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Proceedings of the    Ispat General Hospital                                    YEAR 2011                     Ispat Genera...
Proceedings of the                Ispat General HospitalEditorDr R N MohapatraReviewers                          Publicity...
MessageI am extremely happy to learn that Proceedings of Ispat General Hospital isbeing revived after a gap of nearly two ...
Acknowledgement   We would like to place on record our deep sense of gratitude to ourManaging Director, Shri S N Singh who...
Contents•   Editorial                                                              03Review Article•   Diabetic nephropath...
EditorialBrain Death, its impact on organ donation andresources of critical care units                                    ...
Review ArticlesDiabetic NephropathyKishore C MahantaDeptt. of Internal Medicine                                           ...
Diabetic nephropathy generally goes along with               cytokines such as transforming growth factor-B,other diabetic...
Figure 1. is a schematic summary of the natural        only about 20% go on to develop ESRD. Howeverhistory of diabetic gl...
Laboratory tests that may be done include:             levels, aggressive blood pressure control,     •   BUN             ...
-   Beta blockers are contraindicated in                     ACEi demonstrate slower progression to                       ...
SPECIAL CONSIDERATIONS                                 Survival analysis shows the two modalities are                     ...
3. Transplantation : By far the best treatment for     SummaryESRD from diabetes is kidney transplantation.          The r...
7. Anjali, Jacob J J, Nephropathy in Diabetes;                  and transforming growth factor-beta1 in    practical guide...
24. Jacobsen P, Andersen S, Rossing K, Jensen          dialysed diabetic patients: a prospective    BR, Parving HH. Dual b...
Original PapersPrevalence of phage types & biotypes among Salmonella Typhi andSalmonella Paratyphi A isolates from Rourkel...
suspected of having enteric fever or pyrexia of                   the patients, 768 were males (52.81%) and 686unknown ori...
Most of the phage types of S. Typhi isolates           phage type 40, which itself is a rare and exoticbelonged to biotype...
th(cephotaxime and ceftriaxone) was highly                     Medical Microbiology. 13 ed. Edinburg :encouraging, and can...
Original PapersPredictions of Lengths of Hospital stay of malaria patientsSaroj K Mishra                         Narayan P...
excluded from the study. 700 patients with                     62% were entitled patients (either employees orcomplete dat...
equation was developed by using multiple                    patients are concerned regarding the length ofregressions.    ...
before admission as influencing factors. But a                system. Malaria Journal, 2007; 6:24. doi:major flaw of the s...
Case reportsPeutz- Jeghers Syndrome presenting as acute intestinalobstruction due to Jejunal Intussusception in an adult m...
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  1. 1. Proceedings of the Ispat General Hospital YEAR 2011 Ispat General Hospital, Rourkela Steel Plant, Rourkela
  2. 2. 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
  3. 3. 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)
  4. 4. 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
  5. 5. 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
  6. 6. 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
  7. 7. 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
  8. 8. 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
  9. 9. 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
  10. 10. 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
  11. 11. - 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
  12. 12. 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
  13. 13. 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
  14. 14. 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
  15. 15. 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
  16. 16. 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
  17. 17. 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
  18. 18. 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
  19. 19. 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
  20. 20. 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
  21. 21. 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
  22. 22. 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
  23. 23. 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
  24. 24. 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

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