Proceedings of the Ispat General Hospital

YEAR 2011

Ispat General Hospital,

Rourkela Steel Plant, Rourkela

Proceedings of the

Ispat General Hospital

Editor

Dr R N Mohapatra

Reviewers Publicity

Dr A M Acharya Mr J C Mohapatra

Dr C M Rao Mr R Kumar

Dr K C Mohanta Ms A Satpathy

Dr N K Behera

Dr P Mishra

Dr (Mrs) Prativa Behera

Dr R B Pattnaik

Dr S Mohanty

Dr S K Mishra

Dr S K R Prusty

Dr S N Mohapatra

Message

I am extremely happy to learn that 'Proceedings of Ispat General Hospital' is

being revived after a gap of nearly two decades.

The current edition that heralds a new beginning will surely lay the

foundations for making this journal more meaningful for practicing Doctors.

In fact, with the fast changing scenario in the medical sphere, such

publications have immense value for meeting the education and training

needs of upcoming medical professionals besides providing the basis for

fresh research.

In recent times Ispat General Hospital, administered by Rourkela Steel Plant,

has not only grown in stature as a treatment centre for complicated aliments

but has also established itself as a centre for medical education with the

introduction of post graduate courses (DNB). I am sure this publication will

be of enormous help to the DNB students both as a source of learning and

also a platform to publish their achievements.

I extend my hearty congratulations to the dedicated team of Doctors of Ispat

General Hospital for taking up this endeavour and wish this publication a

grand success in the current edition as well as in future.

S. N. Singh(CEO, RSP & I/c RMD)

Ispat General HospitalRourkela-769005

Dr S.K.Mishra,Director In-Charge,

Medical & Health Services,SAIL, RSP, Rourkela

Acknowledgement We would like to place on record our deep sense of gratitude to our

Managing Director, Shri S N Singh who has constantly encouraged us to

develop as professionals and bring about improvements in every activity

connected to health care. We are particularly grateful to him for his

unstinted support, guidance and encouragement that made this issue of

'The Proceedings of IGH' see the light of the day.

This publication is an endeavour to once again present the efforts and

achievements of the dedicated medical professionals at Ispat General

Hospital before the medical fraternity. The erudite authors of the articles

have contributed significantly in making the proceedings a valuable

compendium truly worth perusing and preserving. The reviewers have also

rendered a commendable service by fine-tuning and adding value to the

content. We sincerely acknowledge the efforts of the authors as well as the

reviewers.

We are also grateful to the Public Relations Department for their support

at each stage of this project, right from conceptualization to coordination

with the publishers, and giving the finishing touches.

The publishers patiently stood by us during the several revisions while

adding their innovative ideas to enhance the quality of this publication. They

deserve our sincere thanks.

Finally I wish to place on record my grateful thanks to all my colleagues for

the generous help and support that they have bestowed at every stage of this

publication.

• Editorial 03

Review Article

• Diabetic nephropathy 04Kishore C Mahanta

Original Papers

• Prevalence of phage types & biotypes among Salmonella Typhi 13and Salmonella Paratyphi A isolates from Rourkela, OrissaSeshadri S Bhattacharya, Usha Das

• Predictions of Length of Hospital stay of malaria patients 17Saroj K Mishra, Narayan P Sahoo, Kishore C Mahanta, Rajalaxmi Mishra

Case reports

• Peutz- Jeghers Syndrome presenting as acute intestinal obstruction 21due to Jejunal Intussusception in an adult male Amulya M Acharya, Sishir R Dash, Manoja K Panigrahi

• Necrotising fasciitis in neonate – case report 25Radhanath Satpathy, Nimain C Nanda, Pitabas Mishra, Rajan K Behera,Pinaki Panigrahi

• Squamous cell carcinoma & basal cell carcinoma with xeroderma 28pigmentosa – a rare presentationAruna M Minz, Niranjan K Behera, Rabi R Panda, Sanghamitra Satpathy,Prativa K Behera, Usha Das

• Multiple brain metastases due to occult Papillary Carcinoma 31of thyroid gland: A Case Report

Rabindra N Mohapatra, Sudhi R Pradhan , Rabi R Panda, Pushpa Kumari, Saropani Hembram

• Unusual case of severe Sepsis 34Rajyabardhan Pattnaik, Sanjib Mohanty, Sradhananda Mohapatra

Clinical imaging

• Choanal Stenosis with single nostril -a rare Case 37Paramananda Rath, Nimai C Nanda, Pitabas Mishra, Sidhesh C Mishra

Residents' Section

• Accidental Breakthrough 39Suman Behera, Pallavi Agarwal

• Practice paper 40

• Down The Memory Lane 44

• Instructions for the Authors 46

• Ispat General Hospital : An Overview

Contents

3

“20,000 liver transplants needed annually in India, only 110 donors in 2009”. This was the news

1headline on April 01 2010 .

Throughout the world, main resources of donor 2, 3

organs are the brain dead patients. But, the sorry state in our country is mainly due to reluctance to accept the concept of brain death, both by the physicians as well as general public. Causes of this reluctance may be due to several reasons related to physicians themselves and relatives of the

2deceased as well. According to Pathak et al., some of the factors responsible for this may be

• Lack of understanding the concept.• Special emotional attachment to the dead

person• Loss of confidence in medical practice• Ethical questions related to earlier organ

transplant procedure• Perceived insufficient participation of

government and medical associations.Concept of clinical death in the form of loss of observable cardio respiratory failure has undergone a sea change due to widespread use of mechanical ventilators that prevent respiratory

3arrest . In 1968, ad hoc committee at Harvard Medical School defined irreversible coma, or brain death, as unresponsiveness and lack of receptivity, the absence of movement and breathing, the absence of brain-stem reflexes, and coma whose

3cause has been identified.

In India, The Transplantation of Human Organs Act, 1994 (Central Act 42of 1994), lays down the definition of death thus: 'Deceased person ' means in whom permanent disappearance of all evidence of life occurs, by reason of brain stem death or in a cardio-pulmonary sense at any time after live birth has taken place. It goes on to state that 'brain-stem death' means the stage at which all functions of the brain stem have permanently and irreversibly ceased. Once brain-stem death has been diagnosed by an authorized committee using specified criteria, the dead person's organs can be removed for transplantation provided legally valid

3, 4consent for this is available.

Continuation of critical care support after brain death, drains out the resource crunch critical care departments of life saving resources, manpower and finance. In fact, it puts a lot of burden on the family members physically, financially and emotionally, for an outcome which is unattainable. In addition, keeping life saving equipments engaged for a brain dead patient may deprive another critically ill patient whose condition is reversible. We, the physicians, should understand that there is no recovery after brain death. We can explain relatives of the deceased that putting their patient on life support system is futile; rather his viable organs can alleviate the disease in a person who can otherwise lead a normal healthy life. In an Indian scenario, the relatives of the deceased can be emotionally appealed that some part of their near and dear ones will still be surviving in the recipient's body.

The purpose of this Editorial is not to go into the intricacies of brain death, rather to sensitise medical professionals and public regarding the fact that brain death is ultimate end of one's journey in this Earth.

It is time to educate ourselves and the public, to assist in understanding the concept of brain death. It is particularly true in hospitals, where load on critical care department is very high.

References:

1. Zee News.Com, uploaded on Thursday, April 01, 2010, 00.03

2. Pathak MK, Tripathy SK, Agrawal P, Chaturvedi R, Yadav S. Clinical Criteria for Diagnosis of Brain death and its Medico-Legal applications (A Review Study). IndMedica-Medico-Legal update.2006; 6(2):3-6

3. Golia AK, Pawar M. The diagnosis of brain death. Indian J Crit Med 2009;13:7-11

4. Pandya SK. Brain death and our transplant law. Paper presented at: The seventh National critical care congress CCCON; 2001 Jan 2-7; Bangalore

Rabindra N.MohapatraDeptt. of Neurosurgery

Address for communication :

Sr. Deputy director, Neurosurgery,

Ispat General Hospital, Rourkela-769005, India

e-mail: ighp@in.com

Brain Death, its impact on organ donation and resources of critical care units

Editorial

4

Diabetic Nephropathy

Kishore C Mahanta

Deptt. of Internal Medicine Address for communication :Dr K.C. Mohanta,

Senior Deputy Director,

Ispat General Hospital, Rourkela -769005, INDIA

Email: kishoremalaria@rediffmail.com

ABSTRACT

Introduction:-

Diabetes has become the common single cause of

Chronic Kidney disease (CKD) leading to End-Stage

Renal Disease (ESRD) in most countries: this is due

to the fact that diabetes, particularly type 2 is

increasing in prevalence and that diabetic

patients are living longer with proper medication.

About 20-30% of patients with type 1/ type 2

diabetes develop evidence of nephropathy.

Recent studies have now demonstrated that the

onset and course of diabetic nephropathy can be

delayed to a very great extent by several

interventions, but these interventions have their

greatest impact if instituted at a very early course

of development of this complication. Recently

there has been a lot of developments in the

treatment of End Stage Renal Failure.

There is a silent epidemic of type 2 diabetes world

over. It is predicted that India will be the diabetic

capital of the world by 2020. With growing

population of type 2 diabetes, the prevalence of

diabetic nephropathy is on the rise. In fact diabetic

nephropathy is the single most common cause of

End Stage Renal Disease (ESRD) today.

Besides patients' miserable sufferings, it

consumes greater financial resources than non

diabetic ESRD. Diabetic ESRD patients do poorly

on dialysis and mortality is higher. There is a

spectrum of co-morbidities such as CV disease,

brain stroke, blindness, gangrene etc which are to

be dealt with while treating such patients with

Renal Replacement Therapy (RRT).

There has been some evidence to suggest that

genetic predisposition to hypertension may

predispose to development of diabetic 1

nephropathy. Pre diabetic individuals, with

impaired glucose tolerance, frequently have

hypertension as one facet of metabolic syndrome.

Genetic factors combined with metabolic and

hemodynamic alterations induce renal damage in

susceptible individuals.

The exact cause of diabetic nephropathy is

unknown, but it is believed that uncontrolled high

blood sugar leads to the development of kidney

damage, especially when high blood pressure is

also present. Not all persons with diabetes

develop this condition.

Each kidney is made up of hundreds of thousands

of filtering units called nephrons. Each nephron

has a cluster of tiny blood vessels called a

glomerulous. Together these structures help

remove waste from the body. Too much blood

sugar can damage these structures, causing them

to thicken and become scarred. Slowly, over time,

more and more blood vessels are destroyed. The

kidney structures begin to leak and protein

(albumin) begins to pass into the urine.

Persons with diabetes who have the following risk

factors are more likely to develop this condition:

• African American, Hispanic, or Americans of

Indian origin

• Family history of kidney disease or high

blood pressure

• Poor control of blood pressure

• Poor control of blood sugars

• Type 1 diabetes before age 20

• Smoking, Alcoholism

• Abnormal lipid levels

Causes:

Review Articles

5

Diabetic nephropathy generally goes along with

other diabetic complications including high blood

pressure, retinopathy and blood vessel changes

(vasculopathy).

The pathophysiology of diabetic nephropathy m a n i f e s t s h i s t o l o g i c a l l y a s d i a b e t i c glomerulosclerosis and is characterized by glomerular basement membrane thickening and mesangial expansion with increased extracellular matrix deposition. Mesangial expansion in diabetic glomerulosclerosis may be considered the result of an imbalance between mesangial matrix protein production and degradation, favor ing matr ix protein accumulat ion. Overproduction of mesangial matrix proteins may be the result of glomerular hypertension and/or hyperglycemia-driven synthesis of prosclerotic

Pathophysiology:

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.

cytokines such as transforming growth factor-B, 2,3angiotensin II, and/or other growth factors.

Alternatively, elevated glucose levels may inhibit matrix protein degradation through non-enzymatic glycosylation and/or through the

4 inhibition of protein degradative pathways. Thus, the mediators of mesangial expansion constitute reasonable therapeutic targets when crafting a treatment strategy for diabetic nephropathy. Understanding the natural history of diabetic glomerulosclerosis is important to design therapeutic interventions, as well as gauging responses to therapy. In this regard, Parving demonstrated the deleterious effect of hypertension on renal function in proteinuric

5,6 diabetics. Of equal or greater value in that report was the demonstration of the expected rate of loss of glomerular filtration rate (GFR) over time, in patients with diabetic nephropathy.

6

Figure 1. is a schematic summary of the natural

history of diabetic glomerulosclerosis, and

demonstrates the relationship between

albuminuria and the loss of GFR over time. The

model is based on the following assumptions: (a)

all macroscopic (dipstick positive) proteinuria is

preceded by a phase of microalbuminuria

(microalbumin 30-300 mg/day); (b) the

appearance of dipstick positive proteinuria

heralds the beginning of a linear, irreversible loss

of GFR; and (c) GFR is lost, on average, at the rate

of 1 ml/min/month.

Clinical diagnosis of diabetic nephropathy

Symptoms :

Examination and Tests

Early stage diabetic nephropathy has no

symptoms. Over time, the kidney's ability to

function starts to decline. Symptoms develop late

in the disease and may include:

• Fatigue

• Foamy appearance or excessive frothing of

the urine

• Frequent hiccups

• General ill feeling

• Generalized itching

• Headache

• Nausea and vomiting

• Poor appetite

• Swelling of the legs

• Swelling, usually around the eyes in the

mornings; general body swelling may

occur with late-stage disease

• Unintentional weight gain (from fluid

buildup)

The earliest clinical evidence of renal involvement

in diabetes is the presence of small amount of

albumin in urine (30-300mg/24 hrs). This is

labeled microalbuminuria. Protein may appear in

the urine for 5 to 10 years before other symptoms

develop. In type 1 Diabetes 80%, who develop

microalbuminuria, will develop macroproteinuria

and around 50% will eventually develop ESRD. In

type 2 Diabetes 20-40% of patient with

microalbuminuria develop overt proteinuria and

only about 20% go on to develop ESRD. However

presence of microalbuminuria in addition to

being a manifestation of renal involvement, is also

a marker of cardiovascular risk. Patients with

sustained microalbuminuria need to be

aggressively managed for cardiovascular risk 7

factors as well.

Screening in individual with type I diabetes should

begin after 5 years disease duration. In type 2 DM,

screening should begin at diagnosis, there after

for the presence of microalbuminuria should be

performed annually.

Screening for microalbuminuria can be

performed by three methods:-

1. Measurement of albumin to creatinine

ratio (ACR) in a random spot collection

2. 24 hr collection with creatinine, allowing

the simultaneous measurement of

creatinine clearance.

3. Screening with reagent tables or dipstick

for microalbumin have sensitivity 95% and

specificity93%. Reagent strips only

indicate concentration and do not correct

the creatinine as the spot albumin-7

creatinine ratio does.

1. Microalbuminuria – Random ACR 30-300

mg on 2 out of 3 occasion

2. Macroalbuminuria- Random ACR >300 mg

or positive protein dipstick

3. Diabetic nephropathy Estimated GFR < 60

ml/min for at least 3 months.

Screening of microalbuminuria is invalid in

following conditions:

In uncontrolled hyperglycaemia, febrile illness,

following strenuous exercise, uncontrolled

hypertension or heart failure and presence of

urinary infection as all these conditions can cause 7transient proteinuria.

High blood pressure often goes along with

diabetic nephropathy. One can have high blood

pressure that develops rapidly or is difficult

to control.

SCREENING FOR MICROALBUMINURIA:-

Definitions :-

7

Laboratory tests that may be done include:

• BUN

• Serum creatinine

The levels of these tests will increase as kidney

damage gets worse. Other laboratory tests that

may be done include:

• 24-hour urine protein

• Blood levels of phosphorus, calcium,

bicarbonate, PTH, and potassium

• Hemoglobin

• Hematocrit

• Protein electrophoresis - urine

A kidney biopsy confirms the diagnosis. However,

clinical diagnosis can be done without a biopsy if

the following three conditions are met with:

1. Persistent protein in the urine

2. Diabetic retinopathy

3. No other kidney or renal tract disease

A biopsy may be done, however, if there is any

doubt in the diagnosis.

Diabetics with heavy proteinuria, but lacking the

disease for a sufficient period of time and/or

retinopathy, may require renal biopsy. These

p a t i e n t s m a y s u f f e r f r o m p r i m a r y

glomerulopathies such as membranous 8

nephropathy, or other glomerular diseases.

Diabetic glomerulopathy is the most common

cause of nephrotic syndrome. Thus, early in the

course of the disease, the serum creatinine is

normal despite heavy proteinuria (> 3 grams/24

hours). In this regard, a diabetic patient

presenting with elevated serum creatinine in the

absence of macroscopic proteinuria should

suggest additional diagnostic possibilities (such as

other glomerulopathies) . The diagnostic utility of

proteinuria is less useful in patients treated with

angiotensin converting enzyme inhibitors (ACEi)

or angiotensin II receptor blockers (ARBs), since

both classes of drugs are known to reduce 9,10

glomerular proteinuria.

MEDICAL THERAPY OF DIABETIC NEPHROPATHY :

The medical therapy of diabetic glomerulo-

sclerosis includes strict control of blood glucose

levels, aggressive blood pressure control,

angiotensin II inhibition, and dietary protein

restriction. Additional therapeutic targets include

microalbuminuria and macroproteinuria. An

approach to each of these parameters is discussed

below.

1. Tight blood glucose control

The DCCT (Diabetes Control and Complications

Trial) demonstrated the importance of tight blood

glucose control in slowing the development of 13

proteinuria in Type 1 diabetics. In this regard,

patients randomized to tight glucose control

(HbA1C levels < 6.5%) versus regular control (8-

9%), demonstrated 39 and 54% lower rates of

development of microalbuminuria and

macroalbuminuria, respectively, over the two

years of the trial.

Similarly the UKPDS(United Kingdom Prospective

Diabetes Study) in Type II diabetes showed a 25%

risk reduction in microvascular complication in

the intensively treated group.

2. Blood pressure control

Hypertension in diabetic patient may be due to

coexisting “essential” hypertension, or due to

myriad of other secondary causes, such as renal

vascular disease. Isolated systolic hypertension

has been attributed to the loss of elastic

compliance of atherosclerotic large vessels. Both

systolic and diastolic hypertension markedly

accelerates the progression of diabetic

nephropathy and aggressive antihypertensive

management is able to greatly decrease the rate

of fall of GFR. Appropriate antihypertensive

intervention can significantly reduce mortality

from 94 to 45% and a reduction in the need for

dialysis and transplantation from 73 to 31% 16

years after development of overt nephropathy.

Choice of antihypertensive therapy:-

One needs to be careful about:-

- Use of ACEI and ARBs as these may lead to

hyperkalemia in patients of advanced renal

insufficiency,

- ACEI are contraindicated in bilateral renal

artery stenosis and in pregnancy.

8

- Beta blockers are contraindicated in

peripheral vascular disease.

Targets for blood pressure control:-

• <130/80 mm hg in absence of proteinuria

• <125/75 mm hg in presence of proteinuria.

3. Angiotensin II inhibition : The ACE inhibitor

trial in diabetic nephropathy was the first

randomized, placebo controlled trial that

showed the beneficial effect of ACE inhibitors

i n t h e t r e a t m e n t o f d i a b e t i c 11 glomerulosclerosis. Subsequent studies have

confirmed this observation for both ACE 10,12 inhibitors and ARBs. Most agree that ACEI

a re f i rst l ine therapy for d iabet i c 10

glomerulosclerosis, but ARBs are regarded by 10 some as equivalent. The beneficial effect of

angiotensin II inhibition may result from:

a) a decline in glomerular hypertension (with 13slowing of mesangial expansion)

b) a reduction in proteinuria (with an

expected decrease in proteinuria-14

associated prosclerotic events), and/or

c) a decrease in angiotensin II stimulated 15,16

TGF-ß synthesis.

4. Dietary protein restriction : In some reports,

dietary protein restriction has been shown to 17slow the loss of GFR in proteinuric diabetics,

although the data are not conclusive. Protein

restricted diets (0.6-0.8 g/kg body wt/day)

decrease glomerular hypertension, the

production of prosclerotic cytokines, 18

proteinuria, and glomerulo-sclerosis, and

remain a viable therapeutic option for

compliant patients.

5. Microalbuminuria : Microalbuminuria

predates the development of macroscopic

proteinuria. Macroscopic proteinuria is a 14major risk factor for progression to ESRD, thus

measures to reverse microalbuminuria may

retard development of clinical nephropathy.

Patients with microalbuminuria treated with

ACEi demonstrate slower progression to 6

macroproteinuria and renal failure. American

Diabetic Association (ADA) guidelines suggest

assessing for microalbuminuria (normal < 30

mg/24 hours or less 30 mcg/mg creatinine for

a spot urine collection) at the time of diagnosis

in all type 2 diabetics, in all type I diabetics with

disease duration > 5 yrs, and annually 19 thereafter in both groups. Early and

aggressive therapy of microalbuminuria, taken

along with angiotensin II inhibition, is

expected to slow disease progression.

6. Macroproteinuria

Heavy proteinuria is a risk factor for progressive 20renal failure, 16 including diabetic nephropathy.

There is abundant evidence that abrogating

proteinuria with dietary and antihypertensive 21

interventions, and/or ACE inhibitors, 1 and/or 22,23 ARBs, results in a slower loss of GFR in

proteinuric states. In this regard, combination

therapy with both ACE inhibitors and ARBs may 24

provide benefit over ACE inhibitors alone.

Finally, nephrotic diabetics treated with ACE

inhibition, and exhibiting a reduction in

proteinuria to < 1 gm / day, demonstrated stable 25

renal function for up to 8 to 15 years. Taken

together, therapeutic measures directed at

reducing macroscopic proteinuria would be

expected to slow the progression of diabetic

nephropathy, and angiotensin II inhibition is the

mainstay of therapy for attaining that goal.

Other aspects of treatment : Treatment of

progressive renal disease includes prevention of

renal osteodystrophy with sodium and phosphate

restriction and use of phosphate binders,

treatment and prevention of anaemia etc.

Avoidance of nephrotoxic drugs in proteinuric

diabetic patients will prevent form onset of acute

kidney injury.

Radiocontrast media are nephrotoxic in diabetic

nephropathy and careful hydration is mandatory

in these cases if it is done.

9

SPECIAL CONSIDERATIONS

Insulin metabolism in CKD : Unutilized insulin is

excreted by kidney normally which accumulates

in CKD. So if we fail to reduce insulin dose as

kidney disease progresses, patients will

experience hypoglycaemia. So reducing insulin

dose and switching to short acting insulin

analogues is recommended in this situation. It is

recommended to avoid long acting Insulins in CKD

patients.

Oral antidiabetic drug: 97% of the most

commonly used oral antidiabetic drug Metformin

is excreted by normal kidney within 12 hrs. In CKD

it will accumulate and lead to lactic acidosis, a

serious condition.

So metformin should be stopped when the eGFR is 2<35 ml/mt/1.73 m correlates to serum creatinine

o f a p p rox m i m ate l y 1 . 7 m g / d l . O l d e r

sulfonylurea(SU) are excreted mainly through

kidney. Only 10% of second line SU are excreted by

kidney but are long acting and may accumulate in

CKD, so we must be cautious while using these.

Meglitinides and Thiazolidinediones are not

excreted by kidneys. These do not cause

hypoglycaemia.

Monitoring glycaemic control in CKD : As kidney

disease develops, the turnover of red blood cells

becomes abnormal. Usually there is prolonged life

span of RBCs, perhaps because the person is

anaemic. So hemoglobin has more time to

become glycated. In such conditions HbA1 in c

kidney disease may be falsely high. Hb may also be

carbamylated with some of the waste products,

which accumulate in uremia and these

compounds will interfere with the measurement

of HbA1 . This is one more reason for HbA1 to be c c

falsely high. Correction of anaemia may lead to 26decrease HbA1 level.c

Renal replacement therapy:

1. Hemodialysis : Hemodialysis and peritoneal

dialysis are the two forms of dialysis used to treat

diabetic patients with end stage renal disease.

Survival analysis shows the two modalities are 27

comparable with regard to patient outcome.

However, when compared to non-diabetics,

diabetic patients on dialysis do substantially 28

worse, with five-year survival rates as low as 5% 29 for elderly type 2 diabetics. With meticulous

management, others have shown three-year 28 survival rates as high as 58%. .The reasons for

poor survival rates relate to the high incidence of

preexisting cardiovascular disease, late referral

both for predialysis care, as well as vascular access

placement, malnutrition, and co-existing vascular

problems (in particular, peripheral vascular 28disease with associated ischemic toes and feet).

Furthermore, diabetes and smoking have been

shown to be significant risk factors for

atherosclerotic heart disease in dialysis patients, 30

similar to what is seen in the general population.

The anemia of chronic renal disease may further

complicate the course of patients with significant

coronary artery disease. Taken together, these

data suggest that the survival of diabetic patients

on hemodialysis may be optimized with

aggressive attention to risk factors for

card iovascu lar d i sease (hypertens ion ,

dyslipidemia, smoking, etc.), awareness and

therapy of diabetic foot problems, and early

nephrology referral (as GFR falls or with

progressive proteinuria) for vascular access

placement and anemia management.

2. Peritoneal dialysis : The second option for renal

replacement therapy in diabetic patients with

ESRD, is peritoneal dialysis. When compared to

hemodialysis, fewer patients are treated with

peritoneal dialysis. Patients opting for peritoneal

dialysis tend to be healthier and more involved in

their medical care. While no clear survival

advantage for peritoneal or hemodialysis has

been demonstrated, patients treated with

peritoneal dialysis may experience labile blood

glucose levels (attributed to the high glucose

concentrations inherent to PD dialysate) and

increased risk of malnutrition (secondary to 31

excessive protein losses in dialysate effluent).

10

3. Transplantation : By far the best treatment for

ESRD from diabetes is kidney transplantation.

Kidney transplantation in diabetics with end-stage

renal disease may include kidney transplantation

a l o n e , o r c o m b i n e d k i d n e y - p a n c re a s

transplantation. The former treats renal failure,

the latter both renal failure and diabetes. Patient

survival following kidney transplantation without

a pancreas has consistently been demonstrated to

be superior to any form of dialysis. Data from the

Organ Procurement and Transplantation Network

reported one-, three-, and five-year patient

survival rates for transplanted diabetics of 90, 79 32

and 66%, respectively. This compares to a two

year survival rate in diabetic patients on 29

hemodialysis of 58%. The improved survival of

renal transplant patients over those treated with

hemodialysis must be interpreted in light of the

fact that they are selected for transplantation,

whereas patients with extensive co-morbidities

tend to remain on dialysis. Living donor

transplants confer an allograft survival advantage

over cadaveric donors, with three-year allograft

survival rates of 88 and 78% for living and 32cadaveric donor transplants, respectively.

However, both modalities are superior to dialysis

with three year patient survival rates of 3 2

a p p r o x i m a t e l y 8 8 - 9 4 % . P r e e m p t i v e

transplantation is renal transplantation that is

performed prior to instituting dialysis. Preemptive

transplantation may confer a survival advantage

that is superior to transplanting patients on

dialysis. In this regard, the time spent on dialysis

prior to transplantation portends worse survival

rates for patients. For example, in patients on

dialysis < 6 months, 12-24 months, or >48 months

had mortality rates of 21%, 41%, and 72%, 33,34,35 respectively. A similar trend for allograft

survival was seen in cadaveric transplants

performed in patients receiving hemodialysis for

more than two years prior to the transplant. In

those studies, the allograft survival rate was only 3639% after ten years.

Summary

The rising incidence of diabetes means that

clinicians can expect to find an increased rate of

diabetic nephropathy, and increasing numbers of

patients requiring renal replacement therapy.

Understanding the natural history of diabetic

nephropathy, the early recognition of diabetic

complications, and timely initiation of therapy to

slow progression are cornerstones in the

management of this condition. Aggressive

treatment of hyperglycemia and hypertension,

the use of angiotensin II inhibitors, and timely

therapy of micro and macroproteinuria are

essential features of optimal therapy. For patients

reaching end stage renal failure, renal

replacement options include dialysis and kidney

transplantation, with transplantation conferring a

substantial survival advantage.

References:

1. Strojek K et al, Nephropathyof type 2

diabetes: Evidence for hereditary factor.

Kidney Int. 51:1602-1607,1997.

2. Hostetter T, Rennke H, Brenner B. The case

for intrarenal hypertension in the

initiation and progression of diabetic and

other glomerulopathies. Am J Med. 1982;

72:375.

3. Ziyadeh F, Han D. Involvement of

transforming growth factor-b and its

receptors in the pathogenesis of diabetic

nephropathy. Kidney Int . 1997; 52:S7-S11.

4. Brownlee M. Biochemistry and molecular

cell biology of diabetic complications.

Nature. 2001; 414(6865):813-20.

5. Parving H, Smidt U, Andersen A, Svendsen

P. Early aggressive antihypertensive

treatment reduces rate of decline in

kidney function in diabetic nephropathy.

Lancet.

1983; 1:1175-1179.

6. Parving HH. Diabetic nephropathy:

prevention and treatment. Kidney Int.

2001; 60(5):2041-55.

11

7. Anjali, Jacob J J, Nephropathy in Diabetes; thpractical guide to Diabetes Mellitus: 4

Edn.;146-148

8. Carstens S, Hebert L, Garancis J, Piering W,

Lemann Jr J. Rapidly progressive

glomerulonephritis superimposed on

diabetic glomerulosclerosis: recognition

and treatment. JAMA. 1982; 247:1453-

1457.

9. Brenner BM. Regarding: “Management of

glomerular proteinuria: a commentary.” J

Am Soc Nephrol. 2004; 15(5):1354-5;

discussion 1356-7.

10. Lewis E, Hunsicker L, Bain R, Rohde R. The

effect of angiotensin converting enzyme

inhibition in diabetic nephropathy. N Engl J

Med. 1993; 329:1456-62.

11. Lewis EJ, Lewis JB. ACE inhibitors versus

angiotensin receptor blockers in diabetic

nephropathy: is there a winner? J Am Soc

Nephrol . 2004; 15(5):1358-60.

12. Hostetter T. Prevention of end-stage renal

disease due to type 2 diabetes. N Engl J

Med. 2001; 345:910-911.

13. Zatz R, Bunn B, Meyer T, Anderson S,

Rennke H, Brenner B. Prevention

o f d i a b e t i c g l o m e r u l o p a t h y b y

pharmacolog ica l amel iorat ion of

glomerular capillary hypertension.

J Clin Invest. 1986; 77:1925.

14. Wilmer WA, Rovin BH, Hebert CJ, Rao SV,

Kumor K, Hebert LA. Management of

glomerular proteinuria: a commentary. J

Am Soc Nephrol. 2003; 14(12):3217-32.

15. Nahman N, Kronenberger J, Sferra T, Clark

K. Transcriptional activation of the TGF-b

gene by angiotensin II: implications for

fibronectin biosynthetic pathways

in human mesangial cells. J Amer Soc

Nephrol. 1997; 8:522A.

16. Siegert A, Ritz E, Orth S, Wagner J.

Differential regulation of transforming

growth factor receptors by angiotensin II

and transforming growth factor-beta1 in

vascular

smooth muscle. J Mol Med . 1999;

77(5):437-45.

17. Zeller K, Whittaker E, Sullivan L, et al. Effect

of restricting dietary protein on the

progression of renal failure in patients with

insulin-dependent diabetes mellitus.

N Engl J Med. 1991; 324:78-84.

18. Klahr S, Levey AS, Beck GJ, et al. The effects

of dietary protein restriction and blood-

pressure control on the progression of

chronic renal disease. Modification of Diet

in Renal Disease Study Group [see

comments]. N Engl J Med . 1994;

330(13):877-84.

19. Molitch ME, DeFronzo RA, Franz MJ, et al.

Nephropathy in diabetes. Diabetes Care.

2004; 27 Suppl 1:S79-83.

20. Breyer JA, Bain RP, Evans JK, et al.

Predictors of the progression of renal

insufficiency in patients with insulin-

dependent diabetes and overt diabetic

nephropathy.

The Collaborative Study Group. Kidney Int.

1996; 50(5):1651-8.

21. Peterson JC, Adler S, Burkart JM, et al.

Blood pressure control, proteinuria, and

the progression of renal disease. The

Modification of Diet in Renal Disease

Study.

Ann Intern Med. 1995; 123(10):754-62.

22. Parving HH, Lehnert H, Brochner-

Mortensen J, Gomis R, Andersen S, Arner P.

The effect of i rbesartan on the

development of diabetic nephropathy in

patients with type 2 diabetes. N Engl J

Med. 2001; 345(12):870-8.

23. Lewis EJ, Hunsicker LG, Clarke WR, et al.

Renoprotective effect of the angiotensin-

receptor antagonist irbesartan in patients

with nephropathy due to type 2 diabetes.

N Engl J Med. 2001; 345(12):851-60.

12

24. Jacobsen P, Andersen S, Rossing K, Jensen

BR, Parving HH. Dual blockade of the renin-

angiotensin system versus maximal

recommended dose of ACE inhibition in

diabetic nephropathy. Kidney Int. 2003;

63(5):1874-80.

25. Wilmer WA, Hebert LA, Lewis EJ, et al.

Remission of nephrotic syndrome in type 1

diabetes: long-term follow-up of patients

in the Captopril Study. Am J Kidney

Dis. 1999; 34:308-14.

26. Mashall S etal, Chronic kidney Disease in

Diabetics: Current best practice and

possibilities for future. Novonordisk

Diabetes Update. Proceedings 2009; 21-28

27. Locatelli F, Pozzoni P, Del Vecchio L. Renal

replacement therapy in patients with

diabetes and end-stage renal disease. J Am

Soc Nephrol. 2004; 15 Suppl 1:S25-9.

28. Schwenger V, Zeier M, Ritz E. How can the

poor outcomes for diabetic dialysis

patients be improved? Semin Dial. 2004;

17(3):186-7.

29. Koch M, Kutkuhn B, Grabensee B, Ritz E.

Apolipoprotein A, fibrinogen, age, and

history of stroke are predictors of death in

dialysed diabetic patients: a prospective

study in 412 subjects. Nephrol Dial

Transplant. 1997; 12(12):2603-11.

30. Cheung AK, Sarnak MJ, Yan G, et al.

Atherosclerotic cardiovascular disease

risks in chronic hemodialysis patients.

Kidney Int. 2000; 58(1):353-62.

31. Xue JL, Everson SE, Constantini EG, et al.

Peritoneal and hemodialysis: II. Mortality

risk associated with initial patient

characteristics. Kidney Int. 2002;

61(2):741-6.

32. Organ Procurement and Transplantation

Network. www.optn.org/latestData/

rptStrat.asp. 2004.

33. Meier-Kriesche HU, Port FK, Ojo AO, et al.

Effect of waiting time on renal transplant

outcome. Kidney Int. 2000; 58(3):1311-7.

34. Mange KC, Joffe MM, Feldman HI. Effect of

the use or nonuse of long-term dialysis on

the subsequent survival of renal

transplants from living donors. N Engl

Med. 2001; 344(10):726-31.

35. Kasiske BL, Snyder JJ, Matas AJ, Ellison MD,

Gill JS, Kausz AT. Preemptive kidney

transplantation: the advantage and the

advantaged. J Am Soc Nephrol. 2002;

13

Original Papers

Prevalence of phage types & biotypes among Salmonella Typhi and Salmonella Paratyphi A isolates from Rourkela, Orissa.

Seshadri S Bhattacharya, Usha Das

Deptt. of Microbiology,

Address for communication :SS Bhattacharya

Deptt. of Microbiology, Ispat General Hospital, Rourkela, Orissa.

Email: sesebha@yahoo.co.in

ABSTRACT

Key words

Introduction

Aim of this study was to highlight the changes in prevalence of phage types encountered among Salmonella isolates from Rourkela. Besides S. Typhi as the main causative agent of enteric fever, S. Paratyphi A has also been emerging with increasing rate as the other causative agent of enteric fever from different parts of India including Rourkela. This retrospective study was carried out between September 2005 and August 2006 with 1454 patients attending out-patient-departments (OPD) and wards of Ispat General Hospital, Rourkela, India. Phage typing and biotyping was performed for randomly chosen isolates of S. Typhi (N=36) and S. Paratyphi A (N=12). A distinctive change has been noticed in the prevalence of phage types compared to their prevalence pattern reported earlier. Phage type 40 was the most commonly encountered phage among S. Typhi isolates followed by type E1. Susceptibility testing was performed for all 112 isolates of Salmonella including 48 strains chosen randomly for phage typing and biotyping. Though 4-5% of Salmonella isolates showed resistance to ciprofloxacin, they were highly sensitive to both aminoglycos ides and th ird generat ion cephalosporins. Diversity among the phage types encountered among S. Typhi isolates was probably due to the diverse origin of those phages. Salmonella enteric serotype Typhi is the most commonly occurring causative agent of

1.2enteric fever in India.

Prevalence; Phage typing; Biotypes; Randomly chosen; Susceptibility testing; Diversity.

Salmonella enteric serotype Typhi is the most commonly occurring causative agent of enteric

1,2 fever in India However, isolation of Salmonella enterica serotype Paratyphi A causing the same disease have been reported with an increasing

3,4 trend. In Rourkela, we have been reporting 5

S.Typhi causing enteric fever since 1996, whereas isolation of S.Paratyphi A causing the same disease has been encountered in this place since

62002.

Phage typing is a major means of epidemiological tracing as strains within a particular serotype may be differentiated into a number of phage types, and may help to define groups of persons who have been infected with the same strain from the same source. Again, combination of biotyping with phage typing gives a finer discrimination of strains in tracing out the source of infection. The use of phage typing and biotyping for epidemiological tracing had been documented

1since 1982 in different parts of India.

Phage typing and biotyping of both Salmonella Typhi and Salmonella Paratyphi A had been

6,7 reported from Rourkela in 2006 and 2007. There was a noticeable change in the prevalence pattern of phage types encountered among S.Typhi isolates in 2005-2006 in comparison to the phage types found in 2004-2005. In this retrospective, hospital based study, we have highlighted the changes in the prevalence pattern of phage types and biotypes among the Salmonella isolates chosen randomly. The susceptibility pattern of Salmonella isolates including the typed strains have also been reported in this communication.

This study was conducted between September 2005 and August 2006. A total of 1454 patients attending out-patient departments (OPDs) and wards of Paediatric and Medicine departments of Ispat General Hospital , Rourkela, Orissa,

.

Materials & methods

14

suspected of having enteric fever or pyrexia of unknown origin (PUO) were included in this study.

A total of 1454 blood samples were included in

this study. Irrespective of repeat sample we have

taken into account only one sample from each

patient. Only positive isolation was considered for

the patients having both positive and negative

results.

Clinical samples of blood were collected in brain

heart infusion broth with sterile precautions and 0

incubated aerobically at 37 C for 48 hours. Three

subcultures were done on blood agar, MacConkey

agar and Salmonella-Shigella agar and incubated 0

aerobically at 37 C for 18-24 hours. In negative

cases subcultures were done for one week.

Isolation of S. Typhi and S. Paratyphi A was 8established by conventional methods.

Identification of these two serotypes was

established by biochemical and serological testing 8,9

with factor sera. Antibiotic susceptibility testing

was performed by Kirby Bauer disk diffusion 10

method, with the modifications recommended

by the National Committee for Clinical Laboratory 11 Standards (NCCLS). Antimicrobials agents tested

were ampicillin, co-trimoxazole, chloromycetin,

gentamicin, amikacin, ciprofloxacin, cephotaxime

and ceftriaxone.

Randomly selected strains of both S. Typhi and

S. Paratyphi A were sent to the National

Salmonella Phage Typing Centre, Lady Hardinge

Medical College, New Delhi, India, for phage

typing and biotyping.

Out of 1454 patients, 1052 were children (72.35%)

and remaining 402 were adults (27.65%). Among

Results

Host organism Phage type Biotype No. of isolates

S. Typhi A I 5

(N=27) D1 I 1

E1 I 17

E9 I 1

J1 I 3

S. Paratyphi A 4 II 3

(N=24) 6 II 21

Table 1. Phage types encountered among S. Typhi ans S. Paratyphi

A isolates in Rourkela between September 2004 and August 2005.

the patients, 768 were males (52.81%) and 686

were females (47.19%).

Of 1454 patients, 112 were positive for Salmonella

isolates giving a per cent positivity of 7.70. Of 112

Salmonella isolates, 92 were S. Typhi strains and

remaining 20 were S. Paratyphi A strains. Almost

75 per cent of isolates were from pediatric

population, among which 52.38% were boys and

47.62% were girls.

In 2004-2005, the predominant phage type

encountered among S. Typhi strains was E1,

followed by phage type A (Table 1). In the present

study (2005-2006), predominant phage type

encountered among S. Typhi isolates was 40,

which itself is a rare and exotic phage type in India.

Second most common phage type of S. Typhi

isolates in this study was E1 and number of Vi-

Negative strains was 4 (Table 2). In both the

studies mentioned, the predominant phage type

found among S. Paratyphi A strains was type 6,

followed by phage types of either 4 or 1.

Host organism Phage type Biotype No. of isolates

S. Typhi A I 1

(N=36) D1 I 1

E1 I 8

J1 I 2

40 II 19

USV-2 II 1

Vi-Negative I 4

S. Paratyphi A 1 II 1

(N=12) 6 II 11

Table 2. Phage types encountered among S. Typhi and S. Paratyphi

A isolates in Rourkela between September 2005 and August 2006.

Antibiotics S. Typhi (%) S. Paratyphi A(%)

(N=92) (N=20)

Ampicillin 82 (89.13) 11 (55)

Co-trimoxazole 74 (80.43) 11 (55)

Chloramphenicol 85 (92.39) 12 (60)

Gentamicin 90 (97.82) 19 (95)

Amikacin 91 (98.91) 20 (100)

Ciprofloxacin 88 (95.65) 19 (95)

Cephotaxime 91 (98.91) 20 (100)

Ceftriaxone 91 (98.91) 19 (95)

Table 3. Susceptibility pattern of S. Typhi and S. Paratyphi

A isolates in Rourkela between September 2005 and August 2006.

15

phage type 40, which itself is a rare and exotic

phage type of S. Typhi in India. It is worth

mentioning that two more rare and exotic phage

types of multi-drug resistant (MDR) S. Typhi

strains, namely type 51 and type 28, caused

outbreaks in Kolkata and Mumbai respectively,

but in case of phage type 40, most of the strains

were not multi-drug resistant. Emergence of Vi-

negative strains among S. Typhi isolates in

Rourkela was another important finding during

the same time.

Till date, not many study-reports are available

regarding phage typing and biotyping of S.

Paratyphi A. A study among the patients (coming

from Indian subcontinents) in Kuwait reported

that 66% of S. Paratyphi A isolates belonged to 13 phage type I. Another study from Nagpur also

showed that the prevalent phage type among S.

Paratyphi A isolates from the local population was 14

type I. The most commonly encountered phage

type of S. Paratyphi A isolates from Rourkela was

type 6, a finding which hardly got any other

contemporary reference in India. From 1992 to

2003, commonest biotype of S. Paratyphi A in 13,14,15 India was type I, but in our study all the

phages of S. Paratyphi A belonged to biotype II.

The commonest biotype encountered among

S. Typhi strains isolated from Kolkata, Nagpur and 12,16,17 Ludhiana was type I, but in our study, biotype I

accounted for 44.4% of S. Typhi isolates and

remaining 55.6% were biotype II.

Susceptibility pattern to ampicillin and

chloramphenicol were very encouraging for 5,6,7 S.Typhi isolates as reported earlier, though it

was not that much inspiring for S.Paratyphi A

isolates in this study. In this study, differences in

per cent susceptibility between S. Typhi and

S. Paratyphi A isolates for ampici l l in,

chloramphenicol and ciprofloxacin were

statistically significant (P<0.05), whereas for the

rest of the antimicrobials tested, differences in per

cent susceptibility were found insignificant

(P>0.05). Although 4-5% resistance to

ciprofloxacin among Salmonella isolates was a

matter of concern, very high susceptibility of

those strains to aminoglycosides (gentamicin and

amikacin) and third generation cephalosporins

1,12

Most of the phage types of S. Typhi isolates

belonged to biotype I, except for phage type 40

and USV-2. All the phage types of S. Paratyphi A

isolates belonged to biotype II (Table 2).

Ampicillin and chloramphenicol sensitivity among

S. Typhi isolates was found very high in our study,

though 40-45% of S. Paratyphi A isolates showed

resistance to these antimicrobials (Table 3).

Isolates of both S. Typhi and S. Paratyphi A showed

remarkably high susceptibility to gentamicin and

amikacin. Resistance to ciprofloxacin was 4-5%

among the isolates of S. Typhi and S. Paratyphi A.

Susceptibility to cefotaxime and ceftriaxone was

very high among the isolates of both S. Typhi and

S. Paratyphi A (Table 3).

Randomly chosen strains of both S.Typhi and S.

Paratyphi A for phage typing and biotyping were

also found remarkably sensitive to the

antimicrobials used in our study. Out of 36 isolates

of S. Typhi, only 2 strains showed resistance to

ciprofloxacin and 1 strain resistant to

cephotaxime. Out of 12 strains of S. Paratyphi A

randomly chosen for phage typing and biotyping,

only 3 strains showed resistance to ampicillin, co-

trimoxazole and chloramphenicol. Interestingly,

all these 3 MDR strains of S. Paratyphi A belonged

to phage type 6.

Phage typing is one of the most important means

of epidemiological tracing. In 1982-89, the order

of frequency of phage types in north and central

India was A, E, O, while in south the second

predominant phage type was O. From 1990

onwards , E1 became the most commonly phage

type except in south India, where phage type O

was the predominant type. In 1992, the order of

frequency had become E1, O, A throughout the

country. However, there was hardly any report of

phage type O from any part of the country since 121994.

In our findings of phage types encountered among

S. Typhi strains from Rourkela, E1 was the most

commonly occurring phage type in 2004-2005

and second-most common phage type in

2005-2006. One strikingly different finding in

2005-2006 study was the highest occurrence of

Discussion

1

16

(cephotaxime and ceftriaxone) was highly

encouraging, and can be used judiciously in case

of ciprofloxacin resistance.

A diversity among phage types of S. Typhi isolates

has been noticed, though in case of S. Paratyphi A,

mostly phage type 6 was encountered. This

diversity of phage types observed in this eastern

part of India might be due to the diverse origin of

these phage types. The diversity of origin of these

phages again may be due to the migration of

population to and from Rourkela, an industrial

(steel) township, with respect to other parts of the

country. Further studies are required regarding

the epidemiological tracing especially for the

exotic phage type 40 of S. Typhi isolates.

References

1. Pillai PK, Prakash K. Current status of drug

resistance and phage types of Salmonella

typhi in India. Indian J Med Res 1993; 97:

154-158.

2. Sanghavi SK, Mane MP, Niphadkar KB.

Multidrug resistant Salmonella serotypes.

Indian J Med Microbiol 1999; 17(2): 88-90.

3. Sood S, Kapil A, Dash N, Das BK, Goel V and

Seth P. Paratyphoid fever in India. Emerg

Infect Dis 1999; 5: 483-484.

4. Chandel DS, Chaudhary R, Dhawan B,

Pandey A, Dey AB. Drug-resistant Salmonella

enterica serotype Paratyphi A in India.

Emerg Infect Dis 2000; 6: 420-421.

5. Bhattacharya SS, Das Usha. Occurrence of

Salmonella typhi infection in Rourkela,

Orissa. Indian J Med Res 2000; 111 : 75-76.

6. Bhattacharya SS, Das Usha. A sudden rise in

occurrence of Salmonella paratyphi A

infection in Rourkela, Orissa. Indian J Med

Microbiol 2007; 25 : 78-79.

7. Das Usha, Bhattacharya SS. Antibiogram,

phage typing & biotyping of Salmonella

Typhi & Salmonella Paratyphi a from

Rourkela, Orissa. Indian J Med Res 2006; 124

: 109-111.

8. Sleigh JD, Duguid JP. Salmonella. In: Collee

JG, Fraser AG, Marmion BP, eds. Practical

6

thMedical Microbiology. 13 ed. Edinburg :

Churchill Livingstone, 1984: 456-81.

9. Baron EJ, Peterson LR, Finegold SM. Bailey , th

and Scott s Diagnostic Microbiology. 9 ed.

St. Louis, Missouri : Mosby, 1994 : 362-85.

10. Bauer AW, Kirby WM, Sherris JC and Truck

M. Antibiotic susceptibility testing by a

standardized single disc method. Am J Clin

Pathol 1996; 45 : 493-6.

11. National Committee for Clinical Laboratory

Standards. Performance standards for thantimicrobial disc susceptibility tests, 6 ed.

Approved standard M2-A6. Wayne, Pa :

National Committee for Clinical Laboratory

Standards; 1997.

12. Saha MR, Palit A, Chatterjee NS, Dutta P,

Mitra U and Bhattacharya SK. A prospective

study of phage types & biotypes of

Salmonella enterica serotype Typhi isolated

from hospitalized children in Kolkata, India.

Indian J Med Res 2003; 117 : 201-204.

13. Panigrahi D, Chugh TD, West PWJ, Dimitrov

TZ, Groover S and Metha G. Antimicrobial

susceptibility, Phage typing and Plasmid

profile of Salmonella enterica serotype

paratyphi A strains isolated in Kuwait. Med

Princ Pract 2003; 12: 252-255.

14. Tankhiwale SS, Agrawal G, Jalgaonkar SV. An

unusually high occurrence of Salmonella

enterica serotype Paratyphi A in patients

with enteric fever. Indian J Med Res 2003;

117: 10-12.

15. Chopra GS, Basu SK and Bhattacharya SR.

Present Phage types and Antibiotic

susceptibility of Salmonellae. Indian J Pathol

Microbiol 1992; 4 : 345-350.

16. Agarwal V, Brahmne RB, Dhanvijay AG,

Jalgaonkar PD, Pathak AA, and Saoji AM.

Antibiogram, phage types and biotypes of

Salmonella Typhi isolated in Nagpur. Indian J

Med Res 1992; 95: 14-16.

17. Kumar R, Aneja KR, Punia AK, Roy P, Sharma

M and Gupta R. Changing pattern of

biotypes, phage types and drug resistance of

Salmonella Typhi in Ludhiana during 1980-

1999. Indian J Med Res 2001; 113: 175-180.

17

Abstract

Introduction:

Malaria is a major cause for hospital admissions in the tropical regions, but there is no objective tool to predict the length of hospital stay (LOS). Analyzing 700 hospitalized patients, a simple equation was devised. LOS was equal to ½ [5+ 5 x Severe anemia + 1 x Jaundice +2 x acute renal failure+3 cerebral malaria + 1 x Type of therapy]; where, presence of the complication is 1 and absence=0 ; Type of therapy : oral anti malaria therapy=1, parenteral =2, and any ICU intervention (ventilator, dialysis etc)=3 . The Length of hospital stay of a malaria patient can be estimated easily and rapidly by a simple formula, which does not require sophist icated investigations. It can be calculated at the time of admission as well as during the course of the disease.

When a patient is admitted to a hospital the most important concern is the survival. The subsequent question which arises in the mind of the health care providers, patients or their relatives, as well as the administrators is the duration of hospital stay of the patient. In malaria prone areas, many of the hospital beds in the referral centres are occupied by patients with malaria. The cost of treatment depends on several factors, one of these being the period of stay. A simple scoring system was devised by Mishra et al to predict the

1 survival of the malaria patients. A large number of the beds are occupied by these patients, during the peak transmission period, making it a major administrative problem. The LOS of admitted patients is one of the indicators of bed occupancy, planning and rotation of staff deployment, etc and

2-4the resource utilization. (Kazembe et al. 2006;

Velip et al. 2006; Van Houdenhoven et al. 2007)

Similarly, from the point of view of the health care

providers and administrators, no tool is available to predict the length of stay for the malaria cases. When confronted by a questioning/ inquisitive relative, the treating doctor only extends a rough estimate depending on his own experience, which is purely subjective. In practical situation, the statements are variable for different doctors and thus totally confusing to the relatives.

In the present study, it is attempted to identify various determinants on LOS, and to develop a mathematical model which can be used objectively for each patient admitted to a hospital. We tried to make it simple and easy to remember. It is attempted that it must be calculated rapidly and must not require too many lab data.

a. Hospital: Ispat General Hospital is situated in Sundargarh district of Orissa. It is a 685 bed hospital under of a Public sector steel plant.

b. It has eleven bed Critical care units. There are facilities for haemodialysis, peritoneal dialysis, blood banking, 24 hour emergency, haematology and biochemical laboratory etc.

c. Catchment area: Patients come from urban areas of Rourkela as well as surrounding villages, forested areas, mining localities etc.

d. Subjects: All patients admitted to the Internal Medicine Dept of Ispat General Hospital, Rourkela with confirmed malaria.

The study has two parts: (a) analysis of the malaria and (b) Multiple regression analysis.

In the first phase, database was collected prospectively in a format which includes age, sex, demographic data, treatment received before admission, biochemical and hematological reports, presence of seizures, treatment details, and the outcome. All those who expired were

Material & Methods:

Predictions of Lengths of Hospital stay of malaria patients

Address for communication :

Dr SK Mishra

Director, Ispat General Hospital,

Rourkela -769005, INDIA

Email: sarojrkl@gmail.com

Original Papers

Saroj K MishraDeptt. of Internal MedicineKishore C MahantaDeptt. of Internal MedicineRajalaxmi Mishra Deptt. of Mathematics,Sushilavati Govt. Womens College, Rourkela

Narayan P SahooDeptt. of Anaesthesia

18

Determinants

Entitled

Sex

Residence area

Acute renal failure

Cerebral malaria

Severe anemia

Jaundice

Complications

Level of treatment

Characteristics

EntitledNE

MaleFemales

RuralUrban

Sr Creatinine >3mg/dlSr Creatinine < 3mg/dl

GCS <10GCS >10

Hb<5.1 GHB>5 g/dl

Bil >3mg/dlBil < 3 mg/dl

UncomplicatedSingleMultiple

Oral drugsParenteral (QBH/AS)

No of patients

433267

512188

257443

29671

61639

18620

139561

390181129

115585

LOS (± SD)

3.99(±2.00)4.95(±2.95)

4.29 (±2.39)4.52(±2.61)

4.62(±2.75)3.91 (±1.73)

8.66 (±4.45) 4.17(±2.14)

7.41(±2.11)4.06(±2.08)

5.89(±2.65)4.37(±2.46)

5.81(±3.33)3.99(±2.03)

2.87(±1.68)4.33(±1.68)6.78(±3.53)

2.97(±21.18)4.62(±2.54)

P value

0.000*

0.299

0.000

0.000

0.000

0.027

0.000

0.000

0.000

Table 1. Characteristics of malaria patients and LOS

excluded from the study. 700 patients with complete data were analysed.

Student's t test was used to differentiate between male vs female; adult vs children; Rural vs urban; patients with acute renal failure (sr Creatinine >3 mg/dl), jaundice (sr Bilirubin > 3 mg/dl), severe anemia (Hb < 5 gm/dl) or cerebral malaria (unarousable coma or GCS <10).

The statistical analysis was done by using OpenEpi version 2.2.1 (2010), an Open Source Epidemiologic Statistics for Public Health, Version 2.2.1. www.OpenEpi.com, accessed on 18 June 2010 The difference is considered to be significant if p < 0.05.

In the second phase Multiple Regressions was performed to find out the relationship of the above parameters and to get a linear equation.

Statistics:

LOS was 8.66 (±4.45) days in presence of acute

renal failure, 7.41(±2.11) days in patients with

cerebral malaria, and 5.89 (±2.65) in presence of

severe anaemia and 5.81 (±3.33) in patients with

jaundice. LOS was longer in patients, who have

come from rural areas, but there was no

difference in males vs females.

After the determinants were identified, a linear

It will be in the form of

LOS = a x + a x + a x + a x + …… + C1 1 2 2 3 3 4 4

In the study we collected the data of those adult patients who survived and were discharged from the hospital. 700 surviving patients were analysed for the prediction of length of hospital stay. Out of these, 188 were females and rest were males.

Observations:

62% were entitled patients (either employees or their dependants, or retired employees of the steel plant: all of these get free medical treatment) and 38% were from different walks of life, including people from villages, township and traders. These patients were treated in the hospital on payment basis. Their income and socio economic conditions varied widely. 60% were from urban areas, and others were from suburbs or villages.

The comparisons of length of stay in different

groups are depicted in the Table-1. As it appears,

the length of stay was significantly longer in

patients with severe anemia, acute renal failure,

cerebral malaria and jaundice.

Thus LOS was 2.87(±1.68) days when the patient

was having uncomplicated malaria, which went

on increasing in presence of complications. Thus

19

patients are concerned regarding the length of stay in a tertiary care hospital and the cost associated with it. We searched the literature to find out the studies related to LOS in malaria patients. But there were only two studies cited in the MEDLINE by Kazembe et al. 2006 and Velip et

2,3 al. 2006. However, several studies have been carried out by Mounsey et al. 1995;. Bannwartet al., 1999; Arrahamyan et al. 2006; Clark et al., 2007 and Diringer et al., 2004 to predict the LOS in other clinical conditions viz, very low weight neonates in nursery, sepsis in ICU settings,

5-9patients after coronary surgery etc.

In a retrospective study in Spain, 1920 episodes of community-acquired pneumonia (CAP) in 27 community hospitals were analyzed by Cabre et

10al. (2007) for inter-hospital variability in length of

hospital stay (LOS), mortality and readmission rates. The overall adjusted LOS (mean+/-S.D.) was

10.0+/-9.8 days. LOS increased according to the Pneumonia Severity Index (PSI) risk class: 7.3 days for class I to 11.3 days for class V (P<0.001).

2Velip et al. (2006) from Goa described the determinants of LOS in malaria patients. The study indicated the importance of altered sensorium, presence of liver involvement, duration of therapy

equation was developed by using multiple regressions.

LOS = 2.441+ 2.565 Severe anemia + 0.447 Jaundice +0.993 acute renal failure

1.405 cerebral malaria +0.657 Level of therapy

The equation was made modified to make it simple and ready to use at bedside.

Thus,

LOS = 2.5+ 2.5 Severe anemia + 0.5 Jaundice +1 acute renal failure

1.5 cerebral malaria + 0.5 Type of therapy

Where, the severe anemia, jaundice, acute renal failure, cerebral malaria are considered as present=1, or absent=0; and level of treatment is oral anti- malaria treatment with chloroquin or quinine =1, parenteral artemisinine or quinine =2,

and any ICU intervention (ventilator, dialysis etc)=3.

Malaria being a disease mostly in the developing countries, the treatment is availed at different levels: (a) at home, (b) at the nearby health facilities and (c) referral centre for severe malaria cases; where the patient is shifted to a hospital far away from own place of residence. Relatives of

Discussion

Factors

Entitled or not

Residence

Severe anemia

Cerebral malaria

Jaundice

Acute renal failure

Level of therapy

Beta

0.186

0.106

2.565

1.405

0.447

0.993

0.657

P value

0.323

0.428

0.000

0.000

0.028

0.006

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 LOS

20

before admission as influencing factors. But a major flaw of the study was that most of the patients were uncomplicated ones. PUBMED search did not show studies on determination of LOS in severe malaria cases. Similarly publications are not available from any tertiary care hospital which manages both uncomplicated and complicated cases.

Some of the parameters in our study were similar to the Goa study. However, we have not been able to find any difference among the males and females, urban vs rural on LOS. But, as expected the LOS is higher in patients with any or more complications. It was noted that all complications are not similar, and they influence the survival in a different weighted capacity. Similarly they also influence the LOS.

When a very sick malaria patient is managed in critical care unit or high dependency unit, survival is the most important concern. In a previous study, Mishra et al. (2007) proposed a simple prediction rule for the survival of the patients with severe malaria by assigning 1,2,3 and 4 to A (anemia), B

(BUN↑ ), C (cerebral malaria) and D (Dyspnoea/ ARDS) respectively. The malaria score for adults (MSA) ranges from 0 to 10. The mortality was 2% for MSA 0 – 2; 10% for MSA 3–4, 40% for MSA 5–6 and 90% for MSA 7 or more. The sensitivity is 89.9% and positive predictive value is 94.1% when 5 is taken as the cut off value.

In the present one, we derived a very simple prediction rule for the LOS. It does not involve sophisticated data collection, estimation or analysis. Still it extends valuable information, which will be helpful to the clinicians. In addition, the formula can be used to modify the result/ prediction in the course of time if any new complication arises.

However, we have analyzed the data of only one year, and that too only among the adults. It is proposed that such studies may be undertaken among children too. It should also be validated in cohorts from different geographical regions.

Acknowledgement: We extend sincere thanks to the staff of IGH and malaria research Unit.

Funding: None, Conflict of interest: None

References:

1. Mishra SK, Panigrahi P, Mishra R, Mohanty S. Prediction of outcome in adults with severe falciparum malaria- a new scoring

system. Malaria Journal, 2007; 6:24. doi: 10.1186/ 1475-1875-6-24.

2. Velip AP, Kulkarni MS, Motghare DD, Vaz FS. Determinants of hospital stay among malaria patients at a tertiary care hospital in Goa. J Communic Dis, 2006; 38: 115-117

3. Kazembe LN, Kleinschmidt I, Sharp BL. Patterns of malaria-related hospital admissions and mortality among Malawian children: an example of spatial modelling of hospital register data Malaria Journal 2006, 5:93 doi:10.1186/1475-2875-5-93

4. Van Houdenhoven M, Nguyen TD, Eijkemans MJ, Steyerberg EW, Tilanus HW, Gommers D, Wullink G, Bakker J, Kazemier G.Optimizing intensive care capacity using individual length-of-stay prediction models. Crit Care. 2007 27; 11 :R42

5. Mounsey JP, Griffith MJ, Heaviside DW, Brown AH, Reid DS. Determinants of LOS in ICU and in hospital after coronary artery surgery. Br Heart J, 1995; 73: 92-98.

6. Arrahamyan L, Demirchyan A, Thomson ME, Hovaguimian H. Determinants of morbidity and ICU stay after coronary surgery. Asian Cardiovasc Thorac Ann, 2006; 14: 114-118.

7. Bannwart BC, Rebello cerebral malaria, Sadeck LSR, Pontes MD, Ramos JLA, Leone C. Prediction of Length of Hospital Stay in Neonatal Units for Very Low Birth Weight Infants. J Perinatology, 1999; 19: 92-96

8. Clark DE, Lucas FL, Ryan LM. Predicting hospital mortality, length of stay, and transfer to long-term care for injured patients. J Trauma, 2007 ;62:592-600.

9. Diringer MN, Reaven NL, Funk SE, Uman GC. Elevated body temperature independently contributes to increased length of stay in neurologic intensive care unit patients. Crit Care Med. 2004 ;32 :1489-95.

10. Cabre M, Bolivar I, Pera G, Pallares R; Pneumonia Study Collaborative Group. Factors influencing length of hospital stay in community-acquired pneumonia: a study in 27 community hospitals. Epidemiol Infect. 2004 Oct;132(5):821-9.Velip AP, Kulkarni MS, Motghare DD, Vaz FS. Determinants of hospital stay among malaria patients at a tertiary care hospital in Goa. J Communic Dis, 2006; 38: 115-117

21

Peutz- Jeghers Syndrome presenting as acute intestinal

obstruction due to Jejunal Intussusception in an adult maleAmulya M Acharya

Sishir R Dash

Manoja K Panigrahi

Deptt. of Surgery

Address for communication :Dr A.M.Acharya, Sr Deputy Director,

Deptt. of Surgery, Ispat General Hospital, Rourkela, Odisha, India

Email:dramulya.acharya@gmail.com

ABSTRACT

Key words:

Introduction:

Peutz – Jeghers syndrome (PJS) is a rare familial

a u t o s o m a l d o m i n a n t d i s o r d e r w i t h

hamartomatous polyposis of G I Tract and melanin

pigmentation around mouth, oral mucosa , lips

and digits. Most common symptoms are

recurrent pain abdomen, anaemia and blood in

stool. Presentation of frank intussusception and

intestinal obstruction in adults is uncommon. We

are reporting a case of Indian adult male

presented to us in acute intestinal obstruction due

to jejuno jejunal intussusception. There were

multiple polyps in the small gut and one large

polyp of 4cm x 8cm was the lead point in triggering

the intussusception. Histopathology confirmed

them as hamartomatous polyps typically seen in

Peutz- Jeghers syndrome. As it is unusual to see

such rare case in clinical practice and scarcity of

literature, we feel to report this for the benefit of

clinicians and students. Awareness of the disease

is helpful for proper diagnosis, early management

and follow up with genetic counseling to the

patient and his family.

Peutz, Jeghers,PJS, polyposis, intestinal polyps,

melanin pigmentation, intussusception

Adult intussusception is rare and do not present

the symptoms of red currant jelly stool that is seen 1 in children. Very rarely multiple intestinal polyps

seen in the familial disorder Peutz- Jeghers

syndrome (PJS) with the typical muco- cutaneous

pigmentation around mouth, oral mucosa lips

and digits. The most common symptoms are

recurrent pain abdomen, anemia, malena and

hematochezia. Here we are reporting a case of PJS

presented as acute intestinal obstruction due to

jejunal intussusception in an Indian adult male.

We are providing some clinical photographs,

histopathology report and added discussion

available from the scarce literature which may be

of educational importance.

A 58 years old Indian male was admitted in the

surgical ward with sudden onset of severe

abdominal pain associated with vomiting of three

days duration. He was found afebrile, anemic and

dehydrated. Pulse 98/min, BP 100 / 70 mm Hg.

Abdomen was distended with diffuse tenderness

and guarding. An ill defined soft immobile mass

(15 x 8 cm) was palpable in the epigastrium. Some

bluish black pigmentation was seen over his

buccal mucosa but could not be correlated with

the acute abdominal condition (Fig.1).

Case report:

Figure 1: Bluish-black pigmentation over buccal mucosa.

Case reports

22

One large polyp of 3.5cm with a 8cm stalk was

found on per rectal examination (Fig.2).

Biochem reports were normal except low protein

(total protein 4g and albumin 1.9g). X-Ray

abdomen showed few air-fluid levels. Ultrasound

of abdomen revealed two concentric echo

structures with classical target sign suggestive of

intussusception (Fig.3a, 3b). Emergency

laparotomy was taken up with a provisional

diagnosis of acute intestinal obstruction.

Laparotomy revealed jejuno-jejunal intussuscep-

tion about one foot distal to duodeno-jejunal

flexture involving two feet long segment of

jejunum. Multiple polyps were seen on the

involved jejunum. There was one large polypoidal

mass of 4cmx8cm which was the lead point in

triggering the intussusceptions (Fig.4a,b).

About two feet of jejunum involving the

intussusception and having multiple polyps was

excised and end to end anastomosis done

followed by rectal polypectomy. Rest of the small

and large gut was thoroughly palpated and found

to be normal. Patient recovered uneventfully.

Histopa-thology of resected jejunum with polyps

showed branching of smooth muscles arising from

muscularis mucosae into the stroma of columnar

and goblet cells which are typical hamartomatous

changes seen in Peutz- Jeghers syndrome (Fig.5).

There was no evidence of atypia or malignancy.

Lymph nodes showed reactive hyperplasia.The case was finally diagnosed as Peutz-

Jeghers syndrome with unusual presentation of

acute intestinal obstruction duo to adult

intussusception.

Figure 2Rectal polyp 3.5cm with 8cm long stalk

Figure 3a US abomen showing target sign of intussusception.

Figure 3b Intussuscipien inside intussusceptum.

Figure 4a Multiple polyps in jejunum.

23

Follow up investigations were carried out. His

upper GI endoscopy and colonoscopy did not

reveal any polyp. Ba-meal follow through was

normal. We could not do the genetic study due to

lack of facilities.

The patient and his family members are now in

regular follow up.

Peutz- Jeghers syndrome (PJS) is a familial disorder

with two distinct features, (a) multiple

hamartomatous polyps of GI tract and (b) melanin

pigmentation around mouth, oral mucosa and

digits. The syndrome first described by Jan Peutz

in 1921 and later published in detail by Harold 2

Jegher in 1949 . First case was reported by 3 A.K.Basu in 1952. The disease is an autosomal

Discussion:

dominant disorder occurs due to subtle loss of 4 chromosome 19p 13.3 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.

Different associated anomalies have been 5reported in PJS. Dormandy et al reported polyps

in bladder, renal pelvis, bronchus and nose . Rarely

polyps in ureter, gallbladder and CBD may occur.

Even ovarian cyst adenoma and Sertoli tumor of

testes are reported.

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 6,7 cases have been reported from India. Malignant

potential of GI tract is very high in these patients,

as reported by various investigators. Giardiello8

et al found 93% cumulative risk of developing

cancer (15.2 fold relative risk, RR) by the age

64years The relative risks (RR) for cancer formation in PJS in relation to general population

are: Small intestine (RR 520), stomach (RR 96),

pancreas (RR 132), colon (RR 84), oesophagus (RR

57), ovary (RR 27), lungs (RR 17), uterus (RR 16)

and breast (RR15).

Giardiello and Trimbath published a review of PJS

and recommended the following management 9.and follow up

• Polypectomy of isolated polyps > 1cm in

stomach, colon

Morbidity and Mortality:

Management:

Figure 5 Branching of smooth muscle into the stroma of the epithelium.

Figure 4b large polypoidal mass which had triggered the intussusception.

24

Resection of intestine segment having

confluence of polyps

• Resection anastomosis for intussusception

• Intra operative push enteroscopy and

polypectomy of >1cm polyps.

1. Annual physical exam. of breast, abdomen,

pelvis( ovary), testes

2. US for pancreas, ovaries, testes annually

3. Mammography / MRI, Pap smear every year

4. Annual complete blood cell count

5. Ba-meal follow through every 2 year

6. EGD & colonoscopy every 2 year

7. Genetic counseling and screening from birth

of all first-degree relatives.

PJS is a rare familial disease involving multiple

polyps of GIT and mucocutaneous pigmentation

around mouth, lips, oral mucosa and digits.

Common C/F are recurrent pain abdomen,

anemia, GI bleeding. Acute Intestinal Obstruction,

Intussusception are common complications.

Development of cancer is relatively high. Early

diagnosis and proper M/M can reduce

complications. Genetic counseling & screening of

family members should be done as there is high

risk of development of cancer.

REFERENCES :

1. Agha FP, Intussusception in adult. Am J

Roentgenol 1986 March;143(3): 527-31

•

9Recommended follow up:

CONCLUSION:

2. Jeghers H, McKusick VA et al. Generalised

intestinal polyposis and melanin spot s of

oral mucosa, lips and digits. N Eng J Med

1949; 241: 993-1005, 1031-6.

3. Basu, A. K.: Familial intestinal polyposis with

pigmentat ion of sk in and mucous

membrane. Lancet 1952, 2: 586-587.

4. Hemminki A, Tomlinson I, Markie D, et al

Localization of susceptibility locus for Peutz-

Jeghers syndrome to 19p using comparative

genomic hybridization and targeted linkage

analysis . Nat Genet 1997; 15: 87-90

5. Dormandy TL, Gastrointestinal polyposis

with mucocutaneous pigmentation ( Peutz-

Jeghers syndrome) N Engl J Med 1957; 256:

1141-6

6. Saxena PK, Arora RK, Mehta, Singh HH.

Peutz-Jeghers syndrome with unusual

features (a case report). J Postgrad Med

1986 ;32:236-8

7. Thakker HH,Joshi A,Despande A, Peutz

Jeghers syndrome presenting as jejuno ileal

intussusception in an adult male: A case

report. Cases J,2009 Aug 2:8865

8. Giardiello FM, Brensinger JD, Tersmette AC ,

Vary high risk of cancer in familial Peutz-

Jeghers syndrome. Gastroenterology , Dec

2000;119(6): 1447-53.

9. Giardiello FM, Trimbath JD, Peutz- Jeghers

syndrome and management recommen-

dations. Cin Gastroenterol Hepatol,2006; 4:

408-15.

10. Clava D,Howe JR. Hamartomatous polyposis

syndrome. Sur Clin North Am 2008 Aug;

88(40) : 779-817

25

Pitabas Mishra Deptt. of Paediatrics

Address for communication :Dr. R. Satpathy, Sr. Consultant,

UNMC NICHD Research Network Email: Globalnet_rkl@yahoo.com

Radhanath Satpathy UNMC NICHD Research Network

Nimain C Nanda Deptt. of Paediatrics

Rajan K BeheraDeptt. of Surgery

Pinaki PanigrahiProfessor and Director, Center for Global Health and DevelopmentCollege of Public Health , University of Nebraska Medical Center, USA

Abstract:

Keyword:

Introduction:

Necrotising Fasciitis (NF) is relatively a rare disease

found in adults. When occur in neonates, its

outcome is usually fatal. Two rare cases of

Necrotizing fasciitis (NF) have been reported with

possible rare association of trisomy.

Necrotising Fasciitis, Neonate

Necrotising fasciitis (NF), otherwise known as the

Flesh Eating Disease, is a term that describes a

disease condition of rapidly spreading infection

usually located in fascial plane of connective tissue 1that results in tissue necrosis . Although the

condition was described earlier, Dr B Wilson 2termed the condition in 1952 . The disease occurs

infrequently and almost can occur in any part of

the body. The spread of infection can be so fast

that it is difficult to stop it with both antimicrobial

drugs and surgery. It is predominantly an adult

disorder. When it occurs in children the course is

usually fatal. Less than a 100 Neonatal NF cases

have been reported in literature. The purpose of

this communication is to report two rare cases of

neonatal NF with fatality.

Case-1 (Figure1) Baby of SA was admitted to

hospital with a big area of ulceration on the back

of 3 days duration. The baby was delivered

normally in hospital and was weighing 2.8 kg. Early

neonatal period was uneventful. It was all along

breastfed. On Day-15, baby had fever and was

crying inconsolably. Next morning, mother

noticed an area of redness on the back that rapidly

spread all over the lower half of the back with

ulceration. On examination, baby was febrile,

irritable, sucking from mother, pink with features

of trisomy and had no other focal sign of infection

than an ulcerated area of 6x4 cm, seen being

surrounded by deep brown dead tissue on the

back. The floor of the ulcer was showing muscles

of the back and oozing of pus. Margin was much

irregular and was looking like punched out ulcer. It

was treated with combination antibiotics, daily

dressing of wound and wound debridement as

and when necessary. Total count was

6400/cm,Hb-14.5/dl, and blood group was B+ve.

Blood culture and wound swab culture did not

reveal any organism. Though, baby improved with

therapy, parents took discharge against medical

advice on D10 and the baby expired at home

after 3 days.

Case-2 (Figure2) Baby of BS, was admitted to

hospital on Day 11 with complaints of unable to

take feed properly, ulceration of mouth of 2 days

duration and a swelling on the back with bluish-

Necrotising Fasciitis In Neonates – Case Report

Case Reports

26

Figure 1 Showing lesion on back

red discoloration and painful to touch of one day

duration. He was born in hospital to a multi-para

mother by normal vaginal delivery and cried soon

after birth. There was premature rupture of

membrane for a week. There was no maternal

fever or any other sickness. Soon after birth, baby

was fed breast milk and had some oral ulceration. 0 On examination baby was febrile (temp 102 F),

lethargic, pale and weighing 2.8kg. Heart rate was

140 and respiration rate was 44/minute. There

was jaundice but no cyanosis. All peripheral

pulsations were felt and capillary refill time was

less than 4 seconds. Ears and anterior fontanel

were normal. Oral thrush was there. A big bluish

red discolored area was on the back measuring

nearly 3''X4” size without any ulceration or oozing

(Fig-2). It had an area of central fluctuation. A

many vesico-pustular lesions were detected on

the peri-umbilical area and back on gluteal region.

Cardiovascular and respiratory systems and

abdominal examination were normal. Neonatal

reflexes were poorly elicitated. Necessary

investigations were done and pulse oxymetry

showed 95 to 99% saturation.

The baby was put on combination antibiotics

(Cefrtriaxone and amikacin) and managed in

pediatric ward. Surgeons saw the baby and

aspirated sero-sangunous fluid on D-2. Baby

continued to be febrile, sick and had abdominal

distention. Wound sloughed out and a raw area

developed by D-4. Vital signs were unstable and

baby was put on IV fluid and pressure amines. By

D-5 there was edema, fever, respiratory distress,

refusal to feed and abdominal distension.

Vancomycin was added to the regimen and

continued for 2weeks. The skins including the

deep tissue were shredded (Fig-2) and wound

debridment was done, the area affected was daily

cleaned and dressed, dead tissues were removed.

Anemia, edema and fever continued for long time

and the baby was somewhat better by 3 weeks

hospital stay.

During the course of stay, the baby continued to

have fever all the time and sick. There was edema

of limbs, abdominal distension and conjugated

hyperbilirubinemia. As the baby developed

anemia and low general condition, it received two

units of blood transfusion. Both medical and

surgical management and crisis management n d

continued for 22 days. On 22 day of

hospitalization, baby had cardiac arrest and could

not be revived.

Necrotising fasciitis is a rare condition in neonates.

Terms like necrotising fasciitis, myonecrosis, and

necrotising adipositis refer to classification by depth of infection. Type 1(polymicrobial) and type

2 (monomicrobial) infections refer to classification based on microbial cause. Historically, necrotizing

infections were classified according to anatomical sites. Fournier gangrene (involving the perineum)

and Ludwig's angina (involving sub-mandibular and sublingual spaces) are examples. These

infections were named after the physicians who

1first described those . NF is frequently

attributable to secondary infections. They are like

omphalitis, mammitis, balanitis, postoperative

complications, and bullous impetigo, and may be

Discussion

Figure 2 Early changes on the back

27

associated with diabetes mellitus, necrotising 3enterocolitis, immunodeficiency, malnutrition

and septicemia. Both the babies were neonates

and were diagnosed in hospital at the interval of

five years, proving the rarity of the condition. If it is

not suspected, the diagnosis is missed. The most

common site of involvement in pediatric patients

is the abdominal wall followed by the thorax, back, 4

extremities with head and neck as unusual sites .

In our case, classically neonates had the back

involvement.

The initial skin presentation ranges from a minimal

rash to erythema, oedema, induration or cellulitis.

These lesions spread rapidly. The overlying skin

may later develop a violaceous discolouration,

peau d'orange appearance, bullae, or necrosis.

Our second case (Fig-2) had the classical

presentation and was detected and treated from ndthe 2 day of occurrence. Continued fever and

tachycardia was seen in both the cases. Marked

tissue oedema, rapid progression of inflammation

and signs of systemic toxicity were seen in the

second case. Death occurred before surgery or

shortly after surgical intervention as a result of

bacter ia l infect ion with sept ic shock,

disseminated intravascular coagulation and/or

multiple organ failure. Our second case died due

to multi-organ failure. Empirical antibiotics to

cover (Cephalosporin and aminoglycoside) gram

positive and negative organism were used, to start

with. Subsequently vancomycin has been used in

second case. We had two different cases, one

presented while skin shredding has occurred (Fig-1)

and the other at the onset of the disease (Fig-2).

Case one, with medico-surgical management had

stable vital signs but died at home on discharge

against medical advice, whereas case two had all

complications of neonatal sepsis and did not

survive after a long duration of hospital stay, thus

showing the fatality.

Early diagnosis and aggressive surgical treatment

reduces risk; however, it is often difficult and

patients are treated for simple cellulitis until they

rapidly deteriorate. Prompt diagnosis with 5

aggressive therapy improves survival . Antibiotic

therapy is mandatory and early surgical

exploration and debridement is critical to ensure a

good outcome. Microbiologically, until blood

culture results are available, wide spectrum

coverage with intravenous antibiotics is started.

These antibiotics should cover S pyogenes, S

aureus, and Gram-negative aerobes and

anaerobes as clinically indicated. Group A Beta

hemolytic streptococci (GABHS) has been

reported widely as a single pathogen. Appropriate

therapy includes IV Penicillin150 000u/kg/day in 4

divided doses, Clindamycin 40mg/kg/day in 4

divided doses and Vancomycin40mg/kg/day in 3-64 divided doses .

References:

1. Medicine Net.com- assessed on 26.10.2010

2. Hsieh WS, Yang PH, Chao HC, Lai JY. Neonatal

necrotizing fasciitis: a report of three cases and

review of the literature. Pediatrics 1999;

103:e53.

3. Antonio FM, Pedro GC; C DM, Carola DM; Luz

Orozco-C, Tamayo-S; Ramon RM Necrotizing

Fasciitis, Report of 39 Pediatric Cases, Arch

Dermatol. 2002; 138: 893-899.

4. Kothari PR and Kulkarni B, Neonatal

Necrotizing Fascitis, Indian Pediatrics: 2004,

41:1070-71

5. Moss RL, Musemeche CA, Kosloske A M.

Necrotising fasciitis in children: prompt

recognition and aggressive therapy improve

survival. J Pediatr Surg 1996 ; 31:1142–6.

6. Textbook of Pediatric Infectious Diseases, 6th

Edition, Saunders, Philadelphia 2009; pg79-791

28

Case Reports

Abstract :

Keywords:

Introduction:

Xeroderma pigmentosum with squamous cell

carcinoma and basal cell carcinoma is rarely

reported. A 22 years female having Xeroderma

Pigmentosum presented with ulcerated and

blacklish pigmented lesion on Sun exposed area of

body. Histopathological examination of the three

different skin biopsy showed squamous cell

carcinoma, basal cell carcinoma & initial phase of

Xeroderma pigmentosum. Case is being

presented because of the rare association of these

tumors with Xeroderma pigmentosum in Indian

scenario. It is also observed for the first time in

IGH, Rourkela.

Xeroderma pigmentosum, squamous cell

carcinoma, basal cell carcinoma

Xeroderma Pigmentosum (XP) is a rare genetically

heterogenous autosomal recessive disorder

resulting from the defect in DNA repair

mechanism i.e. Nucleotide Excision Repair (NER).

It is characterized by photosensitivity, pigmentary

changes, premature skin ageing and various

cutaneous and internal malignancies at an early

age. XP was first described by Herba and Kaposi in 1

1874. It occurs with an estimated frequency of

1:250,000 in US and somehow more common in

2Japan i.e. 1: 40,000 but in Indian scenario its

frequency is not yet calculated because of its

rarity. To our knowledge, dual malignancy i.e.

Squamous Cell Carcinoma (SCC) and Basal Cell

Carcinoma (BCC) associated with XP is rarely

reported in India.

Here we report a case of XP with different stages

of skin manifestations.

22 year female presented with various pigmented

lesion on face and hand (Fig1). Pigmented lesion

on face was since childhood. On examination she

had an ulcerated lesion over forehead with rolled

CASE REPORT:

Squamous cell carcinoma & basal cell carcinoma with

xeroderma pigmentosa – a rare presentation

Aruna M Deptt. of Pathology

Minz Niranjan K of Dermatology

BeheraDeptt.

Rabi R of Pathology

Panda Deptt.

Sanghamitra of Pathology

SatpathiDeptt.

Prativa K of Pathology

BeheraDeptt.

Usha of Microbiology

DasDeptt.

Address for communication : Dr. Aruna Mukti Minz, Specialist,

Department of Pathology,

Ispat General Hospital, Rourkela

e-amil : arunaminz@yahoo.com

Fig1. Pigmented lesions on face

29

out border clinically diagnosed as BCC,

hypertrophied lesion on cheek clinically

diagnosed as actinic keratosis and scarring lesion

on right hand clinically suggestive of SCC. She also

had photophobia .The lesions were progressive

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 4differentiated SCC. (F-4).

Xeroderma Pigmentosum is a rare inherited

disease. The incidence is approximately 1:250,000

in US and somehow more common in Japan i.e. 2 1:40,000. 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 3 XPA is common and XPE is rare. XP patients are at

a high risk for developing skin cancers at an early

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

present as early as 4-5 years of age. As our case

had two varieties of malignancies i.e. SCC and BCC,

she progressed to the third stage of the disease.

Occular problem occurs in 80% cases includes

photophobia, conjunct iv i t is , ectropion

symblephoron with ulceration and malignancies.

Our patient had Photophobia.

Discussion:

Fig 3. Basal Cell Carcinoma (H&E)

stFig2. 1 Stage of Skin Changes of XP

Fig 4. Squamous Cell Carcinoma (H&E)

30

References:

1. Hebra F, Kapsosi M. On diseases of the Skin

including the exanthemata. Vol.3 ( translated by

W.Tay) London: The new Syderham Society

1874;252-8.

2. Robbins JH, Kraemer KH, Lulzner MA, Festoff

BW, Coon HG. Xeroderma Pigmentosum, an

inherited disease with Sun sensitivity, multiple

Cutaneous neoplsia and abnormal DNA repair.

Ann intern Med 1974; 80:221-48.

3. J.I.Harper, R.C.Trembath . Genetics and

Genodermatosis in : Rooks Text book of th

Dermatology.7 Edn. Blackwell 2004; 12.56-

12.61.

4. Lever WF , Schaumberg-Lever G. Congenital

Diseases. In: Lever WF, Schawmberg-Lever G. eds. th

Histopathology of Skin. 9 Edn. Philadelphia: JB

Lippincott 2005; 147-148.

Neurological problems are seen in nearly 20% of

cases which includes microcephaly & Mental

Retardation (MR). De Sanctis cacchione syndrome

refers to the combination of XP & MR and 3cerebellar ataxia, hypogonadism and dwarfism.

In our case, she had absolutely normal

intelligence. Prenatal diagnosis can be made by

amniocentesis.

Xeroderma pigmentosum is a progressive disease

and patient dies due to complications of various

malignancies. So the management of XP patient

needs protection from sunlight by every possible

means. Early and adequate excision &

radiotherapy of all tumors are preferred. Our case

was referred to higher centre for Radiotherapy.

The relatives of known cases must be screened to

detect any genetic defect at early possible stage.

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.

31

Case reports

Abstract :

Keywords:

Introduction:

Case History:

Brain metastases from papillary thyroid

carcinoma (PTC) are extremely rare with a

frequency of only 0.1 to5 percent. Mostly they are

first detected during the course of treatment of

PTC. With the publication of case reports of brain

metastases from clinically silent PTC and

importance of tissue diagnosis to treat this

condition, as it may need radio iodine therapy,

intense thyroid work-up may be needed, in brain

metastases, with unknown primary.

metastases brain, papillary carcinoma thyroid,

silent, occult, unknown primary.

Papillary thyroid carcinoma rarely spreads to 1brain. We, here, report a case of extensive brain

metastases with undetectable primary and

clinically normal thyroid gland. Due to recent

publications, detail thyroid work-up with different

imaging modalities in conjunction with fine

needle aspiration cytology led to suspicion of PTC.

It was corroborated by the tissue diagnosis of

brain lesion. Incidentally, more than 20 countable

metastatic lesions in the brain, is being reported

for the first time.

A 52 years married lady presented at

Neurosurgery department of our hospital with

complaints of weakness of left upper limb for two

months and headache off and on for the same

period. She further revealed that she was having

tingling sensation on her left side limbs at times.

Her higher functions were normal. She was having

gross papilledema on both sides but rest of her

cranial nerves were normal. Her power around

the left shoulder joint, elbow was grade 3/5, at the

wrist and grip of same side was grade 2/5.There

was spasticity in left upper limb but no additional

movements. No sensory deficit could be detected

in her body including her left upper limb, though

she was complaining of tingling sensation. Deep

tendon reflexes were normal all over except in left

upper limb, where they were exaggerated. Her

cortical and cerebellar functions as well as gait

were normal. All other systems, including the

thyroid gland, were normal on clinical

examination. Her hemogram, biochemical reports

and ski gram of cervical spine were within normal

limit. Her computerized tomogram (CT) of the

brain showed multiple ring enhancing lesions

distributed in both the hemispheres and

cerebellum (Figure1). Magnetic Resonance (MR)

imaging and spectroscopy suggested secondary

deposits in brain. With the provisional diagnosis

of multiple metastases of brain, attempt was

made to find out the primary lesion.

Accordingly, she was again examined thoroughly

and investigated with ski gram and CT scan of

Address for communication :Dr.R.N.Mohapatra,

Neurosurgery Department,

Rourkela-769005, India.

e-mail: rkl_rabi@in.com

Multiple brain metastases due to occult Papillary Carcinoma of

thyroid gland: A Case Report

Rabindra N Mohapatra Deptt. of Neurosurgery

Sudhiranjan Pradhan Deptt. of Radiology

Saropani HembramDeptt. Neurosurgery of

Rabiratna PandaDeptt. of pathology

Pushpa Kumari, Deptt. of Ophthalmology

32

chest, ultrasonic examination of abdomen and

pelvis, all of which were unrevealing. Her

mammary glands were normal. On suspicion, she

was advised ultrasonic examination of thyroid,

though the gland was clinically normal. It revealed

one solid nodule of size 6 millimeter (mm) in

diameter on right lobe and the other one on left

side, which was cystic and of same size.

Ultrasound guided fine needle aspiration cytology

(FNAC) was done from both the lesions. FNAC

from the solid nodule was suspicious of papillary

carcinoma.

Thyroid scanning with radio iodine revealed a cold

nodule on right lobe but a normal brain. To clinch

the diagnosis, craniotomy and excision of 2 lesions

from right frontal lobe was done. The excised

specimen was sent for histopathology study,

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

months, the lady is having good cognitive

function, weakness of left half of body improv ed,

needs support to walk and to carry out her day to

day activities. She is on steroid and prophylactic

anticonvulsant only.

Discussion : PTC is the most common thyroid 1, 2, 3

neoplasm. Distant metastases occur in only 5

to 14% cases. The most common sites for distant

metastasis of PTC are the lungs, followed by the

bone. Brain metastasis from PTC is extremely 1, 2, 3, 4, 5

rare. Total 23 cases are reported in literature.1 CT scan, MRI and MR spectroscopy all may help

to diagnose metastases in brain, but they cannot

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 6by the radio isotope. Tco-4 thyroid scanning may

support the diagnosis.

Surgery, radiotherapy, and radioactive iodine

therapy are the available modalities for treatment

of PTC with brain metastases, along with total 1,7

thyroidectomy. But these modalities are

dependent on tissue diagnosis. If primary disease

can be detected initially, it may be possible to

avoid craniotomy and treat the primary disease

early.

Figure1. Contrast enhanced CT scan of brain shows multiple enhancing ring lesions in brain with

surrounding oedema.

Figure2. Histopathology of the brain lesion in low power magnification shows prominent

papillary architecture

33

Median survival of thyroid malignancy, once brain

metastases have occurred varies between 4.7 to 7, 89.4 months.

Metastases from papillary carcinoma of thyroid,

though rare, are being reported by different

authors. When brain metastases are detected

from unknown primary, thyroid gland should be

investigated in detail for the primary lesion

because treatment modalities may be different in

this type of disease. We found ultrasonic

examination followed by fine needle aspiration

cytology to be fruitful procedure in this regard.

References:

1. Saleh FA, Abdullah SA, Wafa AS .Abdullah ST.

Cerebellar mass as a primary presentation of

papillary thyroid carcinoma: case report and

literature review. Head & Neck Oncology

2009; 1:23doi:10.1186/1758-3284-1-23

2. Erem C, Hacihasanoglu A, Sari A, Reis A,

Alhan E, Cobanoglu U, Onder Ersöz H, Ukinç

K. Intrathyroideal papil lary thyroid

carcinoma presenting with a solitary brain

metastasis. Endocrine 2004;25(2): 187-93

3. Jianyi Li, Kenneth D Aldape, Gregory N

Fuller,Suzanne Z Powell. Metastatic Papillary

Thyroid Carcinoma in Brain: Report of Three

Cases. The FASEB Journal 2008; 22:706-25.

4. Tsuguhito O, Yukihiro B, Masamichi H,

Nobuyoshi T, Yasushi T, Yoshio K , Masakiyo F.

Papillary Carcinoma of the Thyroid with

Distant Metastases to the Cerebrum: a Case

Report. Japanese Journal of Clinical

Oncology 2001; 31:112-5

5. Brunicardi FC, Andersen DK, Billiar TR, Dunn

DL, Hunter JG, Matthews JB, Pollock RE,

Schwartz SI: Schwartz's Principles Of Surgery.

8th edition. New York: McGraw-Hill; 2005.

6. Misaki T, Iwata M, Kasagi K, Konishi J. Brain

metastasis from differentiated thyroid

cancer in patients treated with radioiodine

for bone and lung lesions.

Ann Nucl Med 2000;14:111-4.

7. Biswal B M, Bal CS, Singh MS, Padhy AK, Rath

GK. Management of intracranial metastases

of differentiated carcinoma of thyroid.

Journal of Neuro-Oncology 1994, 22:77-81

8. Chiu AC, Delpassand ES, Sherman SI.

Prognosis and treatment of brain metastases

in thyroid carcinoma.

J Clin Endocrinol Metab 1997; 82:3637-42.

Key to the Practice Paper

1c, 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

34

Abstract:

Key words:

Introduction:

Treatment of sepsis is often difficult and

challenging. The problem is aggravated in diabetic

patients. The treatment is based broadly on

diabetic control, broad spectrum antibiotic

therapy, ventilator support, dialysis and other

supportive therapy, may not be sufficient for the

recovery of the patient. Mortality in sepsis with 1

multi-organ failure is around 65%. We report one

unusual case of severe sepsis which ultimately

responded to anti-fungal treatment.

Sepsis, Diabetes, Antifungal.

Sepsis in cases of diabetes has poor outcome.

Diabetic patients are immunocompromised

hence multi organ involvement is much more

frequent then in non diabetics. Infection or

inflammation leads to poor glycemic control which

perpetuates severe infection leading to sepsis and

multi organ failure. Patients treated in ICU with broad

spectrum antibiotics and on ventilator support are

more prone for opportunistic infection like yeast, 2,3fungus, etc.

We report such a case of diabetes mellitus with

severe sepsis who ultimately responded to

empirical anti fungal treatment after adequate

antibiotic therapy and organ support treatment

failed to resolve her condition.

Case Report: A 44 year old female a known case of

Type II diabetes mellitus, hypertension,

hypothyroid was admitted with history of fever,

loose motion for last three days. Fever was not

associated with chills or rigor. It was intermittent

type and low grade. The loose motion was watery

and six to seven times a day. There was no history

of cough, vomiting, itching. At the time of

admission her GCS was 15, pulse 102/ minute

regular, all peripheral pulses were well felt, BP-

80/60 mm Hg, chest was clinically clear, heart

sounds were normal. She was admitted to general

ward. Her hypotension did not respond to fluid

challenge and her sensorium deteriorated, so she

was shifted to ICU. Her chest x-ray showed

shadowing in the left lower zone. She developed

acute renal failure .So she had a central line placed

and fluid replacement was done with frequent

measurement of the central venous pressure. She

was intubated and ventilated in pressure

controlled mode. In spite of adequate fluid

replacement her urine output decreased and

hypotension persisted. So she was put on

inotrope support and peritoneal dialysis started

and continued for 40 two litre exchanges with

indwelling time of 20 minutes for each exchange.

All the investigation reports are in the table no: 1

Unusual case of severe Sepsis

Rajyabardhan PattnaikCritical Care Unit,

Sanjib MohantyDeptt. of Internal Medicine

Sradhananda MohapatraDeptt. of Internal Medicine

Address for correspondence:Dr. Rajyabardhan Pattnaik ,

Critical Care Unit, Ispat General Hospital,

Rourkelae-mail : rajyapattnaik@yahoo.co.in

Case Reports

35

DateInvest 22/8 24/8 27/8 29/8 2/9 5/9 7/9 9/9 12/9 15/9 17/9 21/9

Hb 10.6 10 8.7 7.8 9.2 4.6 11.9 11.3

TLC 5700 18800 22000 34200 34300 19900 35900 13500 13100 10000

FBS 62 300 168 94 198 176 156 204 191 159 172 144

Urea 72 76 41 86 96 44 22

Creat 3.5 4.7 2.9 3.4 2.9 1.6 1.1 1.1 1

Na 125 136 134 137 147 148 150 148 137

K 3.8 3.7 3.4 4.4 3.3 2.8 2.2 2.2 5 3.8

Mg 1.4 2.8 1.8

Bill 1.3 0.8 0.5 0.5

SGPT 40 40 41 31

Platelet 10000 80000 88000 190000 200000

CXR LF LZ Opcty Intnsty Lf MiniOpct perst decrsd pl effsn

Table1. Sequential investigations and their results

Fig3. Skiagram showing shadowing of lungs

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 ventilation

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

patient's 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. There

was dramatic improvement of respiratory effort

and general well being. She was given T' piece trial thon 4 day of anti-fungal treatment and tolerated it

very well. Her tracheostomy was closed on the

During peritoneal dialysis her blood pressure

improved and she started passing adequate urine,

Fig 4. Skiagram shows resolution of chest pathology

36

next day (total 17 days). She was ventilated for 22

days out of 30 days of hospital stay. She was

discharged with a diagnosis of Type-II DM,

hypertension, hypothyroidism, acute renal failure

(peritoneal dialysis was done), sepsis fungal

pneumonia. She was followed up for next 4

months without any complications.

Fungal infection now a days has become a

common cause of infection worldwide.

Candidemia is associated with one of the highest

rate of mortality of any bloodstream infection.

The common risk factors for Candida infections

are previous antimicrobial administration,

prolonged corticosteroid therapy, cancer,

chemotherapy, neutropenia, extensive intra-

abdominal surgery or burn, mechanical

ventilation or admission to ICU indwelling CVP 4,5

line, TPN and haemodialysis .

Anti-fungal agents are Amphoterecin B, Azoles,

and Echinocandins. Amphoterecin B works on the

cell membrane of the fungi and increases

membrane permeability leading to leakage of the

cytoplasm and fungal cell depth. The adverse

effects include nephrotoxicity. Azoles works on

the cell membranes by inhibiting fungal

cytochrome P-450 leading to accumulation of

toxic steroles. There is also much drug interaction

with this drug. But echinocandins, specifically

Caspofungin, disrupts cell wall glucan formation

through non competitive inhibition of the enzyme

complex - (1, 3)-D-glucan synthase, present in

most pathogenic fungi and essential for fungal cell

wall formation. It leads to osmotic instability and 5, 6

ultimate lysis of fungal cell wall and is less toxic 6, 7, 8

with a good safety profile .

A bedside scoring system for early antifungal

treatment in non-neutropenic critically ill patient

with candida colonisation will be helpful. The

variables are multifocal candida species

colonization score 1, surgery on ICU admission

score 1, TPN score 1, severe sepsis score 2. If the

total score is more than 2.5 it helps intensivists to

select patients who will benefit from anti fungal 9

administration.

In our case the risk factor were diabetes mellitus,

broad spectrum antibiotics and prolonged

Discussion:

ventilation. Since the patient could not be weaned

off from ventilator and there was persistent

leucocytosis, the diagnosis of fungal infection was

entertained. Since the patient had acute renal

failure treatment with Amphotericin infusion was

ruled out. So Caspofungin was administered. The

dramatic recovery after caspofungin therapy is a

proof that the patient was having opportunistic

fungal infection which responded well to

antifungal treatment.

References:

1. Todi S, Chatterjee S, Sahu S , Bhattacharyya M.

Epidemiology of severe sepsis: An update

Critical care 2010:14 (suppl 1): 382.

2. Edmond MB, Wallace SE, McClish DK et.al.

nosocomial bloodstream infections in United

States hospitals; A 3 year analysis. Clin infect

Dis 1999;29:239-244.

3. Pfaller MA, Jones RN, Doem GV and the

SENTRY participant group ; Bloodstream

infections due to Candida species ; SENTRY

antimicrobial surveillance program in North

America and Latin America 1997-1998.

Antimicrob Agents Chemother 2000;44:747-

751.

4. Garber G. An overview of fungal infection.

Drugs 2001;61(suppl 1):1-12.

5. Blumberg HM, Jarvis WR, Soucie JM et al and

the NEMIS study group. Risk factor for

candidal bloodstream infection in surgical

intensive care unit patients: Clin Infect Dis

2001; 33: 177-186 Debono M et.al antibiotic

that inhibits fungal cell wall development.

Annu Rev Microbial 1994;48:471-497.

6. Debono M et.al antibiotic that inhibits fungal

cell wall development. Annu Rev Microbial

1994;48:471-497.

7. Keating GM, Jarvis B, Caspofungin, Drugs

2001;61:1121-1129.

8. Sawistowska, Schroder ET, Kerridge D, Perry H.

Echinocandin inhibition of 1,3,-b-D-glucan

Synthase from candida albicans. FEBS Lett

1984; 173: 134-138.

9. Leon C. A bedside scoring system for early

antifungal treatment in non neutropnic

critically ill patients. Crit Care Med

2006;34.730-737.

37

Abstract

Key words

Case Report

Chonal stenosis and atresia is often seen in

immediate neonatal period and presents with

respiratory distress.However single nostril as an

associated anomaly with choanal stenosis has not

yet been reported. In Ispat general hospital

one newborn was delivered with such anomaly

and resusciated successfully.

Choanal stenosis, Single nostril

In Ispat General Hospital,Rourkela a male baby

weighing 2000 gm was delivered to a primi

mother who had an uneventful antenatal

outcome. The baby had respiratory distress with

retraction of chest noticed immediately after

birth. On examination, the baby had a single

nostril. A nasal catheter could pass only ½ to 1

centimetre through the nostril. Some degree of

nasal obstruction was suspected. Even after

frequent suctioning of throat respiratory distress

persisted and baby became cyanosed after few

minutes and started crying. As the baby cried,

cyanosis was relieved and he became pink and

quiet (fig-1, 2, 3). Such repeated attacks of

cyanosis which was being relieved after crying

continued to occur. A diagnosis of choanal atresia

was suspected. The baby was transferred to the

nursery. An oral airway was inserted and secured

to the cheeks with tape (fig-4).This relieved the

respiratory distress.

Address for communication :

Dr. P Rath, Sr. Consultant,Deptt. of Pediatrics and Neonatology,

Ispat General Hospital,Rourkela, Email: paramananda2@yahoo.co.in

Figure 1 Immediately after delivery baby

Clinical imaging

Figure 2 Developing cyanosis

Figure 3 Cyanosis relieved after crying

Sidhesh C MishraDeptt. of E.N.T.

Paramananda Rath, Nimain C Nanda, Pitabas MishraDeptt. of Pediatrics and Neonatology

Choanal Stenosis with single nostril a rare Case

38

Figure 4 airway has been secured

He was kept on IV fluid for two days and then was

given gavage feeding. Congenital defects like

Treacher Collins syndrome, palatal abnormalities,

colobomas, tracheoesophageal fistula, and

congenital heart disease were excluded clinically.

Direct visualization through an otoscope couldn't

demonstrate anything abnormal. Plain radiograph

(antero-posterior view) of nasal and paranasal

region were carried out to rule out any septal

anomaly. A lateral radiograph of head with radio

opaque dye pushed through the nostril showed a

stenotic area (fig-5 arrow marked) in the choanal

region. But the dye could pass through the

stenotic area when pushed with pressure. A

diagnosis of Choanal Stenosis was confirmed.

Baby stayed for ten days in nursery and then was

referred to the pediatric surgeon for reconstructive

surgery which was done successfully.

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 2anomalies . However single nostril associated

with choanal tenosis has not yet been reported.

Newborn babies usually don't 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.

• CT scan can delineate extent of obstruction.

Definitive treatment of choanal atresia/Stenosis

includes

• Transnasal resecn tion by a laser beam.

• Definitive surgical reconstruction.

• Till surgical correction baby's airway to be

maintained by an oral airway and nutrition

maintained by gavage feeding.

• In our case in addition to repair of stenotic

segment cosmetic repair of the nostril was

also needed.

References

1. Pirsig W.Surgery of choanal atrsia in infants

and children:historical notes and updated

reviews,Int J pediatr otorhinolaryngology

II:153,1986

2. Brown K,Rodriguez K,Brown O E.Cummings thOtolaryngology , 4 edition. pp,4099-4109

Discussion

Figure 4 Airway has been secured

39

Residents Section

Accidents in medicine: The idea sends chills down your spine as you conjure up thoughts of

misdiagnoses, mistakenly prescribed drugs, and wrongly amputated limbs. Yet while accidents

in the examining room or on the operating table can be regrettable, even tragic, those that occur

in the laboratory can sometimes lead to spectacular advances, life-saving treatments, and

Nobel Prizes.

A seemingly insignificant finding by one researcher leads to a breakthrough discovery by

another; a physician methodically pursuing the answer to a medical conundrum over many

years suddenly has a "Eureka" moment; a scientist who chooses to study a contaminant in his

culture rather than tossing it out stumbles upon something entirely new.

The story behind the chance discovery of the anti-malarial drug quinine may be more legend

than fact, but it is nevertheless a story worthy of note. The account that has gained the most

currency credits, a South American Indian with being the first to find a medical application for

quinine. According to legend, the man unwittingly ingested quinine while suffering a malarial

fever in a jungle high in the Andes. Needing desperately to quench his thirst, he drank his fill from

a small, bitter-tasting pool of water. Nearby stood one or more varieties of cinchona, which

grows 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 this

man's fever miraculously abated, he brought news of the medicinal tree back to his tribe, which

began to use its bark to treat malaria.

Since the first officially noted use of quinine to fight malaria occurred in a community of Jesuit

missionaries in Lima, Peru in 1630, historians have surmised that Indian tribes taught the

missionaries how to extract the chemical quinine from cinchona bark. In any case, the Jesuits'

use of quinine as a malaria medication was the first documented use of a chemical compound to

successfully treat an infectious disease. To this day, quinine-based anti-malarials are widely used

as effective treatments against the growth and reproduction of malarial parasites in humans.

For all those would-be Nobel Prize-winners, remember the one trait that tied all these lucky

strikers together: openmindedness. As the American physicist Joseph Henry once noted, "The

seeds of great discoveries are constantly floating around us, but they only take root in minds well

prepared to receive them."

Quinine

Keep that mind open

ACCIDENTAL BREAKTHROUGHCompiled by :

Suman Behera (Intern)

Pallavi Agarwal (Intern)

40

1. Transitional epithelium is found in

a. thyroid gland

b. distal urethra

c. Ureter

D. small intestine

2. Narrowest part of male urethra is

A. membranous urethra

b. external urinary meatus

c. penile urethra

d. glandular urethra

3. Red nucleus is a part of

a. Thalamus

b. Pons

c. Cerebellum

d. Mid brain

4. Which is not a part of stomach?

a. Fundus

b. Neck

c. Body

d. Pylorous

5. How many lobes are there in left lungs?

a. 1

b. 2

c. 3

d. 4

6. Iron is absorbed in which part of GI tract

a. stomach

b. duodenum

c. jejunum

d. ileum

7. Vit B12 deficiency can occur in

a. ileal resection

b. strict vegetarians

c. parietal cell atrophy

d. total gasrectomy

e. all of the above

8. Which of the following statements is false

for brain death?

a. respiration should have ceased

permanently

b. heart beat should have ceased

permanently

c. reflex spinal movement of limbs may

be present

d. pupils should have no reaction to light

9. pulmonary vein carries

a. oxygenated blood from lungs to heart

b. oxygenated blood from heart to lungs

c. de oxygenated blood from lungs to heart

d. deoxygenated blood from heart to lungs

10. Nephron is seen in

a. central nervous system

b. kidney

c. spleen

d. liver

11. Mid diastolic murmur is classically seen in

a. mitral stenosis

b. aortic stenosis

c. aortic regurgitation

d. mitral regurgitation

12. Axons of a neuron carry impulse

a. away from the cell body

Residents Section

Practice paper

This practice paper is designed to incite intrusiveness amongst all the doctors and particularly for doctors

desirous to take part in different examinations. Though key to the question paper is given elsewhere, all

are requested to verify the answers from standard text books.

Please choose the most appropriate answer to each question.

41

b. low calcium level

c. a marker of Kalazar

20. In AP view of chest, relative position of

tube and film to the chest are as follows

a. Film is kept anterior and tube is

posterior

b. Tube is kept anterior and film is

posterior

c. Both tube and film are kept on the same

side of chest

21. Risk of radiation is highest with

a. X-ray

b. CT scan

c. MRI

d. ultrasound

22. Most probable diagnosis of the image

below is

a. hydrocephalus

b. encephalocele

c. meningocele

d. microcephaly

23. Which of the following phenotype

describes Bombay blood group?

a. hh

b. HH

c. Ao

d. Bo

b. towards the cell body

c. does not carry impulse

13. pH of vagina is

a. acidic

b. alkaline

c. neutral

13. Billirubin level is estimated

a. to know blood viscosity

b. to know liver function

c. to study pulmonary function

d. to know lipid metabolism

14. Autonomic nervous system deals with all of

the followings except

a. skeletal muscle contraction

b. cardiac function

c. pulmonary function

d. digestive function

15. Largest cell in human body is

a. spermatozoa

b. ovum

c. neutrophil

d. RBC

16. PNDT act deals with

a. drug trading

b. protecting the secrecy of patients

c. sex determination of foetus

d. narcotics

17. In emergency, dying declaration can be

taken by the treating doctor himself

a. true

b. false

18. All of the followings are neoplastic

disorders except

a. glioma

b. antibioma

c. neuroblastoma

d. nephroblastoma

19. Hypokalemia is

a. low potassium level

42

24. Sudden onset, intense headache with neck

stiffness should be investigated

immediately to rule out SAH by

a. lumbar puncture

b. CT scan of brain

c. MRI of brain

d. AP view of skull

25. Two scientists were awarded Noble prize

for their work on one vitamin. Name that

vitamin.

a. Vit B12

b. Vit C

c. Vit B6

d. Vit E

26. All of the followings are signs of upper

motor neuron except

a. up going plantar

b. flaccid muscle tone

c. exaggerated deep tendon reflexes

d. abolished superficial reflex

27. Classical lucid interval is described in

a. extradural hematoma

b. subdural hematoma

c. sub arachnoid hemorrhage

d. ventricular hemorrhage

28. Which of the following statements is false

for TIA?

a. it should be taken seriously because it

heralds major episode ahead

b. it allows time to detect treatable causes

and treat them

c. patient should be counseled only

and asked to report immediately if next

attack occurs.

29. Cauda equine syndrome due to any acute

compression should be considered as

surgical emergency because if delay occurs

a. patient may suffer from permanent loss

of bladder and bowel control

b. permanent motor weakness in lower

limbs and lifelong disablity

c. it may invite litigation

d. all of the above

30. Which of the following act of a doctor does

not make him liable under CPA?

a. Not accepting a cold patient for treatment

b. Fixing surgery at a later date after

accepting the patient for treatment

c. foreign body left in abdomen during

surgery due to the fault of the assisting

nurse.

d. not performing a life saving surgery

because no one is available to sign the

consent form.

31. Which of the following may create problem

for a surgeon under the CPA.

a. consent for surgery taken by the ward

sister

b. consent taken on a printed format used

in the hospital for all surgical patients

(blanket consent)

c. consent signed by the husband of a

40 year old lady

d. consent signed by the father of a 25 year

old newly recruited executive of SAIL.

e. all of the above

f. none of the above

32. Trachea bifurcates at which level?

a. D2

b. D3

c. D4

d. D5

33. Choice of treatment in organo-phospherous

poisoning is

a. PAM

b. atropine

c. neostigmine

d. none of the above

e. all of the above

34. Most dreaded complication of falciparum

malaria is

a. cerebral malaria

b. jaundice

c. association with pregnancy

d. bleeding from nose and gums

43

after full recovery plan for surgery

c. careful and expectant observation

d. conservative

42. which of the followings is most confirmatory

for pregnancy

a. urinary presence of HCG

b. morning sickness

c. ultrasonic observation of cardiac activity

of foetus

d. enlargement of mammary glands

43. Post partum period is the period

a. 2 weeks following delivery

b. 4 weeks following delivery

c. 6 weeks following delivery

d. 8 weeks following delivery

44. All of the followings are complications of

duodenal ulcer except

a. perforation

b. bleeding

c. obstruction

d. malignancy

45. which of the following condition is painful

a. hemorrhoids

b. fissure in ano

c. rectal polyp

d. malena

46. smoking is harmful in all of the following

condition except

a. Berger's disease

b. bronchial asthma

c. ulcerative colitis

d. coronary artery disease

47. Which of the followings are signs of fracture?

a. pain

b. swelling

c. deformity

d. all of the above

35. ACE inhibitors are contraindicated in

a. hypertensive encephalopathy

b. intracerebral hemorrhage

c. acute M.I.

d. bilateral ischemic kidney

36. Which statement is true for Type 2 diabetes?

a. they have insulin deficiency from birth

b. it affects persons above forty only

c. initial treatment is insulin

d. none of the above

e. all of the above

37. Which of the following condition is most

serious?

a. acute MI

b. stable angina

c. unstable angina

d. all are equally serious

38. Treatment of choice in pulse less VT is

a. amiodorone

b. verapramil

c. adenosine

d. DC shock

39. Thrombolysis is contraindicated in

a. non-ST elevation MI

b. unstable angina

c. stable angina

d. all of the above

e. none of the above

40. Life span of corpus luteum is

a. 12 days

b. 14 days

c. 16 days

d. 10 days

41. Management of ruptured ectopic pregnancy is

a. resuscitation and surgery should go side

by side without delay

b. blood transfusion, management of shock,

For Key to Practice Paper, Please see page-33.

44

Pandit Nehru in Ispat general Hospital

Doctors of IGH 1962

Down The Memory Lane

45

A page from the 'proceedings of IGH' published in 1981

Down The Memory Lane

46

1. Letter of submission signed by all the authors

2. 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 words

7. 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- 5

10. Each table on separate sheet.

11. Figures/diagrams on separate sheet.

12. Photographs in envelope appropriately marked.

13. Legends on separate sheet

14. 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. CD's / DVD's of the article if article is submitted in hard copies

1. Online submission is encouraged and preferred.

18. e-mail: editors.ighp@gmail.com

Instructions for the Authors

Rourkela Steel Plant, was the first integrated steel plant in the Public Sector in India. This vision of

Pandit Nehru, the first ‘Temple’ of modern India, began to take shape in the mid-fifties. To

cater to the health need of the massive inflow of workforce to Rourkela a modest beginning was

made in the form of a small medical centre in 1955. In 1956 a First- Aid centre was started in the Steel

Plant 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 612

paramedics. It extends treatment to more than 9 lakh people at its outpatient department, on an

average, in a year. In the inpatient department more than 30 thousand persons get treated annually

out of which about 40% are non-entitled patients.

The hospital has facilities in super specialities like neurosurgery, burn and plastic surgery. The

hospital also provides lifesaving interventions like dialysis, pacemaker implantation and

chemotherapy. Total hip and knee replacement, brain and spinal cord surgery, urological

procedures are routinely taken up apart from laparoscopic and open surgical procedures in

Surgery and Obstetrics department. Laser surgery and phaco-emulsification in Ophthalmology and

bronchoscopic surgery in ENT department make this hospital one of its kind in the entire state of

Odisha.

IGH is equipped with many modern investigating facilities like 3rd generation CT scan, 1.5 Tesla MRI

machine and sophisticated laboratory medicine department comprising Pathology, Microbiology

and Biochemistry departments. Nuclear medicine and blood transfusion facilities greatly facilitate

the treatment of patients.

On the research front, IGH is a WHO recognized research centre for Malaria and the faculty

members of IGH are regularly invited to impart training in other countries. The hospital is equipped

with a molecular laboratory for research work. Paediatric department of the hospital is participating

in research work in the international field in neonatal infection control. Contribution of the hospital

to the future generations of medical professionals is also immense as most of the research work is

published in international medical journals.

This premier hospital is also recognised for imparting post graduate training in most of the

disciplines of medical science. The performance of the students of this Institution is highly

satisfying – 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 steel

plant and their family members. Citizens of Rourkela and nearby districts too reach out to the

hospital. Besides, people of Jharkhand, Chhattisgarh and Madhya Pradesh make IGH their health

destination from time to time.

Ispat General Hospital which has redefined health care in the region epitomises concern and

commitment.

Ispat General Hospital: An Overview

ROURKELA STEEL PLANT