VCFL Sciences Journal

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Table of Contents
UNCOMMON LETHAL COMPLICATION OF A COMMON DISEASE: TYPHOID PANCREATITIS- A RARE CASE REPORT ...................................................................................................... 120 STUDY OF INTRA-OCULAR PRESSURE CHANGES IN APHAKIA AND PSEUDOPHAKIA CASES AFTER CATARACT SURGERY .......................................................................................... 125 CLINICAL PROFILE OF HIV PATIENTS WITH CENTRAL NERVOUS SYSTEM MANIFESTATIONS .................................................................................................................................... 134 PATTERN OF USAGE OF GASTROPROTECTIVE AGENTS IN PATIENTS RECEIVING NONSTEROIDAL ANTI-INFLAMMATORY DRUGS............................................................. 139 STUDY OF CONDUCTION BLOCKS IN ACUTE MYOCARDIAL INFARCTION ......................... 146

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Uncommon Lethal Complication of a Common Disease Typhoid Pancreatitis- A Rare case report
Dr.Akhila.D1, Dr. Mohamed Basha2, Dr. B S prasad3, Dr Akhil .M .Kulkarni4, Dr.Prashanth.S5
1

Senior Resident, Department of Radio diagnosis; 2Assistant Professor

Department of Paediatrics; 3Director of Neonatology; 4Assistant Professor, Department of Radio diagnosis; 5Associate Professor, Department of Neurology, SSIMS & RC, Davangere, Karnataka, India.

Corresponding Author Dr .Akhila.D Email: [email protected]

Abstract Acute pancreatitis is a pancreatic

vague abdominal pain since 2 days. He was diagnosed positive for typhoid fever a week earlier. On examination he had minimally distended abdomen, generalised abdominal

inflammation that recognises Salmonella typhi among its aetiological agents. In this article we describe a case of acute pancreatitis secondary to typhoid fever, evolving towards complete recovery in a preschool child. Salmonella infection must also be considered in cases of non-alcoholic or non-lithiasis pancreatitis.

tenderness and reduced bowel sounds on auscultation. Sub acute intestinal

obstruction was suspected clinically and was referred for imaging investigations. On USG, bulky pancreas measuring 31, 16 and 14mm at the head, body and tail

Keywords Typhoid, Pancreatitis

respectively was noted (fig 1). There were few hypo echoic areas in the tail region of pancreas (fig2) with peripancreatic

Case Report A 4 yr old boy presented to our hospital with history of abdominal distension and

collection measuring 39X28mm (fig3). There was moderate amount of ascites. Overall features were suggestive of pancreatitis.

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Subsequent serum amylase and lipase were analysed and were found to be significantly increased. (S. amylase - 836, S. lipase -1086 ). The patient was managed conservatively with antibiotics, continuous gastric

Asia and south-east Asia, Africa, Latin America. The disease predominantly affects schoolage children (515 years of age), although it does occur in younger children. 3 Salmonella are gram-negative, bacilli. Infections

aspiration and hydration and electrolytes maintained. Thereafter the clinical recovery was uneventful and he recovered

facultatively-anaerobic

caused by Salmonella may present as gastroenteritis, enteric fever, and

completely.

bacteremia, or as symptomless carriers. Transmission of Salmonella occurs by fecal-

Discussion Enteric fever is a systemic infection caused by the human adapted

oral contamination of water and food. The infections are most commonly associated with the consumption of eggs and poultry but may also be related to the ingestion of meat and dairy products. The bacterium grows intracellularly in the intestinal lymphoid tissue, presenting

pathogens Salmonella

entericaserotype

Typhi (S. Typhi) and S. Paratyphi A, B, and C. These organisms are important causes of febrile illness among crowded and

impoverished populations with inadequate sanitation who are exposed to unsafe water and food, and also pose a risk to travelers visiting endemic countries
1

acutely with gastrointestinal symptoms and fever. The classic presentation is that of a prolonged fever, step-ladder in pattern, accompanied by malaise, abdominal pain and constipation in the first two weeks, followed by diarrhea in the third week.
5

Typhoid fever is a common infection that has continued to be a public health problem in many developing countries.2, 3 The World Health Organization (WHO) conservatively puts the annual global incidence of typhoid fever at 21 million cases, with 14% mortality.3 Very high typhoid fever incidence has been found in India and Pakistan4, south-central

The most common complication mentioned is intestinal perforation and bleeding. Other less common complications include

myocarditis,

endocarditis,

pneumonia,

pancrreatitis, cholecystitis, meningitis and psychiatric symptoms.

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capacity is often unavailable, unaffordable, or inconsistently applied 16. Imaging tools are basically used for evaluation of various complications. In the setting of acute abdomen in typhoid fever erect abdominal radiograph and ultrasound abdomen would be the initial investigation of choice. In case of pancreatitis, ultrasound may show massively enlarged and swollen pancreas. A check on blood amylase and lipase show grossly elevated levels. Serum SGOT/SGPT are also raised.

Typhoid pancreatitis is a rare complication and there are few reported cases. Some reports have suggested Salmonella infection would cause pancreatitis; 6-11 Typhus and non-typhus Salmonellae were both reported. The etiology of Salmonella pancreatitis is not clearly understood, and lymphatic or hematogenous invasion has been proposed.13 The biliary tract has been considered a portal of entry for seeding of Salmonella medium.13 as it thrives in bile-rich

Treatment Diagnosis Efforts to develop serologic methods for the diagnosis of typhoid fever that improve on the poor performance of the Widal test still suffer from substantial limitations of both sensitivity and specificity14 . Ciprofloxacin continues to be widely used, but clinicians need to be aware that patients with Salmonella with DCS may not respond adequately17. In this circumstance, third generation cephalosporins such as ceftriaxone may be used. However, the cost and route of less administration suitable for make patient

Serological approaches to the diagnosis of S. Paratyphi A, B, and C have been developed but have not been evaluated or adapted for field use 15. Consequently blood culture, a less sensitive method than bone marrow culture, is often the practical first choice test for both patient diagnosis and for epidemiologic evaluation of S. Typhi and S. Paratyphi burden. However, most enteric fever occurs in low- and middleincome countries where blood culture

ceftriaxone

management in some low- and middleincome countries and the oral third generation cephalosporin cefixime appears to be inferior to other oral agents both in terms of fever clearance time and treatment failure 18. In these circumstances, recent clinical trials suggest that

azithromycin 500mg once daily for 7 days in adults or azithromycin 20mg/kg/day up to a 119

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maximum of 1,000mg/day for 7 days in children is useful for the management of uncomplicated typhoid fever
19

pathogenesis of non-alcoholic or nonlithiasis pancreatitis 22.

. Due to its

pharmacokinetic profile, gatifloxacin has potential as a new agent for managing patients infected with DCS isolates
20

but

carries risk for dysglycemia which may limit its widespread use. Management of a case of typhoid

pancreatitis means treatment both on general hydration and specific lines. and Patients

monitored

electrolytes

maintained. A constant gastric aspiration must be done. In addition to antibiotic patient to be put on polyvalent proteinase inhibitor (trasylol 750,000 units/day). Typhoid pancreatitis as such is a serious complication and carries poor prognosis until and unless it is diagnosed early 21

Conclusion Acute pancreatitis has been associated with typhoid fever. To the best of our

knowledge, there are very few cases reported in the literature with this

association in this age group. Biological or clinical pancreatitis should be considered as a frequent complication of typhoid fever. S. typhi should therefore be added to the list of pathogens implicated in the

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pancreatitis in

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Salmonella

1. Whitaker JA, Franco-Paredes C, del Rio C, Edupuganti S Review Rethinking typhoid fever vaccines: implications for travelers and people living in highly endemic areas. J Travel Med. 2009 JanFeb; 16(1):46-52. 2. Ochiai RL, Acosta CJ, Danovaro-Holliday MC, et al. A study of typhoid fever in five Asian countries: disease burden and implication for controls. Bull World Hlth Org 2008; 86:260268. 3. World Health Organization. Typhoid vaccines: WHO position paper. Weekly Epidemiol Rec No. 6, 2008; 83:4960. 4. Suman K, Shanta of D, Dipika S. and

enteritis.Lancet 1991;337:1611. 9. Coffernils M, Salame M, Paulet P. Salmonellosisassociated and pancreas divisum pancreatitis J Clin

Gastroenterol 1993; 17:270. 10. Andren-Sandberg A, Hojer H.

Necrotizing acute pancreatitis induced by Salmonella infection. Int J

Pancreatol1994; 15:229-230. 11. Hamaguchi H, Okabayashi Y, Yoneda R, Ueno H, Yoon S, Sakaue M, Kasuga M. A case of acute pancreatitis complicating Salmonella enteritis. Int J

Pancreatology1999; 26:189-192. 12. Kune GA, Coster D. Typhoid pancreatic abscess. Med J Aust 1972; 1:417-418. 13. 14 Olsen SJ, Pruckler J, Bibb W, Nguyen TM, Tran MT, Nguyen TM et al Evaluation of rapid diagnostic tests for typhoid fever. J Clin Microbiol. 2004 May; 42(5):1885-9 14. Chart H, Cheasty T, de Pinna E, Siorvanes L, Wain J et al Serodiagnosis

Epidemiology

typhoid

paratyphoid fever in India. J Infect Developing 460 5. Fauci AS, Braunwald E, Kasper DL, Stephan L Hauser, Longo DL, Jameson JL, et al. Salmonellosis. 17th ed. NY: Mc Graw Hill Companies; 2008. 6. Russell IJ, Forgacs P, Geraci JE. Countries. 2008;2(6):454

of Salmonella enterica serovar Typhi and S. enterica serovars Paratyphi A, B and C human infections. J Med Microbiol. 2007 Sep; 56(Pt 9):1161-6. 15. Archibald LK, Reller in LB. Clinical

Pancreatitis complicating typhoid fever. Report of a case. JAMA1976; 235:753754. 7. Murphy S, Beeching NJ, Rogerson SJ, Harries AD.Pancreatitis associated with Salmonella 338:571. 8. Renner F, Nimeth C, Demmelbauer N. High frequency of concomitant enteritis. Lancet 1991;

microbiology

developing

countries. Emerg Infect Dis.2001;7:302 5 16. Crump JA, Kretsinger K, Gay K, et al. Clinical response and outcome of

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with Salmonella paratyphoid fever

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(enteric

enterica serotype Typhi with decreased susceptibility to fluoroquinolones: a United States FoodNet multicenter retrospective cohort study. Antimicrob Agents Chemother. 2008; 52:127884. 17. Pandit A, Arjyal A, Day JN, et al. An open randomised comparison of

fever) Cochrane Database of Systematic Reviews. 2008; 4 Art. No.: CD006083. 19. Dolecek C, La TTP, Rang NN, et al. A multi-center randomised controlled

trial of gatifloxacin versus azithromycin for the treatment of uncomplicated typhoid fever in children and adults in Vietnam. PLoS ONE. 2008;3:e2188 20. S. N. KhoslaTyphoid Fever Its Cause, Transmission And Prevention:162-3 21. Rev Gastroenterol Mex. 2000 JanMar;65(1):30-3.

gatifloxacin versus cefixime for the treatment of uncomplicated enteric fever. PLoS ONE. 2007; 2:e524. 18. Effa EE, Bukirwa H. Azithromycin for treating uncomplicated typhoid and

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VCFL Sciences Journal Photos

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Figure 1: BULKY PANCREASFOR THE AGE WITH HEAD, BODY ANDTAILMEASURING 32, 17, 16 MMRESPEDCTIVELY

Figure 2: HYPOECHOIC AREAS IN BODY OF PANCREAS

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Figure 3: PERIPANCREATIC COLLECTION MEASURING 39X28MM.

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STUDY OF INTRA-OCULAR PRESSURE CHANGES IN APHAKIA AND PSEUDOPHAKIA CASES AFTER CATARACT SURGERY
Dr. Vidya. M. Nadiger1, Dr. Vijayakumar. B. Jatti 2, Dr. Dileep Kumar. R3, Dr. Shanthala4 Dr. Shobha5 1Professor, Department. Of Physiology; 2Associate Professor, 3Postgraduate. Department of Forensic Medicine and Toxicology; 4Professor. Department of Opthalmology; 5Assistant Professor Department of Anatomy; S.S.I.M.S. & R.C., Davangere, Karnataka, India.
Corresponding Author Dr. Vidya. M. Nadiger. Email: [email protected]

difference was seen. No significant relation Abstract Purpose: To highlight any deviation in ocular tension from normal range following cataract extraction and intraocular lens implantation. Setting: Ophthalmology department, was found between age and intraocular pressure. Intraocular pressure was found to be independent on type of surgery. Conclusions: There is no change in

intraocular pressure following cataract extraction with or without intraocular lens.

K.I.M.S., Hubli, Karnataka State. Methods: 50 cases of aphakia and 50 cases of pseudophakia and 50 as control group cases were included on random selection. Intra ocular pressure was recorded at 7 AM, 1 PM and 7 PM preoperatively using the Schiotz tonometer. Postoperatively only one reading was recorded, 6-9 weeks after the surgery. Results: Majority cases of aphakia and pseudophakia were observed to be in the age group of 50-59 years and 60-69 years which contributed 73% in study group and 76% in control group. No significant sex Introduction Eye plays a vital role in the life of any creature on this earth. It has been rightly said that Eyes are the windows of learning through which most of our knowledge and skills are acquired. Keywords Intraocular pressure; Cataract; Aphakia; Pseudophakia; Tonometer.

Following cataract extraction, earlier vision was corrected by thick aphakic glasses but now a days intraocular lenses are used. 125

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Intraocular pressure [IOP] is the tissue pressure of the ocular contents. IOP exists in order to maintain the eyeball in such a state that it can function as an optical instrument. Normal intraocular pressure is between 10 and 22 mmHg greater than the atmospheric pressure with Schiotz

fall of intraocular pressure following only cataract extraction. Aims and Objectives This study was done to attain the following aims and objectives. 1. To study the relationship between intraocular pressure with age and sex. 2. To study the effect of cataract surgery without intraocular lens on intraocular pressure. 3. To study the effect of cataract extraction and implantation of intraocular lens on intraocular pressure.

tonometer. Mean IOP is about 15mm Hg. There is a variation of 1 to 3 mmHg with each cardiac cycle and slower variations with respiration. Any deviation of the intraocular pressure from normal range has untoward effect on eye and may lead to blindness. Factors like genetics, age, sex, refractive error, race etc., exert long-term influence on IOP and factors like diurnal variation, postural variation, exertional influences, lid and eye movement, intraocular conditions, systemic conditions, environmental

Material and Methods The material for this study was taken from the cases attending ophthalmic department of K.I.M.S., Hubli, during September 1997 to July 1998. Fifty cases of aphakia and 50 cases pseudophakia and 50 as control group cases were included on random selection. In order to eliminate the factor which might bias the results, the subjects were selected on following criteria. 1. All the cases were selected randomly without giving any preference to sex, education and socio-economic status. 2. Patients with other ocular diseases like traumatic cataract, glaucoma, diseases of retina, cornea and patients with congenital cataracts were excluded. Except those cases related to age changes were included. 126

conditions, general anesthesia, foods and drugs exert short term influence on IOP. This study was taken up to highlight any deviation in ocular tension from normal range following cataract extraction and intraocular lens implantation. Because

some are under the opinion that there is no change in intraocular pressure following cataract extraction with or without

intraocular lens, where as some authors opine of raise of intraocular pressure following intraocular lens implantation and

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3. Patients with complaint of hypertension and diabetes were included. Family history suggestive of refractive errors and systemic diseases noted. A clinical examination of both the eyes was done and visual acuity was recorded using Snellens chart for the distance and printers type for near vision. Intra ocular pressure was recorded at 7 AM, 1 PM and 7 PM preoperatively using the Schiotz one

recorded at 1 pm and 7 pm preoperatively and at 1 pm postoperatively. All the 100 cases had undergone extra capsular cataract extraction under local anesthesia i.e. peribulbar injection of 2% lignocaine and 0.5% sensorcaine. Cases without complication after cataract

extraction were included. The same Schiotz tonometer was used for all the cases. All the psuedophakos were posterior chamber intraocular lenses. Results and Discussion This prospective study conducted in

tonometer.

Postoperatively

only

reading was recorded, 6-9 weeks after the surgery. The intraocular pressure was recorded with the patient in supine position. A target was fixed and the subject was asked to look at it. The footplate of the tonometer is first cleaned with ether swab and then dried. The eyelids were separated gently and footplate of the tonometer was placed on anesthetized cornea (by using 4%

Department of Ophthalmology in K.I.M.S. Hubli, includes 50 aphakic, 50 pseudophakic and 50 as control group cases. Age incidence: In the present study, the majority cases of aphakia and pseudophakia were observed to be in the age group of 50-59 years and 60-69 years which contributed 73% in study group and 76% in control group. The explanation for the above finding is, aphakia and pseudophakia were the

xylocaine). The indicator needle on the scale gives the reading which is then converted in mmHg by using Friedenwald et al, 1995 conversion table. The reading was taken with a fixed 5.5 gm weight. Any increase in reading beyond 4, additional weight were added to the plunger, like 7.5 and 10 gm. After recording the IOP, 2 drops of antibiotic was administered to avoid infection. In a similar way IOP were

consequences of cataract extraction and cataract extraction with intraocular lens implantation. In the present study only the age dependent cataract or senile cataract were considered. According to Jaffe, most common type of cataract in the human population is the age dependent or senile cataract. 127

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A report from American academy of Ophthalmology 1994-951 states that the prevalence of cataract is 50% in people between the age of 65 & 74 years and it increases to 70% in those over age of 75 years. Sex distribution among study group and Control population: In the present study no significant sex difference was seen. Out of 100 cases studied 41 were males in study group and 29 cases out of 50 cases in control group. Jaffe in his study has cited no sex difference in prevalence of cataract. Intraocular pressure and age in years: According to Duke Elder (1968)2 there is slight rise in IOP as age advances. This is accounted for the tendency of blood pressure to increase with age. A study by Ritch, Sheilds and Krupin3 showed the relationship of IOP and ocular rigidity. Elevated IOP is associated with decreased ocular rigidity and ocular rigidity is reported to decrease with age. According to Franscis HA (1992)4 there is no significant co-relation between IOP and age. Michael Schulzer and Stephen Drance (1987)5 in their co-relational study on IOP, systemic blood pressure and age, found no direct co-relation between age and IOP.

In the present study also, no significant relation was found between age and intraocular pressure. Intraocular pressure and sex: According to Duke Elder (1968)2 and Bruce Shields (1992)6 the intraocular pressure is higher in females vowing to the changes in hormonal pattern. They demonstrate a greater increase in mean intraocular

pressure with age, beginning with onset of menopause [Ritch, Shields and Krupin] 3. A study conducted by C.J. Bulpitt and his colleagues (1975)7 saw no significant difference in the mean IOP between the sexes in their study on IOP and systemic blood pressure. In the present study no significant change was found between the sexes. Intraocular pressure and type of surgery: In the study conducted, the IOP was found to be independent of the type of surgery. It was found to be within normal range in aphakic and pseudophakic eyes. The

intraocular pressure postoperatively was measured by Schiotz tonometer after six to nine weeks of surgery. Out of 50 aphakic eyes 49 of them showed intraocular pressure within normal range. Only one of them showed high IOP postoperatively. Of the 50 pseudophakic eyes 46 of them had intraocular pressure within normal range

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while 3 of them showed hypotension and one of them had high ocular tension. Tubervilte A et al (1983)8 studied 86 eyes undergoing ocular surgery. They found that 32% of the cases developed initial post operative pressure greater than 23 mmHg following extra capsular cataract extraction. Jeffrey G. Gross et al (1988)9 have found increased intraocular pressure in the

intraocular pressure [>21mm Hg] on more than two occasions at 4 months or t least six months period. They were normotensive prior to surgery and underwent extra capsular cataract extraction (ECCE) and ECCE with anterior chamber intraocular lens (IOL). W.J. Ritch et al (1974)13 have reported a rise in intraocular pressure, which occurred with in a few hours after uncomplicated cataract extraction in case study of 10 patients. The measurements of intraocular pressure were done by Perkin hand held applanation tonometer. James E. Miller et al (1957)14 in their study found a variable degree of damage to aqueous out flow mechanism which is of common occurrence following cataract extraction. It is observed that cataract extraction is followed by a state of hypo secretion of aqueous humor lasting from less than 6 weeks to more than 15 months. A group of 111 patients were subjected to repeated tonography and gonioscopy

immediate postoperative period after extra capsular cataract extraction. There was an initial increase in the IOP following

posterior chamber lenses. The readings were taken within 24 hours of the surgery. Orna Geyer, et al (1983)10 have noticed occurrence of hypotony as a late

complication of extra capsular cataract extraction due to detachment of ciliary body. A.C. Hilding 11 in 1955 studied 134 eyes following cataract surgery. He found

reduced post operative ocular tension in nearly all of the 134 eyes after 12th day, up to 3 weeks. The intraocular pressure was found to rise by 22nd day. He states that as ciliary body recovers from the trauma and begins to function normally, the out flow comes under physiologic control, attaining a normal tension again. Robert David et al (1991)12 based on the study conducted, found that 16 of the 746 operations showed consistently raised

before and after cataract surgery to find out the aqueous outflow in the above study. In the present study all 50 patients who underwent cataract extraction 49 of them showed normal intraocular pressure when measured by Schiotz tonometer six to nine weeks after surgery. Only one of them showed high intraocular pressure. This is in 129

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accordance with the study conducted by Alberto Gormaz (1962)15 and A.C. Hilding (1955)11. Ronald L. Radius et al (1984)16 studied change in intraocular pressure in 209 eyes undergoing extraction implantation. extra with They capsular intraocular found cataract lens cataract

range, 3 of them had lower IOP and one of them had higher IOP. Observations of the present study are in accordance with the study conducted by Ronald Radius et al 16 and Kecik T et al 17. Conclusion This study was taken up to highlight the effect of cataract extraction on IOP and also the effect of cataract extraction and intraocular lens implantation on IOP. The materials patients represent who merely those of

extraction and intraocular lens implantation do not cause a statistically significant increase in intraocular pressure and say that there may even be a slight decrease in mean postoperative pressures in eyes undergoing extraction extra with capsular posterior cataract chamber

visited

ophthalmology

department K.I.M.S., Hubli, for relief from cataract. Therefore it does not represent a cross section of the whole population. The majority of cases were observed in the age group of 50-59 and 60-69 years (73%) in study group. No significant sex difference was seen among study group and control group. No significant relation was found between age in years and IOP. No significant change in IOP was found between the sexes. Intraocular pressure was found to be independent on type of surgery.

intraocular lens implantation. Kecik T et al (1991)17 found that there was no essential difference in the behavior of IOP in persons with anterior or posterior chamber lens. John C.E. et al (1997)18 measured IOP by Goldmann applanation tonometer in both eyes of 100 patients who were either bilaterally phakic, unilaterally pseudophakic or bilaterally pseudophakic. They concluded that there is lowering of IOP induced by extra capsular cataract extraction with posterior chamber lens and is stable and it lowers the risk of developing glaucomatous optic nerve damage. In the present study of the 50 pseudophakic eyes, 46 of them showed IOP within normal

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10. Orna G, Victor G, Moshe L. Hypotony as a late complication of ECCE. Am J Ophthalmol 1983; 96(1):112-3. 11. Hilding AC. Reduced ocular tension after cataract surgery. A.M.A. Arch Ophthal 1955; 53:686. 12. Robert D, Linda Z, Daniel BR et al. Diurnal IOP variation an analysis of 690 diurnal curves. Br J Ophthalmol 1991; 76:280. 13. Ritch WJ, Radtke ND, Cohen BE. Early ocular hypertension after cataract

1. American Academy of Ophthalmology. Basic and Clinical Science Course. Lens and Cataract, Section 11, 1994-95. 2. Duke ES. The Physiology of Eye and of Vision. System of Ophthalmology, Vol IV. St. Louis, C.V. Mosby Company, 1968. 3. Ritch, Shields, Krupin. The Glaucomas, basic sciences, 2nd ed. Mosby, 1966;435. 4. Francis HA. Physiology of the Eye. Edited by William M Hart. St. Louis, C.V. Mosby Company, 1992; 264, 266. 5. Schulzer M, Stephen MD. Intraocular pressure, systemic blood pressure and age a co-relative study. Br J Ophthalmol 1987; 71:245-9. 6. Bruce S. Textbook of Glaucoma, 3rd edition. William & Wilkins, 1992; 14, 15,23,56,57, 61. 7. Bulpitt CJ, Charles H, Everitt MG. Intraocular pressure and systemic blood pressure in the elderly. Br J. Ophthalmol 1975; 59:717-20. 8. Tuberville A, Nisserkom L, Tamoda Wood. Post surgical intraocular pressure elevation. J Am Intraocul Implant Soc 1983; 9(3):30912. 9. Jeffery GG, Dale RM, Alan LR, Alfred AF, James SK. Increased intraocular pressure in the immediate postoperative period after extra capsular cataract extraction. Am J Ophthalmol 1988; 105:466-9?

extraction. Br J Ophthalmol 1974; 58:725. 14. James EM, Richard K, Bernard B. Cataract extraction and aqueous outflow. A.M.A. Arch Ophthal 1957; 58:401-6. 15. Alberto Gormaz. Ocular tension after cataract surgery. Am J Ophthalmol 1962; 53:832? 16. Ronald R, Karen S, Kathleen BS et al. Pseudophakia and intraocular pressure. Am J Ophthalmol 1984; 97:738-42.

17. Kecik T, Cixzewska J. Intraocular Pressure in Pseudophakic Eyes. Klin Oezna 1991; 93(9):252-4. 18. John CE. Reduced intraocular pressure after phacoemulsification and posterior chamber intraocular lens implantation. J. Cataract Refract Surg 1997; 23(8):1260-4.

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Table No. 1: Distribution of age groups in the study and control population

Age Groups [in years] 40-49 50-59 60-69 70-74 74+ Total

Study group No. of cases 5 30 43 14 8 100 5% 30% 43% 14% 8% 100% Percentage

Control group No. of cases 2 15 23 5 5 50 4% 30% 46% 10% 10% 100% Percentage

Table No.2: Relation between intraocular pressure variation and age in years
Age in 7 AM years 40-49 50-59 60-69 70-79 79+ Low Normal 5 30 42 18 4 High 2 1 PM Low 1 2 Normal 5 30 41 16 4 High 1 7 PM Low 1 4 1 Normal 5 29 39 17 4 High -

Table No. 3: Relation between intraocular pressure and sex

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Table No 4: Relation between intraocular pressure and type of surgery

Figure: Measuring intraocular pressure using Schiotz tonometer

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Clinical Profile of HIV Patients with Central Nervous System Manifestations

Associate professor, Department of Neurology, S.S.I.M.S & R.C., Davangere, Karnataka, India; 2consultant cardiologist, Nanjappa Hospital, Shimoga, Karnataka, India; 3Professor, Department of Medicine, J.J.M.M.C., Davangere, Karnataka, India; 4Senior resident, Department of Radiology, S.S.I.M.S & R.C., Davangere, Karnataka, India Corresponding Author Dr.Prashanth.S Email: [email protected] Abstract Various central nervous system (CNS) diseases develop among patients with human immunodefeciency virus (HIV) Introduction Neurological diseases are common among patients with HIV infection. More than 50% of HIV infected persons develop

infection. 100 consecutive HIV seropositive patients aged above 18 years, who got admitted with symptoms of central nervous system involvement were included in the study. Clinical profile of these patients were studied. Various CNS diseases in our study were tubercular meningitis (14%), (59%), aseptic

symptomatic neurologic diseases1. The neurological problems that occur in HIV infected individual may be primary to the pathologic process of HIV infection or secondary to opportunistic infections,

neoplasms or side effects of antiretroviral drugs. Besides brain and spinal cord, the peripheral nerves and muscles may be affected. Opportunistic infection become more prevelant with advanced disease and profound immunosuppression. Since many of the conditions are amenable to

cryptococcal

meningitis

meningitis (10%), cerebral abscess (6%), cerebral toxoplasmosis (3%) and

tuberculoma (8%).

Key Words central nervous system manifestations, HIV infection.

treatment, a proper diagnosis and therapy may decrease morbidity and mortality in the already curtailed life span of HIV

patient. The duration of survival and quality of life of these patients can be improved by 134

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early diagnosis and effective treatment including long term suppressive therapy of opportunistic infections. Hence this study is undertaken to study the clinical profile of HIV patients with central nervous system (CNS) manifestations.

Chest x-ray were performed in all cases Computed tomography (CT) scan were done in patients with focal neurological defecits, depressed level of sensorium, features of raised intracranial tension.

Results Materials and Methods 100 consecutive HIV seropositive patients aged above 18 years, who got admitted with symptoms of central nervous system involvement to hospitals attached to J.J.M.Medical college, Davangere. We 100 HIV seropositive patients with central nervous system manifestations were

included in this study. Among these 74 patients were males and 26 females. Age of patients ranged from 21 to 87 years. Maximum number of patients (55%) were between 31 to 40 yrs of age. Majority of the patients belonged to lower(64%) and middle socioeconomic class (28%) and only 8% were from upper socioeconomic class. Various presenting symptoms in our study were fever (69%), headache (91%), vomiting (58%), seizures (18%), altered

studied the clinical profile of these patients. Routine investigations like complete

hemogram, renal function tests, blood sugar, serum electrolytes were performed. When meningoencephalitis were

suspected, lumbar puncture was done and cerebrospinal fluid (CSF) was analysed for: Macroscopy Cell count and cell type using neubars counting chamber. Protein estimation by turbidity method Sugar estimation by Following method.
India ink preparation VDRL Anti toxoplasma antibody Gram staining and Zeihl-Neelson staining CSF culture.

consciousness (59%) and focal neurological defecits (11%). In our study, 73% of patients presented between 3 to 4 weeks of illness prior to admission, 20% presented with illness of more than 4 weeks and 7% presented within 2 weeks of illness. Various CNS diseases in our study were tubercular meningitis (59%), cryptococcal meningitis (14%), aseptic meningitis (10%), cerebral abscess (6%), cerebral 135

Radiological investigations:

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toxoplasmosis (3%) and tuberculoma (8%). Other opportunistic infections were seen in 61% of our patients. These were pulmonary tuberculosis herpes (36%), candidiasis (13%) (44%), and

patients with tubercular meningitis in our study. This is consistent with the study conducted by Shembalkar et al6, and Wadia et al5. however in study conducted by Bishburg et al7, seizures was the common presenting symptom. In our study chest x-ray revealed evidence of pulmonary tuberculosis in 19% of cases. Bishburg et al7 study revealed maximum number of association of pulmonary

zoster

infection

pneumocystis carinii pneumonia (7%). Mortality rate in our study was 18%.

Discussion Neurological diseases are common among patients with HIV infection. More than half of HIV infected persons develop

tuberculosis(80%). In the study by Wadia et al5, there was no chest abnormalities encountered. In our study 14% of patients had

symptomatic neurologic diseases 1. The neurological problems that occur in HIV infected individual may be primary to the pathologic process of HIV infection or secondary to opportunistic infections,

cryptococcal

meningitis.

Cryptococcal

meningitis comprised 12.5% of cases in study conducted by Aquinas et al8. In our study 3% al6 of patients had

neoplasms or side effects of antiretroviral drugs. Among opportunistic infections that involve CNS are progressive etc2. tuberculosis, multifocal some

toxoplasmosis. In study conducted by Shembalkar et 21% had CNS

cryptococcosis,

toxoplasmosis. Dementia is the most important primary neurologic complication of HIV infection. Focal lesions of the central nervous system include cerebral toxoplasmosis, lymphoma, and progressive multifocal Various peripheral

leucoencephalopathy

opportunistic infections are a result of latent or persistent infection requiring life long secondary prophylaxis eg: toxoplasma encephalitis and cryptococcal meningitis3 . In our study 59% patients had tubercular meningitis. Berenguer et al4 reported 59% tubercular meningitis and wadia et al5 reported 91.2% of tubercular meningitis in their series. Headache and fever were the predominant presenting symptoms among

leukoencephalopathy.

neuropathies and myopathies may occur in association with HIV infection or as toxic effects of antiretroviral agents9.

Conclusion 136

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In view of the fact that chronic meningitis was the commonest mode of presentation in our study, we feel that, as a corollary, all patients who present with chronic

The prevalence of neurologic complications associated with HIV disease will increase as more effective therapies allow persons with AIDS to live longer. Early recognition and treatment of these disorders substantially affect patients' quality of life and survival

meningitis should be screened for HIV infection.

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5.Wadia RS, Sawant VS, Pujari S, Pandith M, Kinikar ST, Neurological manifestations of HIV disease in outpatient clinics and in Hospital. 4th Annual conference of Indian Academy of Neurology:1996;130-34. 6.Shembalkar PK, Jadhav MA, Ramleka, IG, Katrak SM. Neurological complication of HIV infection. 4 th Annual conference of Indian Academy of Neurology ACIAN-96:1996;10628. 7.Bishburg E, Sunder AMG, Reichman LB et al. CNS tuberculosis in AIDS and its related complex. Annals of internal medicine, 1986;105:210-213. 8.Aquinas SR, Tarray SD, Ravindran GO, Nagamani D. Cryptococcal meningitis in AIDS - need for early diagnosis. JAPI 1996;44:3. 9.David M. Simpson & Michele Tagliati. Neurologic Manifestations of HIV Infection. Ann Intern Med. 1994;121(10):769-785.

1. Levy RM, Rosenbloom S , Perret LV. Neuroradiologic findings in AIDS a review of 200 cases. American Journal of Radiology. 1986; 147: 977-983. 2. Anthony S, Fauci H, Chifford Lane Human Immunodeficiency Virus disease : AIDS and related disorders: Dennis L. Kasper,Anthony S. Fauci, Dan L. Longo, Eugee Braunwald, Stephen L. Hauser, J. Larry jameson; Harrison principles of internal medicine, Vol.1, 16th Edn. New York: McGraw Hill Companies Inc., 2005; 1076-1139. 3.Das CP, IMS Sawhney: Neurological complications of HIV infection. Neurology India, 1998;46: 82-93. 4.Berenguer T, Moreno S, Laguna F, Viceute T , Adrados M. et al. Tubercular meningitis in patients infected with human immunodeficiency virus. N Engl J Med 1992;326-(10):658-72

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Pattern of Usage Of Gastroprotective Agents In Patients Receiving Nonsteroidal Anti-Inflammatory Drugs

Medical Advisor, Zydus Cadila, Ahemadabad, India; 2Prof & Head, Dept of Pharmacology, A

J Institute of Medical Sciences, Mangalore India; 3Prof & Head, Dept of Pharmacology, Dhanalakshmi Srinivasan Medical College, Perambalur, India; 4 Assistant professor, Dept of pharmacology, Azeezia institute of medical sciences, Meeyannoor, India; professor Dept of Pharmacology, Kasturba Medical College, Mangalore, India.
5

Assistant

Corresponding Author Dr. Ashwini Mandanna M Email: [email protected]

Abstract Background: Non-steroidal anti-inflammatory drugs

Aim: To assess the pattern agents of usage of in patients

gastroprotective

(NSAIDs) are one of the most routinely used drugs. Gastroprotective agents are

receiving NSAIDs in a tertiary care teaching hospital. Methods: Retrospective observational study of

frequently prescribed with NSAIDs due to the increased risk of gastrointestinal gastropathy.

complications-

NSAID

prescriptions from case records from the medical records department of patients admitted with musculoskeletal (MS) pain under orthopedic department of a tertiary care teaching hospital during the period of January 2010 to December 2012. Data was documented proforma methods. & in a specially by designed descriptive

Prostaglandin analogue, misoprostol has been approved for the prevention and treatment of NSAID gastropathy. Due to side effects of misoprostol it is not commonly prescribed. This study tries to assess the pattern of gastroprotective agents used to reduce NSAIDs induced gastrointestinal complications.

analyzed

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anticholinergic agents are not commonly prescribed. Key words: Gastroprotective agents;

Demographic analysis revealed that out of 306 patients most were females (60.5%) and maximum patients were in the age group of 31-60 (73%). Low back ache (29%) was the most common cause of MS pain seeking admission. Analgesics- NSAIDs were prescribed in 300 (98%) patients. The most commonly prescribed agents were

NSAIDs; prescription pattern

Introduction Non-steroidal anti-inflammatory drugs

(NSAIDs) are used in the treatment of arthritis and other musculoskeletal (MS) disorders, and as analgesics in a wide variety of clinical scenarios. (1) They have emerged as the most important cause of peptic ulcer bleeding worldwide. Around 25% of chronic NSAID users will develop ulcer disease and 24% will bleed or perforate. The risk of ulcer formation and bleed depend on various factors including old age, a history of ulcer or ulcer bleeding, severe co morbid illnesses,

diclofenac (70.7%) followed by paracetamol (23.8%). Gastroprotective agents

administration was seen in 287 (94%) of the 306 patients or 97% of the NSAIDs received patients (300). Gastroprotective agents not administered in patient receiving NSAIDs were 3%. Almost all the gastroprotective agents were mostly prescribed with their brand names 285 (>99%). H2 receptor blocker ranitidine was the most commonly used agent, 267 (93%) followed by proton pump inhibitors- pantoprazole 11 (4%), rabeprazole 6 (2%) & omeprazole 3 (1%). All the gastroprotective agents were given per oral. Interpretation & Conclusion: Results of this study agents indicate are that

concomitant use of anticoagulants or corticosteroids, and use of high-dose or multiple NSAIDs. (1-3) NSAIDs inhibit cyclo-oxygenases (COX) and block the formation but not only also of of

proinflammatory

gastroprotective COX-1 isoform. This is a key element in NSAID gastropathy as prostaglandins maintain gastric mucosal blood flow and increase protective mucus as well as bicarbonate production. The discovery of two different cyclo-oxygenases led to the development of drugs 140

gastroprotective

routinely

prescribed with NSAIDs and ranitidine is the most frequently used agent in this tertiary care teaching hospital. The newer proton pump inhibitors or other classes of

gastroprotective agents like antacids and

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preferentially inhibiting the COX-2 isoform, on the proposition that prostaglandins produced by the constitutively expressed COX-1 protect gastric mucosa, whereas the inducible isoform COX-2 is responsible for inflammation and pain. Also enhanced synthesis of leukotrienes may occur by shunting the arachidonic acid metabolism towards the 5-lipoxygenase where in the leukotrienes are supposed to contribute to gastric mucosal injury. (3) There is good evidence that co-prescribing NSAIDs with gastroprotective agents (GPAs) can effectively reduce the risk of ulcer bleeding in high-risk patients. To date, a number of practice guidelines are available to guide clinicians on prescribing GPAs in NSAID users with high ulcer risk.
(1, 4-5)

TYPE

OF

STUDY:

Retrospective

Descriptive hospital based study [Single site]. METHOD OF COLLECTION OF DATA: The source data from medical records department was collected from the period January 2010 to December 2012 (2 years). Both males and females above the age of 18 years and below the age of 65 years who were admitted with complaints of MS pain and treated were included in the study. Ethical committee clearance was obtained for the conduct of the study. Data privacy and confidentiality were maintained at all times. No patient could be traced, and it was also not possible to determine which medical practitioners were involved in the prescribing of the drugs.

This retrospective study was done to analyze and interpret the pattern of co prescription of gastroprotective agents in patients receiving NSAIDs in patients

admitted in an Orthopedic Unit of a tertiary care teaching hospital. Results The orthopedic in-patients diagnosed with Material and methods: Observational study of case records of patients under orthopedic department of a tertiary care hospital during the period of January 2010 to December 2012. SOURCE OF DATA: Medical Records Department. MS pain constituted of 306 patients between the period of January 2010 to December 2012. The analysis of

demographic data showed 185 patients (60.5 %) were female and 121 patients (39.5 %) were male. Most patients were in the age group 31-60 yrs (223, 73%). Out of the 141

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306 patients, 296 (96%) were prescribed NSAIDs. Overall 7 different NSAIDs were prescribed to the patients. Diclofenac was the most commonly prescribed agent (70.7%) followed by paracetamol in (23.8%). Gastroprotective agents administration was seen in 287 (93%) of the 306 patients or 97% of the patients receiving NSAIDs were prescribed with GPAs. The most commonly prescribed GPA was H2 receptor blocker, ranitidine in 267 (93%) of the 287 patients receiving GPAs. All the ranitidine prescribed were in brand name. Other GPAs used were proton pump inhibitors- pantoprazole 11 (4%), rabeprazole 6 (2%) & omeprazole 3 (1%). Almost all the gastroprotective

observed that 97% of the patients receiving NSAIDs were co prescribed with GPA which is much higher than a similar study conducted in orthopedic outpatient

department of an urban, tertiary care, teaching hospital in India & in a study conducted to study GPA co prescription with low dose aspirin in general and specialist outpatient clinics in China (6- 7). The most commonly used GPA in this study was ranitidine where as it was observed in the other studies that proton pump inhibitors (81.19%) were the most common & H2 receptor blockers were a distant second (17.81%) whereas similar to this study the review in China revealed that most of the patients received H2-receptor antagonist. The number of NSAID

agents were mostly prescribed with their brand names 285 (>99%). All the

gastroprotective agents were given per oral. Gastroprotective agent not

prescription without GPA co prescription was low, 3% in this study and in other studies it was observed to be 67% and 51.5%. (6-7).

administered in patient receiving NSAIDs was 3%.

Discussion NSAIDs are the most commonly used analgesics. Prescription understand the audit of help to

Conclusion Several guidelines indicate use of GPAs with NSAIDs to prevent the risk of NSAID gastropathy. In this study the co

attitudes

doctors

towards the disease and its management. The main objective of the study was to assess the co-prescribing pattern of GPAs with NSAIDs in patients diagnosed with MS pain in a tertiary care hospital. It has been

prescription is in accordance with the guidelines. H2 blockers are still the main class of GPAs used. Degree of prescribing drugs in their generic names is very much

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desired. The most preferred route of administration was oral.

Acknowledgements I would like to acknowledge the medical records department for cooperating with us to make this study possible. Conflict of interest None.

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from: FK, Quigley

Vol. 3 Issue.3
URL:

http://cks.nice.org.uk/nsaidsprescribingissues#!scenariorecommendation:3 5. UW medicine. Guidelines for use of NSAIDs and COX-2 selective agents. [Online]. [cited 2012 Aug 31]; Available from:

EM; Practice parameters committee of the American college of of

gastroenterology.

Prevention

NSAID-related ulcer complications. Am J Gastroenterol 2009

Mar;104(2):72838. 2. Ho CW, Tse YK, Wu B, Mulder

URL:http://www.ashp.org/s_ashp/docs /files/GuidelinesNSAID_COX_2Agents. pdf 6. Raghavendra B, Sanji N, Ullal S D, Kamath R, Pai Mrsm, Kamath S, Savur A. Trends in prescribing

CJ, Chan FK. The use of prophylactic gastroprotective therapy in patients with nonsteroidal anti-inflammatory drug- and aspirin-associated ulcer bleeding: a cross-sectional study. Aliment Pharmacol Ther. 2013

gastroprotective agents with non steroidal anti-inflammatory drugs in an orthopaedic outpatient unit of a tertiary care hospital. J Clin Diagn Res. 2009 Jun;3(3):1553-6. 7. Luk H. Use of gastroprotective drugs in patients receiving low-dose

Apr;37(8):819-24. 3. Becker JC, Domschke W, and Pohle T. Current approaches to prevent

NSAID-induced gastropathy COX selectivity and beyond. Br J Clin

Pharmacol. 2004 Dec;58(6):587600. 4. NSAIDs - prescribing issues. [Online]. 2013 [cited 2013 Jun 24] Available

aspirin. J Chin Med Assoc. 2009 Jul;72(7:356-61.)

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PATTERN OF GASTROPROTECTIVE AGENTS USED Gastroprotective agents used Ranitidine Pantoprazole Rabeprazole Omeprazole 287 267 11 6 3 93% 4% 2% 1%

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STUDY OF CONDUCTION BLOCKS IN ACUTE MYOCARDIAL INFARCTION

professor, Department of Neurology, 2Senior resident, Department of Radiology,

S.S.I.M.S & R.C., Davangere, Karnataka, India,; 3Professor, Department of Medicine, J.J.M.M.C., Davangere, Karnataka, India; 4consultant cardiologist, Nanjappa Hospital, Shimoga, Karnataka, India

Corresponding Author Dr.Prashanth.S Email: [email protected]

Abstract Various types of conduction blocks develop following acute myocardial

heart

block(3%),left

anterior

hemiblock[LAHB](4%), right bundle branch block[RBBB]( (3%), left bundle branch block[LBBB](3%), RBBB+LAHB(1%).

infarction (AMI) worsening the outcome of AMI. Hence knowledge about various types of conduction blocks occurring in AMI helps in early recognition of conduction blocks at an early stage, so that pacing appropriate can be

Key Words Conduction infarction, blocks, acute myocardial

treatment

including

instituted at an early stage. 100 consecutive patients with AMI who matched the inclusion criteria were included in the study. Various types of conduction blocks which developed following AMI were analyzed. 25% of patients with AMI developed

Introduction AMI is one of the major problems in todays developing and developed countries. In AMI we come across various complications like ventricular dysfunction, conduction blocks, cardiogenic
1.

shock,

mechanical

conduction blocks. Incidence of various types of conduction blocks were firstdegree atrioventricular (AV) block(7%), second-degree AV block(4%), complete

complications, ventricular arrhythmias, etc prognosis following AMI is worsened in

the presence of these complications.

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Various types of conduction blocks develop following AMI, which worsen the outcome of AMI. Knowledge about various types of conduction blocks occurring in AMI helps in early recognition of conduction blocks at an early stage, so that appropriate treatment including pacing can be instituted at an early stage. This study was undertaken to study the various patterns of conduction blocks occurring in acute myocardial

3. Patients with congenital or rheumatic heart disease 4. Patients blocks 5. Patients with history of intake of drugs causing conduction blocks like clonidine, methyldopa, verapamil, digoxin etc. with previous conduction

Diagnosis of various conduction blocks were made based on the following ECG features: First degree AV block: PR interval of more than 0.20 sec3

infarction.

Materials and Methods 100 consecutive patients of AMI admitted to hospitals attached to JJMMC, Davangere, who matched the inclusion criteria were selected for the study. Various types of conduction blocks which developed

second degree AV block: intermittent failure of AV conduction Mobitz type I: cycle, characterized beginning by with

wenckebach

normal or prolonged PR interval and, with each successive beat, the PR interval lengthens until block of the supraventricular impulse occurs and a beat is dropped. The pause is shorter than PR interval of any two

following AMI were analyzed. Inclusion criteria: patients having acute myocardial infarction as per W.H.O.criteria 2 that is atleast two of the following three elements be present. 1. History of ischaemic type of chest discomfort 2. Evolutionary changes on serially

consecutively conducted beats. The shortest PR interval follows and the longest PR interval precedes the ventricular pause. 3,4 Mobitz type II : here also there is intermittent failure of AV conduction but the PR intervals of all the conducted supraventricular impulses are constant.3

obtained electrocardiograph tracings. 3. A rise and fall in serum cardiac markers.

Exclusion criteria: 1. Patients with old bundle branch block 2. Patients with cardiomyopathy

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3

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Third-degree or complete AV block is characterized by, AV dissociation Slow ventricular rate

it

Broad, notched R waves in lateral precordial leads (V5 and V6) and usually in leads I and aVL.

Absent septal q waves in left sided leads.

Left anterior hemiblock (LAHB) 5,6,7

Small or absent initial r waves in right precordial leads (V1 and V2) followed by

Frontal plane mean QRS axis of -45 to 90 degrees. QRS duration less than 120 msec. qR pattern in leads I and aVL. Late intrinsicoid deflection in aVL (>0.045s) rS pattern in leads II, III, and aVF.

deep S waves. Prolonged intrinsicoid deflection (>60 msec) in V5 and V6. Right bundle branch block (RBBB) 5 QRS duration 120 msec. Broad, notched R waves (rsr, rsR or rSR pattern) in right precordial leads (V1 and V2)

Left Posterior hemiblock (LPHB) 5,6,7

Frontal plane mean QRS axis of +120degress. QRS duration less than 120 msec.

Wide and deep S waves in left precordial leads (V5 and V6). Incomplete RBBB: rsr pattern in lead V1 with a QRS duration between 100 and 120 msec.

Small initial r wave and prominent S wave in leads I and aVL. qR pattern in leads II< III and aVF. Late intrinsicoid defection in aVF

RBBB plus LAHB 5:

(>0.045 s) Exclusion of other causes of right axis deviation.

RBBB plus left axis deviation beyond -45 degrees.

Left bundle branch block(LBBB) 5

RBBB plus LPHB 5: RBBB plus a mean QRS axis deviation to the right of +120 degrees.

QRS duration 120 msec.

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significantly higher among patients who developed complete AV block, RBBB and RBBB+LAHB, which was found to be statistically significant (p = 0.05)

Among the 100 patients, 72% were males and 28% were females. The age of patients ranged from 40 to 79 yrs with a mean age of 57.9yrs (SD10.6). Incidence of various types of conduction blocks in our study were first-degree AV block(7%), second-degree AV block(4%), complete heart block(3%),LAHB(4%), RBBB (3%), LBBB (3%), RBBB+LAHB(1%).

Discussion Conduction blocks are frequent

complications of AMI. The abnormalities in conduction following AMI may be

attributable to one of the following: Ischemia, which results in transient or permanent structural changes of the tissues surrounding the SA and AV junctions. An increase in parasympathetic tone commonly associated with an inferior wall myocardial infarction. An increase in extracellular potassium, which can cause slowing of impulse

Incidence of conduction blocks among various sites of AMI in our study were anteroseptal myocardial infarction(MI) extensive

[17.4%], anterior MI (20%),

anterior wall MI (50%), inferior wall MI (32.3%), anterior+inferior wall MI (25%), inferolateral MI (33.3%).

In our study total mortality rate was 17%. Among patients with conduction blocks mortality rate was 28% and that among patients without conduction blocks was 13.3%. Eventhough mortality rate was

conduction Local release and build up of adenosine, a metabolite of adenosine triphosphate breakdown, which slows the velocity of impulse conduction through the AV node 8.

higher among patients who developed conduction blocks, the difference was not statistically significant (p = 0.08). Mortality rate among patients with various types of conduction blocks were first-degree AV block (14.2%), complete AV block(66.6%), RBBB(66.6%), RBBB+LAHB(100%). LBBB(33.3%), Mortality was

First-degree AV block occur in 4 to 14% of patients with AMI and more often the block is within the AV node 8. In our study, 7% of patients developed first-degree AV block which is comparable with 8.5% reported in

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with a mortality of 66.6% which is comparable with 77% reported by Cohen et al12 . Complete AV block in the setting of inferior infarction usually results from an intranodal or supranodal lesion
1

Among 7 patients one

patient expired with a mortality of 14.2%, in all others it was transient and they had uneventful recovery.

. When it

occurs in anterior infarctions, it results from Mobitz type I second-degree AV block is observed in upto 10% of patients with AMI. Usually it is transient, the block is located within the AV node and is most often caused by an increased vagal tone or less commonly ischemia of the AV junction. It is more commonly seen with inferior wall MI than with anterior involvement
8

extensive septum13 .

necrosis

of

the

ventricular

Incidence of RBBB was 3% and that of LBBB was also 3% in our study, which is same as that reported by Stephen Scheidt & Thomas Kilip14 and it is comparable with the results of Col & Weinberg15 and Rizzon, Biase & Baissus16 . Some studies have noted a
17,18,19

. In our

study 4% of patients developed mobitz type I second-degree AV block, which is

higher incidence of RBBB than LBBB

comparable with 3.5% reported by Meltzer & Kitchell9 and 3.3% by Imperial, carballo & Zimmerman
11

Mortality among patients with RBBB was 66.6% which is comparable with 61% reported by Norris & Croxson 17 and 57% by Hunt & Sloman 18. Mortality among patients with LBBB was 33.3% which is comparable with 33% reported by Rizzon, Biase & Baissus16 , 30% by Stephen Scheidt & Thomas Kilip14 and 29% by Raftery et al 20.

. All the 4 patients had

inferior wall MI in our study and all were transient. None of the patients in our study developed Mobitz type II second-degree AV block. It occurs in less than 1% of patients with AMI, usually indicates damage to the AV junction or bundle of his and is more common in anterior infarctions8 . In our study 3% of patients developed thirddegree AV block which is comparable with 3.3% reported by Imperial, carballo & Zimmerman
11

4% of patients in this study developed LAHB which is comparable with 4.7% reported by James atkins et al21. None of the patients in our study developed LPHB which is usually rare. An incidence of 0.3% was reported by Rizzon, Biase & Baissus16 . Occurrence of LAHB is more common than LPHB because 150

and 4.2%

by Meltzer &

Kitchell9 . Among 3 patients two expired

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left anterior fascicle is highly vulnerable to ischemic or necrotic process because of the unique blood supply from septal branches of the anterior descending coronary artery and its delicate structure15. The incidence of LPHB is rare because the posterior division of the left bundle branch seems relatively invulnerable to coronary artery disease because it has the shortest pathway to the angle of the interventricular septum and the posterior wall and has the largest diameter of the two fascicles. In addition it has a dual blood supply from the anterior and posterior descending coronary arteries15. Since it is larger than the anterior fascicle, in general a larger infarct is required to block it and hence the mortality is markedly increased1. In our study there were no deaths among the patients who developed LAHB. Mortality is increased in these patients, although not as much as in patients with other conduction forms of blocks1.

mortality of 70% and 55.5% by Col & Weinberg15 . None of the patients in our study developed RBBB+LPHB. The

occurrence of RBBB+LAHB is more common than RBBB+LPHB because the anterior

fascicle of left bundle branch and the right bundle branch, apart from its very initial part derive their blood supply exclusively from the penetrating branches of the anterior descending coronary artery16.

Mortality among patients who develop bifascicular blocks is high because of severe pump failure secondary to extensive

myocardial necrosis required to produce such an extensive intraventricular block1.

Conclusion Various patterns of conduction blocks develop following AMI and they have a varied impact on the outcome following AMI. All patients with AMI should be watched carefully for early recognition of conduction blocks and appropriate

intraventricular

Complete AV block is not a frequent complication of either forms of isolated divisional blocks 1.

treatment should be started early thereby reducing mortality.

Acknowledgements: Nil. 1% of patients in the present study developed RBBB+LAHB. But Col & Weinberg15 has reported an incidence of 4.2%. Mortality rate was 100% in our study. Roos and Dunning have reported a 151

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electrocardiography, 10th edn. Philadelphia: Lippincott Williams & Wilkins, 2001.p. 102111.

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Table 1: Incidence of Various Types of Conduction Blocks in the Present Study (N = 100) TYPE OF CONDUCTION BLOCK First-degree AV block Second-degree AV block(type I) Third-degree AV block Left anterior hemiblock(LAHB) Right bundle branch block(RBBB) Left bundle branch block(LBBB) RBBB + LAHB Total NO. OF CASES 7 4 3 4 3 3 1 25 PERCENTAGE 7 4 3 4 3 3 1 25

Table 2: Mortality
GROUP First-degree AV block Second-degree AV block (typeI) Third degree AV block LAHB RBBB LBBB RBBB + LAHB No blocks Total TOTAL No. OF CASES 7 4 3 4 3 3 1 75 100 No. OF DEATHS 1 2 2 1 1 10 17 PERCENTAGE 14.2 66.6 66.6 33.3 100 13.3 17

Table 3: Distribution of Conduction Blocks Among Various Sites Of AMI

First-degree AV block

total No. cases

Complete AV block

Site of AMI

anterior anteroseptal anterolateral Extensive anterior Inferior Inferolateral Inferior+right ventricular extension Anterior+inferior total

25 23 5 6 32 3 2

5 4 3 10 1 1

1 4 1 1

4 -

1 2 -

3 1 -

1 1 -

2 1 -

1 -

4 100

1 25

1 3

RBBB+LAHB

RBBB

LAHB

LBBB

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