ASSOCIATION OF PHYSICIANS

OF BANGLADESH

JOURNAL COMMITTEE

ADVISORY BOARD

National Prof. Nurul Islam

Nation Prof. Brig. (Rtd) Abdul Malik

Prof. M Amanullah

Prof. Md. Tahir

Prof. Nazrul Islam

Prof. Sk. Nesaruddin Ahmed

Prof. Matiur Rahman

Prof. Hazera Mahtab

Prof. Harun ur Rashid

Prof. Mobin Khan

Prof. Tofayel Ahmed

Prof. Md. Fazlul Hoque

Prof. AZM Maidul Islam

Prof. Syed Kamaluddin

Prof. Moyeenuzzaman

EDITORIAL BOARD

Chairman : Prof. Mahmud Hasan

Editor-in-Chief : Prof. Quazi Tarikul Islam

Assistant Editors : Dr. Ahmed Hossain

Dr. Robed Amin

Dr. Kazi Shahnur Alam

Dr. Mamun Al Mahtab

Members : Prof. MA Faiz

Prof. Kaniz Moula

Prof. MA Bashar

Prof. Projesh Kumar Roy

Prof. Nooruddin Ahmed

Prof. Md. Ekhlasur Rahman

Prof. Firoz Ahmed Quraishi

Prof. Md. Ridwanur Rahman

Prof. Md. Zakir Hossain

Prof. Dilip Dhar

Prof. Col Mamun Mostafi

Prof. Md. Faruk Ahmed

Prof. ARM Saifuddin Ekram

Prof. Md. Alamgir Kabir

Prof. Tahmina Begum

Dr. Rubina Yasmin

Ex Officio : Prof. Syed Atiqul Haq

Prof. Md. Mujibur Rahman

Dr. Abdul Wadud Chowdhury

ASSOCIATION OF PHYSICIANS

OF BANGLADESH

EXECUTIVE COMMITTEE 2011-2013

President : Prof. Syed Atiqul Haq

Vice President : Prof. Selimur Rahman

Prof. MA Jalil Chowdhury

Treasurer : Prof. MA Rashid

Secretary General : Prof. Md. Mujibur Rahman

Joint Secretary General : Prof. Golam Rabbani

Organizing Secretary : Dr. Mostafa Zaman

Secretary for Scientific Affairs : Dr. Abdul Wadud Chowdhury

Members : Prof. Mahmud Hasan

Prof. Quazi Deen Mohammad

Prof. Md. Abul Kashem Khandaker

Prof. Chowdhury Ali kawsar

Prof. Khwaza Nazimuddin

Prof. Muhammad Rafiqul Alam

Prof. Md. Azizul Kahhar

Prof. Khan Abul Kalam Azad

Prof. Md. Qamrul Hassan Jaigirdar

Ex-Officio : Prof. AKM Rafiquddin

Prof. AKM Mosharraf

CONTENTS

Original Articles

Dyselectrolytaemia in Acute Stroke Patients, An Observational Study 30-34

MR Siddiqui, QT Islam, MA Haque, MJ Iqbal, A Hossain, YU Rahman, MS Mahbub, AA Sazzad

Presentation and Outcome o Acute Kidney Injury in A Tertiary Military Hospital of Bangladesh 35-40

Mamun Mostafi, MAJ Azizun Nessa, Md Amzad Hossain Fakir, Md Abdul Quddus Bhuyian,

AKM Mijanur Rahman

Study of Correlation of Severity of Hepatic Cirrhosis with Severity of Bone Changes 41-46

Measured By Bmd (Bone Mineral Density)

Md. Ashraful Alam, Nooruddin Ahmed, Shahinul Alam, Mamun Al Mahtab

Incidence of Vasovagal Reaction Among the Blood Donors Attending at Transfusion 47-50

Medicine Department of Dhaka Medical College Hospital

Chowdhury FS, Siddiqui MAE, Rahman KGM, Begum HA, Begum HA, Hoque MM, Nasreen Z

Review Article

Abdominal Tuberculosis - A Review 51-59

Devendra Nath Sarkar, Robed Amin, Hanif Mohammed, MA Azhar, MA Faiz

Case Reports

A Case Report On Decompensated Cirrhosis of Liver With Pregnancy 60-62

Mohammad Mahabubul Alam, Faiz Ahmad Khondakar, Syed Abul Foez,

Mamun Al-Mahtab, Salimur Rahman

Aluminium Phosphide Poisoning with Fatal Effect- A Case Report 63-67

Md Robed Amin, S Shohag, A Basher, Shaker Uddin Ahmed, Shahadath,

Nirmol, Azad, Fazle Rabbi Chowdhury, M A Faiz

should follow the Vancouver format. In the text they

should appear as numbers starting at 1. At the end

of the paper they should be listed (double spaced) in

numerical order corresponding to the orders of

citation in the text. All authors should be quoted for

papers with upto six authors, for papers with more

than six authors the first six only should be quoted

followed by et al.

Abbreviations for titles of medical periodicals should

conform to those used in the latest edition of Index

Medicus. The first and last page numbers for each

reference should be provided. Abstracts and letter

must be identified as such. Authors must check

references against original sources for accuracy.

Examples of reference are given below:

Articles in Journals :

1. Paganini Hill A, Chao A, Ross Rk, Henderson BE.

Aspirin use and chronic disease : a cohort study of

the elderly. BMJ 1989; 299: 1247-50.

2. Parkin DM, Clayton D, Blook RJ, Massyer E, Fried

HP, Iranov E, et al. Childhood Leukaemia in Europe

after Chernobyl : 5 years follow-up. Br J Cancer 1996;

73 : 1006-12.

Chapter in a Book :

1. Phyllyps SJ, Whisnant JP. Hypertension and Stroke.

In : Lurgh JH, Brennes BM, editors. Hypertension :

Pathophysiology, diagnosis and management. 2nd ed.

New York : Raven Press; 1995. p. 465-78.

Tables should be as few as possible and should

present only essential data. Each table should be

type-written on separate sheets, have a title or

caption with Roman numbers. All photographs,

graphs, diagrams should be referred to as figures and

should be numbered consecutively in the text in

Arabic numericals. The legends for illustrations

should be typed on separate sheets. Photographs

and photomicrographs should be unmounted glossy

prints. Photomicrographs should have internal scale

markers, include in the legend the original

magnification and the stain used. Line diagrams and

graphs should be on separate sheets drawn with black

Indian ink on white paper. A photocopy of all

illustrations should be submitted.

Proofs :

Two marked copies of the proofs may be sent to the

principle author which should be read carefully for

error. One corrected copy must be returned to the

editor within the next three days. Major alteration in

the text cannot be accepted.

INSTRUCTION TO AUTHORS

The Journal of Association of Physicians of

Bangladesh publishes original papers, reviews

concerned with recent practice and case reports of

exceptional merit. The Journal considers manuscripts

prepared in accordance with the guidelines laid down

by the international committee of Medical Journal

Editors (BMJ 1988; 296: 401-405). A covering letter

signed by all authors must state that the data have

not been published elsewhere in whole or in part

and all authors agree their publication in Journal of

Association of Physicians of Bangladesh. If the work

has been conducted abroad then the article must be

accompanied by certificate from head of the institute

where the work has been done.

Type scripts :

Three typed copies of the article and one copy in a

3.5" high density floppy diskette processed in

Wordperfect 6.0 or MS Word 6.0 should be submitted

to the Editor. The text should be type-written in double

space on one side of the paper not larger than ISO

A4 with a 5 cm margin and paper should be numbered

consecutively. The first page of the type script should

bear the names of the author(s) and the name and

address of the laboratory or institution where the

work has been carried out, in addition to the title of

the paper. The full address of the principal author to

whom proofs will be sent should be given as footnote,

as should any permanent change of address and/or

appointment. A short (running) title of not more than

45 characters should be given. Please write as

concisely as possible. Amendments should be made

in the texts and not in the margins. All submitted

manuscripts are reviewed by the editors and rejected

manuscripts will not be returned. Ethical aspects will

be considered in the assessment of the paper.

Arrangement :

Papers should be divided into: (a) Title page (b)

Summary (c) Introduction (d) Materials and methods

(e) Results (f) Discussion (g) Acknowledgement (h)

Reference (i) Tables (j) Figures and Captions. The

summary should not exceed 250 words and should

state concisely what was done, the main findings and

how the work was interpreted.

Style :

Abbreviations and symbols must be standard and SI

units should be used throughout. Whenever possible

drugs should be given their approved generic name.

Acronyms should be used sparingly. Statistical

analysis must explain the methods used. Reference

Bangladesh J Medicine 2011; 22 : 30-34

ORIGINAL ARTICLES

Introduction:

Stroke is the most common neurological emergency1.

Stroke is the third most common cause of death in

developed nations after ischaemic heart disease and

cancer.2 The AHA estimates that 780 000 strokes

occur each year; 600 000 of these are new strokes,

and 180 000 are recurrent strokes.3 According to year

book of the department of Medicine at DMCH (2009)

14.7% of total admission was stroke patients. Stroke

is a complex disease that requires the efforts and

skills of all members of the multidisciplinary team.4

A coordinated care of the stroke patient results in

improved outcomes, decreased lengths of stay, and

decreased costs.5 Stroke patient die off either due to

the primary disease or due to complications. Medical

DYSELECTROLYTAEMIA IN ACUTE STROKE

PATIENTS, AN OBSERVATIONAL STUDY

MR SIDDIQUI1, QT ISLAM2, MA HAQUE3, MJ IQBAL4, A HOSSAIN5, YU RAHMAN6, MS MAHBUB7, AA

SAZZAD8

Abstract:

Background: There are many studies on stroke, its associated conditions and their effect on

stroke patient’s outcome, but a few studies on dyselectrolytaemia in stroke patients has been done

in our country, even outside.

Method: a total number of 100 randomly selected, clinically and CT proven acute stroke patients

were studied at medicine units of Dhaka Medical College Hospital. Association of electrolytes

imbalance among acute stroke patient were identified and correlated.

Result: Out of 100 patients 29% were in between 51-60 years age group & 72% were male and

28% were female patients. Majority 53% patients had Ischaemic stroke, 45% Intracerebral

haemorrhage (ICH) and only 2% had Subarachnoid haemorrhage (SAH). 53% of total acute stroke

patient had dyselectrolytaemia. Among 100 acute stroke patients 62.22% of haemorrhagic stroke

(p<0.05) & 43.39% of ischaemic stroke (p>0.05) patients had dyselectrolytaemia. Total 36% of all

stroke patients had serum sodium imbalance & 31% had serum potassium imbalance. In haemorrhagic

stroke & ischaemic stroke patients, hyponatraemia (17% & 13%), hypernatraemia (1% & 3%),

hypokalaemia (19% & 11%), hyperkalaemia (0% & 1%), hypochloraemia (9% & 6%) respectively with

found.

Conclusion: In haemorrhagic stroke, the incidence of dyselectrolytaemia was more than ischaemic

stroke and which were mostly hyponatraemia and hypokalaemia.

Key words: Stroke, dyselectrolytaemia, electrolytes imbalance,

1. FCPS Medicine P-II Course, Dept. of Medicine, DMC.

2. Professor, Dept. of Medicine, DMC.

3. Associate Professor, Dept. of Neurology, DMC.

4. FCPS Medicine P-II Course, DMC.

5. Assistant professor, Dept. of Medicine, DMC.

6. FCPS Medicine P-II Course, DMC.

7. Assistant register, Dept. of Neurology, DMCH.

8. Intern medical officer, Dept. of Medicine, DMCH.

management focus on the prevention of sub acute

complications of stroke, including malnutrition

aspiration, pneumonia, dyselectrolytaemia, UTI,

bowel or bladder dysfunction, DVT, pulmonary

embolism, contractures, joint abnormalities, and skin

breakdown.6 Electrolyte disturbances such as

hypernatraemia or hyponatraemia, resulting from the

syndrome of inappropriate antidiuretic hormone

(SIADH), increase of brain Natriuretic peptides (BNP),

inappropriate fluid intake and loss, can lead to

complications such as seizures or death.4,7 Most

haemorrhagic stroke patients are presented with

headache and vomiting.8 Vomiting is an important

cause of dyselectrolytaemia.2 Complications like

dyselectrolytaemia are more common in acute phase.4

In our country, there are many studies on stroke, its

associated conditions and their effect on stroke

patient’s outcome, but a few studies on electrolytes

disturbance in stroke patients has been done in our

country, even outside.9 In this study, I attempted to

find out the common electrolytes disturbances in

acute stroke patients and its effect on the immediate

outcome of the patients.

Materials & Method:

In this descriptive cross sectional study, a total

number of 100 randomly selected, clinically and CT

proven acute stroke patients were studied from Jan

2010 to June 2010 at medicine units of Dhaka Medical

College Hospital. Patient admitted within 48 hours

of the onset of stroke with CT scan of the brain

showing infarct or haemorrhage was enrolled for this

study. Serum electrolytes level was done in all

patients on admission. Association of electrolytes

imbalance among acute stroke patient were identified

and correlated. All data were collected in individual

case record form. This was done by detailed history

from patients or his / her relatives, complete physical

examination and necessary investigations. Statistical

analysis was carried out by using SPSS v16.0 Windows

statistical software. Descriptive statistics were used

for the interpretation of the findings. Informed and

written consent obtained from all patients or their

guardian. Formal Ethical Clearance was obtained from

the Research Review Committee of Dhaka Medical

College and Hospital.

Result:

Out of 100 patients 29% were in between 51-60 years

age group & 72% were male and 28% were female

patients. According to CT scan findings majority 53%

patients had Ischaemic stroke, 45% Intracerebral

haemorrhage (ICH) and only 2% had Subarachnoid

haemorrhage (SAH). The low income group (63%)

comprises the major percentage of the patients in

our study. 77.7% Haemorrhagic stroke and 75.4%

Ischaemic stroke patients were hypertensive. 53%

(p>0.05) of total acute stroke patient had

dyselectrolytaemia. 62.22% of haemorrhagic stroke

(p<0.05) & 43.39% of ischaemic stroke (p>0.05)

patients had dyselectrolytaemia.

Table-I

Frequency of serum sodium imbalance in stroke patient

Type of stroke Normal Hyponatraemia Hypernatraemia Total

S. Sodium (%) (%) (%) (%)

Intracerebral haemorrhage 27(27%) 17(17%) 1(1%) 45(45%)

Ischaemic stroke 37(37%) 13(13%) 3(3%) 53(53%)

Subarachnoid haemorrhage 0(0%) 2(2%) 0(0%) 2(2%)

Total 64(64%) 32(32%) 4(4%) 100(100%)

n: number of patient, s: serum, normal serum sodium : (135-145mmol/l), hyponatraemia: (<135mmol/l),

hypernatraemia: (>145mmol/l)

This table shows that 32% of all stroke patients had hyponatraemia, Hyponatraemia was most common

among intracerebral haemorrhage patients (17%) followed by ischaemic stroke patients (13%) and all the

patients of subarachnoid haemorrhage had hyponatraemia. Only 4% of all stroke patients had hypernatraemia

which was 3% of ischaemic stroke and 1% of intracerebral haemorrhage. Total 36% of all stroke patients had

serum sodium imbalance during stroke.

Table-II

Association of hyponatraemia in haemorrhagic and ischaemic stroke (n=94)

Type of Stroke Hyponatraemia Normal sodium Total p value

Hemorrhagic 19 27 46

Ischemic 13 37 50 >0.05

Total 32 64 96

n: number of patient

Chi-square test (χ2) was done to measure the level of significant (p value). χ2=1.71, df =1, p=>0.05

There is no significant association between hyponatraemia and type of stroke.

31

Dyselectrolytaemia in Acute Stroke Patients, An Observational Study BJM Vol. 22 No. 2

Table-III

Frequency of serum potassium imbalance in stroke patient

Type of stroke Normal S. Hypokalaemia Hyperkalaemia Total

Potassium (%) (%) (%) (%)

Intracerebral haemorrhage 26(26%) 19(19%) 0(0%) 45(45%)

Ischaemic stroke 41(41%) 11(11%) 0(0%) 53(53%)

Subarachnoid haemorrhage 2(2%) 0(0%) 1(1%) 2(2%)

Total 69(69%) 30(30%) 1(1%) 100(100%)

n: number of patient, s: serum, normal serum potassium : (3.5-5mmol/l) , hypokalaemia: (<3.5mmol/l), hyperkalaemia:

(>5mmol/l)

This table shows that 30% of all stroke patients had hypokalaemia. Hypokalaemia was most common among

intracerebral haemorrhage patients (19%) followed by ischaemic stroke patients (11%). Only 1% of all stroke

patients had hyperkalaemia which was one of the two patients of subarachnoid haemorrhage. Total 31% of all

stroke patients had serum potassium imbalance during stroke.

Table-IV

Association of hypokalaemia in haemorrhagic and ischaemic stroke (n=97)

Type of Stroke Hypokalaemia Normal potassium Total p value

Hemorrhagic 19 26 45

Ischemic 11 41 52 <0.05

Total 30 67 97

n: number of patient

Chi-square test (χ2) was done to measure the level of significant (p value).χ2= 5, df =1, p=<0.05

There is significant association between hypokalaemia and type of stroke.

Table V

Association of various type of dyselectrolytaemia in different type of acute stroke. (n=100)

Various type of Intracerebral Ischaemic Subarachnoid Total (%)

dyselectrolytaemia haemorrhage stroke haemorrhage

Sodium imbalance 18 16 02 36(36)

Hyponatraemia 17 13 02 32(32)

Hypernatraemia 01 03 0 4(4)

Potassium imbalance 19 12 0 31(31)

Hypokalaemia 19 11 0 30(30)

Hyperkalaemia 0 01 0 01(01)

Chloride imbalance 09 07 0 16(16)

Hypochloraemia 09 06 0 15(15)

Hyperchloraemia 00 01 0 01(01)

Bicarbonate imbalance 02 0 0 02(2)

Low bicarbonate 02 0 0 02(02)

High bicarbonate 00 0 0 00(00)

n:number of patient, %:percentage, normal s. sodium : (135-145mmol/l), hyponatraemia: (<135mmol/l), hypernatraemia:

(>145mmol/l), normal s. potassium : (3.5-5mmol/l) , hypokalaemia: (<3.5mmol/l), hyperkalaemia: (>5mmol/l), normal

s. chloride: (96-110mmol/l), hypochloraemia: (<96mmol/l), hyperchloraemia: (>110mmol/l), normal s. bicarbonate:

(24-30mmol/l).

32

BJM Vol. 22 No. 2 Dyselectrolytaemia in Acute Stroke Patients, An Observational Study

This table shows that 36(36%) acute stroke patients

had serum sodium imbalances, 31(31%) had serum

potassium imbalance, 16(16%) had serum chloride

imbalance and only 02(2%) had serum bicarbonate

imbalance. The incidence of serum sodium,

potassium, chloride and bicarbonate imbalances were

higher in intracerebral haemorrhage (18, 19, 09 & 02

patients respectively) than acute ischaemic stroke

(16, 12, 07 & 0 patients respectively).

Discussion:

Stroke incidence rises exponentially with increasing

age. In this present study, maximum number of

patients (29%) were in between 51-60 years age group

followed by (22%) between 61-70 years age group. The

maximum number of male (21% & 16%) and female

(8% & 6%) were also in the above age group

respectively. Bevan H et al 10 in his study of stroke

also found similar picture. A hospital based study

done in DMCH showed that only 1% occurred in <20

years and 26% in 20-45 years and majority are above

45 years.11 72% were male and 28% were female i.e.,

male incidence is 30% higher than female which

coincide with international study. The present study

coincides with the study of Chowdhury et al,12 and

Kurtzke,13 where showed that frequency of stroke is

30% higher in men than women. CT scan findings of

the studied patients show that majority 53% patients

had ischaemic stroke, 45% had intracerebral

haemorrhage and only 2% had subarachnoid

haemorrhage. This study similar with study of Alam

B et al,14 they studied 1020 patients of stroke in

DMCH. Higher rate of haemorrhagic stroke in this

present hospital based study and previous Alam B et

al 14 study in DMCH may be due to the acute

admission is more related to the haemorrhagic stroke.

In this series 53% of our acute stroke patient had

dyselectrolytaemia. Among 45 acute intracerebral

haemorrhage stroke patients 28(62.22%) had

dyselectrolytaemia. There was significant association

between dyselectrolytaemia and acute haemorrhagic

stroke (P=<0.05). Among 53 ischaemic stroke patients

23(43.39%) had dyselectrolytaemia and 30(56.60%) of

them had no electrolytes imbalance, but there was

no statistical significant association between

dyselectrolytaemia and acute ischaemic stroke

(P=>0.05). All of the 2(100%) subarachnoid

haemorrhage patients had dyselectrolytaemia. In a

study by Kusuda K et al,15 found that 52%

haemorrhagic stroke (p=<0.01) and 26% ischaemic

stroke patients had dyselectrolytaemia (p=>0.05). In

this series the percentages of dyselectrolytaemia is

a bit high, may be due to under developed acute

management setup in our hospital.

In this study (table-I), 32% of all stroke patients had

hyponatraemia. Hyponatraemia was most common

among haemorrhagic stroke patients (17%) followed

by ischaemic stroke patients (13%) and all the

patients of subarachnoid haemorrhage had

hyponatraemia. But chi-square test revealed no

statistically significant association between

hyponatraemia and type of stroke (p=>0.05). Only 4%

of all stroke patients had hypernatraemia which was

3% of ischaemic stroke and 1% of haemorrhagic

stroke. Total 36% of all stroke patients had serum

sodium imbalance during stroke. 30% of all stroke

patients had hypokalaemia (table-III). Hypokalaemia

was most common among haemorrhagic stroke

patients (19%) followed by ischaemic stroke patients

(11%). chi-square test revealed significant association

between hypokalaemia and haemorrhagic stroke

(p=<0.05). Only 1% of all stroke patients had

hyperkalaemia which was one of the two patients of

subarachnoid haemorrhage. Total 31% of all stroke

patients had serum potassium imbalance during

stroke. 9% haemorrhagic stroke and 6% ischaemic

stroke patient presented with hypochloraemia during

stroke (p=>0.05). 2% haemorrhagic stroke patient

presented with low bicarbonate level during stroke.

In a study by Kusuda K et al,15 found that 34% acute

stroke patients presented with serum sodium

imbalance and 44% with serum potassium imbalance.

Both hyponatraemia and hypokalaemia were more

common among haemorrhagic stroke patients. All

these findings are consistent with this present study.

Conclusion:

The results of the present study demonstrate that in

haemorrhagic stroke, the incidence of

dyselectrolytaemia was more than ischaemic stroke

and which were mostly hyponatraemia and

hypokalaemia. Early detection and management of

which can improve the overall outcome of stroke

patients.

Conflict of interest: We have no conflict of interest.

References:

1. Bergen DC. The world wide burden of neurologic

disease. Neurology 1996; 47:21-50.

2. Allen CMC, Lueck CJ, Dennis M. Neurological

disease. In Nicholas AB (ed). Davidson’s Principal

and Practice of Medicine, 20th edition. UK Churchill

Livingstone Elsevier, 2006;1131-1235.

3. Rosamond W, Flegal K, Furie K et al. Heart disease

and stroke statistics: 2008 update: a report from

the American Heart Association Statistics Committee

and Stroke Statistics Subcommittee. Circulation

2008;117:25–146.

33

Dyselectrolytaemia in Acute Stroke Patients, An Observational Study BJM Vol. 22 No. 2

4. Summers D, Leonard A, Wentworth D et al.

Comprehensive Overview of Nursing and

Interdisciplinary Care of the Acute Ischemic Stroke

Patient. A Scientific Statement from the American

Heart Association. Stroke 2009;40:2911-44.

5. Alberts MJ, Hademenos G, Latchaw RE et al.

Recommendations for the establishment of primary

stroke centers: Brain Attack Coalition. JAMA

2000;283: 3102–09.

6. Langhorne P, Stott DJ, Robertson L et al. Medical

complications after stroke: a multicenter study.

Stroke 2000;31:1223–29.

7. WHO STEPS Stroke Manual: the WHO STEP wise

approach to stroke surveillance. STEPS Stroke

Surveillance Manual (V2.1); 2006-05-09.

8. Broderick J, Connolly S, Feldmann E et al.

Guidelines for the Management of Spontaneous

Intracerebral Hemorrhage in Adults 2007 Update.

Stroke 2007;38:2001-23.

9. Bhalla A, Sankaralingam S, Ruth Dundas R et al.

Influence of Raised Plasma Osmolality on Clinical

Outcome After Acute Stroke. Stroke 2000;31:

2043-48.

10. Bevan H, Sharma K, Bradly W. Stroke in young

adults. Stroke 1990;21:382-86.

11. Mohammad QD, Alam B, Habib M et al. Prevalence

of stroke in Bangladeshi population-A population

based study. JAFMC 2009;5(1):24-7.

12. Chowdhury SZM. Study of risk factor in

cerebrovascular disease- A study of 100 cases

(Dissertation). BCPS 1991:48.

13. Kurzke JF. Epidemiology of cerebrovascular disease.

In :P.Rowland L, editor. Merrtt’s Neurology.

Philadelphia: LLW;2000:135-76.

14. Alam B, Mohammad QD, Habib M et al. Stroke

evaluation risk factor. Bangladesh J of Neuroscience

1999;15(2):14-8.

15. Kusuda K, Saku Y, Sadoshima S et al. Disterbances

of fluid and electrolyte balance in patients with

acute stroke. Nippon Ronen Igakkai Zasshi

1989;26(3):223-27.

34

BJM Vol. 22 No. 2 Dyselectrolytaemia in Acute Stroke Patients, An Observational Study

PRESENTATION AND OUTCOME O ACUTE KIDNEY

INJURY IN A TERTIARY MILITARY HOSPITAL OF

BANGLADESH

MAMUN MOSTAFI, MAJ AZIZUN NESSA, MD AMZAD HOSSAIN FAKIR, MD ABDUL QUDDUS BHUYIAN,

AKM MIJANUR RAHMAN

Abstract

Introduction: Acute kidney injury (AKI) is a common condition and its incidence is increasing . No

study has been done so far on this subject in the Armed Forces. This retrospective study is

therefore, to find out the incidence, etiology , predisposing factors, diagnostic approach, clinical

course and finally outcome of the patients with AKI in this country, in a selected group of patients.

Methods: This retrospective cross sectional study was conducted in Combined Military Hospital,

Dhaka, from July 2007 to July 2011. Total 105 cases were included in this study. All were adult

and their age of distribution was 18-80 years. Cases were studied in terms of etiology, mode of

presentation, laboratory findings, management and response to treatment or outcome.

Results: Mean age was 47.24+ 18.35 years. Male, female ratio was 3:2. Hypovolemia was the

major (23.8%) etiological factor of AKI in this study due to acute gastroenteritis, 14.28% cases were

due to different non-steroidal anti inflammatory drugs (NSAIDs), 9.52% cases due to rhabdomyolysis

following physical assault and vigorous exercise, 7.61% cases were due to septicaemia, 8.57%

cases were due to glomerulonephritis and 6.66% cases due to acute pyelonephritis.6.66% cases

developed AKI due to falciparum malaria and 5.71% due to obstructive uropathy. Other causes of

AKI in this study are –contrast induced nephropathy 3.8%,postoperative AKI 4.76%,AKI due to

vasculitis 3.8%,2.85% cases due to HELLP syndrome,0.95% case due to snake bite and 0.95% case

due to thrombotic thrombocytopenic purpura(TTP). Oliguria (66.66%) and oedema (64.76%) were

the commonest presentation in this study. Mean blood urea and serum creatinine level on admission

being 9134 mg/dl and 4.292.55 mg/dl respectively. Haemodialysis was done in 44 cases,

continuous renal replacement therapy (CRRT- continuous venovenous haemodialysis) was given in

6 patients, peritoneal dialysis in 5 patients and 49 cases were managed with conservative therapy

alone. Complete recovery occurred in 88 patients, 8 had recovery with residual renal impairment, 6

patients developed end stage renal disease (ESRD) and 3 patients died due to septicaemia and

multi-organ failure (MOF).

Conclusion: Most of the cases of AKI are preventable if we can take due care of some common

health problems like gastroenteritis and at the same time outcome can be rewarding if we can

ensure early reporting, quick diagnosis and appropriate management

Department of Nephrology, Armed Force Medical College, Dhaka

Introduction

Acute kidney Injury (AKI) is one of the most dreadful

disease and therefore, a challenging problem in our

country. AKI has now replaced the term acute renal

failure and a universal definition and staging system

has been proposed to allow earlier detection and

management of AKI.1 The new terminology enables

healthcare professionals to consider the disease as

a spectrum of injury. This spectrum extends from

less severe forms of injury to more advanced injury

when acute kidney failure may require renal

replacement therapy (RRT).1 Clinically AKI is

characterized by a rapid reduction in kidney function

resulting in a failure to maintain fluid, electrolyte

and acid-base homoeostasis.2 Previously there have

been many different definitions of AKI used in the

literature which has made it difficult to determine

the epidemiology and outcomes of AKI. Over recent

years there has been increasing recognition that

relatively small rises in serum creatinine level in a

variety of clinical settings may be associated with

worse outcome. 3, 4Over the years, the

etiology,presentation and management of AKI has

been changed .The study was designed to observe

the recent trends of AKI and its outcome in a tertiary

military hospital.

Materials and Methods

This retrospective cross sectional study was

conducted in Combined Military Hospital, Dhaka,

Bangladesh J Medicine 2011; 22 : 35-40

Bangladesh from July 2007 to July 2011. Total 105

cases were included in this study coming from specific

group of population that is Bangladesh Armed Forces.

Cases were studied in terms of etiology, mode of

presentation, laboratory findings, management and

response to treatment or outcome. Patients already

known to have CKD, with sudden deterioration of

renal function due to some insult or patient with

small sized kidneys as seen by ultrasonogram were

excluded from this study.

Results and Findings

Most patients (33.33%) were from 31-45 years age

group and male female ratio was 3:2 (table-I).

Hypovolemia was the most common (23.8%) etiological

factor of AKI which was mainly due to acute

gastroenteritis. Other important causes of AKI were

NSAIDs (14.28%),rhabdomyolysis (9.52%),septicaemia

(7.61%),glomerulonephritis (8.57%), acute

pyelonephrirtis (6.66%), falciparum malaria (6.66%)

etc (table-II ). Oliguria was the most common (66.66%)

mode of presentation whereas 22.85% were

nonoliguric and 6.66% were anuric . Diarrhoea were

presenting symptoms in 23.8% patients and 32.38%

had shortness of breathing. 66.66%had oedema and

.085% had acidotic breath . 17.14% were hypertensive

and 16.19% were in shock(table-III).Laboratory

findings showed protienuria was present in 41.90%

cases, 40% had WBC, 32.88% had RBC and 26.66%

had RBC cast in their urine(table-IV). Mean blood

urea was 91±34 mg/dl whereas serum creatinine was

4.29±2.55 mg/dl at presentation (table V), which

gradually decreased with time. Mean duration of

hospital stay was 19±10.2 days. 42.85% received

haemodialysis, 5.71% received CRRT whereas

peritoneal dialysis was given in 4.76% patient. 49

patients (46.66%) received conservative management

only(table VII). With these management 88 patients

(83.80%) completely recovered. 8 patients survived

with some residual renal impairment, 6 developed

end stage renal disease (ESRD) three patients expired

due to septicaemia or MOF(table II).

Table-I

Age and Sex Distribution of Patients (n=105).

Age group Male Female Total

(in yrs) (percentage)

18-30 18 6 24 (22.86%)

31-45 21 14 35(33.33%)

46-60 08 10 18(17.14%)

>60 16 12 28(26.67%)

Total 63(60%) 42 (40%) 100%

Table -II

Etiology and Outcome of AKI(n=105).

Cause Number (%) Complete recovery Progression to CKD Death

Hypovolemia 25 (23.8%) 25 - -

NSAIDs 15 (14.28%) 11 4 -

Rhabdomyolysis 10 (9.52%) 10 - -

Septicaemia 8 (7.61%) 6 1 1

Glomerulonephritis 9 (8.57%) 8 - -

Acute pyelonephritis 7(6.66%) 7 - 1

Falciparum Malaria 7 (6.66%) 7 - -

Obstructive Uropathy 6 (5.71%) 5 1 -

Contrast induced -Nephropathy 4 (3.80%) 2 2 -

Post operative 5 (4.76%) 3 2 -

Vasculitis 4 (3.80%) - 4 1

HELLP syndrome 3 (2.85%) 3 - -

Snake Bite 1 (0.95%) 1 - -

TTP 1 (0.95%) 1 - -

36

BJM Vol. 22 No. 2 Presentation and Outcome o Acute Kidney Injury in A Tertiary Military Hospital

Table-III

Mode of Presentation (n=105).

*Presentation Number of patient Percentage

Oliguria 70 66.66%

Non-oliguric 24 22.85%

Anuria 7 6.66%

Diarrhoea 25 23.8%

Shortness of breath 34 32.38%

Oedema 70 66.66%

Haematuria 5 .047%

Shock 17 16.19%

Hypotension 8 7.61%

Hypertension 18 17.14%

Acidotic breath 9 .085%

Loin Pain 8 7.61%

Drowsiness 13 12.4%

Convulsion 6 .057%

*Findings overlap.

Table-IV

Findings of Routine Urine Analysis(n=105).

*Findings Number of patients Percentage

Normal 48 45.71%

Proteinuria 44 41.90%

WBC in urine 42 40%

RBC in urine 34 32.38%

RBC casts 28 26.66%

Granular casts 39 37.14%

*Findings overlap.

Table-V

Blood Biochemistry(at presentation).

Tests Mean Standard

deviation

Blood Urea (mg/dl) 91 34

Serum Creatinine(mg/dl) 4.29 2.55

Serum Sodium (mmol/l) 142 2.46

Serum Potassium (mmol/l) 4.44 1.69

Serum chloride (mmol/l) 99.5 4.09

Serum calcium (mg/dl) 8.6 1.5

Serum phosphate(mg/dl) 5.5 1.2

Serum uric acid(mg/dl) 7.8 1.8

Table -VI

Other investigations.

Investigations *Findings No of patients

(Percentage)

CXR Pulmonary oedema 30 (28.57%)

USG of KUB Renal/ureteric calculi 6 (5.71)%

Plain X-Ray KUB Renal/ureteric calculi 6 (5.71)%

ECG Features of hyperkalaemia 4 (3.81%)

Urine C/S Growth of organism 7 (6.66%)

HBsAg Positive 7 (6.66%)

*Findings overlap.

Table-VII

Types of Management (n=105).

Type of therapy No. of patients Percentage

Haemodialysis 45 42.85%

CRRT(CVVHD) 06 05.71%

Peritoneal dialysis 05 04.76%

Conservative only 49 46.66%

Discussion

The result of the present study showed information

regarding the presentation and prognosis of acute

renal failure in Bangladesh Armed Forces. All the

clinical parameters, available biochemical

estimations, management and prognosis of the

patients with acute renal failure have been studied

in this series.

The clinical spectrum of acute renal failure in this

study is clearly differentiable from those of the

published western reports.5,6,7The age of the patients

included in this study ranges from 18-80 years but

the incidence of AKI found to be high in 31-45 years

age group (33.33%).

In contrast to developed countries where most cases

of AKI are related to trauma and multi-organ failure,

AKI in developing countries is often related to medical

cause.6 In this study hypovolemia mostly due to

diarrhoea and vomiting was the leading cause (23.8%)

of AKI . The next common etiologies were NSAIDs,

contrast AKI and rhabdomyolysis. This is comparable

to observations in India7 where over 60% of AKI cases

are related to gastroenteritis and also to our

country.8,9

Trauma due to road traffic and industrial accidents,

cardiovascular surgery and cardiogenic shock

appeared to proceed acute kidney injury in 60% cases

37

Presentation and Outcome o Acute Kidney Injury in A Tertiary Military Hospital BJM Vol. 22 No. 2

in the developed countries is in sharp contrast to

this study.8,10

Eighteen (17.14%) patients in this study developed

AKI following the ingestion of NSAIDs which they

took for pain of different origin. NSAIDs induced

nephropathy and AKI is not uncommon in military

personnel .They usually take different NSAIDs for

exercise induced injury. However, these patients with

AKI in this study fully recovered after withdrawal of

drug along with adequate hydration and supportive

measures. AKI due to various drugs & chemicals

occurs with increasing frequency in the developed

countries. Increased risk involved in both short and

long-term therapy and is slightly greater among users

of high doses11. Drug induced AKI is not uncommon

in this country. Superstition, self medication and

exploitation of illiterate people by quacks are a

potential risk in this country which needs to be

prevented. NSAIDs users have a three fold greater

risk for developing a first-ever diagnosis of clinical

AKI compared with non-NSAIDs users in the general

population. NSAIDs should be used with special

caution in patients with diabetes mellitus,

hypertension and heart failure.12

Twelve (11.42%) patients developed AKI due to

rhabdomyolysis following physical assault and

vigorous exercise which is not uncommon in military

personnel which simulate to other studies.13,14,15

Septic AKI is common during the first 24 hours after

ICU admission. Patients with septic AKI are generally

sicker, with a higher burden of illness and have greater

abnormalities in acute physiology compared with

patients with nonseptic AKI.16 Moreover, septic AKI

is independently associated with higher odds of death

and longer duration of hospitalization.17 10 (9.52%)

patients developed AKI following septicaemia in our

study.

Acute pyelonephritis is a potentially organ and/or

life threatening infection that characteristically

causes some scarring of the kidney with each infection

and may lead to significant damage to the kidney,

sepsis, or sepsis syndrome/shock/multiorgan system

failure. More than 2,50,000 cases occur in the United

States each year (1995 estimate), and approximately

200,000 patients require hospitalization (1997 data).18

Wide variation exists in the clinical presentation,

severity, options, and disposition of acute

pyelonephritis. Lower UTIs predispose to

pyelonephritis. Diagnosing and managing acute

pyelonephritis is not always straightforward. In the

age range of 5-65 years, it typically presents in the

context of a symptomatic (eg, dysuria, frequency,

urgency, gross haematuria, suprapubic pain) urinary

tract infection (UTI) with classic upper urinary tract

symptoms (eg, flank pain, back pain) with or without

systemic symptoms (eg, fever, chills, abdominal pain,

nausea, vomiting) and signs (eg, fever, costovertebral

angle tenderness) with or without leukocytosis.

However, it can present with nonspecific symptoms.19

In this study 9(8.57%) patients developed AKI due to

acute pyelonephritis, which is comparable to other

studies.18,19

Acute kidney injury (AKI) is one of the most dreaded

complications of severe malaria. As per World Health

Organization criteria, acute kidney injury occurs as a

complication of Plasmodium falciparum malaria in less

than 1% of cases, but the mortality rate in these

cases may be up to 45%.20 We had 7 (6.66%) cases of

AKI following severe falciparum malaria. Soldiers from

operational area in Chittagong hill tracts or African

countries were mostly affected. Most of them were

admitted during leave.

Contrast-induced nephropathy has become a

significant source of hospital morbidity and mortality

with the ever-increasing use of iodinated contrast

media in diagnostic, imaging and interventional

procedures such as angiography in high-risk patients.

It is the third most common cause of hospital-

acquired acute renal failure, after surgery and

hypotension in western countries21 which is a sharp

contrast to our study.

Incidence of post operative AKI varies from 1.1-17%22.

It remains a leading cause of morbidity, mortality

prolonged hospital stay and increased hospital cost23.

We had 5 (4.76%) cases of postoperative AKI, who

had normal renal function preoperatively.

In this study 66.66% patients presented with oliguria

and 10.47% patients presented with anuria. Only 24

(22.85%) patient in this study had non-oliguric renal

failure.

Twenty five (23.8%) patients had dehydration at

presentation indicates that proper replacement of

fluid loss could not made in many cases.

History and clinical examinations are sufficient for

making an etiological diagnosis in most of the cases.

Among laboratory investigations, blood biochemistry

is the main tool for diagnosing AKI.

On routine blood examination in our study Hb% was

11.23 ±2.9 gm/dl was not of any diagnostic help and

was only useful in planning management especially

in case of blood loss. Total and differential leucocyte

count revealed polymorphonuclear leucocytosis in 58

(55.2%) cases indicating infection.

38

BJM Vol. 22 No. 2 Presentation and Outcome o Acute Kidney Injury in A Tertiary Military Hospital

Proteinuria, which was the most common indicator

of renal pathology found in 44 (41.90%) cases.

Haematuria found in 34 (32.38%) cases which was

due to glomerulonephritis or UTI. Pyuria found in 42

(40%) cases indicative of underlying urinary tract

infection, many of which developed in the hospital

during treatment, RBC cast found in 28 (26.66%)

cases gave important clue to glomerulonephritis(table-

IV).

Blood urea, serum creatinine and serum electrolytes

are the most essential guide for diagnosis and

management of AKI patients. Maximum mean urea

level ( 91±34 mg/d1) and creatinine level (4.29±2.55

mg/d1) observed in this study(table-V) is comparable

to that of Razzak et al study which was 61.07±23.26

mg/d1 and 14.7±7 mg/dl respectively.8Electrolyte

imbalance was almost invariable in all patients.

Haemodialysis was done in 42.85% patients which

was the sheet anchor of patient management in this

study(table-VII). Furosemide along with conservative

management was given to 43.80% patients with

positive results. Continuous renal replacement

therapy (CVVHD) was given to 6 haemodynamically

unstable patient, 3 of them died due to multiorgan

failure and other three recovered successfully. Only

5 patients received peritoneal dialysis due to

hypotension or other contraindication to

haemodialysis.

Infections were commonest complication of AKI in

this study. 67.2% patients had to be treated with

antibiotics. Since infection still remains the primary

cause of death, it is possible that the uraemic state

predispose to these infections.

Result of treatment in this study was rewarding. 88

(83.80%) patients were fully recovered. Only 3 (2.85%)

died. 8(7.61%) patients developed some impairment

of renal function and 7(6.66%) developed ESRD. The

mortality rate was 2.85% which is in contradiction to

some western literature where mortality is 28-50%.24

The reason for the rewarding result in this study may

be due to large number of pre-renal etiology

correctable by simple conservative measures, early

reporting, immediate and better management .

Conclusion

Acute kidney injury is potentially life-threatening

and requires intensive treatment. Over the year, the

etiology and outcome of AKI is changing from country

to country and centre to centre. However, the kidneys

usually start working again within several weeks to

months after the underlying cause has been

treated.26 In some cases, chronic renal failure or end-

stage renal disease may develop. Death is most

common when kidney failure is caused by surgery,

trauma, or severe infection in someone with heart

disease, lung disease, or recent stroke.26,27 Old age,

infection, loss of blood from the intestinal tract, and

progression of kidney failure also increase the risk

of death.28 Unlike western countries, our cases

were mostly pre-renal and preventable. Acute

gastroenteritis was the commonest cause of AKI in

this study and then next common was NSAIDs.

Perhaps appropriate intervention in earlier stages of

AKI may have a positive impact on patient outcome

and can reverse the process in most cases and

therefore the mortality can be in the acceptable

range.29

Conflicts of interest: None

References:

1. Webb S, Dobb G “ARF, ATN or AKI? It’s now acute

kidney injury”. Anaesthesia and Intensive Care.

(December 2007). 35 (6): 843–4.

2. Brenner and Rector’s The Kidney. Philadelphia:

Saunders. 2007. ISBN 1-4160-3110-3. 

3. Mehta RL, Kellum JA, Shah SV, et al. “Acute Kidney

Injury Network: report of an initiative to improve

outcomes in acute kidney injury”. Critical Care

(London, England). (2007). 11 (2): R31.

4. Bellomo R, Ronco C, Kellum JA, Mehta RL, Palevsky

P “Acute renal failure - definition, outcome measures,

animal models, fluid therapy and information

technology needs: the Second International

Consensus Conference of the Acute Dialysis Quality

Initiative (ADQI) Group”. Crit Care. (2004). 8 (4):

R204–12.

5. Palevsky PM, Zhang JH, O’Connor TZ, et al.

“Intensity of renal support in critically ill patients

with acute kidney injury”. The New England

Journal of Medicine. (July 2008). 359 (1): 7–20.

6. Schrier RW, Wang W, Poole B, Mitra A “Acute renal

failure: definitions, diagnosis, pathogenesis, and

therapy”. J. Clin. Invest. (2004). 114 (1): 5–14.

7. Prakash J, Tripathi K, Malhotra V, Kumar O,

Srivastava PK. Acute renal failure in eastern India.

Nephrol Dial Transplant. 1995 Nov;10(11):2009-12.

8. Razzak A,Ahmed S,Rahman M, Profile of acute renal

failure in adults. Bang Renal Journal 1983;2:5-8.

9. Nurul M, Harun R, Matiur R. Clinical spectrum of

acute renal failure. IPGMR, Dhaka 1987.

10. Rashid HU,Akhter F,Ahmed E.Outcome of acute

renal failure in Bangladesh.Renal Failure 1993 ;

15(5):603.

11. Perez S, Garcia LA, Raiford DS, et al.Non steroidal

anti inflammatory drugs and risk of hospitalization

for ARF. Arch Intern Med.1996;156,2433-243

39

Presentation and Outcome o Acute Kidney Injury in A Tertiary Military Hospital BJM Vol. 22 No. 2

12. Huerta C, Castellsague J, Varas-Lorenzo C, García

Rodríguez LA .Nonsteroidal anti-inflammatory drugs

and risk of ARF in the general population.Am J

Kidney Dis. 2005;45(3):531.

13. Senert R, Kohl L, Rainone T, Scalea T: Exercise-

induced rhabdomyolysis and ARF. Ann Emerg Med

June 1994;23:1301-6.

14. Ron D, Taitelman U, Michaelson M, et al: Prevention

of acute renal failure in traumatic rhabdomyolysis.

Arch Intern Med 1984;144:277-280.

15. Bywaters EG, Beall D “Crush injuries with

impairment of renal function” Br Med J (1941). 1

(1): 427–32. doi:10.1136/bmj.1.4185.427. 

16. Yegenaga I, Hoste E, Van Biesen W, et al. Clinical

characteristics of patients developing ARF due

to sepsis/systemic inflammatory response

syndrome: resultsof a prospective study.Am J Kidney

Dis 2004, 43:817-824.

17. Oppert M, Engel C, Brunkhorst FM,et al: Acute renal

failure in patients with severe sepsis and septic

shock a significant independent risk factor for

mortality: results from the German Prevalence Study.

Nephrol Dial Transplant 2008, 23:904-909.

18. Czaja CA, Scholes D, Hooton TM, Stamm WE

“Population-based epidemiologic analysis of acute

pyelonephritis”. Clin. Infect. Dis(2007).. 45 (3): 273–

80.

19. Ramakrishnan K, Scheid DC “Diagnosis and

management of acute pyelonephritis in adults”.

Am Fam Physician. (2005). 71 (5): 933–42.

20. Saroj K. Mishra, MD, Bhabani S, Das B S, Malaria

and Acute Kidney Injury . Semin Nephrol. ,

2008.28:395-408

21. Tadhg G. Gleeson; Sudi Bulugahapitiya, Contrast-

Induced Nephropathy, Am J Roentgenol.

2004;183(6) , 2004

22. Kheterpal S, Tremper KK, Englesbe MJ, et al.

Predictors of post-operative renal failure after non

cardiac surgery in patient with previously normal

renal function . Anaesthesiology 2007,107: 892-

902.

23. Reddy VG: Prevention of post-operative acute

renal failure .J postgraduate med 2002,48: 64-70.

24. Woodrow G, Turney JH. Cause of death in acute

renal failure. Nephrol Dial Transplant 1992;7:230-

234.

25. Hoque M, Chowdhury D,Khan MR. Outcome of

acute renal failure in children. Bang J of child

health 1985; 9(1) 5-10.

26. Papadakis, Maxine A.; McPhee, Stephen J.

(2008).Current Medical Diagnosis and

treatment. McGraw-Hill Professional.. 

27. Pannu N, Klarenbach S, Wiebe N, Manns B, Tonelli

M (February 2008). “Renal replacement therapy in

patients with acute renal failure: a systematic

review”. JAMA : the J Am Med 299 (7): 793–805. 

28. Bellomo R, Cass A, Cole L, et al. (October 2009).

“Intensity of continuous renal replacement therapy

in critically ill patients”. New Eng J Med 361 (17):

1627–3.

29. Cole L, Bellomo R, Silvester W, et al. A prospective,

multicentre study of the epidemiology,

management and outcome of severe acute renal

failure in “closed” ICU system. Am J Respir Crit

Care Med 2000; 162: 191-196.

40

BJM Vol. 22 No. 2 Presentation and Outcome o Acute Kidney Injury in A Tertiary Military Hospital

STUDY OF CORRELATION OF SEVERITY OF HEPATIC

CIRRHOSIS WITH SEVERITY OF BONE CHANGES

MEASURED BY BMD (BONE MINERAL DENSITY)

MD. ASHRAFUL ALAM1, NOORUDDIN AHMED2, SHAHINUL ALAM2, MAMUN AL MAHTAB2

Abstract

Background & Aim Metabolic bone disease is common among patients with chronic liver disease

and still it is underestimated complication in liver cirrhosis. The prevalence and presentation of

bone disease in chronic liver diseases have been poorly described except for cholestatic liver

diseases.

This study aims at evaluation of the prevalence and degree of bone changes in patients with

cirrhosis and to correlate severity of hepatic cirrhosis with the severity of bone changes.

Patients and Methods Bone mineral density (BMD) was studied using dual energy X-ray

absorptiometry (DEXA) in 60 subjects of 15-45 years old. Of them 30 subjects are patients with

liver cirrhosis and rest of the 30 subjects were control group without having liver disease or any

other chronic disease. The diagnosis of cirrhosis was based on clinical, biochemical, and

ultrasonographic findings. Patients with renal impairment, cholestatic liver disease, chronic lung

disease, prolonged bed ridden patients or deformity of spine, pelvis or wrist were excluded from the

study. Results of BMD were then correlated with the Child score.

Results Eighteen (60%) patients had decreased bone mineral density (BMD). Of which 15 (50%)

patients have got osteopenia and 3 (10%) patients have got osteoporosis. No correlation was found

between the T-score and Child Paugh score (p =0.236). Significant correlations were found between

BMD and serum bilirubin..

Conclusion Liver cirrhosis is a risk factor for the development of bone loss and there is a high

prevalence of BMD disorders in cirrhotic patients. The severity of bone loss is not related to the

severity of liver disease. Hyperbilirubinemia and low albumin is a contributing factor to altered bone

mineral density in patients with liver cirrhosis

Key words Hepatic osteodystrophy, osteoporosis, DEXA, bone mineral density, cirrhosis

1. Pharmacology Department, Cox’s Bazar Medical College,

2. Department of Hepatology, BSMMU

Introduction

Liver cirrhosis is a debilitating chronic disease

associated with severe complications and raised

mortality. Hepatic bone disease is common among

patients of chronic liver disease. Hepatic

osteodystrophy, and consequent osteopenia and

osteoporosis and increased risk of bone fracture,

represent some of the recently investigated

complications. Initial studies focused on osteoporosis

in patients with primary biliary cirrhosis; more

recently, however, it has been shown that advance

liver cirrhosis of any etiology is a risk factor for

osteopenia and osteoporosis and bone fractures

independent of its aetiology1.

The term hepatic osteodystrophy refers to the

abnormalities of bone metabolism that occur in the

presence of advanced liver disease. Ostemalacia and

osteoporosis are common complications of chronic

liver disease2. Osteoporosis accounts for the majority

of cases whereas osteomalacia is rare in absence of

advanced liver disease and severe malabsorbtion3.

Prevalence of hepatic osteodystrophy in patients with

liver disease varies from 13% to 70%, depending on

the population studied and diagnostic criteria used

to define bone disease4.

With the improvement in survival of patients with

chronic liver disease and with the development of

liver transplantation, the clinical significance of

hepatic osteodystrophy has increased. However, in

many patients with non-cholestatic liver disease

osteodystrophy may remain unrecognized and

untreated5.

Bone density is the best single predictor of future

fracture risk. The advances in bone densitometry and

the development of newer techniques such as dual

Bangladesh J Medicine 2011; 22 : 41-46

energy X-ray absorptiometry (DEXA) made it possible

to rapidly and precisely quantify the amount of bone

in the relevant fracture sites 6. The high level of

precision of this technique allows not only for

diagnosis, but also for monitoring response to

treatment. It is noninvasive, accurate, rapid and

safe7.

In this work we evaluated the prevalence and degree

of bony changes in patients with liver cirrhosis and

studied its relation to the severity of liver disease.

Patients and Methods

Between January 2008 and December 2009, a total of

60 adult subjects of 15-45 years of age were recruited

from the in patient and out patient department of

Hepatology Department, Bangabandhu Sheik Mujib

Medical University. Thirty patients were of cirrhosis

of liver irrespective of etiology. Thirty healthy controls

without having liver disease and absence of other

disease which may cause osteopenia and

osteoporosis.

The diagnosis of liver cirrhosis was made by clinical

features suggestive of cirrhosis of liver,

Ultrasonographic evidence of small sized liver with

coarse echo texture with or without deranged liver

function and/or Endoscopic evidence of esophageal

varices.

Stage of liver disease was assessed using the Child-

Pugh scoring system8. Patients without cirrhosis of

liver, post menopausal women, chronic renal failure,

chronic obstructive pulmonary disease, Patients on

steroid, autoimmune hepatitis, rheumatoid and other

arthritic disease, prolonged bed ridden patients, and

patients of obstructive jaundice were excluded. All

patients were subjected to history taking and clinical

examination, in addition to laboratory investigations:

Serum bilirubin, Serum Albumin, Prothrombin time,

Serum Alkaline phosphates, Endoscopy of upper GIT,

Liver biopsy (Group-I, Child class A group of patient)

and abdominal ultrasound.

The informed patient consent for the study was

obtained.

Bone mineral density evaluation in all patients (both

case and control) was done by using biphotonic

absorbption of X-rays (duel energy X-ray

absorptiometry-DEXA) of whole body. BMD was

expressed as grams per square centimeter. The World

Health Organization (WHO) criteria for osteopenia

and osteoporosis were used to define low BMD9. The

WHO has defined osteopenia as a BMD between -1

and -2.5 standard deviation (SD) and osteoporosis

as a BMD below -2.5 SD of the mean peak value in

young adults (T-score). BMD was also compared to

the mean value in normal subjects of the same age,

sex, and ethnic group (Z-score). A Z-score below -1

SD corresponds to a value in the lowest 25 percentile

of the reference range, a value at which the risk of

fractures is approximately doubled. Z-score could not

be evaluated by the equipment.

Bone status T score

Normal bone density T score < -1 STD

Osteopenia T score between -1 and

- 2.5 STD

Osteoporosis T score < - 2.5 STD

Severe osteoporosis T score < - 2.5 STD and at

least one osteoporotic

fracture

Exclusion of vertebral deformity was done by X-ray

on the LS or by lateral view of the spine during the

DEXA procedure.

Statistical Methods

Individual patient had a code number each. All data

was collected in the structured questionnaire and

entered into a personal computer. Analysis of the

data was done by SPSS (version 13) programme.

Significance of the test was done by ANOVA.

Statistical significance was determined at p-value

<0.05 (significant), and p-value <0.01 (highly

significant).

Results

Age range of healthy subjects was 15-45 years and

mean age was (32.97±7.18) years. Age range of

cirrhosis group was 15-45 years and mean age was

(34.57±9.45) years (Figure-1). In cirrhotic group 25 were

male and 5 were female. In control group 20 were

male and 10 were female. Laboratory parameters of

included patients are presented in (Table 1).

Among the 30 cirrhotic patients, 12 (40%) patient had

normal BMD value, 15 (50%) had osteopenia, and 3

(10%) had osteoporosis. Among 15 osteopenic patients

3(10%) were from Child’s B and 12 (40%) patients

were from Child’s C. All the 3 (10%) ostoporotic

patients were form Child’s C (Table-2).

There is statistically significant difference in BMD

between Cirrhotic group and control group, mean

BMD in control group is 1.29±9.62E-02 and in cirrhotic

group is 1.14±0.109.

42

Study of Correlation of Severity of Hepatic Cirrhosis with Severity BJM Vol. 22 No. 2

Table-I

Laboratory parameters of normal, osteopenic, and osteoporotic groups of patients.

Normal BMD Osteopenia Osteoporosis All

(n=12) (n=15) (n=3) (n=30)

Mean SD Mean SD Mean SD Mean SD

S.Bilirubin (5-20µmol/L) 33.88 24.53 89.59 112.89 40.06 26.10 62.41 84.89

Alk.Phos (50-136U/L) 171.17 97.99 140.4 46.87 95.67 53.78 148.23 73.74

PT (18-22 sec) 24.75 12.09 26.01 10.63 19.60 5.05 24.86 10.73

S.Albumin (30-50 gm/L) 25.00 7.16 25.07 6.87 22.00 2.65 24.73 6.60

S.creatinine (0.6-1.3 mg/dl) 84.63 13.14 89.24 16.55 88.39 15.32 87.31 14.79

ALT (30-65 U/L) 76.2 56.8 60.4 42.8 68.9 76.5 68.9 65.3

Table-II

Distribution of bone mineral density disorders among cirrhotic patients

Patient group Normal Osteopenia Osteoporosis Total

No. % No. % No. % No. %

Child A 0 0 0 0 0 0 0 0

Child B 4 13.33 3 10 0 0 7 23.33

Child C 8 26.67 12 40 3 10 23 76.67

All Patients 12 40 15 50 3 10 30 100

Fig.-1: Difference of BMD in cirrhotic group of patients Fig.-2: Age distribution of patients (n=60)

Fig.-3: DEXA scan

43

Study of Correlation of Severity of Hepatic Cirrhosis with Severity BJM Vol. 22 No. 2

Table-IV

Difference in BMD between Child’s B and Child’s C

group of cirrhotic Patients

Child Pugh Score BMD mean±SD t P value

Child Pugh B 1.17±8.87E-02 0.627 0.563

Child Pugh C 1.140±0.115

Though all three osteoporotic cirrhotic patients were

in child’s pugh C class proportion of patients with

normal, osteopenic and osteoporotic was not different

between child’s B and C (Table-3).

There is no significant difference in BMD between

Child’s B and Child’s C (Table-4).

Among biochemical tests there is no significant

difference in alkaline phosphatase, serum albumin,

prothrombin time, serum creatinine among normal,

osteopenic and osteoporotic group of cirrhotic

patients. But serum bilirubin was found to differ

significantly between these groups

The mean Child score of the normal, osteopenic, and

osteoporotic groups was 2.67 ± 0.492, 2.80 ± 0.414,

and 3.00±0.000, respectively.

Discussion:

Low bone mass and deterioration of bone tissue,

leading to increased bone fragility and risk of fracture,

are the defining characteristics of osteoporosis as

well as osteopenia. In its early asymptomatic stage,

osteopenia and osteoporosis can only be detected by

measuring bone mineral density (BMD). Early

detection of reduced BMD is an important means of

prevention, and dual energy x-ray absorptiometry

(DEXA) is the most helpful modality10. Until relatively

recently, bone biopsies were the only way to identify

the severity and cause of metabolic bone diseases.

Indirect measurement of bone density with DEXA is

the most precise technique (1% to 2% error is

technician dependent). Dual-energy x-ray

absorptiometry (DEXA) remains the gold standard for

measurement of bone density. It is simple to perform,

non invasive and widely available test11. It requires

the least exposure to radiation (10 to 30 mSv) of any

of the other methods that may be used to measure

BMD, such as CT scan12. Fracture risk increases 1.5-

to 3-fold or more for each standard deviation (SD)

decrease in BMD from that of young adult (T score).

Osteopenia is considered to be present when BMD

is between -1 and -2.5 SD; osteoporosis is defined by

the World Health organization (WHO) as BMD more

than -2.5 SD below that of a young adult1.

This study was carried out to see the relation of

severity of hepatic cirrhosis with hepatic

osteoporosis; we investigated thirty cirrhotic patients

irrespective of etiology. The study also included thirty

non liver disease persons as control. BMD were done

in both groups to asses the bony changes. The

cirrhosis patients were included without having any

condition like any rheumatoid and other arthritic

disease, chronic renal failure, chronic obstructive

pulmonary disease, autoimmune hepatitis,

obstructive jaundice. Patients on steroid therapy,

prolonged bed ridden patients and post menopausal

women were also excluded from the study.

Age is recognized as an independent risk factor for

low BMD. So in our study the age range of all the

patients as well as controls were 15-45 years. Among

the patients of cirrhotic group 16 patients were above

36 years of age, 5 patients was in thirties, 9 patients

was below 25 years of age. The mean age of cirrhotic

group was (34.57±9.45) years. The highest incidence

of cirrhosis patients were found at 36-45 age groups.

The control patients were included without liver

disease or having any condition that may cause

osteoporosis. 15 patients were above 36 years of age,

10 patients were in thirties, 5 patients were below

25 years of age. Mean age of control group was

(32.97±7.18) years. (Figure 1).

In this study, among cirrhosis patients male were 25

(83.3%) and female were 5 (16.7%). In control patients

male were 20 (66.7%) and female were 10 (33.3%).

There is male predominance 45 (75%) in the study

population.

In this study, among 30 cirrhotic patients 7(23.33%)

patients were in Child’s group B and 23(76.67%)

patients were in child’s C. Among the 7 Child’s B

patients 4(57%) patients had normal BMD and 3(43%)

patients had osteopenic BMD, no patient had

Table-III

Differences in Child Pugh Score and T score in DEXA scan

Child Pugh Score T score in DEXA Scan χ2 value df P value

Normal Osteopenia Osteoporosis

Child Pugh B 4 3 0 1.677 2 0.432*

Child Pugh C 8 12 3

44

BJM Vol. 22 No. 2 Study of Correlation of Severity of Hepatic Cirrhosis with Severity

osteoporotic BMD. Among the 23 Child’s C patients

8(34.8%) patients had normal BMD, 12(52.2%) patients

had osteopenic BMD and 3(13%) patients had

osteoporotic BMD.

In our study, mean BMD in Control patients was

(Mean ± SD), 1.29 ± 9.62E-02 gm/cm2, minimum BMD

was 1.00 gm/cm2 and maximum 1.38 gm/cm2. Mean

BMD in cirrhotic was (Mean ± SD), 1.14 ± 1.109 gm/

cm2, minimum BMD was 0.976 gm/cm2 maximum

1.360 gm/cm2. This difference is highly significant

(P<0.05) and correlates with a study conducted by

Diamond et al. in 1990, the study demonstrated a

significant decrease in osteoblast surface and bone

formation rate in chronic liver disease studied

compared with that of normal controls13.

In evaluation of patients according to WHO

classification of osteoporosis we found that 60% of

cirrhotic patients had decreased bone mineral density

(10% had osteoporosis and 50% had osteopenia).Our

figure is higher than the study conducted by Cristina

Cijevschi et al. (2005), where they found 38% of

cirrhotic patients have low BMD14.

In our study we could demonstrate the increase in

prevalence and severity of decreased bone mineral

density with the liver dysfunction. In this study we

found a significant positive correlation between serum

albumin which was similar in previous study done by

Alam El Dein R (2003)15 and significant negative

correlation between serum bilirubin level and BMD

values which was similar in previous study done by

Sevic Uretmen et al. (2005)16.

In this study, DEXA was used to asses BMD of whole

body. As age is recognized as an independent risk

factor for low BMD, the use of other criteria rather

than T-score can underestimate its prevalence, so

the T-score was used in our study for evaluation of

BMD disorder. In this study though osteoporosis was

found in 3 patients and osteopenia was found in 12

patients in child’s C class, and no osteoporosis but

3 patients with osteopenia in child’s B, there is no

significant differences in child pugh score and T score

in DEXA scan (Normal, Osteopenia and osteoporosis)

(P=0.432) or T score values (P=0.229).

Mean BMD of Child Pugh B is 11.17±8.87E-02 gm/

cm2 and mean BMD of Child Pugh C is 11.140±0.115

gm/cm2. There is no significant difference in BMD

between Child’s B and Child’s C. Our finding was

similar to the study conducted Francisco J et al. 1998,

where they found no significant differences between

Child’s B and Child’s C. In a study conducted by Chen

CC et al. 1996, found no differences in BMD of lumber

spine in different Child Pugh group of cirrhotic

patients17.

Among the 30 cirrhotic patients 12 (40%) patient have

normal T score in DEXA scan, 15 (50%) has got

Osteopenia, and 3 (10%) are osteoporotic. (Figure10).

There is statistically significant difference in T score

between Cirrhotic group and control group. (P=0.000).

In this study no biochemical variables except serum

bilirubin was found to differ significantly between the

group of cirrhotic patients (normal, Osteopenic or

Osteoporotic).Biochemical variables were alkaline

phosphatase (P=0.360), prothrombin time (P=0.488),

serum albumin (P=0.746), serum creatinine (P= 0.731),

serum bilirubin (P= 0.047).

In this study we tried to see the correlation of severity

of hepatic cirrhosis with bone changes measured by

BMD. We can conclude that liver cirrhosis is a direct

risk factor for the development of bone loss and there

is a high prevalence of BMD disorders in cirrhotic

patients. However no correlation was found between

degree of hepatic dysfunction measured by Child Pugh

score and severity of bone changes.

References

1. Bikle D. Osteoporosis in gastrointestinal, pancreatic,

and hepatic diseases. In: Osteoporosis, Robert M

(ed). Acad Press, Washington 2001: 237-258.

2. Rouillard S, Lane NE. Hepatic osteodystrophy.

Hepatology. 2001; 33:301–307.

3. Riggs BL, Melton LJ 3rd. Involutional osteoporosis.

N Engl J Med. 1986;314:1676–1679.

4. Bernstein CN, Leslie WD, Leboff MS. AGA technical

review on osteoporosis in gastrointestinal diseases.

Gastroenterology 2003; 124; 795-841.

5. Matloff DS, Kaplan MM, Neer RM, Goldberg MT,

Bitman W, Wolfe HJ. Osteoporosis in primary biliary

irrhosis: effects of 25-hydroxyvitamin D treatment.

Gastroenterology 1982;83:97-102.

6. Brunader R, Shelton DK. Radiologic bone assessment

in the evaluation of osteoporosis. Am Fam Physician

2002;65(7):1357-64.

7. Miller PD, Bonnick SL, Rosen C. Guidelines for

the clinical utilization of bone mass measurement

in the adult population. Society for clinical

densitometry. Calcif Tissue Int 1995;57(4):251-2.

8. Pugh RN, Murray Lyon IM, Dawson JL, et al.

Transection of the oesophagus for bleeding

oesophageal arices. Br J Surg 1973;60(8):646-9.

9. Assessment of fracture risk and its application to

screening for postmenopausal osteoporosis. WHO

technical report series 843. Geneva: WHO, 1994.

10. Jenny Heathcote. Osteoporosis in Chronic Liver

Disease Current Gastroenterology Reports 1999,

1:455–458.

11. John C. Southerland and John F. Valentine

Osteopenia and Osteoporosis in Gastrointestinal

45

Study of Correlation of Severity of Hepatic Cirrhosis with Severity BJM Vol. 22 No. 2

Diseases: Diagnosis and Treatment. Current

Gastroenterology Reports 2001, 3:399–407.

12. John Damilakis, Thomas G. Maris, Apostolos H.

Karantanas. An update on the assessment of

osteoporosis causing radiologic techniques. Eur

Radiol (2007) 17: 1591–1602.

13. Diamond T, Stiel D, Lunzer M, Wilkinson M, Roche

J, Posen S. Osteoporosis and skeletal fractures in

chronic liver disease. Gut 1990; 31: 82-87.

14. Cristina Cijesvschi, Catalina Mihai, Eusebiu

Zbranca, Petru Gogalniceanu. Osteoporosis in liver

cirrhosis. Romanian Journal of Gastroenterology

2005; 14: 337-341.

15. Alam El, Dein R. Evaluation of bone mineral density

in cirrhotic patients. Master degree thesis in

internal medicine, Faculty of medicine, Ain Shams

University, 2003: 75-103.

16. Sevinic Uretmen, Mert Gol, Dilek Cimrin, Esra

Irmak. Effects of chronic liver disease on bone

mineral density and bone metabolism markers in

postmenopausal women. Eur Jour Obs & Gyne and

Rep Bio 2005; 123: 67-71.

17. Chen CC, Wang SS, Jeng FS, Lee SD. Metabolic

bone disease of liver cirrhosis: Is it parallel to the

clinical severity of cirrhosis? J Gastroenterol Hepatol

1996; 11: 417-21.

46

BJM Vol. 22 No. 2 Study of Correlation of Severity of Hepatic Cirrhosis with Severity

INCIDENCE OF VASOVAGAL REACTION AMONG THE

BLOOD DONORS ATTENDING AT TRANSFUSION

MEDICINE DEPARTMENT OF DHAKA MEDICAL

COLLEGE HOSPITAL

CHOWDHURY FS1, SIDDIQUI MAE2, RAHMAN KGM3, BEGUM HA4, BEGUM HA5, HOQUE MM6, NASREEN Z7

Abstract:

Introduction: Without blood there may be no blood transfusion. Without donors there may not any

blood. During vasovagal reaction there is chance of accidental fall and injury to blood donor. So

improving the safety of the blood donation experience will reduce the donor injuries and increase

the blood donation, donation frequency and donor satisfaction.

Objective: This study was done to find out the incidence of blood donor reaction- vasovagal reactions

among the blood donors attending at transfusion medicine department of Dhaka Medical College

Hospital and to improve the donor’s safety.

Methodology: This study was done at Transfusion Medicine Department of Dhaka Medical College

Hospital in the period between January 2010 to December 2010. Total 21815 donors of 18 to 55

years of both sexes were selected after reviewing the questionnaire, physical and medical examination

and written consent. Donors were observed for 30 minutes after donation. The needle site was

covered with a bandage and the donor was directed to keep the bandage on for several hours.

Result: In this study, out of 21815 donors 163(8.7%) developed reaction. In163 reactions, 72(44.18%)

were in male and 91 (55.82%) were in female donors. Within 20179 male donors, adverse reactions

occurred in 72 (0.35%) and within 1636 female donors, adverse reactions occurred in 91 (5.56%) The

symptoms were agitation 23 (14.12%), pallor 31 (19.02%), sweating 29 (17.79%), nausea 21 (12.88%),

vomiting 38 (23.21%), cold feeling 12(7.36%), loss of consciousness 9(5.52%),i.e. severe reactions

were 9(5.53%) and mild to moderate reactions were154 (94.47%). Among the reactions 127 (0.89%)

occurred in new donors, 32 (0.49%) occurred in occasional donors and 4 (0.37%) in periodic donors.

Conclusion: Vasovagal reactions are more common in female and new donors.

Key words: Blood donor, vasovagal reaction.

1. Asst. Prof, Transfusion Medicine, National Institute of Kidney Diseases & Urology, Dhaka.

2. Consultant, Cardiology, NITOR.

3. Assoc. Prof. Forensic Medicine, Dhaka Medical College, Dhaka

4. Professor BTC, Dhaka Medical College, Dhaka

5. Associate Professor, BTC, Dhaka Medical College, Dhaka

6. Assistant Professor, BTC, Dhaka Medical College, Dhaka

7. MO, BTC, , Dhaka Medical College Hospital, Dhaka.

Introduction:

Blood transfusion differs from all other medical

activities and therapy that it concerns not only doctors

and patient but also blood donors. Without blood there

may be no blood transfusion. Without donors there

may not any blood. Careful donor selection

contributes vitally to the safety of both donor and

recipient. Work of blood transfusion starts with

collection of blood. Blood donation is not completely

free from risk. The risks of donation are less when

donors are fit and well. Blood must be collected under

the responsibilities of a physician. Any adult

individual who is in good health, free from any recent

serious infection, between 18-55 years, haemoglobin

above 12gm/dl, weight above 50 kg, blood pressure

above100/60 mm Hg and below 200/100 mm Hg, pulse

60-100/ minute, temperature normal can donate

blood after every four months1. Most donor tolerate

giving blood very well but occasionally a donor will

have an adverse reaction to the donation. Most

reactions are vasovagal reactions. The reactions may

be the result of psychological influences caused by

sight of blood, watching others to give blood,

excitement, fear, apprehension or for unexplained

reasons. They may be a neurophysiologic response

to the donation2. Reactions are mild, moderate, and

Bangladesh J Medicine 2011; 22 : 47-50

severe. Mild reactions are signs of shock without loss

of consciousness i.e. anxiety, nervousness, nausea,

vomiting, feeling cold, pallor, sweating, rapid and

thready pulse, hyperventilation. Moderate reactions

are progression of mild reactions with loss of

consciousness. Mild and moderate reactions are

managed by stopping the donations, loosening the

clothes, clearing the airways, rebreathing in a paper

bag, raising the feet end (Trendelenburg position),

cold sponging over forehead or back of the neck,

checking pulse, blood pressure, temperature,

administering oxygen. Severe reactions are signs of

shock with convulsion and vasovagal syncope. Severe

reactions are managed as before after removing from

donor couch to prevent injury3.

Methodology:

Donors were selected after information and

counseling about fulfilling the criteria. Donors were

given a donor questionnaire that included several

basic health and sensitive lifestyle questions

required to protect both the donor and patient. Doctors

reviewed the questionnaire and performed a health

screening examination where pulse, blood pressure,

temperature, haemoglobin, weight were checked.

Donors of both sexes, between 18-55 years, Hb-more

than 12 g/dl, weight above 50 kg, who is in good

physical and mental health, free from any infection

(malaria, hepatitis, typhoid, tuberculosis, syphilis)

were included. Donors with history of allergy,

hypertension (with or without medication), diabetes

(taking insulin), surgery (within 6 months), tooth

extraction (within 6 weeks), immunization (live

vaccine within 4 weeks), blood donation (within 4

months), receiving blood or blood component (within

12 months), delivery, lactation, menstruation,

travelling, drug addiction were excluded. After physical

examination, informed written consent was taken.

With all aseptic precaution about 450ml blood was

collected in blood collecting bag with anticoagulant

taking about 15 minutes4.Donors were observed for

30 minutes after donation. The donors were given light

refreshments to help the donor recover. The needle

site was covered with a bandage and the donor was

directed to keep the bandage on for several hours5.

Results:

Results are given in tables.

Table I

Distribution of donors by sex (n=21815)

Sex of donors No of donors Percentage

Male 20179 92.5

Female 1636 7.5

Table II

Distribution by types of donors depending on

frequency of donation (n=21815)

Types of donors No of donors %

Periodic 1091 5.01

Occasional 6544 29.99

New 14180 65.00

Table-III

Distribution by reaction (n=21815)

Reaction occurred or not No of donors %

Reaction 163 8.74

No reaction 21652 91.26

Table-IV

Distribution by symptoms (n=163)

Symptoms No %

Agitation 23 14.12

Pallor 31 19.02

Sweating 29 17.79

Nausea 21 12.88

Vomiting 38 23.21

Cold feeling 12 7.36

Loss of consciousness 09 5.52

Table-V

Distribution by severity of adverse reactions (n=163)

Severity of reaction No %

Mild to moderate 154 94.47

Severe 09 5.53

Table-VI

Distribution of adverse reactions by sex of donors

(n=21815)

Sex No of reaction No of donor %

Male 72 20179 0.35

Female 91 1636 5.56

Table-VII

Distribution of reactions by types of donor depending

on frequency of donation

Types of donors No of No of %

reactions donor

Periodic 4 1091 0.37

Occasional 32 6544 0.49

New 127 14180 0.89

48

BJM Vol. 22 No. 2 Incidence of Vasovagal Reaction Among The Blood Donors Attending

Discussion:

In this study, total donors were 21815, in which male

were 20179 (92.5%) and female were 1636 (7.5%). Out

of 21815 donors 163 (8.7%) developed vasovagal

reactions. In163 reactions, 72 (44.18%) were in male

and 91 (55.82%) were in female donors. Within 20179

male donors, adverse reactions occurred in 72 (0.35%)

and within 1636 female donors, adverse reactions

occurred in 91 (5.56%) It indicates that reactions are

higher in female. The symptoms were agitation 23

(14.12%), pallor 31 (19.02%), sweating 29 (17.79%),

nausea 21 (12.88%), vomiting 38 (23.21%),cold feeling

12 (7.36%),loss of consciousness 9 (5.52%), i.e.

severe reactions were 9 (5.53%) and mild to

moderate reactions were154 (94.47%). Among the

reactions 127 (0.49%) occurred in new donors, 32

(0.49%) occurred in occasional donors and 4 (0.37) in

periodic donors. Now the conclusion is that vasovagal

reactions are more common in female and new donors.

One study showed that 2% of donors had an adverse

reaction to donation6.Most of these reactions are

minor. Studies have demonstrated that approximately

3% to 10% of blood donors will experience an adverse

reaction or injury after the donation7. In one study

records of 422,231 allogenic whole blood donations

over a 9-month period and assessed for pre-faint and

faint reactions. They found a total of 6,049 adverse

events; a rate of 1.43 %. Of this total, the percent of

mild, moderate or severe reactions was 63%, 29%

and 8% respectively. Predictors of these reactions

were age, sex, blood volume, blood pressure, pulse,

and body mass index. The strongest predictors of a

reaction were donor blood volume of less than 3500

ml, age, and first time donor status8. In one study

the prevalence of moderate to severe reactions was

41 in 10,000 donations; 24% of these reactions were

delayed, and 12% occurred offsite. Delayed reactions

were associated with female gender. Low estimated

blood volume, youth, and first-time donor status were

major risk factors for immediate and delayed

reactions. Women were more likely than men to report

delayed reactions9. Adverse reactions recorded in the

American Red Cross donor hemovigilance program in

2006, adverse reactions occurred at a rate of 7.4, 5.2,

and 3.3 per 10,000 collections for whole blood,

apheresis platelet, and 2-unit automated red

cells10.The donor reaction rate was 12.0 percent (870/

7274). Female donors overall had a higher donor

reaction rate than male donors (16.7% vs. 7.3%). A

model suggested that a change in the blood-unit

volume from 450 to 500 ml would increase donor

reaction rates by 18 percent in either female or male

donors, whereas a reduction in the blood-unit volume

from 500 to 400 ml would decrease donor reaction

rates by 29 and 27 percent in female and male donors,

respectively11. Donors who developed delayed faint

should be indefinitely deferred from blood

donation12.Syncopal reactions most commonly occur

at the refreshment table where preventive safety

measure against trauma could be applied13.

Conclusion:

Reactions can be reduced by proper donor selection.

All donors should be observed for at least 15 min

after donation and should be questioned about their

occupation. Donors in whom fainting would be

especially hazardous to themselves or to others (pilot,

surgeons, bus drivers) should refrain from work or

potentially dangerous hobbies for up to 12 hrs after

giving blood.

Acknowledgement:

Special thanks to all medical and non-medical person

of the department for their service, work, and cordial

help for the study.

Conflicts of interest: None

References

1. Rahman M, Essential Book on Transfusion

medicin,1st edt,2007,p:40-50.

2. Denise M.Harmen, Modern Blood Banking and

Transfusion Practice,3rd edt, Jaypee Brothers, New

Delhi, India,p:217-218.

3. AABB Technical Manual, 15th edt,2005,P:107-108

4. MAYO CLINIC, Division of Transfusion Medicine,

Rochester, Minessota 55905, Blood Donation

Consent Form.

5. Eder AF, Hillyer CD, Dy BA, Notari EP, Benjamin

RJ. “Adverse Reactions to Allogeneic Whole Blood

Donation by 16- and 17-year-olds”. Jama 299 (19):

2279–86

6. “Adverse Effect of Blood Donation, Siriraj

Experience”. American red cross. Retrieved 2008-

06-01.

7. Eder A, Goldman M, Rossmann S, Waxman D,

Bianco C. Selection Criteria to Protect the Blood

Donor in North America and Europe: past (dogma),

present (evidence), and future (hemovigilance).

Transfus med rev. 2009 jul;23(3):205-20.

8. Wiltbank TB, Giordano GF, Kamel H, Tomasulo P,

Custer B. Faint and Prefaint Reactions in Whole

Blood Donors: An Analysis of Predonation

Measurements and Their predictive value.

Transfusion. 2008 sep; 48(9):1799-808.

9. Kamel h, tomasulo p, bravo m, wiltbank t, cusick r,

james rc, custer b. Delayed adverse reactions to blood

donation. Transfusion. 2010 mar; 50(3):556-65.

49

Incidence of Vasovagal Reaction Among The Blood Donors Attending BJM Vol. 22 No. 2

10. Eder AF, Dy BA, Kennedy JM, Notari EP, Strupp

A, Wissel ME, et al. Haimowitz MD, Newman BH,

Chambers LA, Hillyer CD, Benjamin RJ. The

American Red Cross Donor Hemovigilance Program:

Complications of Blood Donation Reported in 2006.

Transfusion. 2008 sep;48(9):1809-19.

11. Newman BH Satz SL, Janowicz NM, Siegfried BA.

Donor Reactions in High-School Donors: The Effects

of Sex, Weight, and Collection Volume. American

Red Cross Blood Services, Southeastern Michigan

Region, Detroit, Michigan 48201, USA.

Newmanb@usa.redcross.org

12. Harvey G. Klein, David J. Anstee, Mollison’s. Blood

Transfusion in Clinical Medicine, 11th edt, 2005,

P:1-12.

13. Newman BH, Graves S, ‘’A study of 178 consecutive

vasovagal syncopal reactions from the prospective

of safety.’’ American Red Cross Blood Service,

Southeast Region, Detroit, USA.

50

BJM Vol. 22 No. 2 Incidence of Vasovagal Reaction Among The Blood Donors Attending

Introduction:

Tuberculosis is an infectious disease that has

plagued mankind since Neolithic times (8000 BC) 1.

It was recognized as a contagious disease by the time

of Hippocrates (400 BC), when it was termed as

‘phthisis’ (Greek Phthinien, meaning to waste away)2

Abdominal TB which may involved the gastrointestinal

tract, peritoneum, lymph nodes or solid viscera,

constitutes up to 12% of extra pulmonary TB and 1-

3% of the total3,4. Abdominal tuberculosis includes

tuberculosis of gastrointestinal tract, peritoneum,

mesenteric lymph node, Liver, Spleen, excluding

genito-urinary system5. Tuberculosis (TB) can involve

any part of the gastrointestinal tract from mouth to

anus, the peritoneum and the pancreatobiliary

system. It can have a varied presentation, frequently

mimicking other common and rare diseases6. TB of

the gastrointestinal tract is the sixth most frequent

form of extra-pulmonary site, after lymphatic,

genitourinary, bone and joint, miliary and meningeal

tuberculosis7. The term Extrapulmonary Tuberculosis

(EPTB) has been used to describe isolated occurrence

of tuberculosis at body sites other than the lung.

However, when an extra-pulmonary focus is evident

in a patient with pulmonary tuberculosis, such

patients have been categorized under pulmonary

tuberculosis as per the guidelines of the World Health

Organization (WHO) 8.

Materials and Methods:

Search strategy and selection criteria

In addition to the review of key papers, we undertook

searches of electronic databases. For PubMed, the

search items were “abdominal tuberculosis”

restricted to the past 25 years. “Gastrointestinal

tuberculosis, tubercular ascites, serositis, iliocaecal

tuberculosis terms were used for search items.”,

abdominal tuberculosis and pathophysiology”, “

tuberculosis of alimentary system and diagnosis”,

“antuitubercular chemotherapy” were search items

without a time restriction. The Cochrane database of

systematic reviews was searched by use of the term

ABDOMINAL TUBERCULOSIS -A REVIEW

DEVENDRA NATH SARKAR ¹, ROBED AMIN ², HANIF MOHAMMED ³, MA AZHAR4, MA FAIZ5

1. Associate Professor of Medicine, Rangpur Medical College, Rangpur, Bangladesh

2. Assistant professor of Medicine, Dhaka Medical College, Dhaka

3. Senior Consultant of Medicine, 250 bed Hospital, Narayanganja, Dhaka

4. Professor and Head, Department of Medicine and Principal, Sir Salimullah Medical College and Mitford

Hospital, Dhaka

5. Professor of Medicine (PRL) Sir Salimullah Medical College, Dhaka

“abdominal tuberculosis”. Articles were selected on

the basis of their effect on abdominal tuberculosis

treatment or control. When more than one paper

illustrated a specific point, the most representative

paper was chosen.

Epidemiology:

Tuberculosis causes some 3 million deaths per year

worldwide and is increasing in developed and

developing countries9. Despite the accelerated efforts

to control the disease for decades, it remains the

seventh leading cause of death globally10. Abdominal

tuberculosis is still highly prevalent in developing

country like India, South Africa, and Saudi

Arabia11,12,13,14,15. In Western countries, with the

development of effective anti-tubercular chemo-

therapy and preventive measure, incidence of

pulmonary tuberculosis was declined but extra-

pulmonary tuberculosis remained constant116,17.

There is considerable variation in the incidence of

abdominal tuberculosis in different ethnic groups.

The disease is endemic in South East Asian and Latin

American countries. In the United Kingdom,

immigrants from Asia are significantly more prone to

this disease compared to the native population18. In

the U.S.A. all forms of tuberculosis are seen amongst

the immigrant population, people residing in the north

American Indian reservations and in patients

suffering from HIV-AIDS.19,20In the era before the

human immunodeficiency virus (HIV) pandemic, and

in studies involving immune-competent adults, it has

been observed that EPTB constituted about 15 to 20

per cent of all cases of TB21-31. In HIV-positive

patients, EPTB accounts for more than 50 per cent of

all cases of TB32-40. The diagnosis of EPTB, especially

involving deeply located in accessible areas is very

difficult..Abdominal tuberculosis is presumed to be

highly prevalent in Bangladesh. There is no extensive

study done in our country regarding abdominal

tuberculosis. One retrospective study was done by

Rouf HMA in general Hospital. Sirajgonj 41with

intestinal obstruction (25%), and 27% chronic

REVIEW ARTICLE

Bangladesh J Medicine 2011; 22 : 51-59

symptoms. Faiz M.A. did another retrospective study

in 1989 in IPGM&R on extra- pulmonary tuberculosis

and found intestinal tuberculosis in 5 cases out of

47 patients having extra-pulmonary tuberculosis42.

Sheldon CD et al. conducted a retrospective study in

east London among Bangladeshi immigrants and

showed the crude incidence in Bangladeshi

community was 7.7cases/100000/year which was

significantly higher than that of European (0.3 cases/

100000/year) 43.

Pathogenesis and pathology:

The disease may develop secondary to primary focus

elsewhere in the body; usually the lungs or it may

originate within intestinal tract from swallowed

sputum or rarely ingestion of cow’s milk44.

The postulated mechanisms by which the tubercle

bacilli reach the gastrointestinal tract are: (i)

haematogenous spread from the primary lung focus

in childhood, with later reactivation; (ii) ingestion of

bacilli in sputum from active pulmonary focus; (iii)

direct spread from adjacent organs; and (iv) and

through lymph channels from infected nodes. The

earlier belief that most cases are due to reactivation

of quiescent foci is being challenged with a recent

study using DNA fingerprinting showing that 40 per

cent cases are due to re-infection. In India, the

organism isolated from all intestinal lesions has been

Mycobacterium tuberculosis and not M.bovis 45,46.

Tuberculosis (TB) can involve any part of the

gastrointestinal tract from mouth to anus, the

peritoneum and the pancreatobiliary system. The

most common site of involvement is the ileo-caecal

region, possibly because of the increased

physiological stasis, increased rate of fluid and

electrolyte absorption, minimal digestive activity and

an abundance of lymphoid tissue at this site. It has

been shown that the M cells associated with Peyer’s

patches can phagocytose BCG bacillis47. In Bhansali’s

series, including 196 patients with gastrointestinal

tuberculosis, ileum was involved in 102 and caecum

in 100 patients48. Of the 300 patients in a study

ileocaecal involvement was present in 16249. The

frequency of bowel involvement declines as one

proceeds both proximally and distally from the

ileocaecal region. Peritoneal involvement may occur

from spread from lymph nodes, intestinal lesions or

from tubercular salpingitis in women. Abdominal

lymph nodal and peritoneal tuberculosis may occur

without gastrointestinal involvement in about one

third of the cases50.

Tuberculous granulomas are initially formed in the

mucosa or the Peyer’s patches. These granulomas

are of variable size and characteristically tend to be

confluent, in contrast to those in Crohn’s disease.

Granulomas are often seen just beneath the ulcer

bed, mainly in the submucosal layer. Submucosal

oedema or widening is inconspicuous. Tubercular

ulcers are relatively superficial and usually do not

penetrate beyond the muscularis51. They may be

single or multiple, and the intervening mucosa is

usually uninvolved. These ulcers are usually

transversely oriented in contrast to Crohn’s disease

where the ulcers are longitudinal or serpiginous52.

Cicatrical healing of these circumferential ‘girdle

ulcers’ results in strictures. Occlusive arterial

changes may produce ischaemia and contribute to

the development of strictures53. Endarteritis also

accounts for the rarity of massive bleeding in cases

of intestinal tuberculosis. Shah et al54 correlated

findings on barium studies and superior mesenteric

angiography in 20 patients. Angiograms were abnormal

in all and showed arterial encasement, stretching

and crowding of vessels, and hypervascularity. In long-

standing lesions there may be variable degree of

fibrosis of the bowel wall which extends from

submucosa into the muscularis. Many sections may

show only non-specific chronic inflammation and no

granulomas. Mesenteric lymph nodes may be

enlarged, matted and may caseate. Characteristic

granulomas may be seen only in the mesenteric

lymph nodes. The reverse, i.e., the presence of

granulomas in the intestine and no granulomas in

the draining lymph nodes is rare50. Hoon et al51

originally classified the gross morphological

appearance of the involved bowel into ulcerative,

ulcerohyperplastic and hyperplastic varieties. Tandon

and Prakash50 described the bowel lesions as

ulcerative and ulcerohypertrophic types. Ulcerative

form has been found more often in malnourished

adults, while hypertrophic form is classically found

in relatively well nourished adults. These ulcerative

and stricturous lesions are usually seen in the small

intestine. Colonic and ileocaecal lesions are

ulcerohypertrophic. The patient often presents with

a right iliac fossa lump constituted by the ileocaecal

region, mesenteric fat and lymph nodes. The

ileocaecal angle is distorted and often obtuse. Both

sides of the ileocaecal valve are usually involved

leading to incompetence of the valve, another point

of distinction from Crohn’s disease. In tuberculous

peritonitis, the peritoneum is studded with multiple

yellow-white tubercles. It is thick and hyperaemic

with a loss of its shiny luster. The omentum is also

thickened58

Intestinal tuberculosis: Intestinal tuberculosis is

usually seen in underdeveloped countries. Organisms

involved are Mycobacterium tuberculosis and

52

BJM Vol. 22 No. 2 Abdominal Tuberculosis -A Review

Mycobacterium Bovis. Primary focus is in intestine

and mesenteric lymph nodal involvement causes Ghon

complex formation. Tuberculous granulomas are

initially formed in the mucosa or the peyer’s patches.

These granulomas are seen just beneath the ulcer

bed mainly in the submucosa. Tuberculous ulcers

are superficial and usually transversely oriented.

Cicatrical healing of these ulcers may produce

strictures. More over occlusive arterial changes

associated with tuberculosis may produce ischemia

and perforation of ulcers as well as aid in development

of strictures.60,61

Ulcerative tuberculosis:It is mostly secondary to

pulmonary tuberculosis and arises as a result of

swallowing tubercle bacilli. There are multiple ulcers

in the terminal ileum, lying transversely, and the

overlying serosa is thickened, reddened, and covered

in tubercles. 62

Hyperplastic tuberculosis:

This variety usually occurs in the ileocecal region,

although solitary or multiple lesions in the distal

ileum are sometimes seen. There is early involvement

of regional lymph nodes which may caseate. Patients

of this variety presented with sub-acute intestinal

obstruction, mass in right iliac fossa, perforation and

some times complete intestinal obstruction. 62. Some

times ileocecal tuberculosis presents as acute

abdomen without any lump in right lower abdomen

or any previous history pointing towards tuberculosis

Tuberculous peritonitis: It is of two varieties according

to mode of presentation. One is acute and other is

chronic. Acute variety presented as acute peritonitis

and on opening peritoneum straw colored fluid come

with tubercles scattered over peritoneum and greater

omentum. Chronic variety presented as pain abdomen,

fever, weight loss, ascites and sometime as abdominal

mass. Source of infection are, mesenteric

lymphadenitis, intestinal tuberculosis, blood borne

from pulmonary tuberculosis62 Peritoneal

tuberculosis occurs in 3 forms: 1) Wet type with

ascites; 2) Encysted (loculated) type with a localized

abdominal swelling; 3) Fibrotic type with abdominal

masses composed of mesenteric and omental

thickening, with matted bowel loops felt as lump(s)

in the abdomen. A combination of these types are

also common.

Tuberculous mesenteric lymphadenitis: These lymph

nodes caseate and can drain their secretion in

peritoneal cavity causing tuberculous peritonitis.The

involved lymph node calcifies in about a year.

Clinical Presentation:

Abdominal tuberculosis is predominantly a disease

of young adults. Two-thirds of the patients are 21-40

yr old and the sex incidence is equal, although some

Indian studies have suggested a slight female

predominanc53. The clinical presentation of

abdominal tuberculosis can be acute, chronic or acute

on chronic. Symptoms and signs of tuberculosis are

non-specific and protean. Weight loss, Fever (low

grade), chronic cough, malaise, anorexia,night sweets

are features developed due to cytokines released by

activated macrophages. i.e. IL-1, TNFa and not by the

organism itself.

Most patients have constitutional symptoms of fever

(40-70%), pain (80-95%), diarrhoea (11- 20%),

constipation, alternating constipation and diarrhoea,

weight loss (40-90%), anorexia and malaise. Pain can

be either colicky due to luminal compromise, or dull

and continuous when the mesenteric lymph nodes

are involved. Other clinical features depend upon the

site, nature and extent of involvement and are

detailed below:

Chronic abdominal pain, sub acute or acute intestinal

obstruction, doughy abdomen and visible peristalsis,

diarrhea alternating with constipation, abdominal

mass may be palpable especially in right iliac fossa

and may present as acute peritonitis when mesenteric

lymph node caseate and secrete its secretion in

peritoneal cavity causing tuberculous peritonitis.

These can mimic with any disease involving

abdominal organs such as inflammatory bowel

disease, colonic cancer, or infectious disease and

ascites of any causes56. The diagnosis of abdominal

tuberculosis is often delayed, increasing the morbidity

associated with this treatable condition57,63-70.

However, its presentation can be vague, non-specific

and can masquerade as other conditions58,71-76.

Some times present as pneumoperitonium especially

in ulcerative type, anemia, chronically ill looking,

malnutrition, hemoptysis in case of associated

pulmonary Tuberculosis and sometimes clubbing.

Patients are mostly unvaccinated and having contact

positive. 77,78-82

Tuberculosis of the oesophagus:

Oesophageal tuberculosis is a rare entity,

constituting only 0.2 per cent of cases of abdominal

tuberculosis47. The patient usually presents with low

grade fever, dysphagia, odynophagia and an ulcer,

most commonly midoesophageal. The disease usually

mimics oesophageal carcinoma and extraoesophageal

focus of tuberculosis may not be evident60.

53

Abdominal Tuberculosis -A Review BJM Vol. 22 No. 2

Gastroduodenal tuberculosis

Stomach and duodenal tuberculosis each constitute

around 1 per cent of cases of abdominal tuberculosis.

Gastroduodenal tuberculosis may mimic peptic ulcer

disease with a shorter duration of history and non

response to anti-secretary therapy61. Most patients

(73%) had symptoms of duodenal obstruction. The

remainder (27%) had a history of dyspepsia and were

suspected of having duodenal ulcers. Duodenal

tuberculosis is often isolated with no associated

pulmonary lesions in more than 80 per cent cases62.

Ileocaecal tuberculosis

Patients complain of colicky abdominal pain,

borborygmi and vomitings. Abdominal examination

may reveal no abnormality or a doughy feel. A well

defined, firm, usually mobile mass is often palpable

in the right lower quadrant of the abdomen.

Associated lymphadenitis is responsible for the

presence of one or more lumps which are mobile if

mesenteric nodes are involved and fixed if para-aortic

or illiac group of nodes are enlarged. The most

common complication of small bowel or ileocaecal

tuberculosis is obstruction due to narrowing of the

lumen by hyperplastic caecal tuberculosis, by

strictures of the small intestine, which are commonly

multiple, or by adhesions. Adjacent lymph nodal

involvement can lead to traction, narrowing and fixity

of bowel loops. In India, around 3 to 20 per cent of all

cases of bowel obstruction are due to

tuberculosis48,63,64. Tuberculosis accounts for 5-9 per

cent of all small intestinal perforations in India, and

is the second commonest cause after typhoid

fever65,66. Tubercular perforations are usually single

and proximal to a stricture53. Acute tubercular

peritonitis without intestinal perforation is usually

an acute presentation of peritoneal disease but may

be due to ruptured caseating lymph nodes48, 66.

Mal-absorption is a common complication. Next to

tropical sprue, it is the most important cause of mal-

absorption syndrome in India. In a patient with mal-

absorption, a history of abdominal pain suggests the

diagnosis of tuberculosis67.

Segmental colonic tuberculosis

Segmental or isolated colonic tuberculosis refers to

involvement of the colon without ileo-cecal region,

and constitutes 9.2 per cent of all cases of abdominal

tuberculosis. It commonly involves the sigmoid,

ascending and transverse colon68. Multifocal

involvement is seen in one third (28 to 44%) of

patients with colonic tuberculosis69,70. The median

duration of symptoms at presentation is less than 1

yr71. Pain is the predominant symptom in 78-90 per

cent of patients and Haematochezia occurs in less

than one third69,72. The bleeding is frequently minor

and massive bleeding is less common. Overall,

tuberculosis accounts for about 4 per cent of patients

with lower gastrointestinal bleeding66.

Rectal and anal tuberculosis

Clinical presentation of rectal tuberculosis is different

from more proximal disease. Haematochezia is the

most common symptom (88%) followed by

constitutional symptoms (75%) and constipation (37%)72. Overall rectal tuberculosis is rare and may occur

in the absence of other lesions in the chest and small

and large bowel73,74. Anal tuberculosis is less

uncommon and has a distinct clinical presentation.

Tubercular fistulae are usually multiple.

Constitutional symptoms were not present in any

patient75. Anal tuberculosis is also seen in pediatric

patients76.

Investigations:

Commonly includes- Routine CBC with raised ESR

.Sputum analysis can reveal associate PTB in less

than 20 percent cases., Mantoux test, Ascitic fluid

examination, X-rays and barium studies, CT scan of

Abdomen with contrast, PCR for tubercular

peritonitis, Diagnostic Laparoscopy for abdominal

tuberculosis in peritoneal siddling and extraluminal

intestinal TB, Endoscopy for upper Gastrointestinal

tuberculosis can be done according to site and

specific area. Chest radiographs may show hilar

lymphadenopathy or tuberculous lesion in case of

concurrent active pulmonary T.B. however a normal

chest radiograph does not rule out the possibility of

abdominal tuberculosis. 77,78,83-91.

X-rays abdomen radiograph can show air fluid levels

and dilated gut loops indicating intestinal obstruction

or air under diaphragm in case of gut perforation. It

can also show calcifications in mesenteric lymph

nodes.77,78,91.

USG abdomen can show mesenteric thickening,

enlarged mesenteric lymph nodes, thickened

omentum, peritoneal ascites with septations, dilated

small bowel loops and bowel wall thickening. It is

also an important tool for USG aspiration of ascitic

fluid. 77,91-97.The following features may be seen,

usually in combination 98.

(i) Intra-abdominal fluid which may be free or

loculated; and clear or complex (with debris and

septae).

(ii) “Club sandwich” or “sliced bread” sign is due to

localized fluid between radially oriented bowel

loop.

54

BJM Vol. 22 No. 2 Abdominal Tuberculosis -A Review

(iii) Lymphadenopathy may be discrete or

conglomerated (matted). The echo texture is

mixed heterogenous. Both caseation and

calcification are highly suggestive of a tubercular

etiology, neither being common in malignancy

related lymphadenopathy.

(iv) Bowel wall thickening is best appreciated in the

ileo-cecal region. The thickening is uniform and

concentric as opposed to the eccentric thickening

in Crohn’s disease and variegated appearance of

malignancy.

(v) Pseudo-kidney sign – involvement of the ileo-

cecal region which is pulled up to a sub-hepatic

position.

Barium studies:

In various studies conducted all over world, the

barium contrast radiography was helpful in about 75%

of patients suspected to have intestinal tuberculosis.

Findings included dilated bowel loops, strictures,

deformed and pulled-up caecum, ulceration of ileum,

bowel wall thickening, and extrinsic compression by

lymph nodes. Thus, contrast barium studies seem to

have a good diagnostic yield, when performed in

patients with suspected intestinal involvement77,78,91.

Barium enema:

The following features 97 may be seen:

(i) Early involvement of the ileocaecal region

manifesting as spasm and oedema of the

ileocaecal valve. Thickening of the lips of the

ileocaecal valve and/or wide gaping of the valve

with narrowing of the terminal ileum

(“Fleischner” or “inverted umbrella sign”) are

characteristic.

(ii) “Conical caecum”, shrunken in size and pulled

out of the iliac fossa due to contraction and

fibrosis of the mesocolon. The hepatic flexure

may also be pulled down.

(iii) Loss of normal ileo-cecal angle and dilated

terminal ileum, appearing suspended from a

retracted, fibrosed caecum (“goose neck

deformity”).

(iv) “Purse string stenosis”– localized stenosis

opposite the ileocaecal valve with a rounded off

smooth caecum and a dilated terminal ileum.

(v) “Sterling’s sign” is characterized by lack of

barium retention in the inflamed segments of

the ileum, caecum and variable length of the

ascending colon, with a normal configured

column of barium on either side.

(vi) “String sign” – persistent narrow stream of barium

indicating stenosis. Both Sterling and String signs

can also be seen in Crohn’s disease and hence

are not specific for tuberculosis.

CT scan:

The most common findings on CT scan highly

suggestive of abdominal tuberculosis are high density

ascites, lymphadenopathy, bowel wall thickening, and

irregular soft tissue densities in the omental area.

Abdominal lymphadenopathy is the commonest

manifestation of tuberculosis on CT. 77,78,91.

Mantoux test:

It is very important adjuvant test in diagnosis of

extrapulmonary T.B. Immunization with BCG vaccine

can cause a positive test, but the reactions are usually

only 5-10 mm and tend to decrease with time. People

with PPD reactions of 15 mm or more are assumed to

be infected with mycobacterium TB even if they are

vaccinated with BCG. False positive result may occur

in persons previously vaccinated with BCG and in

those infected with non tuberculous or atypical

mycobacteria. False negative result may occur in

improper testing technique, concurrent infections,

malnutrition, advanced age, immunologic disorders,

lymphoreticular malignancies, Corticosteroid therapy,

chronic renal failure, HIV infection and fulminant

tuberculosis.79,80,81.

Ascitic fluid examination:

The ascitic fluid in tuberculosis is straw colored with

protein >3g/dl, and total cell count of 150-4000/ ìl,

consisting predominantly of lymphocytes (>70%). The

ascites to blood glucose ratio is less than 0.9650 and

serum ascites albumin gradient is less than 1.1 g/

dl. The yield of organisms on smear and culture is

low. Staining for acid fast bacilli is positive in less

than 3 per cent of cases. A positive culture is obtained

in less than 20 per cent of cases, and it takes 6-8 wk

for the mycobacterial colonies to appear. 82.

Adenosine deaminase (ADA) is an aminohydrolase

that converts adenosine to inosine and is thus

involved in the catabolism of purine bases. The

enzyme activity is more in T than in B lymphocytes,

and is proportional to the degree of T cell

differentiation. ADA is increased in tuberculous ascitic

fluid due to the stimulation of T-cells by mycobacterial

antigens. ADA levels were determined in the ascitic

fluid of 49 patients by Dwivedi et al94. The levels in

tuberculous ascites were significantly higher than

those in cirrhotic or malignant ascites. Taking a cut

off level of 33 U/l, the sensitivity, specificity and

diagnostic accuracy were 100, 97 and 98 per cent

respectively94. In the study by Bhargava et al95, serum

55

Abdominal Tuberculosis -A Review BJM Vol. 22 No. 2

ADA level above 54U/l, ascitic fluid ADA level above

36 U/l and a ascitic fluid to serum ADA ratio >0.985

were found suggestive of tuberculosis96. In co-

infection with HIV the ADA values can be normal or

low. Falsely high values can occur in malignant

ascites. High interferon-levels in tubercular ascites

have been reported to be useful diagnostically83.

Combining both ADA and interferon estimations may

further increase sensitivity and specificity.

PCR (Polymerase chain reaction):

PCR testing of ascitic fluids is a good tool to detect

DNA of mycobacterium tuberculosis82.

Colonoscopy:

It is a very useful tool for identifying colonic and ileo-

cecal tuberculosis. Mucosal nodules (2-6mm) and

ulcers (4-8cm) are pathognomic of tuberculosis.78.Colonoscopy is an excellent tool to diagnose colonic

and terminal ileal involvement but is still often

underutilized. Mucosal nodules of variable sizes (2

to 6 mm) and ulcers in a discrete segment of colon, 4

to 8 cm in length are pathognomic. The nodules have

a pink surface with no friability and are most often

found in the caecum especially near the ileo-cecal

valve. Large (10 to 20 mm) or small (3 to 5 mm) ulcers

are commonly located between the nodules. The

intervening mucosa may be hyperemic or normal70.

Areas of strictures with nodular and ulcerated mucosa

may be seen. Other findings are pseudopolypoid

edematous folds, and a deformed and edematous ileo-

cecal valve. Diffuse involvement of the entire colon

is rare (4%), but endoscopically can look very similar

to ulcerative colitis. Lesions mimicking carcinoma

have also been described70-72. Most workers take up

to 8-10 colonoscopic biopsies for histopathology and

culture. Biopsies should be taken from the edge of

the ulcers. However, there is a low yield on

histopathology because of predominant sub-mucosal

involvement. Granulomas have been reported in 8-

48 per cent of patients and caseation in a third (33-

38%) of positive cases71. A combination of histology

and culture of the biopsy material can be expected to

establish the diagnosis in over 60 per cent of cases.

Diagnostic laparoscopy:

Laparoscopy provides a good deal of visual

confirmation of findings, taking biopsy and collecting

ascitic fluid for further investigations.77

Caseating Granulomas may be found in 85-90 per

cent of the biopsies. The laparoscopic findings in

peritoneal tuberculosis can be grouped into 3

categories :

(i) Thickened peritoneum with tubercles: Multiple,

yellowish white, uniform sized (about 4-5 mm)

tubercles diffusely distributed on the parietal

peritoneum. The peritoneum is thickened,

hyperemic and lacks its usual shiny luster. The

omentum, liver and spleen can also be studded

with tubercles.

(ii) Thickened peritoneum without tubercles.

(iii) Fibro-adhesive peritonitis with markedly

thickened peritoneum and multiple thick

adhesions fixing the viscera.

Diagnosis:

A high clinical index of suspicion and judicious use

of diagnostic procedure can certainly help in timely

diagnosis and treatment and thus reduce the mortality

of this curable but potentially lethal disease9. Many

authors in endemic countries also recommend clinical

trial85, 86.

One or more of the following four criteria along with

high clinical index of suspicion must be fulfilled to

diagnose abdominal tuberculosis—

(1) Histological evidence of tubercle with caseation

necrosis.

(2) Histological demonstration of acid fast bacilli in

a lesion.

(3) Culture of suspected tissue resulting in growth

of M. tuberculosis.

(4) Increased ADA (Adenosine deaminase) in ascitic

fluid ( >37 IU/L)

Management:

Management of all patients with abdominal

tuberculosis should be given standard full course of

ATT. Duration of treatment is different in different

centers. Treatment with three drug regimen for nine

months was also used as anti tuberculous treatment

. Successful treatment of abdominal tuberculosis for

one to one and a half year87 is also the

recommendation in some authors87,88,89.

Previously 18-24 months regime was popular, then 1

year regime and now 6 months of total duration is

considered sufficient for chemotherapy90,91,92.

In Bangladesh, there is a national guide line for

treatment of all kinds of TB patients. It is

recommended total 6 months ATT for the treatment

of abdominal tuberculosis patients93.

All patients of abdominal tuberculosis should receive

conventional anti-tubercular therapy for at least 6

months including initial 2 months of rifampicin,

isoniazid, pyrazinamide, ethambutol and next 4

months of rifampicin and isoniazide93.

56

BJM Vol. 22 No. 2 Abdominal Tuberculosis -A Review

Some authors have recommended the addition of

corticosteroids in patients with peritoneal disease

in order to reduce subsequent complications of

adhesions99

References

1. McDermott LJ, Glassroth J, Mehta JB, Dutt AK,

Tuberculosis Part-1, Dis Mon 1997;43(3):113-80.

2. CDC-Core curriculum on tuberculosis : What the

clinitians should know 4th Edition,US Department

of Health and Human Services:2000

3. Farer LS, Lowell AM, Meador MP. Extra-pulmonary

tuberculosis in the United States. Am J Epidemiol

1979; 109: 5-15

4. Sheer TA, Coyle WJ. Gastrointestinal tuberculosis.

Curr Gastroenterol Rep 2003;5: 273-278.

5. Manohar A, Simjee AE, Haffejee AA, et al. Symptoms

and investigative findings in 145 patients with

tuberculous peritonitis diagnosed by Peritoneoscopy

and biopsy over a five year period. Gut 1990; 31:

1130-2.

6. Peda Veerraju E. Abdominal tuberculosis. In: Satya

Sri S, editor. Textbook of pulmonary and extra

pulmonary tuberculosis. 3rd ed. New Delhi:

Interprint; 1998 p. 250-2.

7. Paustian FF. Tuberculosis of the intestine. In:

Bockus HL, editor. Gastroenterology, vol.11, 2nd ed.

Philadelphia : W.B. Saunders Co.; 1964 p. 311.

8. Maher D, Chaulet P, Spinaci S, Harries A. Treatment

of tuberculosis: guidelines for national programmes.

Geneva: World Health Organization; 1997.

9. Farer LS, Lowell AM, Meador MP. Extra pulmonary

tuberculosis in the United States. Am J Epidemiol

1979; 109: 5-15.

10. World Health Organization, The global burden of

disease: 2004 update. World Health Organization,

Geneva, Switzerland, 2004.

11. Bhansali SK. Abdominal tuberculosis: Experiences

with 300 cases. Am J Gastroe­nterol 1977; 67: 324-

37.

12. Mukhter A. Salmank. Extra pulmonary tuberculosis.

Saudi Med J 1983; 4:327.

13. Yasawy MI, Al-Karawi MA, Mohammed AE.

Alimentary tract tuberculosis. A continuing

challenge to gastroenterologist. Report of 55 cases.

J Gastroenterol Hepatol 1987; 2:137-47.

14. Satti MB, Al-freihi HM, Ibrahim EM, et al. Hepatic

granuloma in Saudi Arabia: A clinical pathologic

study of 59 cases. Am J Gastroenterol 1990; 85:669-

74.

15. Das P. Shukla HS. Clinical diagnosis of abdominal

tuberculosis. Br J Surg 1976 ; 63 : 941-6.

16. Pfaller MA. Application of new technology to the

detection, identification, and antimicrobial

susceptibility testing of mycobacteria. Am J Clin

Pathol 1994; 101:329-37.

17. National survey of tuberculosis notifications in

England and Wales 1978-9. Br Med J 1980; 281:

895-8

18. Palmer KR, Patil DH, Basran GS, et al. Abdominal

tuberculosis in urban Britain: A common disease.

Gut 1985; 26:1296-1305.

19. Rieder, H.L., Cauthcn, G.M., Kelly, G.D., et al.

Tuberculosis in the United States; JAMA 1989,

262,385.

20. Guth, A.A., Kirn, U. The reappearance of abdominal

tuberculosis; Surg Gynecol Obstt; 1991, 172,43

21. Gilinsky NH, Marks IN, Kottler RE, et al . Abdominal

tuberculosis; A 10- year review. S Afr Med J 1983;

64: 849-57.

22. Fanning A. Tuberculosis: 6. Extra pulmonary

disease. CMAJ 1999; 160 : 1597-603.

23. Report from the Medical Research Council

Tuberculosis and Chest Diseases Unit. National

survey of tuberculosis notifications in England and

Wales in 1983: characteristics of disease. Tubercle

1987; 68 : 19-32.

24. Medical Research Council Cardiothoracic

Epidemiology Group. National survey of notifications

of tuberculosis in England and Wales in 1988.

Thorax 1992; 47 : 770-5.

25. Weir MR, Thornton GF. Extra pulmonary

tuberculosis. Experience of a community hospital

and review of the literature. Am J Med 1985; 79 :

467-78.

26. Pitchenik AE, Fertel D, Bloch AB. Mycobacterial

disease: epidemiology, diagnosis, treatment, and

prevention. Clin Chest Med 1988; 9 : 425-41.

27. Snider DE Jr, Roper WL. The new tuberculosis. N

Engl J Med 1992; 326 : 703-5.

28. Snider DE, Onorato M. Epidemiology. In: Rossman

MD, MacGregor RR, editors. Tuberculosis: clinical

management and new challenges. New York: McGraw-

Hill;1995 p. 3-17.

29. Reported tuberculosis in the United States, 1999.

Atlanta: Centers for Disease Control and Prevention,

August 2000.

30. American Thoracic Society. Diagnostic standards

and classification of tuberculosis in adults and

children. Am J Respir Crit Care Med 2000; 161 : 1376-

95.

31. Mohan A, Sharma SK. Epidemiology. In: Sharma

SK, Mohan A, editors. Tuberculosis. New Delhi:

Jaypee Brothers Medical Publishers; 2001 p.14-29.

32. Raviglione MC, Narain JP, Kochi A. HIV-associated

tuberculosis in developing countries: clinical

57

Abdominal Tuberculosis -A Review BJM Vol. 22 No. 2

features, diagnosis and treatment. Bull World Health

Organ 1992; 70 : 515-25.

33. Theuer CP, Hopewell PC, Elias D, Schecter GF,

Rutherford GW, Chaisson RE. Human

immunodeficiency virus infection in tuberculosis

patients. J Infect Dis 1990; 162 : 8-12.

34. Haas DW, Des Prez RM. Tuberculosis and acquired

immunodeficiency syndrome: a historical

perspective on recent developments. Am J Med 1994;

96 : 439-50.

35. Shafer RW, Kim DS, Weiss JP, Quale JM. Extra-

pulmonary tuberculosis in patients with human

immunodeficiency virus infection. Medicine

(Baltimore) 1991; 70 : 384-97.

36. Antonucci G, Girardi E, Armignacco O, Salmaso S,

Ippolito G. Tuberculosis in HIV-infected subjects in

Italy: a multicentre study. The Gruppo Italiano di

Studio Tubercolosi e AIDS. AIDS 1992; 6 : 1007-13.

37. Jones BE, Young SMM, Antoniskis D, Davidson PT,

Kramer F, Barnes PF. Relationship of the

manifestations of tuberculosis to CD4 cell counts

in patients with human immunodeficiency virus

infection. Am Rev Respir Dis 1993; 148 : 1292-7.

38. Lado Lado FL, Barrio Gomez E, Carballo Arceo E,

Cabarcos Ortiz de Barron A. Clinical presentation

of tuberculosis and the degree of immunodeficiency

in patients with HIV infection. Scand J Infect Dis

1999; 31 : 387-91.

39. Lee MP, Chan JW, Ng KK, Li PC. Clinical

manifestations of tuberculosis in HIV-infected

patients. Respirology 2000; 5 : 423-6.

40. Poprawski D, Pitisuttitum P, Tansuphasawadikul

S. Clinical presentations and outcomes of TB among

HIV-positive patients. Southeast Asian J Trop Med

Public Health 2000; 31 (Suppl 1) : 140-2.

41. Rouf HMA. Intestinal tuberculosis in Bangladesh -

study 43 cases. Journal of Bangladesh College of

Physicians and Surgeons. 1990; Vol 7, No.2: 38-

44.

42. Faiz MA, Das KK, Khondaker AK, Tahir M. Extra

pulmonary tuberculosis in Bangladesh - A Review

of 47 cases. Journal of Bangladesh College of

Physicians and Surgeons, 1990; Vol. 17, No.2:1-7.

43. Sheldon CD, Probert CSJ, Cock H, King K, Rompton

DS, Barnes NC, Mayberry JF. Incidence of abdominal

tuberculosis in Bangladeshi migrants in East

London. Tubercle and Lung disease 1993; 74:12-

15. Harrison’s Principles of Internal Medicine (14th

ed.). Mc graw-Hill 1998; 1:1004-14.

44. Raviglione MC, Brien RJ. Tuberculosis. In: Fauci

AS, Braunwald E, Wilson JD, Editors, Prin

Harrison’s ciples of Internal Medicine (14th ed.). Mc

graw-Hill 1998; 1:1004-14.

45. Wig KL, Chitkara NK, Gupta SP, Kishore K,

Manchanda RL. Ileo-cecal tuberculosis with

particular reference to isolation of Mycobacterium

tuberculosis. Am Rev Respir Dis 1961; 84 : 169-78.

46. Vij JC, Malhotra V, Choudhary V, Jain NK, Prasaed

G, Choudhary A, et al. A clinicopathological study

of abdominal tuberculosis. Indian J Tuberc1992; 39

: 213-20.

47. Paustian FF. Tuberculosis of the intestine. In:

Bockus HL, editor. Gastroenterology, vol.11, 2nd ed.

Philadelphia : W.B. Saunders Co.; 1964 p. 311

48. Bhansali SK. Abdominal tuberculosis. Experiences

with 300 cases. Am J Gastroenterol 1977; 67 : 324-

37.

49. Prakash A. Ulcero-constrictive tuberculosis of the

bowel. Int Surg 1978; 63 : 23-9.

50. Hoon JR, Dockerty MB, Pemberton J. Ileocaecal

tuberculosis including a comparison of this disease

with non-specific regional enterocolitis and

noncaseous tuberculated enterocolitis. Int Abstr Surg

1950; 91 : 417- 40.

51. Tandon HD, Prakash A. Pathology of intestinal

tuberculosis and its distinction from Crohn’s

disease. Gut 1972; 13 : 260-9.

52. Anand BS. Distinguishing Crohns disease from

intestinal tuberculosis. Natl Med J India 1989; 2 :

170-5.

53. Kapoor VK. Abdominal tuberculosis. Postgrad Med J

1998; 74 : 459-6.

54. Shah P, Ramakantan R. Role of vasculitis in the

natural history of abdominal tuberculosis - evaluation

by mesenteric angiography. Indian J Gastroenterol

1991; 10 : 127-30.

55. Bhargava DK, Shriniwas, Chopra P, Nijhawan S,

Dasarathy S, Kushwaha AK. Peritoneal tuberculosis:

laparoscopic patterns and its diagnostic accuracy.

Am J Gastroenterol 1992; 87 : 109-12.

56. Gilinsky NH, Marks IN, Kottler RE, et al . Abdominal

tuberculosis; A 10- year review. S Afr Med J 1983;

64: 849-57.

57. Bernhard JS, Bhatia G, Knauer CM. Gastro-

intestinal Tuberculosis Jclin Gastroenterol 2001;

1:397-402.

58. Jadvar H, Mindelzun RE, Olcott EW, Levitt DB. Still

agreat mimicker: abdominal tuberculosis. Am J

Radiology 1997; 168:1455-60.

59. Sharma AK, Agarwal LD, Sharma CS, Sarin YK.

Abdominal tuberculosis in children : experience

over a decade. Indian Peadiatr 1993; 30 : 1149-53.

60. Tassios P, Ladas S, Giannopoulos G, Larion K,

Katsogridakis J, Chalerelakis G, et al. Tuberculous

esophagitis. Report of a case and review of modern

approaches to diagnosis and treatment.

Hepatogastroenterology 1995; 42 : 185-8.

58

BJM Vol. 22 No. 2 Abdominal Tuberculosis -A Review

61. Ali W, Sikora SS, Banerjee D, Kapoor VK, Saraswat

VA, Saxena R, et al. Gastroduodenal tuberculosis.

Aust NZ J Surg 1993; 63 : 466-7.

62. Berney T, Badaoui E, Totsch M, Mentha G, Morel

P. Duodenal tuberculosis presenting as acute ulcer

perforation. Am J Gastroenterol 1998; 93 : 1989-91.

63. Bhansali SK, Sethna JR. Intestinal obstruction : a

clinical analysis of 348 cases. Indian J Surg 1970;

32 : 57-70.

64. Gill SS, Eggleston FC. Acute intestinal obstruction.

Arch Surg 1965; 91 : 589-91.

65. Dorairajan LN, Gupta S, Deo SV, Chumber S, Sharma

L. Peritonitis in India – a decade’s experience. Trop

Gastroenterol 1995; 16 : 33-8.

66. Kapoor VK. Abdominal tuberculosis : the Indian

contribution. Indian J Gastroenterol 1998; 17 : 141-7.

67. Ranjan P, Ghoshal UC, Aggarwal R, Pandey R, Misra

A, Naik S, et al. Etiological spectrum spsoradic

malabsorption syndrome in Northern Indian adults

at a tertiary hospital. Indian J Gastreoenterol 2004;

23 : 94-8.

68. Chawla S, Mukerjee P, Bery K. Segmental

tuberculosis of the colon: a report of ten cases. Clin

Radiol 1971; 22 : 104-9.

69. Arya TVS, Jain AK, Kumar M, Agarwal AK, Gupta

JP. Colonic tuberculosis : a clinical and colonoscopic

profile. Indian J Gastroenterol 1994; 13 (Suppl) A 116.

70. Bhargava DK, Tandon HD, Chawla TC, Shriniwas,

Tandon BN, Kapur BM. Diagnosis of ileocecal and

colonic tuberculosis by colonoscopy. Gastrointest

Endosc 1985; 31 : 68-70.

71. Singh V, Kumar P, Kamal J, Prakash V, Vaiphei K,

Singh K. Clinicocolonoscopic profile of colonic

tuberculosis. Am J Gastroenterol 1996; 91 : 565-8.

72. Puri AS, Vij JC, Chaudhary A, Kumar N, Sachdev

A, Malhotra V, et al. Diagnosis and outcome of

isolated rectal tuberculosis. Dis Colon Rectum 1996;

39 : 1126-9.

73. Chaudhary A, Gupta NM. Colorectal tuberculosis.

Dis Colon Rectum 1986; 29 : 738-41.

74. Gupta OP, Dube MK. Tuberculosis of gastrointestinal

tract: with special reference to rectal tuberculosis.

Indian J Med Res 1970; 58 : 979-84.

75. Shukla HS, Gupta SC, Singh C, Singh PA.

Tubercular fistula in ano. Br J Surg 1988; 75 : 38-9.

76. Wadhwa N, Agarwal S, Mishra K. Reappraisal of

abdominal tuberculosis. J Indian Med Assoc 2004;

102 :31-2.

77. Channa GA. Abdominal Tuberculosis: continuation

of surgical scourge. J CPSP 2008; 18: 393-6.

78. Sood R. Diagnosis of abdominal tuberculosis: Role

of imaging. J Indian Academ Clinical Med 2001; 2.

79. Chandrasoma P, Taylor CR, editors. Concise

pathology. 3rd ed. The Mcgraw-Hill Companies;

1998.p. 607.

80. Levinson W, editor. Medical microbiology and

immunology. 8th ed. The McGraw Hill Companies;

2004.

81. Khan PA, Kundi MZ, editors. Basis of pediatrics.

6th ed. Carvan book centre; 2002.

82. Danish MI, editor. Short text book of medical

diagnosis and management. 5th ed. Karachi: Johar

Publications; 2004.p. 53-5.

83. Sathar MA, Simjer AE, Coovadia YM, Soni PN, Moola

SA, Insam B, et al. Ascitic fluid gamma interferon

concentrations and adenosine deaminase activity

in tuberculous peritonitis. Gut 1995; 36 : 419-21.

84. Lingenfelser T, Zak J, Marks IN et al. Abdominal

tuberculosis: still a potentially lethal disease. Am J

Gastroenterol 1993; 88:744-50.

85. Marshall JB. Tuberculosis of the Gastrointestinal

tract and peritoneum. Am J Gastroenterol 1993;

88:989-99.

86. Anond BS, Nanda R, Sachdev GK. Response of

tuberculosis stricture to antituberculous treatment.

Gut 1988;29:62-9

87. Klimach OE, Prmerod LP. gastrointestinal

tuberculosis. A retrospective review of 109 cases

in a district of General Hospital. Q J Med 1985;

56:569-78.

88. Al-Quorain, et al. Abdominal tuberculosis in Saudi

Arabia: A clinical pathological study of 65 cases.

Am J Gastroenterol 1993; 88:75-79.

89. Schofield PF. Abdominal tuberculosis. Gut 1985;

1275-1278.

90. Channa GA. Abdominal Tuberculosis: continuation

of surgical scourge. J CPSP 2008; 18:393-6

91. Sharma MP, Bhatia V. Abdominal Tuberculosis.

Indian J of Med Res 2004; 120:305-15.

92. Balasurbramaniam R, Nagarajan M, Balambal R,

Tripathy SP, Sundaraman R, Venkatesan P, et al.

randomized controlled clinical trial ofshort course

chemotherapy in abdominal tuberculosis: a five year

report. Int J Tuberc Lung Dis 1997;1:44-51.

93. National Guidelines and Operational Manual for

Tuberculosis Control. 4th ed. National Tuberculosis

Control Programme. Directorate General of Heath

Services, Dhaka, Bangladesh.

94. Dwivedi M, Misra SP, Misra V, Kumar R. Value of

adenosine Deaminase estimation in the diagnosis

of tuberculous ascites. Am J Gastroenterol 1990; 85 :

1123- 5.

95. Bhargava DK, Gupta M, Nijhawan S, Dasarathy S,

Kushwaha AKS. Adenosine deaminase (ADA) in

peritoneal tuberculosis : diagnostic value in ascites

fluid and serum. Tubercle 1990; 71 : 121-6.

96. Balasubramanian R, Ramachandran R, Joseph PE,

Nagarajan M, Thiruvengadam KV, Tripathy SP, et

al. Interim results of a clinical study of abdominal

tuberculosis. Indian J Tuberc 1989; 36 : 117-21.

97. Kapoor VK, Chattopadhyay TK, Sharma LK. Radiology

of abdominal tuberculosis. Australas Radiol 1988; 32

: 365-7.

98. Kedar RP, Shah PP, Shivde RS, Malde HM.

Sonographic findings in gastrointestinal and

peritoneal tuberculosis. Clin Radiol 1994; 49 : 24-9.

99. Sing MM, Bharagava AN, Jain KP. Tuberculous

peritonitis. An evaluation of pathogenic

mechanisms, diagnostic procedures and therapeutic

measures.Engl J Med 1969; 281;1091-94

59

Abdominal Tuberculosis -A Review BJM Vol. 22 No. 2

CASE REPORTS

Introduction

Pregnancy is uncommon in women with advanced

cirrhosis and is associated with an increased risk of

complications such as bleeding from esophageal

varices, liver failure and hepato-renal syndrome1-4.

Esophageal variceal bleeding has been reported in

18% to 32% of pregnant women with cirrhosis and in

up to 50% of those with known portal hypertension4,5.

Among those with preexisting varices, up to 78% will

have gastrointestinal bleeding during pregnancy, with

a mortality rate of 18% to 50%1. Maternal deaths have

been reported in advanced cirrhosis mainly due to

variceal bleeding4. Maternal mortality is likely to

improve with better management of variceal

hemorrhage and liver failure. Up to 24% of pregnant

patients with cirrhosis will also experience hepatic

decompensation, which can lead to rapid clinical

deterioration. When fulminant hepatic failure occurs,

the only treatment available is liver transplantation.

Spontaneous abortion and increased risk of

premature childbirth or stillbirth have been reported

in 15%–20% of pregnancies in women with cirrhosis5.

We are reporting a case of a successful pregnancy

outcome of a woman with decompensated cirrhosis,

caused by hepatitis B virus.

Case Report

The patient, a 28 year old married female got admitted

into Department of Obstetrics & Gynaecology,

Bangabandhu Sheikh Mujib Medical University

(BSMMU) with the complaints of amenorrhoea for last

9 months and gradual abdominal distention and

swelling of both lower limbs for last 5 months.

A CASE REPORT ON DECOMPENSATED CIRRHOSIS

OF LIVER WITH PREGNANCY

MOHAMMAD MAHABUBUL ALAM1, FAIZ AHMAD KHONDAKAR2, SYED ABUL FOEZ1, MAMUN AL-MAHTAB1,

SALIMUR RAHMAN1

Abstract

Pregnancy in women with advanced liver disease is rare. Cirrhosis results in metabolic and hormonal

derangements that lead to anovulation and amenorrhea1. In this paper we described the case of a

successful pregnancy in a young woman with advanced cirrhosis due to hepatitis B virus infection.

Key words: Hepatitis B, liver cirrhosis, viable pregnancy

1. Dept of Hepatology, Bangabandhu Sheikh Mujib Medical University, Dhaka

2. Noakhali Medical College & Hospital, Noakhali.

According to the statement of the patient, she was

relatively well at 5 months back with 4 months of

viable pregnancy. She noticed sudden onset of

vomiting of blood and passage of tarry colored stool

for 3 days. With these complaints she got admitted

in a hospital and was treated conservatively with

blood transfusion. From there she was transferred

to BSMMU and was diagnosed as a case of HBV-

related cirrhosis of liver with 4 months viable

pregnancy. Emergency endoscopy of upper

gastrointestinal tract (UGIT) and oesophageal variceal

ligation (EVL) was done. She was discharged with

diuretics and B-blocker. She continued regular follow

up under an Obstetrician. After 2 months, diuretics

were stopped and swelling of her both lower limbs

and abdomen became worse. The patient

subsequently got admitted into BSMMU again for

better management.

She had no history of jaundice and gave birth of a

healthy child 5 years back. On examination, she was

Fig.-1

Bangladesh J Medicine 2011; 22 : 60-62

conscious and well-cooperative. She was mildly

anaemic, but not ecteric. Pulse rate was 78/min,

regular and blood pressure was 100/70 mm of Hg.

Abdomen was distended, umbilicus everted with

striae graviderum in lower abdomen. Ascites was

evidenced by shifting dullness. No organomegaly was

noted. Other systemic examination revealed normal

study.

Investigations revealed hemoglobin of 11.2 gm/dl

with total leukocyte count of 12000/mm3 (85%

polymorphs and 10% lymphocytes), platelets

1,40,000/mm3, total billirubin 34.0 microm/l, serum

glutamic oxaloacetic transaminase (ALT) 42 U/L (UNL

37U/L), serum glutamic pyruvic transaminase 24 U/

L (AST) (UNL 65 U/L) and alkaline phosphatase 397

U/L (UNL136), serum albumin 2.1 gm/dl and

prothrombin time 16.0 seconds (control 11.8 seconds),

activated partial thromboplastin time 42.0 seconds

(control 28 seconds), fibrin degradation product 10.0

ug/dl (normal <5 ug/dl), D-dimer 1.5 ug/dl (normal

<0.5). She had normal renal function and electrolytes.

Abdominal and pelvic ultrasound (USG) revealed a

shrunken liver, mild spleenomegaly, moderate ascities

and 19 weeks viable twin pregnancy with breech

presentation and marked ascites. She was positive

for HBsAg by ELISA. However, HBeAg by ELISA and

HBV DNA by PCR were not detected in her serum.

Repeat endoscopy of UGIT showed grade II-III

esophageal varices and portal hypertensive

gastropathy (PHG), but no gastric varices. EVL (second

session) of esophageal varices was performed.

She was given propranolol 20 mg twice daily and a

diuretic (combination of frusemide 40mg +

spironolactone 100 mg) ½ tab daily. She underwent

therapeutic paracentesis of massive ascities at 28th

week of gestation.

She eventually gave birth of twin babies. Normal

vaginal delivery was accomplished. Both babies are

in good in health and weight. But mother developed

profuse post-partum bleeding, which was treated with

FFP and inj. Vitamin K. Two units of whole fresh

human blood was also transfused. Bleeding stopped

after 3 days.

Discussion

Infertility is common even in mild forms of chronic

liver diseases. Advanced cirrhosis increases the risk

of maternal and fetal morbidity and mortality1,2. In

such cases, the stage of the liver disease is the most

important determinant of the outcome of the

pregnancy1,2,6,7.

In contrast to cirrhosis due to autoimmune etiology

or alcoholic liver disease, the outcome of pregnancies

in women with other types of chronic liver disease,

especially of viral etiology, is poorly reported and

therefore uncertain8.

Maternal death rate in women with cirrhosis is

reported to be 10.3% to 18% with massive

gastrointestinal bleed as the commonest cause of

death1,3 and liver failure as the next most frequent

cause2. In a review of 117 pregnancies, term pregnancy

without maternal complications was achieved in 50%

of cases, while deterioration in liver function was

observed in 44.4%. Haematemesis occurred on 24

occasions and was responsible for maternal deaths

in 4 % of patients9.

Portal hypertension due to cirrhosis compounds the

physiological increase in circulating blood volume,

elevation in portal pressure and added pressure from

the gravid uterus on the inferior vena cava and can

result in massive bleeding. It is most common during

the 2nd trimester with 20–27% chance of bleeding

from esophageal varices, which is amplified to 62-

78% if there are large size varices1-4,7. Therefore, it

is mandatory to assess such patients for portal

hypertension, which can be done by indirect evidence,

such as the presence of esophageal varices, abdominal

collateral veins, hypersplenism and ascites.

Endoscopic variceal band ligation or sclerotherapy and

beta-blockers are the therapeutic options for such

patients2,3.

There is an increased rate of spontaneous abortion,

premature birth and perinatal deaths in pregnant

woman with advanced cirrhosis. Poor fetal prognosis

is usually explained by poor condition of the mother

in decompensated patients. Though, infants born

alive generally remain well2,3.

In a controlled setting vaginal delivery is usually safe

and early forceps delivery or vacuum extraction should

be considered to prevent any rise in portal pressure

due to prolonged straining during labor2,3. Women

with cirrhosis generally tolerate laparotomy poorly;

therefore the option for caesarean section should be

availed with care and caution. Our patient had an

uncomplicated vaginal delivery with moderate amount

of postpartum bleeding which was controlled with

konakion, FFP and blood transfusion. She did not

have further hepatic decompensation, sepsis or any

other complication.

Conclusion

Data related to the optimal management and outcome

of pregnancy in women with decompensated cirrhosis

secondary to viral etiology is limited. Whether to

advise a pregnancy to a woman with decompensated

cirrhosis is a difficult question to answer. However,

61

A Case Report On Decompensated Cirrhosis Of Liver With Pregnancy BJM Vol. 22 No. 2

careful overall assessment of the severity of the liver

disease as well as of the patient’s psychological

status and desire for children should lead logically

to a resolution of these issues on a case by case

basis. With careful monitoring and advanced

management, successful pregnancy with a good

outcome is a good possibility. The excellent outcome

of the pregnancy in our patient is encouraging and

supports this opinion.

References

1. Tiribelli C, Rigato I. Liver cirrhosis and pregnancy.

Ann Hepatol. 2006;5:201.

2. Aggarwal N, Sawnhey H, Suril V, Vasishta K, Jha

M, Dhiman RK. Pregnancy and cirrhosis of the liver.

Aust N Z J Obstet Gynaecol. 1999;39:503–6.

3. Cerqui AJ, Haran M, Brodribb R. Implications of

liver cirrhosis in pregnancy. Aust N Z J Obstet

Gynaecol. 1998; 38: 93–5.

4. Zeeman GG, Moise KJ., Jr Prophylactic banding of

severe esophageal varices associated with liver

cirrhosis in pregnancy. Obstet Gynecol. 1999;

94:842. doi: 10.1016/S0029-7844(99)00438-X.

5. Lee WM. Pregnancy in patients with chronic liver

disease. Gastroenterol Clin North Am. 1992;

21:889–903.

6. Whelton MJ, Sherlock S. Pregnancy in patients with

hepatic cirrhosis. Management and outcome. Lancet.

1968;2:995–9. doi: 10.1016/S0140-6736(68)91294-4.

7. Garcia-Tsao G. Portal hypertension. Curr Opin

Gastroenterol. 2006;22:254–62. doi: 10.1097/

01.mog.0000218962.93806.9a.

8. Lee MG, Hanchard B, Donaldson EK, Charles C,

Hall JS. Pregnancy in chronic active hepatitis with

cirrhosis. Journal of tropical med & hygiene.

1987;90:245–48.

9. Cheng YS. Pregnancy in liver cirrhosis and/or portal

hypertension. Am J Obs Gynecol. 1977;128:812–22.

62

BJM Vol. 22 No. 2 A Case Report On Decompensated Cirrhosis Of Liver With Pregnancy