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Background: Aim of the present study was to observe the measurements of anterior papillary muscles present in tricuspid valve of human heart. Measurements of anterior papillary muscles in tricuspid valve gains utmost importance in cardiac surgeries because they are the causes of myocardial infarction in recent times because of its variations and detection of these causes by advent in modern technologies which will help in treatment of tricuspid valve diseases. Materials and Methods: This study was carried out on 96 normal formalin fixed human heart specimens. Dissection was performed according to standard techniques. Anterior papillary muscles were observed and length, width and thickness of each muscle were measured and documented. Results: In the present study, numbers of anterior papillary muscles were present with a frequency of 1-3, with most common appearance of 1 muscle in 66 hearts (68.8%) and least common incidence of 3 muscles in 6 hearts (6.3%). Anterior papillary muscles were present in all 96 hearts. In measurements, anterior papillary muscles mean height was 1.49±0.44 cm; mean width was 0.82±0.21 cm and mean thickness was 0.64±0.15 cm respectively. Conclusion: We hope this study will serve to understand the morphometry of anterior papillary muscles better and will help in various surgical procedures and cardiac treatment done on tricuspid valve.

1. Standring S, Borley NR, Collins P, Crossman AR, Gatzoulis MA, Healy JC, et al. Gray’s Anatomy: The Anatomical Basis of Clinical Practice. 40th ed. Philadelphia: Churchill Livingstone Elsevier; 2008. pp. 966-7. 2. Hashimoto K, Oshiumi M, Takakuva H, Sasaki T, Onoguchi K. Congenital mitral regurgitation from absence of the anterolateral papillary muscle. Ann Thorac Surg 2001;72:1386-7. 3. Balachandra N, Rathnam BPP. A Study of the dimensions of the Human Tricuspid valve and attachmentofchordaetendinae. http://www.rguhs.ac.in/digitallibrary/hardbibilo/medical-doc. Accessed on 20-7-2011 at 2.40 pm 4. Gerola LR, Wafae. N, Vieira MC, Juliano Y, Smith R, Prates JC. Anatomic study of the Tricuspid valve in children. Surg Radiol Anat 2001;23:149-53. 5. Negri GR, Didio LJA, Baptista CAC. Papillary muscles and tendinous chords of the right ventricle of the human heart morphological characteristics. Surg Radiol Anat 2001;23:45-9. 6. Motabagani MAB. Comparative, morphometric and histological studies of the Tricuspid valve complex in human and some mammalian hearts. J Anat Soc India 2006;55(1):1-23. 7. Begum JA, Khalil M, Rahman H, Adiluzzaman AA. A morphological and morphometric study of the right ventricular papillary muscles of autopsied heart of Bangladeshi people. Mymensingh Medical Journal 2006;15(2):131-4. 8. Wafae. N, Hayashi. H, Gerola LR, Vieira MC. Anatomical study of the human Tricuspid valve. Surg Radiol Anat 1990;12:37-41. 9. Joudinaud TM, Flecher EM, Duran CMG. Functional terminology for the Tricuspid valve. J Hear Valve Dis 2006 May;15(3):382-8. 10. Ootaki Y, Yamaguchi M, Yoshimuva N, Oka S, Yoshida M, Hasegawa T. Tricuspid valve repair with papillary muscle shortening for severe Tricuspid regurgitation in children. Ann Thorac Surg 2004;78:1486-8.

Introduction: We have studied the effect of multi-vitamin multi-mineral supplementation on polymorphonuclear leukocyte(PMNL) membrane status in Type II Diabetes Mellitus patients. Material and Methods: The study was divided into four groups. Group A- Diabetic patients (DM0). Group B consisted of normal healthy controls (NHC), Group C of Diabetic patients given multi-vitamin multi-mineral supplementation capsules for 30 days (DM30). Group D consisted of diabetics withdrawn from multi-vitamin multi-mineral supplementation for next 30 days (DM60). Fasting blood samples were collected from the respective groups. PMNL Phospholipid phosphorous (PLp), cholesterol, triglyceride lipase, triglycerides, vitamin C, Magnesium and Zinc were estimated by standard methods. Analysis of variance was calculated by applying students “t” test. Results and discussion:- The PMNL cholesterol, triglycerides, phospholipids phosphorous were significantly high (p<0.05) whereas PMNL triglyceride lipase, vitamin C, Zinc and magnesium were significantly low (p<0.05) in DM without multi-vitamin multi-mineral supplementation as compared to NHC . The levels of Cholesterol, triglycerides, Phospholipid phosphorus significantly decreased after 30 days supplementation. Withdrawal of supplementation for next 30 days showed a slight increase in PMNL PLp. A significant increase in PMNL TG lipase activity was seen after multi-vitamin multi-mineral supplementation in diabetic patients. Supplementation of multi-vitamin multi-mineral capsules to diabetic patients showed significant elevation in PMNL Vitamin C, PMNL Mg and PMNL Zn. A significant change was observed in the levels of PMNL Vitamin C, Mg and Zn after withdrawing multi-vitamin multi-mineral supplementation for next 30 days.Conclusion:-This suggests that multi-mineral multi-vitamin supplementation in combination with conventional hypoglycemic treatment may modulate the PMNL function and provide better metabolic control in Type II Diabetes Mellitus patients.

1. Mccarty D, Zommet P;. Global estimates and projections. Melbourne, International Diabetic Institute 1994 Diabetes 1994-2010. 2. David M N; The patho-phyology of diabetic complications:- How does the glucose hypothesis explain? Ann Intern. Med:1996,Vol.174(sept),286-289. 3. Stewart N W, Walker M; Features of syndrome X in first degree relatives of NIDDM patients. Diabetic care;1995;vol; 18(7):pg 1020-1022. 4. Wilson R M; Neutrophils function in Diabetes. Diabet. Med.1986; Nov-Dec 3(6):pg. 509-512. 5. Esmann V; Diabetic leukocyte Review aricle- Enzyme,1972;vol. 13(1):pg; 32-55. 6. Schmitt M, Keller H V, Cottier H; Quantitative and qualitative assessment of human PMNL functions. Beitr Infussionther Klin Ernahr.1926;vol;15:pg 1196-1230. 7. Alexiewicz J M, Kumar D, PMNL in non-insulin dependent diabetes mellitus: abnormalities in metabolism and function. Ann Intern Med.1995 Dec 15;128(12): pg;919-924. 8. Chari S N, Lipid composition and metabolism of PMNL in DM; Diabetes;1984;vol.33;pg586. 9. Boyum A , Isolation of mononuclear cells and granulocytes from human blood. Scand. J. Clin. Lab. Invest.1968; 21,Suppl.1; pg.101-109. 10. Ways and Hanahan, J. Method for lipid extraction Lipid,1986; Rev; 5 :pg. 318. 11. Bagdade J.D., Ways P.O.,Impaired granulocyte adherence. J.Clin. Lab. Med:1970; vol.75;pg 53. 12. Courchaine A. J., Rapid semi-micro method for estimating free and total cholesterol. Clinical Chemistry: 1959;chap.5:pg 609. 13. Kaplan A and Lee V F, Method for estimating free and total cholesterol. and triglycerides.1965; Proc. Soc. Exp, Biol. Med, pg:118- 290. 14. Elsbach P, Rizack M A, Triglyceride lipase estimation. Am. J. Phys., 1963;vol;205 ;pg 1154. 15. Ayekgw et al, A simple colorimetric method for Vitamin C in Serum, 1978;pg 45-50. 16. Gindler E, et al.,Determination of Mg. Clin. Chem.1971; chp.17:pg662. 17. Tetsuo Makino,Determination of Zn. Clin. Chem.Acta.;1991;vol197:pg209-220. 18. Mazor R,Shurtz,Swirskir,Farah R,Kristol B,Shapiro G, Dorlechter F,Cohen Mazor M,Meilin E,Tamaras S,Sela S;Pmnl constitutes a possible link betweeninfection and oxidative stress in diabetic and hyperlipidemic patients.; Atherocslerosis;2008 April;!97(2);937-943. 19. Urberg M and Zemel M B, Evidence for synergism between Cr and nicotinic acid in the control of glucose tolerance in elderly humans. Metabolism ;1987;vol36:pg896. 20. Pote M S, Noronhn J M and Keshvan V, An annatherogenic role of folic acid in experimental diabetes. Jr. Clin. Biol. And Nutr.;1985;vol18(3):pg157. 21. Kautsikos D and Agroyannis B, Biotin for diabetic peripherial neuropathy.Biomedicine and Pharmacotherapy ;1990;vol4(10):pg511. 22. Erikson J and Kohvakka A, Magnesium and ascorbic acid supplementation in diabetes mellitus. Annals of Nutrition and Metabolism; 1995;vol39(4):pg217-233, 23. Paolisso G, Diamore A and Ealibi V, Plasma vit. C affects glucose homeostasis in healthy subjects and NIDDM. Am. Jr. of Physiology;1994; 266(2p+1)E: pg261-128, 1994 24. Caballero B, Vit. E improves the action of insulin. Nutrition Reviews;1993;vol; 51:pg339-340,. 25. Reaven P D, Herold D A and Barnett J, Effects of vit. E on susceptibility of LDL and LDL subfractions to oxidation and on protein glycation in NIDDM. Diabetes Care; 1995;vol18(6):pg 807-816. 26. Holecek V, Racek J and Jerabek Z, Administration of multivitamin combinations and trace elements in diabetes. Casopis Lekaru Ceskych;1095;vol134(3):pg 80-83. 27. Anderson R A, Cromium, glucose tolerance and diabetes. Biological Trace Element Research; 1992;vol32: pg.19-24. 28. Abraham A S and Brook B A, The effects of Chromium supplementation on serum glucose and lipids in patients with and without non-insulin dependent diabetes. Metabolism;1992;vol; 41:pg768-771. 29. Jeejeebhoy K N, Chu R S and Marliss E B, Chromium deficiency, glucose intolerance and neuropathy reversed by chromium supplementation. Am. J. Clin. Nutr.;1977;vol 30:pg531-538. 30. Wangemann M, Seizer A and Leitzmann C, Recommendations on the dietary allowance of magnesium. Magnessium Buletin; 1995;17(3): pg79-85. 31. Honnorat T and Acconunott I M, Effects of diabetic type and treatment on Zinc status in diabetes mellitus. Biological Trace Element Res.; 1992;vol32:312-316. 32. Faure P, Roussei A and Coudray c, Zinc and insulin sensitivity. Biological Trace Element Res.;1995 vol32:pg305-310. 33. Faure P, Be. Hamou P and Perard A, Lipid peroxidation in IDDM with early retinal degenerative lesions: effect of an oral Zn supplementation. Eur.J. Clin. Nutr.;1995;vol 49:pg282-288. 34. Minami T, Ichii M and Okazaki Y, Renal changes of streptozotocin induced diabetic rats and a low Zinc diet. Renal Failure;1995;vol 17:pg3463-3489. 35. Rizzo MR, Abbatecola AM, Barbieri M, Vietri MT, Cioffi M, Grella R, Molinari A, Forsey R, Powell J, Paolisso G. Evidence for anti-inflammatory effects of combined administration of vitamin E and C in older persons with impaired fasting glucose: impact on insulin action. J Am Coll Nutr. 2008 Aug;27(4):505-11.

Background: Spontaneous bacterial peritonitis (SBP) is commonest and severe complication of decompensated cirrhosis. SBP is defined as the infection of ascitic fluid (AF) in the absence of a contiguous source of infection and/or an intra-abdominal inflammatory focus. An AF polymorphonuclear (PMN) leucocyte count ≥ 250/mm3 -irrespective of the AF culture result- is universally accepted nowadays as the best surrogate marker for diagnosing SBP. Without early antibiotic treatment, this complication is associated with high mortality rate, so early diagnosis and treatment of SBP is therefore necessary for survival. Leukocyte esterase dipstick test can rapidly diagnose the SBP. Aim: Objective of our study was to find out the diagnostic accuracy of leukocyte esterase dipstick test for the diagnosis of spontaneous bacterial peritonitis. Methods: This cross-sectional study was conducted from January 2013 to August 2013 at a tertiary care center in central India . All the Patients with cirrhosis and ascites of either gender were included in this study. A total of 104 patients were enrolled for the study. Patients with secondary bacterial peritonitis and those who have received antibiotic therapy during past 10 days of hospital admission were excluded from the study. All the patients underwent abdominal paracentesis. Urine dipstick (Piramal10x test-India) was used as screening test and the results were compared with manual cell counting and ascitic fluid culture. A cut-off of 4+ on dipstick test was considered as positive for SBP. Results: The manual cell count using the above criterion diagnosed 28.9% patients as having SBP. The dipstick results were compared with the PMN counts. Sensitivity, Specificity, Positive predictive value, Negative predictive value and accuracy was 83.3%, 95.9%, 89.3%, 93.4% and 92.3% respectively. Conclusion: Leukocyte esterase dipstick test emerged out as an effective tool for rapid, bedside diagnosis of SBP.

1. Koulaouzidis A, El-Ramli R, Gasem J, Saeed AA. Leukocyte esterase reagent strips for spontaneous bacterial peritonitis: what now? Ann Hepatol. 2008 Jul-Sep; 7(3):255-6. 2. Jepsen P, Vilstrup H, Moller JK, Sorensen HT. Prognosis of patients with liver cirrhosis and spontaneous bacterial peritonitis. Hepatogatroenterology 2003; 50: 2133-36 3. Thanopoulou AC, Koskinas JS, Hadziyinnis SJ. Spontaneous bacterial peritonitis (SBP): Clinical, Laboratory and prognostic feature. A single centre experience. Eur. J. Intern. Med. 2002; 13: 194-198. 4. Rerknimitr R, Rungsangmanoon W, Kongkam P, Kullavanijaya P. Efficacy of leukocyte esterase dipstick test as a rapid test in diagnosis of spontaneous bacterial peritonitis. World J Gastroenterol. 2006;12 (44):7183-7. 5. Wong CL, Holroid-Leduc J, Thorpe KE, Strauss SE. Does this patient have bacterial peritonitis or portal hypertension? How do I perform a paracentesis and analyze the results. JAMA, 2008;299:1166-78. 6. Musa AA, Quortem HA, Ibrahim MD. Rapid diagnosis of meningitis with reagent strips. Lancet, 1995; 345: 1290-91. 7. Azoulay E, Fartoukh M, Galliot R, Baud F, Simonneau G, Le Gall JR, Schlemmer B, Cheveret S. Rapid diagnosis of infectious pleural effusions by use of reagent strips. Clin. Infect. Dis., 2000; 31:914-19. 8. Kutter D, Figueiredo G, klemmer L. Chemical detection of leukocytes in urine by means of a new multiple test strip. J. Clin., Chem. Clin. Biochem. 1987; 25:91-94. 9. Torun S, Dolar E, Yilmaz Y, Keskin M, Kiyici M, Sinirtas M, Sarandol E, Gurel S, Nak SG, Gulten M. Evaluation of leukocyte esterase and nitrite strip tests to detect spontaneous bacterial peritonitis in cirrhotic patients. World J Gastroenterol. 2007 Dec 7;13(45):6027-30. 10. Parsi MA, Atreja A, Zein NN. Spontaneous bacterial peritonitis: Recent data on incidence and treatment. Cleve Clin J. Med. 2004; 71:569-76. 11. Castellote J, Lopez C, Gornals J, et al. Rapid diagnosis of spontaneous bacterial peritonitis by use of reagent strips. Hepatology. 2003;37:893–896 12. Kim DY, Kim JH, Chon CY, et al. Usefulness of urine strip test in the rapid diagnosis of spontaneous bacterial peritonitis. Liver Int. 2005;25:1197–2101 13. Butani RC, Shaffer RT, Szyjkowski RD, Weeks BE, Speights LG, Kadakia SC. Rapid diagnosis of infected AF using leukocyte esterase dipstick testing. Am J Gastroenterol. 2004;99:532–537 14. Sapey T, Mena E, Fort E, et al. Rapid diagnosis of spontaneous bacterial peritonitis with leukocyte esterase reagent strips in a European and in an American center. J Gastroenterol Hepatol. 2005;20:187–192. 15. Thévenot T, Cadranel JF, Nguyen-Khac E, et al. Diagnosis of spontaneous bacterial peritonitis in cirrhotic patients by use of two reagent strips. Eur J Gastroenterol Hepatol. 2004;16:579–583 16. Jha AK et al. Multistix 10SG Leukocyte Esterage Dipstick Testing in Rapid Bedside Diagnosis of Spontaneous Bacterial Peritonitis: A Prospective Study. J of Clin & Exp Hepatology 2012; 2(3): 224-228.

Rhinoliths are uncommon clinical entities reported in practice presenting as unilateral foul smelling nasal discharge and nasal obstruction. These are mineralized foreign bodies in nasal cavity. A case of 43 year old female with left side foul smell nasal discharge and nasal obstruction for the past 10 years diagnosed as rhinolith after thorough clinical examination and confirmed by endoscopy and radiological examination. Endoscopic surgical removal was done. A high index of suspicion is required.

1. Mustafa A, Nishori S. Rhinolith caused from undetected foreign body. A case report. Kosova Journal of Surgery. 2008;2:32–35. 2. Polson CJ. On rhinoliths. J Laryngol Otol 1943;58:79-116.10.1017/S0022215100011002 3. Ezsiás A, Sugar AW. Rhinolith: An unusual case and an update. Ann Otol Rhinol Laryngol 1997. Feb;106(2):135-138 4. Hadi U, Ghossaini S, Zaytoun G. Rhinolithiasis: A forgotten entity. Otolaryngol Head Neck Surg 2002. Jan;126(1):48-51.10.1067/mhn.2002.121018 5. Ireland J. Rhinolith: Report of a case. Archives of Otolaryngology. 1929;10:190–191. 6. Shaw LCK. Rhinolith of endogenous origin: a rare entity. Surgical Practice. 2007;11(1):48–50. 7. Raman V, Padgham N. A case of tooth-filling antral rhinolithiasis presenting with blockage of the osteomeatal complex. British Journal of Radiology. 2007;80(960):e299–e300.

Introduction: The hands and cell phones can harbor various potential pathogens and become an exogenous source of nosocomial infection among hospitalized members. The present study highlights the need of continuous screening of pathogens carried through hands and cell phones and also its proper management. Aims and Objectives: To determine nosocomial infections carried through hands and cell phones of healthcare workers and its management through surface sterilization. Material and Methods: Fifty samples collected from both hands and cell phones of healthcare workers, working in various departments at government hospital, Mandya were subjected to bacteriological analysis. Using sterile cotton tipped applicator moistened with nutrient broth samples were collected from both hands and front, back and the sides of the cell phones. Collected samples were cultured and the resulting isolates were identified. The above procedure was repeated after decontamination of cell phones using 90% alcohol. Results: Out of 50 nursing staff screened, hands swab showed 22% of Staphylococcus aureus, 3% of Streptococcus spp. and 3% of Enterobacter aerogenes where as on mobile phones swab showed 52% of Staphylococcus aureus, 34% of Streptococcus spp. and 4% of Bacillus spp. After decontamination with 90% alcohol only 4 mobile phones showed growth of bacteria which are nonhaemolytic, thus proving the efficacy of decontamination to be nearly 83%. The bacterial isolates were further subjected to antibiotic sensitivity test by disk diffusion as well as well diffusion methods on Muller Hinton agar medium. It is quite interesting to observe that different strains of Staphylococcus aureus recorded varied response to the same antibiotic used in the study. Conclusions: This is an important study carried out to report the varied response of different strains of Staphylococcus aureus against already available/used antibiotics and need of regular checking of hands and handset as a source of inoculum of potential pathogenic bacteria. The difference in genetic set up among the strains can be worked out by further molecular studies.

1. Smyth ETM, McIlvenny G, Enstone JE, Emmerson AM, Humphreys H, Fitzpatrick F, Davies E, Newcombe RG, Spencer RC: Four country healthcare associated infection prevalence survey 2006: overview of the results: Journal of Hospital Infection. 2008; 69(3):230-248. 2. Semmelweis IP, Die Aetilogie, der Begriff und die Prophylaxis des Kindbettfiebers. Budapest: C.A. Hartleben's Verlags-Expedition; 1861. 3. Ulger F, Esen S, Dilek A, Yanik K, Gunaydin M, Hakan L: Are we aware how contaminated our mobile phones with nosocomial pathogens?: Annals of Clinical Microbiology and Antimicrobials. 2009; 8:7-11. 4. Yusha’u M, Bello M, Sule H: Isolation of bacteria and fungi from personal and public mobile cellphones: A case study of Bayero University, Kano (Old Campus): International Journal of Biomedical and Health Sciences. 2010; 6(1):97-102. 5. Popovska K, Zdravkovska M, Blazevska B, Icev K, Eftimovski G: Implementation of proper hand hygiene among microbiological laboratory workers respectively to WHO guidelines: Macedonian Journal of Medical Sciences. 2012; 5(2):147-151. 6. Meltzer B, Nosocomial infections: Docs’ cell phones may spread hospital infections: Outpatients Surgery Magazine. 2003; 11:1-4. 7. Khivsara A, Sushma T, Dhanshree B: Typing of Staphylococcus aureus from mobile phones and clinical samples: Current Science. 2006; 90(7):910-912. 8. Brady RRW, Wasson A, Stirling I, McAllister, Daman NN: Is your phone bugged? The incidence of bacteria known to cause hospital acquired infection on healthcare mobile phones: Journal of Hospital Infection. 2006; 62:123-125. 9. Karabay O, Kocoglu E, Tahtaci M: The role of mobile phone in the spread of bacteria associated with nosocomial infections: The Journal of Infection in Developing Countries. 2007; 1:72-73. 10. Goldblatt JG, Krief I, Haller TD, Milloul V, Sixsmith DM, Srugo I, Potasman I: Use of Cellular Telephones and Transmission of Pathogens by Medical Staff in New York and Israel: Infect Control and Hospital Epidemiolology. 2007; 28:500-503. 11. Akinyemi KO, Atapu AD, Adetona OO, Coker AO: The potential role of mobile phones in the spread of bacterial infections: The Journal of Infection in Developing Countries. 2009; 3(8):628-632. 12. Tolan RW: (2007). Staphylococcus aureus infection. Available at http:www,emedicine.com/2704.htm. 13. Malini J, Harle SA, Padmavathy M, Umapathy BL, Navaneeth BV, Keerthi MJ, Girish MS: Methicillin resistant Staphylococcus aureus carriage among the health care workers in a tertiary care hospital: Journal of Clinical and Diagnostic Research. 2012: 6(5):791-793. 14. Cohen HA, Matalon J: Stethoscope and otoscope - A potential vector of infection: Family Practice 1997; 14: 446-448. 15. Patil P, Hulke S, Thakre A, Gaikwad M: Pen of health care workers as vector of infection: Online Journal of Health and Allied Sciences. 2010; 9(3):15-17. 16. Devine J, Cooke RPD, Wright EP: Is methicillin-resistant Staphylococcus aureus (MRSA) contamination of ward-based computer terminals a surrogate marker for nosocomial MRSA transmission and handwashing compliance?: Journal of Hospital Infection. 2001; 48(1):72-75. 17. Stacey A, Burden P, Croton C, Jone E: Contamination of television sets by Staphylococcus aureus. Journal of Hospital Infection 1998; 39:243- 244. 18. Gunasekara TDCP, Kudavidanage BP, Peelawattage MK, Meedin F, Guruge LD, Nanayakkara G, Nanayakkara M, Fernando SSN: Bacterial contamination of anaesthetists hands, personal mobile phones and wrist watches used during theatre sessions: Sri Lankan Journal of Anaesthesiology 2009; 17(1):11–15. 19. Anon. 1996. The Indian Pharmacopoeia. 3rd edition. Government of India, New Delhi. Ministry of Health and family welfare. 20. Patil PD, Pawar SA: Nosocomials hazards of doctors’ mobile phones: Journal of Theoretical and Experimental Biology 2012; 8:115-121. 21. Bhat SS, Hegde SK, Salian S: Potential of mobile phones to serve as a reservoir in Spread of Nosocomial Pathogens: Online Journal of Health and Allied Sciences. 2011; 10(2):14-16. 22. Goyal R, Das S, Mathur M: Colonization of MRSA among health care workers in a tertiary care hospital of Delhi: Indian Journal of Medical Science. 2002; 56:321-4. 23. MacKintosh CA, Hoffman PN: An extended model for transfer of microorganisms via the hands at laundry. Differences between organisms and the effect of alcohol disinfection: Journal of Hygiene. 1984. 92(3): 345-355. 24. Patrick D, Findon R, Miller TE: Residual moisture determines the level of touch-contact associated bacterial transfer following hand washing: Epidemiology and Infection. 1997; 119:319-325. 25. Oie S, Hosokawa I, Kamiya A: Contamination of room door handles of Methicillin-Sensitive/ Methicillin-Resistant Staphylococcus aureus: Journal Hospital Infection. 2002; 51:140-143. 26. Srikanth P, Rajaram E., Sudharsanam S., Lakshmanan A., Umamaheswari SSM, Kalyani J: The mobile phone in a tropical setting – emerging threat for infection control: Sri Ramachandra Journal of Medicine. 2009; 2(2):18-20. 27. Chamber HF: Community-associated MRSA-resistance and virulence converge: Journal of Medicine. 2005; 352: 1485-1487. 28. Lowy FD: Staphylococcus aureus infections: New England Journal of Medicine. 1998; 339:520-532. 29. Lowy FD: Antimicrobial resistance: the example of Staphylococcus aureus: Journal Clinical Investigation. 2003; 111:1265-2127. 30. Todar M: Pseudomonas aeruginosa in Web Review of Todar's Online Textbook of Bacteriology "The Good, the Bad, and the Deadly" Science Magazine 2004; 304: 1-12. 31. Hughe JM: Study on the efficacy of nosocomial infection control: Infection Control Epidemology. 1988; 34:553-561. 32. Lucet JC, Chevret S, Durand-Zaleski I, Chastang C, Regnier B: Prevalence and risk factors for carriage of methicillin-resistant Staphylococcus aureus at admission to the intensive care unit: results of a multicenter study: Archives of Internal Medicine. 2003; 163:181–188. 33. Harbarth S, Sax H, Fankhauser-Rodriguez C, Schrenzel J, Agostinho A, Pittet D: 2006. Evaluating the probability of previously unknown carriage of MRSA at hospital admission: American Journal of Medicine. 2006; 119:275.e15–23. 34. Huang SS, Rifas-Shiman SL, Warren DK, Fraser VJ, Climo MW, Wong ES, Cosgrove SE, Perl TM, Pottinger JM, Herwaldt LA, Jernigan JA, Tokars JL, Diekema DJ, Hinrichsen VL, Yokoe DS, Platt R: Improving methicillin resistant Staphylococcus aureus surveillance and reporting in intensive care units: Journal of Infectious Disease. 2007; 195:330–338. 35. Bhat SS, Hegde SK, Salian S: Potential of mobile phones to serve as a reservoir in spread of nosocomial pathogens. Online Journal of Health and Allied Sciences. 2011; 10(2):14-16.

Introduction: Cysticercosis is a common tropical disease. One of the uncommon manifestations of cysticercosis is its disseminated form. This is the report of a case of disseminated cysticercosis, with simultaneous involvement of the brain, eyes, muscles and subcutaneous tissues. Such an extensive involvement of cysticercosis is extremely rare. Case Presentation: A 24 year old male presented with a history of abdominal and back pain, one brief episode of tonic clonic seizure and headache. He had multiple asymptomatic pea-sized subcutaneous nodules over the trunk. Serological test for cysticercal antibodies was positive. In Ultrasonography multiple small cystic area seen in muscles of anterior abdominal wall s/o muscular cysticercosis. In Contrast Enhanced CT Scan extensive foci of calcification with non enhancing pea sized hypodense areas seen in abdominal muscles, Psoas, pelvic and thigh muscles s/o cysticercosis. In CT brain multiple hyperdense foci and few hypodense small sized tiny lesions were seen. The patient was treated with albendazole, steroids and phenytoin, and showed improvement during follow up. Conclusion: Wide spread dissemination is a rare complication of cysticercosis. A planned approach to therapy is required.

1. Takayanagui OM, Odashima NS. Clinical aspects of neurocysticercosis. Parasito Int 2006; 55 Suppl: S111 - 5. Epub 2005 Dec 5. 2. Del Brutto, O. H., V. Rajshekhar, A. C. White, Jr., V. C. Tsang, T. E. Nash, O. M. Takayanagui, P. M. Schantz, C. A. Evans, A. Flisser, D. Correa, D. Botero, J. C. Allan, E. Sarti, A. E. Gonzalez, R. H. Gilman, and H. H. Garcia. 2001. Proposed diagnostic criteria for neurocysticercosis. Neurology 57:177-183 3. Wilson M, Bryan RT, Fried JA, et al clinical evaluation of the cysticerciosis enzyme, linked immunoelectrotransfer blot in patients with neurocysticercosis. J Infect Dis. 1991; 164; 1007-1009. 4. Krishnaswami CS. Case of Cysticercus cellulose. Ind Med Gaz. 1912;27:43–44. 5. Wadia N, Desai S, Bhatt M. Disseminated cysticercosis. New observations, including CT scan findings and experience with treatment by praziquantel. Brain. 1988;111:597–614. 6. Pushker N, Bajaj MS, Balasubramanya R. Disseminated cysticercosis involving orbit, brain and subcutaneous tissue. J Infect 2005;51:245-8. 7. Chadha V, Pandey PK, Chauhan D, Das S. Simultaneous intraocular and bilateral extraocular muscle involvement in a case of disseminated cysticercosis. Int Ophthalmol 2005;26:35-7. 8. Baily GG. Cysticercosis. In: Cook GC, Zumla A, editor. Manson's Tropical Disease. 21. London: Saunders; 2003. pp. 1584–1595. 9. Kumar A, Bhagwani DK, Sharma RK, Kavita , Sharma S, Datar S, Das JR. Disseminated cysticercosis. Indian Pediatr. 1996;33:337–339. 10. Sotelo J, Escobedo F, Rodriguez CJ, Torres B, Rubio DF. Treatment of parenchymal brain cysticercosis. N Engl J Med. 1984;310:1001–1007.

Background and objectives: Working and short term memory loss is common in diabetic patients. Though cognitive deficits affect daily activities and differences between genders are not given much importance to assess working and short term memory at bedside. Hence this study was undertaken to compare working and short term memory in type 2 diabetics with gender matched normal subjects. Methodology: Present study was conducted in Al-Ameen Medical College and Government district Hospital, Bijapur on 114 diabetics (male=72, female=42) and 119 normal subjects (male=79, females=40) aged (40-60 yrs.). Cognitive function assessment was done for short term and working memory by using 5 memory tests-AVLT, VFT, VRT, WDST and VST were used. The results were expressed in average total scores (%). χ2 test was used for statistical analysis. Results: Memory scores of all 5 tests decreased in male diabetic patients when compared to normal male subjects and this decrease was statistically significant (P<0.0001). When female diabetes patients were compared with normal female subjects out of 5 memory tests memory scores in 4 tests were decreased (except VRT) and this decrease was found to be statistically significant (P<0.05). Male diabetic patients when compared with female diabetic patients, decrease in memory scores in male diabetic patients was found to be statistically significant in all tests (except in WDST). Interpretation and conclusion: The short term and working memory status in the present study decreased significantly in the male diabetic patients, which may be due to hyperglycemia, hypoglycemia, vascular dementia and insulin resistance, type of diabetes, age of onset, duration and type of therapy. Therefore these observed effects of gender are of potential clinical importance because working and short term memory loss may interfere with day today activities.

1. Andrew J.Sommerfield, Vincent McAulay, Ian J. Deary, Brian M. Frier. Short-Term, Delayed, and Working Memory Are Impaired During Hypoglycemia in Individuals With Type 1 Diabetes. Diabetes care 2003;26:390-396 2. Martha Clare Morris, Dennis A. Evans, Liesi E. Hebert, Julia L. Bienias. Methodological issues in the study of cognitive decline. Am J Epidemiol 1999; 149:789-93. 3. Celile Proast Lima, Haelena Amieva, Jean Francois Dartigues, Helene Jaquirim Gadda. Sensitivity of 4 psychometric tests to measure cognitive changes in brain aging-population based studies. Am J Epidemiol 2007; 165:344-350. 4. Alka M.Kanaya, Elizabeth barrett connor, Ginny Glidengorin, Kristine Yaffe. Change in cognitive function by glucose tolerance status in older adults. Arch Intern Med 2004; 28:64. 5. Coker LH, Shumaker SA. Type 2 Diabetes mellitus and cognition; an understudied issue in women’s health. J Psychosom Res. 2003;54:129-39. 6. R.K.Solanki, Vaibhav Dubey, Deepthi Munshi. Neurocognitive impairment and comorbid depression in patients of Diabetes mellitus. Int J Diabetes Dev Ctries. 2009;29:133-138. 7. Worali G, Moulton N, Briffet E. Effect of Type 2 Diabetes mellitus on cognitive function. J Fam Pract. 1993;36(6):639-43. 8. Ott A, Stolk R P, Van Harskamp F, Pols H A, Hofman A, Breteler M M. Diabetes mellitus and the risk of dementia: The Rotterdam Study. Neurology 1999;53:1937-42. 9. Edward W. Gregg, Kristine Yaffe, Jane A. Cauley, Deborah B. Rolka, Terri L. Blackwell, K.M.Venkatnarayana. Arch Intern Med 2000; 160:174-180.

Several works in different parts of the world have contributed to the etiological and hematological aspects of sickling disorders. The work in this study was planned to correlate hematological profile with blood gas analysis in cases of sickle cell anemia and sickle cell trait .Sickling disorders are associated with an abnormal hemoglobin, vascular obstruction by sickled cells and a resultant shunting of blood across the pulmonary circulation without access to ventilation. An important aspect of the pathophysiology of sickling disorders lies in the maintenance of adequate oxygen delivery in the face of anemia and vascular obstruction, confounded by compensated pulmonary function. Some of the contemporary works on pulse oximetry have thrown light on various other parameters that need to be considered.

1. Agarwal MB, Mehta BC: Sickle syndromes: A study of 44 cases from Bombay .Indian Pediatr 1980;17:793-795 2. Allon M:Renal abnormalities in sickle cell disease. Arch Intern Med 1990;150:501-504. 3. Battle D ,ItsarayoungyuenK, Arruda JAL Kurtzman NA:Hyperkalemic hyperchloremic metabolic acidosis in sickle cell hemoglobinopathies .Am J Med 1982;71:188-192. 4. Bertles JF, Dobler J:Reversible and irreversible sickling, a demonstration by electron microscopy. Blood, 1969; 33:884-898. 5. Bookchin RM ,Tania Blazas ,Landau LC: Determinants of red cell sickling,effects of varying pH and of increasing intracellular hemoglobin concentration by osmotic shrinkage.J Lab Clin Med 1976;87: 597-615. 6. Bromberg PA, Jensen WN: Arterial oxygen saturation in sickle disease. Am Rev Resp Dis 1967;96:400-405. 7. Bromberg PA:Pulmonary aspects of sickle cell disease. Arch Intern Med 1974; 133:652-657. 8. Brown AK, Sleeper LA, Miller ST ,Pagelow CH, Gill FM, Walclawiv MA: Reference values and hematologic changes from birth to five years in patients with sickle cell disease. 9. Buchanan GR ,Glader BE: Leucocyte counts in children with sickle cell disease. Am J Dis child 1978;132:396-398. 10. Bunn HF; The interaction of sicle cell hemoglobin with DPG,CO2 and other hemoglobins, formation of unstable hybrids, Brewer GJ (ed) Hemoglobin and red cell function NY. Plenum 1972:41. 11. Charache S ,Conley CL: Rate of sickling of red cells during deoxygenation of blood from persons with various sickling disorders. Blood 1964;24: 25-48. 12. Dacie JV and Lewis SM: Investigations in hemoglobinopathy. Practical hematology (ed 8) Churchil Livingstone. 1994;12, 266-268. 13. Fabry ME Nagel RL: The effect of deoxygenation on red cell density: significance for the pathophysiology of sickle cell anemia. Blood 1982;60:1370-1377. 14. Lonsdorfer J, Bogui P, Otayeek, Cabannes R: Cardiorespiratory adjustments in chronic hemolytic anemia. Bull Env Physio Pathol Respir Med 1983;19:339-343. 15. Pauling L, Itano HA, Singer SJ, Wells IC: Sickle cell anemia, a molecular disease. Science 1949;110:543-546. 16. Samal GC: Sickle cell crisis,hematological changes. Ind Pediatrics 1985;22:122-124. 17. Sergeant GR, Sergeant BE, Milner PF: The irreversibly sickled cell, a determinant of hemolysis in sickle cell anemia. Br J Hematol 1969;17;527-533. 18. Sproule BJ ,Halden ER, Miller WF: A study of cardiopulmonary alterations in patients with sickle cell disease and its variants.J Clin Invest 1958;37:486-495. 19. Talib VH: A handbook of medical laboratory technology, CBS publishers,1988;Reprint 1996;6 and 9. 20. Varley H, Gowenlock AH, Walker k, Bell M: Practical clinical biochemistry and commoner tests, Heinemann publisher, ed 5,1991;76 and 800. 21. Veda Y, Bookchin RM, Nagel RL: An increased Bohr effect in sickle cell anemia. Blood 1978;53:472-480. 22. Wintrobe MM: Clinical hematology ed 9, Philadelphia,Lea and Febiger 1993;1:1061-1101 Addendum: 23. Felipe O Orliz, Thomas K Aldrich, Ronald L Nagel and Lennette J Benjamin: Accuracy of pulse oximetry and sickle cell disease. Am J Resp and Critical care med 1999;159:447-451. 24. Fitzgerald RK,Johnson A: Pulse oximetry in SCA .Crit Care Med 2001;29(9);1803-6. 25. Loren G Yamamoto: Interpretation of blood gases and pulse oximetry(textbook),2002.

Aim: To understand the frictional forces between the orthodontic brackets and orthodontic wires and to evaluate the frictional resistance of different orthodontic wires. Materials and method: The test was divided into six groups comprising of fifteen samples each. Group I - stainless steel wires, Group II - TMA wires, Group III- low friction TMA wires, Group IV - colored low friction TMA wires aqua, Group V - colored low friction TMA wires purple, Group VI - colored low friction TMA wires honey dew. The measurements of friction between bracket and arch wire were done with the Instron Universal testing machine (model no.4701). The results were subjected to statistical analysis. Results: On analyzing the mean values of Groups I to VI it was clearly evident that the Group II (TMA) has the maximum frictional resistance and Group VI (colored low friction TMA - honey dew) has the lowest frictional resistance. Conclusion: The frictional resistance is highest in TMA, The frictional resistance is lowest in colored low friction TMA honeydew, and the frictional resistance of colored low friction TMA aqua is similar to that of stainless steel.

1. Bednar. J. R, Gruendeman. G. W and Sandrik. J. L, A comparative study of frictional forces between orthodontic brackets and arch wires, American J Orthodontics 1991 vol100 no6 (513 – 522). 2. Drescher.D, Bourauel. C and Schumacher. H. A, Frictional forces between bracket and arch wire, American J Orthodontics 1989 Vol96 no5 (397-404). 3. Burstone. C. J and Goldberg. A. J, Beta titanium: A new orthodontic alloy American J Orthodontics 1980 Feb (121 - 132). 4. Kusy. R. P and Whitley. J. Q, Effects of surface roughness on the coefficients of friction in model orthodontic systems, J. Biomech 1990.vol23 (913-925). 5. Prososki..R. R, Bagby. M. D and Erickson. L. C, Static frictional force and surface roughness of nickel-titanium arch wires, American J Orthodontics 1991 Vol100 no4 (341-348). 6. Tidy. D.C, Frictional forces in fixed appliances, American J Orthodontics 1989 Vol96 no3 (249-254). 7. Burstone. C. J, Farzin - Nia. F, Production of low-friction and coloured TMA by ion implantation, J of Clinical Orthodontics 1995 Jul (453 461). 8. Burstone. C. J, Pryputniewicz. R. J, Holographic determination of centers of rotation produced by orthodontic forces, American J Orthodontics1980 Vol77 (396-405). 9. Andreasen. G. F and Zwanziger. D, A clinical evaluation of the differential force concept as applied to the edgewise bracket, American J Orthodontics 1980 Vol78 no1 (25-40). 10. Andreasen, G. F., and Quevedo, F. R, Evaluation of frictional forces in the 0.022”, 0.028” edgewise bracket in vitro, J Biochem 1970 no3 (151-160). 11. Riley, J. L., Garrett, S. G., and Moon, P. C, Frictional forces of ligated plastic and metal edgewise brackets, J Dental Research 1979 vol58 A21. 12. Kapila.S, Angolkar. P.V, Duncanson. M.G, and Nanda.R.S, Evaluation of friction between edgewise-stainless steel brackets and orthodontic wires of four alloys, American J Orthodontics 1990 Vol98 no2 (117-126). 13. Kusy. R. P, Comparison of nickel-titanium and beta titanium wire sizes to conventional orthodontic arch wire materials, American J Orthodontics 1981 Vol79 no6 (625-629). 14. Kusy .R. P and Whitley. J. Q, Coefficients of friction for arch wires in stainless steel and polycrystalline alumina bracket slots- The dry state, American J Orthodontics 1990 Vol98 no4 (300-312). 15. Michelberger. D .J, Eadie. R. L, Faulkner. M .G, Glover. K. E, The friction and wear patterns of orthodontic brackets and arch wires in the dry state, American J Orthodontics Dentofacial Orthopedics 2000 Vol118 (662-74). 16. Cash. A, Curtis. R, A comparative study of the static and kinetic frictional resistance of titanium molybdenum alloy arch wires in stainless steel brackets, European Journal of Orthodontics 2004 Vol. 26 (105-111). 17. Kusy. R. P, Tobin. E. J, Whitley. J.Q, Sioshansi. P, Frictional coefficients of ion-implanted alumina against ion-implanted beta-titanium in the low load, low velocity, single pass regime, Dental Materials 1992 Vol8 (167-72). 18. Kula. K, Phillips. C, Gibilaro. A, and Proffit. W. R, Effect of ion implantation of TMA archwires on the rate of orthodontic sliding space closure, American J Orthodontics 1998 vol114 no5 (577-580). 19. Kusy. R. P, Tobin. E. J, Whitley .J. Q, Frictional coefficients of ion-implanted alumina against ion-implanted beta-titanium in the low load, low velocity, single pass regime, Dental Materials 1992 Vol8 (167-72). 20. Olga Keith, Kusy. R. P and Whitley. J. Q, Zirconia brackets: An evaluation of morphology and coefficients of friction, American J Orthodontics 1994 Vol106 no6 (605-614). 21. Stannard. J.G, Gau. J. M, and Hanna, Comparative friction of orthodontic wires under dry and wet conditions, American J Orthodontics 1986 Vol89 no6 (485-491). 22. Schwartz. A. M, Tissue changes incident to orthodontic tooth movement, International J Orthodontia 1932 Vol18 (331-352). 23. Storey, E and Smith, R, Force in orthodontics and its relation to tooth movement, Australian J Dentistry 1952 Vol56 (11). 24. Quinn. R. B, Yoshikawa. D. K, A reassessment of force magnitude in orthodontics, American J Orthodotics 1985 Vol88 (252-260). 25. Frank. C. A and Nikolai. R. J, A comparative study of frictional resistances between orthodontic bracket and arch wire, American J Orthodontics 1980 Vol78 no6 (593-609). 26. Riley. J .L, Garrett. S .G, Moon. P .C, Frictional forces of ligated plastic and metal edgewise brackets, J Dental Research 1979 Vol58 A21. 27. Baker. K. L, Nieberg. L. G, Weimer. A.D, Hanna. M, Frictional changes in force values caused by saliva substitution, American J Orthodontics Dentofacial Orthopedics 1987 Vol91 (316-320).

Persistent Mullerian duct syndrome (PMDS) refers to the presence of a uterus and sometimes other Mullerian duct derivatives in a genetically male. We report a case of male with right side cryptorchidism and left inguino scrotal mass with Mullerian duct derivatives (uterus).

1. Odi To, Abdur-Rahman Lo,Nasir AA. Persistent Mullerian duct syndrome ; A case report and review of the literature. Afr J paediatr surg 2010;7:191-3 2. Indian J Radiol Imaging. 2010 February; 20(1): 72–74. Divya Renu, B Ganesh Rao, K Ranganath, and Namitha. 3. Journal of Medical Case Reports 2011, 5:586 Nishikant N Gujar, Ravikumar K Choudhar, Geeta R Choudhari, Nasheen M Bagali, Harish S Mane, Jilani S Awati and Vipin Balachandran. 4. Prakash N, Khurana A, Narula B. Persistent müllerian duct syndrome. Indian J Pathol Microbiol 2009;52:546-8 5. The Journal of Pakistan Medical Association Vol. 57, No. 8, August 2007 Muhammad Shamim Department of Surgery, Fatima Hospital and Baqai Medical University, Karachi.

Background and Objectives: Delay in the application of stomal appliance till the removal of the conventional supporting glass or plastic rods resulted in leakage of faecal matter. The objective of the study was to know the efficacy, safety and compliance of the new technique of loop Stoma Bridge. Methods: Subcutaneously, a closed suction drain tube of 16 or 18 F was placed with the help of trocar .The points of entry and exit of the tube are just beyond the circumference of the flange. Results: Out of the 45 patients studied no major complications were encountered. Emergency and elective procedures were done in 23 and 22 patients respectively. Complications like pain in 14 patients were noticed and in 4 patients serous discharge was seen. None had pain for more than 10 days. Interpretations and Conclusion: It is a safe, cheap method and can be performed easily with low morbidity. The colostomy flange can be applied immediately without faecal leakage.

1. Abcarian H, Pearl RK, Stomas. SurgclinNorth Am 1988:68:1295-1305. 2. Lavery I C technique of colostomy construction and closure. In: Fischer JE, Bland KI, editors Mastery of Surgery. 5th ed. Philadelphia: Lippincott Williams and Wilkins; 2007. p.1439-1448 3. Kodner IJ, Read TE. Intestinal stomas. In: Zinner MJ, Ashley SW,editors. Maingot's Abdominal Operations. 11st ed. United States of America: The McGraw Hill Companies; p. 141–177. 86 1. 4. Lavery IC. Technique of colostomy construction and closure. In: Fischer JE, Bland KI, editors. Mastery of Surgery. 5th ed. Philadelphia: Lippincott Williams and Wilkins; 2007. p. 1439–1448. 5. Dinnick.T. The origins andevolution of colostomy Br j surg 1934 22: 142-153 6. Abcarian H, Pearl RK. Stomas.SurgClin North Am1988;68:1295–1305. 7. Speirs M, Leung E, Hughes D, Robertson I, Donnelly L,Mackenzie I, Macdonald A. Ileostomy rod—is it a bridge toofar? Colorectal Dis 2006;8:484–487. 8. Richardson NG, Leicester RJ. A better bridge for loop stomas.BrJSurg 1996;83:1011. 9. Sudhindran S, Regunath KJ. A better bridge for loop stomas. Br JSurg 1996;83:1797. 10. Habib S, Williams J. A better bridge for loop stomas. Br J Surg1996;83:1161. 11. Nunoo-Mensah JW, Chatterjee A, Khanwalkar D, Nasmyth DG. Loopileostomy: modification of technique. Surgeon 2004;2:287–291. 12. K. Harish , The loop stoma bridge- the new technique. J gastrointest surgery (2008 ) 12:958-961 87 13. Jenkinson LR, Houghton PW, Steele KV, Donaldson LA,Crumplin MK. The Biethium bridge—an advance in stoma care.Ann R CollSurgEngl 1984;66:420–422. 14. Raimes SA, Mathew VV, Devlin HB. Temporary loop ileostomy. JR Soc Med 1984;77:738–741. 15. Wedell J, Banzhaf G, Meier zuEissen P, Schlageter M. Experienceswith a subcutaneous, fully resorbable bridge in construction a doubleloopileo- and colostomy. Chirurg 1990;61:36–38. 16. Atkin G, Scott MA, Mathur P, Mitchell IC. The rectus sling to prevent loop colostomy retraction: a case series. Int Semin Surg Oncol 2005;2:22. 17. Milner CS, Sutton C, Hemingway D. The skin bridge loopcolostomy. Tech Coloproctology 2006;10:137–138.

Background. The tibia is the most common fractured long bone, because of its exposed anatomical location and inadequate muscular envelope. Objectives: Evaluate fracture healing and union time with closed Interlocking nailing with reaming in regards to its functional outcome (klemm and borner criteria) with respect to knee and ankle joint movements, deformity, muscle atrophy and radiological union aiming at early mobility of patients. We report a randomized analysis of 30 patients treated in one center in rural area. Methods: Study done at Orthopaedic Department of NIMS Medical College, Jaipur (Rajasthan) between May 2011and May 2013. The patients included were more than 18 years, only closed diaphyseal fractures considered. Fractures of tibia other than diaphysis and unfit patients were excluded. Mean age was 32.4 years.29 patients had road traffic accident,1patient had history of fall:16 had ipsilateral fibula fracture,6 had contralateral tibia shaft fracture ,3 had head injury,3 had metacarpal fracture,2 had fracture clavicle and one had floating knee. Results: Average union time 4.7 months Complications encountered were 3 delayed union,1 malunion,1superficial infection,1 deep infection and 15 developed anterior knee pain. Conclusion: 90%of the total cases had excellent results,6.66% had good results and 3.33% had fair results.

1. Brown PW, Urban JG. Early weight bearing treatment of fractures of the tibia. An end result of 63 cases. J Bone Joint Surg 1969;51A:59-75. 2. Bach AW, Hansen Jr ST. Plates versus external fixator in severe open tibia shaft fractures. A randomised study. Clin Orthop 1989;241:89-94. 3. Reidt T, Webb JK, Allgower M. Experience with the dynamic compression plate (DCP) in 418 recent fractures of tibial shaft. Injury 1976;7:252-7. 4. Smith JE. Results of early and delayed internal fixation for tibial shaft fractures: A review of 470 fractures. J Bone Joint Surgery 1974;56-B:469-77. 5. Holbrook JL, Swiontkowski MF, Sanders R. Treatment of open fractures of tibial shaft: Ender nailing versus external fixation: A randomized prospective comparison. J Bone Joint Surg 1989;71A:1231-8. 6. Lottes JO. Blind nailing technique for insertion of the triflange medullary nail: Reprot of 300 nailing for fractures of the shaft of the tibia. JAMA 1951; 55:1039-4 7. Nazri MY, Halin YA et al.(2004); Med.J. Malaysia 2004 Dec; 59(5); 665-9.outcome of infection following internal fixation of closed fractures. 8. Klemm k., Borner M. Interlocking nailing of complex fracture of the femur and tibia . Clin. Orthop., 1986.212,89. 9. Lawrence B. Bone, Kenneth D. Johnson.: Treatment of tibial fractures by reaming and intramedullary nailing; Journal of Bone and Joint Surgery, 1986,68A: 877-887. 10. Court Brown C. M, Christie J, Mc Queen M. M.: closed intramedullary tibial nailing; Journal of Bone and Joint Surgery, 1990, 72B: 605-611. 11. Arne Ekeland, B. Jorn. O. Thoresen, Antti’Alho, Kunt Stromsoe, Gunnar Folleras and Aren Haukeb.: Interlocking Intramedullary nailing in the treatment of tibial fractures 1988; CORR, 231 : 208-215. 12. Blachut P. A.,P. J. O'Brien, R. N. Meek, H. M. Broekhuyse.: Interlocking nailing with or without reaming for the treatment of closed fractures of the tibial shaft; Journal of Bone and Joint Surgery, 1997, 79 A: 640-646. 13. Toivanen JA, Vaisto O, Kannus P, Latvala K, Honkonen SE, Jarvinen MJ (2002) Anterior knee pain after intramedullary nailing of fractures of the tibial shaft. A prospective, randomized study comparing two different nail-insertion techniques. J Bone Joint Surg Am 84:580–585 14. Keating JF, O’Brien PI, Blachut PA, Meek RN, Broekhuyse HM (1997) Reamed interlocking intramedullary nailing of open fractures of the tibia. Clin Orthop Relat Res 338:182–191. 15. Bhattacharyya T, Seng K, Nassif NA, Freedman I (2006) Knee pain after tibial nailing: the role of nail prominence. Clin Orthop Relat Res 449:303–307. 16. Hernigou. P. et al..,: Proximal entry for intramedullary nailing of tibia; Journalof Bone and Joint Surgery, 2000, 82B: 33-41. 17. Jarmo. A. K, Toivannen et al.: Anterior knee pain after intramedullary nailingof fractures of tibial shaft; Journal of Bone and Joint Surgery, 2002, 84A: 580-585.

Objectives: Therefore, the present study was planned with an objective to analyze the incidence of postoperative wound infections. An additional objective was to evaluate the efficacy of different measures taken by surgeons prior to Surgery to prevent infection. Methods: Hundred individuals between 18-50 years of age were evaluated based on the surgery’s they underwent at Father Muller Medical College, Mangalore between 2010 – 2012. The data received was recorded in individual patient proform as obtained on admission and on outpatient basis. Results: The overall incidence in this study was 4%. Maximum incidence was observed in 41-50 age group (96%), followed by in the age group of 21-30 yrs (94%).Out of 56 patients with spinal anaesthesia, the incidence of infection was noted in 4 cases. The mean preoperative stay in infected cases was 4.50 days, when compared to 3.06 days in non infected cases whereas mean post operative stay in infected cases was 7.75 days, when compared to 10.16 days. Conclusions: Prophylactic regimens should be recommended for a wide variety of surgical procedures. Marked variations exist in the spectrum of infecting pathogens and in the degree of antimicrobial resistance.

1. McDermott W, Rogers DE. Social ramifications of control of microbial disease. Johns Hopkins Med J. 1982; 151: 301-12. 2. Howe CW, Marston AT. A study on sources of postoperative Staphylococcal infection. Surg Gynecol Obstet.1962;115:266-75. 3. Burke JF. The effective period of preventive antibiotic action in experimental incisions and dermal lesions. Surgery 1961:50:161-8. 4. Kirkland KB, Briggs JP, Trivette SL. The impact of surgical site infections in the 1990’s: attributable mortality, excess length of hospitalization and extra costs. Infect Control Hops Epidemiol 1999No;20(11):725-730. 5. Ketcham AS, Lieberman JE, West JT. Antibiotic prophylaxis in cancer surgery and its value in Staphylococcal carrier patients. Surg Gynecol Obstet. 1963; 117: 1-6. 6. Martson RA, Cobb AG, Bantley G. Stammor compare with Charnley total hip replacement. J Bone J surg 1996;78:178-184. 7. Martson RA, Cobb AG, Bantley G. Stammor compare with Charnley total hip replacement. J Bone J surg 1996;78:178-184. 8. Williams DN, Gustilo RB. The use of preventive antibiotic in Orthopaedic surgery. Clin Orthop Relat Res 1984;190:83-8. 9. Weick JA, Jackson JK, O-Brien TJ, Lurate RB, Russell JM, Dorchak JD. Efficacy of prophylactic antibiotic in arthroscopic surgery. Orthopaedic 1997;20:133-4. 10. Woods RK, Dellinger EP: Current guidelines for antibiotic prophylaxis of surgical wounds. Am Fam Physician 1998 Jun ;57 (11) :2731-2740. 11. Williams DN, Gustilo RB. The use of preventive antibiotic in Orthopaedic surgery. Clin Orthop Relat Res 1984;190:83-8.

Objectives: To report our experience with single-incision laparoscopic surgery (SILS) and to perform a comparison with conventional laparoscopic surgeries. Study Design: Data were prospectively collected for all patients undergoing SILS(n = 23) and compared with data of those undergoing conventional laparoscopic procedures (n = 42) at Lifeline Hospital, Perungudi, Chennai. This included patient demographic data and intraoperative and postoperative outcomes. Interventions: conventional laparoscopic surgeries and SILS. Main Outcome measures: Operative time, conversion to open operation, and length of hospital stay. Results: Operative time was longer with SILS compared with conventional laparoscopic surgeries (P < .001). A correlation was seen between reducing SILS operative time and increasing experience (Pearson’s correlation coefficient, −0.27). Two patients in the SILS group required the addition of extra laparoscopic ports. No patients in the SILS group required conversion to open surgery compared with 4 patients in the standard laparoscopic group. Patients stayed an average of 0.67 days following SILS and 1.62 days following conventional laparoscopic procedures. Conclusions: Single-incision laparoscopic surgery may be equal to conventional laparoscopic surgeries in terms of safety and efficacy. Further randomized studies are required to investigate any significant advantages of this new and attractive technique.

1. Kuhry E, Schwenk W, Gaupset R, Romild U, Bonjer J. Long-term outcome of laparoscopic surgery for colorectal cancer: a Cochrane systematic review of randomised controlled trials. Cancer Treat Rev 2008;34 (6) 498- 504. 2. Keus F, de Jong JA, Gooszen HG, van Laarhoven CJ. Laparoscopic vs open cholecystectomy for patients with symptomatic cholecystolithiasis. Cochrane Database Syst Rev 2006; (4) 6228-6231. 3. Nguyen NT, Reavis KM, Hinojosa MW, Smith BR, Stamos MJ. A single-port technique for laparoscopic extended stapled appendectomy. Surg Innov 2009; 16 (1) 78- 81. 4. Hong TH, Kim HL, Lee YS. et al. Transumbilical single-port laparoscopic appendectomy (TUSPLA): scarless intracorporeal appendectomy. J Laparoendosc Adv Surg Tech A 2009;19 (1) 75- 78. 5. Binenbaum SJ, Teixeira JA, Forrester GJ. et al. Single-incision laparoscopic cholecystectomy using a flexible endoscope. Arch Surg 2009;144 (8) 734- 738. 6. Kuon Lee S, You YK, Park JH, Kim HJ, Lee KK, Kim DG. Single-port transumbilical laparoscopic cholecystectomy: a preliminary study in 37 patients with gallbladder disease. J Laparoendosc Adv Surg Tech A 2009;19 (4) 495- 499. 7. Chow A, Purkayastha S, Aziz O, Paraskeva P. Single-incision laparoscopic surgery for cholecystectomy: an evolving technique. Surg Endosc 2010;24 (3) 709- 714. 8. Reavis KM, Hinojosa MW, Smith BR, Nguyen NT. Single-laparoscopic incision transabdominal surgery sleeve gastrectomy. Obes Surg 2008;18 (11) 1492- 1494. 9. Saber AA, El-Ghazaly TH. Early experience with single incision transumbilical laparoscopic adjustable gastric banding using the SILS port. Int J Surg 2009;7 (5) 456- 459. 10. Bucher P, Pugin F, Morel P. Single port access laparoscopic right hemicolectomy. Int J Colorectal Dis 2008;23 (10) 1013- 1016. 11. Rané A, Rao P, Rao P. Single-port-access nephrectomy and other laparoscopic urologic procedures using a novel laparoscopic port (R-port). Urology 2008;72 (2) 260- 263, discussion 263-264. 12. Honda G, Iwanaga T, Kurata M, Watanabe F, Satoh H, Iwasaki K. The critical view of safety in laparoscopic cholecystectomy is optimized by exposing the inner layer of the subserosal layer. J Hepatobiliary Pancreat Surg 2009;16 (4) 445- 449. 13. Avgerinos C, Kelgiorgi D, Touloumis Z, Baltatzi L, Dervenis C. One thousand laparoscopic cholecystectomies in a single surgical unit using the “critical view of safety” technique. J Gastrointest Surg 2009;13 (3) 498- 503. 14. Seymour NE, Gallagher AG, Roman SA. et al. Virtual reality training improves operating room performance: results of a randomized, double-blinded study. Ann Surg 2002;236 (4) 458- 463, discussion 463-464. 15. Aggarwal R, Ward J, Balasundaram I, Sains P, Athanasiou T, Darzi A. Proving the effectiveness of virtual reality simulation for training in laparoscopic surgery. Ann Surg 2007;246 (5) 771- 779. 16. Aggarwal R, Crochet P, Dias A, Misra A, Ziprin P, Darzi A. Development of a virtual reality training curriculum for laparoscopic cholecystectomy. Br J Surg 2009;96 (9) 1086- 1093. 17. Ishizawa T, Bandai Y, Kokudo N. Fluorescent cholangiography using indocyanine green for laparoscopic cholecystectomy: an initial experience. Arch Surg 2009;144 (4) 381- 382. 18. Uslu HY, Erkek AB, Cakmak A. et al. Trocar site hernia after laparoscopic cholecystectomy. J Laparoendosc Adv Surg Tech A 2007;17 (5) 600- 603. 19. van Gulik TM. Langenbuch's cholecystectomy, once a remarkably controversial operation. Neth J Surg 1986;38 (5) 138- 141. 20. Reynolds W Jr. The first laparoscopic cholecystectomy. JSLS 2001;5 (1) 89- 94. 21. Connor S, Garden OJ. Bile duct injury in the era of laparoscopic cholecystectomy. Br J Surg 2006;93 (2) 158- 168. 22. Fletcher DR, Hobbs MS, Tan P. et al. Complications of cholecystectomy: risks of the laparoscopic approach and protective effects of operative cholangiography: a population-based study. Ann Surg 1999;229 (4) 449- 457. 23. Gallstones and laparoscopic cholecystectomy. NIH Consens Statement 1992;10 (3) 1- 28.

Background: Obesity is associated with enhanced lipid peroxidation. Malondialdehyde (MDA), one of several by-products of lipid peroxidation process, is a biomarker that provides an indication of lipid peroxidation level. The objective of the present study was to estimate the level of MDA in obese individuals. Methods: 30 obese men with BMI between 25-30 Kg/m2 and 30 non-obese men with BMI <25 Kg/m2 were enrolled in the study. Malondialdehyde (MDA) was assessed in both the groups. Results: Plasma MDA activity was significantly increased in the obese subjects when compared with controls. Conclusion: This finding suggests that obesity is an important factor for enhanced oxidative stress in individuals.

1. Haslam W, James P: “Obesity”. Lancet 2005, 366:1197-1197. 2. Pérez-Escamilla, R.; Obbagy, J.E.; Altman, J.M.; Essery, E.V.; McGrane, M.M.; Wong, Y.P.; Spahn, J.M.; Williams, C.L. Dietary energy density and body weight in adults and children:A systematic review. J. Acad. Nutr. Diet. 2012, 112, 671–684. 3. Coutinho, G.V.; Coutinho, F.R.; Faiad, J.Z.; Takii, M.S.; de Limareis, S.R.; Ignácio-Souza, L.M.; Paiva, A.A.; Latorraca, M.Q.; Gomes-da-Silva, M.H.; Martins, M.S. Intrauterine protein restriction combined with early postnatal overfeeding was not associated with adult-onset obesity but produced glucose intolerance by pancreatic dysfunction. Nutr. Metab. 2013, 10, 5. 4. Winter, Y.; Sankowski, R.; Back, T. Genetic determinants of obesity and related vascular diseases. Vitam. Horm. 2013, 91, 29–48. 5. Delrue, M.A.; Michaud, J.L. Fat chance: Genetic syndromes with obesity. Clin. Genet. 2004, 66, 83–93. 6. Nielsen S, Jensen MD. (1997) Obesity and cardiovascular disease: is body structure a factor? Curr Opin Lipidol; 8: 200 -204. 7. Evans JL, Goldfine BA, Maddux BA, Grodsky GM. (2002) Oxidative stress and stress-activated signalling pathways: a unifying hypothesis of type 2 diabetes. Endocr Rev; 23: 599-622 8. Vincent HK, Taylor AG. (2006) Biomarkers and potential mechanisms of obesity-induced oxidant stress in humans. Int J Obes; 30: 400- 418. 9. Nourooz-zadeh J, Tajaddini Sarmadi J, MC Carthy. S. et al. elevated levels of authentic plasma hydroperoxides in NIDDM, Diabetes 1995;44: 1054-1058. 10. Vincent HK, Taylor AG. (2006) Biomarkers and potential mechanisms of obesity-induced oxidant stress in humans. Int J Obes; 30: 400- 418. 11. Vincent HK, Innes KE, Vincent KR. (2007) Oxidative stress and potential interventions to reduce oxidative stress in overweight and obesity. Diabetes Obes Metab; 9: 813-839. 12. Spiteller G. (2007) The important role of lipid peroxidation processes in aging and age dependent diseases. Mol Biotechnol; 37: 5-12. 13. Cheng Z, Li Y. (2007) What is responsible for the initiating chemistry of iron-mediated lipid peroxidation: an update. Chem Rev; 107: 748-766. 14. Sattler W, Malle E, Kostner GM. Methodological approaches for assessing lipid and protein oxidation and modification in plasma and isolated lipoproteins. Methods Mol Biol 1998; 110: 167. 15. Selvakumar C, Maheshwari U, Suganthi, Archana. (2012) Oxidant-Antioxidant disturbance in men classified as obese according to the preliminary WHO guidelines for Asians. J. Stress Physiol. Biochem. Vol. 8 No. 1, 172-181. 16. Mates JM, Perez-Gomez C, Nunez de Castro I. (1999) Antioxidant enzymes and human diseases. Clin Biochem; 32: 595–603.

Purpose: To report the initial experience, complications and short term visual outcomes of patients undergoing 23 Gauge Transconjunctival Pars Plana Vitrectomy. Methods: This was a Retrospective non comparative case series evaluating the first 50 consecutive cases of 23 Gauge Transconjunctival Pars Plana Vitrectomy done by a single surgeon in a Tertiary Eye Care centre. The outcome measures included best corrected visual acuity at 6weeks compared to the Pre Operative Visual acuity, Intraoperative complications and difficulties and Post Operative complications. The relevant information was retrieved from the case records and follow up records of these patients. Results: Out of the 50 eyes studied, Visual Acuity at 6 weeks improved in 39 (78%); remained unchanged in 8 (16%) and worsened in 3 (6%). Suturing of at least one of the ports was done in 18 eyes (36%).Intraoperative Retinal breaks occurred in 2 eyes. The Post operative complications noted in the post operative period up to 6 wks were vitreous hemorrhage (8%) ,cataract formation (6%),post operative uveitis (6%) and retinal redetachment (2%). 1 case had to be converted into a 20 Gauge vitrectomy due to the development of choroidal effusion. Conclusion: 23 Gauge Transconjunctival Vitrectomy is an effective surgical technique for a variety of Vitreoretinal surgical indications. The safety and efficacy compared well with that in the published literature.

1. Holladay JT. Proper method for calculating average visual acuity. JRefract Surg. 1997;13:388–391. 2. Eckardt C. Transconjunctival sutureless 23-gauge vitrectomy .Retina 2005;25:208 –211. 3. Fine HF, Iranmanesh R, Iturralde D, Spaide RF. Outcomes of 77 consecutive cases of 23-gauge transconjunctival vitrectomy surgery for posterior segment disease. Ophthalmology 2007;114:1197–2000. 4. Janet J. Chieh, Adam H. Rogers,Torsten W. Wiegand, Caroline R. Baumal,,Elias Reichel, Jay S. Duker. Short-term safety of 23-gauge single-step transconjunctival vitrectomy surgery .Retina 2009;29:1486–1490. 5. Lott MN, Manning MH, Singh J, Zhang H, Singh H, MarcusDM. 23-Gauge vitrectomy in 100 eyes: short-term visual outcomes and complications. Retina 2008;28:1193–1200. 6. Omesh P. Gupta, Allen C. Ho, Peter K. Kaiser, Carl D. Regillo, Sanford Chen, David S. Dyer,Pravin U. Dugel, Sunil Gupta, And John S. Pollack Am J Ophthalmol 2008;146:193–197. 7. Spandau Ulrich & Heimann Heinrich. Practical Handbook for Small-Guage Vitrectomy: A Step-by-Step Introduction to Surgical Techniques :Springer-Verlag Berlin and Heidelberg GmbH & Co. K, Berlin, 2012.

Introduction: Sacral fractures occur in approximately 45% of all pelvic fractures. From conservative to surgical, various treatment modalities are available to treat sacral fracture. The post treatment outcome also depends on various factors. Aims and Objectives: To study the modalities of treatment employed in the management of sacral and sacro-iliac joint injuries (Conservative and Operative) and to compare the results and outcomes of conservative vs. operative interventions employed in the management of sacral factures and sacro-iliac joint injuries. Materials and methods: total 32 patients were selected during the study period and were followed for 6 months post treatment to study the outcome. Majeed Scoring system was used to study post treatment functional assessment. Results: post injury displacement was seen in Denis type 3 fracture and vertical shaer fractures. And the displacement ids much reduced after treatment (both surgical and conservative). Mean ambulatory time in patients managed surgically and conservatively was nearly equal. In surgical procedure plating was required in most of the patients as compared to iliosacral screw and external fixator. It was also observed that patient managed surgically scored better Majeed score as compared to conservatively managed patients. But the difference was not significant. Conclusion: sacral fracture can be managed conservatively and surgically depending upon the post injury displacement. Outcome can be improved by selecting appropriate treatment modality.

1. Hasenboehler EA, Stahel PF, Williams A. Prevalence of sacral dysmorphia in a prospective trauma population: Implications for a "safe" surgical corridor for SI-screw placement. Presented at: 75th Annual meeting of the American Academy of Orthopaedic Surgeons; March 5-9, 2008; San Francisco, CA 2. Vaccaro AR, Lim DH, Brodke DS, Harris M, Chapman J, Schildhauer T, et al. Diagnosis and management of sacral spine fractures. J Bone Joint Surg Am 2004;86:166-75. 3. Majeed SA. Grading the outcome of pelvic fractures. J Bone Joint Surg [Br] 1989;71-B: 304-6 4. Latenser BA, Gentilello LM, Tarver AA, Thalgott JS, Batdorf JW. Improved outcome with early fixation of skeletally unstable pelvic fractures. J Trauma. 1991 Jan;31(1):28-31. 5. Kellam JF, McMurtry RY, Paley D, Tile M. The unstable pelvic fracture: operative treatment. Orthop Clin North Am 1987;18:25-41. 6. Matta JM, Tornetta P, III. Internal fixation of unstable pelvic ring injuries. Clin Orthop. 1996;129-140.

Aims and Objectives: To assess the practice and trends of blood transfusion services at our institute in elective orthopaedic surgeries, and to work out Surgical Blood Order Schedule at our institute by means of Cross Match Transfusion Ratio (C/T ratio), Transfusion Index (TI), Transfusion Probability (%T) and Mead’s criteria and to develop suggestions to improve the efficiency of blood utilisation and reduce the unnecessary cross matching as well as wastage of blood bank resources. Materials and Methods: Patients (male and female) of the age group of 20- 80 years under elective orthopaedic surgery were enrolled in the study. Patients, who received blood transfusion during intraoperative period and within 24 hours postoperatively, during one year duration, were included in the study and frequency of utilization of blood in different elective orthopaedic surgeries was noted. Results and Conclusion: A total of 159 patients with an age group of 20-80 years were evaluated in one year duration. Two hundred forty two units of blood were cross matched and only seventy eight units were transfused to seventy one patients. Sixty eight percent of the units cross-matched were not transfused. Five out of six elective procedures had a C/T ratio higher than 2.5 and all of the procedures under study had a low Transfusion Index (TI<0.5).

1. Blood Transfusion Safety cited in The Clinical Use of Blood. WHO, Geneva. Pg. 16-17, 101-102, 126-127. 2. Bhutia SG, Srinivasan K, Ananthakrishnan N, Jayanthi S, Ravishankar M.Blood utilization in elective surgery-requirements, ordering and transfusion practices. Nati Med J India 1997 Jul-Aug; 10(4): 164-8. 3. Chawla T, Kakepoto GN, Khan MA. An audit of blood cross-match ordering practices at the Aga Khan University Hospital: first step towards a Maximum Surgical Blood Ordering Schedule. J Pak Med Assoc. 2001 Jul; 51(7): 251-4. 4. Vibhute M, Kamnath SK, Shetty A. Blood utilization in elective general surgery cases: requirements, ordering a transfusion practices. J Post grad Med, 2000 Jan-March; 46(1): 13-7. 5. Fredman B, Oberman H, Chanwick A, et al.The maximum surgical blood order schedule and surgical blood use in the United States. Transfusion 1976; 16: 380-387. 6. Friedman BA. An analysis of surgical blood use in United States hospitals with application to the maximum surgical blood order schedule. Transfusion, 1979 May-Jun; 19(3): 268-78. 7. Gupta AK et al. The Blood transfusion trends in a Delhi Hospital. Indian J. Intern Med 1995; 5:66-71. 8. The British Committee for Standards in Haematology Blood Transfusion Task Force. Guidelines for implementation of a maximum surgical blood order system schedule. Clin Lab Haematol. I; 12:321-7. 9. Juma T Baraka A, Abu-Lisan M, Afsar SK. Blood ordering habits for elective surgery: Time for change. Int Hospital Federations 1990; 26 :16-19. 10. Mintz PD, Nordine RB, Henry JB et al. Expected Hemotherapy in elective surgery. New York State J Med 1976; 76; 532-537. 11. Sarma DP. Use of blood in elective surgery. JAMA 1980; 243; 1536-1538.

Aims and Objectives: To assess the practice and trends of blood transfusion services at our institute in elective orthopaedic surgeries, and to work out Surgical Blood Order Schedule at our institute by means of Cross Match Transfusion Ratio (C/T ratio), Transfusion Index (TI), Transfusion Probability (%T) and Mead’s criteria and to develop suggestions to improve the efficiency of blood utilisation and reduce the unnecessary cross matching as well as wastage of blood bank resources. Materials and Methods: Patients (male and female) of the age group of 20- 80 years under elective orthopaedic surgery were enrolled in the study. Patients, who received blood transfusion during intraoperative period and within 24 hours postoperatively, during one year duration, were included in the study and frequency of utilization of blood in different elective orthopaedic surgeries was noted. Results and Conclusion: A total of 159 patients with an age group of 20-80 years were evaluated in one year duration. Two hundred forty two units of blood were cross matched and only seventy eight units were transfused to seventy one patients. Sixty eight percent of the units cross-matched were not transfused. Five out of six elective procedures had a C/T ratio higher than 2.5 and all of the procedures under study had a low Transfusion Index (TI<0.5).

1. Blood Transfusion Safety cited in The Clinical Use of Blood. WHO, Geneva. Pg. 16-17, 101-102, 126-127. 2. Bhutia SG, Srinivasan K, Ananthakrishnan N, Jayanthi S, Ravishankar M.Blood utilization in elective surgery-requirements, ordering and transfusion practices. Nati Med J India 1997 Jul-Aug; 10(4): 164-8. 3. Chawla T, Kakepoto GN, Khan MA. An audit of blood cross-match ordering practices at the Aga Khan University Hospital: first step towards a Maximum Surgical Blood Ordering Schedule. J Pak Med Assoc. 2001 Jul; 51(7): 251-4. 4. Vibhute M, Kamnath SK, Shetty A. Blood utilization in elective general surgery cases: requirements, ordering a transfusion practices. J Post grad Med, 2000 Jan-March; 46(1): 13-7. 5. Fredman B, Oberman H, Chanwick A, et al.The maximum surgical blood order schedule and surgical blood use in the United States. Transfusion 1976; 16: 380-387. 6. Friedman BA. An analysis of surgical blood use in United States hospitals with application to the maximum surgical blood order schedule. Transfusion, 1979 May-Jun; 19(3): 268-78. 7. Gupta AK et al. The Blood transfusion trends in a Delhi Hospital. Indian J. Intern Med 1995; 5:66-71. 8. The British Committee for Standards in Haematology Blood Transfusion Task Force. Guidelines for implementation of a maximum surgical blood order system schedule. Clin Lab Haematol. I; 12:321-7. 9. Juma T Baraka A, Abu-Lisan M, Afsar SK. Blood ordering habits for elective surgery: Time for change. Int Hospital Federations 1990; 26 :16-19. 10. Mintz PD, Nordine RB, Henry JB et al. Expected Hemotherapy in elective surgery. New York State J Med 1976; 76; 532-537. 11. Sarma DP. Use of blood in elective surgery. JAMA 1980; 243; 1536-1538.

Background and Objectives: Working and short term memory loss is common in poorly controlled diabetic patients. Though cognitive deficits affect daily activities much importance is not given to assess working and short term memory at bedside. Hence this study was undertaken to correlate blood glucose level with working and short term memory in type 2 diabetics compared with age and gender matched normal subjects. Methodology: Present study was conducted in Al-Ameen Medical College and Government district Hospital, Bijapur on 114 diabetics aged (40-60 yrs.) and 119 normal subjects aged (40-60 yrs.). Cognitive function assessment was done for short term and working memory by using 5 memory tests. For short term memory- AVLT, VFT and VRT and for working memory – WDST and VST were used. The results were expressed in average total scores(%). T test and Correlation-regression analysis were used for statistical analysis. Results: Significant decrease in working and short term memory was observed in diabetic patients. In diabetes patients mean FBS was found to be 146+29.2mg% compared to the mean FBS levels of normal subjects (97.9+12.6mg %). In diabetes patients mean PPBS was found to be 194+39mg % compared to the mean PPBS levels of normal subjects (133+11.1mg %). Memory scores in all 5 tests were found to be decreased correlating negatively with the FBS and PPBS levels. Interpretation and Conclusion: The short term and working memory status in the present study decreased significantly in the diabetic patients, which may be due to hyperglycemia, hypoglycemia, vascular dementia and insulin resistance. Therefore these observed effects of FBS and PPBS levels are of potential clinical importance because working and short term memory loss could interfere with day today activities.

1. Andrew J.Sommerfield, Vincent McAulay, Ian J. Deary, Brian M. Frier. Short-Term, Delayed, and Working Memory Are Impaired During Hypoglycemia in Individuals With Type 1 Diabetes. Diabetes care 2003;26:390-396 2. Martha Clare Morris, Dennis A. Evans, Liesi E. Hebert, Julia L. Bienias. Methodological issues in the study of cognitive decline. Am J Epidemiol 1999; 149:789-93. 3. Celile Proast Lima, Haelena Amieva, Jean Francois Dartigues, Helene Jaquirim Gadda. Sensitivity of 4 psychometric tests to measure cognitive changes in brain aging-population based studies. Am J Epidemiol 2007; 165:344-350. 4. R.K.Solanki,Vaibhav Dubey, Deepthi Munshi. Neurocognitive impairment and comorbid depression in patients of Diabetes mellitus. Int J Diabetes Dev Ctries. 2009; 29:133-138. 5. Carol E. Greenwood, Stacey Hebblewaite, Randall J Kaplan, David J A Jenkins. Carbohydrate induced memory impairment in adults with Type 2 Diabetes. Diabetes care 2003; 26:1961-1966. 6. Toth C, Schmidt AM, Tuor UI, Francis G, Foniok T, Brussee V, et al.. Diabetes, leukoencephalopathy and rage. Neurobiol Dis 2006; 23:445–461. 7. Aragno M, Mastrocola R, Medana C, Restivo F, Catalano MG, Pons N, et al.. Up-regulation of advanced glycated products receptors in the brain of diabetic rats is prevented by antioxidant treatment. Endocrinology 2005; 146:5561–5567. 8. Biessels GJ, Kappelle AC, Bravenboer B, Erkelens DW, Gispen WH. Cerebral function in diabetes mellitus. Diabetologia 1994; 37:643–650. 9. Lupien S, Lecours AR, Lussier I, Schwartz G, Nair NP, Meaney MJ. Basal cortisol levels and cognitive deficits in human aging. J Neurosci 1994;14:2893–2903. 10. Rachel A. Whitmer, Andrew J. Karter, Kristine Yaffe, Charles P. QuesenherryJr, Joseph V. Selby. Hypoglycemic episodes and risk of dementia in older patients with Type 2 diabetes mellitus. JAMA 2009;301:1565-1572. 11. Sherin Antony, Peeyushkumar T, Jobin Matthew, T R Anju, C S Palose. Hypoglycemia induced memory changes in cholinergic receptor expression in the cerebellum of diabetic rats. Journal of Biomedical Science 2010;17:7.

Introduction: Sacral fractures occur in approximately 45% of all pelvic fractures. Neurological deficit has been reported in some cases of sacral fracture. Aims and Objectives: To study the extent of neurological involvement and neurological deficit in different types of sacral fractures in accordance with the Gibbons classification. Materials and method: present study was conducted in tertiary care institute with total 32 patients of sacral fracture. Gibbons grading system was used to assess neurological deficit. Results: 15.7%% patients had neurological deficit. In Denis classification fractures neurological deficit was found in type 2 and 3 patients. Neurodeficit found in 37.5% of vertical shear type of sacral fracture. Conclusion: neurodeficit occours in some cases of sacral fracture. And it is common in sever grade of Denis classification and vertical shear fracture.

1. Mehta S, Auerbach JD, Born CT, Chin KR. Sacral fractures. J Amer Acad Orthop Surg. 2006; 14(12):656-665 2. Denis F, Davis S, Comfort T. Sacral fractures: an important problem. Retrospective analysis of 236 cases. Clin Orthop. 1988;227:67-81. 3. Gibbons KJ, Soloniuk DS, Razack N. Neurological injury and patterns of sacral fractures. J Neurosurg. 1990;72:889-93. 4. Mehta S, Auerbach JD, Born CT, Chin KR. Sacral fractures. J Amer Acad Orthop Surg. 2006; 14(12):656-665. 5. Robles LA. Transverse sacral fractures. Spine J. 2009; 9(1):60-69 6. Vaccaro AR, Kim DH, Brodke DS, et al. Diagnosis and management of sacral spine fractures. Instr Course Lect. 2004; 53:375-385. 7. Taguchi T, Kawai S, Kaneko K, Yugue D. Operative management of displaced fractures of the sacrum. J Orthop Sci.1999;4(5):347-52. 8. Mouhsine E, Wettstein M, Schizas C, Borens O, Blanc CH, Leyvraz PF, Theumann N, Garofalo R. Modified triangular posterior osteosynthesis of unstable sacrum fracture. Eur Spine J. 2006 Jun;15(6):857-63. 9. Schildhauer TA, Josten Ch, Muhr G. Triangular osteosynthesis of vertically unstable sacrum fractures: a new concept allowing early weight-bearing. J Orthop Trauma. 2006 Jan;20(1 Suppl):S44-51. 10. Bellabarba C, Schildhauer TA, Vaccaro AR, Chapman JR.Complications associated with surgical stabilization of high-grade sacral fracture dislocations with spino-pelvic instability. Spine (Phila Pa 1976). 2006 May 15;31(11 Suppl):S80-8; discussion S104. 11. Zelle BA, Gruen GS, Hunt T, Speth SR. Sacral fractures with neurological injury: is early decompression beneficial? Int Orthop. 2004 Aug;28(4):244-51.

Objective: To evaluate the hypoglycemic activity of Tramadol in streptozocin induced diabetic rats. Methods: In this study, 18 albino rats (Three groups each containing six rats)were included for the study. After 4 days of streptozocin injection those rats that develop fasting blood sugar >200mg/dl will be selected for the study. The study groups will be divided as follows, Group-1 (CONTROL): Distilled water 0.5ml (oral), Group-2 (STANDARD): Streptozocin (60mg/kg) i.v. and Group-3 (TEST): Streptozocin(60mg/kg) i.v.+ Tramadol(0.45mg/kg). Fasting blood glucose levels from experimental animals will be measured on 1, 3, 7, 14 and 28th day by capillary blood glucose method by using glucometer(ACUCHEK). Results: In this study after inducing diabetes with streptozotocin(60mg/kg) diabetes was induced and test drug has showed significant hypoglycemic activity comparing to standard drug Glimepiride.

1. Alberti KG, Zimmet PZ. New diagnostic criteria and classification of diabetes-again.Diabet Med. 1998;15:535–6 2. Raffa RB, Friderichs E, Reimann W, Shank RP, Codd EE, Vaught JL. Opioid and nonopioid components inde- pendently contribute to the mechanism of action of trama- dol, an ‘atypical’ opioid analgesic. J Pharmacol Exp Ther.1992;260:275-285. 3. Akbarzadeh A, Norouzian D, Mehrabi MR, Jamshidi Sh, Farhangi A, Verdi AA, Mofidian SM, Rad BL Department of Pilot Biotechnology of Pasteur Institute of Iran, 69-pasteur, Ave, 13164 Tehran, Iran. 4. Indian Journal of Clinical Biochemistry : IJCB [2007, 22(2):60-64] Type: Journal Article. 5. Devreese, K. and G. Leroux-Roels, 1993. Laboratory assessment of five glucose meters designed for self-monitoring of blood glucose concentration. Eur. J. Chn. Chem. Clin. Biochem., 31: 829-837. 6. Y. Harati, MD, C. Gooch, MD, M. Swenson, MD, S. Edelman, MD, D. Greene, MD, P. Raskin, MD, P. Donofrio, MD, D. Cornblath, MD, R. Sachdeo, MD, C. O. Siu, PhD and M. Kamin, MD. Double‐blind randomized trial of tramadol for the treatment of the pain of diabetic neuropathy: doi: 10.1212/WNL.50.6.1842 Neurology June 1998 vol. 50 no. 6 1842-1846.

Objective: To study the clinical profile, the pattern of presentation, treatment and the outcome in scorpion sting envenomation at a tertiary care hospital. Methods: A total of 120 children were prospectively studied. The data included demographics, the time of presentation to the hospital, the clinical features, and the premedication which was given before the arrival of the subjects at the hospital, response to the oral Prazosin and the hospital outcome. Results: Local pain, sweating and peripheral circulatory failure were the common clinical presentations. Complications like acute pulmonary oedema, myocarditis, shock and encephalopathy were also seen. These were treated with a combination of Prazosin with either inotropes or vasodilators. Mortality was seen in 3(2.5%) children. Oral Prazosin, a postsynaptic alpha –1 blocker, is a highly effective drug for scorpion sting envenomation. Conclusion: Scorpion sting envenomation is an acute life threatening emergency and an early presentation to the hospital and an early intervention with proper medication( Prazosin) can hasten the recovery in the scorpion sting victim.

1. Bosnak M, Ece A, Yolbas I, Bosnak V, Kaplan M, Gurkan F,Scorpion sting envenomation in children in southeast Turkey. Wilderness Environ Med. 2009 Summer;20(2):118-24. 2. Mahadevan S. Scorpion sting. Indian Pediatr 2000; 37: 504-513. 3. Santhanakrishnan BR, Ranganathan G, Ananthasubramanian P.Cardiovascular manifestations of scorpion stings in children. Indian Pediatr 1977; 14: 353-356. 4. Ismail M. The scorpion-envenoming syndrome. Toxicon 1995; 3: 825-858. 5. N. Osnaya-Romero*, T. de Jesus Medina-HernaÂndez, S.S. Flores-HernaÂndez, G. LeoÂn-Rojas, Clinical symptoms observed in children envenomated by scorpion stings, at the children's hospital from the State of Morelos, Mexico, Toxicon 39 (2001) 781±785 6. Sofer S, Gueron M. Vasodilators and hypertensive encephalopathy following scorpion envenomation in children. Chest 1990; 97: 118-120. 7. Bawaskar HS, Bawaskar PH. Cardiovascular manifestations of scorpion sting in India (Review of 34 children). Ann Trop Pediatr 1991; 11:381-387. 8. Santhanakrishnan BR, Balagopal Raju V. Management of scorpion sting in children. Trop Med Hyg 1974; 77: 133-135. 9. Biswal N, Murmu Uday C, Mathai B, Balachander J, Srinivasan S.Management of scorpion sting envenomation. Pediatrics Today 1999;2(4): 420-426. 10. Murthy KRK, Vakil AE, Yeolekar RE. Insulin administration reverses the metabolic and echocardiographic changes in acute myocarditis which is induced by Indian red scorpion (B. tamulus) venom in experimental dogs. Ind Heart J 1990; 42: 35-37. 11. Bawaskar HS, Bawaskar PH. Utility of scorpion antivenom vs Prazosin in the management of severe Mesobuthus tamulus (Indian red scorpion) envenoming at a rural setting. J Assoc Physicians India.2007; 55: 14-21. 12. Miller R, Awarn A, Maxwell BB, Masson DT. Sustained reduction of cardiac impedence and preload in congestive cardiac failure with antihypertensive Prazosin. New Engl J Med 1977; 297: 303-307. 13. Bawaskar HS, Bawaskar PH. Scorpions sting: a review of 121 cases. J Wilderness Medicine 1991; 2: 164-174. 14. Vasconcelos F, Lanchote VL, Bendhack LN, et al.. Effects of voltagegated Na+ channel toxin from Tityus serrulatus venom on rat arterial blood pressure and plasma catecholamines. Comp Biochem Physiol C Toxicol Pharmacol. 2005; 141: 85-92. 15. Bawaskar HS, Bawaskar PH. Management of cardiovascular manifestations of poisoning by the Indian red scorpion (Mesobuthus tamulus). Br Heart J 1992; 68: 478-480. 16. Biswal N, Bashir RA, Murmu Uday C, Mathai B, Balachander J, Srinivasan S. Outcome of scorpion sting envenomation after a protocol guided therapy. Indian J Pediatr 2006; 73: 577-582. 17. Bosnak M, Levent YH, Ece A, Yildizdas D, Yolbas I, Kocamaz H, et al.. Severe scorpion envenomation in children: management in the pediatric intensive care unit. Hum Exp Toxicol 2009; 28(11): 721-728. 18. Bawaskar HS, Bawaskar PH. Prazosin in the management of cardiovascular manifestations of scorpion sting. Lancet 1986; 1:510-511. 19. Bawaskar HS, Bawaskar PH. Indian red scorpion envenomation.Indian J Pediatr 1998; 65: 383-391. 20. Prasad R, Mishra OP, Pandey N, Singh TB. Scorpion sting envenomation in children: Factors affecting the outcome. Indian J Pediatr 2011; 78(5): 544-548. 21. Graham RM, Hettinger WA. Drug therapy-Prazosin. New Engl J Med 1979; 300: 232-235. 22. Bawaskar HS, Bawaskar PH. Vasodilators: Scorpion envenoming and the heart (An Indian experience). Toxicon 1994; 32: 1031-1040.

Congenital diaphragmatic hernia (CDH) usually presents immediately in neonatal period with respiratory distress. However, delayed presentation has been reported. The morbidity and mortality of congenital diaphragmatic hernia is related to the severity of lung hypoplasia, pulmonary hypertension and associated anomalies. This report highlights the importance of high index of suspicion through clinical examination and noninvasive diagnostic modalities. CDH presenting after neonatal period if diagnosed early, and treated appropriately poses less challenges in management.

1. Congenital diaphragmatic hernia: delayed presentation with asymptomatic spleenic herniation. Arvind Sehgal, Jagdish Chandra, Varinder Singh, A.K.Dutta and Deepak Bagga. Department of pediatrics and pediatrics surgery, kalawati saran childrens hospital and Lady Hardinge medical college, new delhi. 2. Congenital diaphragmatic hernia presenting after neonatal period Adejuyigbe, AM Abubakar Nigerian journal of pediatrics 1998. 3. Congenital diaphragmatic hernia: prevalence and management Hasan K. Gatea FICMS Ped. Surgery Faik T.Al Gailani DMRD Radiologist Raghad J. Abulhab FICMS Ped. Surgery Fac Med Baghdad, 2010; 4. Numanoglu A, Steiner Z. Delayed presentation of congenital diaphragmatic hernia. South Afr J Surg 1997; 35: 74-76. 5. Lynch JM, Adkins JC, Wiener ES. Incaarcerated congenital diaphragmatic hernia with small bowel obstruction. J Pediat Surg 19825; 17: 534-40. 6. Malone PS, Brain AJ, Kiely EM, Spitz L. Congential diaphragmatic defects that present late. Arch Disease Child 1989; 64: 1532-44. 7. Berman L, Stringer D, Sigmund H Ein, Shandling B. The late presenting pediatrics Bochdalek hernia. J Pediat surg 1988;23 :735-39.

Infection continues to account for a major proportion of maternal, fetal and neonatal mortality and morbidity worldwide. The shared relationship between mothers and their newborns leads to common risk factors and etiologies of infectious diseases. Neonatal sepsis continues to be one of the leading causes of neonatal mortality in India. Neonatal sepsis is defined as a clinical syndrome of bacteremia with systemic signs and symptoms of infection in the first 4 weeks of life. The present study has been undertaken to understand the pattern of maternal vaginal flora in labour and its relation with neonatal sepsis. Knowledge of the significant organisms in the genital tract of the pregnant woman and the peripartal risk factors can help us to develop strategies to control the transmission from mother to child or from environment to the neonate. Prevention of these infections could be practiced through screening programs for mothers vaginorectal colonization, identification of pathogenic organisms and administration of antibiotic prophylaxis to mothers or high risk neonates. Early treatment with appropriate antibiotics would minimize the risk of severe morbidity and mortality besides reducing the emergence of multidrug resistant organisms in intensive care units by rational antibiotic use.

1. Staffan Bergstrom.Infection –related morbidities in the mother,fetus and neonate.Journal of Nutrition 2003 ;133(5 ):1656-1660. 2. Grace J Chan, Anne CC Lee,Abdullah H Baqui,Jingwentan,Robert E Black.Risk of early onset neonatal infection with maternal infection or colonization : a global systematic review and meta analysis.Plos Med 2013;10(8);e 1001502. 3. GoldenbergR, HauthJ, Andrews W .intrauterine infection and preterm delivery. NEngl J Med 2000;342 :1500-1507. 4. National Neonatal forum of India.National Neonatal Perinatal Database-report for year 2002- 2003,NewDelhi; NNF India ;2004 5. Michela Paolucci, Maria Paola Landini,VittorioSambri.How can the microbiologist help in diagnosing neonatal sepsis? International Journal of Pediatrics.Volume2012,article ID 120139,14 page 6. S Vergnano, MSharland,PKazembe,CM Wansambo et al. .Neonatal sepsis :an international perspective. Arch dis child Fetal Neonatal Ed 2005 ;90:F220-224. 7. Goperlud CP, Ohm MJ, Galask RP. Anaerobic and aerobic flora of the cervix during pregnancy and puerperium .Am J Obstet Gynecol 1976; 126 :858. 8. Larsen B,GalaskR.Vaginal microbial flora:composition and influence of host physiology .Ann Intern Med 1982 ;96:926-30. 9. CC Ekwempu,RV Lawande,LJ Egler.Microbial flora of the lower genital tract of women in labour in Zaria.J ClinPathol 1981; 34:82-83. 10. Balaka B,Agbere AD,Baeta S, Kessie K,Assimadi K. Bacterial flora in the genital tract in the last trimester of pregnancy.J Gynecol Obstet BiolReprod (Paris ) 2003 ;32 (6 ) : 555-61. 11. Vidhya Ayengar,Madhulika ,S.N .Vani .Neonatal sepsis due to verticsl transmission from maternal genital tract.The Indian journal of Pediatrics 1991; 58:661-664. 12. Basavaraj M Kerur,B Vishnu Bhat, B.N.Harish, S.Habeebullah, C.Udaykumar. Maternal genital bacteria and surface colonization in early neonatal sepsis.Indian journal of pediatrics 2006;73:29-32. 13. Tessy .A.Joseph, ,Suma P Pyati ,Norman Jacobs.Neonatal early onset Escherichia Coli disease.Arch Pediatr Adolesc med 1998 ;152:35-40. 14. Mahmood A,Karamat K.A ,Butt .T.Neonatal sepsis : high antibiotic resistance of the bacterial pathogens in a neonatal intensive care unit in Karachi .J Pak Med Assoc 2002 ;52 (8): 348-350. 15. KuruvillaK.A,Pillai S,Jesudason M,Jana .A.K.Bacterial profile of sepsis in a neonatal unit in South India.Indian Pediatrics 1998; 35:351-58. 16. J.de.louvois,Rosalinde Hurley,Valerie .C.Stanley.Microbial flora of the lower genital tract during pregnancy: relationship to morbidity.J.clin.Path 1975,28,731-735. 17. Bartlett Jg,Moon Ne,Goldstein PR.Cervical and vaginal bacterial flora : ecologic niches in the female lower genital tract.Am J obstet Gynecol 1978;130:658-61. 18. Tallur SS,Kasturi AV,Nadgir SD,Krishna BV.Clinico-bacteriological study of neonatal septicemia in Hubli.Indian J Pediatr 2000 Mar;67 (3 ) :169-74. 19. Vinodkumar CS,Neelagund YF,Kalsurmath Suneeta ,Banapurmath Sudha,Kalappannavar NK,Basavarajappa KG.Perinatal risk factors and microbial profile of neonatal septicemia :a multicentred study.J obstet Gynecol India 2008 ;58 (1 ) :32-40. 20. S.Khurshid Anwer ,Sultan Mustafa,Sallem Pariyani,Shamim Ashraf.Neonatal sepsis; an etiological study.J Pak Med Assoc 2000 ;50(3) : 91-94. 21. Betty Chacko,Inderpreet Sohi.Early onset neonatal sepsis.Indian journal of pediatrics 2005 ;72(1): 23-26. 22. Abdelrahman M Elmashad, Hala A Ismael,Ibstesam K.Afifi.Prevalence of methicillin –resistant staphylococcus –aureus in neonatal sepsis and detection of other accompanied diagnostic markers. Egyptian journal of medical microbiology 2009; 18(4 ): 67-76. 23. Feng-Ying .C.Lin,Leonard E Weisman ,James Troendle,Karen Adams.Prematurity is the major risk factor for late –onset group B streptococcus disease.Journal of Infectious disease 2003 ;188: 267-71. 24. Ghanshyam D Kumbhar,V.G.Ramachandran,Piyush gupta.Bacteriological analysis of blood culture isolates from neonates in a tertiary care hospital in India.J Health Population Nutr 2002 ;20(4):343-347. 25. Gyawali Narayan,Raj Kumari Sanjana.Bacteriological profile and antibiogram of neonatal septicemia.Indian J Pediatr 2013 ;80 (5): 371-374. 26. Elizabeth A.Marchant,Guilaine K.Boyce,Manish Sadarangani,Pascal M.Lavoie. Neonatal sepsis due to coagulase –negative staphylococci.Clinical and developmental immunology 2013;article ID 586076,10 pages.

Predicting the severity of critically ill patients is as essential as management of the patient in intensive care unit . Several scoring systems have been tried in the past with regular modifications. Acute physiological and chronic health examination scoring system (APACHE IV) was used in predicting the mortality and outcome in critically ill patients. APACHE IV scoring system was compared with the older scoring systems, LODS, MPM II0 and MPM II24, . Various statistical tools were used to assess the correlation, significance, and predictability. A total of 181 patients were included in the study. APACHE IV score had the best calibration and discrimination MPM II0 score had good calibration and fairly good discrimination MPM II24 score had the least significant discrimination and calibration.

1. Azoulay E, Adrie C, De Lassence A, Pochard F, Moreau D, Thiery G et al.Determinants of postintensive care unit mortality: a prospective multicenter study. Crit Care Med 2003 Feb;31(2):428-32 2. Pittet D, Tarara D, Wenzel RP: Nosocomial bloodstream infection in critically ill patients: excess length of stay, extra costs, and attributable mortality.JAMA 1994 May 25; 271(20):1598-601. 3. Shadnia S, Darabi D, Pajoumand A, Salimi A, Abdollahi M. A simplified acute physiology score in the prediction of acute organophosphate poisoning outcome in an intensive care unit. Hum ExpToxicol2007 Aug;26(8):623–27. 4. Nguyen HB, Banta JE , Cho TW, Van Ginkel C, Burroughs K, Wittlalake WA et al. Mortality predictions using current physiologic scoring systems in patients meeting criteria for early goal-directed therapy and the severe sepsis resuscitation bundle. 5. Luo XP, Wang HH, Hu SF, Wu SJ, Xie GH, Cheng BL et al. Comparison of three different organ failure assessment score systems in predicting outcome of severe sepsis. 6. Pittet D, Tarara D, Wenzel RP: Nosocomial bloodstream infection in critically ill patients: excess length of stay, extra costs, and attributable mortality. JAMA 1994 May 25; 271(20):1598-601.

Background and objective: Alcoholism is common and serious problem. Alcohol most commonly consumed in the form of ethanol. The effects of alcohol are mainly caused by altering the function of membrane proteins in many different cell types especially cells of GIT, urinary tract, cardiovascular and nervous system. Alcohol also causes alcoholic peripheral neuropathy. Material and Methods: The study was conducted in the department of physiology MR Medical College Gulbarga. The study was conducted in chronic alcoholic’s subject and there age matched control and in three groups of 30 subjects in each groups. Group I – Normal healthy control, Group II – chronic alcoholic without neuropathy, Group III – chronic alcoholic with neuropathy. Nerve conduction study was carried out by using RMS- EMG,EP machine manufactured by Recorders and Medicare System (P) Ltd. The data was statistically analyses by using student unpaired’ test. Result: Motor and sensory nerve conduction velocity was compared with chronic alcoholic and healthy aged matched controls. The both sensory and motor nerve conduction was significantly decreased in chronic alcoholic without neuropathy and with neuropathy. Conclusion: From our study we conclude that alcohol addiction has adverse effect on the NCV Thus helps in early diagnosis as well as prognosis of alcoholic neuropathy

1. Morse R.M, Flavin D.K. “The definition of alcoholism. The Joint Committee of the National Council on Alcoholism and Drug Dependence and the American Society of Addiction Medicine to study the definition and criteria for the Diagnosis of Alcoholism” JAMA: the journal of American Medical Association ( August 1992) 268 (8): 1012 – 4. 2. Ramon Estruch, jose M. Nicolas, Alcohol, alcohol abuse and alcoholism; Vol.28.No5.pp 543- 550 (1993) 3. Fiona Barter and Andrew R. Tanner: Neuropathy in an alcoholic population; Postgraduate Medical Journal (1987)63, 1033-1036. 4. Dr. Bill Boggan: Effects of Ethyl Alcohol on organ Function, Alcohol Chemistry and you; Alcohol and Alcoholism, vol.36 no 5, 2001. 5. Shy M.E. Peripheral neuropathies. In: Goldman L, Ausiello D, eds. Cecil Medicine.23rd ed. Philadelphia, Pa: Saunders Elsevier; 2007: chapter 446. 6. Christopher C.H.Book; B vitamin deficiency and neuropsychiatric syndromes in alcohol misuse; Alcoholand Alcoholism Vol 33,No4,pp.317-336,1998. 7. Mawdsley C and Mayer R.F: Nerve Conduction in Alcoholic Polyneuropathy, Brain (1965) 88, vol. 2,335-356 8. Taraksd S Ramchndran: Alcohol related neuropathy, Medscae drugs disease and procedure ,June 2009. 9. Coers C and Hildebrand J (1965) : Latent neuropathy in diabetes and alcoholism. Electromyographic and histological study. Neurology (Minneap) 15, 19 – 38. 10. Juul – Jensen, Mayer R.F(1966) : Threshod stimulation for nerve conduction studies in man. Archives of Neurology,15,410 -419. 11. Walsh .J.C and McLeod J.G.(1970): Alcoholic neuropathy An electrophysiological and histological study. Journal of Neurological Science,10,457 -469. 12. M.Lefebvre D’Amour, B.T. Shahani: The importance of studying sural nerve conduction and late responses in the evaluation of alcoholic subjects; Neurology 1979; 29,1600-1604 13. J.P Ballantyne, S Hansen: Quantitative electrophysiological study of alcoholic neuropathy.Journal of Neurology, Neurosurgery and Psychiatry,1980 May,43 (5),427-432 14. Matti Hillbom and Arne Wennberg; Prognosis of alcoholic polyneuropathy; Journal of Neurology, Neurosurgery and Psychiatry,1984:47,699-703. 15. T.G.H.C.Ferdinandis, and H. J .De Silva (2007) illicit alcohol consumption and neuropathy – A preliminary study in Sri Lanka; Alcohol and Alcoholism Vol.43, No.2,pp.171 -173 16. Eileen Blackstock, Geoffrey Rushworth and Dennis Gath; Electrophysiological studies in Alcoholism; Journal of Neurology, Neurosurgery and Psychiatry, 1972,35,326-334. 17. E.B.Casey and Pamel; Electrophysiological evidence of distal lesion in alcoholic neuropathy, Journal of Neurology, Neurosurgery and Psychiatry, 1972, 35,624 -630 18. Hell D, Six P, Vitamin B1 deficiency in chronic alcoholics and its clinical correlation salked R Schweiz Med Wochenschr.1976 Oct 23; 106(43) 19. Thompson, Warren and R Gregory Lande, ‘Alcholism’ Mediscape drugs, disease and procedures, Feb18 2011 20. Robert D.Hienze, Danielle A. Bowers Acute ethanol effects on sensory/motor function in baboons with a history of chronic ethnol ingestion; Drug and Alcohol Dependence, Vol.30, issue 1,April 1992, pp85 -100.

Background and objective: The present study was undertaken to assess the pulmonary function tests in chronic alcoholics. Alcohol has multitude of effects on many organ systems producing distinct clinical entities, particularly in lung, heart, liver and central nervous system. Material and Methods: The study was done using computerized medspiror. It includes 50 male chronic alcoholics of 20 - 60 years age and 50 normal male healthy subjects who served as age matched controls. The following lung function viz FVC, FEV1/FVC ratio, PEFR was carried out and subjected for statistical significance. Analysis was carried out by ‘t’ unpaired test. Result: The results of the study revealed statistically significant (P<0.05) decline in FVC and FEV1/FVC ratio, PEFR in chronic alcoholics as compared to normal control group, suggesting chronic alcoholism definitely affects pulmonary functions with the manifestations of both obstructive as well as restrictive pattern. Conclusion: Thus we conclude that alcoholism adversely affects pulmonary functions. (1).

1. Arther S.Banner: Pulmonary function is chronic alcoholism. American review of respiratory 1973;108:851-857. 2. Banner A.S: Alcohol and the lung. Chest 1980; 77: 460-461. 3. Henry O. Heinemann: Alcohol and the lung. Editiorial 1976; 229-35. 4. Michale D Lebowitz : Respiratory symptoms and disease related to alcohol consumption. American review of respiratory disease 1981; 123:16-19. 5. Lange, Steffen groth, Jann Mortenson et al: Pulmonary function is influenced by heavy alcohol consumption. American review of respiratory disease 1988; 137: 1119-1123. 6. George E. Burch, Nicholas P. De Pasquale: Alcoholic lung disease an hyptesis. American heart journal. Feb 1967; 73(2):47-50. 7. Rankin J,G. Hale, J.S. Wilkinson et al ; Relationship between smoking and pulmonary disease in alcoholism Med. J. 1969;1;730 8. Bernice H. Cohen, David D. Celentano, GarryA Chase et al; Alcohol consumption and airway obstruction. American Review of respiratory diseases. 1980; 121;205-15. 9. Laurenzi G.A. Guanery J.J; the study of the mechanism of pulmonary resistance to infection – the relationship of bacterial clearance to ciliary and alveolar macrophage function. American Rev. Respiratory Disease,1966; 93;134 10. Kilburn K.H; Cilia and mucus transport as determinants of the response of lung air pollutants. Arch. Environ Health, 1967; 14:77 11. Green G.M ; Pulmonary clearance of infection agents. Ann. Rev. Med. 1968; 19; 315. 12. Gee JBJ, Kaskin J. Dunconbe MP et al: The effects of ethanol on sum metabolic features of phagocytosis in the alveolar macrophage. Journal Reticuloendothial Society. 1974; 15:61 13. Grenn G.M, Kass E.H; The influence of bacterial species in pulmonary resistance to infection in mice subjected to hypoxia, cold stress and ethanolic intoxication. Br. Journal of Exp. Pathol 1965; 46;360. 14. T.H. Beaty, B.H. Cohen, C.A.Newill et al ; Impaired function as a risk factor for mortality American Journal of Epidemology,1982;116;102 -13 15. Colp C. R.Prk and William, et al; Pulmonary function studies in pneumonia. American Review. Respiratory disease1962; 85;808 16. Wagner m, Heinemann HO; Effect of ethanol on phospholipids metabolism by the rat lung. Am.J. of Physiology, 1975:229;1316. 17. Ruff F, Hughes JMB, Stanly N, et al: Regional lung function in patients with hepatic cirrhosis. J. clinical Investigation.1971; 50; 2403. 18. Naimark A : Cellular dynamics and lipid metabolism in lung. Fed. Proc. 1967;32 19. Tierny D.F, Clemants J.A. Trahan H.J; Rates of replacement of lecitihins and alveolar instability in rat lungs. American Journal of Physiology.1967; 213;671. 20. Young S.L, Tierney D.F: Dipalmitoye lecitihin secretion and metabolism by the rat lung. American Journal of Physiology. 1972;222;1539 21. King R.J; The surfactant system of the lung Fed.Proc.1974: 33 2238 22. Shimoda, Kohanos, Takao A et al: Investigation of the mechanism of alcohol induced asthma. Journal of Allergy Clinical Immunology,1997, 74 – 84.