Priyanka V, Dayanand V P, Bhaskara B
Introduction: In the present study we compared ropivacaine and bupivacaine with adjuvant morphine for perineal surgeries. Aims: The aim of this study is to compare isobaric 3ml of 0.5% Ropivacaine and 3ml of isobaric 0.5% Bupivacaine with 100µ morphine in both the group sintrathecally for elective Perineal surgeries. Onset and duration of sensory block, onset and duration of motor block, maximum height of sensory block, quality of anaesthesia, time of request for analgesia, time for ambulation, time for urination, sedation score, VAS score, hemodynamic parameters and adverse effects if any were studied. Methods: This study was conducted in 120 patients scheduled for elective Perineal surgeries were randomly divided into two groups of 60 each. Group B received isobaric 3ml of 0.5% Bupivacaine and Group R received 3ml of 0.5% Ropivacaine with 100µ morphine intrathecally in both groups. Onset and duration of sensory block, onset and duration of motor block, maximum height of sensory block, quality of anaesthesia, time of request for analgesia, time for ambulation, time for urination, sedation score, VAS score, hemodynamic parameters and adverse effects if any were studied Results: There was significant difference between the two groups in mean time to onset of sensory block,duration of sensory block, duration of motor block and time to walk in mins. Total duration of sensory block was 155.50±4.19 min in group R and 199.83±11.12 min in group B, which is significant. (P ˂0.001). Duration of motor block was 159.83 min in group R and 182.83min in group B which is clinically and statistically significant (P<0.001). Conclusion: Ropivacaine 3 ml of 0.5% with 100µ morphine provides comparable quality of sensory block but has slower onset and significantly shorter duration of motor block compared to Bupivacaine.
1. Malinovsky JM, Charles F. Kick O, Intrathecalanaesthesia: Ropivacaine verus bupivacaine, Anaesth-analgesia 2000;91:1457-60. 2. NevalBoztug, Zeiye Bigat, Bilge Karsli, NurdanSaykal, Ertugrul Erotog: Comparison of Ropivacaine and Bupivacaine for intrathecalanaesthesia during outpatient arthoscopic surgery, Journal of Clinical anaesthesia 2006; 18:521-525. 3. Gautier PE, de Kock M, van Steenberge, A. Intrathecal Ropivacaine for Ambulatory Surgery. Anaesthesilogoy 1999; 91; 1239-45. 4. HelenaKallio, Eljas-Veli T, Snall, comparison of intrathecal plain solutions containing Ropivacaine 20 or 15 mg versus Bupivacaine 10 mg, Anaesthesia-analgesia 1999;3;713-717. 5. Mc. Namee DA, Mc. Clelland AM, Scott. S, et al. Spinal Anaesthesia: Comparison of plain Ropivacaine 5 mg/ml with Bupivacaine 5 mg/ml for major Orthopeadic Surgery. Br.J. Anaesth 2002;89;702-6 6. Erturk E, Tutuncu C, Eroglu A, Gokben M, Clinical Comparison of 12 mg Ropivacaine and 8 mg Bupivacaine both with 20ug fentanyl in spinal anaesthesia for major orthopaedic surgery in geriatric patients. Eub 2010; 19(2): 142-7. 7. Mantouvalou M, Ralli S, Arnaoutoglou H, Tziris G, Papadopoulos G. Spinalananestheisa: Comparison of plain Ropivacaine,Bupivacaine and Levobupivacaine for lower abdominal surgery, ActaAnaesthesiologica Belgica 2008;59:65-71. 8. Ogun C.O, Kirgiz E.N, Duman A, Okesil S, Akyurek C, Comparison of Intrathecal isobaric bupicacaine-morphine and ropivacaine-morphine for Caesarean delivery, British journal anaesthesia 2003; 90(5): 659-664. 9. P.D.W.Fettes, G.Hocking, M.K.Peterson, J.F.Luck and J.A.W.Wildsmith. Comparison of plain and hyperbaric solutions of ropivacaine for spinal anaesthesia. British Journal of Anaesthesia 94(1): 107-11 (2005). 10. HannuKokki, PaulaYlonen, Merja Laisalmi, MarjaHeikkinen. Isobaric Ropivacaine 5 mg/ml for Spinal Anesthesia in Children. AnesthAnalg 2005; 100:66-70. 11. JackW.vanKleef, Bernadette Th. Veering and Anton G. L.Burm. Spinal Anesthesia with Ropivacaine: A Double- Blind Study on the Efficacy and Safety of 0.5% and 0.75% Solutions in Patients Undergoing Minor Lower Limb Surgery. AnesthAnalg 1994; 78:1125-30. 12. Jean-Marc Malinovsky, Florence Charles,Ottmar Kick, MD, Jean-Yves Lepage, MyriamMalinge, Antoine Cozian, MD, Olivier Bouchot, Michel Pinaud, Intrathecal Anesthesia: Ropivacaine Versus BupivacaineAnesthesia and analgesia, December 2000 vol. 91 no. 61457-1460 13. P. Gautier, M. De Kock, L. Huberty, T. Demir, M. Izydorczic and B. Vanderick, Comparison of the effects of intrathecalropivacaine, levobupivacaine, and bupivacaine for Caesarean section, British Journal of Anaesthesia (2003) 91 (5): 684-689
Guruswamy N T, Habeeb Khan, Pavan Hegde
Background: Hyponatremia(serum sodium<135mEq/L)has been found to be the major electrolyte abnormality in children admitted with pneumonia in various studies throughout the world. Hyponatremia increases morbidity and mortality of children if not evaluated and treated appropriately. Hyponatremia in pneumonia was found to be mainly dilutional and secondary to Syndrome of Inappropriate secretion of Antidiuretic Hormone(SIADH).Objectives: This is a prospective study to know the incidence of hyponatremia and SIADH in children with severe pneumonia, morbidity and mortality due to hyponatremia and its management in children with severe pneumonia. Materials and Methods: The study group comprised of 60 children in the age group of 2 months to 5 years admitted with severe pneumonia as defined by modified WHO-BTS guidelines and confirmed radiologically. Investigations were done on the day of admission for serum electrolytes. In patients who were clinically euvolemic and had an initial serum sodium value <135mEq/L, work up for diagnosis of SIADH was done. Renal function tests were also done. Statistical analysis was done to know the frequency of hyponatremia, morbidity and mortality associated with hyponatremia. Results: Of the 60 children enrolled in the study, 28(46.7%) children had hyponatremia. Of the 28 hyponatremic children, 18(64.3%) had dilutional hyponatremia secondary to SIADH. The duration of hospitalization was significantly prolonged in children who had hyponatremia. There were 3 mortalities and all the 3 had hyponatremia, of which 2 were found to have SIADH. Conclusion: Almost half of the children with severe pneumonia developed hyponatremia which was predominantly due to SIADH. Hence careful fluid management is needed in children with pneumonia.
1. Zar HJ, Madhi SA. Childhood pneumonia-progress and challenges. S Afr Med J 2006; 96:890-900 2. Rudan I, Boschi-Pinto C, Biloglav Z. Epidemiology and etiology of childhood pneumonia. Bull World Health Organ 2008; 86 (5):408-16 3. Sakellaropoulou A, Hatzistilianou M, Eboriadou M, Athanasiadou-Piperopoulou F. Hyponatremia in cases of children with pneumonia. Arch Med Sci 2010; 6(4):578-583. 4. Dreyfuss D, Leviel F, Paillard M, Rahmani J, Coste F. Acute infectious pneumonia is accompanied by latent vasopressin-dependent impairement of renal water excretion. Am Rev Respir Dis 1988; 138(3):583-9. 5. Singhi S, Dhawan A. Frequency and significance of electrolyte abnormalities in Pneumonia. Indian Pediatr1992; 29:735-40. 6. Prasad SVSS, Singhi S, Chugh KS. Hyponatremia in sick children seeking Paediatric emergency care. Indian Pediatr 1994; 31:287-94. 7. WHO. Acute respiratory infections in children: case management in small hospitals in developing countries: A manual for doctors and other senior health workers. Geneva. Switzerland: 1990. 8. World Health Organization. Technical basis for the WHO recommendations on the management of pneumonia in children at first level health facilities. Geneva: WHO; 1991. WHO document WHO/ARI/91.20. 9. Harris M, Clark J, Coote N et al. British Thoracic Society guidelines for the management of community acquired pneumonia in children: update 2011. Thorax 2011; 66:ii 1-ii 23 10. Roberts KE. Pediatric fluid and electrolyte balance: critical care case studies. Crit Care Nurs Clin North Am. 2005;17: 361-73. 11. Moritz ML, Ayus JC. Disorders of water metabolism in children: hyponatremia and hypernatremia. Pediatr Rev 2002; 23:371–80. 12. Sorensen JB, Andersen MK, Hansen HH. Syndrome of inappropriate secretion of antidiuretic hormone (SIADH) in malignant disease.J Intern Med 1995; 238:97–110. 13. Gross P. Clinical management of SIADH. Ther Adv Endocrinol Metab 2012; 3(2):61–73 14. Shann F, Germer S. Hyponatraemia associated with pneumonia or bacterial meningitis. Arch Dis Child 1985; 60:963-966. 15. Dhawan A, Narang A, Singhi S. Hyponatraemia and the inappropriate ADH syndrome in pneumonia. Ann Trop Paediatr 1992; 12: 455-62. 16. Don M, Valerio G, Korppi M, Canciani M. Hyponatremia in pediatric community-acquired pneumonia. Pediatr Nephrol 2008;23:2247-53 17. Singhi S, Prasad SVSS, Chugh KS. Hyponatremia in Sick Children: A Marker of Serious Illness. Indian Pediatr 1994; 31:19-25.
R A Suryawanshi
Tertiary sediments along west coast of Maharashtra (India) are about 60 m. above the present sea-level and occurrence of lateritic gravel beds and bouldery, pebbly gravels below the sea-level suggest sea level changes around Ratnagiri (Rajguru and Marathe, 1984). Occurrences of lignite bed over laterite, developed on Deccan basalt clearly indicate that the lignite is younger than the laterite of early Tertiary age. Sedimentlogical and pollen studies revel creek or estuarine environment of deposition. The angiosperm pollens and their modern equivalent conform non marine environment of deposition.
1. Germeraad, J.H., Hopping, C.A. and Muller, J., (1968) Palynology of Tertiary Sediments from Tropical Areas. Rev. Paleobot. Polynol., (6), pp. 189 – 348. 2. Leidelmeyer, P., (1966) The Paleocene and Lower Eocene Pollen Flora of Guyana, Leidse Geol. Meded., 36, pp. 49 - 70. 3. Muller, J., (1968) Palynology of the Pedawan and Plateau Sandstone Formation (Cretaceous - Eocene) in Sarawak, Malaysia. Micropalaeontol., 14, pp. 1-37. 4. Potonie R. (1970) Synopsis der Guttungen Sporae - Dispersae III Beih. Geol. Jb., 39, pp. 1 - 189. 5. Phadtare, N.R., (1982) Floristic Studies on the Lignitic Beds of Ratnagiri District, Ph.D. Thesis, Univ. of Bombay, p. 275. 6. Phadtare, N.R. and Kulkarni, A.R., (1980) Palynological Investigation on Ratnagiri Lignite, Maharashtra. Geophytol. 10, pp. 158 - 170. 7. Phadtare, N.R. and Kulkarni, A.R., (1984) Affinity of the Genus Quilonipollenites with the Malasia Palm Eugeissana Griffith. Pollen at Spores, 26, pp. 217 - 226. 8. Rajguru, S.N. and Marathe, A.R., (1984) Neotectonic Activity Around Ratnagiri, Western India, Proc. Symp. Quat. Episodes, Dept. Geol. M.S.Univ., Baroda. pp. 1-6. 9. Rao, K.P. and Ramanujam, C.G.K., (1976) A palynological Approach to the study of Quilon Beds of Kerala State in South India. Curr. Sci. 44, 730 - 732. 10. Saxena, R.K., (1991) A Catalogue of Fossil Plants from India. Part 5A, B. Birbal Sahni Inst. Palaeobot., Lucknow, p. 147. 11. Van der Ham, R.W.J.M., (1989) New Observations on the Pollen of Ctenolophon Oliver (Ctenolophonaceas) with remark on the Evolutionary History of the genus. Rev. Paleobot. Palynol., 59, pp. 153 - 160. 12. Venkatachala, B.S. and Kar, R.K., (1969) Palynology of the Tertiary Sediments of Kutch - 1: Spores and Pollen from Bore Hole No. 14, Palaeobotanist, 17, pp. 157-178. 13. Suryawanshi R.A. (1984) Use of microfossils to decipher the paleo- environment of tertiary sediments of Ratnagiri, Maharashtra (India) International Research Journal of Earth Sciences. Vol .2 (8) pp7-9.
Sangeeta Chippa, V S Prasannakumar Reddy, N Bhavani, Bijan Mukhopadhyay, Aaradhana Giri, Avanthi Sathineedi
Objective: To study the epidemiodemiological factors related to intrauterine fetal death and to study the associated maternal and fetal risk factors. Methods: This observational study was carried out at M. N. R. Medical college and Hospital, Sangareddy over a period of 2 years. All pregnant women diagnosed as singleton intrauterine fetal death with gestational age more than 20 weeks were included in the study. Women with Multiple pregnancy and intrapartum fetal deaths were excluded from the study. Data was analysed with respect to age, parity, gestational age, blood group, previous history of intrauterine fetal death and associated risk factors. Results: 41 patients were included in the study. 90% of fetal deaths were seen in young women between 20 to 30yrs age. Majority (51.2%) women were primigravida and 56% were diagnosed as having intrauterine fetal death at 26 to 31 weeks of gestation. Preeclampsia, severe oligohydramnios, antepartum haemorrhage and congenital anomalies were the major associated risk factors. Other less common risk factors seen in the study were Rh isoimmunisation, eclampsia and hand prolapse. In 19.51% women no risk factor was identified and the cause remained unexplained. Conclusion: majority of risk factors associated with intrauterine fetal death are preventable. Although congenital anomalies remain unavoidable, prenatal diagnostic tests and early detection of anomalies by antenatal screening tests may reduce the prevalence of late fetal death and associated psychological trauma to the parents. Early detection and treatment of high risk women may reduce the risk of unexplained fetal deaths.
1. Anjali Choudhary, Vineeta Gupta. Epidemiology of intrauterine fetal deaths: A study in Tertiary referral centre in uttarakhand. J. of dental and medical sciences2014;13(3):03-06 2. Richardus, Jan H, Graafmans, Wilcoe, Verloove- Vanoriele. The perinatal mortality rate as an indicator of quality of care in international comparisons. Medical care 1998;36(1):54-66 3. Mehrunnisa Khaskheli, Shahla Baloch, Imdad A. Khushk, Shaheen Sharf Shah. Pattern of fetal deaths at a University Hospital of Sindh. J. Ayub. Med Coll. Abottabad 2007;19(2):32-34. 4. Lamia A. Shaaban, Rihab A. Al Saleh, Buthina M. Al Wafi, Rajaa M. Al Raddadi. Associated riskfactors with antepartum intrauterine fetal death. Saudi Med J.2006 ; 27(1): 76-79. 5. Ratmond EG, Cnattingius S, Kiely JL. Effects of maternal age and parity and smoking on the risk stillbirths. Br. J. Obstet Gynae Col 1994 ; 101:301-306. 6. Al Kadri ,Hanah Tamim, Hani. Factors contributing to intrauterine fetal death. Archives of Obstetrics andGynaecol 2012; 286 (5) : 1109. 7. Nayak SR, Garg Nidhi. Determinants of antepartum fetal death. J. ObstetGynecolIndia ; 60 (6) : 494-497. 8. Koerjo R, Bhutta S, J Noorani KJ et al. An audit of trends of perinatal mortality at the Jinnah Postgraduate Medical centre, Karachi. J. Pak Med Assoc 2007; 57: 168-172.
Febe R Suman, Lawrence D’Cruze, Rithika Rejendran, Suresh Varadarajan
Background: Thrombocytopenia is a common haematologic abnormality in dengue which demands platelet transfusion. Platelet transfusion though life saving has its own hazards so that unnecessary usage is to be avoided. There is a need to find out a laboratory parameter which can predict platelet recovery. Aims and objectives: We aim to study the platelet and immature platelet dynamics and the immature platelet fraction Methods: This is a observational descriptive study done in 2012 on all the dengue patients who were positive for NS1 antigen or IgM antibody or both and treated at Sri Ramachandra Medical Center. The values of platelet and IPF were retrieved for day 1st, 3rd, 5th and 7th day of admission Association between values of IPF and significant clinical change in platelet values during the subsequent 48 hrs is done. A sensitivity analysis was carried out to ascertain the cut-off of IPF on the corresponding days which yielded increase in platelet values of over 20,000 in the subsequent 48 hours. Results: There is statistically significant (P < 0.01) improvement in platelet values within 48 hours when the IPF is more than 6.1% If the IPF value is more than 6.25% and10.6% there is 67% and100% chance of platelet recovery within 48 hours respectively. Conclusion: IPF is an additional parameter to predict platelet recovery, so that prophylactic platelet transfusion can be deferred and also the hazards associated with it.
1. Sri Chaikul T, Nimmannitya S. Haematology in dengue and dengue haemorrhagic fever. Baillieres Best pract. Res. Clin. Haematol, 2000; 13: 261-276. 2. RN Makroo, Raina V, Kumar P, Kanth R K.Role of Platelet Transfusion in the managmenet of dengue patients in a tertiary care hospital. Asian J Transf. Science, 2007; 1:4-7 3. Ingram M, Coopersmith A. Reticulated platelets following acute blood loss. Br J haematol, 1969, 17:225-229. 4. Briggs C, Kunka S, Hart D, Oguni S, Madin SJ . Assessment of an immature platelet fraction (IPF) in peripheral thrombocytopenia. Br J Haematol, 2004; 126: 93-99. 5. Saigo K, Sakota Y, Masuda Y, Matsunaga K, Takenokuchi M, Nishimura K et al. Automatic detection of immature platelets for decision making regarding platelet transfusion indications..Transfus Apher Sci, 2008; 38(2):127-132. 6. Dadu, T., Sehgal, K., Joshi, M, Khodaiji, S. Evaluation of the immature platelet fraction as an indicator of platelet recovery in dengue patients. International Journal of Laboratory Hematology, 2013; 2013; 49(7)10.1111/ijlh.12177. 7. Carol B, Ian L, Punamar K et al, Performance evaluation of the Sysmex haematology XN modular system. J Clin Pathol, 2012; 0:1-7. 8. Francisca R F , Guerreiro A , Romelia P.G., Marin H.P., Daniella M.L.IVOCB Dengue: Profile of haematological and biochemical dynamics. Rev. Bras Haematol, 2012; 34:1-10 9. Irfan A, Fayyaz A M, Aamir H, Shahida A R S. Dengue fever; cliniciopathologic correlations and their associations with poor outcome. Professional Med J, 2011; 18:57-63. 10. Banerjee M, Chatterjee T, Choudhary G.S., Srinivas. V, Kataria V.K. Dengue: A clinic haematological profile. MJAFI, 2008; 64: 333-336. 11. Ahmed S, alin Ashraf S, Ilyas M, Tariq WZ, Chotani RA. Dengue fever out break: A clinical management experience. JCPSP, 2008; 18: 8 -12 12. Sara JB, Bethau P, Mare F, Lemke KP, Peter A S et al. Platelet production and platelet destruction assessing mechanisms of treatment effect in immune thrombocytopenia (ITP). Blood, 2010; 11:321-398. 13. Briggs C, Hart D, Kunka S, Ogunr S, Machin S J, et al. Transfusion Medicine. Transfusion Medicine, 2006; 16:101-109. 14. Rolf Hinzmann. The clinical significance of the measurement of immature platelets. Sysmex lab info, 2005. 15. Abe Y, Wada H, Tomatsu H, Sakaguchi A, Nishioka J, Yabu Y et al. A simple technique to determine thrombopoiesis level using immature platelet fraction (IPF). Thromb Res, 2006; 118: 463-467. 16. Jung H, Jeon H K, Kim H J, Kim S H. Immature platelet fraction. Establishment of a reference interval and diagnostic measure for thrombocytopenia. Korean J Lab Med, 2010; 30:451-459. 17. Sehgal K K, Tina D, Chokseyo, Dalal R J, Shahnaz K J. Reference range evaluation of complete blood count parameters with emphasis on newer research parameters on the complete blood count analyzer Sysmex XE 2100. Indian J. Pathol Microbiol, 2013; 56:120-124 18. Sachdev R, Tiwari AK, Goel S, Raina V, Sethi M. Establishing biological reference interval for novel platelet parameters (immature platelet fraction, high immature platelet fraction, platelet distribution width, platelet large cell ratio, platelet-X, platelet crit and platelet distribution width) and their correlations among each other. Indian J Pathol Microbiol, 2014; 57:231-5.
Priya Subashchandrabose, Vasudevan Kasturirengan, Monica Vincent Bonipace, Sarada Venkatesan
Bombay blood group is a very rare phenotype within ABO group and is inherited in an autosomal recessive pattern. This phenotype necessitates extreme caution while blood transfusion as these individuals can be given either autologous transfusion or blood from other Bombay group individuals only. Review of literature reveals that Bombay blood group is reported to be associated with congenital disorder of Glycosylation Type 2c, leukocyte adhesion deficiency type 2 and Rambam–Hasharon syndrome. To the best of author’s knowledge, there are no other syndromic associations described so far. We report a case of incidentally identified Bombay blood group in a 12 year old female child during routine pre operative evaluation for drainage of cerebellar abscess. She had a constellation of clinical findings which include Bombay blood group, congenital anomalies (Bilateral Microtia with Supra aural fistula), history of mild delay in developmental milestones and recurrent infections (Mastoiditis).
1. Bhende YM, Deshpande CK, Bhatia HM. A new blood group character related to the ABO system. Lancet 1952; 1:903-4. 2. Dauber A, Ercan A, Lee J, James P, Jacobs PP, Ashline DJ, et al. Congenital disorder of fucosylation type 2c (LADII) presenting with short stature and developmental delay with minimal adhesion defect. Hum Molec Genet. 2014; 23:2880-7. 3. Sturla L, Puglielli L, Tonetti M, Berninsone P, Hirschberq CB, De Flora A et al. Impairment of the Golgi GDP-L-fucose transport and unresponsiveness to fucose replacement therapy in LAD II patients. Pediatr Res. 2001; 49 (4): 537–42. 4. Frydman M, Vardimon D, Shalev E, Orlin JB. Prenatal diagnosis of Rambam–Hasharon syndrome. Prenat Diagn. 1996; 16: 266–9. 5. Oriol R, Candelier JJ, Mollicone R. Molecular genetics of H. Vox Sang 2000;78:105-8. 6. Das PK, Nair SC, Harris VK, Rose D, Mammen JJ, Bose YN, et al. Distribution of ABO and Rh-D blood groups among blood donors in a tertiary care center in South India. Trop Doct 2001; 31:47-8. 7. Khan MQ. Bombay blood group: a case report. Pacific J Sci Tech 2009; 10:333-7. 8. Koda Y, Soejima M, Johnson PH, Smart E, Kimura H. Missense mutation of FUT1 and deletion of FUT2 are responsible for Indian Bombay phenotype of ABO blood group system. Biochem Biophys Res Commun. 1997; 238:21–5. 9. Lubke T, Marquardt T, Etzioni A, Hartmann E, Von Figura K, Körner C. (May 2001). Complementation cloning identifies CDG-IIc, a new type of congenital disorders of glycosylation, as a GDP-fucose transporter deficiency. Nat Genet. 2001; 28 (1):73–6. 10. Frydman M, Etzioni A, Eidlitz-Markus T, Avidor I, Varsano I, Shechter Y et al. Rambam–Hasharon syndrome of psychomotor retardation, short stature, defective neutrophil motility, and bombay phenotype. Am J Med Genet. 1992; 44:297–302.
Karunashree, Padma Vijayashree, Bijan Kumar Mukhopadhyay, Sangeeta Chippa4, N. Bhavani, Prasanna Kumar Reddy, Chitra Patil
Introduction: Diabetes mellitus type -2 is one of the common metabolic disorder we face in our day to day life. it is characterized by high blood glucose level. Adenosine deaminase (ADA) is the enzyme which catalyses the irreversible deamination of adenosine to inosine. Objective: To estimate the level of serum adenosine deaminase (ADA), fasting blood glucose and lipid profile in patients with uncomplicated type -2 diabetes mellitus through case control study and also to know any correlation between plasma glucose values with ADA and lipid profile. Method: This study was conducted in Dept. of Obstetrics and Gynaecology, MNR Medical College and Hospital, Sangareddy, Medak. We took total 50 patients in our study, out of which 25 patients were with uncomplicated type-2 diabetes mellitus and other 25 were as healthy control group. Blood sample were taken and Adenosine deaminase levels were measured colourimetrically, based on the method described by Giusti and Galanti. Other routine investigation like- FBS,PPBS,lipid profile, Blood urea, Serum creatinine were also measured. Results: elevation of the serum ADP were found in diabetic patients as compared to controls and also strong correlations were found between serum ADA, lipid profile and plasma glucose levels. Conclusions: ADA level is significantly related with the type -2 diabetes mellitus. Any change of ADA level is an indirect expression of tissue adenosine levels. In pathophysiology of diabetes, ADA has its multimetabolic effects.
1. Sheetz M.J King GL. Molecular understanding of hyperglycaemia’s adverse effects for diabetic complications, JAMA 2002; 288:2579-88. 2. Wild S ‘Roglic G, Green A, et al Global prevalence of diabetes: estimates for the years 2000 and projections for 2030. Diabetes care 2004; 27: 1047-53. 3. Stain Johanson. Metabolic roles of adenosine. Thesis 2007; Karolinska Institute. 4. World Health Organization Diabetes updated march 2013-WHO media criteria. 5. Denis Mcgarry J. Dysregulation of fatty acid metabolism in the etiology of type-2 Diabetes. Banting Lecture 2001. Diabetes 2002; 51(1):7-18. 6. Kurtul N, Akarsu E, Aktaran S. The relationship between serum total sialic acid levels and adenosine deaminase activity in obesity. Saudi Med J 2006, 27, 170-2. 7. Bottini E, Gerlini G, Lucirini N, Amante A, Gloria Bottini F. Evidence of selective interaction between adenosine deaminase and acid phosphatase polymorphisms in fetuses carried by diabetic women. Hum Genet. 1991, 87,199-200. 8. Hoshino T, Yamada K, Masuoda K, Tsuboi L, Itoh K, Nonaka K. Elevated adenosine deaminase activity in the serum of patients with Diabetes Mellitus. Diabetes Res Clin Prac 1994, 25 97-102. 9. Singh LS, Sharma R, Alloxan Diabetes regulates adenosine deaminase activity in mice: tissue and age specific correlation. Biochem Mol Biol Int 1998, 46, 55-61. 10. Gitangali G, Neerja. The effect of Hyperglycemia on some Biochemical parameters in Diabetes Mellitus. JCDR 2010, 4, 3181-6. 11. Erkilic K, Evereklioglu C, Cekmen M. Adenosine deaminase enzyme activity is increased and negatively correlates with catalase, SOD, and GSH in patients Behcet’s Disease” Original contributions/ clinical and laboratory investigations. Mediators Inflamm 2003, 12, 107-16. 12. Shiva Prakash M, Chennaiah S, Murthy YSR. Altered Adenosine Deaminase activity in type 2 Diabetes Mellitus. JICAM 2006,7, 114-117. 13. Selva Kumar C, Kalaivani R, study of adenosine Deaminase and serum protein Bound sialic acid levels in alcoholic Liver Disease. Int J Biol Med Res. 2011, 2754-756. 14. Nisha Subhas Chandra Ramani, Krishna Murthy N, Raghavendra Prasad BN et al. Role of Adenosine Deaminase to predict glycemic status in type -2 Diabetes mellitus. Jclin Bio med Sci 2012, 2, 123-2. 15. John N. Fain, Paul W.Weiser. Effects of adenosine deaminase on cyclic adenosine monophosphate accumulation, lipolysis and glucose metabolism of fat cells. The Journal of Biological Chemistry 1975; 250 (3): 1027-1034. 16. Peter Arner, Jan Ostman, Relationship between the tissue level of cyclic AMP and the fat cell size of human adipose tissue. Journal of Lipid Research 1978; 19:613-618. 17. Madhavi Reddy A, Rao Y.N, Yogendra Singh, Alpana Saxsena. Adenosine Deaminase and protein Tyrosine Phosphatase activities in liver and peritoneal macrophages of streptozocin induced diabetic mice. Indian Journal of Clinical Biochemistry. 1995; 10 (2): 66-71. 18. Anjali C. Warrier, Narasimha Y.Rao, Tarun K. Mishra et al. Evaluation of Adenosine Deaminase activity and lipid peroxidation levels in Diabetes Mellitus. Indian Journal of Clinical Biochemistry. 1995; 10 (1): 9-13. 19. Mustafa Araz, Yuksel, Ozdemir, Mehmet, Tarakcyoolu et al. Elevated Adenosine Deaminase Activity is not implicated in microvascular complications of type 2 Diabetes Mellitus Except HbA1c. Turkish Journal of Endocrinology and Metabolism. 2000; 4(3) : 95-99. 20. Mazzone T, 2000: Current concepts and controversies in the pathogenesis, prevention of the macrovascular treatment complications of diabetes. J.Lab 21. Samantha P, Venkateswrlu M, Siva Probodh V. Lipid profile levels in type-2 diabetes mellitus from the tribal population of Adilabad, Andhra Pradesh, India. Journal of clinical and Diagnostic Research. 2012 may (suppl-2) Vol-6(4) : 590-592. 22. Idogun ES, Unuigbe EL, Ogunro PS, Akinola OT, Fanodu AA, Assessment of the serum lipids in Nigerians with type-2 Diabetes Mellitus complications. Pak.J.Med.Sci. (part-1) 2007: 23(5) : 708-12. 23. Albrki WM,Elzouki ANY, EL –Mansoury ZM, Tashani OA, Lipid profiles in Libian Type 2 diabetes. J.Sci.Appls 2007: 1(1) : 18-23. 24. Bijlani PK, Shah Kokila Raheja BS, HDL cholesterol in Diabetics. JAPI 1984; 32. 25. H.Surekha Rani, G. Madhvi, V rama Chandra Rao, B.K Sahay and A. Jyothy. Risk factors for coronary Heart Disease in type 2 Diabetes Mellitus. Indian Journal of clinical Biochemistry 2005, 20 (2): 75-80.
Priti Bagade, Anagha Jinturkar
Background: Systemic Lupus erythmatosus is a autoimmune disease mostly affecting Women of child bearing age. SLE are at higher risk for exacerbations of the disease during pregnancy, spontaneous abortions, intrauterine foetal death, pre-eclampsia and eclampsia, preterm delivery and intrauterine growth retardation. Objective: pregnancy is a challenge for lupus patients and their physicians. This case report is focused on the disease course, gestational outcome and management of patients with SLE during pregnancy. Methods: Here we describe the successful management of patient with SLE, registered at second trimester of pregnancy, with antinuclear antibody and antiphospholipid antibody positive, with intra uterine growth restriction with good maternal and fetal outcome. Conclusion: As the treatment of systemic lupus erythematosus (SLE) improves, and with better understanding of the disease more women with this disease are able to become pregnant. Pregnancy outcomes have improved dramatically over the last 40 years. However, fetal and maternal complications still exist. Careful planning of pregnancy coupled with multidisciplinary monitoring and treatment substantially decreases the risks for the mother and the infant.
1. Cunningham F. Gary, et al. Williams obstetrics. 21st Ed., New York: McGraw Hill; 2001 .p. 1146-1152 2. National study of the complications of lupus in pregnancy. Am J Obstet Gynecol 2008;199:127. Clowse ME, Jamison M, Myers E, James e1-6. 3. Clowse ME, Magder LS, Witter F, Petri M. The impact of increased lupus activity on obstetric outcomes. Arthritis Rheum 2005;52:514-21. 4. Megan E. B. Clowse,1 Laurence Magder,2 Frank Witter,3 and Michelle Petri. Hydroxychloroquine in Lupus Pregnancy, ARTHRITIS and RHEUMATISM. Vol 54, No. 11, November 2006, pp 3640–3647. 5. Josephine Patricia Dhar, MD and Robert J. Sokol, MD. Lupus and Pregnancy: Complex yet Manageable, Clin Med Res. Dec 2006; 4(4): 310–321 6. Dhar JP, Sokol RJ. Lupus and pregnancy: Complex yet manageable. Clin Med Res 2006;4:310-21. 7. Stojan G1, Baer AN.Flares of systemic lupus erythematosus during pregnancy and the puerperium: prevention, diagnosis and management. Expert Rev Clin Immunol. 2012 Jul;8(5):439-53. doi: 10.1586/eci.12.36. 8. Merkel PA, Chang Y, Pierangeli SS, Convery K, Harris EN, Polisson RP. The prevalence and clinical associations of anticardiolipin antibodies in a large inception cohort of patients with connective tissue diseases. Am J Med 1996;101:576-83. 9. A Doria1, A. Tincani2 and M. Lockshin3(Tandon A, Ibañez D, Gladman DD, Urowitz MB. The effect of pregnancy on lupus nephritis. Arthritis Rheum 2004;50:3941-6. 10. Rai R, Cohen H, Dave M, Regan L. Randomised controlled trial of aspirin and aspirin plus heparin in pregnant women with recurrent miscarriage associated with phospholipid antibodies (or antiphospholipid antibodies). BMJ 1997;314:253-7. IN FOC. 11. Stone S, Hunt BJ, Khamashta MA, Bewley SJ, Nelson-Piercy C. Primary antiphospholipid syndrome in pregnancy: an analysis of outcome in a cohort of 33 women treated with a rigorous protocol. J Thromb Haemost 2005; 3: 243–5. 12. Michael D. Lockshin, M.D., Maurice L. Druzin, M.B., Stephanie Goei, Tasneem Qamar, M.A., Margret S. Magid, M.D., Lois Jovanovic, M.D., and Michael Ferenc, M.D. Antibody to Cardiolipin as a Predictor of Fetal Distress or Death in Pregnant Patients with Systemic Lupus Erythematosus. N Engl J Med 1985; 313:152-156. 13. Vyas V, Shukla D, Patil S, Mohite S. Caesarean section in a case of systemic lupus erythematosus. Indian J Anaesth 2014;58:193-5 14. Donaldson LB, De Alvarez RR. Further observations on lupus erythematosus associated with pregnancy. Am J Obstet Gynecol. 1962;83:1461–73. 15. Ellis FA, Bereston ES. Lupus erythematosus associated with pregnancy and menopause.AMA Arch Derm Syphilol. 1952;65:170–6. 16. Cervera R, Font J, Carmona F, Balasch J. Pregnancy outcome in systemic lupus erythematosus: good news for the new millennium. Autoimmun Rev. 2002;1:354–9.
Jaykar R D, Ubale B P, Shende P Shweta, Vikram Ramamurthy
Background: The evolution of scientific knowledge in microbiological field has provided an opportunity to explode new methods of therapy, which have changed and improved surgical practice remarkably during 20th century. Surgical infection, particularly surgical site infection (SSI), has always been a major complication of surgery and trauma and has been documented for 4000-5000 years. Cases: 800 patients have been studied in this study. Department of microbiology helped us in conducting this study. Every Patient who underwent clean and clean contaminated surgery was studied.
1. Richard Cobb inguinal hernia : oxford textbook of surgery : edited by Peter J. Morris and Ronald A Mall; vol. 1 29.1 : 1399-1405 2. Robert J. Fitzgibbons, Jr Charles J. Fillipi and Thomas H. Quinn : Schwartz principles of surgery 8th edition , chapter 36, inguinal hernia : 1353-1392 3. Statistics by country for inguinal hernia 4. Jack Abradinson, Hernias, maingots abdominal operation Michel J. Zinner Seymous I. Schwartz Harold Rllis, vol. 1, 14, 1779-572 5. Sameer S. Awad MD : evidence based approach to hernia surgery : the American journal of surgery 188 ( supplement to December 2004) 6. Bellon J M, Bajo A, Handunrille N et al. fibroblast from transversalis fascia of young patient with direct inguinal hernia show constitutive MMP – over expression annals of surgery 2001; 233 (2) ; 287-291 7. Q 8. Robert J. Fitzgibbons et al. laparoscopic inguinal herniorraphy : results of a multi-central trial annals of surgery 1995; 221 9. David C Dunn, Donald Menzies. J 2 : the history of hernia repair. Hernia repair : the laparoscopic approach chapter 2 ; 3-9 10. Zieren j. Zieren H. Jacobi A frank A. Wenger Muller Jochen: prospective randomized study comparing laparoscopic and open tension free inguinal hernia repair with shouldice’s repair. the American journal of surgery april 1998 ; 175 ; 330-332
B Easwaran, N Sivaprahasam, G P Sekar, B Selvaraj
Majority of the tuberculous intestinal perforation are associated with a distal stricture and are considered to be blow outs due to distension. Perforations not associated with strictures or adhesive bands which can cause proximal dilatation are only considered as true perforations. Some of the perforations are associated with initiation of antituberculous therapy. Herewith we report 2 cases of tuberculous ileal perforation which are associated with neither strictures nor antituberculous therapy. Hence these are considered as spontaneous and true.
1. H. D. Tandon, A. Prakash. Pathology of intestinal tuberculosis and its distinction from Crohn's disease Gut, 1972, 13, 260-269. 2. Ha HK, Ko GY, Yu ES, Yoon K, et al. Intestinal tuberculosis with abdominal complications: radiologic and pathologic features. Abdom Imaging 1999;24:32. 3. W. G. Prout. Multiple tuberculous perforations of ileum Gut, 1968, 9, 381-382 4. Dasgupta A, Singh N, Bhatia A. Abdominal tuberculosis. A Histopathological study with special reference to intestinal perforation and mesenteric vasculopathy. J Lab Phys 2009; 1: 56–61. 5. Gupta RL. Abdominal Tuberculosis. In: GI Surgery Annual. Vol 2. Ed. Chattopadhya TK. New Delhi: Saku Printing House 2001; 51–60. 6. Kapoor VK. Abdominal tuberculosis. Postgrad Med J 1998; 74 : 459-6. 7. Bhansali SK. Abdominal tuberculosis. Experiences with 300 cases. Am J Gastroenterol 1997; 67: 324–337. 8. Kakar A, Aranya RC, Nair SK Acute perforation of small intestine due to tuberculosis. Aust N Z J Surg. 1983 Aug;53(4):381-3. 9. Nagi B, Lal A, Kochhar R, et al. Perforations and fistulae in gastrointestinal tuberculosis. Acta Radiol. 2002;43: 501–506. 10. Seabra J, Coelho H, Barros H, et al. Acute tuberculosis perforation of the small bowel during antituberculosis therapy. J Clin Gastroenterol. 1993;16: 320–2. 11. Gilinsky NH, Marks IN, Kottler RE, et al. Abdominal tuberculosis: a 10-year review. S Afr Med J. 64:849–857. 12. Tabrisky J, Lindstrom RR, Peters R, et al. Tuberculous enteritis: review of a protean disease. Am J Gastroenterol. 1975;63:49–57. 13. Dorairajan LN, Gupta S, Deo SV, Chumber S, Sharma L. Peritonitis in India – a decade’s experience. Trop Gastroenterol 1995; 16 : 33-8. 14. Kapoor VK. Abdominal tuberculosis : the Indian contribution. Indian J Gastroenterol 1998; 17 : 141-7. 15. Talwar S, Talwar R, Prasad P. Tuberculous perforations of the small intestine. Int J Clin Pract. 1999 Oct-Nov;53(7):514-8. 16. Sweetman, W. R., and Wise, R. A. (1959). Acute perforated tuberculous enteritis: surgical treatment. Ann. Surg., 149, 143-148. 17. Sanjay Gupta, Mayank Jayant, Robin Kaushik Free tubercular perforation of the ileum. World J Emerg Med 2013;4(3):235–236. 18. N.O. Aston and A.M. de Costa Tuberculous perforation of the small bowel Postgraduate Medical Journal (1985) 61, 251-252.
Jaykar R D, Jadhav S C, Ganakwar R G, Lakhpatre S B
Background: The evolution of scientific knowledge in microbiological field has provided an opportunity to explode new methods of therapy, which have changed and improved surgical practice remarkably during 20th century. Surgical infection, particularly surgical site infection (SSI), has always been a major complication of surgery and trauma and has been documented for 4000-5000 years. Cases: 800 patients have been studied in this study. Department of microbiology helped us in conducting this study. Every Patient who underwent clean and clean contaminated surgery was studied.
1. Brachman PS, Dan BB, Haley RW, Hooton TM, Garner JS, Allen JR. Nosocomial surgical infections: incidence and cost. Surg Clin North Am 1980;60:15-25 2. Cruse PJE, Foord R. The epidemiology of wound infection. A ten year prospective study of 62,939 wounds. Surg Clin North Am 1980; 60:27-40. 3. Olson M, O’Connor MO, Schwartz ML. A 5 year prospective study of 20,193 wounds at the Minneapolis VA Medical Center. Ann Surg 1984:199:253-259. 4. Green JW, Wenzel RP. Postoperative wound infection: a controlled study of increased duration of hospital stay and direct cost of hospitalization. Ann Surg 1977; 185:264-8. 5. Adrian Barbul and David T. Efron. Wound healing. In Schwartz’s Principles of Surgery, 9th edition United States of America, The McGraw-Hill Companies, Inc. 2010;222. 6. Garner JS, Dixon RE, Aber RC. Epidemic infections in surgical patients. AORN J 1981;34:700-24 7. Aber RC, Garner JS. Postoperative wound infections. In: Wenzel RP, ed. Handbook of hospital acquired infections. Boca Raton, Florida: CRC Press, Inc 1981:303-16 8. Schwartz J T and Saunders D E: Microbial penetration of surgical gown materials Surg. Gynaec Obst. 150; 507-512, 1980. 9. Cruse P J E, Foord R a: Five-year prospective study of 23, 649 surgical wounds Arch. Surg. 107; 206-210, 1973. 10. Lilani SP, Jangale N, Chowdhary A, Daver GB. Surgical site infection in clean and clean-contaminated cases. Indian J Med Microbiol 2005; 23(4):249-52. 11. Kowli S S, Nayak M H.Mehta A P. Bhalerao R A: Hospital infection. Ind. J. Surg. 475-86, 1985.
The severity of complications in pediatric foreign body aspiration is often underestimated as they are rarely reported. Complications are more severe in patients who have tracheo-bronchial aspiration for prolonged time. Rigid bronchoscopy is a common procedure in pediatric age group. Pneumothorax and tracheo-broncheal stenosis are rare complications noticed after rigid bronchoscopy done for pediatric foreign body aspirations. Here are 3 case reports of complications noticed after bronchoscopy. First two cases developed pneumothorax post bronchoscopy and intercostal tube drainage was sufficient in their management. Third case had undergone 3 repeat rigid bronchoscopic procedures in one month duration. At 6 months follow up he had developed mild bronchial stenosis manifesting as intermittent wheezy respiration without respiratory distress . The case was managed conservatively.
1. Reddy V. Anesthetic management of 18 month old child for rigid bronchoscopy: A difficult case scenario. Perspectives in Medical Research. 2014 jan; 2(1):41-42. 2. Hasdiraz L,Oguzkaya F,Bilgin M,Bicer C. Complication of bronchoscopy for foreign body removal:experience of 1035 cases. Ann Saudi Med. 2006;26(4):283-87. 3. Merrill W, Michels MD. Pneumothorax and Mediastinal Emphysema Complicating Tracheostomy. Arch Otolaryngol.1939;29(5):842-52. 4. Ciftci A O, Bingol KM, Enocak ME, Tanyel F C, Buyukpamukcu N. Bronchoscopy for evaluation of foreign body aspiration in children. J Pediatr Surg.2003;38:1170-76. 5. Campisi P, Forte V. Rigid endoscopy of airway:Basic technique.Chapter 9. Operative endoscopy and endoscopic surgery in infant and children.Taylor and fransis group.2012: 57-59. 6. Smith ME, Elstad MR. Bronchology. Chapter 84. Ballengers otorhinolaryngology : Head and Neck surgery. Snow Wackym. 17th edition.2006:966-67. 7. Burkey BB, Gardy S L, Rohde S L.Airway control and laryngotracheal stenosis in adults. Chapter 78. Ballengers otorhinolaryngology: Head and Neck surgery. Snow Wackym. 17th edition.2006:909-11. 8. Puchalalski J. Tracheal and bronchial stenosis: etiologies, bronchoscopic interventions and outcomes. Pakisthan Journal of Chest Medicine.2012 jan-mar;18(1):38-46.
Laxmi Rachkonda, Suresh Rawte, Surabhi Ruiwale
Introduction: Antepartum Haemorrhage (APH) is defined as bleeding from or into the genital tract after 28th week of pregnancy till the end of 2nd stage of labour. APH is a grave obstetrical emergency and is one of the leading causes of maternal and perinatal morbidity and mortality. APH can be due to placenta praevia, abruptio placentae, indeterminate causes or local causes of genital tract. This study is carried out to have a statistical impression of the consequences of antepartum haemorrhage on mother and foetus in a tertiary care center (MGM Hospital, Aurangabad, India). Objectives: This is a prospective observational study carried out in MGM Medical College, Aurangabad, India from January 2014 to June 2014. Results: During the study period, there were 1211 deliveries, out of which complete data from 50 diagnosed patients with antepartum haemorrhage were studied. In my study the incidence of antepartum haemorrhage was 4.1%. Out of 50 deliveries, 21 (42%) were diagnosed with placenta praevia, 29 (58%) had abruptio placentae as causes of antepartum haemorrhage. The mean age was 25 years. 76% of the patients were registered. During the antenatal period 52% had anaemia, 30% had oligohydramnios, 18% had malpresentation, 28% had hypertensive disorder in present pregnancy.80% have delivered by LSCS. 70% were preterm LSCS. The postnatal complications were PPH (16%), HELLP syndrome (6%), DIC (6%), Shock (4%). 66% required blood transfusion.53% of the live babies were low birth weight.46% were admitted to NICU. 16% had birth asphyxia 13% had IUGR. The perinatal mortality was 40%. Conclusion: From this study it was evident that, Antepartum Haemorrhage has serious life threatening complications and if diagnosed earlier in pregnancy and proper antenatal care is provided the maternal and perinatal outcome is surely to improve.
1. Konar H.D.C. Dutta’s textbook of obstetrics.seventh edition.Kolkata.2011.p.241-251. 2. Suresh. S. Rawte, Srinivas Gadappa. High risk cases in obstetrics. First edition.2014.p.289-313. 3. S Singhal,Nymphaea,S Nanda. Maternal And Perinatal Outcome In Antepartum Haemorrhage: A Study At a Tertiary Care Referral Institute. The Internet Journal Of Gynaecology And Obstetrics.2007; volume 9 number 2. 4. Rosalba Giordano, Alessandra Cacciatore, Pietro Cignini, Roberto Vigna, and Mattea Romano. Antepartum Haemorrhage. Journal of Prenatal Medicine; An International Journal of Prenatal Diagnosis and Fetal Maternal Medicine.2010.volume 4(1).page 12-16. 5. B. Bako, B. M. Audu, C. M. Chama,O. Kyari, A. Idrissa. An 8 year Clinical Review Of Antepartum Haemorrhage At The University Of Maiduguri Teaching Hospital,Maidugiri. BOMJ.July-December 2008.Volume 5 Issue 2. 6. S Bhandari, EA Raja, A Shetty and S Bhattacharya. Maternal and perinatal consequences of antepartum haemorrhage of unknown origin.BJOG:An International Journal of Obstetrics and Gynaecology. January 2014.Volume 121, Issue 1, pages 44–52,DOI: 10.1111/1471-0528.12464. 7. F Sheikh, S Khokhar, P Sirichand, R Shaikh. A Study of Antepartum Haemorrhage: Maternal And Perinatal Outcome. Medical Channel.April-June 2010. Volume 16, No 2. 8. A Maurya,S Arya. Study of Antepartum Haemorrhage and its maternal and perinatal outcome. International Journal of Scientific and Research Publications, Volume 4, Issue 2, February 2014. ISSN 2250-3153. 9. C Calvert, S Thomas, C Ronsmans, K Wagner, A Adler, V Filippi. Identifying Regional Variation in the Prevalence of Postpartum Haemorrhage: A Systematic Review and Meta-Analysis. PLOS ONE. July 23, 2012. DOI: 10.1371/journal.pone.0041114 10. Amoa AB, Augurea L, Klufio CA. Antepartum Haemorrhage at the Port Moresby General Hospital: a retrospective study of 130 consecuitive cases. P N G Medical Journal. 1992 Mar; 35(1):17-22. 11. Ajayi RA, Soothill PW, Campbell S, Nicolaides KH. Antenatal testing to predict outcome in pregnancies with unexplained antepartum haemorrhage. British Journal of Obstetrics and Gynaecology. 1992 Feb; 99(2):122-5. 12. Pagano, R; Adey, F D; Butterfield, L J. The management of antepartum haemorrhage (excluding placenta praevia). The Australian and New Zealand Journal of Obtetrics and Gynaecology. Vol. 23 Issue 1 Feb 1983. 13. A Bener, NM Saleh, MT Yousafzai. Prevalence and associated risk factors of ante-partum hemorrhage among Arab women in an economically fast growing society. Medical and dental consultant association of Nigeria.volume 15 issue 2. 16th June 2012.pages 185-189. DOI: DOI: 10.4103/1119-3077.97315. 14. Atsuko Sekiguchi, Akihito Nakai, Ikuno Kawabata, Masako Hayashi, and Toshiyuki Takeshita. Location of Placenta Previa Affect Preterm Delivery Risk Related to Antepartum Hemorrhage. International Journal Of medical Sciences. Volume 10 issue 12.24th September 2013. Pages 1683-1688. DOI: 10.7150/ijms.6416.
R V Desai, R A Suryawanshi
Attempt of this study is to use GIS for drainage analysis of Urmodi river basin of Satara district of Maharashtra. This river is tributary of Krishna, which originates at Kas Lateritic plateau of Bamnoli range. The aim of this paper is to understand a geomorphological change that has been taken place and to understand the geological role in these changes. GIS is a tool which is very useful and important in this case for assessment of drainage analysis. With the help of rosette diagram we tried to find out the structural control of different order streams of this basin for which Geo Rose software is used. All the parameters indicate steep slopes at higher altitude with high stream frequency on hard laterite and compact non porous basalt at lower level. There is structural, geomorphological and lithological control on basin development.
1. Coates D. R. (1958) Quantitative Geomorphology of Small Drainage Basins of Southern Indiana. Department of Geology, Columbia University, Tech. Report 10. 2. Chorley, R.J., E.G. Donald Malm and H.A. Pogorzelski,. “A new standard for estimating drainage basin shape”, Amer. Jour. Sci., 255: 138141. (1957). 3. Chow, V.T. Maidment D.R. and Mayse W., (1988), Applied Hydrology, New York, McGraw Hill. 4. Duncan, R. A., Pyle, D. G., 1988. Raid eruption of the Deccan Traps at the Cretaceous/Tertiary boundary. Nature, 333, 841-843. 5. Horton, R.E.: Drainage basin characteristics. Trans. Am. Geophys. Union 13: 350-360. (1932). 6. Horton, R.E., 1945, “Erosional development of streams and their drainage basins: hydrophysical approach to quantitative morphology”, Bull. Geol. Soc. Amer., 5, pp 275370. 7. Medlicott H. B. and Blanford W. T. (1879) A Manual of the Geology Of India Geol. Surv. India, pp 348-370 8. Miller, V.C.: A quantitative geomorphic study of drainage basin characteristic in the clinch, Mountain area, Verdinia and Tennesser, Projet NR 389-042,Tech. Rept.3 Columbia University, Department of Geology, ONR, Geography Branch, New York. (1953). 9. Sayyad, M.R.G. and Hundekari, S.M., Quaternary Int., 2006, 156-157, 189-199 10. S. A. Schumm, (1956), Evolution of drainage systems and slopes in Badlands at Perth Amboy, New Jersey, Geological Society of America, Bulletin, 67, 1956, 597-646. 11. Stanly Schumm, (1956), The relation of drainage basin relief to sediment loss. (intrnet publish) 12. Strahler A.N. 1952, Hypsometric (area - altitude) analysis of erosional topography. Bull Geol. Soc. Am 63, 1117- 1142 13. Strahler A.N. 1957, “Quantitative Analysis Of Watershed Geomorphology”, Trans. Amer. Geophys. Union., 38, pp 913-920 14. Strahler A. N. (1964) Quantitative geomorphology of drainage basin and channel networks. Section 4-II. In: V.T. Chow (Ed.), Handbook of Applied Hydrology, McGraw-Hill, New York. 15. Strahler, A.N. and A.H. Strahler. A Textbook of Physical Geography, John Wiley and Sons, New York. (2002). 16. Thornbury W.D., (1990), “Principle of Geomorphology”, Second edition, Willey Eastern Limited, New Delhi. 17. Widdowson M and Cox K G 1996 Uplift and erosional history of the Deccan Traps, India: Evidence from laterites and drainage patterns of the Western Ghats and Konkan coast; Earth Planet. Sci. Lett. 137 57–69. 18. Widdowson, M. (1997). Tertiary palaeosurfaces of the SW Deccan, Western India: implications for passive margin uplift. In: Palaeosurfaces: Recognition, Reconstruction and Paleoenvironmental Interpretation, 120 (Ed. by M. Widdowson), Geol. Soc. Lond. Spec. Publ. 221–248. 19. Widdowson M and Gunnell Y 1999 Lateritization, geomorphology and geodynamics of a passive continental margin: The Konkan and Kanara coastal lowlands of western peninsular India; Spec. Publ. Int. Assoc. Sediment. 27 245–274. 20. Wilkins, A., Subbarao, K.V., Walsh, G., 1994. Weathering regimes in Deccan basalts. In: Subbarao, K.V. (Ed.), Volcanism. Wiley Eastern Ltd, New Delhi, pp. 217–232. 21. Wood P.R.1960, Geology and groundwater fractures of the butte valley region, Sisikiyan Country, California USA, U.S.G.S. water supply paper No-1461, 150 pp
Sibaprashad Pattanayak, Subrata Pramanik, Sanjit Kumar Nayak, Sivashankar Behuria
Background: Krukenberg tumors in pregnancy are relatively very rare and their management can present a great dilemma for the obstetrician and oncologist. The situation becomes further complicated when the primary is bilateral lobular breast cancers. Case Report: We present the case of a G2P1 who presented to us at 34 weeks of gestation with bilateral massive Krukenberg tumors. She also had bilateral lobular cancers of breasts. Despite at surgery and chemotherapy she died 3 months postpartum. Conclusion: Early detection followed by surgery and chemotherapy could possibly result in a favorable outcome with such patients.
1. Jiang R, Tang J, Cheng X, Zang RY. Surgical treatment for patients with different origins of Krukenberg tumors: outcomes and prognostic factors. Eur J Surg Oncol 2009;35:92-7. 2. Yada-Hashimoto N, Yamamoto T, Kamiura S, Seino H, Ohira H, Sawai K, et al. Metastatic ovarian tumors: a review of 64 cases. Gynecol Oncol 2003;89:314-7. 3. De Waal YR, Thomas CM, Oei AL, Sweep FC, Massuger LF. Secondary ovarian malignancies: frequency, origin, and characteristics. Int J Gynecol Cancer 2009;19:1160-5. 4. Demopoulos RI, Touger L, Dubin N. Secondary ovarian carcinoma: a clinical and pathological evaluation. Int J Gynecol Pathol 1987; 6:166-75. 5. Young RH, Scully RE. Metastatic tumors in the ovary: a problem-oriented approach and review of the recent literature. Semin Diagn Pathol 1991; 8:250-76. 6. Brown DL, Zou KH, Tempany CMC, Frates MC, Silverman SG, McNeil BJ, Kurtz AB et al. Primary versus secondary ovarian malignancy: imaging findings of adnexal mass in the Radiology Diagnostic Oncology Group Study. Radiology 2001; 219:213-8. 7. Powari M, Dey P, Gupta SK, Saha S. Metastatic tumours of the ovary: a clinico-pathological study. Indian J Pathol Microbiol. 2003; 46:412-5. 8. Moore RG, Chung M, Granai CO, Gajewski W, Steinhoff MM. Incidence of metastasis to the ovaries from nongenital tract primary tumors. Gynecol Oncol. 2004; 93:87-91. 9. Le Bouedec G, de Latour M, Levrel O, Dauplat J. Krukenberg tumors of breast origin. 10 cases. Presse Med. 1997; 26:454-7. 10. Johansson M. Clinical aspects of metastatic ovarian cancer of extragenital origin. Acta Obstet Gynecol Scand 1960; 39:681-97. 11. Osborne MP, Pitts RM. Therapeutic oophorectomy for advanced breast cancer: the significance of metastases to the ovary and of ovarian cortical stromal hyperplasias. Cancer 1961;14:126-30 12. White TT. Carcinoma of the breast and pregnancy; analysis of 920 cases collected from the literature and 22 new cases. Ann Surg 1954; 139: 9–18. 13. Sophie E. McGrath, Alistair Ring. Chemotherapy for breast cancer in pregnancy: evidence and guidance for oncologists, Ther Adv Med Oncol. Mar 2011; 3(2): 73–83. doi: 10.1177/1758834010392445 14. Jiang R, Tang J, Cheng X, Zang RY. Surgical treatment for patients with different origins of Krukenberg tumors: outcomes and prognostic factors. Eur J Surg Oncol 2009;35:92-7.
Objectives: 1) To study the knowledge of breast feeding among mothers. 2) To study the practice methods of breast feeding followed among mothers. Materials and Method: Observational study done over 3 months at Sri Adichunchangiri institute of medical sciences, B.G. Nagara. Study period: January 2009 till April 2009. Cases studied: 300. Using simple questionare regarding knowledge of breast feeding and practices followed to mothers who delivered at Sri Adichunchangiri institute of medical sciences, B.G. Nagara, in the study period. WHO BFHI Guidelines were used in the questionnaire. Results: In my study of all mothers who delivered at Sri Adichunchangiri institute of medical sciences, B.G. Nagara in the study period, 60% of mothers had NO knowledge, 43.3% with average knowledge and 16.6 % with good knowledge of breast feeding. About breast feeding practices, 33.3% of mothers followed good practices, 16.6 % of the mothers were average and 50% of the mothers were not following good breast feeding practices. Morethan hospital staff, elderly person at family and neighbours influence the practice of breast feeding among mothers. Conclusion: Large proportion of mothers are still lacking the knowledge of good breast feeding and practice methods. Antenatal counselling and demonstration of breast feeding advantages and techniques ante natally and post natally would help to achieve WHO goals in a long run.
1. WHO reference number: WHO_MPS_10.03, WHO technical consultation on postpartum and postnatal care. 2. The Baby-Friendly Hospital Initiative-WHO-UNICEF-1991.Ten steps to successful breastfeeding 3. WHO reference number: WHO/FHE/MSM/94.11 Rev.1.Practcal guide for Mother-Baby Package: Implementing safe motherhood in countries.
N Sivaprahasam, S Vijayalakshmi, S Kalitathinam, R Balasubramaniam
Introduction: Perforated peptic ulcer is a life threatening emergency and a means to predict severity of disease is welcome. Many scoring systems to predict outcome in patients with peritonitis are available. Materials and Methods: To evaluate the usefulness of Mannheim Peritonitis Index, in patients with perforated peptic ulcer a prospective study was done from June 2003 to May 2004 at Govt. Rajaji Hospital attached to Madurai Medical College, Madurai. 37 patients were studied. Results: No patient with a score <15 died, whereas 3 out of 4 (75%) with a score >25 died. Conclusion: MPI is useful in prediction outcome in patients with perforated peptic ulcer. Increasing MPI score indicates poor prognosis and higher mortality.
1. Wacha H, Linder MM, Feldmann U, Wesch G, Gundlach E, Steifensand RA. Mannheims peritonitis index – prediction of risk of death from peritonitis. Theoretical Surgery 1987; 1:169-177. 2. Ermolov AS, Bagdat’ev VE, Chudotvortseva EV, Rozhnov AV. Evaluation of the Mannheim Peritonitis Index. Vestn Khir Im I I Grek 1996; 155:22-3. 3. Függer R, Rogy M, Herbst F, Schemper M, Schulz F. Validation study of the Mannheim Peritonitis Index. Chirurg 1988; 59:598-601. 4. Notash AY, Salimi J, Rahimian H, Fesharaki MH, Abbasi A. Evaluation of Mannheim peritonitis index and multiple organ failure score in patients with peritonitis. Indian J Gastroenterol 2005; 24:197-200. 5. Billing A, Fröhlich D, Schildberg FW. Prediction of outcome using the Mannheim peritonitis index in 2003 patients. Peritonitis Study Group. Br J Surg 1994;81:209-13 6. Bohnen J, Boulanger M, Meakins JL, McLean AP. Prognosis in generalized peritonitis. Relation to cause and risk factors. Arch Surg 1983; 118:285-90. 7. Giessling U, Petersen S, Freitag M, Kleine-Kraneburg H,Ludwig K. Surgical management of severe peritonitis. Zentralbl Chir 2002; 127:594-7. 8. Schein M, Saadia R, Freinkel Z, Decker GAG. Aggressive treatment of acute severe diffuse peritonitis from intestinal origin. World J Surg 1983; 7:762-6. 9. Farthmann EH, Schöffel U. Principles and limitations of operative management of intraabdominal infections. World J Surg 1990; 14:210-7. 10. F. Ntirenganya, G. Ntakiyiruta, I. Kakande: Prediction of Outcome Using the Mannheim peritonitis Index in Patients with Peritonitis at Kigali University Teaching Hospital. East and Central African Journal of Surgery 2012 vol17 (2): 52-64 11. John Boey, Samuel k.Y. Choi, T. Alagaratnam, A. Poon, Risk Stratification in Perforated Duodenal Ulcers 1987 Annals of surgery vol 201 (1): 22-26 12. Feliciano DV. Do perforated duodenal ulcers need an acid-decreasing surgical procedure now that omeprazole is available? Surg Clin North Am. 1992;72(2):369–380 13. Ng EK, Lam YH, Sung JJ, et al: Eradication of Helicobacter pylorus prevents recurrence of ulcer after simple closure of duodenal ulcer perforation: Randomized controlled trial. Ann Surg 231:153, 2000. 14. Matsuda M, Nishiyama M, Hanai T, et al. Laparoscopic omental patch repair for perforated peptic ulcer. Ann Surg. 1995; 221:236–240. 15. Lau W-Y, Leung K-L, Kwong K-H, et al. A randomized study comparing laparoscopic versus open repair of perforated peptic ulcer using suture or sutureless technique. Ann Surg. 1996; 224:131–138. 16. Dubois F. New surgical strategy for gastroduodenal ulcer: laparoscopic approach. World J Surg. 2000; 24:270–276. 17. Lagoo S, McMahon RL, Kakihara M, et al. The sixth decision regarding perforated duodenal ulcer. JSLS. 2002; 6:359–368. 18. Donovan AJ, Berne TV, Donovan JA. Perforated duodenal ulcer: an alternative therapeutic plan. Arch Surg. 1998; 133:1166–1171. 19. Nirula R, Gastro duodenal perforation. Surg Clin North Am. 2014 Feb;94(1):31-4 20. Leeman MF, Skouras C, Paterson-Brown S. The management of perforated gastric ulcers. Int J Surg. 2013; 11(4):322-4. 21. M.M.Correia, L.C.S Thuler et.al. Prediction of death using the Mannheim Peritonitis index in oncologic patients. Revista Brasileira de Cancerologia, 2001, 47(1): 63-68 22. Arpan Mishra, Dhananjaya Sharma, V.K.Raina, A simplified prognostic scoring system for peptic ulcer perforation in developing countries. Indian J Gastroenterology, 2002, 22: 49-53 23. Christian Ohmann, Dietmar H. Wittmann, Hannes Wacha and the Peritonitis Study Group. Prospective evaluation of prognostic scoring systems in peritonitis Eur J Surg 159: 267-274, 1993.
Salma Shaziya, Mozimul Haq Siddiqui
History of foreign body aspiration presumably is as old as mankind. 90% of foreign bodies aspirated are bronchial and only 10% foreign bodies are laryngeal or tracheal. Our first case is unique in sense aspiration was due to fruit gel chocolate which clinically presented as a catastrophic event due subglottic obstruction and child’s life was saved with tracheal aspiration following intubation. The second case was unique in sense unlike usual severe symptoms following subglottic foreign body aspirations this child presented with time lapse of seven days after aspiration and only stridor as symptom.
1. Khan N S , Khan A R , Din S, Sattar F. Management of subglottic foreign body: A therapeutic challenge.JPMI.2011;18(4): 658-61 2. Cotton R T, Rutter J M. Foreign Body Aspiration. Kendig’s disorders of the respiratory tract in children.Chapter41.Chernick and boat.W.B.Saunders.Philadelphia.2006; 610-15. 3. Kaur K, Sonkhya N, Bapna A S. Foreign bodies in the tracheobronchial tree: a prospective study of fifty cases. Indian Journal of Otolaryngotogy and Head and Neck Surgery. 2002 mar; 54(1):30-34. 4. Gupta A K,Parida P K, Bansal S, Kumar S. Tracheal foreign body: an unusual history and presentation. Internet Journal of Pediatrics and Neonatology. 2005;6:1-5 5. Pawar R T, Thakin G V, Amit T, Anup G. An unusual presentation of impacted foreign body in the larynx: A case report. International journal of recent trends in science and technology. 2013; 7(3)100-102. 6. Fraga J C et al. Bronchoscopic removal of foreign body from airway through tracheostomy or tracheotomy. J pediatr. 2003; 79(4):369-72.
S G S Rajesh Reddy V, Shiddalingesh Salimath, Torvi Janaki R
This case report illustrates anaphylactic/anaphylactoid reaction in form of generalized rash and laryngospasm after administration of a single dose of 1mg ondansetron intravenously. It was used as a preanesthetic medication in a 7yr old female child with left sided pyothorax/fibrothorax posted for minithoracotomy (decortitectomy). Awareness on this rare but fatal adverse reaction to this commonly used drug helps in early recognition and prompt management of event
1. Ross AK, Ferrero-Conover D. Anaphylactoid reaction due to the administration of ondansetron in a pediatric neurosurgical patient. Anesth Analg 1998; 87: 779-80. 2. Mehra KK, Gogtay NJ, Ainchwar R, Bichile LS. Hypersensitivity to intravenous ondansetron. J Med Case Rep 2008; 2: 274. 3. Sharma A, Raina V. Generalised seizures following ondansetron. Ann Oncol 2001; 12(1): 131-132. 4. Tolan MM, Fuhram TM, Tsueda K, Lipmann SB. Perioperative extrapyramidal reactions associated with ondansetron. Anesthesiology 1999; 90 (1): 340-341. 5. Kataja V, de Bruijn KM. Hypersensitivity reactions associated with 5-hydroxytryptamine (3)-receptor antagonists: a class effect? Lancet 1996; 347(9001):584-585. 6. Bousquet PJ, Co-Minh HB, Demoly P. Isolated urticaria to ondansetron and successful treatment with granisetron. Allergy 2005; 60(4):543-544.
Savitha H C, Usha D, Sanjay Kumar C, Deepthi H R
Objective: To assess the maternal, neonatal complications and outcome in pregnancy with gestational diabetes mellitus. Materials and Methods: A total of 72 GDM cases were studied retrospectively at MIMS Mandya over a period of 3yrs. Antenatal and perinatal data were obtained from patient’s medical records. All diabetic pregnant women also suffering from other disorders which directly or indirectly may affect the outcome of pregnancy were excluded from the study. Results: Out of total 20,468 deliveries, GDM was seen in 72cases(0.35%). 62% of the patients were above 25yrs of age and 68% were multiparous. 69% of the patients required insulin for glycemic control. Higher incidence of preeclampsia (44.4%), polyhydramnions(23.6%), PROM(8.3%) and preterm delivery(8.3%) was noted. Common neonatal complications were macrosomia (29.17%) and hypoglycaemia (9.7%). Increased rate of caesarean section was also noted (62%). Conclusion: GDM is recognised to be associated with increased rates of adverse maternal and neonatal outcomes, which are supported by the findings of our study. Even mild form of GDM seems to have significant consequences for women and their offspring and is recommended to be aggressively treated. Early diagnosis and strict control of blood sugar levels throughout the pregnancy can significantly reduce maternal and neonatal complications.
1. Position Statement AD; American Diabetes Association. Gestational diabetes mellitus. Diabetes Care 2004 Jan;27(Suppl 1):S88-S90. 2. Karcaaltincaba D, Kandemir O, Yalvac S, Güvendag-Guven S, Haberal A. Prevalence of gestational diabetes mellitus and gestational impaired glucose tolerance in pregnant women evaluated by National Diabetes Data Group and Carpenter and Coustan criteria. Int J Gynaecol Obstet 2009 Sep; 106(3):246-249. 3. Sendag F, Terek MC, Itil IM, Oztekin K, Bilgin O. Maternal and perinatal outcomes in women with gestational diabetes mellitus as compared to nondiabetic controls. J Reprod Med 2001 Dec; 46(12):1057-1062. 4. Reece EA. The fetal and maternal consequences of gestational diabetes mellitus. J Matern Fetal Neonatal Med 2010 Mar; 23(3):199-203. 5. O’Sullivan JB. Diabetes mellitus after GDM. Diabetes 1991; 29 Suppl 2: 131-5. 6. National Diabetes Data Group. Classification: and diagnosis of diabetes mellitus and other categories of glucose intolerance. Diabetes 1979; 28: 1039- 57. 7. Konje JC. Diabetes Mellitus. Gestational Diabetes. In: Luesley DM, Baker PM, editors. Obstetrics and gynaecology. An evidence based test for MRCOG. 1st edition. New York: Distributed in the United States of America by Oxford University Press 2004. p. 47, 174. 8. Khan A, Jaffarey SN. Screening for gestational diabetes. Medical Channel 1997; 3: 8-12. 9. Randhawa MS, Moin S, Shoaib F. Diabetes mellitus during pregnancy: a study of fifty cases. Pakistan J Med Sci 2003; 19: 277-82. 10. Perveen N, Saeed M. Gestational diabetes and pregnancy outcome: Experience at Shaikh Zayed Hospital. Mother and Child 1996; 34: 83-8. 11. Samad N, Hassan JA, Shera AS, Maqsood A. Gestational diabetes mellitus-screening in a developing country. J Pak Med Assoc 1996; 46: 249-52. 12. Jovanovic-Peterson L, Peterson CM. Nutritional management of the obese pregnant women. Nutrition and the MD 1991; 17: 1. 13. Gillmer MDG, Hurley PA. Diabetes and endocrine disorders in pregnancy. In: Edmonds DK, editor. Dewhurst’s Textbook of obstetrics and gynaecology for postgraduates. 6th ed. Oxford: Blackwell Science 1999. p. 197-209. 14. Falls J, Millo L. Endocrine disorders of pregnancy. In: Bankowski BJ, Hearne AE, Lambrou NC, Fox HE, Wallach EE, editors. The Johns Hopkins Manual of Gynecology and Obstetrics. 2nd ed. Philadelphia: Lippincott Williams and Wilkins, A Wolter Kluwer Company 2002. p. 162-75. 15. Jovanovic-Peterson L, editor. Medical management of pregnancy complicated by diabetes, 2nd ed. Alexandria, VA: Amarican Diabetic Association; 1995. 16. Usmani AT, Waheed N. Pregnancy complicated with diabetes: A one year experience. J Pak Institute Med Science 1995; 6: 342-5. 17. Mannan J, Bhatti MT, Kamal K. Outcome of pregnancies in diabetic mothers: A descriptive study. Pak J Obstet Gynaecol 1996; 9:35-40. 18. Ferchiou M, Zhioua F, Hadhri N, Hafsia S, Mariah S. Predictive factors of macrosomia in diabetic pregnancies. Rev Fr Gynecol Obstet 1994; 89: 73-6. 19. Diabetes Control and Complications Trial Research Group. The effect of pregnancy on microvascular complications in the diabetes control and complications trial. Diabetes Care 2000; 23: 1084-91. 20. Gellis SS, Hsia DYY. The infant of diabetic mothers. Am J Dis Child 1959; 97: 1. 21. Kitzmiller JL, Cloherty JP, Younger MD. Diabetic pregnancy perinatal morbidity. Am J Obstet Gynaecol 1978; 131: 560-80.
Rajesh C Sambutwad, Vasant Wagh, V S Rathod, A Mudey
Background: Tuberculosis (TB) is a contagious disease. Like the common cold, it spreads through the air. Only people who are sick with TB in their lungs are infectious..The last two-three decades have seen increasing interest in the quantitative study of socioeconomic factors and health system factors as determinants of health outcomes in the field of public health. Aim: Correlation between TB result and socio economic class and area of leaving Objective: 1) finding the treatment outcome according to the socio economic group. 2)to find out the area wise treatment outcome of tuberculosis patient Method: Community based longitudinal study was conducted. All the participant are tose who visit to hospitals Tb and chest department and register for the tuberculosis treatment. Social economic class we uses for rural area Modified Prasads classification and urban area Kuppuswamis method of classification. Result: Most of the patients are from rural area 81.5% of total participant and urban area only 18.4% .cure rate also higher in urban area that was 78.9%.Defolter rate was higher in rural area 2.3%. According to social class most patient belong to class IV 64.5%, cure rate was 100% in SEC I. Conclusion: The area and SEC class where we work hard for the better result of Tb treatment outcome.
1. History of TB Control TBC INDIA Director General of Health Services 2. TBC INDIA ,Ministry of Health and Family Welfare INDIA 3. Palomino – Leão – Ritacco Tuberculosis 2007 From basic science to patient care TuberculosisTextbook.comFirst Edition 4. Golub JE, Mohan CI, Gomstock GW, Chaisson RE. Active case finding of Tuberculosis: Historical perspective and future prospects. Int J Tuber Lung Dis 2005 5. TBC India directorate General of Health Services Ministry of Health and Family Welfare 6. Dye C, Lönnroth K, Jaramillo E, Williams BG, Raviglione M. Trends in tuberculosis incidence and their determinants in 134 countires. Bull World Health Organ. 2009;87:683–91 7. Stuckler D, Basu S, McKee M. Drivers of inequality in millennium development goal progress: A statistical analysis. PLoS Med. 2010;7:e1000241. 8. Ma,de Lourdes Garcia tuberculosis epidmology and control in Vercrwz,Maxico international Jurnal of epidmology 1999,28:135-140 9. Ranjani Ramachandran et al mycobacteremia in tuberculosis patients with hiv infection Ind J Tub,2002,50, 29 10. Kedir Wajisso et al assessment of hiv sero-prevalence among registered tuberculosis patients in arsi zone department of community health faculty of medicine, addis ababa university april 2003 addis ababa