC, Khopkar U. An approachto the iagnosisofneutrophilicdermatoses:Ahistopathological perspective. Indian J Dermatol Venereol Leprol 2007;73:222-30 20. Lisa M. Kroonen. Erythema Multiforme: Case Report and Discussion. JABFP 1998;11(1):63-65 21. Fabbri P, Panconesi E. Erythema multiforme(minus and maius) and drug intake. ClinDermatol 1993;11:479-489 22. Massimiliano Scalvenzi, Franco Palmisano, Maria Carmela Annunziata, Ernesto Meza, Immacolata Cozzolino, Claudia Costa. Subcornea lPustular Dermatosis in Childhood: A Case Report and Review of Literature. Case reports in Dermatological Medicine 2013. Article id 424797(http://dx.doi.org/10.1155/2013/424797) 23. ValentinaDimitrova, IvelinaYordanova, Dimitar Gospodinov Department. GeneralisedMorphea: A Case Report. J of IMAB 2007;13(1):68-70 (doi:10.5272/jimab.2007131.64) 24. I. Kolm, N. Eggmann, J. Kamarashev, K. Kerl, L.E. French, G.F.L. Hofbauer. Lichenoid Drug Eruption following Intravenous Application of orally Formulated Diamorphine, a semi-synthetic heroine. Case Report Dermatol2013;5:176-180 (DOI:10.1159/000353305) 25. Billet A, Viseux V, Chaby G, Dascotte-Barbeau E, Gontier MF, Denoeux JP, Lok C. Perforating granuloma annulare with transfollicular perforation. Ann DermatolVenereol 2005;132(8-9):678-81 26. RajatKandhari, V Ramesh, Avninder Singh. A Generalised,Non Pruritic Variant of Lichen Amyloidosis: A case Report and a Brief Review.Indian J Dermatol 2013;58(4):328 (doi: 10.4103/0019-5154.113995) 27. Weslermark P, Ridderström E, Vahlqulsl A. Macular posterior pigmentary incontinence; its relation to macular amyloidosus and nostalgia paresthetica. Acta Derm Venereol. 1996; 76:302–4. [PubMed] 28. Chang YT, Wong CK, Chow KC, Tsai CH. Apoptosis in primary cutaneous amyloidosis. Br J Dermatol. 1999; 140:210–5. [PubMed] 29. A. Mert, H. Kumbasar, R. Ozaras, S. Erten, L. Tasli, F. Tabak, R. Ozturk. Erythema nodosum: an evaluation of 100 cases. Clinical and Experimental Rheumatology 2007; 25: 563-570 30. Taralakshmi VV, Pankayalakshmi VV, Arumugam S, Subramanian S. Mycetoma caused by Madurellamycetomii in Madras. Aust J Dermatol. 1978; 19:125–9. [PubMed] 31. UsmaIftikhar, Muhammad Nadeem, ShahbazAman, AtifHasnainKazmi. Scrofuloderma:A common type of cutaneous tuberculosis.A case report. Journal of Pakistan Association of Dermatologists2011;21:61-65 32. Joshi R. Clues to histopathological diagnosis of treated leprosy. Indian J Dermatol. 2011 Sep-Oct; 56(5): 505–509 33. Revankar SG. Dematiaceous fungi. Mycoses 2007; 50:91-101. 34. Sharma NL, Mahajan V, Sharma RC, Sharma A. Subcutaneous pheohyphomycosis in India--a case report and review. Int J Dermatol 2002; 41:16-20. 35. Pradhan SV, Talwar OP, Ghosh A, Swami RM, KC Shiva Raj, Gupta S. Chromoblasomycosis in Nepal: A study of 13 cases. Indian J DermatolVenereolLeprol 2007; 73:176-8 36. JA Aviles Izquierdo, D.Velazquez – Tarjuelo, M. Lecona-Echevarria, P Lazaro-Ochaita. Dermoscopic features of Eccrineporoma. Actas Dermosifiliogr 2009;100:133-6 37. NemotoI,AkiyamaN,AoyagiS,NomuraT,Shimizu H. Eccrineporocarcinoma and eccrineporoma arising in a scar. Br J Dermatol 2004; 150:1232-3 38. RR Joshi, a Nepal, A Ghimire, SKarki. Eccrineporoma in neck of a child- a rare presentation. Nepal Med Coll J2009; 11(1):73-74
Kuljit Kaur, R. D. Shrivastav, Veena Rahatgaonkar, U. T. Bhosale
Aim: To Study the fetal and maternal outcome in patients with eclampsia. Background: In modern Obstetrics, the prevalence of eclampsia and its complication is high, so we decided to study pregnancy outcome in all eclampsia patients. Methodology: A Retrospective study carried out in department of Obstetrics and Gynecology in Bharati Medical College and Hospital, Sangli. Cases of eclampsia from May 2008 to May 2012 included in study. Analysis done regarding age of women, parity , gestational age, number of convulsion, time of convulsion, mode of delivery and fetal outcome. Results: 84.6% patients are primigravidas.88.4% came with antepartum eclampsia. Only 15.3% patients had postpartum eclampsia. Fetal outcome being intrauterine death in 46.1 % and preterm delivery in 26.9 %. Conclusion: Our observation states Antepartum eclampsia is more common in primigravidas between age group 20-25 years. With gestational age between 24-28 weeks and 32 to 36 weeks with poor fetal and maternal outcome. In our study we found all cases were unbooked and not received Antenatal care indicating the failure of adequate health care delivery in rural areas of western Maharashtra. Fetal outcome is better in patients with early intervention by lower segment caesarean section.
1. Tuffnell DJ, Jankowisz D, Lindow SW, Lyons G, Mason GC, Rusell LF, Walker JJ 2005. Outcomes of severe pre-eclampsia / eclampsia in Yorkshire 1999/2003 BJOG: An International Journal of Obstetrics and Gynaecology 112: 875-880. 2. Ikechebelu et al JI, Okoli CC 2002. Review of eclampsia at the Nnamdi Azikiwe University Teaching Hospital, Nnewi. (January1996-December 2000) Journal of Obstetrics and Gynaecology 22:287-280. 3. Mattar, F, Sibai BM. Eclampsia. VIII. Risk Factors for maternal morbidity. Am J Obstet Gynecol. 1990; 163:1049-55. 4. Konje JC, Obisesan KA, Odukoya OA et al. Presentation and management of eclampsia. Int J Gynecol Obstet. 1992; 38:31-5. 5. Swain S, Ojha KN. Maternal and perinatal mortality due to eclampsia. Indian Pediatr. 1993; 30(6):771-3. 6. The WHO Application of ICD-10 to deaths during pregnancy, childbirth and the puerperium: ICD-MM.2013; p13. 7. Chesley LC. Hypertensive disorders in pregnancy. Newyork: Appleteon Centuary Crofts 1978:p2. 8. Chhabra S, Kakani A. Maternal mortality due to eclamptic and non-eclamptic hypertensive disorders: a challenge. J Obstet Gynaecol. 2007; 27(1):25-9. 9. Choudhary P. Eclampsia: a hospital based retrospective study. Kathmandu Univ Med J (KUMJ). 2003; 1(4):237-41. 10. Sibai BM, Abdella TN, Spinnato JA, Anderson GD. Eclampsia. V. The incidence of nonpreventable eclampsia. Am J Obstet Gynecol. 1986; 154(3):581-6. 11. MacKay AP, Berg CJ, Atrash HK. Pregnancy-related mortality from preeclampsia and eclampsia. Obstet Gynecol. 2001; 97(4):533-8. 12. Urassa D, Carlstedt A, Nystrom L, Msamanga G. Management of hypertension in pregnancy as aquality indicator of antenatal care in rural Tanzania. Afr J Reproductive Health. 2003; 7:69-76. 13. Moodley J. Maternal deaths associated with hypertensive disorders of pregnancy: a population-based study. hypertension in pregnancy. 2005; 23(3):247-56. 14. Sibai BM. Diagnosis, prevention, and management of eclampsia. Obstet Gynecol. 2005; 105(2):402-10. 15. Onuh SO, Aisien AO. Maternal and fetal outcome in eclamptic patients in Benin City, Nigeria. J Obstet Gynaecol. 2004; 24(7):765-8. 16. Noraihan MN, Sharda P, Jammal AB. Report of 50 cases of eclampsia. J Obstet Gynaecol Res. 2005; 31(4):302-9. 17. Urassa DP, Carlstedt A, Nystrom L, Massawe SN, Lindmark G. Eclampsia in Dar es Salaam, Tanzania -incidence, outcome, and the role of antenatal care. Acta Obstet Gynecol Scand. 2006; 85(5):571-8. 18. Sibai BM. Eclampsia. VI. Maternal-perinatal outcome in 254 consecutive cases. Am J Obstet Gynecol. 1990;163(3):1049-54; discussion 54-5.
V. R. Lokhande
Abstract: The case of a 30 years old male presenting with pain and swelling over the manubrium sternii with no constitutional symptoms is presented here. The patient was immunocompetent and found to have tuberculous affection of sternum with lung involvement as well based on imaging and histopathology. He was treated with anti tuberculous therapy for 9 months and responded well with complete resolution of the lesions. A one year follow up has revealed no recurrence so far. This case highlights the importance of rare presentations of TB in immunocompetent individuals.
1. Tuli SM. Tuberculosis of rare sites, girdle and flat bones. In: Tuli SM (ed). Tuberculosis of the Skeletal System. Bursal Sheaths. 2nd ed. Delhi: Jaypee Brothers Medical Publishers, 2000: 159-160. 2. Cherif E, Ben Hassine L, Boukhris I, Khalfallah N. Sternal tuberculosis in an immunocompetent adult. BMJ Case Rep. 2013 Apr 10; 2013. 3. Zhao X1, Chen S, Deanda A Jr, Kiev J. A rare presentation of tuberculosis. Am Surg. 2006 Jan; 72(1):96-7. 4. Watts RA, Paice EW, White AG. Spontaneous fracture of the sternum and sternal tuberculosis. Thorax 1987; 42: 984-985 5. McLellan DG1, Philips KB, Corbett CE, Bronze MS. Sternal osteomyelitis caused by mycobacterium tuberculosis: case report and review of the literature.Am J Med Sci. 2000 Apr; 319(4):250-4. 6. Shah J1, Patkar D, Parikh B, Parmar H, Varma R, Patankar T, Prasad S Tuberculosis of the sternum and clavicle: imaging findings in 15 patients Skeletal Radiol. 2000 Aug; 29(8):447-53. 7. A. Khali, C. Le Breton, M Tsart et al. Utility of CT scan for the diagnosis of chest wall tuberculosis Eur. Radiol. 9 ( 1638- 1642), 1999 8. WHO. Treatment of Tuberculosis guidelines. 4th Edition 2010.
Venukumar Lachmaya Rangu, Rupali Venukumar Rangu, Nitin Akhade
Abstract: Corneal transplantation remains a major treatment option for restoring sight among those suffering from corneal blindness. The number of corneal transplants done is far less than the actual requirement in India. This is largely due to the inadequate numbers of corneas collected. Medical students can be involved in the motivation of patients and relatives to pledge their eyes and to do grief counseling for donating eyes. The aim of the study was to assess the perception and willingness of 400 first-year medical students towards eye donation in Maharashtra. They were administered a pretested semi-structured questionnaire on eye donation. Data were analyzed using Epi-Info software package 6.04 version. The majority (99.6%) of students knew that eyes can be donated after death but only 40% knew that the ideal time of donation was within six hours of death. Most participants (83.5%) were willing to donate eyes, 89.5% students were aware that there is shortage of donated eyes in India. Nobility in the act of eye donation was the main motivational force for eye donation according to 86.2% of students. Perceived reasons for not pledging eyes by the people were: lack of awareness (31.8%), objection by family members (27.7%), unsuitability to donate because of health problem (16.6%) and the unacceptable idea to separate the eye from the body (15.1%). Mass media such as television, newspapers, magazines and posters were important sources of information on eye donation. Perceived reasons for not donating eyes need to be considered while creating awareness about eye donation in the community.
1. Krishnaiah S, Kovai V, Nutheti R, Shamanna BR, Thomas R, Rao GN. Awareness of eye donation in the rural population of India. Indian J Ophthalmol 2003; 52:73-8. 2. Dandona L, Dandona R, Naduvilath TJ, McCarty CA, Nanda A, Srinivas M, et al . Is current eye- care policy focus almost exclusively on cataract adequate to deal with blindness in India? Lancet 1998; 351:1312-6. 3. Rekhi GS, Kulshreshtha OP. Common causes of blindness: A pilot study in Jaipur, Rajasthan. Indian J Ophthamol 1991; 39:108-11. 4. Dandona L, Dandona R, Srinivas M, Giridhar P, Vilas K, Prasad MN, et al. Blindness in Indian state of Andhra Pradesh. Invest Ophthalmol Vis Sci 2001; 42:908-16. 5. Dandona L, Dandona R, John RK. Estimation of blindness in India from 2000 through 2020: Implications for the blindness control policy. Natl Med J India 2001; 14:327-34. 6. Ministry of Health and Family Welfare, Government of India. Eye care services - eye banking. [Cited on 2006 Oct 13]. Available from: http:/mohfw.nic.in.b/index.html#vision. 7. Bardell T, Hunter DJ, Kent WD, Jain MK. Do medical students have the knowledge needed to maximize organ donation rates? Can J Surg 2003; 46:453-7. 8. Kannan KA. Eye donation movement in India. J Indian Med Assoc 1999; 97:318-9. 9. Priyadarshan B, Srinivasan M, Padmavathi A, Selvam R, Nirmalan PK. Awareness of eye donation in an adult population of southern India. A pilot study. Indian J Ophthalmol 2003; 51:101-4. 10. Singh P, Kumar A, Pandey CM, Chandra H. Level of awareness about transplantation, brain death and cadaveric organ donation in hospital staff in India. Prog Transplant 2002; 12:289-92. 11. Golchet G, Carr J, Harris MG. Why don't we have enough cornea donors? A literature review and survey. Optometry 2000; 71: 318-28. 12. Dandona R, Dandona L, Naduvilath TJ, McCarty CA, Rao GN. Awareness of eye donation in an urban population in India. Aust NZ J Ophthalmol 1999; 27:166-9. 13. Tandon R, Verma K, Vanathi M, Pandey RM, Vajpayee RB. Factors affecting eye donation from post-mortem cases in a tertiary care hospital. Cornea 2004; 23:597-601. 14. Phadke KD, Anandh U. Ethics of paid organ donation. Pediatr Nephrol 2002; 17:309-11.
Venkateshwarlu Nandyala, Gandiah P., Govind Das, Harish Kumar J., P Anand G. Reddy, Sandeep Kumar G
Abstract: Thirty cases of SJS-TEN were reported during a seven year period between 01-01-2007 and 31-12-2013 were analysed. Eighteen were males, anti-epileptics were the culprits in 11 cases (Phenytoin sodium was responsible in 6, carbamazepine in 4 while sodium valproate was responsible in 1 case. Ofloxacin was responsible in 4 ciprofloxacin and cefixime in one each case whereas another 8 cases it was NSAIDs. Two ayurvedic medications were also noted in our study. 12 patients received 3 days therapy of pulse dose dexamethasone therapy, 6 patients received pulse dose Methyl Prednisolone 7 patients received regular dexamethasone treatment while remaining 5 did not get any steroid. All cases received supportive therapy, barrier nursing and prophylactic antibiotics. Cases who received Pulse dose steroid treatment recovered fast and hospital stay was reduced, while two patients in non-steroid group died and remaining 3 recovered very slowly. Short term (3 days) pulse steroid therapy is well tolerated and recovery is very fast as compared to regular steroid therapy or therapy without steroid. However as the sample size is small we recommend a large study preferably a double blind study.
1. Sharma VK, Sethuraman G, Minz A. Stevens Johnson syndrome, toxic epidermal necrolysis and SJS-TEN overlap: A retrospective study of causative drugs and clinical outcome. Indian J Dermatol Venereol Leprol 2008; 74: 238-40. 2. Sharma VK, Sethuraman G. Adverse cutaneous reactions to drugs: An overview. J Postgrad Med 1996; 42: 15-22. 3. Roujeau JC, Kelly JP, Naidi L et al. Medication use and the risk of Stevens - Johnson syndrome or toxic epidermal necrolysis. N Engl J Med 1995; 333: 1600-7. 4. Lyell A: Toxic epidermal necrolysis: an eruption resembling scalding of the skin. Br J Dermatol 1956, 68:355-361. 5. Bastuji-Garin S, Rzany B, Stern RS, Shear NH, Naldi L, Roujeau JC. Clinical classification of cases of toxic epidermal necrolysis, Stevens-Johnson syndrome, and erythema multiforme. Arch Dermatol 1993; 129: 92-6. 6. Roujeau JC. The spectrum of Stevens-Johnson syndrome and toxic epidermal necrolysis: A clinical classification. J Invest Dermatol 1994; 102: 28S-30. 7. Li LF, Ma C. Epidemiological study of severe cutaneous adverse drug reactions in a city district in China. Clin Exp Dermatol 2006; 31: 642-7. 8. Borchers AT, Lee JL, Naguwa SM, Cheema GS, Gershwin ME. Stevens-Johnson syndrome and toxic epidermal necrolysis. Autoimmun Rev 2008; 7: 598-605. 9. Khambaty MM, Hsu SS. Dermatology of the patient with HIV. Emerg Med Clin North Am 2010; 28: 355-68. 10. Garcia-Doval I, LeCleach L, Bocquet H, Otero XL, Roujeau JC. Toxic epidermal necrolysis and Stevens-Johnson syndrome: Does early withdrawal of causative drugs decrease the risk of death? Arch Dermatol 2000; 136: 323-7. 11. Bastuji-Garin S, Fouchard N, Bertocchi M, Roujeau JC, Revuz J, Wolkenstein P. SCORTEN: a severity-of-illness score for toxic epidermal necrolysis. J Invest Dermatol 2000; 115: 149–153. 12. Yetiv JZ, Bianchine JR, Owen JA Jr. Etiologic factors of the Stevens-Johnson syndrome. South Med J 1980; 73: 599-602. 13. Stern RS, Chan HL. Usefulness of case report literature in determining drugs responsible for toxic epidermal necrolysis. J Am Acad Dermatol 1989; 21: 317-22. 14. Ruiz-Maldonado R. Acute disseminated epidermal necrosis types 1, 2, and 3: study of sixty cases. J Am Acad Dermatol 1985; 13: 623-35. 15. Gui llaume J-C, Roujeau J-C, Revuz J, Penso D, Touraine R. The culprit drugs in 87 cases of toxic epidermal necrolysis (Lyell’s syndrome). Arch Dermatol 1987; 123: 1166-70. 16. R oujeau J-C, Guillaume J-C, Fabre J-P, Penso D, Flechet ML, Girre JP. Toxic epidermal necrolysis (Lyell syndrome): incidence and drug etiology in France, 1981–1985. Arch Dermatol 1990; 126: 37-42. 17. Schöpf E, Stühmer A, Rzany B, Victor N, Zentgraf R, Kapp JF. Toxic epidermal necrolysis and Stevens-Johnson syndrome: an epidemiologic study from West Germany. Arch Dermatol 1991; 127: 839-42. 18. C orreia O, Chosidow O, Saiag P, Bastuji-Garin S, Revuz J, Roujeau J-C.Evolving pattern of drug-induced toxic epidermal necrolysis. Dermatology 1993; 186: 32-7. 19. C han HL, Stern RS, Arndt KA, et al. The incidence of erythema multiforme, Stevens-Johnson syndrome, and toxic epidermal necrolysis: a population- based study with particular reference to reactions caused by drugs among outpatients. Arch Dermatol 1990; 126:43-7 20. Barvaliya M, Sanmukhani J, Patel T, Paliwal N, Shah H, Tripathi C. Drug-induced Stevens-Johnson syndrome (SJS), toxic epidermal necrolysis (TEN), and SJSTEN overlap: A multicentric retrospective study. J Postgrad Med 2011; 57: 115-9. 21. Naveen KN, Pai VV, Rai V, Athanikar SB. Retrospective analysis of Steven Johnson syndrome and toxic epidermal necrolysis over a period of 5 years from northern Karnataka, India. Indian J Pharmacol 2013; 45: 80-2. 22. Saka B, Kombaté K, Mouhari‑Toure A, Akakpo S, Tchangai‑Walla K, Pitché P. Stevens‑Johnson syndrome and toxic epidermal necrolysis in a teaching hospital in Lomé, Togo: Retrospective study of 89 cases. Med Trop (Mars) 2010; 70: 255‑8. 23. Kannenberg SM, Jordaan HF, Koegelenberg CF, Von Groote‑Bidlingmaier F, Visser WI. Toxic epidermal necrolysis and Stevens‑Johnson syndrome in South Africa: A 3‑year prospective study. QJM 2012; 105: 839‑46. 24. Fagot JP, Mockenhaupt M, Bouwes‑Bavinck JN, Naldi L, Viboud C, Roujeau JC, et al. Nevirapine and the risk of Stevens‑Johnson syndrome or toxic epidermal necrolysis. AIDS 2001; 15: 1843‑8. 25. Rzany B, Mockenhaupt M, Stocker U, Hamouda O, Schöpf E. Incidence of Stevens‑Johnson syndrome and toxic epidermal necrolysis in patients with the acquired immunodeficiency syndrome in Germany. Arch Dermatol 1993; 129: 1059. 26. Tejas K. Patel, Manish J. Barvaliya1, Dineshchandra Sharma, Chandrabhanu Tripathi1 Systematic review of Stevens‑Johnson syndrome and toxic epidermal necrolysis; Indian Journal of Dermatology, Venereology, and Leprology | May-June 2013 | Vol 79 | Issue 3; 389-398 27. Thomas Harr, Lars E French Toxic epidermal necrolysis and Stevens-Johnson Syndrome Orphanet Journal of Rare Diseases 2010, 5:39 28. Brown KM, Silver GM, Halerz M, Walaszek P, Sandroni A, Gamelli RL. Toxic epidermal necrolysis: does immunoglobulin make a difference? J Burn Care Rehabil 2004; 25: 81–88. 29. Halebian PH, Corder VJ, Madden MR, Finklestein JL, Shires GT. Improved burn center survival of patients with toxic epidermal necrolysis managed without corticosteroids. Ann Surg 1986; 204: 512–513. 30. Fine JD. Management of acquired bullous skin diseases (correspondence). N Engl J Med 1996; 334: 864–865. 31. Chave TA, Mortimer NJ, Sladden MJ, Hall AP, Hutchinson PE. Toxic epidermal necrolysis: current evidence, practical management and future directions. Br J Dermatol 2005; 153: 241–253. 32. Nesbitt LT. Minimizing complications from systemic glucocorticosteroid use. Dermatologic Clinics 1995; 13: 925–939. 33. Guibal F, Bastuji-Garin S, Chosidow O, Saiag P, Revuz J, Roujeau JC. Characteristics of toxic epidermal necrolysis in patients undergoing long-term glucocorticoid therapy. Arch Dermatol 1995; 131: 669–672. 34. Rasmussen JE. Update on the Stevens-Johnson syndrome. Cleve Clin J Med 1988; 55: 412–414. 35. Nesbitt LT. Minimizing complications from systemic glucocorticosteroid use. Dermatologic Clinics 1995; 13: 925–939. 36. Sherertz EF, Jegasothy BV, Lazarus GS. Phenytoin hypersensitivity reaction presenting with toxic epidermal necrolysis and severe hepatitis. J Am Acad Dermatol 1985; 12: 178–181. 37. Barman KD, Verma KK, Agrawal S, Agarwalla A, Rijal A. Stevens-Johnson syndrome with idiopathic thrombocytopenic purpura treated with dexamethasone pulse therapy. J Dermatol 2003; 30: 54–58.
Jaykar R.D., Jadhav S.C., Agrawal S.G
Background: The frequency of pancreatic fistulas is low. Only 0.4% of patients develop this complication after an acute episode. However, the incidence of these complications increases in patients with other complications after acute pancreatitis—4.5% in patients with pancreatic pseudocysts (4.5%) and 40% in patients with infected necrosis after surgical debridement. Treatment is conservative for most patients.1 Case: We report a case of Spontaneous Pancreatico-cutaneous (Pancreatico-umbilical) Fistula in a 30 year male complaining of pain in abdomen in epigastrium, lump in abdomen and spontaneous discharge of pus from umbilicus followed by disappearance of lump. Patient was known case of Acute Pancreatitis with pseudocyst formation since 4 months. Abdominal ultrasound contrast CT scan abdomen revealed. “Severe acute pancreatitis with focal necrosis in tail region with multiple peripancreatic collection. Multiple organised intra-abdominal infective collection. Organised collection in anterior abdominal wall with sinus tract formation in umbilical region”. Review CT scan abdomen with Fistulogram revealed “Small fistulous tract in midline extending from umbilicus and communicating with peritoneal cavity”. The patient was treated conservatively with higher antibiotics and patient recovered uneventfully and discharged.
1. Eric H. Jensen, Daniel Borja-Cacho, Waddah B. Al Refaie and Selwyn M. Vickers. Exocrine Pancreas. In: Townsend, Beauchamp, Evers, Mattox, Editors. Sabiston Text book of surgery: The Biological Basis of Modern Surgical Practice. 19th Ed; Saunders an Imprint of Elsevier; 2012. 56, P.1526. 2. William E. Fisher, et al. Pancreas. In: Charles Brunicardi, Dana K. Anderson… [et al.]. Editors. Schwartz’s Principles of surgery: 9th Ed; The McGraw-Hill Companies; 2010. 33, P. 1167-1245. 3. John A. Windsor, Benjamin P.T. Loveday. Complications of Acute Pancreatitis (including pseudocyst) In: Michael J. Zinner, Stanley W. Ashley. Editors. Maingots abdominal operations: 12th Ed; The McGraw-Hill Companies; 2013. 55, P. 1123. 4. Satyajit Bhattacharya. The Pancreas. In: Norman S. Williams, Christopher J.K. Bulstrode, P Ronan O'connell, Editors. Bailey and Love’s Short Practice of Surgery. 26th Ed. CRC press; 2013. 68, P.1126. 5. Roger Saadia, M.D. Fistulas of the pancreas. In: Holzheimer RG, Mannick JA, Editors. Surgical Treatment: Evidence-Based and Problem-Oriented; Munich: Zuckschwerdt; 2001. Part VIII. 6. Boerma D, Rauws EA, van Gulik TM, Huibregtse K, Obertop H, Gouma DJ.: Endoscopic stent placement for pancreaticocutaneous fistula after surgical drainage of the pancreas. Br J Surg. 2000 Nov; 87(11):1506-9.
Venkateshwarlu Nandyala, Gandiah P., Indira G., Anand Gopal Reddy P.
Abstract: Tropical pulmonary eosinophilia is one of the many pulmonary infiltrates with eosinophilia. We are presenting a case with features of lung abscess in left lung field. The diagnosis was suspected and proved retrospectively after successful treatment with diethyl carbamazine (DEC). There was an elevation of gamma-glutaryl transpeptidase levels in our case, which may have a role in pulmonary infiltrates in tropical eosinophilia.
1. Ottesen EA, Nutman TB (1992): Tropical pulmonary eosinophilia Annu Rev Med. 1992; 43:417. . Pub Med 2. Vijayan VK (2007): Tropical pulmonary eosinophilia: pathogenesis, diagnosis and management; Curr Opin Pulm Med. 2007 Sep; 13(5):428-33. 3. Ong RKC, Doyle RL (1998) Tropical pulmonary eosinophilia. Chest 1998; 113:1673–9. 4. Andrea K. Boggild, Jay S. Keystone, and Kevin C. Kain (2004) Tropical Pulmonary Eosinophilia: A Case Series in a Setting of Nonendemicity Clinical Infectious Diseases 2004; 39:1123–8 5. Obaray A, Khan F, Azueta V, et al.(1982): Tropical eosinophilia presenting as acute bronchial asthma: case report with clinical, physiologic, and histologic features before and after treatment. Heart Lung 1982; 11:464–8. 6. Jiva TM, Israel RH, Poe RH.(1996): Tropical pulmonary eosinophilia masquerading as acute bronchial asthma. Respiration 1996; 63:55–8. 7. Jones DA, Pillai DK, Rathbone BJ, et al (1983) Persisting “asthma” in tropical pulmonary eosinophilia. Thorax 1983; 38:692–3. 8. Frimodt-Moller C, Barton RM. A pseudo-tuberculosis condition associated with eosinophilia. Indian Med Gaz 1940; 75: 607-13. 9. Rom WN, Vijayan VK, Cornelius MJ, et al.(1990) Persistent lower respiratory tract inflammation associated with interstitial lung disease in patients with tropical pulmonary eosinophilia following conventional treatment with diethylcarbamazine. Ann Rev Respir Dis 1990; 142:1088–92.
D. B. Katikar, R. D. Jaykar, Mahendra Kamble, Sumeet
Background: Meningocele is sac protruding from the spinal column, Myelomeningocele is most severe type of spina bifida, which is commonly encountered by surgeon in new born due to failure of caudal neurulation. The incidence of meningocele is 0.2-2/1000 live births, and 15-25% of neonates with myelomeningocele have hydrocephalus at birth. Hence required significant amount of medical intervention, about 80-90% of them need shunt procedure. Methods: For all patients evaluation plan was as follows: Detail clinical history followed by thorough clinical examination. Investigations: Routine laboratory investigation required for pre anesthetic checkup such as Hemogram, Blood sugar level, Serum electrolytes, Blood urea level, Serum creatinine, Serum bilirubin; Ultrasonography (local, abdomen and pelvis, cranium); CT scan head. Consent: A written informed consent for surgery as per the risk was obtained from parents of patients. Pre-Operative Treatment: One dose of pre-operative antibiotic i.v Ceftriaxone 100mg/kg before operation. Anaesthesia: General anaesthesia Procedure: a) Low pressure V.P Shunt was used. b) Skin closure with 2-0 Nylon in both the procedures. Post-operative Treatment: All the patients from both the study groups were given- Antibiotics - I.V Ceftriaxone 100mg/kg x 5 days I.V Amikacin 15mg/kg x 5 days Local care -dressing on day 3, 5 and on wards if required Postoperative: Each patient’s operative time requirement for both study groups was recorded. The operative time was considered as the time from skin incision to the application of dressing. Patients were discharged after the operation as per their comfort and instructed to follow up on for suture removal. Patients were followed up at every week for two week, then on fourth week, eighth week and three months after discharge on outpatient department basis. Problems expected during postoperative period were: 1. Local wound infection. 2. Non healing of the wound. 3. Dehiscence of the wound. 4. Meningitis. 5. Ventriculitis. 6. Shunt failure. Local infection leading to septicaemia: In our comparative study, we had compared 40 patients of meningocele with hydrocephalus operated in one stage group and in two stage group. All patients were infants with age less than seven days. The meningocele sac was more commonly situated in lumbosacral region in our study groups. Our average operative time for single stage group was 105 min and average operative time for two stage group was 135 mins. The average hospital stay for single stage group was 10 days and two stage group was 22 days. We had two mortalities in our study, one each for both groups. Both the children developed septicemia and meningitis in spite of aggressive antibiotics treatment, they succumbed. We had complications like fever, local wound dehiscence and cerebrospinal fluid leak, none of which were life threading and all got corrected with appropriate treatment. The incidence in both group was almost similar. Both the procedure appeared to be equally safe and the complication rates were similar. The operative timing and hospital stay was less in one stage procedure which makes it economical and emotional burden lessens for the patients family. If the child appears to be fit and undergoes one stage procedure, it appears to be safe economical and without additional complication. Conclusion: Our comparative study revealed as 1. Mean operative time was less in one stage procedure than two stage procedure. 2. Hospital stay in one stage procedure was less than two stage procedure. 3. Complications rate in both the group were comparable. 4. One stage procedure enhanced flap survival and prevented CSF leakage. 5. It can be safely done, 6. It is economical and shortens hospital stay. 7. It avoided need for second aneasthetic administration. 8. It leads to reduction in hospital burden and patient morbidity. 9. Complication such as CSF leakage, wound dehiscence and shunt infection were comparable. Children who are having meningocele and hydrocephalus can be operated by either one stage procedure or two stage procedure. Both the procedures appear to be equally safe and the complication rate was similar. The operative timing and hospital stay was less in one stay procedure which makes economical and emotional burdens less for the patient’s family. If the child appears to be fit, and undergoes one stage procedure, it appears to be safe, economical and without additional complication. A bigger sample size would be needed to validate their finding. Simultaneous surgery had the advantages of exposing these children to ones rather than twice for anaesthesia.
1. Leach J, Kerr R, William N, Bulstrode C, O’ Conell P. 2008 in Baily and Love’ short Practice of Surgery. 25th ed., Edward Arnold, UK: 625. 2. Gocer AI, Tuna M, Gezercan Y, et al. Multiple anterolateral cervical meningoceles associated with neurofibromatosis. Neurosurg Rev 22:124-126, 1999. 3. Salomao JF. Cervical meningocele in association with spinal abnormalities. Childs Nerv Syst 21:4-5; author reply 6, 2005 4. McLone DG, Dias L, Kaplan WE, Sommers MW. Concepts in the management of spina bifida. Concepts Pediatr Neurosurg 1985; 5:97-105. 5. Lorber J. Systematic ventriculographic studies in infants born with meningomyelocele and encephalocele. The incidence and development of hydrocephalus. Arch Dis Child 1961; 36:381-9. 6. Stein SC, Schut L. Hydrocephalus in meningomyelocele. Childs Brain 1979:5:413-9. 7. Francis W, Gamache, Jr. Treatment of hydrocephalus in patients with Meningomyelocele or encephalocele : a recent series. Child's Nerv Syst (1995) 11:487 - 488. 8. Park TS: Mylomeningocele In: Albright AL, Pollack F, Adelson PD (eds). Principles and practice of padiatric neurosurgery. Thieme, New York: 1999: 291 -321. 9. 13 14 J Pediatr Neurosci. 2011 October; 6(Suppl1): S11–S22. 10. Drake JM, Sainte-Rose C: The Shunt Book. Cambridge, MA: Blackwell Science, 1995, pp 3-12. 11. Fisher RG: Surgery of the congenital anomalies, in Walker AE (ed): A History of Neurological Surgery. Baltimore: Williams and Wilkins, 1951, pp 334-347. 12. Al-Rodhan NR, Fox JL: Al-Zahrawi and Arabian neurosurgery, 936-1013 AD. Surg Neurol 26:92-95, 1986. 13. Vesalius A: De Humani Corporis Fabrica Librorum Epitome. Basileae: Joannis Oporini, 1543 47. Walker ML, MacDonald J, Wright LC: The history of ventriculoscopy: where do we go from here? Pediatr Neurosurg 18: 218-223, 1992. 14. Drake JM, Sainte-Rose C: The Shunt Book. Cambridge, MA: Blackwell Science, 1995, pp 3-12. 15. Milhorat, TH: Hydrocephalus: historical notes, etiology and clinical diagnosis, in McLauren RL (ed): Pediatric Neuro-surgery. New York: Grune and Stratton, 1984, pp 197-210. 16. Roth PA, Cohen AR: Management of hydrocephalus in infants and children, in Tindall GT, Cooper PR, Barrow DL (eds): The Practice of Neurosurgery. Baltimore: Williams and Wilkins, 1996, Vol 3, pp 2707-2711. 17. West C: Lectures on the Diseases of Infancy and Childhood. London: Longman, 1848. 18. Willis T: Cerebri Anatomie. Londini: Roycroft, 1664. 19. Mccullough DC: History of the treatment of hydrocephalus, in Scott MR (ed): Hydrocephalus. Baltimore: Williams and Wilkins, 1990, Vol 3, pp 1-10. 20. Milhorat, TH: Hydrocephalus: historical notes, etiology and clinical diagnosis, in McLauren RL (ed): Pediatric Neuro-surgery. New York: Grune and Stratton, 1984, pp 197-210. 21. Key A, Retzius G: Studien in der Anatomie des Nervensystems und des Bindegewebes. Stockholm: Samson and Wallin, 1875-76. 22. Weed, LH: Certain anatomical and physiological aspects of the meninges and cerebrospinal fluid. Brain 58:383-397, 1935. 23. Sato H, Matsumoto S: Hydrocephalus: Historical review, in Matsumoto S, Tamaki N (eds): Hydrocephalus: Pathogenesis and Treatment. Tokyo: Springer-Verlag, 1991, pp 3-6. 24. Putnam T: Surgical treatment of infantile hydrocephalus. Surg Gynecol Obstet 76:171-182, 1943. 25. Keen WW: Surgery of the Lateral Ventricles. Verhandl d Xinternat Med Kngr III Chir: 108, 1891. 26. Davidoff LE: Treatment of hydrocephalus. Arch Surg 18: 1737-1762, 1929. 27. Anton G, von Bramann F: Balkenstich bei Hydrozephalien, Tumoren und bei Epilepsie. Munchen Med Wchnschr 55: 1673-1677, 1908 28. Parkin A: The treatment of chronic hydrocephalus by basal drainage. Lancet 2:1244, 1893. 29. Glynn TJ: Case of hydrocephalus: trephining: opening of fourth ventricle: recovery. Lancet 2:1106, 1895. 30. Payr E: Drainage der Hirnventrikel Mittelst frei Transplantirter Blutgefasse; Bemerkungen ueber Hydrocephalus. Arch Klin Chir 87:801-885, 1908. 31. Kausch W: Die Behandlung des Hydrocephalus der Cleinen Kinder. Arch Klin Chir 87:709-796, 1908. 32. Heile B: Zur Behandling des Hydrocephalus. Dtsche Med Wchnschr 24:1468-1470, 1908. 33. Putnam T: Surgical treatment of infantile hydrocephalus. Surg Gynecol Obstet 76:171-182, 1943. 34. Scarff JE: Nonobstructive hydrocephalus. Treatment by endo-scopic cauterization of the choroid plexuses. Am J Dis Child 63:297-334, 1942. 35. Dandy WE: An operative procedure for hydrocephalus. Bull Johns Hopkins Hosp 33:189, 192. 36. Stookey B, Scarff J: Occlusion of the aqueduct of sylvius by neoplastic and non-2neoplastic processes with a rational surgical treatment for relief of the resultant obstructive hy drocephalus. Bull Neurol Inst NY 5:348-377, 1936. 37. Torkildsen A: A new palliative operation in cases of inoperable occlusion of the sylvian aqueduct. Acta Chir Scand 82: 117-125, 1939. 38. Matson DD: Current treatment of hydrocephalus. N Engl J Med 255:933-936, 1956. 39. Matson DD: A new operation for the treatment of communicating hydrocephalus: report of a case secondary to generalized meningitis. J Neurosurg 6:238-247, 1949. 40. Pudenz RH: The surgical treatment of hydrocephalus, in Fields WS (ed): Disorders of the Developing Nervous System. Springfield, IL: Thomas, 1961, pp 468-489. 41. Pudenz RH, Russell FE, Hurd AH, et al: Ventriculo-auriculostomy. A technique for shunting cerebrospinal fluid into the right auricle. Preliminary report. J Neurosurg 14:171-179, 1957. 42. Ames RH: Ventriculo-peritoneal shunts in the management of hydrocephalus. J Neurosurg 27:525-529, 1967. 43. Raimondi AJ, Matsumoto S: A simplified technique for performing the ventriculoperitoneal shunt. Technical note. J Neurosurg 26:357-360, 1967. 44. Miles, M.. Children with spina bifida and hydrocephalus in Africa: can medical, family and community resources improve the life chances?Disability and Society 2006-09; 17: 643-658. 45. Dahlgren, Ryan M.; Baron, Eli M.; and Vaccaro, Alexander R., "Pathophysiology, diagnosis, and treatment of spinal meningoceles and arachnoid cysts" (2007). Department of Orthopaedic Surgery Faculty Papers. Paper 4 Spine Surgery, 18(3):148-153, 2006. 46. W. Bruce Cherny, MD Barrow Quarterly - Volume 16, No 4, 2000. 47. Hamid R, Philippa new filed. Pediatric neuroanestheisa phallusephalus. pediatric emergencies : Anesthesiology clincs of north america volume 19 : number 2 June 2001. 48. Bell WO, Arbit E, Fraser RA: one-stage meningomyelocele closure and ventriculpoperitoneal shunt placement, Surgery Neurology (1987)27:233-236. 49. Lorber J. Systematic ventrulographic studies in infants born with meningomyelocele and encephalocele. The incidence and development of hydrocephalus. Arch Dis Child 1961;36:381-9. 50. Ashish Wakhlu, Sunita Saxena, R.K. Tandon, Single stage Treatment of Spina Bifida with hydrocephalus based on a Prediction Rule Derived from preoperative Cranial Ultrasound, Pediatr Nerosurg 2009, 45:271. 51. Huballah MY, Hofman HJ: early repair of Meningomyelocele and simultaneously insertion of VP Shunt technique and result, Neurosurgery 1987 20; 21, 23. 52. Shandip K Sinha Anjan Dhua, Mohit Kumar Mathurm Sudhir Singh, Manoj Modi, Simmi K Ratan. Neural tube defect repair and ventriculoperitoneal shunting: indications and outcome Journal of Neonatal Surgery volume 1 (2), Apr-Jun 2012. 53. IS Oktem, Menku A, Ozdemir A. when ventriculoperitoneal shunt placement should be performed in cases with myelomeningocele and hydrocephalus. Turkish Neurosurger 2008, Vol : 18, No.4, 387-391. 54. Parent AD, McMillan T: Contemporaneous shunting with repair of myelopmeningocle pediatr neurosurg 1995: 22:132-135. 55. Chadduck WM, Reding DL: Experience with simultaneous ventriculoperitoneal shunt and meningocele repair. J. Pediatr Surg 1988:23:913-916. 56. Machado HR, Santos de Oliviera R: Simultaneous repair of myelomeningocele and shunt insertion. Childs Nerv Syst 2004; 20:107-109. 57. Miller PD, Polack IF, Pang D: comparison of simultaneous versus delayed ventriculoperitoneal shunt insertion in children undergoing meningomyelocele repair. J. Child Neuro 1996; 11:370-372. 58. Epstein NE, Rosenthal AD, Zito J, Ospi of M: shunt placement and myelomeningocele repair: simultaneous versus sequential shunting review of 12 cases. Childs nerv syst 1985; 1:145-147. 59. Caldarelli M, Di Rocco C, La Marca F: Shunt complications in the first post operative year in children with meningomyelocele. Childs Nerv Syst 1996:12:748-754.
Sreejith M. G., Peter George
Background: Dengue fever (DF), is the most common mosquito borne arbo-viral infection in humans. The high mortality associated with DF mandates early diagnosis and therapeutic interventions. Aims: To study the utility of clinic-laboratory parameters in serologically diagnosed cases of DF and to correlate with serological tests with the progression of disease. Material and methods: This is are prospective study done among patients, admitted to a tertiary care facility in South India between 1rstMarch and 31rst August 2013, with the diagnosis of Dengue fever (DF) either by dengue NS1 or Ig-M positive test. Their clinical and laboratory parameters were compared for the diagnostic utility withthat of NS1 or Ig-M dengue tests in relation to the day of performing the tests. Results: 200 serologically diagnosed DF patients were evaluated with 145 positive for NSI antigen and 55 for Ig-M antibody. 114 patients were male and 86 females. Clinical features of fever with headache, body ache and myalgia were present in 90%, whereas retro-orbital pain in only 40 % of cases. High grade fever and headache were the most specific clinical feature(92%). Almost 94% of NS1 positive cases presented within 4 days of onset of fever. Among NS1 positive cases leucopoenia alone had a sensitivity of 55% and specificity 48% with PPV 73%. Thrombocytopenia had sensitivity 89% with PPV 70.45%. Anicteric hepatitis had sensitivity of 75% and specificity 40%. Combination of clinical features with 2 out of four laboratory parameters (high haematocrit, leucopenia, thrombocytopenia, anicteric hepatitis) increased sensitivity to 94%. The chances of developing complications were very less during the first 4 days (3%) and the sensitivity of NS1 was 0-40% after 5 days of symptom, but IGM was 70-100%. Conclusion: During the early stages of disease we observed the diagnostic efficacy of clinico-laboratory parameters is similar to NS1 antigen. In a developing country with limited resources, were DF is endemic the routine use of expensive serological investigations is questionable.
1. WHO, World Health Organization (2000).Scientific working group ondengue. Meeting report, Geneva, Switzerland, 3–5 April 2000. WHO: Geneva. 2. Kyle JL, Harris E. Global spread and persistence of dengue. Annu Rev Microbiol 2008;62:71-92. 3. Kalayanarooj S, Vaughn DW, Nimmannitya S, Green S, Suntayakorn S, Kunentrasai N, Viramitrachai W, Ratanachu-eke S, Kiatpolpoj S, Innis BL, Rothman AL, Nisalak A, Ennis FA. Early clinical and laboratory indicators of acute dengue illness. J Infect Dis 1997;176:313-21. 4. Potts JA, Rothman AL. Clinical and laboratory features that distinguish dengue from other febrile illnesses in endemic populations. Trop Med Int Health 2008;13:1328-40. 5. Lee MS, Hwang KP, Chen TC, Lu PL, Chen TP. Clinical characteristics of dengue and dengue hemorrhagic fever in a medical centre of southern Taiwan during the2002 epidemic. J Microbiol Immunol Infect 2006;39:121-9. 6. Teixeira MG, Barreto ML. Diagnosis and management of dengue. BMJ 2009; 339:b4338. 7. WHO Regional Office for Southeast Asia. Comprehensive guidelines for prevention and control of dengue and dengue haemorrhagic fever. Revised and expanded version. SEARO Technical Publication Series, New Delhi, India 2011. 8. Rigau-Pérez JG, Gubler DJ, Vorndam AV, Clark GG. Dengue surveillance--United States, 1986-1992. MMWR CDC Surveill Summ 1994; 43:7. 9. Blacksell SD, Mammen MP Jr, Thongpaseuth S, et al. Evaluation of the Panbio dengue virus nonstructural 1 antigen detection and immunoglobulin M antibody enzyme-linked immunosorbent assays for the diagnosis of acute dengue infections in Laos. DiagnMicrobiol Infect Dis 2008; 60:43. 10. Fry SR, Meyer M, Semple MG, Simmons CP, Sekaran SD, Huang JX, et al. The diagnostic sensitivity of dengue rapid testassays is significantly enhanced by using a combined antigen and antibody testingapproach. PLoSNegl Trop Dis 2011;5:e1199. 11. Halstead SB. The XXth century dengue pandemic: need for surveillance and research. World Health Stat Q 1992;45:292–8. 12. Chaterji S, Allen JC Jr, Chow A, Leo YS, Ooi EE. Evaluation of the NS1 rapid test and the WHO dengue classification schemes for use as bedside diagnosis of acute dengue fever in adults. Am J Trop Med Hyg. Feb 2011;84:224-8. 13. Monath TP. Dengue: the risk to developed and developing countries. Procular, a normal plasma AST level was a strong negative predictor NatlAcadSci USA 1994;91:2395–400. 14. Global Health Atlas. Geneva, World Health Organization (http://apps.who.int/globalatlas/default.asp, accessed 26 December2010). 15. Günther J et al. Distribution of dengue cases in the state of Oaxaca, Mexico, during the period 2004–2006. Journal of ClinicalVirology, 2009;45:218–222. 16. Amélia PA et al. Dengue epidemic in Belém, Pará, Brazil, 1996–1997. Emerging Infectious Diseases, 2000, 6(3). 17. García-Rivera EJ, Rigau-Pérez JG. Dengue severity in the elderly in Puerto Rico. Pan American Journal of Public Health, 2003;13:362–368 18. Singh MP, Majumdar M, Singh G, Goyal K, Preet K, Sarwal A, Mishra B, Ratho RK. 19. NS1 antigen as an early diagnostic marker in dengue: report from India. Diagn Microbiol Infect Dis. 2010;68:50-4. 20. Sabin AB. Research on dengue during World War II. Am J Trop Med Hyg 1952; 1:30. 21. Rigau-Pérez JG. The early use of break-bone fever (Quebrantahuesos, 1771) and dengue (1801) in Spanish. Am J Trop Med Hyg1998; 59:272. 22. Simmons CP, Farrar JJ, Nguyen vV, Wills B (April 2012). "Dengue". N Engl J Med366 (15): 1423–32. 23. Chen LH, Wilson ME (October 2010). "Dengue and chikungunya infections in travelers". Current Opinion in Infectious Diseases (5): 438–44. 24. Wolfff K, Johnson RA 0(eds.) (2009). "Viral infections of skin and mucosa". Fitzpatrick's color atlas and synopsis of clinical dermatology (6th ed.). New York: McGraw-Hill Medical. pp. 810–2. 25. Schwartz E, Mendelson E, Sidi Y. Dengue fever among travelers. Am J Med 1996; 101:516. 26. Kalayanarooj S, Vaughn DW, Nimmannitya S, et al. Early clinical and laboratory indicators of acute dengue illness. J Infect Dis 1997; 176:313. 27. Potts JA, Rothman AL. Clinical and laboratory features that distinguish dengue from other febrile illnesses in endemic populations. Trop Med Int Health 2008; 13:1328. 28. Trofa AF, DeFraites RF, Smoak BL, et al. Dengue fever in US military personnel in Haiti. JAMA 1997; 277:1546. 29. Souza LJ, Alves JG, Nogueira RM, GicovateNeto C, Bastos DA, Siqueira EW, et al, Aminotransferase changes and acute hepatitis in patients with dengue fever: analysis of 1,585 cases. Braz J Infect Dis 2004; 8:156-163. 30. Kuo CH, Tai DI, Chang-Chien CS, Lan CK, Chiou SS, Liaw YF. Liver biochemical tests and dengue fever. Am J Trop Med Hyg 1992; 47:265-270 31. Trung DT, Thao le TT, Hien TT, Hung NT, Vinh NN, Hien PT, et al. Liver involvement associated with dengue infection in adults in Vietnam. Am J Trop Med Hyg 2010; 83:774-780.
Tejaswita Kajale, Abhay Pawar, Channapatana
Abstract: The world is getting modernized and industrialized day by day. As a result vehicles and engines are increasing. But energy sources used in these engines are limited and decreasing gradually. This situation leads to seek an alternative fuel for diesel engine is biodiesel. Biodiesel is a non-toxic, biodegradable and renewable alternative fuel that can be used in diesel engines with little modification. Biodiesel is currently expensive. It could be produced from low-cost Neem seed oils. The objective of this study was to investigate the effect of the biodiesel produced from high free fatty acid feed stocks on engine performance and emissions. Biodiesel performance and testing is done in C.I. engine. Neem oil was extracted from neem seed by solvent extraction. Refractive index, density, viscosity, ash content, Saphonification value, iodine number was studied. Biodiesel has been prepared from NEEM oil by esterification and transesterification. It was examined for physical and chemical properties and chemical properties. HC, CO, NOx, SOx, and particulate matter was studied. The conversion of the biodiesel fuel's energy to work was equal to that from diesel fuel. The results also clearly indicate that the engine running with biodiesel and blends have higher NOx emission by up to 20%. However, the emissions of the CI engine running on neat biodiesel (B100) were reduced by up to 15%, 40% and 30% for CO, CO2 and THC emissions respectively, as compared to diesel fuel at various operating conditions.
1. Bobade S.N and Khyade V.B, Detail study on the Properties of Pongamia Pinnata (Karanja) for the Production of Biofuel, Research Journal of Chemical Sciences, 2012, 2(7), 16-20. 2. Mishra Sruti Ranjan, Mohanty Mahendra Kumar, Pattanaik Ajay Kumar, Preparation Of Biodiesel from Crude oil of Simarouba glauca using CaO as a Solid Base Catalyst, Research Journal of Recent Sciences, 1, 2012, 49-53. 3. Agarwal AK. Biofuels (alcohols and biodiesel) applications as fuels in internal combustion engines. Progr Energy Combust Sci 2007, 32,233−71. 4. Demirbas A. Biodiesel production from vegetable oils via catalytic and non-catalytic supercritical methanol transesterification methods. Progr Energy Combust Sci 2005, 31,466−87. 5. Graboski MS, McCormick RL. Combustion of fat and vegetable oil derived fuels in diesel engines. Progr Energy Combust Sci 1998, 24,125−64. 6. Komninos NP, Rakopoulos CD. Modeling HCCI combustion of biofuels: A review. Renew Sustain Energy Rev 2012,16,1588–610. 7. Dorado, M. P., Ballesteros, E., Arnal, J.M.; Gomez, J., Lopez, F.J. Exhaust emissions from a Diesel engine fueled with transesterified waste olive oil. Fuel 2003, 82, 1311–1315. 8. Utlu, Z., Kocak, M.S. The effect of biodiesel fuel obtained from waste frying oil on direct injection diesel engine performance and exhaust emissions. Renew. Energy 2008, 33, 1936–1941. 9. S. P. Singh, Dipti Singh, Biodiesel Production Through The use Of Different Sources and Characterization of Oils and Their Esters as the Substitute of Diesel: A Review, Renewable and Sustainable Energy Reviews, 14, 2010, 200-216. 10. Graboski, M. S. and R. L. McCormick. Combustion of fat and vegetable oil derived fuels in diesel engines. Prog. Energy Combust. Sci., 1998, 24, 125-164. 11. Chang, D. Y. Z. and J. H. Van Gerpen. Fuel properties and engine performance for biodiesel prepared from modified feed stocks. 1997, SAE Paper No. 971684. 12. Schumacher, L. G. and J. H. Van Gerpen, Research needs resulting from experiences of fueling of diesel engines with biodiesel. In Liquid Fuels and Industrial Products from Renewable Resources Proceedings of the Third Liquid Fuel Conference,1996, 207-216, 13. Schmidt, K. and J. H. Van Gerpen, The effect of biodiesel fuel composition on diesel combustion and emissions.1996, SAE Paper No. 961086. 14. Zhang Y. and J. H. Van Gerpen., Combustion analysis of esters of soybean oil in a diesel engine. 1996,SAE Paper No. 960765. 15. Chang, D. Y. Z., J. H. Van Gerpen, I. Lee, L. A. Johnson, E. G. Hammond, and S. J. Marley. Fuel properties and emissions of soybean oil esters as diesel fuel. JAOCS, 1996, 73(11), 1549-1555. 16. Sharp, C. A. Characterization of biodiesel exhausts emissions for EPA 211(b). Final report for National Biodiesel Board. Southwest Research Institute, San Antonio, Texas.1998. 17. Wang R, Hanna MA, Zhou WW, Bhadury PS, Chen Q, Song BA, Yang S Production and selected fuel properties of biodiesel from promising non-edible oils: Euphorbia lathyris L., Sapium sebiferum L,and Jatropha curcas L. Bioresour. Technol.2011, 102(2), 1194-1199. 18. Fukuda H, Kondo A, Noda H, Biodiesel fuel production by transesterification of oils. J. Biosci. Bioeng. 2001, 92(5): 405-416. 19. Kusdiana D, Saka S, Kinetics of transesterification in rapeseed oil to biodiesel fuel as treated in supercritical methanol. Fuel, 2001, 80(5), 693-698. 20. Ma F, Hanna MA, Biodiesel production: a review1. Bioresour. Technol. 1998, 70(1), 1-15. 21. Schuchardt U, Sercheli R, Vargas RM, Transesterification of vegetable oils: a review. J. Braz. Chem. Soc. 1998, 9(3), 199-210. 22. Mittelbach M, Diesel fuel derived from vegetable oils, VI: Specifications and quality control of biodiesel. Bioresour. Technol.1996, 56(1), 7-11. 23. Zhang Y, Dube M, McLean D, Kates M, Biodiesel production from waste cooking oil: 1. Process design and technological assessment. Bioresour. Technol.2003, 89(1), 1-16. 24. Berrios M, Siles J, Martin M, Martin A, A kinetic study of the esterification of free fatty acids (FFA) in sunflower oil. Fuel, 2007, 86(15), 2383-2388. 25. Berchmans HJ, Hirata S, Biodiesel production from crude Jatropha curcas L. seed oil with a high content of free fatty acids. Bioresour. Technol. 2008, 99(6): 1716-1721. 26. Jain S, Sharma M, Kinetics of acid base catalyzed transesterification of Jatropha curcas oil. Bioresour. Technol. 2010, 101(20): 7701-7706. 27. Lu H, Liu Y, Zhou H, Yang Y, Chen M, Liang B ,Production of biodiesel from Jatropha curcas L. oil. Comput. Chem. Eng. 200933(5):1091-1096. 28. Research and Development Report, Tree Born Oilseeds by National Oilseeds and Vegetable Oils, Development Board, Government of India, 2009. 29. S. P. Singh, Dipti Singh, Biodiesel Production Through The use Of Different Sources and Characterization of Oils and Their Esters as the Substitute of Diesel: A Review, Renewable and Sustainable Energy Reviews, 14, 2010, 200-216.
Prashant Bade, Varsharani Kendre, Yallapa Jadhav, Atul Wadagale
Background: According to WHO, the optimal caesarean delivery rate is 10-15%.However the caesarean rate is much higher in India. The increased caesarean rate has resulted in increased economical burden on health care and possibly increased maternal morbidity. Objectives: To study various indications for caesarean sections performed at Govt. Medical College and Hospital, Latur. To suggest recommendations to reduce the caesarean section rate. Materials and Methods: This study is a record based cross sectional study, conducted at Government Medical College and Hospital, Latur. All women who underwent caesarean section from March 2013 to august2013 were included in the study .Data was entered in MS Excel and analyzed with percentages and chi square test using SPSS ver.21. Results: Caesarean section rate observed in our study was 23.97 %. It was significantly more common in the age group of 21-30years, women with parity 2 and rural women. The primary LSCS rate was 41.99% and that of repeat LSCS was 58.01%.The Emergency LSCS rate was significantly higher (74.22%) than elective LSCS rate. The commonest indication for LSCS was previous LSCS (24.8%) followed by, cephalopelvic disproportion (17.6%), failure to progress (16.6%), and fetal distress (11.7%). Conclusions: In this study, caesarean section rate is higher than WHO standard and previous LSCS was the most common indication. So reduction in overall caesarean section rate can be met through reduction of elective LSCS with the promotion of trial of labour and by improving maternal health. Interpretation: Though the benefits of the caesarean section cannot be denied, unnecessary caesarean sections should be avoided.
1. Belizan JM, Althabe F, Barros FC, Alexander S. Rates and implications of caesarean section in Latin America: ecological study. Br Med J 1999; 319:1397-400. 2. Porreco RP, Thorp JA. The cesarean birth epidemic:trends, causes, and solutions. Am J Obstet Gynecol 1996; 175:369-74. 3. Caesarean section on the rise (editorial). Lancet 2000; 356:1697. 4. J Health Popul Nutr 2001 Dec; 19(4):306-312 5. World Health Organisation. Appropriate technology for birth. Lancet 1985; 2:436-7. 6. Adv. Appl. Sci. Res., 2013; 4(4):196-202 7. UNICEF, WHO, UNFPA, New York: United Nations Children’s Fund, 1997, 1 8. IJMCH, 2012; 14(3):2-7. 9. Sudha Salhan, Textbook of Obstetrics, pg.683-685 10. D.C. Dutta, Textbook of obstetrics,7th edition pg.588-594. 11. M. Wagner, Int J Gynaecol Obstet., 2001, 75, S25. 12. Wagner, Lancet, 2000, 356,1677 13. Shiono PH, McNellis D, Rhoads GG. Reasons for rising cesarean delivery rates: 1978-1984. Obstet Gynecol 1987;69:696-700. 14. Centers for Disease Control. Rates of caesarean delivery: United States. MMWR 1993;42:285. 15. Bottoms SF, Rosen MG, Sokol RJ. The increase in the cesarean birth. N Engl J Med 1980;302:559-63. 16. Kambo I, Bedi N, Dhillon BS, Saxena NC. A critical appraisal of cesarean section rates at teaching hospitals in India. Int J Gynecol Obstet 2002; 79: 151-8. 17. Gilliam M, Rosenberg D, Davis F. The likelihood of placenta previa with greater number of cesarean deliveries and higher parity. Obstet Gynecol 2002; 99:976-80. 18. Leung AS, Leung EK, Paul RH. Uterine rupture after previous cesarean delivery: maternal and fetal consequences. Am J Obstet Gynecol 1993; 169:945-950. 19. Mollison J, Porter M, Campbell D et al. Primary mode of delivery and subsequent pregnancy. Br J Obstet Gynecol 2005; 112:1061-5.
K. S. Nemade, M. M. Meshram
Abstract: Palmaris longus muscle is a very well known muscle for variations. It can be absent, digastric, duplicated, having proximal tendon. These variations are important in grafting surgeries like tendon transfer, ptosis correction, lip augmentations which use the muscle as a graft. Here, we reported a rare variation of palmaris longus in the form of proximal tendon, middle belly and distal tendon which is continuous with palmar aponeurosis. In the same cadaver, plantaris muscle also dissected to note the variation.
1. Hollinshead WH. Anatomy for surgeons: Back and limbs. Jocker Harpe, New York: p, 413; 1956. 2. Oommen A, Rajarajeshwari. Palmaris longus- upside down!!! J. anat. Soc. India. 2002; 51(2): 232-233. 3. Reimann AF, Daseler EH, Anson BJ, Beaton LE. The palmaris longus muscle and tendon. A study of 1600 extremities. Anat Rec 1944; 89: 495-505. 4. Rawat JS, John B. Reverse palmaris longus muscle: a case report. Indian J orthop.2003;37(2): 5. Thejodhar P, Bhagath Kumar Potu, Rakesh G. Vasavi. Unusual palmaris longus muscle. Indian J Plast Surg. 2008; 41(1) Jan-Jun: 95-96. 6. Vanderhooft E. The frequency of and relationship between the palmaris longus and plantaris tendons. Am. J. orthop. 1996 Jan; 25(1):38-41. 7. William PL, Bannister LH, Dyson M, Berry MM, Collins P, Duseek JE, Pergusson MWJ. Gray Anatomy In: The muscular system. 38th Edn. Churchill Livingstone, London: p. 846; 1995.
Socioeconomic status (SES) refers to an individual’s position within a hierarchical social structure, which is one of the important determinants of health status. Composite scales are generally used to measure the SES, which has a combination of social and economic variables. Several studies namely hospital and community based require assessment of socio-economic status of an individual / family. This reflects the affordability of health services, necessities and purchasing power of the same. Several methods or scales have been proposed for classifying different populations by socioeconomic status: Rahudkar scale 1960, Udai Parikh scale 1964, Jalota Scale 1970, Kulshrestha scale 1972, Kuppuswamy scale 1976, Shrivastava scale 1978, Bharadwaj scale 2001.1-7 However, social transformation and fast growing economy have rendered these scales ineffective in measuring the SES over the years. The Kuppuswamy scale proposed in 1976, measures the SES of an individual based on three variables namely, education and occupation of the head of the household and income of the family.5 Of the three variables, education and occupation of the head of the household do not change frequently with time. However, the steady inflation and the resultant devaluation of the rupee necessitate periodic revisions of the income variable. The previous revisions of the scale were done in the years 1998 and 2007.8,9
1. Rahudkar WB. A scale for measuring socio-economic status of Indian farm families. Nay Agril Coll Mag 1960; 34. 2. Parikh U, Trivedi G. Manual of socio-economic status scale (Rural), Manasayan, Delhi, 1964. 3. Alota S, Pandey RN, Kapoor SD, Singh RN. Socio-economic status questionnaire (urban), psycho- Centre, New Delhi, 1970. 4. Kulshrestha SP, Day P. Socio-economic status scale (Urban) form-A, National Psychological Corporation, Agra, 1972. 5. Kuppuswamy B. Manual of Socioeconomic Status (urban), Manasayan, Delhi, 1981. 6. Srivastava GP. Socio-economic status scale (Urban), National Psychological Corporation, Agra, 1978. 7. Bhardwaj RL. Manual for socio-economic status scale. National Psychological Corporation, Agra, 2001. 8. Mishra D, Singh HP. Kuppuswamy’s socioeconomic status scale—a revision. Indian J Pediatr. 2003; 70:273–4. 9. Kumar N, Shekhar C, Kumar P, Kundu AS. Kuppuswamy’s socioeconomic status scale-updating for 2007. Indian J Pediatr.2007; 74:1131–2. 10. Petro BK, Jeyashree K, Gupta PK. Kuppuswamy’s Socioeconomic Status Scale 2010—The Need for Periodic Revision. Indian J Pediatr.2012; 79(3):395–6 11. http://labourbureau.nic.in/indexes.htm accessed on 25th March 2014