This document summarizes diabetic nephropathy, which is the leading cause of chronic kidney disease worldwide. It begins with an introduction discussing the rising prevalence of diabetes and its associated kidney complications. The causes and pathophysiology of diabetic nephropathy are then explained, focusing on how high blood sugar and blood pressure damage the filtering units of the kidney over time. Natural history and progression to end-stage renal disease are depicted in a figure. Early detection through screening and aggressive management of risk factors are emphasized to delay kidney damage progression in diabetic patients.

1. Proceedings of the
Ispat General Hospital
YEAR 2011
Ispat General Hospital,
Rourkela Steel Plant, Rourkela

2. 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

3. 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)

5. 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.
Dr S.K.Mishra,
Director In-Charge,
Ispat General Hospital Medical & Health Services,
Rourkela-769005 SAIL, RSP, Rourkela

6. Contents
• Editorial 03
Review Article
• Diabetic nephropathy 04
Kishore C Mahanta
Original Papers
• Prevalence of phage types & biotypes among Salmonella Typhi 13
and Salmonella Paratyphi A isolates from Rourkela, Orissa
Seshadri S Bhattacharya, Usha Das
• Predictions of Length of Hospital stay of malaria patients 17
Saroj K Mishra, Narayan P Sahoo, Kishore C Mahanta, Rajalaxmi Mishra
Case reports
• Peutz- Jeghers Syndrome presenting as acute intestinal obstruction 21
due to Jejunal Intussusception in an adult male
Amulya M Acharya, Sishir R Dash, Manoja K Panigrahi
• Necrotising fasciitis in neonate – case report 25
Radhanath Satpathy, Nimain C Nanda, Pitabas Mishra, Rajan K Behera,
Pinaki Panigrahi
• Squamous cell carcinoma & basal cell carcinoma with xeroderma 28
pigmentosa – a rare presentation
Aruna M Minz, Niranjan K Behera, Rabi R Panda, Sanghamitra Satpathy,
Prativa K Behera, Usha Das
• Multiple brain metastases due to occult Papillary Carcinoma 31
of thyroid gland: A Case Report
Rabindra N Mohapatra, Sudhi R Pradhan , Rabi R Panda, Pushpa Kumari,
Saropani Hembram
• Unusual case of severe Sepsis 34
Rajyabardhan Pattnaik, Sanjib Mohanty, Sradhananda Mohapatra
Clinical imaging
• Choanal Stenosis with single nostril -a rare Case 37
Paramananda Rath, Nimai C Nanda, Pitabas Mishra, Sidhesh C Mishra
Residents' Section
• Accidental Breakthrough 39
Suman Behera, Pallavi Agarwal
• Practice paper 40
• Down The Memory Lane 44
• Instructions for the Authors 46
• Ispat General Hospital : An Overview

7. Editorial
Brain Death, its impact on organ donation and
resources of critical care units
Address for communication :
Sr. Deputy director, Neurosurgery,
Rabindra N.Mohapatra
Ispat General Hospital, Rourkela-769005, India
Deptt. of Neurosurgery
e-mail: ighp@in.com
“20,000 liver transplants needed annually in India, Continuation of critical care support after brain
only 110 donors in 2009”. This was the news death, drains out the resource crunch critical care
1
headline on April 01 2010 . departments of life saving resources, manpower
Throughout the world, main resources of donor and finance. In fact, it puts a lot of burden on the
2, 3
organs are the brain dead patients. But, the sorry family members physically, financially and
state in our country is mainly due to reluctance to emotionally, for an outcome which is unattainable.
accept the concept of brain death, both by the In addition, keeping life saving equipments
physicians as well as general public. Causes of this engaged for a brain dead patient may deprive
reluctance may be due to several reasons related to another critically ill patient whose condition is
physicians themselves and relatives of the reversible. We, the physicians, should understand
2
deceased as well. According to Pathak et al., some that there is no recovery after brain death. We can
of the factors responsible for this may be explain relatives of the deceased that putting their
patient on life support system is futile; rather his
• Lack of understanding the concept.
viable organs can alleviate the disease in a person
• Special emotional attachment to the dead who can otherwise lead a normal healthy life. In
person an Indian scenario, the relatives of the deceased
• Loss of confidence in medical practice can be emotionally appealed that some part of
• Ethical questions related to earlier organ their near and dear ones will still be surviving in the
transplant procedure recipient's body.
• Perceived insufficient participation of The purpose of this Editorial is not to go into the
government and medical associations. intricacies of brain death, rather to sensitise
Concept of clinical death in the form of loss of medical professionals and public regarding the fact
observable cardio respiratory failure has that brain death is ultimate end of one's journey in
undergone a sea change due to widespread use of this Earth.
mechanical ventilators that prevent respiratory It is time to educate ourselves and the public, to
3
arrest . In 1968, ad hoc committee at Harvard assist in understanding the concept of brain death.
Medical School defined irreversible coma, or brain It is particularly true in hospitals, where load on
death, as unresponsiveness and lack of receptivity, critical care department is very high.
the absence of movement and breathing, the
absence of brain-stem reflexes, and coma whose References:
3
cause has been identified. 1. Zee News.Com, uploaded on Thursday, April
In India, The Transplantation of Human Organs Act, 01, 2010, 00.03
1994 (Central Act 42of 1994), lays down the 2. Pathak MK, Tripathy SK, Agrawal P,
definition of death thus: 'Deceased person ' means Chaturvedi R, Yadav S. Clinical Criteria for
in whom permanent disappearance of all evidence Diagnosis of Brain death and its Medico-
of life occurs, by reason of brain stem death or in a Legal applications (A Review Study).
cardio-pulmonary sense at any time after live birth IndMedica-Medico-Legal update.2006;
has taken place. It goes on to state that 'brain-stem 6(2):3-6
death' means the stage at which all functions of the
brain stem have permanently and irreversibly 3. Golia AK, Pawar M. The diagnosis of brain
ceased. Once brain-stem death has been death. Indian J Crit Med 2009;13:7-11
diagnosed by an authorized committee using 4. Pandya SK. Brain death and our transplant
specified criteria, the dead person's organs can be law. Paper presented at: The seventh
removed for transplantation provided legally valid National critical care congress CCCON; 2001
3, 4
consent for this is available. Jan 2-7; Bangalore
3

8. Review Articles
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 predispose to development of diabetic
1
Diabetes has become the common single cause of nephropathy. Pre diabetic individuals, with
Chronic Kidney disease (CKD) leading to End-Stage impaired glucose tolerance, frequently have
Renal Disease (ESRD) in most countries: this is due hypertension as one facet of metabolic syndrome.
to the fact that diabetes, particularly type 2 is Genetic factors combined with metabolic and
increasing in prevalence and that diabetic hemodynamic alterations induce renal damage in
patients are living longer with proper medication. susceptible individuals.
About 20-30% of patients with type 1/ type 2 Causes:
diabetes develop evidence of nephropathy. The exact cause of diabetic nephropathy is
Recent studies have now demonstrated that the unknown, but it is believed that uncontrolled high
onset and course of diabetic nephropathy can be blood sugar leads to the development of kidney
delayed to a very great extent by several damage, especially when high blood pressure is
interventions, but these interventions have their also present. Not all persons with diabetes
greatest impact if instituted at a very early course develop this condition.
of development of this complication. Recently
Each kidney is made up of hundreds of thousands
there has been a lot of developments in the
of filtering units called nephrons. Each nephron
treatment of End Stage Renal Failure.
has a cluster of tiny blood vessels called a
Introduction:- glomerulous. Together these structures help
There is a silent epidemic of type 2 diabetes world remove waste from the body. Too much blood
over. It is predicted that India will be the diabetic sugar can damage these structures, causing them
capital of the world by 2020. With growing to thicken and become scarred. Slowly, over time,
population of type 2 diabetes, the prevalence of more and more blood vessels are destroyed. The
diabetic nephropathy is on the rise. In fact diabetic kidney structures begin to leak and protein
nephropathy is the single most common cause of (albumin) begins to pass into the urine.
End Stage Renal Disease (ESRD) today. Persons with diabetes who have the following risk
Besides patients' miserable sufferings, it factors are more likely to develop this condition:
consumes greater financial resources than non • African American, Hispanic, or Americans of
diabetic ESRD. Diabetic ESRD patients do poorly Indian origin
on dialysis and mortality is higher. There is a • Family history of kidney disease or high
spectrum of co-morbidities such as CV disease, blood pressure
brain stroke, blindness, gangrene etc which are to • Poor control of blood pressure
be dealt with while treating such patients with • Poor control of blood sugars
Renal Replacement Therapy (RRT). • Type 1 diabetes before age 20
There has been some evidence to suggest that • Smoking, Alcoholism
genetic predisposition to hypertension may • Abnormal lipid levels
4

9. Diabetic nephropathy generally goes along with cytokines such as transforming growth factor-B,
other diabetic complications including high blood angiotensin II, and/or other growth factors.2,3
pressure, retinopathy and blood vessel changes Alternatively, elevated glucose levels may inhibit
(vasculopathy). matrix protein degradation through non-
enzymatic glycosylation and/or through the
Pathophysiology: 4
inhibition of protein degradative pathways. Thus,
The pathophysiology of diabetic nephropathy the mediators of mesangial expansion constitute
manifests histologically as diabetic reasonable therapeutic targets when crafting a
glomerulosclerosis and is characterized by treatment strategy for diabetic nephropathy.
glomerular basement membrane thickening and Understanding the natural history of diabetic
mesangial expansion with increased extracellular glomerulosclerosis is important to design
matrix deposition. Mesangial expansion in therapeutic interventions, as well as gauging
diabetic glomerulosclerosis may be considered responses to therapy. In this regard, Parving
the result of an imbalance between mesangial demonstrated the deleterious effect of
matrix protein production and degradation, hypertension on renal function in proteinuric
favoring matrix protein accumulation. diabetics.5,6 Of equal or greater value in that report
Overproduction of mesangial matrix proteins may was the demonstration of the expected rate of
be the result of glomerular hypertension and/or loss of glomerular filtration rate (GFR) over time,
hyperglycemia-driven synthesis of prosclerotic in patients with diabetic nephropathy.
Fig 1. Graphic presentation of the natural history of diabetic glomerulosclerosis. Initially there is glomerular hyper
filtration and microalbuminuria. Microalbuminuria is followed by macroalbuminuria (dipstick positive
proteinuria), the onset of macroproteinuria heralds the beginning of a relentless decline in GFR at the rate
approximately 1ml/mt/month (at a BP of 140/90 mm hg). If GFR is 70ml/mt at onset of macroalbuminuria
and dialysis is indicated at a GFR of 10ml/mt, 65 months would pass from the onset of proteinuria to the need
for renal replacement therapy. The goal of therapy is to slow the rate of loss of GFR. Reducing the rate of loss
of GFR from 1 ml/minute/month to 0.5 ml/min/month would translate into a doubling of the time for the
need for dialysis (130 months). Modified from Molitch, Diabetes Care 17:756, 1994.
5

10. Figure 1. is a schematic summary of the natural only about 20% go on to develop ESRD. However
history of diabetic glomerulosclerosis, and presence of microalbuminuria in addition to
demonstrates the relationship between being a manifestation of renal involvement, is also
albuminuria and the loss of GFR over time. The a marker of cardiovascular risk. Patients with
model is based on the following assumptions: (a) sustained microalbuminuria need to be
all macroscopic (dipstick positive) proteinuria is aggressively managed for cardiovascular risk
7
preceded by a phase of microalbuminuria factors as well.
(microalbumin 30-300 mg /day); (b) the SCREENING FOR MICROALBUMINURIA:-
appearance of dipstick positive proteinuria Screening in individual with type I diabetes should
heralds the beginning of a linear, irreversible loss begin after 5 years disease duration. In type 2 DM,
of GFR; and (c) GFR is lost, on average, at the rate screening should begin at diagnosis, there after
of 1 ml/min/month. for the presence of microalbuminuria should be
Clinical diagnosis of diabetic nephropathy performed annually.
Symptoms : Screening for microalbuminuria can be
Early stage diabetic nephropathy has no performed by three methods:-
symptoms. Over time, the kidney's ability to 1. Measurement of albumin to creatinine
function starts to decline. Symptoms develop late ratio (ACR) in a random spot collection
in the disease and may include: 2. 24 hr collection with creatinine, allowing
• Fatigue the simultaneous measurement of
• Foamy appearance or excessive frothing of creatinine clearance.
the urine 3. Screening with reagent tables or dipstick
• Frequent hiccups for microalbumin have sensitivity 95% and
• General ill feeling specificity93%. Reagent strips only
• Generalized itching indicate concentration and do not correct
• Headache the creatinine as the spot albumin-
7
• Nausea and vomiting creatinine ratio does.
• Poor appetite Definitions :-
• Swelling of the legs 1. Microalbuminuria – Random ACR 30-300
• Swelling, usually around the eyes in the mg on 2 out of 3 occasion
mornings; general body swelling may 2. Macroalbuminuria- Random ACR >300 mg
occur with late-stage disease or positive protein dipstick
• Unintentional weight gain (from fluid 3. Diabetic nephropathy Estimated GFR < 60
buildup) ml/min for at least 3 months.
Examination and Tests Screening of microalbuminuria is invalid in
The earliest clinical evidence of renal involvement following conditions:
in diabetes is the presence of small amount of In uncontrolled hyperglycaemia, febrile illness,
albumin in urine (30-300mg/24 hrs). This is following strenuous exercise, uncontrolled
labeled microalbuminuria. Protein may appear in hypertension or heart failure and presence of
the urine for 5 to 10 years before other symptoms urinary infection as all these conditions can cause
develop. In type 1 Diabetes 80%, who develop transient proteinuria.7
microalbuminuria, will develop macroproteinuria High blood pressure often goes along with
and around 50% will eventually develop ESRD. In diabetic nephropathy. One can have high blood
type 2 Diabetes 20-40% of patient with pressure that develops rapidly or is difficult
microalbuminuria develop overt proteinuria and to control.
6

11. Laboratory tests that may be done include: levels, aggressive blood pressure control,
• BUN angiotensin II inhibition, and dietary protein
• Serum creatinine restriction. Additional therapeutic targets include
microalbuminuria and macroproteinuria. An
The levels of these tests will increase as kidney
approach to each of these parameters is discussed
damage gets worse. Other laboratory tests that
below.
may be done include:
1. Tight blood glucose control
• 24-hour urine protein
The DCCT (Diabetes Control and Complications
• Blood levels of phosphorus, calcium,
Trial) demonstrated the importance of tight blood
bicarbonate, PTH, and potassium
glucose control in slowing the development of
• Hemoglobin 13
proteinuria in Type 1 diabetics. In this regard,
• Hematocrit patients randomized to tight glucose control
• Protein electrophoresis - urine (HbA1C levels < 6.5%) versus regular control (8-
A kidney biopsy confirms the diagnosis. However, 9%), demonstrated 39 and 54% lower rates of
clinical diagnosis can be done without a biopsy if development of microalbuminuria and
the following three conditions are met with: macroalbuminuria, respectively, over the two
years of the trial.
1. Persistent protein in the urine
Similarly the UKPDS(United Kingdom Prospective
2. Diabetic retinopathy
Diabetes Study) in Type II diabetes showed a 25%
3. No other kidney or renal tract disease
risk reduction in microvascular complication in
A biopsy may be done, however, if there is any the intensively treated group.
doubt in the diagnosis.
2. Blood pressure control
Diabetics with heavy proteinuria, but lacking the
Hypertension in diabetic patient may be due to
disease for a sufficient period of time and/or
coexisting “essential” hypertension, or due to
retinopathy, may require renal biopsy. These
myriad of other secondary causes, such as renal
patients may suffer from primary
vascular disease. Isolated systolic hypertension
glomerulopathies such as membranous
8
has been attributed to the loss of elastic
nephropathy, or other glomerular diseases. compliance of atherosclerotic large vessels. Both
Diabetic glomerulopathy is the most common systolic and diastolic hypertension markedly
cause of nephrotic syndrome. Thus, early in the accelerates the progression of diabetic
course of the disease, the serum creatinine is nephropathy and aggressive antihypertensive
normal despite heavy proteinuria (> 3 grams/24 management is able to greatly decrease the rate
hours). In this regard, a diabetic patient of fall of GFR. Appropriate antihypertensive
presenting with elevated serum creatinine in the intervention can significantly reduce mortality
absence of macroscopic proteinuria should from 94 to 45% and a reduction in the need for
suggest additional diagnostic possibilities (such as dialysis and transplantation from 73 to 31% 16
other glomerulopathies) . The diagnostic utility of years after development of overt nephropathy.
proteinuria is less useful in patients treated with Choice of antihypertensive therapy:-
angiotensin converting enzyme inhibitors (ACEi)
One needs to be careful about:-
or angiotensin II receptor blockers (ARBs), since
both classes of drugs are known to reduce - Use of ACEI and ARBs as these may lead to
9,10
glomerular proteinuria. hyperkalemia in patients of advanced renal
MEDICAL THERAPY OF DIABETIC NEPHROPATHY : insufficiency,
The medical therapy of diabetic glomerulo- - ACEI are contraindicated in bilateral renal
sclerosis includes strict control of blood glucose artery stenosis and in pregnancy.
7

12. - Beta blockers are contraindicated in ACEi demonstrate slower progression to
6
peripheral vascular disease. macroproteinuria and renal failure. American
Targets for blood pressure control:- Diabetic Association (ADA) guidelines suggest
assessing for microalbuminuria (normal < 30
• <130/80 mm hg in absence of proteinuria
mg/24 hours or less 30 mcg/mg creatinine for
• <125/75 mm hg in presence of proteinuria. a spot urine collection) at the time of diagnosis
3. Angiotensin II inhibition : The ACE inhibitor in all type 2 diabetics, in all type I diabetics with
trial in diabetic nephropathy was the first disease duration > 5 yrs, and annually
randomized, placebo controlled trial that thereafter in both groups. 19 Early and
showed the beneficial effect of ACE inhibitors aggressive therapy of microalbuminuria, taken
in the treatment of diabetic along with angiotensin II inhibition, is
glomerulosclerosis.11 Subsequent studies have expected to slow disease progression.
confirmed this observation for both ACE 6. Macroproteinuria
inhibitors and ARBs.10,12 Most agree that ACEI
Heavy proteinuria is a risk factor for progressive
a re f i rs t l i n e t h e ra p y fo r d i a b e t i c
10 renal failure, 16 including diabetic nephropathy.20
glomerulosclerosis, but ARBs are regarded by
There is abundant evidence that abrogating
some as equivalent.10 The beneficial effect of
proteinuria with dietary and antihypertensive
angiotensin II inhibition may result from: 21
interventions, and/or ACE inhibitors, 1 and/or
a) a decline in glomerular hypertension (with ARBs,22,23 results in a slower loss of GFR in
slowing of mesangial expansion)13 proteinuric states. In this regard, combination
b) a reduction in proteinuria (with an therapy with both ACE inhibitors and ARBs may
24
expected decrease in proteinuria- provide benefit over ACE inhibitors alone.
14
associated prosclerotic events), and/or Finally, nephrotic diabetics treated with ACE
inhibition, and exhibiting a reduction in
c) a decrease in angiotensin II stimulated
15,16 proteinuria to < 1 gm / day, demonstrated stable
TGF-ß synthesis. 25
renal function for up to 8 to 15 years. Taken
4. Dietary protein restriction : In some reports, together, therapeutic measures directed at
dietary protein restriction has been shown to reducing macroscopic proteinuria would be
slow the loss of GFR in proteinuric diabetics,17 expected to slow the progression of diabetic
although the data are not conclusive. Protein nephropathy, and angiotensin II inhibition is the
restricted diets (0.6-0.8 g/kg body wt/day) mainstay of therapy for attaining that goal.
decrease glomerular hypertension, the
Other aspects of treatment : Treatment of
production of prosclerotic cytokines,
18 progressive renal disease includes prevention of
proteinuria, and glomerulo-sclerosis, and
renal osteodystrophy with sodium and phosphate
remain a viable therapeutic option for
restriction and use of phosphate binders,
compliant patients.
treatment and prevention of anaemia etc.
5. Microalbuminuria : Microalbuminuria
Avoidance of nephrotoxic drugs in proteinuric
predates the development of macroscopic
diabetic patients will prevent form onset of acute
proteinuria. Macroscopic proteinuria is a
kidney injury.
major risk factor for progression to ESRD,14 thus
measures to reverse microalbuminuria may Radiocontrast media are nephrotoxic in diabetic
retard development of clinical nephropathy. nephropathy and careful hydration is mandatory
Patients with microalbuminuria treated with in these cases if it is done.
8

13. SPECIAL CONSIDERATIONS Survival analysis shows the two modalities are
27
Insulin metabolism in CKD : Unutilized insulin is comparable with regard to patient outcome.
excreted by kidney normally which accumulates However, when compared to non-diabetics,
diabetic patients on dialysis do substantially
in CKD. So if we fail to reduce insulin dose as 28
worse, with five-year survival rates as low as 5%
kidney disease progresses, patients will
for elderly type 2 diabetics.29 With meticulous
experience hypoglycaemia. So reducing insulin
management, others have shown three-year
dose and switching to short acting insulin
survival rates as high as 58%.28 .The reasons for
analogues is recommended in this situation. It is
poor survival rates relate to the high incidence of
recommended to avoid long acting Insulins in CKD
preexisting cardiovascular disease, late referral
patients.
both for predialysis care, as well as vascular access
Oral antidiabetic drug: 97% of the most placement, malnutrition, and co-existing vascular
commonly used oral antidiabetic drug Metformin problems (in particular, peripheral vascular
is excreted by normal kidney within 12 hrs. In CKD disease with associated ischemic toes and feet).28
it will accumulate and lead to lactic acidosis, a Furthermore, diabetes and smoking have been
serious condition. shown to be significant risk factors for
So metformin should be stopped when the eGFR is atherosclerotic heart disease in dialysis patients,
30
<35 ml/mt/1.73 m2 correlates to serum creatinine similar to what is seen in the general population.
of approxmimately 1.7 mg /dl. Older The anemia of chronic renal disease may further
sulfonylurea(SU) are excreted mainly through complicate the course of patients with significant
kidney. Only 10% of second line SU are excreted by coronary artery disease. Taken together, these
kidney but are long acting and may accumulate in data suggest that the survival of diabetic patients
CKD, so we must be cautious while using these. on hemodialysis may be optimized with
Meglitinides and Thiazolidinediones are not aggressive attention to risk factors for
excreted by kidneys. These do not cause c a rd i o va s c u l a r d i s e a s e ( hy p e r te n s i o n ,
hypoglycaemia. dyslipidemia, smoking, etc.), awareness and
therapy of diabetic foot problems, and early
Monitoring glycaemic control in CKD : As kidney
nephrology referral (as GFR falls or with
disease develops, the turnover of red blood cells
progressive proteinuria) for vascular access
becomes abnormal. Usually there is prolonged life
placement and anemia management.
span of RBCs, perhaps because the person is
anaemic. So hemoglobin has more time to 2. Peritoneal dialysis : The second option for renal
become glycated. In such conditions HbA1c in replacement therapy in diabetic patients with
kidney disease may be falsely high. Hb may also be ESRD, is peritoneal dialysis. When compared to
carbamylated with some of the waste products, hemodialysis, fewer patients are treated with
peritoneal dialysis. Patients opting for peritoneal
which accumulate in uremia and these
dialysis tend to be healthier and more involved in
compounds will interfere with the measurement
their medical care. While no clear survival
of HbA1c. This is one more reason for HbA1c to be
advantage for peritoneal or hemodialysis has
falsely high. Correction of anaemia may lead to
been demonstrated, patients treated with
decrease HbA1c level.26
peritoneal dialysis may experience labile blood
Renal replacement therapy: glucose levels (attributed to the high glucose
1. Hemodialysis : Hemodialysis and peritoneal concentrations inherent to PD dialysate) and
dialysis are the two forms of dialysis used to treat increased risk of malnutrition (secondary to
31
diabetic patients with end stage renal disease. excessive protein losses in dialysate effluent).
9

14. 3. Transplantation : By far the best treatment for Summary
ESRD from diabetes is kidney transplantation. The rising incidence of diabetes means that
Kidney transplantation in diabetics with end-stage clinicians can expect to find an increased rate of
renal disease may include kidney transplantation diabetic nephropathy, and increasing numbers of
alone, or combined kidney-pancreas patients requiring renal replacement therapy.
transplantation. The former treats renal failure, Understanding the natural history of diabetic
the latter both renal failure and diabetes. Patient nephropathy, the early recognition of diabetic
survival following kidney transplantation without complications, and timely initiation of therapy to
a pancreas has consistently been demonstrated to slow progression are cornerstones in the
be superior to any form of dialysis. Data from the management of this condition. Aggressive
Organ Procurement and Transplantation Network treatment of hyperglycemia and hypertension,
reported one-, three-, and five-year patient the use of angiotensin II inhibitors, and timely
survival rates for transplanted diabetics of 90, 79 therapy of micro and macroproteinuria are
32
and 66%, respectively. This compares to a two essential features of optimal therapy. For patients
year survival rate in diabetic patients on reaching end stage renal failure, renal
29
hemodialysis of 58%. The improved survival of replacement options include dialysis and kidney
renal transplant patients over those treated with transplantation, with transplantation conferring a
hemodialysis must be interpreted in light of the substantial survival advantage.
fact that they are selected for transplantation, References:
whereas patients with extensive co-morbidities
1. Strojek K et al, Nephropathyof type 2
tend to remain on dialysis. Living donor
diabetes: Evidence for hereditary factor.
transplants confer an allograft survival advantage Kidney Int. 51:1602-1607,1997.
over cadaveric donors, with three-year allograft
2. Hostetter T, Rennke H, Brenner B. The case
survival rates of 88 and 78% for living and
for intrarenal hypertension in the
cadaveric donor transplants, respectively. 32 initiation and progression of diabetic and
However, both modalities are superior to dialysis other glomerulopathies. Am J Med. 1982;
with three year patient survival rates of 72:375.
32
approximately 88-94%. Preemptive 3. Ziyadeh F, Han D. Involvement of
transplantation is renal transplantation that is transforming growth factor-b and its
performed prior to instituting dialysis. Preemptive receptors in the pathogenesis of diabetic
transplantation may confer a survival advantage nephropathy. Kidney Int . 1997; 52:S7-S11.
that is superior to transplanting patients on 4. Brownlee M. Biochemistry and molecular
dialysis. In this regard, the time spent on dialysis cell biology of diabetic complications.
prior to transplantation portends worse survival Nature. 2001; 414(6865):813-20.
rates for patients. For example, in patients on 5. Parving H, Smidt U, Andersen A, Svendsen
dialysis < 6 months, 12-24 months, or >48 months P. Early aggressive antihypertensive
had mortality rates of 21%, 41%, and 72%, treatment reduces rate of decline in
33,34,35
respectively. A similar trend for allograft kidney function in diabetic nephropathy.
survival was seen in cadaveric transplants Lancet.
performed in patients receiving hemodialysis for 1983; 1:1175-1179.
more than two years prior to the transplant. In 6. Parving HH. Diabetic nephropathy:
those studies, the allograft survival rate was only prevention and treatment. Kidney Int.
39% after ten years.36 2001; 60(5):2041-55.
10

15. 7. Anjali, Jacob J J, Nephropathy in Diabetes; and transforming growth factor-beta1 in
practical guide to Diabetes Mellitus: 4th vascular
Edn.;146-148 smooth muscle. J Mol Med . 1999;
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discussion 1356-7. chronic renal disease. Modification of Diet
10. Lewis E, Hunsicker L, Bain R, Rohde R. The in Renal Disease Study Group [see
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11. Lewis EJ, Lewis JB. ACE inhibitors versus Nephropathy in diabetes. Diabetes Care.
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Nephrol . 2004; 15(5):1358-60. Predictors of the progression of renal
12. Hostetter T. Prevention of end-stage renal insufficiency in patients with insulin-
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16. 24. Jacobsen P, Andersen S, Rossing K, Jensen dialysed diabetic patients: a prospective
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12

17. Original Papers
Prevalence of phage types & biotypes among Salmonella Typhi and
Salmonella Paratyphi A isolates from Rourkela, Orissa.
Address for communication :
Seshadri S Bhattacharya, Usha Das SS Bhattacharya
Deptt. of Microbiology,
Deptt. of Microbiology,
Ispat General Hospital, Rourkela, Orissa.
Email: sesebha@yahoo.co.in
ABSTRACT fever in India.1,2 However, isolation of Salmonella
Aim of this study was to highlight the changes in enterica serotype Paratyphi A causing the same
prevalence of phage types encountered among disease have been reported with an increasing
Salmonella isolates from Rourkela. Besides S. trend.3,4 In Rourkela, we have been reporting
5
Typhi as the main causative agent of enteric fever, S.Typhi causing enteric fever since 1996, whereas
S. Paratyphi A has also been emerging with isolation of S.Paratyphi A causing the same
increasing rate as the other causative agent of disease has been encountered in this place since
enteric fever from different parts of India 2002.6
including Rourkela. This retrospective study was Phage typing is a major means of epidemiological
carried out between September 2005 and August tracing as strains within a particular serotype may
2006 with 1454 patients attending out-patient- be differentiated into a number of phage types,
departments (OPD) and wards of Ispat General and may help to define groups of persons who
Hospital, Rourkela, India. Phage typing and have been infected with the same strain from the
biotyping was performed for randomly chosen same source. Again, combination of biotyping
isolates of S. Typhi (N=36) and S. Paratyphi A with phage typing gives a finer discrimination of
(N=12). A distinctive change has been noticed in strains in tracing out the source of infection. The
the prevalence of phage types compared to their use of phage typing and biotyping for
prevalence pattern reported earlier. Phage type epidemiological tracing had been documented
40 was the most commonly encountered phage since 1982 in different parts of India.1
among S. Typhi isolates followed by type E1. Phage typing and biotyping of both Salmonella
Susceptibility testing was performed for all 112 Typhi and Salmonella Paratyphi A had been
isolates of Salmonella including 48 strains chosen reported from Rourkela in 2006 and 2007.6,7 There
randomly for phage typing and biotyping. Though was a noticeable change in the prevalence pattern
4-5% of Salmonella isolates showed resistance to of phage types encountered among S.Typhi
ciprofloxacin, they were highly sensitive to both isolates in 2005-2006 in comparison to the phage
a m i n o g l yco s i d e s a n d t h i rd ge n e rat i o n types found in 2004-2005. In this retrospective,
cephalosporins. Diversity among the phage types hospital based study, we have highlighted the
encountered among S. Typhi isolates was changes in the prevalence pattern of phage types
probably due to the diverse origin of those and biotypes among the Salmonella isolates
phages. Salmonella enteric serotype Typhi is the chosen randomly. The susceptibility pattern of
most commonly occurring causative agent of Salmonella isolates including the typed strains
1.2
enteric fever in India. have also been reported in this communication.
Key words Materials & methods
Prevalence; Phage typing; Biotypes; Randomly This study was conducted between September
chosen; Susceptibility testing; Diversity. 2005 and August 2006. A total of 1454 patients
Introduction attending out-patient departments (OPDs) and
Salmonella enteric serotype Typhi is the most wards of Paediatric and Medicine departments of
commonly occurring causative agent of enteric Ispat General Hospital , Rourkela, Orissa,
13

18. suspected of having enteric fever or pyrexia of the patients, 768 were males (52.81%) and 686
unknown origin (PUO) were included in this study. were females (47.19%).
A total of 1454 blood samples were included in Of 1454 patients, 112 were positive for Salmonella
this study. Irrespective of repeat sample we have isolates giving a per cent positivity of 7.70. Of 112
taken into account only one sample from each
patient. Only positive isolation was considered for Host organism Phage type Biotype No. of isolates
the patients having both positive and negative S. Typhi A I 1
results. (N=36) D1 I 1
E1 I 8
Clinical samples of blood were collected in brain
J1 I 2
heart infusion broth with sterile precautions and
0 40 II 19
incubated aerobically at 37 C for 48 hours. Three
USV-2 II 1
subcultures were done on blood agar, MacConkey
Vi-Negative I 4
agar and Salmonella-Shigella agar and incubated
0 S. Paratyphi A 1 II 1
aerobically at 37 C for 18-24 hours. In negative
(N=12) 6 II 11
cases subcultures were done for one week.
Table 2.
Isolation of S. Typhi and S. Paratyphi A was Phage types encountered among S. Typhi and S. Paratyphi
established by conventional methods. 8 A isolates in Rourkela between September 2005 and August 2006.
Identification of these two serotypes was
established by biochemical and serological testing Antibiotics S. Typhi (%) S. Paratyphi A(%)
8,9
with factor sera. Antibiotic susceptibility testing (N=92) (N=20)
was performed by Kirby Bauer disk diffusion Ampicillin 82 (89.13) 11 (55)
10
method, with the modifications recommended Co-trimoxazole 74 (80.43) 11 (55)
by the National Committee for Clinical Laboratory Chloramphenicol 85 (92.39) 12 (60)
Standards (NCCLS).11 Antimicrobials agents tested Gentamicin 90 (97.82) 19 (95)
were ampicillin, co-trimoxazole, chloromycetin, Amikacin 91 (98.91) 20 (100)
gentamicin, amikacin, ciprofloxacin, cephotaxime Ciprofloxacin 88 (95.65) 19 (95)
and ceftriaxone. Cephotaxime 91 (98.91) 20 (100)
Ceftriaxone 91 (98.91) 19 (95)
Randomly selected strains of both S. Typhi and
S. Paratyphi A were sent to the National Table 3.
Susceptibility pattern of S. Typhi and S. Paratyphi
Salmonella Phage Typing Centre, Lady Hardinge A isolates in Rourkela between September 2005 and August 2006.
Medical College, New Delhi, India, for phage Salmonella isolates, 92 were S. Typhi strains and
typing and biotyping. remaining 20 were S. Paratyphi A strains. Almost
Results 75 per cent of isolates were from pediatric
population, among which 52.38% were boys and
Out of 1454 patients, 1052 were children (72.35%)
47.62% were girls.
and remaining 402 were adults (27.65%). Among
In 2004-2005, the predominant phage type
Host organism Phage type Biotype No. of isolates encountered among S. Typhi strains was E1,
S. Typhi A I 5 followed by phage type A (Table 1). In the present
(N=27) D1 I 1 study (2005-2006), predominant phage type
E1 I 17 encountered among S. Typhi isolates was 40,
E9 I 1 which itself is a rare and exotic phage type in India.
J1 I 3 Second most common phage type of S. Typhi
S. Paratyphi A 4 II 3 isolates in this study was E1 and number of Vi-
(N=24) 6 II 21 Negative strains was 4 (Table 2). In both the
studies mentioned, the predominant phage type
Table 1.
Phage types encountered among S. Typhi ans S. Paratyphi
found among S. Paratyphi A strains was type 6,
A isolates in Rourkela between September 2004 and August 2005. followed by phage types of either 4 or 1.
14

19. Most of the phage types of S. Typhi isolates phage type 40, which itself is a rare and exotic
belonged to biotype I, except for phage type 40 phage type of S. Typhi in India. It is worth
and USV-2. All the phage types of S. Paratyphi A mentioning that two more rare and exotic phage
isolates belonged to biotype II (Table 2). types of multi-drug resistant (MDR) S. Typhi
Ampicillin and chloramphenicol sensitivity among strains, namely type 51 and type 28, caused
1,12
S. Typhi isolates was found very high in our study, outbreaks in Kolkata and Mumbai respectively,
though 40-45% of S. Paratyphi A isolates showed but in case of phage type 40, most of the strains
resistance to these antimicrobials (Table 3). were not multi-drug resistant. Emergence of Vi-
Isolates of both S. Typhi and S. Paratyphi A showed negative strains among S. Typhi isolates in
remarkably high susceptibility to gentamicin and Rourkela was another important finding during
amikacin. Resistance to ciprofloxacin was 4-5% the same time.
among the isolates of S. Typhi and S. Paratyphi A. Till date, not many study-reports are available
Susceptibility to cefotaxime and ceftriaxone was regarding phage typing and biotyping of S.
very high among the isolates of both S. Typhi and Paratyphi A. A study among the patients (coming
S. Paratyphi A (Table 3). from Indian subcontinents) in Kuwait reported
Randomly chosen strains of both S.Typhi and S. that 66% of S. Paratyphi A isolates belonged to
Paratyphi A for phage typing and biotyping were phage type I.13 Another study from Nagpur also
also found remarkably sensitive to the showed that the prevalent phage type among S.
antimicrobials used in our study. Out of 36 isolates Paratyphi A isolates from the local population was
14
of S. Typhi, only 2 strains showed resistance to type I. The most commonly encountered phage
ciprofloxacin and 1 strain resistant to type of S. Paratyphi A isolates from Rourkela was
cephotaxime. Out of 12 strains of S. Paratyphi A type 6, a finding which hardly got any other
randomly chosen for phage typing and biotyping, contemporary reference in India. From 1992 to
only 3 strains showed resistance to ampicillin, co- 2003, commonest biotype of S. Paratyphi A in
trimoxazole and chloramphenicol. Interestingly, India was type I,13,14,15 but in our study all the
all these 3 MDR strains of S. Paratyphi A belonged phages of S. Paratyphi A belonged to biotype II.
to phage type 6. The commonest biotype encountered among
S. Typhi strains isolated from Kolkata, Nagpur and
Discussion Ludhiana was type I,12,16,17 but in our study, biotype I
Phage typing is one of the most important means accounted for 44.4% of S. Typhi isolates and
of epidemiological tracing. In 1982-89, the order remaining 55.6% were biotype II.
of frequency of phage types in north and central Susceptibility pattern to ampicillin and
India was A, E, O, while in south the second chloramphenicol were very encouraging for
1
predominant phage type was O. From 1990 S.Typhi isolates as reported earlier,5,6,7 though it
onwards , E1 became the most commonly phage was not that much inspiring for S.Paratyphi A
type except in south India, where phage type O isolates in this study. In this study, differences in
was the predominant type. In 1992, the order of per cent susceptibility between S. Typhi and
frequency had become E1, O, A throughout the S. Paratyphi A isolates for ampicillin,
country. However, there was hardly any report of chloramphenicol and ciprofloxacin were
phage type O from any part of the country since statistically significant (P<0.05), whereas for the
12
1994. rest of the antimicrobials tested, differences in per
In our findings of phage types encountered among cent susceptibility were found insignificant
S. Typhi strains from Rourkela, E1 was the most (P>0.05). Although 4-5% resistance to
commonly occurring phage type in 2004-2005 ciprofloxacin among Salmonella isolates was a
and second-most common phage type in matter of concern, very high susceptibility of
2005-2006. One strikingly different finding in those strains to aminoglycosides (gentamicin and
2005-2006 study was the highest occurrence of amikacin) and third generation cephalosporins
15

20. th
(cephotaxime and ceftriaxone) was highly Medical Microbiology. 13 ed. Edinburg :
encouraging, and can be used judiciously in case Churchill Livingstone, 1984: 456-81.
of ciprofloxacin resistance. 9. Baron EJ, Peterson LR, Finegold SM. Bailey
, th
A diversity among phage types of S. Typhi isolates and Scott s Diagnostic Microbiology. 9 ed.
has been noticed, though in case of S. Paratyphi A, St. Louis, Missouri : Mosby, 1994 : 362-85.
mostly phage type 6 was encountered. This 10. Bauer AW, Kirby WM, Sherris JC and Truck
diversity of phage types observed in this eastern M. Antibiotic susceptibility testing by a
part of India might be due to the diverse origin of standardized single disc method. Am J Clin
these phage types. The diversity of origin of these Pathol 1996; 45 : 493-6.
phages again may be due to the migration of 11. National Committee for Clinical Laboratory
population to and from Rourkela, an industrial Standards. Performance standards for
(steel) township, with respect to other parts of the antimicrobial disc susceptibility tests, 6th ed.
6
country. Further studies are required regarding Approved standard M2-A6. Wayne, Pa :
the epidemiological tracing especially for the National Committee for Clinical Laboratory
exotic phage type 40 of S. Typhi isolates. Standards; 1997.
References 12. Saha MR, Palit A, Chatterjee NS, Dutta P,
Mitra U and Bhattacharya SK. A prospective
1. Pillai PK, Prakash K. Current status of drug
study of phage types & biotypes of
resistance and phage types of Salmonella
Salmonella enterica serotype Typhi isolated
typhi in India. Indian J Med Res 1993; 97:
from hospitalized children in Kolkata, India.
154-158.
Indian J Med Res 2003; 117 : 201-204.
2. Sanghavi SK, Mane MP, Niphadkar KB.
13. Panigrahi D, Chugh TD, West PWJ, Dimitrov
Multidrug resistant Salmonella serotypes. TZ, Groover S and Metha G. Antimicrobial
Indian J Med Microbiol 1999; 17(2): 88-90. susceptibility, Phage typing and Plasmid
3. Sood S, Kapil A, Dash N, Das BK, Goel V and profile of Salmonella enterica serotype
Seth P. Paratyphoid fever in India. Emerg paratyphi A strains isolated in Kuwait. Med
Infect Dis 1999; 5: 483-484. Princ Pract 2003; 12: 252-255.
4. Chandel DS, Chaudhary R, Dhawan B, 14. Tankhiwale SS, Agrawal G, Jalgaonkar SV. An
Pandey A, Dey AB. Drug-resistant Salmonella unusually high occurrence of Salmonella
enterica serotype Paratyphi A in India. enterica serotype Paratyphi A in patients
Emerg Infect Dis 2000; 6: 420-421. with enteric fever. Indian J Med Res 2003;
5. Bhattacharya SS, Das Usha. Occurrence of 117: 10-12.
Salmonella typhi infection in Rourkela, 15. Chopra GS, Basu SK and Bhattacharya SR.
Orissa. Indian J Med Res 2000; 111 : 75-76. Present Phage types and Antibiotic
susceptibility of Salmonellae. Indian J Pathol
6. Bhattacharya SS, Das Usha. A sudden rise in
Microbiol 1992; 4 : 345-350.
occurrence of Salmonella paratyphi A
16. Agarwal V, Brahmne RB, Dhanvijay AG,
infection in Rourkela, Orissa. Indian J Med
Jalgaonkar PD, Pathak AA, and Saoji AM.
Microbiol 2007; 25 : 78-79.
Antibiogram, phage types and biotypes of
7. Das Usha, Bhattacharya SS. Antibiogram,
Salmonella Typhi isolated in Nagpur. Indian J
phage typing & biotyping of Salmonella Med Res 1992; 95: 14-16.
Typhi & Salmonella Paratyphi a from
17. Kumar R, Aneja KR, Punia AK, Roy P, Sharma
Rourkela, Orissa. Indian J Med Res 2006; 124 M and Gupta R. Changing pattern of
: 109-111. biotypes, phage types and drug resistance of
8. Sleigh JD, Duguid JP. Salmonella. In: Collee Salmonella Typhi in Ludhiana during 1980-
JG, Fraser AG, Marmion BP, eds. Practical 1999. Indian J Med Res 2001; 113: 175-180.
16

21. Original Papers
Predictions of Lengths of Hospital stay of malaria patients
Saroj K Mishra Narayan P Sahoo
Deptt. of Internal Medicine Deptt. of Anaesthesia
Address for communication :
Kishore C Mahanta Dr SK Mishra
Deptt. of Internal Medicine Director, Ispat General Hospital,
Rajalaxmi Mishra Rourkela -769005, INDIA
Deptt. of Mathematics, Email: sarojrkl@gmail.com
Sushilavati Govt. Womens College, Rourkela
Abstract providers and administrators, no tool is available
Malaria is a major cause for hospital admissions in to predict the length of stay for the malaria cases.
the tropical regions, but there is no objective tool When confronted by a questioning/ inquisitive
to predict the length of hospital stay (LOS). relative, the treating doctor only extends a rough
Analyzing 700 hospitalized patients, a simple estimate depending on his own experience, which
equation was devised. LOS was equal to ½ [5+ 5 x is purely subjective. In practical situation, the
Severe anemia + 1 x Jaundice +2 x acute renal statements are variable for different doctors and
failure+3 cerebral malaria + 1 x Type of therapy]; thus totally confusing to the relatives.
where, presence of the complication is 1 and In the present study, it is attempted to identify
absence=0 ; Type of therapy : oral anti malaria various determinants on LOS, and to develop a
therapy=1, parenteral =2, and any ICU mathematical model which can be used
intervention (ventilator, dialysis etc)=3 . The objectively for each patient admitted to a
Length of hospital stay of a malaria patient can be hospital. We tried to make it simple and easy to
estimated easily and rapidly by a simple formula, remember. It is attempted that it must be
which does not require sophisticated calculated rapidly and must not require too many
investigations. It can be calculated at the time of lab data.
admission as well as during the course of the Material & Methods:
disease.
a. Hospital: Ispat General Hospital is situated in
Introduction: Sundargarh district of Orissa. It is a 685 bed
When a patient is admitted to a hospital the most hospital under of a Public sector steel plant.
important concern is the survival. The subsequent b. It has eleven bed Critical care units. There are
question which arises in the mind of the health facilities for haemodialysis, peritoneal
care providers, patients or their relatives, as well dialysis, blood banking, 24 hour emergency,
as the administrators is the duration of hospital haematology and biochemical laboratory etc.
stay of the patient. In malaria prone areas, many
c. Catchment area: Patients come from urban
of the hospital beds in the referral centres are
areas of Rourkela as well as surrounding
occupied by patients with malaria. The cost of
villages, forested areas, mining localities etc.
treatment depends on several factors, one of
these being the period of stay. A simple scoring d. Subjects: All patients admitted to the Internal
system was devised by Mishra et al to predict the Medicine Dept of Ispat General Hospital,
1
survival of the malaria patients. A large number of Rourkela with confirmed malaria.
the beds are occupied by these patients, during The study has two parts: (a) analysis of the malaria
the peak transmission period, making it a major and (b) Multiple regression analysis.
administrative problem. The LOS of admitted In the first phase, database was collected
patients is one of the indicators of bed occupancy, prospectively in a format which includes age, sex,
planning and rotation of staff deployment, etc and demographic data, treatment received before
2-4
the resource utilization. (Kazembe et al. 2006; admission, biochemical and hematological
Velip et al. 2006; Van Houdenhoven et al. 2007) reports, presence of seizures, treatment details,
Similarly, from the point of view of the health care and the outcome. All those who expired were
17

22. excluded from the study. 700 patients with 62% were entitled patients (either employees or
complete data were analysed. their dependants, or retired employees of the
Statistics: steel plant: all of these get free medical
treatment) and 38% were from different walks of
Student's t test was used to differentiate between
life, including people from villages, township and
male vs female; adult vs children; Rural vs urban;
traders. These patients were treated in the
patients with acute renal failure (sr Creatinine >3
hospital on payment basis. Their income and socio
mg/dl), jaundice (sr Bilirubin > 3 mg/dl), severe
economic conditions varied widely. 60% were
anemia (Hb < 5 gm/dl) or cerebral malaria
from urban areas, and others were from suburbs
(unarousable coma or GCS <10).
or villages.
The statistical analysis was done by using OpenEpi
The comparisons of length of stay in different
version 2.2.1 (2010), an Open Source
groups are depicted in the Table-1. As it appears,
Epidemiologic Statistics for Public Health, Version
2.2.1. www.OpenEpi.com, accessed on 18 June the length of stay was significantly longer in
2010 The difference is considered to be patients with severe anemia, acute renal failure,
significant if p < 0.05. cerebral malaria and jaundice.
In the second phase Multiple Regressions was Thus LOS was 2.87(±1.68) days when the patient
performed to find out the relationship of the was having uncomplicated malaria, which went
above parameters and to get a linear equation. on increasing in presence of complications. Thus
Determinants Characteristics No of patients LOS (± SD) P value
Entitled Entitled 433 3.99(±2.00) 0.000*
NE 267 4.95(±2.95)
Sex Male 512 4.29 (±2.39) 0.299
Females 188 4.52(±2.61)
Rural 257 4.62(±2.75)
Residence area 0.000
Urban 443 3.91 (±1.73)
Sr Creatinine >3mg/dl 29 8.66 (±4.45)
Acute renal failure Sr Creatinine < 3mg/dl 671 4.17(±2.14) 0.000
GCS <10 61 7.41(±2.11)
Cerebral malaria GCS >10 639 4.06(±2.08) 0.000
Hb<5.1 G 18 5.89(±2.65)
Severe anemia HB>5 g/dl 620 4.37(±2.46) 0.027
Bil >3mg/dl 139 5.81(±3.33)
Bil < 3 mg/dl 561 3.99(±2.03)
Jaundice 0.000
Uncomplicated 390 2.87(±1.68)
Single 181 4.33(±1.68)
Complications Multiple 129 6.78(±3.53) 0.000
Oral drugs 115 2.97(±21.18)
Level of treatment Parenteral (QBH/AS) 585 4.62(±2.54) 0.000
Table 1. Characteristics of malaria patients and LOS
It will be in the form of LOS was 8.66 (±4.45) days in presence of acute
LOS = a1x1 + a2x2 + a3x3 + a4x4 + …… + C renal failure, 7.41(±2.11) days in patients with
cerebral malaria, and 5.89 (±2.65) in presence of
Observations:
severe anaemia and 5.81 (±3.33) in patients with
In the study we collected the data of those adult jaundice. LOS was longer in patients, who have
patients who survived and were discharged from
come from rural areas, but there was no
the hospital. 700 surviving patients were analysed
difference in males vs females.
for the prediction of length of hospital stay. Out of
these, 188 were females and rest were males. After the determinants were identified, a linear
18

23. equation was developed by using multiple patients are concerned regarding the length of
regressions. stay in a tertiary care hospital and the cost
LOS = 2.441+ 2.565 Severe anemia + 0.447 associated with it. We searched the literature to
Jaundice +0.993 acute renal failure find out the studies related to LOS in malaria
1.405 cerebral malaria +0.657 Level of patients. But there were only two studies cited in
therapy the MEDLINE by Kazembe et al. 2006 and Velip et
2,3
The equation was made modified to make it al. 2006. However, several studies have been
simple and ready to use at bedside. carried out by Mounsey et al. 1995;. Bannwart
Thus, et al., 1999; Arrahamyan et al. 2006; Clark et al.,
2007 and Diringer et al., 2004 to predict the LOS in
LOS = 2.5+ 2.5 Severe anemia + 0.5 Jaundice +1
other clinical conditions viz, very low weight
acute renal failure
neonates in nursery, sepsis in ICU settings,
1.5 cerebral malaria + 0.5 Type of therapy 5-9
patients after coronary surgery etc.
Where, the severe anemia, jaundice, acute renal
In a retrospective study in Spain, 1920 episodes of
failure, cerebral malaria are considered as
community-acquired pneumonia (CAP) in 27
present=1, or absent=0; and level of treatment is
community hospitals were analyzed by Cabre et
oral anti- malaria treatment with chloroquin or 10
al. (2007) for inter-hospital variability in length of
quinine =1, parenteral artemisinine or quinine =2,
Factors Beta P value
Entitled or not 0.186 0.323
Residence 0.106 0.428
Severe anemia 2.565 0.000
Cerebral malaria 1.405 0.000
Jaundice 0.447 0.028
Acute renal failure 0.993 0.006
Level of therapy 0.657 0.000
LOS= 2.441+ 2.565 Severe anemia + 0.447 Jaundice +0.993 acute renal failure
1.405 cerebral malaria +0.657 Level of therapy
simplifying the equation for ready bedside use
LOS = 2.5+ 2.5 Severe anemia + 0.5 Jaundice +1 acute renal failure
+ 1.5 cerebral malaria + 0.5 Level of therapy
or,
LOS = ½ [5+ 5 x Severe anemia + 1 x Jaundice +2 x acute renal failure
+3 x cerebral malaria + 1 x Level of therapy]
Where, presence =1 , and absence = 0 for severe anemia, jaundice, acute renal failure and cerebral malaria.
For level of therapy oral chloroquin or quinine =1, parenteral artemisinine or quinine =2, and any ICU
intervention (ventilator, dialysis etc)=3
Table-2.: Multiple regression showing influence of factors on LOS
and any ICU intervention (ventilator, dialysis hospital stay (LOS), mortality and readmission
etc)=3. rates. The overall adjusted LOS (mean+/-S.D.) was
Discussion 10.0+/-9.8 days. LOS increased according to the
Malaria being a disease mostly in the developing Pneumonia Severity Index (PSI) risk class: 7.3 days
countries, the treatment is availed at different for class I to 11.3 days for class V (P<0.001).
2
levels: (a) at home, (b) at the nearby health Velip et al. (2006) from Goa described the
facilities and (c) referral centre for severe malaria determinants of LOS in malaria patients. The study
cases; where the patient is shifted to a hospital far indicated the importance of altered sensorium,
away from own place of residence. Relatives of presence of liver involvement, duration of therapy
19

24. before admission as influencing factors. But a system. Malaria Journal, 2007; 6:24. doi:
major flaw of the study was that most of the 10.1186/ 1475-1875-6-24.
patients were uncomplicated ones. PUBMED 2. Velip AP, Kulkarni MS, Motghare DD, Vaz FS.
search did not show studies on determination of Determinants of hospital stay among
LOS in severe malaria cases. Similarly publications malaria patients at a tertiary care hospital in
are not available from any tertiary care hospital Goa. J Communic Dis, 2006; 38: 115-117
which manages both uncomplicated and 3. Kazembe LN, Kleinschmidt I, Sharp BL.
complicated cases. Patterns of malaria-related hospital
Some of the parameters in our study were similar admissions and mortality among Malawian
to the Goa study. However, we have not been able children: an example of spatial modelling of
to find any difference among the males and hospital register data Malaria Journal 2006,
females, urban vs rural on LOS. But, as expected 5:93 doi:10.1186/1475-2875-5-93
the LOS is higher in patients with any or more 4. Van Houdenhoven M, Nguyen TD,
complications. It was noted that all complications Eijkemans MJ, Steyerberg EW, Tilanus HW,
are not similar, and they influence the survival in a Gommers D, Wullink G, Bakker J, Kazemier
different weighted capacity. Similarly they also G.Optimizing intensive care capacity using
influence the LOS. individual length-of-stay prediction models.
When a very sick malaria patient is managed in Crit Care. 2007 27; 11 :R42
critical care unit or high dependency unit, survival 5. Mounsey JP, Griffith MJ, Heaviside DW,
is the most important concern. In a previous study, Brown AH, Reid DS. Determinants of LOS in
Mishra et al. (2007) proposed a simple prediction ICU and in hospital after coronary artery
rule for the survival of the patients with severe surgery. Br Heart J, 1995; 73: 92-98.
malaria by assigning 1,2,3 and 4 to A (anemia), B 6. Arrahamyan L, Demirchyan A, Thomson
(BUN↑ ), C (cerebral malaria) and D (Dyspnoea/ ME, Hovaguimian H. Determinants of
ARDS) respectively. The malaria score for adults morbidity and ICU stay after coronary
(MSA) ranges from 0 to 10. The mortality was 2% surgery. Asian Cardiovasc Thorac Ann,
for MSA 0 – 2; 10% for MSA 3–4, 40% for MSA 5–6 2006; 14: 114-118.
and 90% for MSA 7 or more. The sensitivity is 7. Bannwart BC, Rebello cerebral malaria,
89.9% and positive predictive value is 94.1% when Sadeck LSR, Pontes MD, Ramos JLA, Leone
5 is taken as the cut off value. C. Prediction of Length of Hospital Stay in
In the present one, we derived a very simple Neonatal Units for Very Low Birth Weight
prediction rule for the LOS. It does not involve Infants. J Perinatology, 1999; 19: 92-96
sophisticated data collection, estimation or 8. Clark DE, Lucas FL, Ryan LM. Predicting
analysis. Still it extends valuable information, hospital mortality, length of stay, and
which will be helpful to the clinicians. In addition, transfer to long-term care for injured
the formula can be used to modify the result/ patients. J Trauma, 2007 ;62:592-600.
prediction in the course of time if any new 9. Diringer MN, Reaven NL, Funk SE, Uman GC.
complication arises. Elevated body temperature independently
However, we have analyzed the data of only one contributes to increased length of stay in
year, and that too only among the adults. It is neurologic intensive care unit patients. Crit
proposed that such studies may be undertaken Care Med. 2004 ;32 :1489-95.
among children too. It should also be validated in 10. Cabre M, Bolivar I, Pera G, Pallares R;
cohorts from different geographical regions. Pneumonia Study Collaborative Group.
Acknowledgement: We extend sincere thanks to Factors influencing length of hospital stay in
the staff of IGH and malaria research Unit. community-acquired pneumonia: a study in
Funding: None, Conflict of interest: None 27 community hospitals. Epidemiol Infect.
2004 Oct;132(5):821-9.Velip AP, Kulkarni
References: MS, Motghare DD, Vaz FS. Determinants of
1. Mishra SK, Panigrahi P, Mishra R, Mohanty hospital stay among malaria patients at a
S. Prediction of outcome in adults with tertiary care hospital in Goa. J Communic
severe falciparum malaria- a new scoring Dis, 2006; 38: 115-117
20

25. Case reports
Peutz- Jeghers Syndrome presenting as acute intestinal
obstruction due to Jejunal Intussusception in an adult male
Amulya M Acharya Address for communication :
Sishir R Dash Dr A.M.Acharya, Sr Deputy Director,
Deptt. of Surgery, Ispat General Hospital,
Manoja K Panigrahi Rourkela, Odisha, India
Deptt. of Surgery Email:dramulya.acharya@gmail.com
and digits. The most common symptoms are
ABSTRACT recurrent pain abdomen, anemia, malena and
Peutz – Jeghers syndrome (PJS) is a rare familial hematochezia. Here we are reporting a case of PJS
autosomal dominant disorder with presented as acute intestinal obstruction due to
hamartomatous polyposis of G I Tract and melanin jejunal intussusception in an Indian adult male.
pigmentation around mouth, oral mucosa , lips We are providing some clinical photographs,
and digits. Most common symptoms are histopathology report and added discussion
recurrent pain abdomen, anaemia and blood in available from the scarce literature which may be
stool. Presentation of frank intussusception and of educational importance.
intestinal obstruction in adults is uncommon. We Case report:
are reporting a case of Indian adult male
A 58 years old Indian male was admitted in the
presented to us in acute intestinal obstruction due
surgical ward with sudden onset of severe
to jejuno jejunal intussusception. There were
abdominal pain associated with vomiting of three
multiple polyps in the small gut and one large
days duration. He was found afebrile, anemic and
polyp of 4cm x 8cm was the lead point in triggering
dehydrated. Pulse 98/min, BP 100 / 70 mm Hg.
the intussusception. Histopathology confirmed
Abdomen was distended with diffuse tenderness
them as hamartomatous polyps typically seen in
and guarding. An ill defined soft immobile mass
Peutz- Jeghers syndrome. As it is unusual to see
(15 x 8 cm) was palpable in the epigastrium. Some
such rare case in clinical practice and scarcity of
bluish black pigmentation was seen over his
literature, we feel to report this for the benefit of
buccal mucosa but could not be correlated with
clinicians and students. Awareness of the disease
the acute abdominal condition (Fig.1).
is helpful for proper diagnosis, early management
and follow up with genetic counseling to the
patient and his family.
Key words:
Peutz, Jeghers,PJS, polyposis, intestinal polyps,
melanin pigmentation, intussusception
Introduction:
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 Figure 1:
pigmentation around mouth, oral mucosa lips Bluish-black pigmentation over buccal mucosa.
21

26. One large polyp of 3.5cm with a 8cm stalk was
found on per rectal examination (Fig.2).
Figure 3b
Intussuscipien inside intussusceptum.
Figure 2 triggering the intussusceptions (Fig.4a,b).
Rectal polyp 3.5cm with 8cm long stalk
About two feet of jejunum involving the
Biochem reports were normal except low protein
intussusception and having multiple polyps was
(total protein 4g and albumin 1.9g). X-Ray
excised and end to end anastomosis done
abdomen showed few air-fluid levels. Ultrasound
followed by rectal polypectomy. Rest of the small
of abdomen revealed two concentric echo
and large gut was thoroughly palpated and found
structures with classical target sign suggestive of
to be normal. Patient recovered uneventfully.
intussusception (Fig.3a, 3b). Emergency
Histopa-thology of resected jejunum with polyps
laparotomy was taken up with a provisional
showed branching of smooth muscles arising from
diagnosis of acute intestinal obstruction.
muscularis mucosae into the stroma of columnar
Laparotomy revealed jejuno-jejunal intussuscep-
and goblet cells which are typical hamartomatous
tion about one foot distal to duodeno-jejunal
changes seen in Peutz- Jeghers syndrome (Fig.5).
flexture involving two feet long segment of
There was no evidence of atypia or malignancy.
jejunum. Multiple polyps were seen on the
Lymph nodes showed reactive hyperplasia.
involved jejunum. There was one large polypoidal The case was finally diagnosed as Peutz-
mass of 4cmx8cm which was the lead point in Jeghers syndrome with unusual presentation of
acute intestinal obstruction duo to adult
intussusception.
Figure 3a US abomen showing target sign Figure 4a Multiple polyps in jejunum.
of intussusception.
22