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    • Proceedings of the Ispat General Hospital YEAR 2011 Ispat General Hospital, Rourkela Steel Plant, Rourkela
    • Proceedings of the Ispat General HospitalEditorDr R N MohapatraReviewers PublicityDr A M Acharya Mr J C MohapatraDr C M Rao Mr R KumarDr K C Mohanta Ms A SatpathyDr N K BeheraDr P MishraDr (Mrs) Prativa BeheraDr R B PattnaikDr S MohantyDr S K MishraDr S K R PrustyDr S N Mohapatra
    • MessageI am extremely happy to learn that Proceedings of Ispat General Hospital isbeing revived after a gap of nearly two decades.The current edition that heralds a new beginning will surely lay thefoundations for making this journal more meaningful for practicing Doctors.In fact, with the fast changing scenario in the medical sphere, suchpublications have immense value for meeting the education and trainingneeds of upcoming medical professionals besides providing the basis forfresh research.In recent times Ispat General Hospital, administered by Rourkela Steel Plant,has not only grown in stature as a treatment centre for complicated alimentsbut has also established itself as a centre for medical education with theintroduction of post graduate courses (DNB). I am sure this publication willbe of enormous help to the DNB students both as a source of learning andalso a platform to publish their achievements.I extend my hearty congratulations to the dedicated team of Doctors of IspatGeneral Hospital for taking up this endeavour and wish this publication agrand success in the current edition as well as in future. S. N. Singh (CEO, RSP & I/c RMD)
    • Acknowledgement We would like to place on record our deep sense of gratitude to ourManaging Director, Shri S N Singh who has constantly encouraged us todevelop as professionals and bring about improvements in every activityconnected to health care. We are particularly grateful to him for hisunstinted support, guidance and encouragement that made this issue ofThe Proceedings of IGH see the light of the day. This publication is an endeavour to once again present the efforts andachievements of the dedicated medical professionals at Ispat GeneralHospital before the medical fraternity. The erudite authors of the articleshave contributed significantly in making the proceedings a valuablecompendium truly worth perusing and preserving. The reviewers have alsorendered a commendable service by fine-tuning and adding value to thecontent. We sincerely acknowledge the efforts of the authors as well as thereviewers. We are also grateful to the Public Relations Department for their supportat each stage of this project, right from conceptualization to coordinationwith the publishers, and giving the finishing touches. The publishers patiently stood by us during the several revisions whileadding their innovative ideas to enhance the quality of this publication. Theydeserve our sincere thanks. Finally I wish to place on record my grateful thanks to all my colleagues forthe generous help and support that they have bestowed at every stage of thispublication. Dr S.K.Mishra, Director In-Charge,Ispat General Hospital Medical & Health Services, Rourkela-769005 SAIL, RSP, Rourkela
    • Contents• Editorial 03Review Article• Diabetic nephropathy 04 Kishore C MahantaOriginal Papers• Prevalence of phage types & biotypes among Salmonella Typhi 13 and Salmonella Paratyphi A isolates from Rourkela, Orissa Seshadri S Bhattacharya, Usha Das• Predictions of Length of Hospital stay of malaria patients 17 Saroj K Mishra, Narayan P Sahoo, Kishore C Mahanta, Rajalaxmi MishraCase reports• Peutz- Jeghers Syndrome presenting as acute intestinal obstruction 21 due to Jejunal Intussusception in an adult male Amulya M Acharya, Sishir R Dash, Manoja K Panigrahi• Necrotising fasciitis in neonate – case report 25 Radhanath Satpathy, Nimain C Nanda, Pitabas Mishra, Rajan K Behera, Pinaki Panigrahi• Squamous cell carcinoma & basal cell carcinoma with xeroderma 28 pigmentosa – a rare presentation Aruna M Minz, Niranjan K Behera, Rabi R Panda, Sanghamitra Satpathy, Prativa K Behera, Usha Das• Multiple brain metastases due to occult Papillary Carcinoma 31 of thyroid gland: A Case Report Rabindra N Mohapatra, Sudhi R Pradhan , Rabi R Panda, Pushpa Kumari, Saropani Hembram• Unusual case of severe Sepsis 34 Rajyabardhan Pattnaik, Sanjib Mohanty, Sradhananda MohapatraClinical imaging• Choanal Stenosis with single nostril -a rare Case 37 Paramananda Rath, Nimai C Nanda, Pitabas Mishra, Sidhesh C MishraResidents Section• Accidental Breakthrough 39 Suman Behera, Pallavi Agarwal• Practice paper 40• Down The Memory Lane 44• Instructions for the Authors 46• Ispat General Hospital : An Overview
    • EditorialBrain Death, its impact on organ donation andresources of critical care units Address for communication : Sr. Deputy director, Neurosurgery,Rabindra N.Mohapatra Ispat General Hospital, Rourkela-769005, IndiaDeptt. of Neurosurgery e-mail: ighp@in.com“20,000 liver transplants needed annually in India, Continuation of critical care support after brainonly 110 donors in 2009”. This was the news death, drains out the resource crunch critical care 1headline on April 01 2010 . departments of life saving resources, manpowerThroughout the world, main resources of donor and finance. In fact, it puts a lot of burden on the 2, 3organs are the brain dead patients. But, the sorry family members physically, financially andstate in our country is mainly due to reluctance to emotionally, for an outcome which is unattainable.accept the concept of brain death, both by the In addition, keeping life saving equipmentsphysicians as well as general public. Causes of this engaged for a brain dead patient may deprivereluctance may be due to several reasons related to another critically ill patient whose condition isphysicians themselves and relatives of the reversible. We, the physicians, should understand 2deceased as well. According to Pathak et al., some that there is no recovery after brain death. We canof the factors responsible for this may be explain relatives of the deceased that putting their patient on life support system is futile; rather his • Lack of understanding the concept. viable organs can alleviate the disease in a person • Special emotional attachment to the dead who can otherwise lead a normal healthy life. In person an Indian scenario, the relatives of the deceased • Loss of confidence in medical practice can be emotionally appealed that some part of • Ethical questions related to earlier organ their near and dear ones will still be surviving in the transplant procedure recipients body. • Perceived insufficient participation of The purpose of this Editorial is not to go into the government and medical associations. intricacies of brain death, rather to sensitiseConcept of clinical death in the form of loss of medical professionals and public regarding the factobservable cardio respiratory failure has that brain death is ultimate end of ones journey inundergone a sea change due to widespread use of this Earth.mechanical ventilators that prevent respiratory It is time to educate ourselves and the public, to 3arrest . In 1968, ad hoc committee at Harvard assist in understanding the concept of brain death.Medical School defined irreversible coma, or brain It is particularly true in hospitals, where load ondeath, as unresponsiveness and lack of receptivity, critical care department is very high.the absence of movement and breathing, theabsence of brain-stem reflexes, and coma whose References: 3cause has been identified. 1. Zee News.Com, uploaded on Thursday, AprilIn India, The Transplantation of Human Organs Act, 01, 2010, 00.031994 (Central Act 42of 1994), lays down the 2. Pathak MK, Tripathy SK, Agrawal P,definition of death thus: Deceased person means Chaturvedi R, Yadav S. Clinical Criteria forin whom permanent disappearance of all evidence Diagnosis of Brain death and its Medico-of life occurs, by reason of brain stem death or in a Legal applications (A Review Study).cardio-pulmonary sense at any time after live birth IndMedica-Medico-Legal update.2006;has taken place. It goes on to state that brain-stem 6(2):3-6death means the stage at which all functions of thebrain stem have permanently and irreversibly 3. Golia AK, Pawar M. The diagnosis of brainceased. Once brain-stem death has been death. Indian J Crit Med 2009;13:7-11diagnosed by an authorized committee using 4. Pandya SK. Brain death and our transplantspecified criteria, the dead persons organs can be law. Paper presented at: The seventhremoved for transplantation provided legally valid National critical care congress CCCON; 2001 3, 4consent for this is available. Jan 2-7; Bangalore 3
    • Review ArticlesDiabetic NephropathyKishore C MahantaDeptt. of Internal Medicine Address for communication : Dr K.C. Mohanta, Senior Deputy Director, Ispat General Hospital, Rourkela -769005, INDIA Email: kishoremalaria@rediffmail.comABSTRACT predispose to development of diabetic 1Diabetes has become the common single cause of nephropathy. Pre diabetic individuals, withChronic Kidney disease (CKD) leading to End-Stage impaired glucose tolerance, frequently haveRenal Disease (ESRD) in most countries: this is due hypertension as one facet of metabolic syndrome.to the fact that diabetes, particularly type 2 is Genetic factors combined with metabolic andincreasing in prevalence and that diabetic hemodynamic alterations induce renal damage inpatients are living longer with proper medication. susceptible individuals.About 20-30% of patients with type 1/ type 2 Causes:diabetes develop evidence of nephropathy. The exact cause of diabetic nephropathy isRecent studies have now demonstrated that the unknown, but it is believed that uncontrolled highonset and course of diabetic nephropathy can be blood sugar leads to the development of kidneydelayed to a very great extent by several damage, especially when high blood pressure isinterventions, but these interventions have their also present. Not all persons with diabetesgreatest impact if instituted at a very early course develop this condition.of development of this complication. Recently Each kidney is made up of hundreds of thousandsthere has been a lot of developments in the of filtering units called nephrons. Each nephrontreatment of End Stage Renal Failure. has a cluster of tiny blood vessels called aIntroduction:- glomerulous. Together these structures helpThere is a silent epidemic of type 2 diabetes world remove waste from the body. Too much bloodover. It is predicted that India will be the diabetic sugar can damage these structures, causing themcapital of the world by 2020. With growing to thicken and become scarred. Slowly, over time,population of type 2 diabetes, the prevalence of more and more blood vessels are destroyed. Thediabetic nephropathy is on the rise. In fact diabetic kidney structures begin to leak and proteinnephropathy is the single most common cause of (albumin) begins to pass into the urine.End Stage Renal Disease (ESRD) today. Persons with diabetes who have the following riskBesides patients miserable sufferings, it factors are more likely to develop this condition:consumes greater financial resources than non • African American, Hispanic, or Americans ofdiabetic ESRD. Diabetic ESRD patients do poorly Indian originon dialysis and mortality is higher. There is a • Family history of kidney disease or highspectrum of co-morbidities such as CV disease, blood pressurebrain stroke, blindness, gangrene etc which are to • Poor control of blood pressurebe dealt with while treating such patients with • Poor control of blood sugarsRenal Replacement Therapy (RRT). • Type 1 diabetes before age 20There has been some evidence to suggest that • Smoking, Alcoholismgenetic predisposition to hypertension may • Abnormal lipid levels 4
    • Diabetic nephropathy generally goes along with cytokines such as transforming growth factor-B,other diabetic complications including high blood angiotensin II, and/or other growth factors.2,3pressure, retinopathy and blood vessel changes Alternatively, elevated glucose levels may inhibit(vasculopathy). matrix protein degradation through non- enzymatic glycosylation and/or through thePathophysiology: 4 inhibition of protein degradative pathways. Thus,The pathophysiology of diabetic nephropathy the mediators of mesangial expansion constitutemanifests histologically as diabetic reasonable therapeutic targets when crafting aglomerulosclerosis and is characterized by treatment strategy for diabetic nephropathy.glomerular basement membrane thickening and Understanding the natural history of diabeticmesangial expansion with increased extracellular glomerulosclerosis is important to designmatrix deposition. Mesangial expansion in therapeutic interventions, as well as gaugingdiabetic glomerulosclerosis may be considered responses to therapy. In this regard, Parvingthe result of an imbalance between mesangial demonstrated the deleterious effect ofmatrix protein production and degradation, hypertension on renal function in proteinuricfavoring matrix protein accumulation. diabetics.5,6 Of equal or greater value in that reportOverproduction of mesangial matrix proteins may was the demonstration of the expected rate ofbe the result of glomerular hypertension and/or loss of glomerular filtration rate (GFR) over time,hyperglycemia-driven synthesis of prosclerotic in patients with diabetic nephropathy.Fig 1. Graphic presentation of the natural history of diabetic glomerulosclerosis. Initially there is glomerular hyper filtration and microalbuminuria. Microalbuminuria is followed by macroalbuminuria (dipstick positive proteinuria), the onset of macroproteinuria heralds the beginning of a relentless decline in GFR at the rate approximately 1ml/mt/month (at a BP of 140/90 mm hg). If GFR is 70ml/mt at onset of macroalbuminuria and dialysis is indicated at a GFR of 10ml/mt, 65 months would pass from the onset of proteinuria to the need for renal replacement therapy. The goal of therapy is to slow the rate of loss of GFR. Reducing the rate of loss of GFR from 1 ml/minute/month to 0.5 ml/min/month would translate into a doubling of the time for the need for dialysis (130 months). Modified from Molitch, Diabetes Care 17:756, 1994. 5
    • Figure 1. is a schematic summary of the natural only about 20% go on to develop ESRD. Howeverhistory of diabetic glomerulosclerosis, and presence of microalbuminuria in addition todemonstrates the relationship between being a manifestation of renal involvement, is alsoalbuminuria and the loss of GFR over time. The a marker of cardiovascular risk. Patients withmodel is based on the following assumptions: (a) sustained microalbuminuria need to beall macroscopic (dipstick positive) proteinuria is aggressively managed for cardiovascular risk 7preceded by a phase of microalbuminuria factors as well.(microalbumin 30-300 mg /day); (b) the SCREENING FOR MICROALBUMINURIA:-appearance of dipstick positive proteinuria Screening in individual with type I diabetes shouldheralds the beginning of a linear, irreversible loss begin after 5 years disease duration. In type 2 DM,of GFR; and (c) GFR is lost, on average, at the rate screening should begin at diagnosis, there afterof 1 ml/min/month. for the presence of microalbuminuria should beClinical diagnosis of diabetic nephropathy performed annually.Symptoms : Screening for microalbuminuria can beEarly stage diabetic nephropathy has no performed by three methods:-symptoms. Over time, the kidneys ability to 1. Measurement of albumin to creatininefunction starts to decline. Symptoms develop late ratio (ACR) in a random spot collectionin the disease and may include: 2. 24 hr collection with creatinine, allowing • Fatigue the simultaneous measurement of • Foamy appearance or excessive frothing of creatinine clearance. the urine 3. Screening with reagent tables or dipstick • Frequent hiccups for microalbumin have sensitivity 95% and • General ill feeling specificity93%. Reagent strips only • Generalized itching indicate concentration and do not correct • Headache the creatinine as the spot albumin- 7 • Nausea and vomiting creatinine ratio does. • Poor appetite Definitions :- • Swelling of the legs 1. Microalbuminuria – Random ACR 30-300 • Swelling, usually around the eyes in the mg on 2 out of 3 occasion mornings; general body swelling may 2. Macroalbuminuria- Random ACR >300 mg occur with late-stage disease or positive protein dipstick • Unintentional weight gain (from fluid 3. Diabetic nephropathy Estimated GFR < 60 buildup) ml/min for at least 3 months.Examination and Tests Screening of microalbuminuria is invalid inThe earliest clinical evidence of renal involvement following conditions:in diabetes is the presence of small amount of In uncontrolled hyperglycaemia, febrile illness,albumin in urine (30-300mg/24 hrs). This is following strenuous exercise, uncontrolledlabeled microalbuminuria. Protein may appear in hypertension or heart failure and presence ofthe urine for 5 to 10 years before other symptoms urinary infection as all these conditions can causedevelop. In type 1 Diabetes 80%, who develop transient proteinuria.7microalbuminuria, will develop macroproteinuria High blood pressure often goes along withand around 50% will eventually develop ESRD. In diabetic nephropathy. One can have high bloodtype 2 Diabetes 20-40% of patient with pressure that develops rapidly or is difficultmicroalbuminuria develop overt proteinuria and to control. 6
    • Laboratory tests that may be done include: levels, aggressive blood pressure control, • BUN angiotensin II inhibition, and dietary protein • Serum creatinine restriction. Additional therapeutic targets include microalbuminuria and macroproteinuria. AnThe levels of these tests will increase as kidney approach to each of these parameters is discusseddamage gets worse. Other laboratory tests that below.may be done include: 1. Tight blood glucose control • 24-hour urine protein The DCCT (Diabetes Control and Complications • Blood levels of phosphorus, calcium, Trial) demonstrated the importance of tight blood bicarbonate, PTH, and potassium glucose control in slowing the development of • Hemoglobin 13 proteinuria in Type 1 diabetics. In this regard, • Hematocrit patients randomized to tight glucose control • Protein electrophoresis - urine (HbA1C levels < 6.5%) versus regular control (8-A kidney biopsy confirms the diagnosis. However, 9%), demonstrated 39 and 54% lower rates ofclinical diagnosis can be done without a biopsy if development of microalbuminuria andthe following three conditions are met with: macroalbuminuria, respectively, over the two years of the trial. 1. Persistent protein in the urine Similarly the UKPDS(United Kingdom Prospective 2. Diabetic retinopathy Diabetes Study) in Type II diabetes showed a 25% 3. No other kidney or renal tract disease risk reduction in microvascular complication inA biopsy may be done, however, if there is any the intensively treated group.doubt in the diagnosis. 2. Blood pressure controlDiabetics with heavy proteinuria, but lacking the Hypertension in diabetic patient may be due todisease for a sufficient period of time and/or coexisting “essential” hypertension, or due toretinopathy, may require renal biopsy. These myriad of other secondary causes, such as renalpatients may suffer from primary vascular disease. Isolated systolic hypertensionglomerulopathies such as membranous 8 has been attributed to the loss of elasticnephropathy, or other glomerular diseases. compliance of atherosclerotic large vessels. BothDiabetic glomerulopathy is the most common systolic and diastolic hypertension markedlycause of nephrotic syndrome. Thus, early in the accelerates the progression of diabeticcourse of the disease, the serum creatinine is nephropathy and aggressive antihypertensivenormal despite heavy proteinuria (> 3 grams/24 management is able to greatly decrease the ratehours). In this regard, a diabetic patient of fall of GFR. Appropriate antihypertensivepresenting with elevated serum creatinine in the intervention can significantly reduce mortalityabsence of macroscopic proteinuria should from 94 to 45% and a reduction in the need forsuggest additional diagnostic possibilities (such as dialysis and transplantation from 73 to 31% 16other glomerulopathies) . The diagnostic utility of years after development of overt nephropathy.proteinuria is less useful in patients treated with Choice of antihypertensive therapy:-angiotensin converting enzyme inhibitors (ACEi) One needs to be careful about:-or angiotensin II receptor blockers (ARBs), sinceboth classes of drugs are known to reduce - Use of ACEI and ARBs as these may lead to 9,10glomerular proteinuria. hyperkalemia in patients of advanced renalMEDICAL THERAPY OF DIABETIC NEPHROPATHY : insufficiency,The medical therapy of diabetic glomerulo- - ACEI are contraindicated in bilateral renalsclerosis includes strict control of blood glucose artery stenosis and in pregnancy. 7
    • - Beta blockers are contraindicated in ACEi demonstrate slower progression to 6 peripheral vascular disease. macroproteinuria and renal failure. AmericanTargets for blood pressure control:- Diabetic Association (ADA) guidelines suggest assessing for microalbuminuria (normal < 30• <130/80 mm hg in absence of proteinuria mg/24 hours or less 30 mcg/mg creatinine for• <125/75 mm hg in presence of proteinuria. a spot urine collection) at the time of diagnosis3. Angiotensin II inhibition : The ACE inhibitor in all type 2 diabetics, in all type I diabetics with trial in diabetic nephropathy was the first disease duration > 5 yrs, and annually randomized, placebo controlled trial that thereafter in both groups. 19 Early and showed the beneficial effect of ACE inhibitors aggressive therapy of microalbuminuria, taken in the treatment of diabetic along with angiotensin II inhibition, is glomerulosclerosis.11 Subsequent studies have expected to slow disease progression. confirmed this observation for both ACE 6. Macroproteinuria inhibitors and ARBs.10,12 Most agree that ACEI Heavy proteinuria is a risk factor for progressive a re f i rs t l i n e t h e ra p y fo r d i a b e t i c 10 renal failure, 16 including diabetic nephropathy.20 glomerulosclerosis, but ARBs are regarded by There is abundant evidence that abrogating some as equivalent.10 The beneficial effect of proteinuria with dietary and antihypertensive angiotensin II inhibition may result from: 21 interventions, and/or ACE inhibitors, 1 and/or a) a decline in glomerular hypertension (with ARBs,22,23 results in a slower loss of GFR in slowing of mesangial expansion)13 proteinuric states. In this regard, combination b) a reduction in proteinuria (with an therapy with both ACE inhibitors and ARBs may 24 expected decrease in proteinuria- provide benefit over ACE inhibitors alone. 14 associated prosclerotic events), and/or Finally, nephrotic diabetics treated with ACE inhibition, and exhibiting a reduction in c) a decrease in angiotensin II stimulated 15,16 proteinuria to < 1 gm / day, demonstrated stable TGF-ß synthesis. 25 renal function for up to 8 to 15 years. Taken4. Dietary protein restriction : In some reports, together, therapeutic measures directed at dietary protein restriction has been shown to reducing macroscopic proteinuria would be slow the loss of GFR in proteinuric diabetics,17 expected to slow the progression of diabetic although the data are not conclusive. Protein nephropathy, and angiotensin II inhibition is the restricted diets (0.6-0.8 g/kg body wt/day) mainstay of therapy for attaining that goal. decrease glomerular hypertension, the Other aspects of treatment : Treatment of production of prosclerotic cytokines, 18 progressive renal disease includes prevention of proteinuria, and glomerulo-sclerosis, and renal osteodystrophy with sodium and phosphate remain a viable therapeutic option for restriction and use of phosphate binders, compliant patients. treatment and prevention of anaemia etc.5. Microalbuminuria : Microalbuminuria Avoidance of nephrotoxic drugs in proteinuric predates the development of macroscopic diabetic patients will prevent form onset of acute proteinuria. Macroscopic proteinuria is a kidney injury. major risk factor for progression to ESRD,14 thus measures to reverse microalbuminuria may Radiocontrast media are nephrotoxic in diabetic retard development of clinical nephropathy. nephropathy and careful hydration is mandatory Patients with microalbuminuria treated with in these cases if it is done. 8
    • SPECIAL CONSIDERATIONS Survival analysis shows the two modalities are 27Insulin metabolism in CKD : Unutilized insulin is comparable with regard to patient outcome.excreted by kidney normally which accumulates However, when compared to non-diabetics, diabetic patients on dialysis do substantiallyin CKD. So if we fail to reduce insulin dose as 28 worse, with five-year survival rates as low as 5%kidney disease progresses, patients will for elderly type 2 diabetics.29 With meticulousexperience hypoglycaemia. So reducing insulin management, others have shown three-yeardose and switching to short acting insulin survival rates as high as 58%.28 .The reasons foranalogues is recommended in this situation. It is poor survival rates relate to the high incidence ofrecommended to avoid long acting Insulins in CKD preexisting cardiovascular disease, late referralpatients. both for predialysis care, as well as vascular accessOral antidiabetic drug: 97% of the most placement, malnutrition, and co-existing vascularcommonly used oral antidiabetic drug Metformin problems (in particular, peripheral vascularis excreted by normal kidney within 12 hrs. In CKD disease with associated ischemic toes and feet).28it will accumulate and lead to lactic acidosis, a Furthermore, diabetes and smoking have beenserious condition. shown to be significant risk factors forSo metformin should be stopped when the eGFR is atherosclerotic heart disease in dialysis patients, 30<35 ml/mt/1.73 m2 correlates to serum creatinine similar to what is seen in the general population.of approxmimately 1.7 mg /dl. Older The anemia of chronic renal disease may furthersulfonylurea(SU) are excreted mainly through complicate the course of patients with significantkidney. Only 10% of second line SU are excreted by coronary artery disease. Taken together, thesekidney but are long acting and may accumulate in data suggest that the survival of diabetic patientsCKD, so we must be cautious while using these. on hemodialysis may be optimized withMeglitinides and Thiazolidinediones are not aggressive attention to risk factors forexcreted by kidneys. These do not cause c a rd i o va s c u l a r d i s e a s e ( hy p e r te n s i o n ,hypoglycaemia. dyslipidemia, smoking, etc.), awareness and therapy of diabetic foot problems, and earlyMonitoring glycaemic control in CKD : As kidney nephrology referral (as GFR falls or withdisease develops, the turnover of red blood cells progressive proteinuria) for vascular accessbecomes abnormal. Usually there is prolonged life placement and anemia management.span of RBCs, perhaps because the person isanaemic. So hemoglobin has more time to 2. Peritoneal dialysis : The second option for renalbecome glycated. In such conditions HbA1c in replacement therapy in diabetic patients withkidney disease may be falsely high. Hb may also be ESRD, is peritoneal dialysis. When compared tocarbamylated with some of the waste products, hemodialysis, fewer patients are treated with peritoneal dialysis. Patients opting for peritonealwhich accumulate in uremia and these dialysis tend to be healthier and more involved incompounds will interfere with the measurement their medical care. While no clear survivalof HbA1c. This is one more reason for HbA1c to be advantage for peritoneal or hemodialysis hasfalsely high. Correction of anaemia may lead to been demonstrated, patients treated withdecrease HbA1c level.26 peritoneal dialysis may experience labile bloodRenal replacement therapy: glucose levels (attributed to the high glucose1. Hemodialysis : Hemodialysis and peritoneal concentrations inherent to PD dialysate) anddialysis are the two forms of dialysis used to treat increased risk of malnutrition (secondary to 31diabetic patients with end stage renal disease. excessive protein losses in dialysate effluent). 9
    • 3. Transplantation : By far the best treatment for SummaryESRD from diabetes is kidney transplantation. The rising incidence of diabetes means thatKidney transplantation in diabetics with end-stage clinicians can expect to find an increased rate ofrenal disease may include kidney transplantation diabetic nephropathy, and increasing numbers ofalone, or combined kidney-pancreas patients requiring renal replacement therapy.transplantation. The former treats renal failure, Understanding the natural history of diabeticthe latter both renal failure and diabetes. Patient nephropathy, the early recognition of diabeticsurvival following kidney transplantation without complications, and timely initiation of therapy toa pancreas has consistently been demonstrated to slow progression are cornerstones in thebe superior to any form of dialysis. Data from the management of this condition. AggressiveOrgan Procurement and Transplantation Network treatment of hyperglycemia and hypertension,reported one-, three-, and five-year patient the use of angiotensin II inhibitors, and timelysurvival rates for transplanted diabetics of 90, 79 therapy of micro and macroproteinuria are 32and 66%, respectively. This compares to a two essential features of optimal therapy. For patientsyear survival rate in diabetic patients on reaching end stage renal failure, renal 29hemodialysis of 58%. The improved survival of replacement options include dialysis and kidneyrenal transplant patients over those treated with transplantation, with transplantation conferring ahemodialysis must be interpreted in light of the substantial survival advantage.fact that they are selected for transplantation, References:whereas patients with extensive co-morbidities 1. Strojek K et al, Nephropathyof type 2tend to remain on dialysis. Living donor diabetes: Evidence for hereditary factor.transplants confer an allograft survival advantage Kidney Int. 51:1602-1607,1997.over cadaveric donors, with three-year allograft 2. Hostetter T, Rennke H, Brenner B. The casesurvival rates of 88 and 78% for living and for intrarenal hypertension in thecadaveric donor transplants, respectively. 32 initiation and progression of diabetic andHowever, both modalities are superior to dialysis other glomerulopathies. Am J Med. 1982;with three year patient survival rates of 72:375. 32approximately 88-94%. Preemptive 3. Ziyadeh F, Han D. Involvement oftransplantation is renal transplantation that is transforming growth factor-b and itsperformed prior to instituting dialysis. Preemptive receptors in the pathogenesis of diabetictransplantation may confer a survival advantage nephropathy. Kidney Int . 1997; 52:S7-S11.that is superior to transplanting patients on 4. Brownlee M. Biochemistry and moleculardialysis. In this regard, the time spent on dialysis cell biology of diabetic complications.prior to transplantation portends worse survival Nature. 2001; 414(6865):813-20.rates for patients. For example, in patients on 5. Parving H, Smidt U, Andersen A, Svendsendialysis < 6 months, 12-24 months, or >48 months P. Early aggressive antihypertensivehad mortality rates of 21%, 41%, and 72%, treatment reduces rate of decline in 33,34,35respectively. A similar trend for allograft kidney function in diabetic nephropathy.survival was seen in cadaveric transplants Lancet.performed in patients receiving hemodialysis for 1983; 1:1175-1179.more than two years prior to the transplant. In 6. Parving HH. Diabetic nephropathy:those studies, the allograft survival rate was only prevention and treatment. Kidney Int.39% after ten years.36 2001; 60(5):2041-55. 10
    • 7. Anjali, Jacob J J, Nephropathy in Diabetes; and transforming growth factor-beta1 in practical guide to Diabetes Mellitus: 4th vascular Edn.;146-148 smooth muscle. J Mol Med . 1999; 8. Carstens S, Hebert L, Garancis J, Piering W, 77(5):437-45. Lemann Jr J. Rapidly progressive 17. Zeller K, Whittaker E, Sullivan L, et al. Effect glomerulonephritis superimposed on of restricting dietary protein on the diabetic glomerulosclerosis: recognition progression of renal failure in patients with and treatment. JAMA. 1982; 247:1453- insulin-dependent diabetes mellitus. 1457. N Engl J Med. 1991; 324:78-84. 9. Brenner BM. Regarding: “Management of 18. Klahr S, Levey AS, Beck GJ, et al. The effects glomerular proteinuria: a commentary.” J of dietary protein restriction and blood- Am Soc Nephrol. 2004; 15(5):1354-5; pressure control on the progression of discussion 1356-7. chronic renal disease. Modification of Diet 10. Lewis E, Hunsicker L, Bain R, Rohde R. The in Renal Disease Study Group [see effect of angiotensin converting enzyme comments]. N Engl J Med . 1994; inhibition in diabetic nephropathy. N Engl J 330(13):877-84. Med. 1993; 329:1456-62. 19. Molitch ME, DeFronzo RA, Franz MJ, et al. 11. Lewis EJ, Lewis JB. ACE inhibitors versus Nephropathy in diabetes. Diabetes Care. angiotensin receptor blockers in diabetic 2004; 27 Suppl 1:S79-83. nephropathy: is there a winner? J Am Soc 20. Breyer JA, Bain RP, Evans JK, et al. Nephrol . 2004; 15(5):1358-60. Predictors of the progression of renal 12. Hostetter T. Prevention of end-stage renal insufficiency in patients with insulin- disease due to type 2 diabetes. N Engl J dependent diabetes and overt diabetic Med. 2001; 345:910-911. nephropathy. 13. Zatz R, Bunn B, Meyer T, Anderson S, The Collaborative Study Group. Kidney Int. Rennke H, Brenner B. Prevention 1996; 50(5):1651-8. of diabetic glomerulopathy by 21. Peterson JC, Adler S, Burkart JM, et al. p h a r m a co l o g i ca l a m e l i o rat i o n o f Blood pressure control, proteinuria, and glomerular capillary hypertension. the progression of renal disease. The J Clin Invest. 1986; 77:1925. Modification of Diet in Renal Disease 14. Wilmer WA, Rovin BH, Hebert CJ, Rao SV, Study. Kumor K, Hebert LA. Management of Ann Intern Med. 1995; 123(10):754-62. glomerular proteinuria: a commentary. J 22. Parving HH, Lehnert H, Brochner- Am Soc Nephrol. 2003; 14(12):3217-32. Mortensen J, Gomis R, Andersen S, Arner P. 15. Nahman N, Kronenberger J, Sferra T, Clark The effect of irbesartan on the K. Transcriptional activation of the TGF-b development of diabetic nephropathy in gene by angiotensin II: implications for patients with type 2 diabetes. N Engl J fibronectin biosynthetic pathways Med. 2001; 345(12):870-8. in human mesangial cells. J Amer Soc 23. Lewis EJ, Hunsicker LG, Clarke WR, et al. Nephrol. 1997; 8:522A. Renoprotective effect of the angiotensin- 16. Siegert A, Ritz E, Orth S, Wagner J. receptor antagonist irbesartan in patients Differential regulation of transforming with nephropathy due to type 2 diabetes. growth factor receptors by angiotensin II N Engl J Med. 2001; 345(12):851-60.11
    • 24. Jacobsen P, Andersen S, Rossing K, Jensen dialysed diabetic patients: a prospective BR, Parving HH. Dual blockade of the renin- study in 412 subjects. Nephrol Dial angiotensin system versus maximal Transplant. 1997; 12(12):2603-11. recommended dose of ACE inhibition in 30. Cheung AK, Sarnak MJ, Yan G, et al. diabetic nephropathy. Kidney Int. 2003; Atherosclerotic cardiovascular disease 63(5):1874-80. risks in chronic hemodialysis patients.25. Wilmer WA, Hebert LA, Lewis EJ, et al. Kidney Int. 2000; 58(1):353-62. Remission of nephrotic syndrome in type 1 31. Xue JL, Everson SE, Constantini EG, et al. diabetes: long-term follow-up of patients Peritoneal and hemodialysis: II. Mortality in the Captopril Study. Am J Kidney risk associated with initial patient Dis. 1999; 34:308-14. characteristics. Kidney Int. 2002; 61(2):741-6.26. Mashall S etal, Chronic kidney Disease in 32. Organ Procurement and Transplantation Diabetics: Current best practice and Network. www.optn.org/latestData/ possibilities for future. Novonordisk rptStrat.asp. 2004. Diabetes Update. Proceedings 2009; 21-28 33. Meier-Kriesche HU, Port FK, Ojo AO, et al.27. Locatelli F, Pozzoni P, Del Vecchio L. Renal Effect of waiting time on renal transplant replacement therapy in patients with outcome. Kidney Int. 2000; 58(3):1311-7. diabetes and end-stage renal disease. J Am 34. Mange KC, Joffe MM, Feldman HI. Effect of Soc Nephrol. 2004; 15 Suppl 1:S25-9. the use or nonuse of long-term dialysis on28. Schwenger V, Zeier M, Ritz E. How can the the subsequent survival of renal poor outcomes for diabetic dialysis transplants from living donors. N Engl patients be improved? Semin Dial. 2004; Med. 2001; 344(10):726-31. 17(3):186-7. 35. Kasiske BL, Snyder JJ, Matas AJ, Ellison MD,29. Koch M, Kutkuhn B, Grabensee B, Ritz E. Gill JS, Kausz AT. Preemptive kidney Apolipoprotein A, fibrinogen, age, and transplantation: the advantage and the history of stroke are predictors of death in advantaged. J Am Soc Nephrol. 2002; 12
    • Original PapersPrevalence of phage types & biotypes among Salmonella Typhi andSalmonella Paratyphi A isolates from Rourkela, Orissa. Address for communication :Seshadri S Bhattacharya, Usha Das SS Bhattacharya Deptt. of Microbiology,Deptt. of Microbiology, Ispat General Hospital, Rourkela, Orissa. Email: sesebha@yahoo.co.inABSTRACT fever in India.1,2 However, isolation of SalmonellaAim of this study was to highlight the changes in enterica serotype Paratyphi A causing the sameprevalence of phage types encountered among disease have been reported with an increasingSalmonella isolates from Rourkela. Besides S. trend.3,4 In Rourkela, we have been reporting 5Typhi as the main causative agent of enteric fever, S.Typhi causing enteric fever since 1996, whereasS. Paratyphi A has also been emerging with isolation of S.Paratyphi A causing the sameincreasing rate as the other causative agent of disease has been encountered in this place sinceenteric fever from different parts of India 2002.6including Rourkela. This retrospective study was Phage typing is a major means of epidemiologicalcarried out between September 2005 and August tracing as strains within a particular serotype may2006 with 1454 patients attending out-patient- be differentiated into a number of phage types,departments (OPD) and wards of Ispat General and may help to define groups of persons whoHospital, Rourkela, India. Phage typing and have been infected with the same strain from thebiotyping was performed for randomly chosen same source. Again, combination of biotypingisolates of S. Typhi (N=36) and S. Paratyphi A with phage typing gives a finer discrimination of(N=12). A distinctive change has been noticed in strains in tracing out the source of infection. Thethe prevalence of phage types compared to their use of phage typing and biotyping forprevalence pattern reported earlier. Phage type epidemiological tracing had been documented40 was the most commonly encountered phage since 1982 in different parts of India.1among S. Typhi isolates followed by type E1. Phage typing and biotyping of both SalmonellaSusceptibility testing was performed for all 112 Typhi and Salmonella Paratyphi A had beenisolates of Salmonella including 48 strains chosen reported from Rourkela in 2006 and 2007.6,7 Thererandomly for phage typing and biotyping. Though was a noticeable change in the prevalence pattern4-5% of Salmonella isolates showed resistance to of phage types encountered among S.Typhiciprofloxacin, they were highly sensitive to both isolates in 2005-2006 in comparison to the phagea m i n o g l yco s i d e s a n d t h i rd ge n e rat i o n types found in 2004-2005. In this retrospective,cephalosporins. Diversity among the phage types hospital based study, we have highlighted theencountered among S. Typhi isolates was changes in the prevalence pattern of phage typesprobably due to the diverse origin of those and biotypes among the Salmonella isolatesphages. Salmonella enteric serotype Typhi is the chosen randomly. The susceptibility pattern ofmost commonly occurring causative agent of Salmonella isolates including the typed strains 1.2enteric fever in India. have also been reported in this communication.Key words Materials & methodsPrevalence; Phage typing; Biotypes; Randomly This study was conducted between Septemberchosen; Susceptibility testing; Diversity. 2005 and August 2006. A total of 1454 patientsIntroduction attending out-patient departments (OPDs) andSalmonella enteric serotype Typhi is the most wards of Paediatric and Medicine departments ofcommonly occurring causative agent of enteric Ispat General Hospital , Rourkela, Orissa, 13
    • suspected of having enteric fever or pyrexia of the patients, 768 were males (52.81%) and 686unknown origin (PUO) were included in this study. were females (47.19%).A total of 1454 blood samples were included in Of 1454 patients, 112 were positive for Salmonellathis study. Irrespective of repeat sample we have isolates giving a per cent positivity of 7.70. Of 112taken into account only one sample from eachpatient. Only positive isolation was considered for Host organism Phage type Biotype No. of isolatesthe patients having both positive and negative S. Typhi A I 1results. (N=36) D1 I 1 E1 I 8Clinical samples of blood were collected in brain J1 I 2heart infusion broth with sterile precautions and 0 40 II 19incubated aerobically at 37 C for 48 hours. Three USV-2 II 1subcultures were done on blood agar, MacConkey Vi-Negative I 4agar and Salmonella-Shigella agar and incubated 0 S. Paratyphi A 1 II 1aerobically at 37 C for 18-24 hours. In negative (N=12) 6 II 11cases subcultures were done for one week. Table 2.Isolation of S. Typhi and S. Paratyphi A was Phage types encountered among S. Typhi and S. Paratyphiestablished by conventional methods. 8 A isolates in Rourkela between September 2005 and August 2006.Identification of these two serotypes wasestablished by biochemical and serological testing Antibiotics S. Typhi (%) S. Paratyphi A(%) 8,9with factor sera. Antibiotic susceptibility testing (N=92) (N=20)was performed by Kirby Bauer disk diffusion Ampicillin 82 (89.13) 11 (55) 10method, with the modifications recommended Co-trimoxazole 74 (80.43) 11 (55)by the National Committee for Clinical Laboratory Chloramphenicol 85 (92.39) 12 (60)Standards (NCCLS).11 Antimicrobials agents tested Gentamicin 90 (97.82) 19 (95)were ampicillin, co-trimoxazole, chloromycetin, Amikacin 91 (98.91) 20 (100)gentamicin, amikacin, ciprofloxacin, cephotaxime Ciprofloxacin 88 (95.65) 19 (95)and ceftriaxone. Cephotaxime 91 (98.91) 20 (100) Ceftriaxone 91 (98.91) 19 (95)Randomly selected strains of both S. Typhi andS. Paratyphi A were sent to the National Table 3. Susceptibility pattern of S. Typhi and S. ParatyphiSalmonella Phage Typing Centre, Lady Hardinge A isolates in Rourkela between September 2005 and August 2006.Medical College, New Delhi, India, for phage Salmonella isolates, 92 were S. Typhi strains andtyping and biotyping. remaining 20 were S. Paratyphi A strains. AlmostResults 75 per cent of isolates were from pediatric population, among which 52.38% were boys andOut of 1454 patients, 1052 were children (72.35%) 47.62% were girls.and remaining 402 were adults (27.65%). Among In 2004-2005, the predominant phage typeHost organism Phage type Biotype No. of isolates encountered among S. Typhi strains was E1,S. Typhi A I 5 followed by phage type A (Table 1). In the present(N=27) D1 I 1 study (2005-2006), predominant phage type E1 I 17 encountered among S. Typhi isolates was 40, E9 I 1 which itself is a rare and exotic phage type in India. J1 I 3 Second most common phage type of S. TyphiS. Paratyphi A 4 II 3 isolates in this study was E1 and number of Vi- (N=24) 6 II 21 Negative strains was 4 (Table 2). In both the studies mentioned, the predominant phage type Table 1. Phage types encountered among S. Typhi ans S. Paratyphi found among S. Paratyphi A strains was type 6, A isolates in Rourkela between September 2004 and August 2005. followed by phage types of either 4 or 1. 14
    • Most of the phage types of S. Typhi isolates phage type 40, which itself is a rare and exoticbelonged to biotype I, except for phage type 40 phage type of S. Typhi in India. It is worthand USV-2. All the phage types of S. Paratyphi A mentioning that two more rare and exotic phageisolates belonged to biotype II (Table 2). types of multi-drug resistant (MDR) S. TyphiAmpicillin and chloramphenicol sensitivity among strains, namely type 51 and type 28, caused 1,12S. Typhi isolates was found very high in our study, outbreaks in Kolkata and Mumbai respectively,though 40-45% of S. Paratyphi A isolates showed but in case of phage type 40, most of the strainsresistance to these antimicrobials (Table 3). were not multi-drug resistant. Emergence of Vi-Isolates of both S. Typhi and S. Paratyphi A showed negative strains among S. Typhi isolates inremarkably high susceptibility to gentamicin and Rourkela was another important finding duringamikacin. Resistance to ciprofloxacin was 4-5% the same time.among the isolates of S. Typhi and S. Paratyphi A. Till date, not many study-reports are availableSusceptibility to cefotaxime and ceftriaxone was regarding phage typing and biotyping of S.very high among the isolates of both S. Typhi and Paratyphi A. A study among the patients (comingS. Paratyphi A (Table 3). from Indian subcontinents) in Kuwait reportedRandomly chosen strains of both S.Typhi and S. that 66% of S. Paratyphi A isolates belonged toParatyphi A for phage typing and biotyping were phage type I.13 Another study from Nagpur alsoalso found remarkably sensitive to the showed that the prevalent phage type among S.antimicrobials used in our study. Out of 36 isolates Paratyphi A isolates from the local population was 14of S. Typhi, only 2 strains showed resistance to type I. The most commonly encountered phageciprofloxacin and 1 strain resistant to type of S. Paratyphi A isolates from Rourkela wascephotaxime. Out of 12 strains of S. Paratyphi A type 6, a finding which hardly got any otherrandomly chosen for phage typing and biotyping, contemporary reference in India. From 1992 toonly 3 strains showed resistance to ampicillin, co- 2003, commonest biotype of S. Paratyphi A intrimoxazole and chloramphenicol. Interestingly, India was type I,13,14,15 but in our study all theall these 3 MDR strains of S. Paratyphi A belonged phages of S. Paratyphi A belonged to biotype II.to phage type 6. The commonest biotype encountered among S. Typhi strains isolated from Kolkata, Nagpur andDiscussion Ludhiana was type I,12,16,17 but in our study, biotype IPhage typing is one of the most important means accounted for 44.4% of S. Typhi isolates andof epidemiological tracing. In 1982-89, the order remaining 55.6% were biotype II.of frequency of phage types in north and central Susceptibility pattern to ampicillin andIndia was A, E, O, while in south the second chloramphenicol were very encouraging for 1predominant phage type was O. From 1990 S.Typhi isolates as reported earlier,5,6,7 though itonwards , E1 became the most commonly phage was not that much inspiring for S.Paratyphi Atype except in south India, where phage type O isolates in this study. In this study, differences inwas the predominant type. In 1992, the order of per cent susceptibility between S. Typhi andfrequency had become E1, O, A throughout the S. Paratyphi A isolates for ampicillin,country. However, there was hardly any report of chloramphenicol and ciprofloxacin werephage type O from any part of the country since statistically significant (P<0.05), whereas for the 121994. rest of the antimicrobials tested, differences in perIn our findings of phage types encountered among cent susceptibility were found insignificantS. Typhi strains from Rourkela, E1 was the most (P>0.05). Although 4-5% resistance tocommonly occurring phage type in 2004-2005 ciprofloxacin among Salmonella isolates was aand second-most common phage type in matter of concern, very high susceptibility of2005-2006. One strikingly different finding in those strains to aminoglycosides (gentamicin and2005-2006 study was the highest occurrence of amikacin) and third generation cephalosporins 15
    • th(cephotaxime and ceftriaxone) was highly Medical Microbiology. 13 ed. Edinburg :encouraging, and can be used judiciously in case Churchill Livingstone, 1984: 456-81.of ciprofloxacin resistance. 9. Baron EJ, Peterson LR, Finegold SM. Bailey , thA diversity among phage types of S. Typhi isolates and Scott s Diagnostic Microbiology. 9 ed.has been noticed, though in case of S. Paratyphi A, St. Louis, Missouri : Mosby, 1994 : 362-85.mostly phage type 6 was encountered. This 10. Bauer AW, Kirby WM, Sherris JC and Truckdiversity of phage types observed in this eastern M. Antibiotic susceptibility testing by apart of India might be due to the diverse origin of standardized single disc method. Am J Clinthese phage types. The diversity of origin of these Pathol 1996; 45 : 493-6.phages again may be due to the migration of 11. National Committee for Clinical Laboratorypopulation to and from Rourkela, an industrial Standards. Performance standards for(steel) township, with respect to other parts of the antimicrobial disc susceptibility tests, 6th ed. 6country. Further studies are required regarding Approved standard M2-A6. Wayne, Pa :the epidemiological tracing especially for the National Committee for Clinical Laboratoryexotic phage type 40 of S. Typhi isolates. Standards; 1997.References 12. Saha MR, Palit A, Chatterjee NS, Dutta P, Mitra U and Bhattacharya SK. A prospective 1. Pillai PK, Prakash K. Current status of drug study of phage types & biotypes of resistance and phage types of Salmonella Salmonella enterica serotype Typhi isolated typhi in India. Indian J Med Res 1993; 97: from hospitalized children in Kolkata, India. 154-158. Indian J Med Res 2003; 117 : 201-204. 2. Sanghavi SK, Mane MP, Niphadkar KB. 13. Panigrahi D, Chugh TD, West PWJ, Dimitrov Multidrug resistant Salmonella serotypes. TZ, Groover S and Metha G. Antimicrobial Indian J Med Microbiol 1999; 17(2): 88-90. susceptibility, Phage typing and Plasmid 3. Sood S, Kapil A, Dash N, Das BK, Goel V and profile of Salmonella enterica serotype Seth P. Paratyphoid fever in India. Emerg paratyphi A strains isolated in Kuwait. Med Infect Dis 1999; 5: 483-484. Princ Pract 2003; 12: 252-255. 4. Chandel DS, Chaudhary R, Dhawan B, 14. Tankhiwale SS, Agrawal G, Jalgaonkar SV. An Pandey A, Dey AB. Drug-resistant Salmonella unusually high occurrence of Salmonella enterica serotype Paratyphi A in India. enterica serotype Paratyphi A in patients Emerg Infect Dis 2000; 6: 420-421. with enteric fever. Indian J Med Res 2003; 5. Bhattacharya SS, Das Usha. Occurrence of 117: 10-12. Salmonella typhi infection in Rourkela, 15. Chopra GS, Basu SK and Bhattacharya SR. Orissa. Indian J Med Res 2000; 111 : 75-76. Present Phage types and Antibiotic susceptibility of Salmonellae. Indian J Pathol 6. Bhattacharya SS, Das Usha. A sudden rise in Microbiol 1992; 4 : 345-350. occurrence of Salmonella paratyphi A 16. Agarwal V, Brahmne RB, Dhanvijay AG, infection in Rourkela, Orissa. Indian J Med Jalgaonkar PD, Pathak AA, and Saoji AM. Microbiol 2007; 25 : 78-79. Antibiogram, phage types and biotypes of 7. Das Usha, Bhattacharya SS. Antibiogram, Salmonella Typhi isolated in Nagpur. Indian J phage typing & biotyping of Salmonella Med Res 1992; 95: 14-16. Typhi & Salmonella Paratyphi a from 17. Kumar R, Aneja KR, Punia AK, Roy P, Sharma Rourkela, Orissa. Indian J Med Res 2006; 124 M and Gupta R. Changing pattern of : 109-111. biotypes, phage types and drug resistance of 8. Sleigh JD, Duguid JP. Salmonella. In: Collee Salmonella Typhi in Ludhiana during 1980- JG, Fraser AG, Marmion BP, eds. Practical 1999. Indian J Med Res 2001; 113: 175-180. 16
    • Original PapersPredictions of Lengths of Hospital stay of malaria patientsSaroj K Mishra Narayan P SahooDeptt. of Internal Medicine Deptt. of Anaesthesia Address for communication :Kishore C Mahanta Dr SK MishraDeptt. of Internal Medicine Director, Ispat General Hospital,Rajalaxmi Mishra Rourkela -769005, INDIADeptt. of Mathematics, Email: sarojrkl@gmail.comSushilavati Govt. Womens College, RourkelaAbstract providers and administrators, no tool is availableMalaria is a major cause for hospital admissions in to predict the length of stay for the malaria cases.the tropical regions, but there is no objective tool When confronted by a questioning/ inquisitiveto predict the length of hospital stay (LOS). relative, the treating doctor only extends a roughAnalyzing 700 hospitalized patients, a simple estimate depending on his own experience, whichequation was devised. LOS was equal to ½ [5+ 5 x is purely subjective. In practical situation, theSevere anemia + 1 x Jaundice +2 x acute renal statements are variable for different doctors andfailure+3 cerebral malaria + 1 x Type of therapy]; thus totally confusing to the relatives.where, presence of the complication is 1 and In the present study, it is attempted to identifyabsence=0 ; Type of therapy : oral anti malaria various determinants on LOS, and to develop atherapy=1, parenteral =2, and any ICU mathematical model which can be usedintervention (ventilator, dialysis etc)=3 . The objectively for each patient admitted to aLength of hospital stay of a malaria patient can be hospital. We tried to make it simple and easy toestimated easily and rapidly by a simple formula, remember. It is attempted that it must bewhich does not require sophisticated calculated rapidly and must not require too manyinvestigations. It can be calculated at the time of lab data.admission as well as during the course of the Material & Methods:disease. a. Hospital: Ispat General Hospital is situated inIntroduction: Sundargarh district of Orissa. It is a 685 bedWhen a patient is admitted to a hospital the most hospital under of a Public sector steel plant.important concern is the survival. The subsequent b. It has eleven bed Critical care units. There arequestion which arises in the mind of the health facilities for haemodialysis, peritonealcare providers, patients or their relatives, as well dialysis, blood banking, 24 hour emergency,as the administrators is the duration of hospital haematology and biochemical laboratory etc.stay of the patient. In malaria prone areas, many c. Catchment area: Patients come from urbanof the hospital beds in the referral centres are areas of Rourkela as well as surroundingoccupied by patients with malaria. The cost of villages, forested areas, mining localities etc.treatment depends on several factors, one ofthese being the period of stay. A simple scoring d. Subjects: All patients admitted to the Internalsystem was devised by Mishra et al to predict the Medicine Dept of Ispat General Hospital, 1survival of the malaria patients. A large number of Rourkela with confirmed malaria.the beds are occupied by these patients, during The study has two parts: (a) analysis of the malariathe peak transmission period, making it a major and (b) Multiple regression analysis.administrative problem. The LOS of admitted In the first phase, database was collectedpatients is one of the indicators of bed occupancy, prospectively in a format which includes age, sex,planning and rotation of staff deployment, etc and demographic data, treatment received before 2-4the resource utilization. (Kazembe et al. 2006; admission, biochemical and hematologicalVelip et al. 2006; Van Houdenhoven et al. 2007) reports, presence of seizures, treatment details,Similarly, from the point of view of the health care and the outcome. All those who expired were 17
    • excluded from the study. 700 patients with 62% were entitled patients (either employees orcomplete data were analysed. their dependants, or retired employees of theStatistics: steel plant: all of these get free medical treatment) and 38% were from different walks ofStudents t test was used to differentiate between life, including people from villages, township andmale vs female; adult vs children; Rural vs urban; traders. These patients were treated in thepatients with acute renal failure (sr Creatinine >3 hospital on payment basis. Their income and sociomg/dl), jaundice (sr Bilirubin > 3 mg/dl), severe economic conditions varied widely. 60% wereanemia (Hb < 5 gm/dl) or cerebral malaria from urban areas, and others were from suburbs(unarousable coma or GCS <10). or villages.The statistical analysis was done by using OpenEpi The comparisons of length of stay in differentversion 2.2.1 (2010), an Open Source groups are depicted in the Table-1. As it appears,Epidemiologic Statistics for Public Health, Version2.2.1. www.OpenEpi.com, accessed on 18 June the length of stay was significantly longer in2010 The difference is considered to be patients with severe anemia, acute renal failure,significant if p < 0.05. cerebral malaria and jaundice.In the second phase Multiple Regressions was Thus LOS was 2.87(±1.68) days when the patientperformed to find out the relationship of the was having uncomplicated malaria, which wentabove parameters and to get a linear equation. on increasing in presence of complications. Thus Determinants Characteristics No of patients LOS (± SD) P value Entitled Entitled 433 3.99(±2.00) 0.000* NE 267 4.95(±2.95) Sex Male 512 4.29 (±2.39) 0.299 Females 188 4.52(±2.61) Rural 257 4.62(±2.75) Residence area 0.000 Urban 443 3.91 (±1.73) Sr Creatinine >3mg/dl 29 8.66 (±4.45) Acute renal failure Sr Creatinine < 3mg/dl 671 4.17(±2.14) 0.000 GCS <10 61 7.41(±2.11) Cerebral malaria GCS >10 639 4.06(±2.08) 0.000 Hb<5.1 G 18 5.89(±2.65) Severe anemia HB>5 g/dl 620 4.37(±2.46) 0.027 Bil >3mg/dl 139 5.81(±3.33) Bil < 3 mg/dl 561 3.99(±2.03) Jaundice 0.000 Uncomplicated 390 2.87(±1.68) Single 181 4.33(±1.68) Complications Multiple 129 6.78(±3.53) 0.000 Oral drugs 115 2.97(±21.18) Level of treatment Parenteral (QBH/AS) 585 4.62(±2.54) 0.000 Table 1. Characteristics of malaria patients and LOSIt will be in the form of LOS was 8.66 (±4.45) days in presence of acute LOS = a1x1 + a2x2 + a3x3 + a4x4 + …… + C renal failure, 7.41(±2.11) days in patients with cerebral malaria, and 5.89 (±2.65) in presence ofObservations: severe anaemia and 5.81 (±3.33) in patients withIn the study we collected the data of those adult jaundice. LOS was longer in patients, who havepatients who survived and were discharged from come from rural areas, but there was nothe hospital. 700 surviving patients were analysed difference in males vs females.for the prediction of length of hospital stay. Out ofthese, 188 were females and rest were males. After the determinants were identified, a linear 18
    • equation was developed by using multiple patients are concerned regarding the length ofregressions. stay in a tertiary care hospital and the costLOS = 2.441+ 2.565 Severe anemia + 0.447 associated with it. We searched the literature to Jaundice +0.993 acute renal failure find out the studies related to LOS in malaria 1.405 cerebral malaria +0.657 Level of patients. But there were only two studies cited in therapy the MEDLINE by Kazembe et al. 2006 and Velip et 2,3The equation was made modified to make it al. 2006. However, several studies have beensimple and ready to use at bedside. carried out by Mounsey et al. 1995;. BannwartThus, et al., 1999; Arrahamyan et al. 2006; Clark et al., 2007 and Diringer et al., 2004 to predict the LOS inLOS = 2.5+ 2.5 Severe anemia + 0.5 Jaundice +1 other clinical conditions viz, very low weight acute renal failure neonates in nursery, sepsis in ICU settings, 1.5 cerebral malaria + 0.5 Type of therapy 5-9 patients after coronary surgery etc.Where, the severe anemia, jaundice, acute renal In a retrospective study in Spain, 1920 episodes offailure, cerebral malaria are considered as community-acquired pneumonia (CAP) in 27present=1, or absent=0; and level of treatment is community hospitals were analyzed by Cabre etoral anti- malaria treatment with chloroquin or 10 al. (2007) for inter-hospital variability in length ofquinine =1, parenteral artemisinine or quinine =2, Factors Beta P value Entitled or not 0.186 0.323 Residence 0.106 0.428 Severe anemia 2.565 0.000 Cerebral malaria 1.405 0.000 Jaundice 0.447 0.028 Acute renal failure 0.993 0.006 Level of therapy 0.657 0.000 LOS= 2.441+ 2.565 Severe anemia + 0.447 Jaundice +0.993 acute renal failure 1.405 cerebral malaria +0.657 Level of therapy simplifying the equation for ready bedside use LOS = 2.5+ 2.5 Severe anemia + 0.5 Jaundice +1 acute renal failure + 1.5 cerebral malaria + 0.5 Level of therapy or, LOS = ½ [5+ 5 x Severe anemia + 1 x Jaundice +2 x acute renal failure +3 x cerebral malaria + 1 x Level of therapy] Where, presence =1 , and absence = 0 for severe anemia, jaundice, acute renal failure and cerebral malaria. For level of therapy oral chloroquin or quinine =1, parenteral artemisinine or quinine =2, and any ICU intervention (ventilator, dialysis etc)=3 Table-2.: Multiple regression showing influence of factors on LOSand any ICU intervention (ventilator, dialysis hospital stay (LOS), mortality and readmissionetc)=3. rates. The overall adjusted LOS (mean+/-S.D.) wasDiscussion 10.0+/-9.8 days. LOS increased according to theMalaria being a disease mostly in the developing Pneumonia Severity Index (PSI) risk class: 7.3 dayscountries, the treatment is availed at different for class I to 11.3 days for class V (P<0.001). 2levels: (a) at home, (b) at the nearby health Velip et al. (2006) from Goa described thefacilities and (c) referral centre for severe malaria determinants of LOS in malaria patients. The studycases; where the patient is shifted to a hospital far indicated the importance of altered sensorium,away from own place of residence. Relatives of presence of liver involvement, duration of therapy 19
    • before admission as influencing factors. But a system. Malaria Journal, 2007; 6:24. doi:major flaw of the study was that most of the 10.1186/ 1475-1875-6-24.patients were uncomplicated ones. PUBMED 2. Velip AP, Kulkarni MS, Motghare DD, Vaz FS.search did not show studies on determination of Determinants of hospital stay amongLOS in severe malaria cases. Similarly publications malaria patients at a tertiary care hospital inare not available from any tertiary care hospital Goa. J Communic Dis, 2006; 38: 115-117which manages both uncomplicated and 3. Kazembe LN, Kleinschmidt I, Sharp BL.complicated cases. Patterns of malaria-related hospitalSome of the parameters in our study were similar admissions and mortality among Malawianto the Goa study. However, we have not been able children: an example of spatial modelling ofto find any difference among the males and hospital register data Malaria Journal 2006,females, urban vs rural on LOS. But, as expected 5:93 doi:10.1186/1475-2875-5-93the LOS is higher in patients with any or more 4. Van Houdenhoven M, Nguyen TD,complications. It was noted that all complications Eijkemans MJ, Steyerberg EW, Tilanus HW,are not similar, and they influence the survival in a Gommers D, Wullink G, Bakker J, Kazemierdifferent weighted capacity. Similarly they also G.Optimizing intensive care capacity usinginfluence the LOS. individual length-of-stay prediction models.When a very sick malaria patient is managed in Crit Care. 2007 27; 11 :R42critical care unit or high dependency unit, survival 5. Mounsey JP, Griffith MJ, Heaviside DW,is the most important concern. In a previous study, Brown AH, Reid DS. Determinants of LOS inMishra et al. (2007) proposed a simple prediction ICU and in hospital after coronary arteryrule for the survival of the patients with severe surgery. Br Heart J, 1995; 73: 92-98.malaria by assigning 1,2,3 and 4 to A (anemia), B 6. Arrahamyan L, Demirchyan A, Thomson(BUN↑ ), C (cerebral malaria) and D (Dyspnoea/ ME, Hovaguimian H. Determinants ofARDS) respectively. The malaria score for adults morbidity and ICU stay after coronary(MSA) ranges from 0 to 10. The mortality was 2% surgery. Asian Cardiovasc Thorac Ann,for MSA 0 – 2; 10% for MSA 3–4, 40% for MSA 5–6 2006; 14: 114-118.and 90% for MSA 7 or more. The sensitivity is 7. Bannwart BC, Rebello cerebral malaria,89.9% and positive predictive value is 94.1% when Sadeck LSR, Pontes MD, Ramos JLA, Leone5 is taken as the cut off value. C. Prediction of Length of Hospital Stay in In the present one, we derived a very simple Neonatal Units for Very Low Birth Weightprediction rule for the LOS. It does not involve Infants. J Perinatology, 1999; 19: 92-96sophisticated data collection, estimation or 8. Clark DE, Lucas FL, Ryan LM. Predictinganalysis. Still it extends valuable information, hospital mortality, length of stay, andwhich will be helpful to the clinicians. In addition, transfer to long-term care for injuredthe formula can be used to modify the result/ patients. J Trauma, 2007 ;62:592-600.prediction in the course of time if any new 9. Diringer MN, Reaven NL, Funk SE, Uman GC.complication arises. Elevated body temperature independentlyHowever, we have analyzed the data of only one contributes to increased length of stay inyear, and that too only among the adults. It is neurologic intensive care unit patients. Critproposed that such studies may be undertaken Care Med. 2004 ;32 :1489-95.among children too. It should also be validated in 10. Cabre M, Bolivar I, Pera G, Pallares R;cohorts from different geographical regions. Pneumonia Study Collaborative Group.Acknowledgement: We extend sincere thanks to Factors influencing length of hospital stay inthe staff of IGH and malaria research Unit. community-acquired pneumonia: a study inFunding: None, Conflict of interest: None 27 community hospitals. Epidemiol Infect. 2004 Oct;132(5):821-9.Velip AP, KulkarniReferences: MS, Motghare DD, Vaz FS. Determinants of1. Mishra SK, Panigrahi P, Mishra R, Mohanty hospital stay among malaria patients at a S. Prediction of outcome in adults with tertiary care hospital in Goa. J Communic severe falciparum malaria- a new scoring Dis, 2006; 38: 115-117 20
    • Case reportsPeutz- Jeghers Syndrome presenting as acute intestinalobstruction due to Jejunal Intussusception in an adult maleAmulya M Acharya Address for communication :Sishir R Dash Dr A.M.Acharya, Sr Deputy Director, Deptt. of Surgery, Ispat General Hospital,Manoja K Panigrahi Rourkela, Odisha, IndiaDeptt. of Surgery Email:dramulya.acharya@gmail.com and digits. The most common symptoms areABSTRACT recurrent pain abdomen, anemia, malena andPeutz – Jeghers syndrome (PJS) is a rare familial hematochezia. Here we are reporting a case of PJSautosomal dominant disorder with presented as acute intestinal obstruction due tohamartomatous polyposis of G I Tract and melanin jejunal intussusception in an Indian adult male.pigmentation around mouth, oral mucosa , lips We are providing some clinical photographs,and digits. Most common symptoms are histopathology report and added discussionrecurrent pain abdomen, anaemia and blood in available from the scarce literature which may bestool. Presentation of frank intussusception and of educational importance.intestinal obstruction in adults is uncommon. We Case report:are reporting a case of Indian adult male A 58 years old Indian male was admitted in thepresented to us in acute intestinal obstruction due surgical ward with sudden onset of severeto jejuno jejunal intussusception. There were abdominal pain associated with vomiting of threemultiple polyps in the small gut and one large days duration. He was found afebrile, anemic andpolyp of 4cm x 8cm was the lead point in triggering dehydrated. Pulse 98/min, BP 100 / 70 mm Hg.the intussusception. Histopathology confirmed Abdomen was distended with diffuse tendernessthem as hamartomatous polyps typically seen in and guarding. An ill defined soft immobile massPeutz- Jeghers syndrome. As it is unusual to see (15 x 8 cm) was palpable in the epigastrium. Somesuch rare case in clinical practice and scarcity of bluish black pigmentation was seen over hisliterature, we feel to report this for the benefit of buccal mucosa but could not be correlated withclinicians and students. Awareness of the disease the acute abdominal condition (Fig.1).is helpful for proper diagnosis, early managementand follow up with genetic counseling to thepatient and his family.Key words:Peutz, Jeghers,PJS, polyposis, intestinal polyps,melanin pigmentation, intussusceptionIntroduction:Adult intussusception is rare and do not presentthe symptoms of red currant jelly stool that is seen 1in children. Very rarely multiple intestinal polypsseen in the familial disorder Peutz- Jegherssyndrome (PJS) with the typical muco- cutaneous Figure 1:pigmentation around mouth, oral mucosa lips Bluish-black pigmentation over buccal mucosa. 21
    • One large polyp of 3.5cm with a 8cm stalk wasfound on per rectal examination (Fig.2). Figure 3b Intussuscipien inside intussusceptum. Figure 2 triggering the intussusceptions (Fig.4a,b). Rectal polyp 3.5cm with 8cm long stalk About two feet of jejunum involving theBiochem reports were normal except low protein intussusception and having multiple polyps was(total protein 4g and albumin 1.9g). X-Ray excised and end to end anastomosis doneabdomen showed few air-fluid levels. Ultrasound followed by rectal polypectomy. Rest of the smallof abdomen revealed two concentric echo and large gut was thoroughly palpated and foundstructures with classical target sign suggestive of to be normal. Patient recovered uneventfully.intussusception (Fig.3a, 3b). Emergency Histopa-thology of resected jejunum with polypslaparotomy was taken up with a provisional showed branching of smooth muscles arising fromdiagnosis of acute intestinal obstruction. muscularis mucosae into the stroma of columnarLaparotomy revealed jejuno-jejunal intussuscep- and goblet cells which are typical hamartomatoustion about one foot distal to duodeno-jejunal changes seen in Peutz- Jeghers syndrome (Fig.5).flexture involving two feet long segment of There was no evidence of atypia or malignancy.jejunum. Multiple polyps were seen on the Lymph nodes showed reactive hyperplasia.involved jejunum. There was one large polypoidal The case was finally diagnosed as Peutz-mass of 4cmx8cm which was the lead point in Jeghers syndrome with unusual presentation of acute intestinal obstruction duo to adult intussusception. Figure 3a US abomen showing target sign Figure 4a Multiple polyps in jejunum. of intussusception. 22
    • dominant disorder occurs due to subtle loss of chromosome 19p 13.3 4 due to defect in serine/ threonine kinase gene (STK11/LKB 1). Sporadic PJS can rarely occur. The incidence of PJS is one in 60,000 – 3,00,000 population and not specific to any sex or race. The polyps in PJS most commonly found in jejunum, ileum; but can occur in any part of GI tract. The melanin spots found small flat, brown or dark blue and commonly found around the mouth, lips, and buccal mucosa. The pigmented spots may fade after puberty. Figure 4b large polypoidal mass which had triggered the intussusception. Different associated anomalies have been reported in PJS. Dormandy et al 5 reported polypsFollow up investigations were carried out. His in bladder, renal pelvis, bronchus and nose . Rarelyupper GI endoscopy and colonoscopy did not polyps in ureter, gallbladder and CBD may occur.reveal any polyp. Ba-meal follow through was Even ovarian cyst adenoma and Sertoli tumor ofnormal. We could not do the genetic study due to testes are reported.lack of facilities. Morbidity and Mortality: Small intestine obstruction and intussusception occurs in 43% cases of Peutz-Jeghers syndrome but usually seen in children. In our case an adult male presented with frank jejuno-jejunal intussusception and intestinal obstruction due to an unusual large polyp of 4x8 cm. Very few such cases have been reported from India.6,7 Malignant potential of GI tract is very high in these patients, as reported by various investigators. Giardiello 8 et al found 93% cumulative risk of developing cancer (15.2 fold relative risk, RR) by the age Figure 5 Branching of smooth muscle into the stroma of the epithelium. 64years The relative risks (RR) for cancer formation in PJS in relation to general populationThe patient and his family members are now in are: Small intestine (RR 520), stomach (RR 96),regular follow up. pancreas (RR 132), colon (RR 84), oesophagus (RRDiscussion: 57), ovary (RR 27), lungs (RR 17), uterus (RR 16)Peutz- Jeghers syndrome (PJS) is a familial disorder and breast (RR15).with two distinct features, (a) multiple Management:hamartomatous polyps of GI tract and (b) melaninpigmentation around mouth, oral mucosa and Giardiello and Trimbath published a review of PJSdigits. The syndrome first described by Jan Peutz and recommended the following managementin 1921 and later published in detail by Harold and follow up 9. 2Jegher in 1949 . First case was reported by • Polypectomy of isolated polyps > 1cm in 3A.K.Basu in 1952. The disease is an autosomal stomach, colon 23
    • • Resection of intestine segment having 2. Jeghers H, McKusick VA et al. Generalised confluence of polyps intestinal polyposis and melanin spot s of oral mucosa, lips and digits. N Eng J Med • Resection anastomosis for intussusception 1949; 241: 993-1005, 1031-6. • Intra operative push enteroscopy and 3. Basu, A. K.: Familial intestinal polyposis with polypectomy of >1cm polyps. pigmentation of skin and mucousRecommended follow up: 9 membrane. Lancet 1952, 2: 586-587. 4. Hemminki A, Tomlinson I, Markie D, et al 1. Annual physical exam. of breast, abdomen, Localization of susceptibility locus for Peutz- pelvis( ovary), testes Jeghers syndrome to 19p using comparative 2. US for pancreas, ovaries, testes annually genomic hybridization and targeted linkage analysis . Nat Genet 1997; 15: 87-90 3. Mammography / MRI, Pap smear every year 5. Dormandy TL, Gastrointestinal polyposis 4. Annual complete blood cell count with mucocutaneous pigmentation ( Peutz- 5. Ba-meal follow through every 2 year Jeghers syndrome) N Engl J Med 1957; 256: 1141-6 6. EGD & colonoscopy every 2 year 6. Saxena PK, Arora RK, Mehta, Singh HH. 7. Genetic counseling and screening from birth Peutz-Jeghers syndrome with unusual of all first-degree relatives. features (a case report). J Postgrad Med 1986 ;32:236-8CONCLUSION: 7. Thakker HH,Joshi A,Despande A, PeutzPJS is a rare familial disease involving multiple Jeghers syndrome presenting as jejuno ilealpolyps of GIT and mucocutaneous pigmentation intussusception in an adult male: A casearound mouth, lips, oral mucosa and digits. report. Cases J,2009 Aug 2:8865Common C/F are recurrent pain abdomen, 8. Giardiello FM, Brensinger JD, Tersmette AC ,anemia, GI bleeding. Acute Intestinal Obstruction, Vary high risk of cancer in familial Peutz-Intussusception are common complications. Jeghers syndrome. Gastroenterology , DecDevelopment of cancer is relatively high. Early 2000;119(6): 1447-53.diagnosis and proper M/M can reduce 9. Giardiello FM, Trimbath JD, Peutz- Jegherscomplications. Genetic counseling & screening of syndrome and management recommen-family members should be done as there is high dations. Cin Gastroenterol Hepatol,2006; 4:risk of development of cancer. 408-15.REFERENCES : 10. Clava D,Howe JR. Hamartomatous polyposis 1. Agha FP, Intussusception in adult. Am J syndrome. Sur Clin North Am 2008 Aug; Roentgenol 1986 March;143(3): 527-31 88(40) : 779-817 24
    • Case ReportsNecrotising Fasciitis In Neonates – Case ReportRadhanath Satpathy Nimain C Nanda Pitabas MishraUNMC NICHD Deptt. of Paediatrics Deptt. of PaediatricsResearch NetworkPinaki Panigrahi Rajan K BeheraProfessor and Director, Deptt. of SurgeryCenter for Global Health and DevelopmentCollege of Public Health , University ofNebraska Medical Center, USA Address for communication : Dr. R. Satpathy, Sr. Consultant, UNMC NICHD Research Network Email: Globalnet_rkl@yahoo.comAbstract: of 3 days duration. The baby was deliveredNecrotising Fasciitis (NF) is relatively a rare disease normally in hospital and was weighing 2.8 kg. Earlyfound in adults. When occur in neonates, its neonatal period was uneventful. It was all alongoutcome is usually fatal. Two rare cases of breastfed. On Day-15, baby had fever and wasNecrotizing fasciitis (NF) have been reported with crying inconsolably. Next morning, motherpossible rare association of trisomy. noticed an area of redness on the back that rapidly spread all over the lower half of the back withKeyword: ulceration. On examination, baby was febrile,Necrotising Fasciitis, Neonate irritable, sucking from mother, pink with featuresIntroduction: of trisomy and had no other focal sign of infectionNecrotising fasciitis (NF), otherwise known as the than an ulcerated area of 6x4 cm, seen beingFlesh Eating Disease, is a term that describes a surrounded by deep brown dead tissue on thedisease condition of rapidly spreading infection back. The floor of the ulcer was showing musclesusually located in fascial plane of connective tissue of the back and oozing of pus. Margin was muchthat results in tissue necrosis1. Although the irregular and was looking like punched out ulcer. Itcondition was described earlier, Dr B Wilson was treated with combination antibiotics, dailytermed the condition in 1952 2. The disease occurs dressing of wound and wound debridement asinfrequently and almost can occur in any part of and when necessary. Total count wasthe body. The spread of infection can be so fast 6400/cm,Hb-14.5/dl, and blood group was B+ve.that it is difficult to stop it with both antimicrobial Blood culture and wound swab culture did notdrugs and surgery. It is predominantly an adult reveal any organism. Though, baby improved withdisorder. When it occurs in children the course is therapy, parents took discharge against medicalusually fatal. Less than a 100 Neonatal NF cases advice on D10 and the baby expired at homehave been reported in literature. The purpose of after 3 days.this communication is to report two rare cases of Case-2 (Figure2) Baby of BS, was admitted toneonatal NF with fatality. hospital on Day 11 with complaints of unable toCase-1 (Figure1) Baby of SA was admitted to take feed properly, ulceration of mouth of 2 dayshospital with a big area of ulceration on the back duration and a swelling on the back with bluish- 25
    • Figure 1 Showing lesion on back Figure 2 Early changes on the backred discoloration and painful to touch of one day Vancomycin was added to the regimen andduration. He was born in hospital to a multi-para continued for 2weeks. The skins including themother by normal vaginal delivery and cried soon deep tissue were shredded (Fig-2) and woundafter birth. There was premature rupture of debridment was done, the area affected was dailymembrane for a week. There was no maternal cleaned and dressed, dead tissues were removed.fever or any other sickness. Soon after birth, baby Anemia, edema and fever continued for long timewas fed breast milk and had some oral ulceration. and the baby was somewhat better by 3 weeksOn examination baby was febrile (temp 102 0 F), hospital stay.lethargic, pale and weighing 2.8kg. Heart rate was During the course of stay, the baby continued to140 and respiration rate was 44/minute. There have fever all the time and sick. There was edemawas jaundice but no cyanosis. All peripheral of limbs, abdominal distension and conjugatedpulsations were felt and capillary refill time was hyperbilirubinemia. As the baby developedless than 4 seconds. Ears and anterior fontanel anemia and low general condition, it received twowere normal. Oral thrush was there. A big bluish units of blood transfusion. Both medical andred discolored area was on the back measuring surgical management and crisis management ndnearly 3X4” size without any ulceration or oozing continued for 22 days. On 22 day of(Fig-2). It had an area of central fluctuation. A hospitalization, baby had cardiac arrest and couldmany vesico-pustular lesions were detected on not be revived.the peri-umbilical area and back on gluteal region. DiscussionCardiovascular and respiratory systems and Necrotising fasciitis is a rare condition in neonates.abdominal examination were normal. Neonatal Terms like necrotising fasciitis, myonecrosis, andreflexes were poorly elicitated. Necessary necrotising adipositis refer to classification byinvestigations were done and pulse oxymetry depth of infection. Type 1(polymicrobial) and typeshowed 95 to 99% saturation. 2 (monomicrobial) infections refer to classificationThe baby was put on combination antibiotics based on microbial cause. Historically, necrotizing(Cefrtriaxone and amikacin) and managed in infections were classified according to anatomicalpediatric ward. Surgeons saw the baby and sites. Fournier gangrene (involving the perineum)aspirated sero-sangunous fluid on D-2. Baby and Ludwigs angina (involving sub-mandibularcontinued to be febrile, sick and had abdominal and sublingual spaces) are examples. Thesedistention. Wound sloughed out and a raw area infections were named after the physicians whodeveloped by D-4. Vital signs were unstable and first described those 1 . NF is frequentlybaby was put on IV fluid and pressure amines. By attributable to secondary infections. They are likeD-5 there was edema, fever, respiratory distress, omphalitis, mammitis, balanitis, postoperativerefusal to feed and abdominal distension. complications, and bullous impetigo, and may be 26
    • associated with diabetes mellitus, necrotising Early diagnosis and aggressive surgical treatmententerocolitis, immunodeficiency, malnutrition3 reduces risk; however, it is often difficult andand septicemia. Both the babies were neonates patients are treated for simple cellulitis until theyand were diagnosed in hospital at the interval of rapidly deteriorate. Prompt diagnosis with 5five years, proving the rarity of the condition. If it is aggressive therapy improves survival . Antibioticnot suspected, the diagnosis is missed. The most therapy is mandatory and early surgicalcommon site of involvement in pediatric patients exploration and debridement is critical to ensure ais the abdominal wall followed by the thorax, back, good outcome. Microbiologically, until blood 4extremities with head and neck as unusual sites . culture results are available, wide spectrumIn our case, classically neonates had the back coverage with intravenous antibiotics is started.involvement. These antibiotics should cover S pyogenes, SThe initial skin presentation ranges from a minimal aureus, and Gram-negative aerobes andrash to erythema, oedema, induration or cellulitis. anaerobes as clinically indicated. Group A BetaThese lesions spread rapidly. The overlying skin hemolytic streptococci (GABHS) has beenmay later develop a violaceous discolouration, reported widely as a single pathogen. Appropriatepeau dorange appearance, bullae, or necrosis. therapy includes IV Penicillin150 000u/kg/day in 4Our second case (Fig-2) had the classical divided doses, Clindamycin 40mg/kg/day in 4presentation and was detected and treated from divided doses and Vancomycin40mg/kg/day in 3-the 2nd day of occurrence. Continued fever and 4 divided doses6.tachycardia was seen in both the cases. Marked References:tissue oedema, rapid progression of inflammation 1. Medicine Net.com- assessed on 26.10.2010and signs of systemic toxicity were seen in the 2. Hsieh WS, Yang PH, Chao HC, Lai JY. Neonatalsecond case. Death occurred before surgery or necrotizing fasciitis: a report of three cases andshortly after surgical intervention as a result of review of the literature. Pediatrics 1999;b a c te r i a l i nfe c t i o n w i t h s e pt i c s h o c k , 103:e53.disseminated intravascular coagulation and/ormultiple organ failure. Our second case died due 3. Antonio FM, Pedro GC; C DM, Carola DM; Luzto multi-organ failure. Empirical antibiotics to Orozco-C, Tamayo-S; Ramon RM Necrotizingcover (Cephalosporin and aminoglycoside) gram Fasciitis, Report of 39 Pediatric Cases, Archpositive and negative organism were used, to start Dermatol. 2002; 138: 893-899.with. Subsequently vancomycin has been used in 4. Kothari PR and Kulkarni B, Neonatalsecond case. We had two different cases, one Necrotizing Fascitis, Indian Pediatrics: 2004,presented while skin shredding has occurred (Fig-1) 41:1070-71and the other at the onset of the disease (Fig-2). 5. Moss RL, Musemeche CA, Kosloske A M.Case one, with medico-surgical management had Necrotising fasciitis in children: promptstable vital signs but died at home on discharge recognition and aggressive therapy improveagainst medical advice, whereas case two had all survival. J Pediatr Surg 1996 ; 31:1142–6.complications of neonatal sepsis and did not 6. Textbook of Pediatric Infectious Diseases, 6thsurvive after a long duration of hospital stay, thus Edition, Saunders, Philadelphia 2009; pg79-791showing the fatality. 27
    • Case ReportsSquamous cell carcinoma & basal cell carcinoma withxeroderma pigmentosa – a rare presentationAruna M Minz Niranjan K Behera Rabi R PandaDeptt. of Pathology Deptt. of Dermatology Deptt. of PathologySanghamitra Satpathi Prativa K BeheraDeptt. of Pathology Deptt. of Pathology Address for communication :Usha Das Dr. Aruna Mukti Minz, Specialist,Deptt. of Microbiology Department of Pathology, Ispat General Hospital, Rourkela e-amil : arunaminz@yahoo.com 2Abstract : Japan i.e. 1: 40,000 but in Indian scenario itsXeroderma pigmentosum with squamous cell frequency is not yet calculated because of itscarcinoma and basal cell carcinoma is rarely rarity. To our knowledge, dual malignancy i.e.reported. A 22 years female having Xeroderma Squamous Cell Carcinoma (SCC) and Basal CellPigmentosum presented with ulcerated and Carcinoma (BCC) associated with XP is rarelyblacklish pigmented lesion on Sun exposed area of reported in India.body. Histopathological examination of the three Here we report a case of XP with different stagesdifferent skin biopsy showed squamous cell of skin manifestations.carcinoma, basal cell carcinoma & initial phase of CASE REPORT:Xeroderma pigmentosum. Case is being 22 year female presented with various pigmentedpresented because of the rare association of these lesion on face and hand (Fig1). Pigmented lesiontumors with Xeroderma pigmentosum in Indian on face was since childhood. On examination shescenario. It is also observed for the first time in had an ulcerated lesion over forehead with rolledIGH, Rourkela.Keywords:Xeroderma pigmentosum, squamous cellcarcinoma, basal cell carcinomaIntroduction:Xeroderma Pigmentosum (XP) is a rare geneticallyheterogenous autosomal recessive disorderresulting from the defect in DNA repairmechanism i.e. Nucleotide Excision Repair (NER).It is characterized by photosensitivity, pigmentarychanges, premature skin ageing and variouscutaneous and internal malignancies at an earlyage. XP was first described by Herba and Kaposi in 11874. It occurs with an estimated frequency of1:250,000 in US and somehow more common in Fig1. Pigmented lesions on face 28
    • and getting aggravated after sun exposure. Family history was not significant. Systemic examination was unremarkable and intelligence was normal. Skin biopsies were taken from the face and hand lesions. Histopathological examination showed three different lesions. Biopsy from cheek showed features suggestive of first stage of skin changes of XP i.e. hyperkeratosis, thinning of stratum malpighi with hyper-pigmentation (F-2), biopsy from forehead showed features of BCC (F-3) and biopsy from hand showed features of well differentiated SCC.4 (F-4). Fig2. 1st Stage of Skin Changes of XP Discussion: Xeroderma Pigmentosum is a rare inherited disease. The incidence is approximately 1:250,000 in US and somehow more common in Japan i.e. 1:40,000.2 The defect is autosomal recessive genetic defect in which NER enzymes are mutated leading to reduction in or elimination of NER. There are seven groups of XP i.e. XPA to XPH and one more type which is XP variant. Out of these XPA is common and XPE is rare.3 XP patients are at a high risk for developing skin cancers at an early Fig 3. Basal Cell Carcinoma (H&E) age as compared to normal individual and these cancers are commonly BCC, SCC & malignant melonoma. In our case, the patient had both BCC and SCC. The disease typically passes through three stages. The first stage appears after the age of six months characterized by different erythema, scaling and freckle like area of increased pigmentation on the sun exposed areas. The second stage is characterized by skin atrophy, telangiectasis and mottled hyper-pigmentation. The third stage is presented by numerous malignancies including SCC, BCC, malignant melanoma and fibrosarcoma. These cancers may Fig 4. Squamous Cell Carcinoma (H&E) present as early as 4-5 years of age. As our case had two varieties of malignancies i.e. SCC and BCC,out border clinically diagnosed as BCC, she progressed to the third stage of the disease.hypertrophied lesion on cheek clinically Occular problem occurs in 80% cases includesdiagnosed as actinic keratosis and scarring lesion photophobia, conjunctivitis, ectropionon right hand clinically suggestive of SCC. She also symblephoron with ulceration and malignancies.had photophobia .The lesions were progressive Our patient had Photophobia. 29
    • Neurological problems are seen in nearly 20% of References:cases which includes microcephaly & Mental 1. Hebra F, Kapsosi M. On diseases of the SkinRetardation (MR). De Sanctis cacchione syndrome including the exanthemata. Vol.3 ( translated byrefers to the combination of XP & MR and W.Tay) London: The new Syderham Societycerebellar ataxia, hypogonadism and dwarfism.3 1874;252-8.In our case, she had absolutely normal 2. Robbins JH, Kraemer KH, Lulzner MA, Festoffintelligence. Prenatal diagnosis can be made by BW, Coon HG. Xeroderma Pigmentosum, anamniocentesis. inherited disease with Sun sensitivity, multiple Cutaneous neoplsia and abnormal DNA repair.Xeroderma pigmentosum is a progressive disease Ann intern Med 1974; 80:221-48.and patient dies due to complications of various 3. J.I.Harper, R.C.Trembath . Genetics andmalignancies. So the management of XP patient Genodermatosis in : Rooks Text book ofneeds protection from sunlight by every possible th Dermatology.7 Edn. Blackwell 2004; 12.56-means. Early and adequate excision & 12.61.radiotherapy of all tumors are preferred. Our case 4. Lever WF , Schaumberg-Lever G. Congenitalwas referred to higher centre for Radiotherapy. Diseases. In: Lever WF, Schawmberg-Lever G. eds.The relatives of known cases must be screened to th Histopathology of Skin. 9 Edn. Philadelphia: JBdetect any genetic defect at early possible stage. Lippincott 2005; 147-148. Editorial Declaration Copy right of the manuscripts, letters and photographs published in the Proceedings of Ispat General Hospital is vested with the contributors of the material. "Authors and contributors are free to publish or present their research work anywhere else only under intimation to the editors of this publication. 30
    • Case reportsMultiple brain metastases due to occult Papillary Carcinoma ofthyroid gland: A Case ReportRabindra N Mohapatra Sudhiranjan Pradhan Rabiratna PandaDeptt. of Neurosurgery Deptt. of Radiology Deptt. of pathologyPushpa Kumari, Saropani Hembram Address for communication :Deptt. of Ophthalmology Deptt. of Neurosurgery Dr.R.N.Mohapatra, Neurosurgery Department, Rourkela-769005, India. e-mail: rkl_rabi@in.comAbstract : complaints of weakness of left upper limb for twoBrain metastases from papillary thyroid months and headache off and on for the samecarcinoma (PTC) are extremely rare with a period. She further revealed that she was havingfrequency of only 0.1 to5 percent. Mostly they are tingling sensation on her left side limbs at times.first detected during the course of treatment of Her higher functions were normal. She was havingPTC. With the publication of case reports of brain gross papilledema on both sides but rest of hermetastases from clinically silent PTC and cranial nerves were normal. Her power aroundimportance of tissue diagnosis to treat this the left shoulder joint, elbow was grade 3/5, at thecondition, as it may need radio iodine therapy, wrist and grip of same side was grade 2/5.Thereintense thyroid work-up may be needed, in brain was spasticity in left upper limb but no additionalmetastases, with unknown primary. movements. No sensory deficit could be detected in her body including her left upper limb, thoughKeywords: she was complaining of tingling sensation. Deepmetastases brain, papillary carcinoma thyroid, tendon reflexes were normal all over except in leftsilent, occult, unknown primary. upper limb, where they were exaggerated. HerIntroduction: cortical and cerebellar functions as well as gaitPapillary thyroid carcinoma rarely spreads to were normal. All other systems, including thebrain.1 We, here, report a case of extensive brain thyroid gland, were normal on clinicalmetastases with undetectable primary and examination. Her hemogram, biochemical reportsclinically normal thyroid gland. Due to recent and ski gram of cervical spine were within normalpublications, detail thyroid work-up with different limit. Her computerized tomogram (CT) of theimaging modalities in conjunction with fine brain showed multiple ring enhancing lesionsneedle aspiration cytology led to suspicion of PTC. distributed in both the hemispheres andIt was corroborated by the tissue diagnosis of cerebellum (Figure1). Magnetic Resonance (MR)brain lesion. Incidentally, more than 20 countable imaging and spectroscopy suggested secondarymetastatic lesions in the brain, is being reported deposits in brain. With the provisional diagnosisfor the first time. of multiple metastases of brain, attempt wasCase History: made to find out the primary lesion.A 52 years married lady presented at Accordingly, she was again examined thoroughlyNeurosurgery department of our hospital with and investigated with ski gram and CT scan of 31
    • which revealed predominantly papillary architecture with evidence of malignancy (Fig2). The lady was referred to a premier oncology center for consideration of radiotherapy (RT). While she was undergoing radiation therapy her general condition deteriorated and she withdrew her consent, for thyroidectomy and radio iodide therapy, (after receiving 30 Gy RT over 10 sittings). She had undergone Tco4-thyroid scan, which revealed photon deficient area in both the lower poles of thyroid, diffuse increased tracer concentration in both hemispheres of brain. These were highly suggestive of PTC with metastatic deposit in brain. At the end of 3 Figure1. Contrast enhanced CT scan of brain shows multiple enhancing ring lesions in brain with months, the lady is having good cognitive surrounding oedema. function, weakness of left half of body improv ed, needs support to walk and to carry out her day tochest, ultrasonic examination of abdomen and day activities. She is on steroid and prophylacticpelvis, all of which were unrevealing. Her anticonvulsant only.mammary glands were normal. On suspicion, she Discussion : PTC is the most common thyroidwas advised ultrasonic examination of thyroid, 1, 2, 3 neoplasm. Distant metastases occur in only 5though the gland was clinically normal. It revealed to 14% cases. The most common sites for distantone solid nodule of size 6 millimeter (mm) in metastasis of PTC are the lungs, followed by thediameter on right lobe and the other one on left bone. Brain metastasis from PTC is extremelyside, which was cystic and of same size. 1, 2, 3, 4, 5Ultrasound guided fine needle aspiration cytology rare. Total 23 cases are reported in literature. 1(FNAC) was done from both the lesions. FNAC CT scan, MRI and MR spectroscopy all may helpfrom the solid nodule was suspicious of papillary to diagnose metastases in brain, but they cannotcarcinoma. help to identify the primary lesion. As PTC is not known to cause metastases to brain, frequently detail work-up of thyroid gland is neglected, when it is clinically silent. Ultrasonic examination of the thyroid gland followed by FNAC may help to clinch the pathology, as in our case. Radio Iodine uptake is very rare in brain metastases from PTC, probably due to the poor penetration of blood brain barrier by the radio isotope. 6 Tco-4 thyroid scanning may support the diagnosis. Surgery, radiotherapy, and radioactive iodine Figure2. Histopathology of the brain lesion in low power magnification shows prominent therapy are the available modalities for treatment papillary architecture of PTC with brain metastases, along with total 1,7Thyroid scanning with radio iodine revealed a cold thyroidectomy. But these modalities arenodule on right lobe but a normal brain. To clinch dependent on tissue diagnosis. If primary diseasethe diagnosis, craniotomy and excision of 2 lesions can be detected initially, it may be possible tofrom right frontal lobe was done. The excised avoid craniotomy and treat the primary diseasespecimen was sent for histopathology study, early. 32
    • Median survival of thyroid malignancy, once brain Thyroid Carcinoma in Brain: Report of Threemetastases have occurred varies between 4.7 to Cases. The FASEB Journal 2008; 22:706-25.9.4 months. 7, 8 4. Tsuguhito O, Yukihiro B, Masamichi H,Metastases from papillary carcinoma of thyroid, Nobuyoshi T, Yasushi T, Yoshio K , Masakiyo F.though rare, are being reported by different Papillary Carcinoma of the Thyroid withauthors. When brain metastases are detected Distant Metastases to the Cerebrum: a Casefrom unknown primary, thyroid gland should be Report. Japanese Journal of Clinicalinvestigated in detail for the primary lesion Oncology 2001; 31:112-5because treatment modalities may be different in 5. Brunicardi FC, Andersen DK, Billiar TR, Dunnthis type of disease. We found ultrasonic DL, Hunter JG, Matthews JB, Pollock RE,examination followed by fine needle aspiration Schwartz SI: Schwartzs Principles Of Surgery.cytology to be fruitful procedure in this regard. 8th edition. New York: McGraw-Hill; 2005.References: 6. Misaki T, Iwata M, Kasagi K, Konishi J. Brain metastasis from differentiated thyroid1. Saleh FA, Abdullah SA, Wafa AS .Abdullah ST. cancer in patients treated with radioiodine Cerebellar mass as a primary presentation of for bone and lung lesions. papillary thyroid carcinoma: case report and literature review. Head & Neck Oncology Ann Nucl Med 2000;14:111-4. 2009; 1:23doi:10.1186/1758-3284-1-23 7. Biswal B M, Bal CS, Singh MS, Padhy AK, Rath2. Erem C, Hacihasanoglu A, Sari A, Reis A, GK. Management of intracranial metastases Alhan E, Cobanoglu U, Onder Ersöz H, Ukinç of differentiated carcinoma of thyroid. K. Intrathyroideal papillary thyroid Journal of Neuro-Oncology 1994, 22:77-81 carcinoma presenting with a solitary brain 8. Chiu AC, Delpassand ES, Sherman SI. metastasis. Endocrine 2004;25(2): 187-93 Prognosis and treatment of brain metastases3. Jianyi Li, Kenneth D Aldape, Gregory N in thyroid carcinoma. J Clin Endocrinol Metab 1997; 82:3637-42. Fuller,Suzanne Z Powell. Metastatic PapillaryKey to the Practice Paper1c, 2b, 3d, 4b, 5b, 6b, 7e, 8b, 9a, 10b, 11a, 12a, 13a, 14a, 15b, 16c, 17a, 18b, 19a, 20b, 21b, 22a, 23a, 24b, 25a,26b, 27a, 28c, 29d, 30a, 31e, 32a, 33b, 34a, 35d, 36d, 37a, 38d, 39d, 40b, 41a, 42c, 43c, 44d, 45b, 46c, 47d 33
    • Case ReportsUnusual case of severe SepsisRajyabardhan Pattnaik Sanjib Mohanty Sradhananda MohapatraCritical Care Unit, Deptt. of Internal Medicine Deptt. of Internal Medicine Address for correspondence: Dr. Rajyabardhan Pattnaik , Critical Care Unit, Ispat General Hospital, Rourkela e-mail : rajyapattnaik@yahoo.co.inAbstract: antibiotic therapy and organ support treatment failed to resolve her condition.Treatment of sepsis is often difficult andchallenging. The problem is aggravated in diabetic Case Report: A 44 year old female a known case ofpatients. The treatment is based broadly on Type II diabetes mellitus, hypertension,diabetic control, broad spectrum antibiotic hypothyroid was admitted with history of fever,therapy, ventilator support, dialysis and other loose motion for last three days. Fever was notsupportive therapy, may not be sufficient for the associated with chills or rigor. It was intermittent type and low grade. The loose motion was wateryrecovery of the patient. Mortality in sepsis with 1 and six to seven times a day. There was no historymulti-organ failure is around 65%. We report one of cough, vomiting, itching. At the time ofunusual case of severe sepsis which ultimately admission her GCS was 15, pulse 102/ minuteresponded to anti-fungal treatment. regular, all peripheral pulses were well felt, BP-Key words: 80/60 mm Hg, chest was clinically clear, heartSepsis, Diabetes, Antifungal. sounds were normal. She was admitted to generalIntroduction: ward. Her hypotension did not respond to fluid challenge and her sensorium deteriorated, so sheSepsis in cases of diabetes has poor outcome. was shifted to ICU. Her chest x-ray showedDiabetic patients are immunocompromised shadowing in the left lower zone. She developedhence multi organ involvement is much more acute renal failure .So she had a central line placedfrequent then in non diabetics. Infection or and fluid replacement was done with frequentinflammation leads to poor glycemic control which measurement of the central venous pressure. Sheperpetuates severe infection leading to sepsis and was intubated and ventilated in pressuremulti organ failure. Patients treated in ICU with broad controlled mode. In spite of adequate fluidspectrum antibiotics and on ventilator support are replacement her urine output decreased andmore prone for opportunistic infection like yeast, hypotension persisted. So she was put onfungus, etc.2,3 inotrope support and peritoneal dialysis startedWe report such a case of diabetes mellitus with and continued for 40 two litre exchanges withsevere sepsis who ultimately responded to indwelling time of 20 minutes for each exchange.empirical anti fungal treatment after adequate All the investigation reports are in the table no: 1 34
    • DateInvest 22/8 24/8 27/8 29/8 2/9 5/9 7/9 9/9 12/9 15/9 17/9 21/9Hb 10.6 10 8.7 7.8 9.2 4.6 11.9 11.3TLC 5700 18800 22000 34200 34300 19900 35900 13500 13100 10000FBS 62 300 168 94 198 176 156 204 191 159 172 144Urea 72 76 41 86 96 44 22Creat 3.5 4.7 2.9 3.4 2.9 1.6 1.1 1.1 1Na 125 136 134 137 147 148 150 148 137K 3.8 3.7 3.4 4.4 3.3 2.8 2.2 2.2 5 3.8Mg 1.4 2.8 1.8Bill 1.3 0.8 0.5 0.5SGPT 40 40 41 31Platelet 10000 80000 88000 190000 200000CXR LF LZ Opcty Intnsty Lf Mini Opct perst decrsd pl effsn Table1. Sequential investigations and their results so inotropes were stopped. Her blood sugar was well controlled with intermediate insulin. She had received six units of whole blood and six units of platelet rich plasma during her hospital stay for her anemia and thrombocytopenia. All care was taken to correct her electrolyte imbalance. In spite of good glucose control, improvement of anemia and correction of electrolyte imbalance and improvement of sensorium she could not be weaned off from ventilator and had persistent leucocytosis. As she needed prolonged ventilationFig3. Skiagram showing shadowing of lungs and tracheostomy was done on day five of ventilation. Her nutrition was improved with enteral feeding. Her antibiotics were upgraded but still she could not be weaned off from ventilator and leucocytosis persisted. There was radiological deterioration of the chest shadowing. In spite of two weeks broad antibiotic therapy patients respiratory effort was poor and leucocytosis persisted. So empirical antifungal started with caspofungin with loading dose of 70mg followed by 50mg daily for six days. ThereFig 4. Skiagram shows resolution of chest pathology was dramatic improvement of respiratory effort and general well being. She was given T piece trialDuring peritoneal dialysis her blood pressure on 4th day of anti-fungal treatment and tolerated itimproved and she started passing adequate urine, very well. Her tracheostomy was closed on the 35
    • next day (total 17 days). She was ventilated for 22 ventilation. Since the patient could not be weaneddays out of 30 days of hospital stay. She was off from ventilator and there was persistentdischarged with a diagnosis of Type-II DM, leucocytosis, the diagnosis of fungal infection washypertension, hypothyroidism, acute renal failure entertained. Since the patient had acute renal(peritoneal dialysis was done), sepsis fungal failure treatment with Amphotericin infusion was ruled out. So Caspofungin was administered. Thepneumonia. She was followed up for next 4 dramatic recovery after caspofungin therapy is amonths without any complications. proof that the patient was having opportunisticDiscussion: fungal infection which responded well toFungal infection now a days has become a antifungal treatment.common cause of infection worldwide. References:Candidemia is associated with one of the highest 1. Todi S, Chatterjee S, Sahu S , Bhattacharyya M.rate of mortality of any bloodstream infection. Epidemiology of severe sepsis: An updateThe common risk factors for Candida infections Critical care 2010:14 (suppl 1): 382.are previous antimicrobial administration,prolonged corticosteroid therapy, cancer, 2. Edmond MB, Wallace SE, McClish DK et.al.chemotherapy, neutropenia, extensive intra- nosocomial bloodstream infections in Unitedabdominal surgery or burn, mechanical States hospitals; A 3 year analysis. Clin infectventilation or admission to ICU indwelling CVP Dis 1999;29:239-244. 4,5line, TPN and haemodialysis . 3. Pfaller MA, Jones RN, Doem GV and theAnti-fungal agents are Amphoterecin B, Azoles, SENTRY participant group ; Bloodstreamand Echinocandins. Amphoterecin B works on the infections due to Candida species ; SENTRYcell membrane of the fungi and increases antimicrobial surveillance program in Northmembrane permeability leading to leakage of the America and Latin America 1997-1998.cytoplasm and fungal cell depth. The adverse Antimicrob Agents Chemother 2000;44:747-effects include nephrotoxicity. Azoles works on 751.the cell membranes by inhibiting fungal 4. Garber G. An overview of fungal infection.cytochrome P-450 leading to accumulation of Drugs 2001;61(suppl 1):1-12.toxic steroles. There is also much drug interaction 5. Blumberg HM, Jarvis WR, Soucie JM et al andwith this drug. But echinocandins, specifically the NEMIS study group. Risk factor forCaspofungin, disrupts cell wall glucan formation candidal bloodstream infection in surgicalthrough non competitive inhibition of the enzyme intensive care unit patients: Clin Infect Discomplex - (1, 3)-D-glucan synthase, present in 2001; 33: 177-186 Debono M et.al antibioticmost pathogenic fungi and essential for fungal cell that inhibits fungal cell wall development.wall formation. It leads to osmotic instability and Annu Rev Microbial 1994;48:471-497. 5, 6ultimate lysis of fungal cell wall and is less toxic 6. Debono M et.al antibiotic that inhibits fungal 6, 7, 8with a good safety profile . cell wall development. Annu Rev MicrobialA bedside scoring system for early antifungal 1994;48:471-497.treatment in non-neutropenic critically ill patient 7. Keating GM, Jarvis B, Caspofungin, Drugswith candida colonisation will be helpful. The 2001;61:1121-1129.variables are multifocal candida species 8. Sawistowska, Schroder ET, Kerridge D, Perry H.colonization score 1, surgery on ICU admission Echinocandin inhibition of 1,3,-b-D-glucanscore 1, TPN score 1, severe sepsis score 2. If the Synthase from candida albicans. FEBS Letttotal score is more than 2.5 it helps intensivists to 1984; 173: 134-138.select patients who will benefit from anti fungaladministration. 9 9. Leon C. A bedside scoring system for early antifungal treatment in non neutropnicIn our case the risk factor were diabetes mellitus, critically ill patients. Crit Care Medbroad spectrum antibiotics and prolonged 2006;34.730-737. 36
    • Clinical imagingChoanal Stenosis with single nostril a rare CaseParamananda Rath, Nimain C Nanda, Pitabas Mishra Address for communication :Deptt. of Pediatrics and Neonatology Dr. P Rath, Sr. Consultant, Deptt. of Pediatrics and Neonatology,Sidhesh C Mishra Ispat General Hospital,Rourkela,Deptt. of E.N.T. Email: paramananda2@yahoo.co.inAbstractChonal stenosis and atresia is often seen inimmediate neonatal period and presents withrespiratory distress.However single nostril as anassociated anomaly with choanal stenosis has notyet been reported. In Ispat general hospitalone newborn was delivered with such anomalyand resusciated successfully.Key words Figure 1 Immediately after delivery babyChoanal stenosis, Single nostrilCase ReportIn Ispat General Hospital,Rourkela a male babyweighing 2000 gm was delivered to a primimother who had an uneventful antenataloutcome. The baby had respiratory distress withretraction of chest noticed immediately afterbirth. On examination, the baby had a singlenostril. A nasal catheter could pass only ½ to 1centimetre through the nostril. Some degree ofnasal obstruction was suspected. Even after Figure 2 Developing cyanosisfrequent suctioning of throat respiratory distresspersisted and baby became cyanosed after fewminutes and started crying. As the baby cried,cyanosis was relieved and he became pink andquiet (fig-1, 2, 3). Such repeated attacks ofcyanosis which was being relieved after cryingcontinued to occur. A diagnosis of choanal atresiawas suspected. The baby was transferred to thenursery. An oral airway was inserted and securedto the cheeks with tape (fig-4).This relieved therespiratory distress. Figure 3 Cyanosis relieved after crying 37
    • referred to the pediatric surgeon for reconstructive surgery which was done successfully. Discussion Choanal atresia was first reported in 1830 and is often seen in newborn period and occurs in 1 in 1 5000 to 8000 live births .It is usually associated with anomalies likeCHARGE (Coloboma, Heart defect, Atresia choaenae, Retardation of growth and genital anomalies), polydactyly, nasal- auricular and palatal deformities and other cranial anomalies2. However single nostril associated Figure 4 Airway has been secured with choanal tenosis has not yet been reported. Newborn babies usually dont have mouth breathing.In choanal atresia they try to breath through mouth.When they close their mouth or are breast fed respiratory distress and cyanosis occurs. Choanal atresia can be unilateral or bilateral(20%) and may be associated with other anomalies stated above. Diagnosis of choanal atresia is done by • Typical clinical presentation. • Direct visualization of the atretic area by otoscope. • Taking a radiograph while pushing radioopaque dye through nasal opening- atretic or stenotic area can be visualized. Figure 4 airway has been secured • CT scan can delineate extent of obstruction. Definitive treatment of choanal atresia/StenosisHe was kept on IV fluid for two days and then was includesgiven gavage feeding. Congenital defects like • Transnasal resecn tion by a laser beam.Treacher Collins syndrome, palatal abnormalities, • Definitive surgical reconstruction.colobomas, tracheoesophageal fistula, and • Till surgical correction babys airway to becongenital heart disease were excluded clinically. maintained by an oral airway and nutritionDirect visualization through an otoscope couldnt maintained by gavage feeding.demonstrate anything abnormal. Plain radiograph • In our case in addition to repair of stenotic(antero-posterior view) of nasal and paranasal segment cosmetic repair of the nostril wasregion were carried out to rule out any septal also needed.anomaly. A lateral radiograph of head with radio Referencesopaque dye pushed through the nostril showed a 1. Pirsig W.Surgery of choanal atrsia in infantsstenotic area (fig-5 arrow marked) in the choanal and children:historical notes and updatedregion. But the dye could pass through the reviews,Int J pediatr otorhinolaryngologystenotic area when pushed with pressure. A II:153,1986diagnosis of Choanal Stenosis was confirmed. 2. Brown K,Rodriguez K,Brown O E.CummingsBaby stayed for ten days in nursery and then was Otolaryngology , 4th edition. pp,4099-4109 38
    • Residents Section ACCIDENTAL BREAKTHROUGH Compiled by : Suman Behera (Intern) Pallavi Agarwal (Intern)Accidents in medicine: The idea sends chills down your spine as you conjure up thoughts ofmisdiagnoses, mistakenly prescribed drugs, and wrongly amputated limbs. Yet while accidentsin the examining room or on the operating table can be regrettable, even tragic, those that occurin the laboratory can sometimes lead to spectacular advances, life-saving treatments, andNobel Prizes.A seemingly insignificant finding by one researcher leads to a breakthrough discovery byanother; a physician methodically pursuing the answer to a medical conundrum over manyyears suddenly has a "Eureka" moment; a scientist who chooses to study a contaminant in hisculture rather than tossing it out stumbles upon something entirely new.QuinineThe story behind the chance discovery of the anti-malarial drug quinine may be more legendthan fact, but it is nevertheless a story worthy of note. The account that has gained the mostcurrency credits, a South American Indian with being the first to find a medical application forquinine. According to legend, the man unwittingly ingested quinine while suffering a malarialfever in a jungle high in the Andes. Needing desperately to quench his thirst, he drank his fill froma small, bitter-tasting pool of water. Nearby stood one or more varieties of cinchona, whichgrows from Colombia to Bolivia on humid slopes above 5,000 feet. The bark of the cinchona,which the indigenous people knew as quina-quina, was thought to be poisonous. But when thismans fever miraculously abated, he brought news of the medicinal tree back to his tribe, whichbegan to use its bark to treat malaria.Since the first officially noted use of quinine to fight malaria occurred in a community of Jesuitmissionaries in Lima, Peru in 1630, historians have surmised that Indian tribes taught themissionaries how to extract the chemical quinine from cinchona bark. In any case, the Jesuitsuse of quinine as a malaria medication was the first documented use of a chemical compound tosuccessfully treat an infectious disease. To this day, quinine-based anti-malarials are widely usedas effective treatments against the growth and reproduction of malarial parasites in humans.Keep that mind openFor all those would-be Nobel Prize-winners, remember the one trait that tied all these luckystrikers together: openmindedness. As the American physicist Joseph Henry once noted, "Theseeds of great discoveries are constantly floating around us, but they only take root in minds wellprepared to receive them." 39
    • Residents SectionPractice paperThis practice paper is designed to incite intrusiveness amongst all the doctors and particularly for doctorsdesirous to take part in different examinations. Though key to the question paper is given elsewhere, allare requested to verify the answers from standard text books.Please choose the most appropriate answer to each question.1. Transitional epithelium is found in 7. Vit B12 deficiency can occur in a. thyroid gland a. ileal resection b. distal urethra b. strict vegetarians c. Ureter c. parietal cell atrophy D. small intestine d. total gasrectomy e. all of the above2. Narrowest part of male urethra is A. membranous urethra 8. Which of the following statements is false for brain death? b. external urinary meatus a. respiration should have ceased c. penile urethra permanently d. glandular urethra b. heart beat should have ceased3. Red nucleus is a part of permanently a. Thalamus c. reflex spinal movement of limbs may b. Pons be present c. Cerebellum d. pupils should have no reaction to light d. Mid brain 9. pulmonary vein carries a. oxygenated blood from lungs to heart4. Which is not a part of stomach? b. oxygenated blood from heart to lungs a. Fundus c. de oxygenated blood from lungs to heart b. Neck d. deoxygenated blood from heart to lungs c. Body 10. Nephron is seen in d. Pylorous a. central nervous system5. How many lobes are there in left lungs? b. kidney a. 1 c. spleen b. 2 d. liver c. 3 11. Mid diastolic murmur is classically seen in d. 4 a. mitral stenosis6. Iron is absorbed in which part of GI tract b. aortic stenosis a. stomach c. aortic regurgitation b. duodenum d. mitral regurgitation c. jejunum 12. Axons of a neuron carry impulse d. ileum a. away from the cell body 40
    • b. towards the cell body b. low calcium level c. does not carry impulse c. a marker of Kalazar13. pH of vagina is 20. In AP view of chest, relative position of a. acidic tube and film to the chest are as follows b. alkaline a. Film is kept anterior and tube is c. neutral posterior b. Tube is kept anterior and film is13. Billirubin level is estimated posterior a. to know blood viscosity c. Both tube and film are kept on the same b. to know liver function side of chest c. to study pulmonary function 21. Risk of radiation is highest with d. to know lipid metabolism a. X-ray14. Autonomic nervous system deals with all of b. CT scan the followings except c. MRI a. skeletal muscle contraction d. ultrasound b. cardiac function 22. Most probable diagnosis of the image c. pulmonary function below is d. digestive function15. Largest cell in human body is a. spermatozoa b. ovum c. neutrophil d. RBC16. PNDT act deals with a. drug trading b. protecting the secrecy of patients c. sex determination of foetus d. narcotics17. In emergency, dying declaration can be taken by the treating doctor himself a. true a. hydrocephalus b. false b. encephalocele18. All of the followings are neoplastic c. meningocele disorders except d. microcephaly a. glioma 23. Which of the following phenotype b. antibioma describes Bombay blood group? c. neuroblastoma a. hh d. nephroblastoma b. HH19. Hypokalemia is c. Ao a. low potassium level d. Bo 41
    • 24. Sudden onset, intense headache with neck 30. Which of the following act of a doctor does stiffness should be investigated not make him liable under CPA? immediately to rule out SAH by a. Not accepting a cold patient for treatment a. lumbar puncture b. Fixing surgery at a later date after b. CT scan of brain accepting the patient for treatment c. MRI of brain c. foreign body left in abdomen during d. AP view of skull surgery due to the fault of the assisting nurse.25. Two scientists were awarded Noble prize for their work on one vitamin. Name that d. not performing a life saving surgery vitamin. because no one is available to sign the a. Vit B12 consent form. b. Vit C 31. Which of the following may create problem c. Vit B6 for a surgeon under the CPA. d. Vit E a. consent for surgery taken by the ward sister26. All of the followings are signs of upper b. consent taken on a printed format used motor neuron except in the hospital for all surgical patients a. up going plantar (blanket consent) b. flaccid muscle tone c. consent signed by the husband of a c. exaggerated deep tendon reflexes 40 year old lady d. abolished superficial reflex d. consent signed by the father of a 25 year27. Classical lucid interval is described in old newly recruited executive of SAIL. a. extradural hematoma e. all of the above b. subdural hematoma f. none of the above c. sub arachnoid hemorrhage 32. Trachea bifurcates at which level? d. ventricular hemorrhage a. D228. Which of the following statements is false b. D3 for TIA? c. D4 a. it should be taken seriously because it d. D5 heralds major episode ahead b. it allows time to detect treatable causes 33. Choice of treatment in organo-phospherous and treat them poisoning is c. patient should be counseled only a. PAM and asked to report immediately if next b. atropine attack occurs. c. neostigmine29. Cauda equine syndrome due to any acute d. none of the above compression should be considered as e. all of the above surgical emergency because if delay occurs 34. Most dreaded complication of falciparum a. patient may suffer from permanent loss malaria is of bladder and bowel control a. cerebral malaria b. permanent motor weakness in lower limbs and lifelong disablity b. jaundice c. it may invite litigation c. association with pregnancy d. all of the above d. bleeding from nose and gums 42
    • 35. ACE inhibitors are contraindicated in after full recovery plan for surgery a. hypertensive encephalopathy c. careful and expectant observation b. intracerebral hemorrhage d. conservative c. acute M.I. 42. which of the followings is most confirmatory d. bilateral ischemic kidney for pregnancy36. Which statement is true for Type 2 diabetes? a. urinary presence of HCG a. they have insulin deficiency from birth b. morning sickness b. it affects persons above forty only c. ultrasonic observation of cardiac activity c. initial treatment is insulin of foetus d. none of the above d. enlargement of mammary glands e. all of the above 43. Post partum period is the period37. Which of the following condition is most a. 2 weeks following delivery serious? b. 4 weeks following delivery a. acute MI c. 6 weeks following delivery b. stable angina d. 8 weeks following delivery c. unstable angina 44. All of the followings are complications of d. all are equally serious duodenal ulcer except38. Treatment of choice in pulse less VT is a. perforation a. amiodorone b. bleeding b. verapramil c. obstruction c. adenosine d. malignancy d. DC shock 45. which of the following condition is painful39. Thrombolysis is contraindicated in a. hemorrhoids a. non-ST elevation MI b. fissure in ano b. unstable angina c. rectal polyp c. stable angina d. malena d. all of the above 46. smoking is harmful in all of the following e. none of the above condition except a. Bergers disease40. Life span of corpus luteum is b. bronchial asthma a. 12 days c. ulcerative colitis b. 14 days d. coronary artery disease c. 16 days d. 10 days 47. Which of the followings are signs of fracture? a. pain41. Management of ruptured ectopic pregnancy is b. swelling a. resuscitation and surgery should go side by side without delay c. deformity b. blood transfusion, management of shock, d. all of the aboveFor Key to Practice Paper, Please see page-33. 43
    • Down The Memory LanePandit Nehru in Ispat general Hospital Doctors of IGH 1962 44
    • Down The Memory Lane A page from the proceedings of IGH published in 198145
    • Instructions for the Authors1. Letter of submission signed by all the authors2. Type of articles- Original article -2000 words, case reports- 800 words, guide line of IGH for management of emergency cases 2500 words, article of historical interest -500 words, case reports in Image -200 words, Review articles on invitation.3. Figures - Maximum 2 colour photographs per 500 words except case report in images where 4 photographs can be submitted.4. Three copies of manuscript with copies of illustrations attached to each.5. Title page Title of manuscript Full name(s) and department(s) Name, Address, Telephone, and e-mail address of corresponding author (first author). Number of pages, number of figures and number of tables.6. Abstract (objectives, methods, results, conclusion) along with title, and key words7. Article proper (double spaced on A/4 size paper) with reference no. immediately following the description as superscript.8. Acknowledgements (separate sheet).9. References (double spaced, separate sheet, Vancouver style). Maximum number of references for Original articles - 15,Guide lines-15,Case reports - 6, Article of historical interest or true stories which can inspire young doctors -5.Case reports in images- 510. Each table on separate sheet.11. Figures/diagrams on separate sheet.12. Photographs in envelope appropriately marked.13. Legends on separate sheet14. Since proceedings of IGH is our in house publication, articles are not copyright protected by this publication. Authors can publish their articles in other journals as per the prevailing rules of RSP.15. Statement regarding Ethics Committee Approval and informed consent from subjects.*16. CDs / DVDs of the article if article is submitted in hard copies1. Online submission is encouraged and preferred.18. e-mail: editors.ighp@gmail.com 46
    • Ispat General Hospital: An OverviewRourkela Steel Plant, was the first integrated steel plant in the Public Sector in India. This vision ofPandit Nehru, the first ‘Temple’ of modern India, began to take shape in the mid-fifties. Tocater to the health need of the massive inflow of workforce to Rourkela a modest beginning wasmade in the form of a small medical centre in 1955. In 1956 a First- Aid centre was started in the SteelPlant and in the year 1959, the building, which houses the present day Ispat General Hospital(IGH), came into existence.As the years passed IGH kept pace with times and technology adding new facilities to its repertoire.Today IGH is a 700-bedded state of the art hospital with a pool of 125 competent doctors and 612paramedics. It extends treatment to more than 9 lakh people at its outpatient department, on anaverage, in a year. In the inpatient department more than 30 thousand persons get treated annuallyout of which about 40% are non-entitled patients.The hospital has facilities in super specialities like neurosurgery, burn and plastic surgery. Thehospital also provides lifesaving interventions like dialysis, pacemaker implantation andchemotherapy. Total hip and knee replacement, brain and spinal cord surgery, urologicalprocedures are routinely taken up apart from laparoscopic and open surgical procedures inSurgery and Obstetrics department. Laser surgery and phaco-emulsification in Ophthalmology andbronchoscopic surgery in ENT department make this hospital one of its kind in the entire state ofOdisha. IGH is equipped with many modern investigating facilities like 3rd generation CT scan, 1.5 Tesla MRImachine and sophisticated laboratory medicine department comprising Pathology, Microbiologyand Biochemistry departments. Nuclear medicine and blood transfusion facilities greatly facilitatethe treatment of patients.On the research front, IGH is a WHO recognized research centre for Malaria and the facultymembers of IGH are regularly invited to impart training in other countries. The hospital is equippedwith a molecular laboratory for research work. Paediatric department of the hospital is participatingin research work in the international field in neonatal infection control. Contribution of the hospitalto the future generations of medical professionals is also immense as most of the research work ispublished in international medical journals.This premier hospital is also recognised for imparting post graduate training in most of thedisciplines of medical science. The performance of the students of this Institution is highlysatisfying – an eloquent testimony to the quality of training they are receiving here.At present Ispat General Hospital caters to the complete health needs of employees of the steelplant and their family members. Citizens of Rourkela and nearby districts too reach out to thehospital. Besides, people of Jharkhand, Chhattisgarh and Madhya Pradesh make IGH their healthdestination from time to time.Ispat General Hospital which has redefined health care in the region epitomises concern andcommitment.
    • ROURKELA STEEL PLANT