Journal of Medical Society, Jan. 2011

GUEST EDITORIAL 

“Undergraduate Medical Education” 

1 

Dr. Matum Moirangthem 

2 

Dr. L. Prasad 

Graduate Medical education is aimed 

towards training of medical students to 

become a physician of first hand contact who 

is capable of looking after the preventive, 

creative and rehabilitative aspects of 

medicine 1 . A graduate who has completed the 

medical course can opt for a number of career 

opportunities. The graduate can take up a job 

in a government hospital. The person can 

also become a teacher in a medical college. 

He/she may like to do post graduation to 

become a specialist or researcher. Although, 

the options are many, the basic training in 

graduate medical education should provide an 

experience of the essential requirement for 

health care. 

For undergoing medical course, the 

students have to follow certain guidelines and 

a curriculum which is a plan of educational 

experiences and activities provided to the 

learners by the institution. The curriculum 

indicates selection and organization of content. 

It also suggests certain pattern of learning and 

teaching along with a programme for 

evaluation of learning objectives. On the basis 

of the curriculum, the basic concept of 

undergraduate medical education should be 

health oriented teaching instead of disease 

oriented teaching. For this, there is a need for 

more flexibility and it is necessary to remove 

the compartmentalization of the curriculum 

into pre, para and clinical subjects at least as 

an overall view, even though for the sake of 

convenience different parts of training 

1 

Associate Prof. Dept. of Anatomy, RIMS. 

2 

Associate Prof. Dept. of Medicine, RIMS. 

programme may be developed predominantly 

to these group of subjects. For achieving the 

aim, it will be desirable to expose the medical 

students to health problems throughout the 

period of undergraduate training 2 . 

However, if the country’s medical 

education is minutely examined; there 

appears to be an overwhelming emphasis in 

promoting the production of medical 

manpower as evidenced by the ever 

increasing number of medical colleges. On 

the other hand, the quality of medical training 

programme has not drawn the attention it 

deserves. The training programme should be 

considered satisfactory only if it is relevant and 

responsive to the needs of the people. On 

detailed study of the curriculum and ongoing 

training programmes, certain querries come 

up, which are outlined hereunder: 

a) Is the curriculum need- base? It can 

be examined by analyzing the common 

disease spectrum seen at outpatient and 

inpatient setups at health centres, district 

hospitals, general practioners and medical 

college hospitals. Do the training programmes 

match fairly with the common health problems 

encountered? 

b) Whether the departments could 

identify their departmental goals, objectives 

and core abilities? Has it been documented 

and available to the medical students? 

c) What type of teaching-learning 

process is going on? Is it active or passive? 

d) Are the medical students given the 

integrated learning schedule? 

JMS * Vol 25 * No. 1 * January, 2011 1

GUEST EDITORIAL 

e) Do the medical graduates possess 

the basic skills to plan and manage community 

health programme and have clear cut idea 

about their role in different national health 

programmes? 

f) Do the basic doctors possess the 

requisite skills to manage efficiently with 

confidence- (i) Clinical emergencies and (ii) 

medico-legal situations? 

g) Have they acquired the managerial 

and leadership skills to lead the health team 

of primary health centre or any health care 

set up? Do they care cost-effective 

therapeutics? 

h) Have they developed humanistic 

attitude in medical practice 

- Good communication with patients, 

ethical issues, privacy and dignity of 

patients 

- Acting as role models of kind and 

compassionate attitude towards 

patients 

- Helping family members in managing 

the chronically ill patients 

- Taking care of religions and cultural 

values of patients 

There are a few aspects of ongoing 

undergraduate medical teaching programme 

besides much broader areas like existing 

internship programmes, methods of teaching 

and use of newer and effective teaching aids. 

National Health policy (NHP) decries the 

wrong priorities that crept into health care 

services of the country and clearly points to 

prepare doctors who will serve rural and who 

will not give emphasis on curative aspects of 

medicine alone. The NHP also says that 

medical personnel should work as a member 

of an integrated team with social motivation 

to deal with day today problems within the 

existing constraints and professional 

competence 3 . 

Keeping in view of the existing curriculum 

and ongoing training prgrammes and National 

Health Policy, it may be worthwhile to think of 

a strategy for any change in the curricula. The 

suggestions may include faculty sensitisation, 

discussion with students’ representatives, 

identification of tasks of a medical graduate, 

review and revision of question papers and 

affiliating University’s approval for any change. 

Some of the starting points for changes can 

be – developing problem, base exercises, 

introduction of integrated teachings in selected 

topics or areas of relevance, surprise casualty 

postings, medico-legal management posting 

and setting of question papers balance in 

term of course content and relevancy. 

Apart from this, to achieve successful 

changes, the Medical Education Unit/cell be 

entrusted for many activities including – coordination 

and helping departments in 

developing “learning objectives” 

- Identifying core abilities 

- Modifying teaching-learning methods 

- Curricula construction/development 

- Restructuring evaluation tools and 

techniques 

- Support in implementation of teaching 

innovations 

- Monitoring of changes by feed back from 

students and faculty, and modification if 

needed. 

References 

1. Medical Council of India. Regulation on 

Undergraduate Medical Education, 1997; The 

Gazette of India, May 1997. 

2. Medical Council of India. Regulation on 

Undergraduate Medical Education, New Delhi; 

MCI, 1979. 

3. National Health Policy: Ministry of Health and 

Family Welfare, New Delhi; Government of 

India: 1983. 

2 

JMS * Vol 25 * No. 1 * January, 2011

ORIGINAL ARTICLE 

Comparative study of angiotensin converting enzyme inhibitor versus beta 

blocker on endothelial-dependent flow mediated vasodilation in patients with 

essential hypertension 

1 

Dhanaraj Singh Chongtham, 2 Sridhar G, 3 Anil Grover, 4 Rohit Manoj, 1 Ksh. Birendra Singh 

Abstract 

Objective : To compare the endothelialdependent 

flow mediated vasodilation of 

angiotensin converting enzyme (ACE) 

inhibitor versus beta blocker in patients with 

essential hypertension. Methods : In this 

prospective study twenty patients with recently 

detected essential hypertension who were not 

yet started on any anti hypertensive drugs and 

who fulfilled the inclusion criteria were included 

in the study. Baseline brachial artery flow 

mediated vasodilatation (FMD) studies were 

done non invasively by a single person for all 

the subjects. After the baseline FMD studies 

all the 20 patients were divided into two groups 

of ten each at random. One group was started 

on ACE inhibitor Ramipril and the other group 

was started on beta blocker Atenolol. After 8 

weeks, repeat FMD studies were conducted 

and after one week of washout period the 

subjects were then crossed over from one 

group to the other in order to be started on the 

second study medication. After 8 weeks of 

completion of second drug therapy, FMD 

studies were again repeated. Results : There 

were 13 male patients (65%) and 7 female 

patients (35%) with age ranging from 42-58 

years. At the and of 8 weeks of therapy with 

1. Associate Professor, Department of Medicine, 

Regional Institute of Medical Sciences, Imphal. 2. 

Former Senior Resident 3. Former Additional 

Professor 4. Associate Professor, Cardiology Department, 

PGIMER, Chandigarh. 

Correspondence author 

Dr. Dhanaraj Singh Chongtham, Associate Professor, 

Department of Medicine, RIMS, Imphal Email 

dhanarajcardiology@yahoo.co.in 

Ramipril, a net Systolic Blood pressure 

reduction of 4.6% from baseline was 

observed (P


more than 50 years ago and flow dependent 

dilation has been suggested as the principal 

response in a variety of physiological vascular 

adaptations such as collateralization and long 

term diameter adaptation to increased flow 

loads. 4 The principal mediator of FMD is 

endothelium derived nitric oxide (NO). Indeed, 

endothelial denudation or treatment with a 

nitric oxide synthetase inhibitor abolishes FMD 

in a variety of arterial vessels. 5 The same effect 

has been shown in venous system also. 6 Over 

the past decade a non invasive technique has 

evolved to evaluate flow-mediated 

vasodilation, an endothelial dependent function 

in the brachial artery. 7 The reproducibility and 

accuracy of the same has also been 

confirmed. 8 

Hypertension is one of the commonest result 

of endothelial dysfunction and also an 

important cause of morbidity and mortality 

in general population. 9 With proven 

endothelial dysfunction associated with 

hypertension, FMD has not been extensively 

studied in hypertensive subjects with or 

without any other risk factors for coronary 

artery disease [CAD]. 

Various anti hypertensive agents have been 

used to evaluate their effects on endothelial 

function through FMD in CAD patients. 10,11 

Angiotensin converting enzyme [ACE] 

inhibitors and calcium channel blockers[CCB] 

have been shown to be useful in improving 

endothelial dysfunction in hypertensive 

patients. 12,13 

Beta-blockers have been shown to be of 

immense benefit in patients with coronary 

artery disease, congestive heart failure [CHF] 

and hypertension, which are secondary to 

endothelial dysfunction. Effect of Betablockers 

on endothelial function through FMD 

in hypertensive subjects has rarely been 

studied. 

Methods 

Twenty patients with recently detected 

essential hypertension who were not yet 

started on any antihypertensive drugs were 

taken up for the study from cardiology OPD, 

PGI, Chandigrah after obtaining written 

informed consent. 

4 

Inclusion criteria 

Patients with essential hypertension (Supine 

measurement after 10 minutes of rest) with 

blood pressure recordings of more than 140/ 

90 mmHg on 3 occasions at 1-week intervals 

were included in the study. They were never 

treated with antihypertensive medications 

before inclusion in to the study. 

Exclusion criteria 

1. Patients more than 60 years of age. 

2. Patients with hypercholesterolemia (total 

cholesterol > 250 mg/dL). 

3. Patients with diabetes mellitus. 

4. Patients with cardiac and/or cerebral 

ischemic vascular disease. 

5. Patients with impaired renal function. 

6. Pre-menopausal women. 

7. Secondary forms of hypertension detected 

by suitable diagnostic procedures. 

8. All current smokers were excluded from 

the study except ex-smokers who have 

left smoking at least 2 years before the 

study. 

All the patients were taken up for the baseline 

brachial artery flow studies (FMD) by a noninvasive 

method using ultrasound system for 

2-dimensional (2D) imaging, fitted with an 

internal ECG monitor and a high frequency 

vascular transducer operated at 10 MHz. The 

study was conducted after overnight fasting 

with patients in supine position at a room 

temperature of 22 to 25 0 C after resting for 30 

minutes. Transducer was placed 

approximately 5 cm proximal to elbow joint at 

a fixed point for imaging brachial artery in the 

longitudinal plane. A segment with clear 

anterior and posterior intimal interfaces was 

selected for continuous 2-D gray scale 

imaging. 

Diameter measurement was taken from one 

intimal surface to the other, measured at end 

diastole taking beginning of R wave on ECG 

interface. Brachial artery flow was measured 

from the mid point of the lumen using pulse 

Doppler. A single person made all the 

measurements. After taking baseline 

measurements, blood pressure cuff tied at 



forearm was inflated to about 50 mmHg above 

systolic blood pressure. After 5 minutes of 

cuff inflation, the cuff was deflated rapidly. 

Scans were recorded from 30 seconds before 

to 120 seconds after the release of occlusion 

including a flow velocity recording 15 seconds 

after the cuff release. For diameter 

measurements readings were taken from 30 

to 90 seconds after cuff deflation and the 

greatest diameter was considered. 

The 20 patients after their baseline FMD 

studies were divided in to two groups of ten 

each at random. One group was started on 

ACE inhibitor Ramipril the dose of which was 

titrated as per the requirements to keep blood 

pressure under control at twice a week 

intervals. The other group was started on 

Beta Blocker Atenolol the dose of which was 

again titrated as above. 

After 8 weeks of initiation of drugs for both the 

groups respectively repeat FMD studies were 

conducted. The patients in each group were 

again taken up for FMD studies after one week 

of washout period (at the end of 9 weeks). 

The patients were then crossed over from one 

group to the other in order to be started on the 

second study medication. 

20 patients 

10 patients on Atenolol 

Atenolol (8 weeks) 

10 patients on Ramipril Ramipril (8 weeks) 

(8 weeks) 

The doses of Ramipril/Atenolol were again 

titrated as per blood pressure readings 

measured at twice a week intervals. After 8 

weeks of completion of second drug therapy, 

FMD studies were again repeated. The 

maximum dose of Ramipril administered was 

10 mg and that of Atenolol 100 mg. 

As it was a cross over study patients 

themselves acted as their own controls. 

The recorded parameter readings were 

tabulated at the end of the study and subjected 

to statistical analysis. 

Results 

There were 13 male patients (65%) and 7 

female patients (35%). The age of subjects 

ranged from 42 to 58 years and the duration 

of hypertension was 1 month to 30 months at 

the time of enrolment. The Basal Metabolic 

Table 1: Baseline characteristics of patients. 

Table 4: Corelation between of Hypertension, 

FMD & Hyperaemia 

Baseline Ramipril Washout Atenolol 

Mean FMD 9.63 ± 1.8 16.48 ± 2.9 11.10 ± 2.4 15.91 ± 2.3 

% change mean FMD 71% 43% 

Change in hyperaemia 25.91 ±3.1 38.89 ±4.2 23.97 ± 3.8 42.88 ± 4.8 

% change in hyperaemia 50% 79% 

Mean SD Minimum Maximum 

AGE (Yrs) 50.80 + 2.4 4.95 42 58 

Duration of Hypertension 

(months) 9.75±3.0 7.35 1.00 30.00 

BMI (Kg/m 2 ) 21.19±1.8 1.37 18.80 23.20 

Mean baseline 

vessel size [mm] 3.87±1.3 1.1 3.1 4.8 

Table 2: Change from Baseline in Systolic BP and 

Diastolic BP in Ramipril and Atenolol treatment 

group (n=20) 

Table 3: Ramipril and Atenolol Within and 

between Treatment Comparison (n=20) 

Mean SD % change Statistical 

Significance 

Baseline 9.63+1.8 4.11 71% P


Table 5: Correlation of Duration of Hypertention 

and Flow Mediated Dilatation (FMD) 

Correlation (r) 

Statistical significance 

Duration HTN and Baseline FMD -0.074 P=0.756 (NS) 

Duration HTN and Ramipril FMD -0.134 P=0.573 (NS) 

Duration HTN and Atenolol FMD 0.039 P=0.869 (NS) 

Table 6: Correlation of duration of Hypertention 

and Hyperaemia 

Correlation (r) 

Statistical 

Significance 

Duration HTN and Baseline Hyperaemia -0.019 P=0.937 (NS) 

Duration HTN and Ramipril Hyperaemia 0.048 P=0.840 (NS) 

Duration HTN and Atenolol Hyperaemia -0.051 P=0.830 (NS) 

Note: HTN means Hypertension 

index (BMI) of the subject ranged from 18.80 

to 23.28 and the mean baseline vessel size 

ranged from 3.1 to 4.8 mm (Table 1). 

The mean systolic blood pressure was 161.1+ 

3.4 mm Hg and diastolic blood pressure was 

89.8+1.1 mm Hg at baseline. 

At the end of 8 weeks of therapy with Ramipril, 

the mean systolic blood pressure decreased 

to 153.7+2.8 mm Hg, A net reduction of 4.6% 

from baseline, which was statistically 

significant (p< 0.001). The diastolic blood 

pressure also decreased to 86.4+1.0 mm Hg 

with Ramipril, a net reduction of 3.8% from 

baseline, which was also statistically 

significant (p= 0.012) (Table-2). 

At the end of 8 weeks of Atenolol therapy, the 

systolic blood pressure dropped to 151.1+2.0 

mm Hg, a net reduction of 6.2%. It was 

statistically significant (p< 0.001). So was the 

case with diastolic blood pressure, which 

significantly dropped to 83.1+1.1 mm Hg, a net 

reduction of 7.5% from baseline (p< 0.001) 

(Table-2). 

Though the net reduction in blood pressure 

with both the drugs was statistically significant 

from baseline, comparative analysis of net fall 

between Ramipril and Atenolol groups was 

statistically insignificant (p=0.072)(Table-2). 

There was a significant increase in the vessel 

diameter post blood pressure cuff release i.e. 

flow mediated vasodilation post 8 weeks of 

Ramipril therapy. There was a 71% increase 

in the vessel diameter in response to 

increased flow of blood post Ramipril therapy, 

which was statistically very significant (p< 

0.001). The same was the case with 

hyperaemia (increased blood flow) also which 

increased 50% as compared to baseline 

post 8 weeks of Ramipril therapy (p=0.001) 

(Table-3). 

There was a significant increase in the FMD 

post Atenolol therapy also, which showed a 

net increase of 43% in vessel diameter as 

compared to the washout period or baseline 

diameter (p=0.008). A significant increase in 

hyperaemia was also seen which amounted 

to a net increase of 79% as compared to 

baseline/washout period (p=0.002)(Table-3). 

However, when Ramipril and Atenolol groups 

were directly compared with each other for 

FMD and hyperaemia, the result were not 

statistically significant (p=0.802 for FMD and 

0.618 for hyperaemia (Table 3). 

There was no significant correlation between 

duration of hypertension with either baseline 

FMD or hyperaemia (r=-0.074, p=0.756 and 

r= -0.019, p=0.937 respectively). 

There was also no significant correlation with 

duration of hypertension and FMD or 

hyperaemia post therapy with Ramipril or 

Atenolol ( Table 4,5&6). 

Discussion 

The relationship of functional alterations of 

blood vessels to the pathogenesis of elevated 

blood pressure is not yet fully known. 

Enhanced vasoconstrictor response is one 

of the features often referred to in relation to 

the mechanisms of elevated blood pressure. 

Another functional change often described is 

an impairment of endothelium dependent 

vascular relaxation. At the level of medium to 

small arteries, this vascular relaxation is 

attenuated in hypertensive subjects. 14 

In addition to this in early 90’s a basic doubt 

was expressed whether endothelium has 

anything to do in hypertension as conflicting 

reports regarding endothelium dependent 

vasodilatation in patients with essential 

hypertension was published. 2, 15 Most of these 

studies have used invasive procedures for 

evaluation of endothelial function 

A non invasive method has been developed 

for the measurement of the dilation of a large 

6 



artery in response to an increase in flow and 

shear stress by ultrasound. 16 By means of this 

method an impairment of flow-mediated 

dilation of the brachial artery has been shown 

in uncomplicated hypertensive patients. 17 The 

brachial artery dilator response can also be 

used to investigate the reversibility of 

endothelial dysfunction in hypertensive 

patients which has been very scarcely studied. 

In the present study we tried to evaluate the 

effect of a angiotensin converting enzyme 

inhibitor (Ramipril) and beta blocker (Atenolol) 

on endothelium dependent flow mediated 

vasodilatation through noninvasive brachial 

artery Doppler studies in patients with 

essential hypertension in an open labelled 

cross over manner. 

In a number of related studies where in FMD 

was compared before and after therapy with 

antihypertensive medications for a duration 

ranging from 8 weeks to 2 years, variable 

results were obtained with different class of 

antihypertensive agents. 18-21 The only 

common factor was that impaired endothelial 

dependent vasodilatation was present in 

hypertensive patients as compared to 

normotensive control population. We could 

not confirm the same as we had not included 

any control normotensive population and 

already a number of studies had proven the 

same fact. 20,21 

Despite being a randomized efficacy trial, no 

control population was needed as being a 

cross over study patients acted as their own 

controls. Our study population number is 

comparable to other similar studies by 

Tzemos and Colleagues 18 where the number 

was 12 and that of Ghiadoni and colleagues 

where the number was 28. 19 Mean age of our 

population [50.80±2.4 years] and sex ratio is 

also comparable to other related studies by 

Croeger and colleagues where it was 45±2 

years and Taddei and colleagues where it was 

51±2 years respectively. 12,22 None of our study 

population was smoker as it was our 

exclusion criteria. But 4 of the male patients 

were ex smokers; quit smoking more than 2 

years before. 

Mean duration of hypertension was 9.75+3.0 

months which was much lower when 

compared to other studies where it ranged from 

12 to 46 months. 10,18,19 The mean baseline 

vessel diameter was 3.87+1.3 mm which was 

slightly lesser as compared to a related study 

by Ghiadoni and colleagues 19 [4.3 mm] 

perhaps due to the western population with 

higher BMI in that study. 

The maximum dose of Ramipril administered 

was 10mg/day and that of Atenolol was 

100mg/day in incremental doses as per the 

blood pressure response. We did not use any 

diuretic in addition to the study drugs as done 

by Tzemos and colleagues 18 who used 50 mg 

of Atenolol with 25 mg hydrochlorothiazide in 

all patients. Instead we titrated the dose of 

either of our study medication at twice weekly 

intervals to achieve adequate blood pressure 

control. 

There was a significant reduction in both 

systolic as well as diastolic blood pressure 

with both our study drugs at the end of 8 weeks 

of therapy. Similar blood pressure reduction 

was also shown in other studies using ACE 

inhibitors or â blockers for a duration ranging 

from 8 weeks to 2 years. 18,19,21 This assumes 

significance as 8 weeks of therapy with 

Captopril or Enalapril did not result in 

significant reduction in blood pressure in one 

of the studies akin to our study. 12 Instead when 

both the drugs were compared with each other 

for extent of blood pressure reduction, the 

result was statistically insignificant (p = 0.072). 

So, both the drugs were equally capable of 

reducing blood pressure in the same time 

duration. 

The same results were observed in a number 

of studies using various antihypertensive 

drugs of different classes as well as different 

antihypertensive medications of the same 

class of drugs. 10,12,18.19 

There was a significant increase in brachial 

artery diameter post shear and hypoxic stress 

on endothelium in the form of cuff occlusion 

and release from 9.63 ± 1.8% to 16.48 ± 2.9% 

a net increase of 71% (P


net FMD increment was statistically not 

significant (p=0.802). 

Extensive review of internet and English 

medical literature did not reveal any study 

where Ramipril was directly studied and 

compared with any other anti hypertensive 

drug regarding reversal or improvement of 

endothelial dysfunction utilizing non invasive 

FMD studies. 

Newer ACE inhibitors such as Perindopril 19 , 

Quinapril and Cilazapril have been adequately 

tested for endothelial function through noninvasive 

FMD studies. Lisinopril is also studied 

in normolipidemic hypertensive patients with 

regards to endothelial function assessed by 

FMD either alone or in combination with statin 

therapy. 21 Quinapril has also been shown to 

be superior to Enalapril in improving 

endothelial dysfunction because of its higher 

tissue specificity and higher tissue 

concentrations. 10 

Ramipril is a widely used ACE inhibitor in 

hypertension, CHF and diabetic population the 

efficacy of which has been amply proven in 

each of the above. 23 We have shown it to be 

efficacious in improving endothelial function 

as well in addition to controlling blood 

pressure in present study. It is not a contention 

nor is the data which says that ACE inhibitors 

do not have class effect and Ramipril is 

showing what others have shown. 29 One of 

the peculiar results of our study was that 

Atenolol significantly improved FMD. This drug 

was not shown to be beneficial in other similar 

studies. 18,19 

It is well established that endothelium 

dependent vasodilatation is impaired in 

patients with essential hypertension. 3 We 

hypothesized that longer the duration of 

hypertension and severe the hypertension, 

more severe or more impaired would be the 

FMD in lieu of much severe endothelial 

dysfunction. However we discovered that 

there was no positive correlation between 

duration of hypertension and baseline FMD 

or FMD following Ramipril and Atenolol 

therapy. We, nevertheless, observed that FMD 

at baseline was positively correlated with the 

diastolic blood pressure at base line. [r=0.511, 

P=0.021]. 

This may be because of the fact that 

endothelial dysfunction is an all or none 

phenomenon irrespective of the duration of 

hypertension or else endothelial dysfunction 

itself is a primary cause of hypertension. 

Diabetes, dyslipidemia, insulin resistance, 

hyperglycemia, renal insufficiency are all 

shown to be associated with endothelial 

dysfunction. Our study was not empowered 

to show any correlation between total 

cholesterol, LDL, HDL, triglycerides, 

creatinine and fasting glucose levels with 

baseline FMD. This was because of the fact 

that dyslipidemia, diabetes and renal failure 

were our exclusion criteria. 

Smoking is known to cause endothelial 

dysfunction and as most of our study 

population was non smokers and few were 

ex-smokers, no correlation could be drawn 

between smoking status and FMD. 

Conclusions 

Both Ramipril and Atenolol improve the 

endothelial dysfunction associated with 

essential hypertension. Demonstration of 

normal endothelial independent vasodilatation 

by agents such as sublingual nitroglycerine 

or intravenous sodium nitroprusside 

administration would have further 

authenticated our results. This was a limitation 

of our study. 

Whether improvement in endothelial function 

is merely due to decrease in blood pressure 

alone or linked with class effect of these 

drugs needs to be validated by larger and 

long-term studies. 

8 



References 

1. Luscher TF, Vanhoutte PM. The endothelium: 

Modulator of cardiovascular function. 

BocaRaton, Fla: CRC Press; 1990. 

2. Panza JA, Quyyumi AA, Brusch JE, Epstein 

SE. Abnormal endothelium dependent 

vascular relaxation in patients with essential 

hypertension. NEJM 1990; 323: 22-27. 

3. Muiesan ML, Salvetti M, Monteduro C, 

Rizzoni D, Zulli R et al. Effect of treatment 

on flow dependent vasodilation of the brachial 

artery in essential hypertension. 

Hypertension 1999; 33: 575-580. 

4. Rodband S. Vascular Caliber. Cardiology 

1975; 60: 4-49. 

5. Joannides R, Haffeli WE, Linder L et al. Nitric 

oxide is responsible for flow dependent dilation 

of human peripheral conduit arteries in Vivo. 

Circulation 1995; 91: 1314-1319. 

6. Grover A, Padginton C, Wilson MF et al. 

Insulin attenuates nor epinephrine induced 

venoconstriction. Hypertension 1995; 22: 

779-784. 

7. Anderson EA, Mark AL. Flow-mediated and 

reflex changes in large peripheral artery tone 

in humans. Circulation 1989; 79: 93-100. 

8. Sorensen KE, Celermajer DS, 

Georgakopoulos D, Hatcher G, Betteridge J, 

Deanfield JE. Impairment of endothelium – 

dependent dilation is an early event in children 

with familial hyper cholesterolemia and is 

related to LP(a) level. J Clin Invest 1994; 93: 

50-55. 

9. 1997 Heart and Stroke Statistical Update. 

Dallas: American Heart Association, 1996. 

10. Anderson TJ, Elstein E, Haber H, 

Charbonneau F. Comparative study of ACEinhibition, 

angiotensin II antagonism and 

calcium channel blockade on flow mediated 

vasodilation in patients with coronary disease. 

BANFF study. J Am Coll Cardiol 2000; 35: 

60-66. 

11. Anderson TJ, Overhisen RW, Haber H, 

Charbonneau F. A comparative study of four 

antihypertensive agents on endothelial 

function in patients with coronary artery 

disease. J Am Coll Cardiol 1998; 31: 1147- 

1154. 

12. Croeger MA, Roddy MA. Effect of captopril 

and enalapril on endothelial function in 

hypertensive patients. Hypertension 1994; 

24: 499-505. Schiffrin EL, Deng L-Y. Structure 

and function of resistance arteries in 

hypertensive patients treated with b Blockers 

or calcium channel antagonists. J Hypertens 

1996; 27: 1046-1053. 

13. Schiffrin EL, Deng LY, Lorochelle P. Effects 

of a b-Blocker or a converting enzyme 

inhibitor on small arteries in essential 

hypertension. Hypertension 1994; 23: 83-91. 

14. Cockcroft JR, Chowienczyk PJ, Benjamin N, 

Ritter JM. Preserved endothelium dependent 

vasodilatation in patients with essential 

hypertension. NEJM 1994; 330: 1036-10400. 

15. Celermajer DS, Sorensen KE, Gooch VM et 

al. Non-invasive detection of endothelial 

dysfunction in children and adults at risk of 

atherosclerosis. Lancet 1992; 340: 1111-1115. 

16. Celermajer DS. Endothelial dysfunction. Does 

it matter? Is it reversible? J Am Coll Cardiol 

1997; 30: 325-333. 

17. Tzemos N, Lim PO, Mac Donald T. Nebivolol 

reverses endothelial dysfunction in essential 

hypertension. A randomized, double blind, 

crossover study. Circulation 2001; 104: 511- 

514. 

18. Ghiadoni L, Magagna A, Versari D, Kardasz 

I, Huang Y et al. Different effect of 

antihypertensive drugs on conduit artery 

endothelial function. Hypertension 2003; 41: 

1281-1286. 

19. On YK, Kim CH, Oh BH, Lee MM, Park YB. 

Effects of angiotensin converting enzyme 

inhibitor and calcium antagonist on 

endothelial function in patients with essential 

hypertension. Hypertension Res 2002; 25: 

365-371. 

20. Danaoglu Z, Kultursay H, Kayikcioglu M, Can 

L, Payzin S. Effect of Statin therapy added 

to ACE inhibitors on blood pressure control 

and endothelial function in normolipidemic 

hypertensive patients. Anadolu Kardiyol Derg 

2003; 3: 338-339. 

21. Taddei S, Virdis A, Mattei P, Salvetti A. 

Vasodilation to acetyl choline in primary and 

secondary forms of hypertension. 

Hypertension 1993; 21: 929-933. 

22. Yusuf S, Sleight P, Pogue J, et al. The Heart 

Outcomes Prevention Evaluation Study 

investigators: Effects of an angiotensinconverting-inhibitor, 

Ramipril, on death from 

cardiovascular causes, myocardial infarction, 

and stroke in high-risk patients. N Engl J 

Med 2000; 342: 145-153. 



Corelation of carotid intimal medial thickness with coronary artery 

disease 

1 

Yogesh Ghimirey, 2 Dhanraj S. Chongtham, 2 Ksh. Birendra Singh, 3 T. Jeeten Kumar Singh, 

4 

S.Subaschandra Singh, 5 M. Kulachandra Singh 

Abstract 

Objective: To study the carotid intimal 

medial thickness (IMT) in patients with 

coronary artery disease (CAD) and to 

establish a correlation of carotid intimal 

thickness with coronary artery disease. 

Methods: One hundred patients, >45years, 

were divided into two groups : group 1 - with 

CAD and group 2 - without CAD and carotid 

artery scanning was performed with high 

resolution 7.5 MHz linear array transducer 

by trained radiologist in Department of 

Radiology, Regional Institute of Medical 

Sciences (RIMS),Imphal. The two groups 

were compared in terms of the number of 

risk factors, average IMT and maximum IMT. 

Values were expressed as mean±standard 

error or a percentage .Student’s unpaired t 

- test and Chi square test were used where 

appropriate. Risk factor count of each 

subject was calculated as the sum of 

conventional risk factors (diabetes mellitus, 

hypertension, dyslipidemia and smoking). All 

statistical analyses were performed using 

SPSS version 15.0 software. Results: The 

average IMTs in Group1 and Group 2 were 

found to be between 0.45mm-1.35mm with 

a mean of 0.83 and 0.25mm-1.00mm with 

a mean of 0.58 respectively. The difference 

1 - PG Student, 2 - Assoc Prof., 3 - Asst. Prof., 5 - 

Prof. & Head, Dept. of Medicine, 4 - Asst. Prof. Dept. 

of Radiodiagnosis, Regional Institute of Medical 

Sciences, Imphal. 

Corresponding author : 

Dr. T. Jeetenkumar Singh, Medicine Department, 

RIMS, dr.jeeten@yahoo.co-in 

in average IMT between the two groups was 

highly significant (p


Materials & Methods 

One hundred patients with age > 45 years, 

irrespective of sex from the medicine wards 

and the outpatient department of the Institute 

were enrolled in the study. They were 

divided into two groups; group1 comprised 

fifty patients with established CAD and 

group 2 comprised fifty randomly selected 

conformable individuals without any history 

of CAD. Diagnosis of CAD was established 

in group1 by a history of documented 

myocardial infarction/stable angina/unstable 

angina or one coronary artery with more 

then 50% stenosis at coronary angiography. 

All patients underwent clinical evaluation 

and biochemical tests. Carotid artery 

scanning was performed with a high 

resolution 7.5MHz linear array transducer 

(Sinoline Versa Plus-Siemens).Two values 

of the carotid IMT were obtained for each 

individual, the average and maximum of 

these two values were considered for 

further analysis. All Statistical analysis were 

done using SPSS version 15.0 Software. 

Results 

The baseline characteristics of the study 

subjects shows no statistical difference 

between the groups. The age of the patients 

ranged from 45 to 84 years in group 1 and 

46 to 87 years in group 2 with a mean of 64 

± 11.9 in group 1 and 60 ± 9.5 in group 2 

respectvely (p = 0.667). There were 

31(62%) males and 19 (38%) females in 

group 1 and 28(56%) males and 22(44%) 

females in group 2 respectively(p = 0.389 

and 0.33). There were 30(60%) 

hypertensive patients in group 1 and 

22(44%)hypertensive subjects in group 2 (p 

= 0.91). 23(46%)subjects in group 1 and 

14(28%) subjects in group 2 had 

dyslipidemia (p = 0.786). 14(28%) subjects 

in group 1 and 28(56%) subjects in group 2 

had diabetes mellitus (p = 0.603).21(42%) 

subjects in group 1 and 17(34%) subjects 

in group 2 weresmokers (p = 0.612) 

(Table-1). 

In the body mass index distribution in CAD 

patiens (group1), 28 patiens (56%) had BMI 

20-24 and 12 subjects (23%) had a BMI 25- 

Table 1. Baseline characteristics of study groups 

Variable Group1 Group2 P Value 

No. of patients 50 50 

Age(years) 64±11.49 60±9.5 0.667 

Males 31(62%) 28(56%) 0.389 

Females 19(38%) 22(44%) 0.33 

Hypertension 30(60%) 22(44%) 0.91 

Diabetes mellitus 14(28%) 28(56%) 0.603 

Dyslipidemia 23(46%) 14(28%) 0.786 

Smoking 21(42%) 17(34%) 0.612 

Table 2. Body mass index (BMI) distribution in 

CAD patients(group 1). 

BMI Males Females Total % 

30 1 1 2 4 

Mean 23.6±3.1 22.2±3.5 

Table 3. Average and maximum carotid intimal 

medial thickness in group 1 and group 2. 

Carotid IMT (mm) Group1 Group2 P value 

Average IMT(mm) 

Mean 0.83 0.58


maximum IMT mean value in group 1 was 

0.93 (0.50-1.50) and 0.67 (0.30-1.20) in 

group 2 with a P value of < 0.001 (Table 3). 

Out of the four risk factors (hypertension, 

diabetes, dyslipidemia and smoking), that 

was considered in the study maximum 

subjects (72) had 1 or 2 risk factors where 

as 19 subjects had 3 risk factors. 8 subjects 

did not have any coronary risk factors where 

as 1 had all the risk factors (Table 4). 

Discussion 

Several studies have shown that carotid IMT 

is strongly associated with cardiovascular 

risk factors.It possibly reflects the 

cumulative deleterious effects of various 

cardiovascular risk factors over time. In the 

Chennai Urban Population Study a 

significantly raised mean IMT values in 

Diabetic patients(0.95±0.31mm) compared 

to non-diabetic subjects (0.74±0. 14mm; 

p


References 

1. Gaziano JM.Global Burden of Cardiovascular 

Disease. Libby, Bonow,Mann,Zipes, Editors. 

Braunwald’s Heart Disease-A textbook of 

Cardiovascular Medicine,8 th Edition, Replika 

Press Pvt Limited,India; 2008:1-21. 

2. Schoen FJ.Blood vessels. Kumar, Abbas, 

Fausto, Editors.Robbins and Cotran-Pathologic 

basis of disease.7 th Edition,Elsevier,India; 

2006:511-554. 

3. David S, Philip JA Robinson,JeremyPR, Jenkins 

Richard WW, Paul AA, Peter W, John MS. 

Textbook of Radiology and Imaging.7 th 

Edition,Churchill Livingston, Philadelphia; 2003: 

460-475. 

4. Mohan V, Ravikumar R,Shanthirani S,Deepa 

R.Intima-media thickness of the carotid artery 

in South Indian Diabetic and non-diabetic 

subjects: The Chennai Urban Population 

Study(CUPS).Diabetologia 2000;43:494-499. 

5. Burke GL, Evans GW,Riley WA,Sharrett 

AR,Howard G,Barnes RW.Arterial wall 

thickness is associated with prevalent 

cardiovascular disease in middle-aged adults: 

The Atherosclerosis Risk in Communities 

(ARIC) Study. Stroke 1995;26:386-391. 

6. Gupta G,Bhargava K,Bansal M, Tandon S, 

Kasliwal RR.Carotid Intima Media Thickness 

and Coronary Artery Disease:An Indian 

perspective. Asian Cardiovasc Thorac Ann2003; 

11:217-221. 

7. Visona A, Pesavento R, Lusiani L,Bonanome 

A,Cernetti C,Rossi M.Intimal medial thickening 

of common carotid artery as indicator of 

coronary artery disease.Angiology 1996;47:61- 

66. 

8. Geroulakos G,Gorman DJ, Kalodiki E, Sheridan 

DJ,Nicolaides AN. The Carotid Intima-Media 

Thickness as a marker of the presence of severe 

symptomatic coronary artery disease. Eur 

Heart J 1994;15:781-785. 



Clinical profile and management of deep neck space infections 

1 

Aniruddha Majumder, 2 O. Priyokumar Singh, 3 S.Thingbaijam, 4 H. Priyoshakhi Devi, 5 R.K. Bedajit 

Abstract 

Objective: To study the clinical profile and 

different modalities of treatment in deep neck 

space infections. 

Method: A prospective study of fifty 

consecutive cases of deep neck space 

infection that were treated in the department 

of ENT, Regional Institute of Medical 

Sciences, Imphal (Manipur) during a period 

of two years from August 2004 and July 2006 

were evaluated for the clinical profile, 

laboratory findings and results of medical and 

surgical managements. Patients with proven 

deep neck space infection and abscess of all 

age group were included in the study 

irrespective of sex, religion, duration of illness 

and severity of the condition. Results: Deep 

neck space infections were most prevalent in 

the 3 rd and 4 th decades of life, males affecting 

more than females. Pain in and around the 

neck was the most common presenting 

symptom (76% of the cases) and swelling of 

the neck was the most common examination 

finding (90% of the cases) in the present study. 

The most common location of the abscess 

was at the parapharyngeal space (44% of the 

cases). Out of the 50 cases treated, only 3 

patients (6%) developed complications in the 

form of mediastinitis. 

1. RMO cum Clinical Tutor, Dept. of ENT, NRS Medical 

College, Kolkata, 2. Registrar, .3 Associate Professor, 

4. Professor, 5. Asst. Prof., Department of 

Otorhinolaryngology, Regional Institute of Medical 

Sciences, Imphal, 

Corresponding author 

Dr. HP Devi, Professor, Department of ENT, RIMS 

14 

Conclusion: Deep neck space infections are 

potentially life threatening conditions affecting 

any age or sex group. If diagnosed early and 

treated promptly, complications may be 

avoided. Infections with evidences of 

suppuration are better treated with both 

surgical drainage and medical therapy. 

Key words: Deep neck space infections, 

mediastinitis. 

Introduction 

Deep neck space infections affect the potential 

spaces of the neck bounded by the deep 

cervical fascia of the neck. In the pre-antibiotic 

era, infections of the deep neck spaces were 

fairly common and were a source of 

considerable morbidity and mortality. Although 

the advent of modern antibiotics has reduced 

the overall incidence of deep neck space 

infections, they still occur in the general 

population, with a definite potential for 

significant morbidity and even mortality if not 

diagnosed and treated promptly. 

Infections of the deep neck spaces are 

challenging to the physicians because of 

several reasons. Complex anatomy and deep 

location in close proximity with several 

important vital structures are the main factors. 

The deep neck spaces have a real and 

potential avenue of communication with each 

other allowing easy and fast spread of 

infections to the adjacent spaces. Moreover, 

certain deep neck space infections can extend 

to other parts of the body (e.g. Mediastinum, 

coccyx). To gain access to these spaces, the 



superficial tissues and various vital structures 

must be crossed with potential risk of injuring 

these structures. 

Materials and Methods 

Fifty consecutive cases of deep neck space 

infection that were treated in the department 

of ENT, Regional Institute of Medical 

Sciences, Imphal (Manipur) during a period 

of two years from August, 2004 and July, 2006 

were evaluated for the clinical profile, 

laboratory findings and results of medical and 

surgical managements. Patients with proven 

deep neck space infection and abscess of all 

age group were included in the study 

irrespective of sex, religion, duration of illness 

and severity of the condition. Patients with 

pure peritonsillar abscess, superficial 

infections of the external neck wounds 

(surgical or traumatic) and abscess related 

to fractures were excluded from the study. 

The diagnosis was made from the typical 

clinical findings and the laboratory tests. 20 

cases were treated medically with broad 

spectrum antibiotics and other supportive 

treatments. 30 cases were treated with both 

medical and surgical procedures. 

Results 

The youngest patient in the study was a 3 

months old male child and the eldest a 60 

years old male patient. Most of the cases were 

in the third and fourth decades of life, of which 

maximum cases 16 (32%) were in the age 

group between 31 and 40 years. The mean 

age of the patients in the present study was 

31.3 years ± 13.9 (S.D. -13.9). Out of the 50 

cases, 29 (58%) were male and 21 (42%) 

were female. (Table 1) 

Table 2. Shows the presenting complaints of 

the cases. The symptoms included pain in 

and around the neck in 38 (76%), fever in 32 

(64%), and swelling in the neck in 31 (62%) 

patients. 

Table 3 shows the distribution of clinical 

examination findings. Neck swelling was the 

commonest examination finding which was 

seen in 4 (90%) followed by dental 

abnormality in the form of carious tooth and 

periodontal disease in 15 (30%). Trismus 

Table 1. Age distribution. 

Age (years) No. of patients Percentage 

(n=50) 

< 1 1 2% 

1-10 4 8% 

11-20 4 8% 

21-30 15 30% 

31-40 16 32% 

41-50 8 16% 

51-60 2 4% 

Total 50 100% 

Table 2. Presenting complaints. 

Symptoms No. of patients Percentage 

(n=50) 

Pain 38 76% 

Fever 32 64% 

Swelling neck 31 62% 

Dysphagia/ 

odynophagia 21 42% 

Respiratory difficulty 7 14% 

Toothache 3 6% 

Table 3. Clinical examination findings. 

Signs 

No. of patients Percentage 

(n=50) 

Neck swelling 45 90% 

Dental abnormality 15 30% 

Fluctuance 14 28% 

Oropharyngeal 

abnormalities 11 22% 

Trismus 9 18% 

Laryngeal 

abnormalities 9 18% 

was seen only in 9 (18%) of the cases. 

Fig 1 shows the distribution of cases in relation 

to the anatomical sites. In the present study, 

parapharyngeal space was most commonly 

involved (44%), followed by submandibular 

space (28%) and retropharyngeal space 

(20%). Mediastinum was involved in only 3 

cases (6%) and in 14% of the cases, multiple 

spaces were involved. 

Figure 2 shows distribution of cases 

according to the aetiology. Out of the 50 



cases, aetiology was not established in 20 

(40%). Among the known etiological factors, 

dental origin was seen in 14 (28%), 

oropharyngeal infections in 6 (12%), trauma 

and foreign body impaction in 4 (8%). 

Fig. 1. Pie chart showing distribution of cases 

according to the location of abscess. 

isolated was Streptococcus pyogenes (56%), 

followed by Klebsiella sp. (28%), 

Staphylococcus aureus (16%), Neisseria sp. 

(4%) and Haemophilus sp. (4%). 

Table 4. Pathogens isolated from the neck 

abscesses. 

Pathogens No.of cases Percentage 

(n=25) 

Streptococcus 

pyogenes 14 56 

Klebsiella 7 28 

Staphylococcus 

aureus 4 16 

Neisseria sp. 1 4 

Haemophilus sp. 1 4 

Fig. 2. Distribution of cases according to the 

aetiology 

In the present study, complications in the form 

of mediastinitis were seen in only 3 patients 

(6%) with no mortality. 

Figure 3 shows the treatment modalities in 

the present study. Out of the 50 cases, 20 

patients (40%) were managed conservatively 

with intravenous antibiotics and other 

supportive treatments. The remaining 30 

cases (60%) were managed by combination 

therapy, i.e. surgical interventions and 

antibiotics and other supportive measures. 

Discussion 

Fig 3. Treatment modalities. 

Out of the 50 cases, culture and sensitivity 

test was done in 35 cases out of which culture 

was positive in 25 cases (71.42%). Table IV 

shows the pathogens isolated from the 

abscesses. The commonest organism 

16 

Deep neck infection can occur in any age as 

suggested in the present study. The youngest 

patient in the present study was a 3 months 

old boy while the eldest being a 60 years old 

male. The most common age range affected 

by deep neck space infection was 31 – 40 

years and the mean age in the present was 

31.3 years a finding similar in line with 

others 1,2,3 . 

Deep neck space infections were more 

common in the males than females. In the 

present study, we found that 58% of the cases 

were males and 42% of the cases were 

females. The present study findings are 

comparable to the findings of other studies 1,3 . 

In the present study, pain in the neck was the 

most common symptom in 38 (76%) followed 

by fever in 32 (64%) smilar to other studies 1,4,5 . 



Swelling in the neck was the most common 

physical finding in the present study seen in 

45 (90%) cases. Next commonest finding was 

dental pathologies which were seen in 15 

(30%) of the cases. Similar findings were 

reported in other studies 1,6,7 . 

Parapharyngeal abscess (44%) was the 

commonest type of deep neck space 

abscess in the present study followed by 

submandibular space infection (28%) and 

retropharyngeal abscess (20%). The present 

findings are comparable to the findings of other 

studies 3,7,8 . 

In the present study the etiology of the deep 

neck space abscesses were identified in 60% 

of the cases (30 out of 50 cases). Among the 

known etiological factors, dental infection was 

the most common factor which was seen in 

28% of the cases, followed by recent infection 

of tonsils or pharynx (24% of the cases). 

Etiology was unknown in 40% of the cases. 

Wang et al 9 . Found in their study that upper 

respiratory tract infection was the most 

common source followed by the odontogenic 

origin. Sethi and Stanley 4 in their series of 64 

cases found that in 61% of the cases the 

causative factors could be detected but in 

39% of the cases etiology was unknown. 

Out of the fifty cases in the present study, 

culture and sensitivity was done in 35 cases 

out of those 35 cases 25 cases were culture 

positive. In aerobic culture Streptococcus 

pyogene (56%) and Klebsiella (28%) were the 

most common organism isolated. 

Staphylocoocus aureus was isolated in 4 

cases (16%). Neisseria sp. and Haemophilus 

influezae was isolated in 1 case (4%) each. 

Sethi and Stanley 4 found in their study that 

Streptococcus sp. as the most common 

pathogen. This is similar with the study done 

by Kamath et al 7 . 

Management of the deep neck space 

infections involved broad spectrum antibiotics 

with or without surgical drainage. In the 

present study of 50 cases, 20 patients (40%) 

were managed conservatively with antibiotics 

and other supportive medications, and the rest 

30 cases (60%) were managed with both 

surgical drainage and broad spectrum 

antibiotics. A group of 20 patients who were 

managed conservatively belong to children 

and young age group. Our experience 

suggests that some patients with apparent 

abscess formation may also respond 

favourably to antimicrobial therapy only without 

surgical intervention. Our findings and 

observations in the treatment of deep neck 

space infections are similar with the study 

conducted by Beck 10 and Levitt 11 . De Marie et 

al 12 had described successful resolution of 

neck space infections, including patients with 

frank abscess, with conservative therapy only. 

In the present study of 50 cases, 47 patients 

(94%) were discharged without complications. 

Mean abscess related hospital stay was 9.5 

days. In the present series, 3 cases (6%) 

developed complications in the form of 

mediastinitis, out of which one patient died of 

the complication giving a mortality rate of 2%. 

This is comparable to the mortality rate of 3% 

quoted by Kamath et al 7 . Mediastinal 

involvement calls for prompt management 

with high dose intravenous antibiotics, 

thoracotomy and drainage as it is the major 

cause of mortality. 

Conclusion 

Deep neck space infections are potentially life 

threatening conditions affecting any age or sex 

group. Most of the cases are in their 3 rd or 4 th 

decade of life with a male preponderance. 

Early diagnosis and timely interventions are 

the mainstay of management of deep neck 

space infections and fatal complications can 

be avoided. Infections with evidences of 

suppuration are better treated with both 

surgical drainage and medical therapy. 



References 

1. Tom MB and Rice DH: Presentation and 

management of neck abscess: A retrospective 

analysis. Laryngoscope 1998; 98: 877-881. 

2. Chen MK, Wen SY, Chang CC, Huang TM and 

Hsiao CH: predisposing factors of life 

threatening deep neck infection: Logistic 

Regression Analysis of 214 cases. The Journal 

of Otolaryngology 1998; 27: 141-144. 

3. Parhiscar A and Gadyhar EL: Deep neck 

abscess: A retrospective review of 210 cases. 

Ann Otol Rhinol Laryngol 2001; 110: 1051-1054. 

4. Sethi DS and Stanley RE: Parapharyngeal 

abscesses. The Journal of Laryngology and 

otology 1991; 105: 1025-1030. 

5. Tanti Pei, Changyin L, Huang CY, Hsum CC, 

Wang CR and Yienlin T: Deep neck infections 

in children. J. Microbiol Immunol Infect 2001; 

34:287-292. 

6. Broughton RA: Nonsurgical management of 

deep neck infections in children. Paediatric 

Infect Disease Journal 1992; 11: 14-19. 

7. Kamath MP, Shetty AB, Hegde MC, 

Sreedharam S, Bhojwani K, Padmanabhan K, 

Agarwal S, Mathew M and Kumar R: 

Presentation and management of deep neck 

space abscess. Indian journal of 

Otolaryngology and Head and Neck Surgery 

2003; 55(4): 270-274. 

8. Gadyhar EL, Jeffery HA, Ashok Shaha, Frank 

EL and Brooklyn NY: Changing trends in deep 

neck abscess : a retrospective study of 

hundred and ten patients. Oral med oral pathol 

1994 ; 77:446-450. 

9. Wang FL, Wen RK, Shih MT and Huang KJ: 

Characterization of life threatening deep cervical 

space infection: A review of one hundred ninety 

six cases. Americal Journal of Otolaryngology 

2003; 24(2): 111-117. 

10. Beck AL: The influence of chemotherapeutic 

and antibiotic drugs on the incidence and 

course of deep neck space infection. Ann Otol 

Rhinol Laryngol 1952; 61: 515-532. 

11. Levitt GW : The surgical treatment of deep neck 

infections. Laryngoscope 1971; 81(3): 403-411. 

12. de Marie S, Tjon A, Tham RT, Vander MAC, 

Meerdink G, Vanfurth R, Vander MJW: Clinical 

infections and nonsurgical treatment of 

parapharyngeal space infections complicating 

throat infection. Rev Infect Dis. 1989; 11: 975- 

982. 

18 



A comparative study between cemented and uncemented bipolar 

hemiarthroplasty in the treatment of fresh fracture of femoral neck in the 

elderly patients 

1 

Umesh Singh T., 1 Kesho Singh Th., 2 Sanjib Waikhom, 3 S.N.Chishti, 4 S.N.Singh, 5 Ch.A.K.Singh 

Abstract 

Objective : To evaluate the differences in 

functional outcomes of the two treatment 

groups (Cemented and Uncemented bipolar 

hemiarthroplasty) for the treatment of fresh 

fractures of femoral neck in elderly patients 

attending RIMS hospital, Manipur. Material 

and Methods: The study was carried out in 

30 consecutive elderly patients attending 

Emergency and Outpatient department (OPD) 

of our institute with fresh fracture (


The use of Bipolar prosthesis is considered 

as a suitable compromise between unipolar 

hemiarthroplasty and total hip replacement. 5 

Bipolar hemiarthroplasty for femoral neck 

fracture in the elderly is a sound treatment 

modality as restoration of function, relief of pain 

and early mobilization are achieved with 

acceptable rate of complications, compared 

with conventional hemiarthroplasty. 

Charnley J 6 for the first time reported on the 

clinical use of cemented (Polymethylmethacrylate, 

PMMA) femoral prostheses. 

Various authors have observed that 

hemiarthroplasty of the hip with cemented 

femoral prosthesis is a technically easy 

procedure that allow immediate and excellent 

prosthetic fixation. The purpose of this study 

is to analyse the differences in patient 

outcome after hemiarthroplasty for femoral 

neck fracture using uncemented press fit or 

cemented bipolar prostheses. 

Material And Methods: 

The study group comprises of 30 consecutive 

patients of which 19 were women and 11 were 

men with mean age of 73 years ( range 60-85 

years) attending the Emergency and 

Outpatient Department(OPD) of Regional 

Institute of Medical Sciences (RIMS), Imphal 

between the period of June 2006 to November 

2008 with fresh fractures (< 21 days) of the 

femoral neck. All the fractures were either 

Garden type III or type IV and are treated with 

Bipolar hemiarthroplasty. The patients were 

alternately allocated into one of the 2 groups 

of equal sample size. Group 1 consists of 15 

patients and treated with uncemented bipolar 

prosthesis using press fit technique and group 

2 had the same number of the patients but 

treated with cemented bipolar prostheses. 

Both the groups were comparable in mean 

age, sex, pre fracture level of activity. And the 

patients with pathological fractures, medical 

co morbidities and infections in and around 

operative site were excluded and the 

procedures followed were in accordance with 

the ethical standard of the institute. All the 

patients were assessed pre-operatively with 

radiographs of pelvis showing both hips in AP 

and lateral views. The fractures were 

classified using Garden’s classification. Of the 

20 

30 displaced fractures, 4 were of Garden’s 

type III and 26 of type IV. 

CEMENTED 

UNCEMENTED 

Figure 1: Uncemented bipolar prosthesis 

Figure 2: Cemented bipolar prosthesis. 

All the patients were operated under spinal 

anaesthesia using a posterior Moore’s 

approach to the Hip using uncemented or 

cemented bipolar prostheses. The cement 

used was DePuy Medium viscosity bone 

cement (Johnson &Johnson company). 

Post operatively mobilization started from 2 nd 

day. Reduction and position of the prosthesis 

was confirmed radiologically. Suction drain 

was removed on 2 nd day. The patients were 

discharged on 10 th post operative day with the 

advice not to squat. The patients were followed 

up for a minimum of 2 years, every month for 

the first 6 months and then at and interval of 6 

months. Functional outcomes were assessed 

using the Harris’s Hip Scoring System. 7 

Results: 

There are 10 males and 5 females in the 

uncemented group and 9 males and 6 

females in the cemented group. The mean 

age in the uncemented group was 73 years 

(range 60-85 years) and in the cemented 

group was 73.3 years (range 60-85 years). 

The commonest size of prostheses used was 

45 mm (Table 1). 

The average operating time of uncemented 

groups was 64 minutes as against 90.3 

minutes for cemented group (the difference 

in mean was statistically significant, 

p < 0.0001 ). The average blood loss in the 

cemented group was 436.7 ml and 306 ml in 

the uncemented group; a significant difference 



TABLES 

Table 1: Size of prostheses used. 

SIZES CEMENTED UNCEMENTED 

39 mm 2 1 

41 mm 2 3 

43 mm 2 2 

45 mm 8 8 

51 mm 1 1 

Table 2: Comparison of the operating time, intraoperative 

blood loss and intraoperative 

blood transfusion and length of hospital 

stay. 

MEAN CEMENTED UNCEMENTED Student 

VALUE 

t-Test 

Operating time 

( minutes) 90.3 64 P= 0.0001 

Intra-operative 

blood loss ( ml) 436.7 306 P=0.0025 

Intra-operative blood 

transfusion ( units) 1.26 1.13 P=0.00056 

Hospital stay 

( days) 23.7 22.8 P > 0.05 

Table 3: Complications. 

COMPLICATIONS CEMENTED UNCEMENTED 

Hypotension during surgery 4 1 

Dislocation 1 0 

Fissuring of proximal femur 1 0 

Urinary tract infection 2 2 

TOTAL 08 03 

Table 4: Post-operative Harris Hip score gradings. 

SCORE RANGE GRADING CEMENTED NCEMENTED 

(Points) n ( % ) n ( % ) 

90-100 Excellent 1 (6.7) 1 (6.7) 

80-89 Good 9 (60) 4 (26.7) 

Table 5: comparison of functional results. 

RESULTS CEMENTED UNCEMENTED Chi Square 

n ( % ) N( % ) test 

Thigh pain 2 ( 13.3) 7 (46.7) p = 0.0001 

Groin pain 3 (20) 2 (13.3) p > 0.05 

Range of CEMENTED UNCEMENTED Student t-test 

motion 

Flexion 104 o 103 o p > 0.05 

Abduction 38 o 38 o p > 0.05 

Table 6: comparison of Radiographic 

results. 

RESULTS CEMENTED UNCEMENTED Chi Square 

n ( % ) n ( % ) test 

Femoral stem 

loosening 3 (20) 6 (40) p = 0.025 

Heterotopic 

calcification 4 (26.7) 2 (13.3) p = 0.05 

Acetabular 

erosion 2 (13.3) 3 (20) p = 0.225 

Protrusio 

acetabuli 0 ( 0) 1 (6.7) p > 0.05 

statistically ( p =0.0025 ). The mean unit of 

blood transfused for the uncemented group 

was 1.13 units as against 1.26 units of the 

cemented group; a finding of statistically 

significance (p=0.00056). The average 

hospital stay was 23.7 days and 22.8 days 

respectively for cemented and uncemented 

groups (Table 2). The difference was not 

significant statistically (p > 0.05) 

Complications of operation were analysed and 

noted in table 3. 

The occurrence of heterotopic calcification 

was more common in the cemented group. 4 

and 2 patients in cemented and uncemented 

group respectively. There was one late 

periprosthetic femoral fracture distal to the tip 

of a well fixed uncemented stem secondary 

to a fall. 

Final functional outcome was assessed using 

Harris Hip scoring system at 2 years post 

operative. The cemented group had a higher 

score (80 versus 74, cemented versus 

uncemented, p = 0.01; table 4).In the final 

analysis cemented group had functionally and 

radiographically better outcome than 

uncemented although perioperative 

complications were marginally more in 

cemented group (Table 5,6). 

Discussion 

Cementing the femoral prostheses can 

provide excellent immediate fixation of the 

prosthesis ( even in osteoporotic bone ) so 

that the patients can start mobilization and 

weight bearing soon after surgery. Lo W H et 

al 8 studied the result of using cemented 

versus uncemented Bateman bipolar 

hemiarthroplasty for femoral neck fractures 



and concluded that better results were obtained 

using a cemented bipolar hemiarthroplasty. 

They found a statistically significant higher 

post operative Harris hip score. Emery RJH 

et al 9 also found similar good results with 

cemented prostheses following a randomized 

trial of cemented Thompson and uncemented 

Moore stem bipolar hemiarthroplasty. In the 

present study, we also found significantly 

higher Harris hip score in the cemented group 

than in the uncemented group (p = 0.01). 

Our study also showed more than three fold 

increase in incidence of thigh pain in the 

uncemented group and was similar to that 

reported by Lo W H et al 8 . Femoral stem 

loosening was responsible for the thigh pain 

in the both groups.Again, increased incidence 

of femoral loosening in the uncemented group 

in our study was attributed to the failure of 

achieving ‘ pressfit’ ( a technical defect) and 

the ability of the stem to rotate in the medullary 

canal in the absence of fixation with cement 

producing a variable version upon weight 

bearing. This observation was also put forward 

by Khan R J et al 10. The incidence of 

acetabular erosion in cemented group in our 

study was comparable with the finding of John 

D et al 11 , use of cement didn’t significantly 

increase the chance of acetabular erosion and 

protrusion of the prosthesis in the acetabulum. 

In fact more incidence of acetabulum erosion 

/ protrusio acetabuli was found in the 

uncemented group in the present study. The 

observation of increased operating time and 

increased blood loss in the cemented group 

is well comparable with many contemporary 

studies 8,9 . 

As regards to wound infection in relation with 

surgical approach, Chan RNW et al 12 found 

an increased incidence of wound infection in 

posterior approach as it is the site in a 

contaminated area. The absence of wound 

infection in our present study which used 

posterior approach to hip may be related to 

proper maintenance of suction drain, careful 

bladder management, trained surgeon 

performing the procedure shortening the 

operating time with proper surgical technique 

and meticulous selection of prophylactic as 

well as post operative antibiotics. Godsiff SP 

et al 13 also found no incidence of wound 

infection while comparing cemented and 

uncemented femoral components in the ring 

hip prosthesis of 58 patients but using 

posterior approach. Although this study 

involves a smaller number of participants, over 

all the rate of dislocation of 3.3 % is consistent 

with or even lower than those of many 

contemporary series (2% by John D et al 11 ). 

Maini PS et al 14 found that open reduction is 

required in all dislocations of cemented bipolar 

prostheses, We found no difficulty in reducing 

the dislocated cemented prosthesis by routine 

closed method and the patients did well later. 

Our finding compares well with that of Barnes 

CL et al 15 . There was more heterotopic 

calcification in the cemented group than in the 

uncemented group. Lo WH et al 8 also showed 

significant increase in the incidence of 

heterotopic calcification in the cemented 

group than in the uncemented group. 

In our study no death occurred during 

hospitalization or follow up period which is also 

the finding of at least on series by Vugt ABV et 

al 16 involving 22 patients. Zero mortality rate 

in either group may be partly explained by the 

facts of smaller number of participants, shorter 

follow up period and most importantly 

exclusion of patients with major medical comorbidities. 

Conclusion 

Bipolar hemiarthroplasty is a common 

surgical treatment option for the treatment of 

femoral neck fractures in the elderly. 

Cemented bipolar hemiarthroplasty offers the 

major advantage of immediate weight bearing 

mobilization after surgery. The immediate 

stability afforded by cementing the prosthesis 

results in freedom from pain and a sense of 

security in the early post-operative period with 

consequent improvement in morale. 

22 



References 

1) Khan RJ, Macdowell A, Crossman P, Keene 

GS. Cemented or uncemented 

hemiarthroplasty for displaced intracapsular 

fractures of hip – a systemic review. Injury 2002; 

33(1): 13-17. 

2) Garden RS. Low angle fixation in fractures of 

the femoral neck. J Bone Joint Surg 1961; 43- 

B: 647-663. 

3) Bently G. Impacted fractures of the neck of the 

femur. J Bone Joint surg 1968; 50-B:551-561. 

4) Sorlide O, Morster A, Raugstad TS. Internal 

fixation versus primary prosthetic replacement 

in acute femoral neck fractures: a prospective 

randomized clinical study. Br. J Surg 1979; 66: 

56-60. 

5) Bateman JE. Single-Assembly total hip 

prostheses: A preliminary report. Orthop Dig 

1974; 2: 15-22. 

6) Charnley J. Acrylic Cement in Orthopaedics 

Surgery. E and S Livingstone, Edinburg; 1970. 

7) Harris WH.Traumatic arthritis of the hip after 

dislocation and acetabular fracture: treatment 

by mold arthroplasty. J Bone Joint Surg 

[Am]1969;51-A:737-55. 

8) Lo W H, Chen WM, Huang CK, Chen TH, Chiu 

FY, Chen CM. Bateman bipolar 

hemiarthroplasty for displaced femoral neck 

fractures. Uncemented versus cemented. Clin 

Orthop Relat Res 1994; 302: 75-87. 

9) Emery RJH, Broughton NS, Desai K,Bulstrode 

CJK, Thomas TL. Bipolar hemiarthroplasty for 

subcapital fracture of femoral neck: a 

prospective randomized trial of cemented 

Thompson and uncemented Moore stems. J 

Bone Joint Surg 1991; 73-B: 322-324. 

10) Khan RJ, Macdowell A, Crossman P, Keene 

GS. Cemented or uncemented 

hemiarthrosplasty for displaced intracapsular 

fractures of hip-a systemic review. Injury 2002; 

33(1): 13-17. 

11) John D, Micheal D. Treatment of fractures of 

the femoral neck by replacement with the 

Thompson prosthesis. J Bone Joint Surg 1976; 

58-B: 279-286. 

12) Chan RNW, Bath and Hoskinson J. Thompson 

prostheses for fracture neck of femur: a 

comparison of surgical approaches. J Bone 

Joint Surg 1975; 57-B: 437-443. 

13) Godsiff SP, Emery RJH, Heywood-Waddington 

MB, Thomas TL. Cemented versus uncemented 

femoral components in the ring hip arthroplasty. 

J Bone Joint Surg 1992; 74-B: 822-824. 

14) Maini PS, Talwar N, Nijhawn VK, Dhawan M. 

Results of cemented bipolar hemiarthroplasty 

for fracture of the femoral neck: 10 years study. 

Indian J Orthop 2006; 40: 154-156. 

15) Barnes CL, Berry DJ, Sledge CB. Dislocation 

after bipolar hemiarthroplasty of the hip. J 

Arthroplasty 1995; 10: 667-669. 

16) Vugt ABV, Osterwijk WM, Goris RJA. 

Osteosynthesis versus endoprosthesis in the 

treatment of unstable intracapsular hip fractures 

in the elderly: a randomized clinical trial. Arch 

Orthop Trauma Surg 1994; 113: 39-45. 

17) Asif N, Sherwani MKA. Bipolar 

hemiarthroplasty of the hip: a review of eighty 

cases. Ind J Orthop 1999; 33: 23-25. 

18) Browett JP. The uncemented Thompson 

prosthesis. J Bone Joint Surg 1981; 63-B: 634- 

635. 



A clinical study of measurement of axial length of the eye by A-scan 

ultrasonography in the indigenous people of Manipur 

1 

A. Suchitra Devi, 2 Lhingkhohat Haokip, 1 Ibohal Salam, 3 Rajkumari Bigyabati, 4 Phani Sarkar 

Abstract 

Objective : To find out the axial length of the 

eyeball and the correlation between the axial 

length and the power of IOL in the indigenous 

population of Manipur. Methods : 500 patients 

aged 10 years to 90 years attending RIMS Eye 

OPD and those admitted in Eye ward from 

October 2005 to September 2007 were 

enrolled for the study. Echorule S. No. 1714 

(Biomedix) A- scan ultrasonography was used 

to measure the axial length of the eye. The 

findings obtained were tabulated and analysed 

according to sex, age, laterality of the eyes 

and upon their caste/ ethnicity. Results : The 

average axial length was 22.51 mm±0.83. The 

mean axial length of men was 22.73 mm±0.87 

and 22.38 mm ±0.79 for women. The finding 

of shorter axial length is responsible for high 

power of IOL calculated before cataract 

surgery. Conclusion : The axial length of the 

eyeball is shorter in the indigenous people of 

Manipur(22.51±0.83) compared to the normal 

value of 23.6 mm. The finding of shorter axial 

length is responsible for high power of IOL 

calculated before Cataract surgery. 

Key words : Axial length, biometric procedure, 

indigenous population 

1. Associate Prof. of Ophthalmology, RIMS 2. 

Ophthalmologist, J.N. Hospital, Imphal 3. Postgraduate 

Trainee In Ophthalmology, RIMS 4. Asst. 

Prof. of Ophthalmology, Agartala Medical College 


Dr. A. Suchitra Devi, 

Associate Prof., Department of Ophthalmology, 

RIMS 

Introduction 

The axial length of the eye can be measured 

by the following methods: 

1. Ultrasonic method 

2. Radiologic method 

3. Optical method 

Ultrasonic method is the most easy and 

accurate method which is commonly done by 

A-scan. 1,2,3 The accuracy of axial length 

measured by A-scan is generally taken to be 

within 0.1 mm and a high degree of accuracy 

of measurement is mandatory especially 

when used in calculating IOL power as an 

error of 1 mm leads to miscalculation of 2.5 

D to 3.5 D. 9 

Ultrasound are waves of high frequencies 

greater than 20 KHZ. These high frequencies 

produce short wavelength (


reflected predictably. It is this property that 

makes ultrasound useful for diagnostic 

1, 12, 13 

purpose. 

A frequency of 10MHZ is used in diagnostic 

ophthalmic ultrasonography. 12 

Material and methods 

The study was conducted on 500 patients 

aged 10 years to 90 years attending Eye OPD 

and / those admitted in the Eye Ward, RIMS 

Hospital, Imphal from October 2005 to 

September 2007. The biometric procedure 

was explained to the patients. Echorule S No 

1714 (Biomedix) A- scan ultrasonography was 

used to measure the axial length of the eye. 

The instrument settings were properly 

checked before commencement of 

examination. Anaesthetic drops (4% 

Xylocaine) are instilled into both the eyes of 

the patient. The eye was inspected for 

presence of excess of fluid (e.g. anaesthetic 

drops or tears). Then the tip of the probe was 

cleaned with rectified spirit, and procedure of 

measurement was started step by step. 

Step I:- The patient was seated upright in a 

chair near the Echorule so that that the screen 

was easily seen. 

Step Ii:- The transducer was held with right 

hand and the palm rest on the patient ’ s face 

for stability. 

Step III:- The patient gazed steadily at fixation 

target while the two lids were wide open with 

the left hand. 

Step IV:- The transducer was brought near the 

cornea directed along the optical axis and just 

touched cornea gently. 

Step V:- The transducer should not be on the 

cornea for more than 10 seconds, nor slide 

over. If repositioning is required the probe 

should be removed from the cornea, realigned 

and the contact re-established. 

StepVI :- The transducer is pulled back from 

the cornea once the Echorule in Automatic 

mode beeps twice and the scan is evaluated 

for anterior chamber depth to see if cornea 

has been pressed or not and the foot switch 

is depressed to save the reading. The patient 

was asked to blink to keep the cornea moist. 

Step VII:- The procedure was repeated until 

at least 3 high quality readings were obtained 

from the right eye and the same procedure 

was repeated on the left eye. After the 

completion of the procedures antibiotic eye 

drops were instilled into both the eyes. 

Results 

The data was processed through SPSS-13 

version with some well known statistical 

formulae like x 2 – test, F-test and correlating 

co-efficient “r”, wherever was found suitable 

and necessary, and interpretation was made 

accordingly. 

Table 1. Comparison of Mean ± S.D. of age & axial 

length of eyes between sex 

Male (185) Female (315) t- values p- values 

Mean± S.D. Mean± S.D. 

Age (year) 37.16±19.23 37.33±19.77 0.092 0.927 

Right eye 22.75±0.88 22.41±0.84 4.336 0.000*** 

Left eye 22.71±0.89 22.35±0.78 4.654 0.000*** 

Both eyes 22.73±0.86 22.38±0.78 4.629 0.000*** 

* - Significant at 5% Probability level 

** - Significant at 1% Probability level 

*** - Significant at 0% Probability level 

Table 1 reveals comparison of mean with 

standard deviation of age in years and axial 

length of eyes between male and female. 

Further, it shows corresponding test-values 

along with p-values. 

Insignificant values of p (= 0.927) for age 

highlights that there is an uniform structure of 

age over the sex and therefore age is blind in 

the present study. However very highly 

significant p- values (=0.000) for sex indicates 

that male has certainly more longer axial length 

than that of his counterpart female. This is 

true in right, left and both eyes. 

Table 2. Results of the correlation 

co- efficient “r” 

Between 

r-values 

Age & right eye -0.061 

Age & left eye -0.061 

Age & both eyes -0.063 

Right & left eyes 0.887** 

Right & both eyes -0.972** 

Left & both eyes 0.970** 



Association between age of the patient and 

axial length of the eye as well as between the 

eyes were examined by the formulacorrelation 

“r” and the results are shown on 

the table-2. There is a negative correlation 

between age and axial length which means 

that axial length decreases as age advances 

which is true in both eyes as well as mean of 

both eyes. Nevertheless, their associationship 

is not significant statistically. 

Table-4. Results of the independent t-test 

On the contrary, direct/ positive correlation is 

witnessed between the eyes and it is found to 

be very highly significant. It implies that longer 

axial length of one eye certainly corresponds 

to longer axial length of another eye and viceversa. 

Table 3. Comparison of Mean ± S.D. of age & axial 

length of eyes among the age groups (Yr) 

Comparison of mean ± S.D. of axial length of 

right, left eyes and mean of both eyes are 

made for each age group which are displayed 

in table-3 and their test in significant results 

are set forth in table-4. 

The highest axial length for the right eye is 

22.67 mm which belongs to age group 21- 30 

years and the lowest axial length of 20.52 mm 

to those of 10-20 years. Also in case of left 

eye, the highest axial length is 22.61 mm, 

belonging to age group 21-30 years and lowest 

axial length of 21.49 mm to those of 81-90 

years. 

At the same time, highest axial length for 

average of both eyes is 22.64 mm belonging 

to age group 21- 30 years and lowest (21.67 

mm) to 81-90 years. 

Discussion 

During the past 10 years or so, it has been 

observed that IOL power in the indigenous 

people of Manipur is comparatively higher than 

26 

the average people of the country. Thus the 

present study was undertaken to find out the 

correlation between the axial length and the 

power of IOL. It is accepted that a longer axial 

length results in lower IOL power and 

viceversa. 1,3,4,5. 

In the present study we observed that the 

average axial length was 22.51mm±0.83 

which is on the shorter side from the average 

value of 23.6mm.The mean axial length of 

men was 22.73mm±0.87 and 22.38mm±o.79 

for women comparable to Larsen JS 8 findings 

of longer axial length in men(23.82mm) than 

in women(23.02mm). Wong TY et al 14 also 

found longer axial length in men (23.80mm 

±1.20) than in women (23.40mm±1.37). 

WickremansingbeS et al 13 found no major 

difference between the axial length of the right 

eye 23.13mm±1.15 and left eye 23.19mm±19 

and in this study we also observed that the 



axial length of the right eye is 22.54mm±0.87 

and that of the left eye is 22.49mm±0.84. The 

finding of shorter axial length in the indigenous 

people of Manipur may be due to shorter built 

and consequently smaller eyes. 

Conclusion 

It is concluded that the axial length of the 

eyeball is shorter in the indigenous people of 

Manipur which is responsible for higher power 

of IOLs calculated before cataract surgery. 

References 

1. BinkhorstRD ,Troutman RC. The accuracy of 

ultrasonic measurement of axial length of the 

eye. Ophthalmic Surgery 1981;Vol 12:353-365. 

2. Byrne SF, Green RL. Axial length 

measurements. In: Ultrasound of eye and 

orbit.2nd ed. Missouri: Mosby;2002.p.244-271. 

3. Cass K, Thrompson CM, TromansC,Wood IC. 

Evaluation of the validity and reliability of 

ultrasound biometry with a single use 

disposable cover. Br J Ohpthalmol 

2002;86(3):344-9. 

4. Diamond JF, Ossoinig KC. Contact A-scan 

ultrasonography. In: Peyman GA, Sounders 

DR, Goldberg MF,editors. Principles and 

practice of Ophthalmology. 3rd ed. New Delhi: 

Jaypee Brothers;1987.p.1403-1450. 

5. Giers U, Epple C. Comparison of A-scan device 

accuracy.J Cataract Refract Surg 1990;16(2): 

235-43. 

6. Hauff W. Biometry- An exact method for the 

measurement of the axial length of the eye. 

Wien KlinWochenshr 1983;95(8):271-4. 

7. Hoffer KJ. Axial dimension of the human 

cataractous lens. Arch Ophthalmol 1993; Vol 

III: 914-918. 

8. Larsen JS. Axial length of the emmetropic eye 

and its relation to the head size. 

ActaOphthalmolCopenh 1979; 57(1): 76-83. 

9. Norman SJ, Mark SJ, Gary SJ. Intraocular lens 

implants. In: Cataract surgery and its 

complications. 6 th ed. Asia: Mosby Harcourt 

Pvt.Ltd;1990. p. 161-171. 

10. Shammas HJ. Axial length measurement and 

its relation to intraocular lens power 

calculations. J Am Intraocul Implant Soc 1982; 

8(4): 346-9. 

11. Siahmed K, Muriare M, Brasseur G. Optic 

biometry in intraocular lens calculation for 

cataract surgery. J FrOphthalmol 2001; 24(9): 

922-6. 

12. Sihota R, Tandon R, editors. Ancillary 

investigations. In: Parson , s Disease of the 

Eye.19 th ed. New Delhi:Elsevier Harcourt Pvt. 

Ltd; 2003.p. 139-140. 

13. Wickremansingbe S, Foster PL, Uranchimeg 

D, Lee PS, Devereux JG, Alsbirk PH, et al. 

Ocular biometry and refraction in Mongolian 

adults. Ivos 2004; Vol 45:3. 

14. Wong TY, Forter PJ, Ng TP, TielschJm, 

Johnson GJ,Seah SKL. Variations in ocular 

biometry in adult Chinese population in 

Singapore. Ivos 2001; Vol 42: 1. 



A preliminary study on hypoglycemic effect of aqueous extract of 

Portulaca oleracea leaves in normal albino rats 

1 

M. Medhabati Devi, 2 N. Meena Devi, 1 U. Dharmaraj Meetei, 1 L. Tarinita Devi 

Abstract 

Objective: To study the hypoglycemic effect 

of Portulaca oleracea in normal albino rats. 

Methods: The albino rats were divided into 

five groups of six animals each receiving 

different treatments consisting of vehicle, 

aqueous extract of P. oleracea leaves (250, 

500 and 1000 mg/kg, p.o.) and the standard 

antidiabetic drug, glibenclamide (0.5 mg/kg, 

p.o.). Blood glucose level was estimated using 

glucose oxidase method before and 2 h after 

the administration of drugs. Results: The 

aqueous extract of P. oleracea leaves showed 

significant reduction in blood glucose level 

(P


hypoglycemic affect of P. oleracea in normal 

rats. 

Materials And Methods 

Animals: Healthy albino rats of wistar strain 

of either sex weighing between 100-200 gm 

obtained from central animal house, RIMS, 

Imphal were used for the study. The animals 

were kept in polypropylene cages in the 

departmental animal house. They were 

acclimatized for ten days and fed on standard 

laboratory diets with water ad libitum. 

Laboratory practice: The institutional ethics 

committee of RIMS, Imphal approved the 

protocol of the study. 

Preparation of plant extract : The fresh 

aerial parts of Portulaca oleracea were 

collected from South Eastern region of 

Manipur during the months of June-July, 2009 

identified and authenticated. The plant 

materials were cleaned and dried under 

shade. Then the leaves were separated and 

powdered by a mechanical grinder and stored 

in air tight container for future use. 

Preparation of aqueous extract was done by 

the method described by Khosla et al 8 . 38gm 

of the powdered dry leaves of the plant was 

extracted with distilled water using a soxhlet 

apparatus. The brownish extract obtained was 

evaporated, shade-dried, scraped out, 

weighed and stored in glazed porcelain jar for 

future use. The yield was 35.2%. 

The hypoglycemic effect of P.oleracea leaf 

extract was studied in normal albino rats. 30 

albino rats were used for the experiment. They 

were divided into 5 groups with six animals in 

each group and kept fast for 18 h with free 

access to water. Care was taken to prevent 

corpophagy. Blood samples were collected 

from lateral tail vein for glucose estimation. 

Then the animals were treated as follows: 

Group 

A (control) 

B (test) 

C (test) 

D (test) 

E (standard) 

Drugs 

2% gum acacia in distilled water 

P.oleracea (250 mg/kg, p.o.) 



Glibenclamide (0.5 mg/kg, p.o.) 

Test and standard drugs were administered 

orally using 2% aqueous gum acacia 

suspension as vehicle with the help of feeding 

tube. The blood samples were collected from 

lateral tail vein before and 2 h after drug 

administration. The dose of the standard drug 

glibenclamide was calculated on the basis of 

human dose, based on surface area by 

extrapolation method 9 . Blood glucose was 

estimated by glucose oxidase method 10 . The 

period of 2 h is based on the finding that the 

maximum hypoglycemic effect of 

glibenclamide was found around 2 h of 

administration. Results were analysed by oneway 

ANOVA followed by Dunnett’s ‘t’ test. 

P


Table 1. Effect of Portulaca oleraca on blood glucose level in normal albino rats 

Group Dose (mg/kg, p.o.) Blood glucose level (mg/dl) 

Before drug After drug (2 h) % decrease 

A (control) : 2% gum 10 ml/kg 99.66 ± 0.94 100.20 ± 2.64 

acacia in dist.water 

B (test) P.oleracea 250 97.83 ± 2.91 91.33±1.37* 6.60 

C (test) P.oleracea 500 95.50 ± 3.40 69.53±3.50** 27.22 

D (test) P.oleracea 1000 93.66 ± 1.10 53.50 ± 2.98** 42.87 

E (standard) Glibenclamide 0.5 97.16 ± 2.33 55.40 ± 2.58** 42.98 

One way ANOVA F 3.54 21.51 

df 5,24 5,24 

Values are mean ±SEM, n=6 in each group, * P


9. Ghosh MN: Fundamentals of experimental 

Pharmacology: Scientific Book Agency, 

Kolkata, 4 th Edn, 176-83, 2008. 

10. Barham D and Trinder P: An improved colour 

reagent for the determination of blood glucose 

by the oxidase system, Analyst. 1972; 97: 

142-5. 

11. Xu X, Yu L and Chen G: Determination of 

flavanoids in Portulaca oleracea L. by Capillary 

electrophoresis with electrochemical 

detection. J. Pharm Bio med Anal. 2006, 41 

(2) : 493-99. 

12. Beretz A, Antom R and Stoclet: Flavonoid 

compounds are potent inhibitors of cyclic 

phosphodiesterease, Experimentia. 1977; 34: 

1054-55. 

13. Oliver B: Oral hypoglycemic plants in west 

Africa, J Ethnopharm. 1980; 2: 119-27. 



Evaluation of psychosocial variables in patient of attempted suicide in RIMS 

1 

Anup Kumar Debnath, 2 N. Heramani Singh, 3 R.K. Lenin Singh, 1 T. Hemachand Singh, 4 L. Roshan Singh 

Abstract 

Objective: To evaluate psychosocial variables 

in individuals who attempted suicide and 

attended Regional Institute of Medical 

Sciences Hospital, Imphal. Method: The study 

was cross-sectional in which 50 patients who 

attempted suicide and attended RIMS Hospital 

and fulfilled the inclusion criteria were included 

in the study which was conducted from 

November 2004 to October 2005. A semistructured 

interview schedule was used to find 

out the sociodemographic profile. Present 

State Examination was used for symptom 

elicitation and ICCD-10 was used for 

confirming the diagnosis. Results: Males 

(64%) outnumbered females. Sixty-four 

patient had psychiatric illness, depressive 

episode (28%) being the most common 

diagnosis followed by Alcohol Dependence 

Syndrome (9%). Conclusion: Depressive 

episode was found to be commonest 

psychiatric illness in patients who attempted 

suicide. 

Key words: Attempted suicide, depressive 

episode, alcohol dependence syndrome. 

Introduction 

Suicidal behavior or suicidality can be 

conceptualized as a continuum ranging from 

1. Ex PG student, 2. Professor & HOD, 3-Associate 

Professor, Dept. of Psychiatry, RIMS 4. Assistant 

Professor, Department of Clinical Psycology, Regional 

Institute of Medical Sciences, Imphal-795004, Manipur 


Dr. N. Heramani Singh, 

Prof. Department of Psychiatry, RIMS, Imphal – 795001. 

32 

ideation to completed suicide. 1 Suicide is a 

complex phenomenon with numerous 

influences including the individual’s 

personality, biology, culture and social 

environment as well as the macro-economic 

and political context. 2 Suicide is among the 

leading causes of death for young adults. It is 

among the top three causes of death in the 

population aged 15-34 years. This represents 

a massive loss to society of young persons 

in their productive years of life. 3 As anywhere 

else, in India, suicide is among the top ten 

causes of death. It is also among the three 

commonest causes of death in India between 

16 to 35 years range. 4 Data on suicide 

attempts indicate suicide attempts may be 

upto 20 times higher than the number of 

completed suicide. 3 This study was an attempt 

to find out the psychosocial characteristics 

and psychiatric morbidity among the patient 

who attempted suicide in Manipur. 

Material and Methods: 

The study was conducted in the Department 

of Psychiatry, RIMS Hospital, Imphal, for a 

period of one year from November 2004 to 

October 2005. After obtaining informed 

consent, first 50 patients who attended RIMS 

Hospital following attempted suicide, 

irrespective of age and sex, were selected for 

the study. Patients who had no reliable 

informant or those who were discharged, left 

against medical advice or expired before 

completion of interview were excluded from 

the study. 

Assessment tools used were, a semi- 



structured interview schedule for collection of 

information on sociodemographic variables, 

present State Examination (PSE) 5 and 

Suicidal Intent Questionnaire 6 for symptom 

elicitation and confirmation to the diagnosis 

was done using ICD-10diagnostic criteria. 

Statistical analysis was performed using chisquare 

test. 

Results: 

Table I : Frequency distribution of present 

psychiatric illness 

Present Psychiatric illness 

No. of patients 

M F Total (%) 

Depressive episode 9 5 14 (28%) 

Alcohol dependence 9 0 9 (18%) 

Adjustment disorder with 

depressive reaction 4 3 7 (14%) 

Schizophrenia 1 1 2 (4%) 

No psychiatric diagnosis 9 9 18 (36%) 

Total 32 18 50 

Table-II : Sexwise frequency distribution of 

psychiatric illness, family history of psychiatric 

illness physical ailments. 

No. of patients 

Variables Present Absent 

M (%) F (%) M (%) F (%) 

Present Psychiatric 

diagnosis 23(71.8%) 9(50%) 9(28.12%) 9(50%) 

Past psychiatric 

diagnosis 15(46.8%) 6(33.3%) 17(53.1%) 12(66.6%) 

Family history of 

psychiatric illness 6(18.7%) 10(55.5%) 26(81.2%) 8(44.4%) 

Physical ailments 9(28.1%) 13(70.2%) 23(71.8%) 5(27.7%) 

Out of the total 50 patients who attempted 

suicide 32 (64%) were males and 18 (36%) 

were females. Majority of the patients 28 

(56%) who attempted suicide belonged to 21- 

30 years age group. There were 11 (22%) 

patients in the age group < 20 years and it 

constituted the second commonest group. 

Out of the total 50 patiens 32 (64%) had 

psychiatric illness. The psychiatric disorder 

found in order of frequency were Depressive 

episode 14 (28%) alcohol dependence 

syndrome 9 (18%) adjustment disorder 7 

(14%) and schizophrenia 4%. 

Family history of psychiatric illness was found 

in 16 (32%) of patients. The family history of 

psychiatric illness was more common in 

females (55.55%). This finding was 

statistically significant (P


Conclusion: 

The present study showed that majority of 

those attempt suicide suffer from psychiatric 

illness which Department disorder 

happened to be commonest. Family history 

of psychiatric illness and presence of 

comorbid physical illness may be important 

risk factor. 

Reference: 

1. Lonqvist JK: Suicide, New Oxford Text Book of 

Psychiatry; Gelder MG, Ibor JJLJ and Nancy 

CA: Oxford University Press, New York, 1 st 

Edition, 1, 1033-1039, 2000. 

2. Kwame M, Mark S, and Crawford M: Suicide in 

ethnic minority groups, British Journal of 

Psychiatry; 183: 100-101, 2003. 

3. World Health Organisation (2001a), World 

Health Report 2001; Mental health: New 

understanding, New hope, Geneva: World 

Health Organisation, 37- 39, 2001. 

4. Unni KES: Human self destructive behavior, 

Text Book of Postgraduate Psychiatric; Vyas 

JN and Ahyja N: Jaypee Brothers Medical 

Publishers (P) Ltd., New Delhi, 2nd edition, 2, 

526-556,1999 

5. Wing JK, Copper JE and Satorious N: 

Measurement and classification of psychiatric 

symptoms – An instruct manual for the PSE 

and Catego program; Cambridge University 

Press, London, 1974 

6. Gupta SC, Anand R and Trivedi JK: Development 

of a suicidal intent Questionnaire, Inian Journal 

of psychiatry: 25(1):57-62,1983 

7. Rao AV: Attempted suicide in psychiatric 

patients, Indian Journal of Psychiatric;7:253- 

264,1965 

8. Kumar PNS: Age and gender related analysis 

of psychological factors in attempted suicide: 

study from a medical intensive care unit, Indian 

Journal of Psychiatry; 40(4): 338-345,1998 

9. Sharma RC: Attempted suicide in Himachal 

Pradesh, Indian Journal of Psychiatry; 40(1): 

50-54, 1998. 

10. Bland RC, Neuman SC and Dysk RJ: The 

epidemiology of parasuicide in Edmonton, 

Canadian Journal of Psychiatry; 39:391-396, 

1994 

11. Colman I, Newman SC, Schopflocher D, Bland 

RC and Dyck RJ: A multivariate study of 

predictors of repeat parasuicide, Acta 

Psychiatric Scandinavica; 109;306-312, 2004 

12. Latha KS, Bhat SM and D Sourza P: Suicide 

attempters in a general hospital unit in India: 

34 

their socio-demographic and clinical 

profilemphasis on cross-cultural aspects, Acta 

Psychiatrica Scandinavica;94:26-30,1996 

13. Kumar CTS and Chandrasekaran R: A study of 

psychological and clinical factors associated 

with adolescent suicide attempts, Indian Journal 

of Psychiatry and personality disorders in 

survivors following their first suicide attempt, 

Indian Journal of Psychiatry; 42(3):237-242, 

2000 

14. Chandrasekaran R, Gynanaseelan J, Sahai A, 

Swaminathan RP and Perme B: Psychiatric and 

personality disorders in survivors following their 

first suicide attempt, Indian Journal of 

Psychiatry; 45(11):45-48,2003 

15. Fawcett J, Schefner W, Clark D, Hedeker D, 

Gibbons R and Coryell W: Clinical predictors 

of suicide in patients with major affective 

disorders: A controlled prospective study. 

American Journal of Psychiatry; 144:35-40,1987 

16. Srivastava MK, Sahoo RN, Ghotekar LH, Dutta 

S, Danabalan M, Dutta TK and Das AK: Risk 

factors associated with attempted suicide: a 

case control study, Indian Journal of Psychiatry; 

46(1):33-38,2004 

17. Kumar PNS, Kuruvilla K, Dutta S, John G and 

Jayaseelan: Psychological aspects of 

attempted suicide: study from a medical 

intensive care unit, Indian Journal of 

Psychological Medicine: 18(2):32-40,1995 

18. Balfoursclare A and Hamilton CM: Attempted 

suicide in Glasgov, British Journal of Psychiatry; 

109:609-615,1963 

19. Barraclough BM: The suicides in epilepsy, Acta 

Psychiatrica Scandinavica;76: 339-345,1987 

17. Kumar PNS, Kuruvilla K, Dutta S, John G and 

Jayaseelan: Psychological aspects of 

attempted suicide: study from a medical 

intensive care unit, Indian Journal of 

Psychological Medicine: 18(2):32-40,1995 

18. Balfoursclare A and Hamilton CM: Attempted 

suicide in Glasgov, British Journal of Psychiatry; 

109:609-615,1963 

19. Barraclough BM: The suicides in epilepsy, Acta 

Psychiatrica Scandinavica;76: 339-345,1987 


cmyk 


Identification of prognostic factors of fertility in Manipur 

1 

R.K. Narendra, 2 Ch. Mem Chanu, 3 W. Jibol Singh. 

Abstract 

Objective: To identify the significant 

prognostic variables and their causal effects 

on the fertility pattern of Manipur society. 

Besides it is proposed to prove that the 

multiple regression model fits the data well. 

Methods: The present study is based on a 

primary data of 1080 eligible Manipuri women 

representing entire Manipur state. Average 

number of live birth ever born per woman is 

considered as mean fertility which is analysed 

with socio-demographic and behavioural 

factors, by regression technique. Results: 

Mean ± SD of fertility of Manipuri women is 

2.54 ± 1.52 live births. Out of 17 prognostic 

variables considered, 7 are identified as 

indispensible causal factors to high fertility. 

Conclusion: The multiple regression model 

with stepwise method is a quite suitable 

technique to identify risk factors for high fertility. 

They are religion, duration of marriage, 

number of family members, number of eligible 

couple, type of family, educational level and 

availability of separate room, that explained 

1. Professor and Head, Unit of Biostatistics, RIMS, 

Imphal 2. Research Scholar, Unit of Biostatistics, 

Manipur University ,Imphal, 3. Reader and Head, 

Statistics Dept., B.M. College, Sawombung Imphal- 

East. 


Professor and Head, Unit of Biostatistics , RIMS, 

Imphal, e-mail: biostatrims@yahoo.com 

fertility by 62%. All the prognostic factors 

except availability of separate room (P =0.026) 

are highly significant (P =0.000). The final 

multiple regression model fits the data well 

(P =0.000). 

Key words : Fertility, socio-demographic and 

behavioural factors, multiple regression 

model. 

Introduction 

Population growth indulges chain reaction of 

manifold problems that most people face 

today in this fertile world. There are at least 

2,00,000 more people alive today than 

yesterday and tomorrow, there will be at least 

another 2,00,000 more too 1 . Human beings 

would be sunk in the human ocean if the 

present population trend is not controlled in a 

stable stage. Thus fertility study becomes a 

necessity of paramount importance. In fact, 

human fertility is a complex biological process 

and it constitutes an essential aspect of 

population dynamics. The study of socioeconomic, 

demographic and behavioural 

factors contributing to higher fertility level 

assumes a great importance in view of the 

increasing population growth experienced in 

most of the developing countries now and its 

level still varies within and between countries. 

Thus the present study is initiated to identify 

the significant prognostic factors to fertility and 

to fit a regression model based on a primary 

data of Manipuri women considering with 

some of the important socio-demographic and 

behavioural factors. 




The present study is based on a primary data 

of 1080 eligible couples representing entire 

Manipur state. The type of study is so called 

cross sectional comparative study and 

stratified random sampling with proportional 

allocation as a sampling procedure. The 

survey is conducted during May 2007 to Feb 

2008 with April 30, 2007 as reference date. 

Personal interview method and pre-designed 

semi-structural schedule are adopted as 

procedure and tool of the survey respectively. 

Model: 

A multiple regression model is 

36 

Y= β o 

+ 

+ ; i =1, 2, 3…17 

where Y is the predicted value of fertility and 

represent best fitting regression weights 

with intercept as the value of Y when all 

predictor variables x i are zero together with a 

residual variable. 

Variable specification: 

(a) Response variable ( Y ): No. of live birth 

ever born (b) Predictor variables ( X i ): PR 

(Place of residence; rural=1, urban=0) TY 

(Type of family; nuclear= 1, joint= 0 ), ASR 

(Availability of separate room; yes =1, no= 0), 

HR (Religion; Hindu =1, others= 0), MR 

(Religion; Muslim=1,others=0), AMW (Age at 

marriage of wife); PAW (Present age of wife); 

DM (Duration of marriage); TFM(Total family 

member); EC (no. of eligible couple); EH 

(Educational level of husband), EW 

(Educational level of wife), DNS (Desire no. 

of son); FI (Family income); OH (Occupation 

of husband; govt. employed=1, others=0); 

OW (Occupation of wife; govt. employed=1, 

others =0); AC (Attitude of contraceptive; yes 

=1, no =0) 

Results 

Again the value of R 2 = 0.621 through Enter 

method highlights that the 17 predictors 

considered can explained the response 

variable (fertility) by 62.1% and Durbin-Watson 

Table 1 : Estimated regression parameters 

Un standardized 

Coefficients 

Standardized 

Coefficients 

B Std. Error Beta t P-value 

(Constant) 1.557 .355 4.380 .000 

PR .093 .064 .029 1.440 .150 

TF .302 .072 .097 4.224 .000 

ASR -.277 .123 -.044 -2.255 .024 

HR -.021 .068 -.007 -.308 .758 

MR 2.292 .228 .447 10.054 .000 

AMW -.011 .007 -.038 -1.549 .122 

PAW .007 .005 .029 1.474 .141 

DM .071 .005 .289 12.981 .000 

TFM .192 .017 .340 11.486 .000 

EC -.692 .082 -.238 -8.444 .000 

EH .004 .010 .009 .381 .703 

EW -.021 .008 -.065 -2.616 .009 

DNS .052 .028 .038 1.871 .062 

FI 1.47E-006 .000 .008 .330 .742 

OH .070 .069 .021 1.014 .311 

OW .040 .090 .009 .451 .652 

AC -.170 .199 -.036 -.858 .391 

R 2 = 0.621; d= 1.920 

Table 2 : Estimated regression 

parameters (after excluding outliers 

cases) 

Un standardized Standardized 

Coefficients Coefficients P- 

value 

B Std. Error Beta t 

(Constant) 1.492 .356 4.197 .000 

PR .085 .065 .026 1.308 .191 

TF .303 .072 .097 4.222 .000 

ASR -.281 .122 -.046 -2.301 .022 

HR -.014 .068 -.004 -.204 .838 

MR 2.392 .230 .467 10.394 .000 

AMW -.011 .007 -.039 -1.589 .112 

PAW .006 .005 .025 1.241 .215 

DM .071 .006 .289 12.957 .000 

TFM .190 .017 .337 11.371 .000 

EC -.665 .082 -.230 -8.119 .000 

EH .004 .010 .010 .409 .683 

EW -.019 .008 -.060 -2.383 .017 

DNS .052 .028 .038 1.858 .063 

FI -7.97E-007 .000 -.004 -.177 .859 

OH .086 .069 .026 1.241 .215 

OW .039 .090 .009 .434 .664 

AC -.083 .202 -.017 -.412 .681 

R 2 = 0.623; d= 1.878 



Table3: Estimated regression 

parameters by Stepwise method 

Model Un standardized Standardized t P-value 

Coefficients Coefficients 

B Std . Error Beta 

1 (Constant) 2.212 .037 59.369 .000 

MR 3.336 .119 .651 27.974 .000 

2 (Constant) 1.402 .056 24.901 .000 

MR 3.015 .106 .589 28.335 .000 

DM .091 .005 .368 17.697 .000 

3 (Constant) .974 .088 11.027 .000 

MR 2.875 .107 .561 26.885 .000 

DM .092 .005 .375 18.329 .000 

TFM .072 .012 .128 6.212 .000 

4 (Constant) 1.322 .093 14.227 .000 

MR 2.585 .108 .505 24.033 .000 

DM .086 .005 .349 17.553 .000 

TFM .171 .015 .304 11.076 .000 

EC -.730 .079 - .252 -9.268 .000 

5 (Constant) 1.004 .113 8.899 .000 

MR 2.551 .107 .498 23.919 .000 

DM .080 .005 .324 15.95 .000 

TFM .203 .017 .359 12.207 .000 

EC -.742 .078 -.257 -9.516 .000 

TF .342 .070 .11 4.87 .000 

6 (Constant) 1.298 .134 9.691 .000 

MR 2.529 .106 .494 23.848 .000 

DM .076 .005 .307 14.938 .000 

TFM .197 .017 .349 11.901 .000 

EC -.708 .078 -.245 -9.092 .000 

TF .326 .070 .105 4.671 .000 

EW -.025 .006 -.08 -4.008 .000 

7 (Constant) 1.553 .176 8.825 .000 

MR 2.544 .106 .497 23.985 .000 

DM .076 .005 .309 15.015 .000 

TFM .196 .017 .347 11.849 .000 

EC -.703 .078 -.243 -9.045 .000 

TF .297 .071 .095 4.183 .000 

EW -.024 .006 -.076 -3.814 .000 

ASR -.268 .121 -.043 -2.225 .026 

‘‘d’’=1.920, which is very close to 2, reveals 

that the residuals are quite independents. The 

fitted model is also highly significant as 

evidenced by P = 0.000. 

Through outlier checking 15 observations viz., 

24, 56, 70, 96, 123, 246, 318, 364, 485, 681, 

694, 727, 746 and 1035 out of the total 

observations (1080) are scanned and 

excluded for further analysis. 

After excluding outliner cases, R 2 value is 

slightly increased to 0.623 while “d” slightly 

decreases to 1.878. Highly significant P-value 

(i.e.0.000) indicates the model fits the data 

well. 

In order to study the causal effects of 17 

predictors on mean fertility, further analysis is 

carried out in 7 steps by stepwise method and 

findings are set forth on table-3. In the last 

model i.e., model-7, there are 7 predictors 

which are identified as the most important 

ones out of the 17 predictors considered. They 

are Muslim religion (MR), duration of marriage 

(DM), total family member (TFM), eligible 

couple (EC), type of family (TF), educational 

level of wife (EW) and availability of separate 

room (ASR). All the predictors except 

availability of separate room are highly 

significant even at 0.000 probability level. Of 

course, R 2 value monotonically increases 

from model-1 (0.424) to model-7 (0.619) and 

the last fitted model is found to be highly 

significant (F = 245.604, P = 0.000). 

Discussion 

A highly significant regression co-efficient 

2.544 of Muslim religion implies that Muslim 

has contributed higher fertility than that of the 

women of other religion groups. This is 

because of the fact the Muslim society is 

conservative, less educated as well as 

restriction on birth control by religion belief. 

This is in agreement with some of the 

scholars 2, 3, 4 . The mean fertility rate for Hindus 

is 4.2 and for Muslims,5.8 5 . The Mysore 

population study 6 finds that Muslim women 

have more children at all age groups than 

Hindu women. Here the duration of marriage 

is termed as the time interval between the 

date of effective marriage of the couple and 

reference date which has a positive significant 

impact on fertility level ( = 0.076). 

Next to duration of marriage, total family 

member(TFM) also has a positive impact 



( =0.196) while no. of eligible couple(EC) in 

the family has negative impact ( = -0.703). 

On contrary, nuclear family has higher fertility 

than that of joint family ( =0.297).This is 

because of the fact that in nuclear family, 

couples are usually free to cohabitation. In 

contrast, in joint family structure young 

couples are frequently separated with less 

coital frequencies that result less chance of 

conception 7 . The educational level of women 

has negative impact ( = -0.024) on fertility, 

it implies that fertility among educated women 

is lower as compared with illiterate or less 

educated women. Educated women are quite 

enlightened that they do not allow fertility rate 

up, as long as that is considered absolutely 

necessary by the couple. Usually, later the 

marriage of educated women higher is the use 

of family planning devices. Lastly availability 

of separate room (ASR) has a negative 

impact ( = -0.268) on fertility. 

Conclusion 

The mean fertility of the study population is 

found to be 2.54 with S.D. of 1.52. After 

scanning the variables according to their 

degree of importance, the predictors viz., 

religion, duration of marriage, total no. of family 

member, no. of eligible women, type of family, 

educational level, and availability of separate 

room are treated as importance to explain the 

variability of fertility. These factors can explain 

62% of the total variation in mean fertility of 

the population under study. The model fits the 

data well. 

References 

1. Martin W. The big problem. Available at http:// 

www.mwillett.org/politics/bigprobl.htm. 

Assessed on 15.09.2009. 

2. Narendra RK. A statistical study of components 

of birth–intervals in relation to Manipuri women. 

Ph.D thesis, Patna University, Patna; 1984. 

3. Binota M. A study of fertility and mortality in 

relation to socio-economic development of 

Manipur: A case study of Imphal. Ph.D thesis, 

Manipur University, Canchipur; 1989. 

4. Sharat N. A contribution to determinants of birth 

interval and fertility of Manipuri women: A case 

study of Imphal. Ph.D. thesis, Manipur 

University, Canchipur; 2002. 

5. Sharif AS. Human development report, National 

council for applied economic research. Delhi: 

Oxford University press; 1999. 

6. United Nations . The Mysore population 

studies: A cooperative project of the United 

Nations and the Government of India, 

Population Studies 1961, No. 34 ST/SOA/ 

SERIES/A/34, New York. 

7. Nag M. Family type and fertility – Proceedings 

of WPC; UN. Belgrade; 1965: 160-3. 

38 



Malonaldehyde (MDA) status in human semen of different fertility potential 

1 

Jayshree Phurailatpam, 2 A.R.Chaudhari 

Abstract 

Objective: Human spermatozoa produce 

reactive oxygen species and are susceptible 

to peroxidative damage arousing intense 

interest about the role of oxidative stress in 

causing male infertility. Malonaldehyde (MDA) 

one of the end-products of lipid peroxidation 

has been suggested to be a good chemical 

marker for oxidative damage. Methods: In this 

study, we have measured MDA levels in 150 

semen samples (Normozoospermia-50, 

Oligozoospermia-50, Azoospermia -50) of 

males within the age range of 21-45 years 

attending the Reproductive unit, Department 

of Physiology, MGIMS, Sewagram. Results: 

Comparative studies between the three 

groups showed a positive correlation between 

MDA levels and normal Sperm count indicating 

the role of spermatozoa in the generation of 

MDA. The presence of abnormal levels of MDA 

in the azoospermic group may indicate some 

contributory generation of MDA by cellular 

elements like immigrant leucocytes present 

in the semen even in the absence of 

spermatozoa. A negative correlation have 

been found between MDA levels and motility 

of spermatozoa. Conclusion: The present 

1. Senior tutor, Department of Physiology, RIMS, 

Imphal, Manipur. 2. Professor, Department of 

Physiology, Mahatma Gandhi Institute of Medical 

Sciences, Sevagram, Wardha. 

Corresponding author: 

Dr Jayshree Phurailatpam, 

Senior Tutor/Demonstrator, Dept of Physiology, 

Regional Institute of Medical Sciences, Imphal, 

Manipur. 

Email:jayshreeshar@yahoo.co.in 

study shows that the increased presence of 

abnormal spermatozoa in Oligozoospermic 

males excessively generate reactive oxygen 

species, compromising the anti-oxidizing 

power of the seminal plasma thereby 

damaging the spermatozoa and reducing their 

motility significantly with adverse effects on 

male fertility. Understanding this promises 

beneficial effects of Antioxidant therapy in the 

management of male infertility. 

Key words: Human semen, Oxidative stress, 

MDA, male infertility. 

Introduction 

Reproduction is an important aspect of all 

living beings and there is an immense interest 

about the role of oxidative stress in causing 

human male infertility. A free radical defined 

as a molecular species capable of 

independent existence and containing one or 

more unpaired electrons making them 

relatively active, are formed as a natural by 

product of Oxygen metabolism. They serve 

the purpose of burning down bacteria and 

refuse body matter but when out of control, 

they become toxic and start damaging the 

body tissues by a process called Oxidative 

Stress. Oxidative stress has been implicated 

in a wide range of tissue injuries and diseases 

such as Myocardial Infarction, 

Atherosclerosis, Aging, Rheumatoid Arthritis 

and Parkinson’s disease besides causing 

male infertility 1 . It has been demonstrated that 

human spermatozoa produce reactive oxygen 

species (ROS) like Hydrogen peroxide (H 2 

O 2 

) 

& Superoxide. The presence of high amount 

of unsaturated fatty acids in the semen and 



the membrane of the spermatozoon as well 

as their tendency to undergo spontaneous lipid 

peroxidation makes them highly susceptible 

to peroxidative damage by these free 

radicals 2 . Exposure in physiological amounts 

is important for maintaining normal functions 

of the spermatozoa by stimulating DNA 

compaction and promoting a redox regulated 

c-AMP- mediated pathway that is central to 

the induction of sperm capacitation, acrosome 

reaction and fusion with the oocyte 

membrane 3 . However excessive exposure 

stimulates DNA fragmentation and 

peroxidative damage to the highly sensitive 

plasma membrane of the spermatozoa 

leading to a loss of sperm function 4 . Therefore 

the balancing amount of ROS produced and 

the amount scavenged at any moment will 

determine whether a given sperm function will 

be promoted or jeopardized. Thus, 

assessment of Oxidative stress is vital for 

elucidating the fertility status as clinicians can 

then identify the subgroups of patients that will 

respond to therapeutic strategies. 

Malonaldehyde (MDA) is a stable end-product 

of lipid peroxidation has been suggested to 

be a good chemical marker for oxidative 

damage and is considered a direct indicator 

of lipid peroxidation-induced injury by ROS 5,6 . 

The onset of lipid peroxidation in susceptible 

sperm leads to the progressive accumulation 

of lipid hydroxides in the sperm plasma 

membrane, which then decompose to form 

MDA. Thus the aim of the present study was 

to investigate the status of Malonaldehyde 

(MDA) in seminal fluid of subjects with different 

fertility potential. 

Material and Methods 

Sample: 

Semen samples from 150 male partners (21- 

45 years of age) of infertile couples attending 

the Reproductive Biology unit, Dept. of 

Physiology, MGIMS, Sevagram. 

Collection of sample: 

Following three days absolute abstinence, 

semen obtained by masturbation or coitus 

interruptus is collected in a dry wide-mouth 

container. Use of Condoms is avoided as they 

may contain a spermicide. The collected 

samples are then subjected to semen 

40 

analysis and the MDA level estimated with the 

Thiobarbiturate- Tri cyclic acid (TBA-TCA) 

assay by spectrophotometer determination. 

Semen analysis: 

After complete liquefaction, semen samples 

are analysed for the following parameters: 

• Volume: Standard graduated glass 

cylinder 

• pH: pH paper 

• Viscosity 

• Spermatozoa concentration : SQA IIB (fig. 

I) 

• Motility: SQA IIB 

• Morphology of spermatozoa: SQA IIB 

• Total functional sperm count (TFSC): SQA 

IIB 

• Sperm motility Index (SMI): SQA IIB 

Grouping of subjects: 

The semen samples were then classified in 

accordance to the WHO criteria into the 

following groups 7 : 

Normozoospermia: 

Sperm count > 20 millions /ml of semen. 

Motility: > 25% grade A motility or > 50% grade 

A +B motility 

Morphology: > 30% normal head-forms of 

sperms 

Oligozoospermic: 

Sperm count < 20 millions /ml of semen. 

Asthenoteratozoospermia: 

Sperm count > 20 millions /ml of semen 

Motility :< 25% grade A 

Morphology: < 30% normal head-forms of 

sperms. 

Azoospermia: 

Not a single sperm/ HPF. 

Volume > 0.0ml 

ESTIMATION of MDA in SEMEN: 

TBA-TCA assay by spectrophotometer 

determination of MDA 8 . 

0.5 ml of Standard or test sample pipette out 



+ 2.5 ml of 20% TCA + 1ml of 0.67% TBA 

Vortexed Boiling water bath x 30 mins 

cooled in cold water x 10mins. 4ml n Butyl 

alcohol Vigorous shaking Chromogen 

Centrifuge x 10mins at 3000rpm 

Supernatant optical density measured in 

spectrophotometer at 530 nm with Butanol 

blank (fig.II). 

Calculations: 

Conc. of 

MDA = OD (TEST) X Standard 

Level OD of standard/test (nmoles/ml) 

Observations and results 

The present study involving 150 semen 

samples from subjects between 21-45 years 

of age shows 50 normal seminogram in 

terms of sperm count, motility & morphology; 

and 100 abnormal seminogram (50- 

oligoasthenoteratozoospermic=21Oligozoospermia 

+ 29 Asthenozoospermia; 50- azoospermic). 

Maximum percentage of the population was 

found to be between 20-25 years of age. 

Volume: The seminal volume was not 

significantly different in Normozoospermic 

(3.23ml) and Asthenoteratozoospermic 

(2.1ml) groups and was similar between the 

latter and Oligozoospermic (2.77ml) group. 

The study shows average volume of semen 

to vary between 2-4 ml in all the groups and 

the mean volume was closer to the value of 

2.5 ml in all the groups except 

asthenozoospermic group where it was 

significantly low (2.1 ml). Still, the mean 

volume was more than the minimum accepted 

TABLE I 

Group Volume in ml pH 

(mean + SD) 

Normozoospermia (50) 3.23+1.19 7.49+0.177 

Oligozoospermia(21) 2.77+0.79 7.55+0.129 

Asthenoteratozoospermia(29) 2.1+0.84 7.5+0.179 

Azoospermia(50) 2.76+0.98 7.45+0.177 

TABLE II 

Group Count Motility Morphology TFSC SMI MDA 

millions/ml % % Nmoles/ml 

Normospermia (50) 93.72+37.5 61.4+7.8 40.12+7.6 39.9+20 254.9+99.9 2.77+0.38 

Asthenozoospermia(29) 30.93+8.99 34.9+9.2 22.4+3.66 4.35+4.2 99.6+37.4 4.33+0.65 

Oligospermia(21) 8+6.61 13.1 +8.7 12.33+5.6 1.33+1.8 29.6+22.3 

Azoospermia(50) - - - - - 5.66+1.42 

volume for fertility (2ml) in all the groups 

indicating that semen volume is not a major 

factor in impairing the fertility potential of a 

person. The volume is observed to decline 

gradually after 35 years of age in all the groups. 

Presence of genito-urinary lesions was also 

found to be associated with impaired semen 

quality. 

pH: The pH in all the 

groups did not show 

any statistically 

significant difference 

suggesting the 

presence of precise 

mechanisms for its 

maintenance within a 



narrow range and indicating little role in 

maintaining motility and viability. 

MDA: Results were analysed by Students‘t’ 

test for significance of MDA levels observed 

between different groups and correlation 

coefficient calculated. The observations are 

presented in table I& II and figures a,b,c. 

The seminal MDA levels however was 

significantly different (p


References: 

1. Esterbauer H., K. H. Cheeseman,. 

Superoxide Dismutase. Chem. Phys. 

Lipids 1993; 197,103. 

2. Jones R and Mann T. Toxicity of 

exogenous fatty acid peroxidase towards 

spermatozoa. J. Reprod Fertil; 

1977:50:255-260. 

3. Griveau JF, Le Lannou D. Reactive 

Oxygen Species and human 

spermatozoa: physiology and pathology. 

Int J Androl, 1997; 20:61-9. 

4. Diezel WS, Engel N, Sonnichsen and 

Horne WE. Lipid peroxidation products 

in human spermatozoa detection and 

pathological significance. Andrologia 

1980:12:167-171. 

5. Hellstrom WJ, Bell M, Wang R, Sikka Sc. 

Effect of sodium nitroprusside on sperm 

motility, viability and lipid peroxidation. 

Fertil steril 1994; 61:1117-22. 

6. Bell M, Sikka S, Rajasekharan M, 

Hellstrom W.Time course of hydrogen 

peroxide induced changes in the lipid 

peroxidation of human sperm 

membranes.Adv contracept Deliv syst 

1992;8:144-50. 

7. W.H.O. laboratory manual for the 

examination of the human semen and 

semen cervical mucus interaction. 

Cambridge Univ. Press, 1987. 

8. Ledwozyw A, Michalak J, Stephen A, 

Kadziolka A. TBA-TCA assay by 

spectrophotometer determination of MDA 

.Clin. Chem. Acta: 1986:155:275-284. 

9. Yu BP Cellular defences against damage 

from reactive oxygen species. Physiol 

Rev, 1994;74:139-62 

10. Zini A, De Lamerande E and Gagnon C: 

ROS in semen of infertile patients- levels 

of SOD and Catalase like activities in 

seminal plasma and spermatozoa. Int J 

Androl 1993:16:183-188. 

11. Aitken R J, Clarkson JS: cellular basis of 

defective sperm function and its 

association with genesis of reactive 

oxygen species by human spermatozoa. 

J. Reprod Fertil 1987:81; 459-462. 

12. Iwasiki I, Gagnon C; Formation of ROS 

in spermatozoa in infertile patients. Fertl 

Steril. 1992:57:409-416. 

13. Lenzi A, Picardo M, Gandini L, Passi S 

and Dundero F. Glutathione treatment of 

Dyspermia- Effect of lipoperoxidation?. 

Mol. Rep. and Dev.:1994; 37:345-362. 

14. Sharma RK, Agarwal A. Role of reactive 

oxygen species in male infertility. Urology, 

1996:48(6):835-50. 



Intradialytic complications of hemodialysis 

1 

Loukrakpam Sharatchandra Singh, 2 Shivendra Singh, 3 T. Brojen Singh, 4 Sanjeev Kumar Behura 

4 

Biplab Ghosh, 4 Sashidhar Shreeniwas 

Abstract 

Aim of study: To study the intradialytic 

complications of hemodialysis. Methods: 275 

patients of renal failure comprising of 125 

acute renal failure and 150 chronic renal failure 

patients who were registered for conventional 

hemodialysis during the period of May 1, 2007 

and May 15, 2008 were taken up for the 

intradialytic complications of hemodialysis 

regardless of age, sex,race and cause of renal 

failure. Special emphasis has been given for 

complications related to vascular access sites 

like femoral, arterio-venous and internal jugular 

venous punctures. During the study period 

there were 1075 bicarbonate dialyses on 

these patients. Most of the ARF and CRF 

patients were dialysed by femoral vein access. 

Among the patients on CRF, 10 patients were 

on arterio-venous fistula and 8 were on 

internal jugular venous catheterizations. 

Results: In the ARF patients, common 

intradialytic complications were hypotension 

(12.2%), vomiting (5.2%), headache (5.2%), 

rigor (2.4%), hypertension (1.2%), nausea 

(1%), cramps (0.8%), oedema (0.9%), fever 

(0.6%), first-use syndrome (0.4%), 

hypoglycemia (0.4%), and itching (0.2%). In 

the CRF group, common complications were 

hypertension (11.4%), hypotension (10.48%), 

1. Assoc. Prof. 3. Asst. Prof., Department of Madicine, 

RIMS, Imphal 2.Lecturer 4. Sr. Resident, Department 

of Nephrology Institute of Medical Sciences, Banaras 

Hindu University, Varanasi, Uttar Pradesh – 221005. 


Loukrakpam Sharatchandra Singh, Assoc. Prof., 

Department of Medicine, RIMS, Imphal 

44 

vomiting (8.7%), rigor (5.7%), chest pain 

(4.6%), nausea (3.1%), headache (3.1%), 

fever (1.6%), cramps (0.71%), itching (0.35%) 

and haematoma (0.35%). Intracerebral 

hemorrhage and migration of fractured 

catheter tip were noted in one patient each. 

Conclusion: There is a need for a special 

attention for the diagnosis and management 

of intradialytic complications of hemodialysis 

because such complications could be 

managed successfully without the need of 

subsequent termination of dialysis procedure. 

Key words: Hemodialysis, Conventional, 

Bicarbonate, Complications, Acute renal 

failure, Chronic renal failure. 

Introduction 

Hemodialysis is a life-saving treatment that 

has only been routinely applied for end stage 

renial disease (ESRD) for the past 40 years. 1 

Pioneering physicians such as Merrill, 

Scribner and Schreiner 2 successfully 

supported patients through the oligoanuric 

phase of acute kidney injury. Haemodialysis 

should be initiated at a level of residual renal 

function above which the major symptoms 

of uremia usually supervene. Among the 

accepted criteria for initiating dialysis in the 

United States are residual creatinine 

clearances of 15 mL/min and 10 mL/min for 

diabetics and non-diabetics respectively. 

Clinical practice guidelines suggest that 

dialysis be initiated at a creatinine clearance 

between 9 and 14 mL/min. 5 At best, with 

current Haemodialysis technology, thriceweekly 

sessions of 5 hours each will achieve 



the equivalent urea clearance of 

approximately 20 mL/min in a 70-kg individual. 

The current guidelines of creatinine 

clearances of 15 mL/min and 10 mL/min or 

of serum creatinine concentrations of 6 mg/ 

dL and 8 mg/dL for diabetics and nondiabetics 

respectively are reasonable criteria for 

initiating Haemodialysis. The clinical 

spectrum of hemodialysis associated 

complications has changed over the 

decades. Our study highlights the acute 

intradialytic complications of conventional 

hemodialysis including uncommon 

conditions like migration of fractured catheter 

and intracerebral hemorrhage. 

Fig.1. CT scan showing Intracerebral hemorrhage 

developed during hemodialysis in a CRF patient 

Materials and methods 

The study on intradialytic complications of 

hemodialysis consists of 275 patients of renal 

failure (125 ARF and 150 CRF patients) 

regardless of age, sex,race and cause during 

the period of May 1, 2007 and May 15, 2008 at 

BHU, Banaras. A special emphasis for 

complications related to vascular access sites 

was considered. Femoral vein cannulations 

were done in 123 and 132 patients of ARF 

and CRF patients respectively. Internal jugular 

vein cannulations were done in 2 and 8 

patients of ARF and CRF patients respectively. 

10 patients of CRF were on Cimino-Brescia 

arterio-venous fistula. There were 1075 

dialyses in these patients. Bicarbonate 

hemodialysis was done in all of these patients. 

TR-FX (Torray Med Co. Ltd) conventional 

hemodialysis machine was used for 

hemodialysis in these patients at the dialysate 

and blood flow rates of 500 and 250 ml/minute 

respectively. 

Results 

In the ARF patients, common intradialytic 

complications were hypotension (12.2%), 

vomiting (5.2%), headache (5.2%) and rigor 

(2.4%). (Table 1). In the CRF group, common 

complications were hypertension (11.4%), 

hypotension (10.48%), vomiting (8.7%), rigor 

(5.7%), chest pain (4.6%), nausea (3.1%), 

headache (3.1%), and fever (1.6%)(Table 1). 

Intracerebral hemorrhage (Fig. 1) and 

migration of catheter tip (Fig.2) were noted in 

one patient each. 

Figure 2. Broken portion of femoral venous catheter 

impacted in external iliac vein removed by 

venotomy 

Table 1. Intradialytic complications of 

hemodialysis in ARF (n=125, 510 dialyses) and 

CRF (n=150, 565 dialyses) patients. 

Complication Number (%) in Number (%) in 

ARF patients ARF patients 

(n=125, 510 (n=150, 565 

dialyses) dialyses) 

Hypotension 61(12.2%) 59 (10.48%) 

Vomiting 26(5.2%) 49 (8.7%) 

Headache 05(5.2%) 17(3.1%) 

Rigor 12 (2.4%) 32 (5.7%) 

Hypertension 06(1.2%) 64(11.4%) 

Nausea 05 (1%) 17 (3.1%) 

Cramps 04(0.8%) 04 (0.71%) 

Fever 03 (0.6%) 09(1.6%) 

First-use syndrome 04 (0.78%) - 

Hypoglycemia 02 (0.4%), - 

Itching 01 (0.19%) 02 (0.35%) 

Restlessness 01 (0.19%) - 

Oedema 01 (0.19%) - 

Chest pain - 26 (4.6%), 

Dyspnoea - 02 (0.35%) 

Femoral haematoma - 02 (0.35%) 

Intracerebral hemorrhage - 01(0.17%) 

Migration of catheter tip - 01 (0.17%) 



Discussion 

Hypotension is the most common acute 

complication (20% - 50%) of HD followed by 

muscle cramps (20%), nausea, vomiting (5- 

15%), dialysis disequilibrium(10%-20%), 

headache (5%), chest pain (2-5%), itching 

(5%), fever and chills (


hemodialysis patients—Nebraska and 

Maryland, 1998. JAMA 1998; 280(15):1299- 

1300. 

11. Eaton JW, Leida MN. Hemolysis in chronic 

renal failure. Semin Nephrol 1985; 5:133-139. 

12. De Wachter DS, Verdonck PR, De Vos 

JY, Hombrouckx RO. Blood trauma in plastic 

haemodialysis cannulae. Int J Artif 

Organs 1997; 20(7):366-70. 

13. Sica DA, Harford AM, Zawada ET. 

Hypercalcemic hypertension in hemodialysis. 

Clin Nephrol 1984;22:102-4. 

14. Zucchelli P, Santoro A, Zucchala A. Genesis 

and control of hypertension in hemodialysis 

patients. Semin Nephrol 1988;8:163-8. 

15. Singh S, Prakash J, Shukla VK, Sharatchandra 

Singh Lk. Intravenous Catheter associated 

complications. J Assoc Physicians Ind 

2010;58:186-7. 



Evaluation of Adenosine deaminase (ADA) activity in the diagnosis of 

tuberculous pleural effusion in children 

1 

Nedup D Bhutia, 2 Y.Tomba Singh, 3 Ch. Shyamsunder, 4 Th.Satyakumar, 5 M.Amuba Singh, 

4 

Sunibala Keithellakpam 

Abstract 

Objective: To evaluate the Adenosine 

deaminase (ADA) activity and to find out its 

specificity, sensitivity and the cut off value in 

the diagnosis of tubercular pleural effusion in 

children. Material and Methods: The study 

was carried out in 54 consecutive patients with 

pleural effusion of age < 13 years attending 

Outpatient Department (OPD) and 

Emergency Department of Regional Institute 

of Medical Sciences, Imphal. The patients 

were classified into two groups i.e. Group A ( 

Tubercular pleural effusion) and Group B ( Non 

tubercular pleural effusion) and the pleural fluid 

were studied for Adenosine deaminase (ADA) 

activity, its cut off value, sensitivity & specificity 

for the diagnosis of tubercular pleural effusion. 

Results: Group A (tubercular) consisted of 35 

patients (23 males & 12 females) with a mean 

age of 5.14 and group B (non tubercular) with 

19 patients (11 males & 8 females) and a 

mean age of 6.43 3.15 (years). The mean 

ADA activity value in group A was of 

114.7461.25 IU/L and group B has the mean 

of 30.896.66 IU/L ( p value < 0.001). Using a 

cut-off value of 40 IU/L, the sensitivity and 

specificity in the diagnosis of tubercular pleural 

1. Post Graduate Trainee, 2. Associate Professor, 3. 

Assistant Professor, 4. Registrar, Department of 

Pediatrics, RIMS, 5. Professor, Department of 

Biochemistry, RIMS. 


Dr. Nedup Bhutia, Department of Pediatrics, RIMS, 

Imphal. Pin - 795004, 

Phone – 91-9002890142 

effusion were 94.28 % and 89.47 % 

respectively. Conclusion: The present study 

shows that by using ADA value of 40 IU/L as 

the cut off value, we can ascertain the 

diagnosis of tubercular pleural effusion in 

children. Estimation of ADA level in pleural fluid 

is one of the reliable tests for the diagnosis of 

tubercular pleural effusion as it is adequately 

sensitive and specific, also easy, quick and 

economical to perform with high accuracy. 

Key words: Tuberculosis, pleural effusion, 

Adenosine deaminase. 

Introduction 

Tuberculosis, one of the oldest diseases 

known to affect humans, is caused by bacteria 

belonging to the Mycobacterium tuberculosis 

complex. The WHO estimates that 

tuberculosis today kills more children and 

adults than any other infectious diseases and 

that it kills 100,000 children each year. 1 

Children are the victims of adults and 

adolescents with tuberculosis. Child to child 

transmission of Mycobacterium tuberculosis 

is virtually unknown. Nahmias et al 1 refer 

tuberculosis as an “ADULTOSIS” – a disease 

inflicted by adults on children and not by 

children on adults. In pediatric outpatient 

department, 5 to 8 % attendance is accounted 

by tuberculosis. 2 

Adenosine deaminase (ADA) is an enzyme 

present in a great number of plants and 

animals, found from simple invertebrates to 

human beings. It is an important enzyme that 

48 



catalyzes the deamination of adenosine and 

deoxyadenosine into their respective inosine 

nucleosides. ADA is considered as indicator 

of cellular immunity and fundamental for 

differentiation of lymphocytes. In humans, the 

lack of this enzyme results in severe 

lymphopenia and immunodeficiency, bringing 

the risk of an early death for the affected 

individuals. It is found in several human 

diseases, lymphocytic effusion, including 

those consequent of tuberculosis, neoplasm 

and some acute viral infections. This suggests 

that a high ADA activity is indirectly related to 

the subsets of T cell lymphocytes involved in 

the inflammatory response. 3 The 

determination of the ADA level in the suspected 

pleural fluid appears to be the most promising 

marker because of the ease, rapidity and cost 

effectiveness of the ADA assay. 

Pleural fluid Adenosine deaminase (ADA) can 

be used as a rapid and accurate method for 

the early diagnosis of tuberculous pleurisy, 

thereby expediting the initial decision making 

over the therapeutic and management plans, 

especially in developing countries where the 

disease is highly prevalent and resources are 

limited. 4 

The present work tries to evaluate the 

Adenosine deaminase (ADA) activity and to 

find out its specificity, sensitivity and the cut 

off value in the diagnosis of tubercular pleural 

effusion in children. 

Material and methods 

The study group comprises of 54 consecutive 

patients with pleural effusion, of which 35 were 

tubercular (group A) and 19 were non 

tubercular (group B) attending Out Patient 

Department (OPD) and Emergency 

Department of Paediatrics, RIMS hospital, 

Imphal during the period between August 2007 

to July 2009. Patient with age 13 years were 

excluded and the procedures followed were 

in accordance with the ethical standards of 

the Institute. Those 54 cases of pleural 

effusion were divided into: Group A: 

Tuberculous pleural effusion (35); Group B: 

Non-tuberculous pleural effusion (19). Group 

B include Nephrotic syndrome- 6; malignant 

pleural effusion-1; cardiac cause – 4; other 

causes-8. 

The diagnosis of tuberculous pleural effusion 

was made on detailed history, clinical 

examination, chest X-ray, pleural fluid analysis 

for cytology, protein, acid fast bacilli and 

Montoux test. 

Adenosine deaminase (ADA) hydrolyses 

adenosine to ammonia and inosine. The 

ammonia formed further reacts with a phenol 

and hypochlorite in alkaline medium to form a 

blue colored complex with sodium 

nitroprusside acting as a catalyst. Intensity of 

the blue colored complex formed is directly 

proportional to the amount of ADA present in 

the sample. 

Adenosine + H 2 

O ADA 

Ammonia + Inosine 

Ammonia + Phenol+ Hypochlorite alkaline medium Blue Indophenol 

complex 

Collection of pleural fluid sample for 

determination of Adenosine deaminase (ADA) 

was done with a sterile 10 ml dispovan syringe 

with standard precautions. In the present 

study, ADA was estimated by using 

colorimetric method described by Guisti G 

and Galanti B (1984) by using commercially 

available reagent kit manufactured by 

Microxpress Tulip Diagnostics (p) Ltd., India. 

Results 

Group A (tubercular) consisted of 35 patients 

(23 males & 12 females) with a mean age of 

5.14 group B (non tubercular) with 19 patients 

(11 males & 8 females) and a mean age of 

6.43 3.15 (years). The mean ADA activity value 

in group A was of 114.7461.25 IU/L and group 

B has the mean of 30.896.66 IU/L ( p value < 

0.001 ) as shown in Table 1. 

Using 7 different values of positive criterion or 

cut off values, sensitivity ( true positive rate), 

specificity (true negative rate), positive 

predictive value (PPV) and negative predictive 

value (NPV) were calculated for estimating the 

most appropriate cut-off value level for the 

diagnosis of tubercular pleural effusion. 

Using a cut-off value of 40 IU/L, the sensitivity 

and specificity in the diagnosis of tubercular 

pleural effusion were 94.28 % and 89.47 % 

respectively.(Table 2). 



Tables - 

Table - 1 : ADA values (mean S.D) in different 

groups. 

Category ADA values(IU/L) P-Value 

Group A 114.74 61.25 < 0.001 

Group B 30.89 6.66 (Highly 

significant) 

Table - 2: Test performance characteristics for 

7 different values of ADA positivity. 

Positivity sensitivity specificity PPV NPV 

criterion 

(value) 

30 100 36.84 74.47 100 

35 100 68.42 77.79 100 

40 94.28 89.47 94.28 89.47 

45 91.42 100 100 86.36 

50 91.42 100 100 86.36 

55 85.71 100 100 79.16 

60 77.14 100 100 70.37 

Discussion 

The determination of the ADA level in the 

suspected pleural fluid appears to be the most 

promising marker because of the case, 

rapidity and cost effectiveness of the ADA 

assay. Strict distinction between the adult and 

childhood patterns of tuberculosis should be 

avoided. 5 

In the present study the ADA activity was found 

to be highest in tubercular pleural effusion with 

a mean ADA of 114.7461.25 U/L comparing to 

those with non tubercular pleural effusion with 

the mean ADA value of 30.896.66 U/L (p value 

< 0.001). Bañales JL et al 6 also conducted a 

similar study and found that ADA activity of 

tubercular pleural effusion was more than that 

of non tubercular with mean of 123.25 U/L and 

30.36 U/L respectively. Nukuyucu Z et al 7 also 

measured ADA activity in children with 

tubercular pleural effusion with mean serum 

ADA activity of 74.0668.5 U/L. Their findings 

were found lower than our present findings. 

Gupta BK 8 found significantly higher ADA 

activity (mean of 77.68 U/L and p < 0.001) in 

comparison to other effusions. He also found 

ADA value > 50.75 IU/L with sensitivity and 

specificity of 100% and 94.1% respectively 

and considered ADA value as low cost and 

easy routine investigation for tuberculous 

pleural effusion. His study is concordant to 

our present study. Valdes L et al 9 also found 

ADA value of 47 U/L as the cut off value in the 

diagnosis of tubercular pleural effusion in 

children which was almost similar with our 

study with cut off value of 40 U/L. Sharma SK 

et al 10 also conducted ADA estimation and with 

the cut off value of 35 IU/L with the sensitivity 

and specificity of ADA were 83.3% and 66.6% 

respectively. Even though the cut off ADA value 

used in their study is lower than our present 

study but it is also concordant to our finding 

concluding that ADA level in tubercular pleural 

fluid was significantly higher than other pleural 

effusion. 

In the present study it is found that the ADA 

value of 40 IU/L is considered best as the 

reference limit for diagnosis of tubercular 

pleural effusion with the sensitivity of 94.28% 

and specificity of 89.47% and the positive 

predictive value of 94.28% and negative 

predictive value of 89.47%. It is also concluded 

that unilateral pleural effusion occurred more 

frequently than bilateral pleural effusion in both 

the groups. 

Conclusion 

The determination of Adenosine deaminase 

(ADA) level in the suspected pleural fluid 

appears to be the most promising marker 

because of the ease, rapidity and cost 

effectiveness of the ADA assay. However 

study should be carried out on large number 

of patients to reach a better conclusion. 

50 



References 

1. Klein M, Michael DI. Mycobacterial Infections. 

In : Pediatric respiratory medicine, Taussig- 

Landau, Le Souf, M Morgan Sly(Eds),2 nd 

Edn.,1999;New York, 702-724. 

2. Gupte S : Pediatric Pulmonology. In : The short 

Textbook of Pediatrics, Daljit Singh, Suraj Gupte, 

Jaypee Brothers Medical Publishers (P) Ltd, 

New Delhi, 10 th Edn.,2004,264-277. 

3. Tuon FF, Da Silva VI, Leila GM, Ho YL. The 

usefulness of ADA in the diagnosis of 

tuberculous pericarditis. Rev Inst Med Trop S 

Paulo 2007;49(3):165-170. 

4. Kataria YP, Khurshid I. Adenosine Deaminase 

in the diagnosis of tuberculous pleural effusion. 

Chest 2001;120:334-336. 

5. Khurshid R, Shore N, Saleem M, Naz M, 

Zameer N. Diagnostic significance of Adenosine 

deaminase in pleural tuberculosis. Pak J Physiol 

2007;3(2):23-25. 

6. Bañales JL, Pineda PR, Fitzgerald JM, Rubio 

H, Selman M, Lezama MS. Adenosine 

deaminase in the diagnosis of tuberculous 

pleural effusions. A report of 218 patients and 

review of the literature. Chest1991; 99:355-357. 

7. Nukuyucu Z, Karakurt ,Bilaloglu E, Karacan C, 

Tezic T. Adenosine deaminase in childhood 

pulmonary tuberculosis : diagnostic value in 

serum, J Trop Pediatr 1999;45(4):245-7. 

8. Gupta BK: Evaluation of pleural fluid and serum 

Adenosine deaminase levels in differentiating 

transudative from exudative effusions, Ind J. Tub 

1990; 49: 97- 100. 

9. Valdes L, San Jose E, Alvarez D, Valle JM. 

Adenosine deaminase isoenzymes analysis in 

pleural effusion: Diagnostic role and relevance 

to the origin of increased ADA in tuberculous 

pleurisy. Eur Repir J 1996; 9(4):747-51. 

10. Sharma SK, Suresh Y,Mohan A, Kaur P, Saha 

P, Kumar A, Pande JN. A prospective study of 

sensitivity and specificity of Adenosine 

deaminase estimation in the diagnosis of 

tuberculous pleural effusion. Indian J Chest Dis 

Allied Sci 2001;43:149-155. 



The vertebral level of termination of the spinal cord in human foetuses 

1 

M. Matum, 2 Th. Naranbabu, 2 N. Saratchandra, 2 Ch. Rajendra, 3 Ch. Arunchandra 

introduction 

The caudal termination of the human spinal 

cord relative to the vertebral level has been 

well studied in the adult with accurate 

precision. They subsequently found the level 

of termination of the human spinal cord 

anywhere between the last thoracic and the 

third lumbar vertebrae, though the majorities 

of the cases end opposite the the first and 

second lumbar vertebrae 1 . 

In foetuses, spinal cord occupies the whole 

length of the vertebral canal, then later on the 

level of termination of the spinal cord gradually 

decreases from below upwards as the 

gestational week advances. However, there 

are varied opinion about the level of termination 

of spinal cord at birth viz: spinal cord 

terminates at the level of third lumbar vertebra 

at birth 2,3,4,5,6 and it ends at the lower border 

of the second lumbar vertebra 7 . However, 

Rao 8 recorded in one of the foetuses of the 

South India as early as 214mm Crown 

Rump (CR) length at the level of first lumbr 

vertebra. 

Hence, there seems to be a slight differences, 

regarding the level of termination of the spinal 

cord in foetuses particularly amongst different 

races. 

1. Associate Prof. 2. Professor and 3. Ex. Prof. Anat. 

Deptt. of Anatomy, RIMS, Imphal. 


Dr. M. Matum, 

Associate Professor 

Department of Anatomy, RIMS, Imphal 

52 

Aims and objects 

The present study is to find out the level of 

termination of the spinal cord in the foetuses 

of Meiteis of Manipur. 


This study was conducted in the Department 

of Anatomy, RIMS, Imphal in one hundred and 

twentyfive foetuses who died before and soon 

after birth after obtaining due permission from 

the ethical committee. These foetuses were 

collected from the Department of Obstretrics 

and Gaenecology, RIMS Hospital, Imphal with 

due permission from the concerned parties 

and authorities. Any foetus showing gross 

maceration and malformation was excluded 

from the study. Age of the foetuses were 

determined from the LMP and CR length. 

All the foetuses were fixed in 10% formalin. 

Fixed foetus was kept in prone position with 

abdominal support in a basin. A midline incision 

extending from the cervical region to the tip of 

the coccyx was given and skin was reflected 

on either side. Extensor muscles were also 

reflected.To expose the spinal cord, the 

pedicles of the vertebrae were cut near the 

bodies of the vertebrae and carefully removed 

along with laminae. The dura matter was slitted 

longitudinally and the lower extremity of the 

conus medullaris was exposed. The 

relationship of this point to the underlying 

vertebrae or inter vertebral disc was determined 

by counting the pedicles or inter vertebral disc 

between second and third cervical vertebrae 

from above downwards. Photographs of the 

dissected foetuses were also taken. 



Observation 

constant dispropotional increase in the relative 

length of the lumbar region over the cervical 

The caudal limit of the spinal cord showed to 

region and thoracic region. Initially the cervical 

change constantly in different age of the 

region is the longest until 6 to 8 month of 

foetuses. Also the foetuses of the same age 

gestation when it is equalled in length by the 

group showed variation at the level of the 

lumbar vertebrae. At term the cervical region 

conus medullaris. The finding of the study, 

is about four- fifth of the lumbar and in adult 

from foetuses divided into VII groups, is shown 

only two-thirds. The spinal cord also follows 

in Table I. In this finding, the figure like L 1.5 

this pattern but later on to a lesser degree. 

would mean the middle of the first lumbar 

They also observed that the lumbar cord and 

intervertebral disc and L 2 

the middle of the 

column grow faster than other regions, 

second lumbar vertebra. 

although the growth of the cord is relatively 

The finding of the study shows a rapid ascent 

of the conus medullaris before 16 th week of 

gestation when the spinal cord ends opposite 

the middle of the first sacral vertebra. 

Thereafter the cord continues to ascend at 

much slower rate till its terminal reaches 

between the first and third lumbar 

intervertebral disc at term. 

lower than that of the vertebral column. There 

is also equal rate of growth of the vertebral 

column and the spinal cord throughout the 

period of childhood. But, both the components 

of lumbar axis contineud to lengthen more 

than other axial regions. They also claimed 

that the most rapid ascend of the conus 

medullaris takes place between 11 and 17 

weeks of gestation. A. J. Barson 7 found the 

TABLE -I 

rapid ascent of the conus medullaris to the 

LEVEL OF TERMINATION OF THE SPINAL CORD 

fourth lumbar vertebra at 19th week stage. 

Groups Gestational No.of Termination Of The present study shows the rapid ascent of 

Week Observation The Spinal Cord the spinal cord in the first half gestation 

I 13-15 9 C 0 

– s 1 particularly upto 16th weeks of gestation. 

II 16-20 13 S 1 – 

L 4 

III 21-25 16 L 5 

–L 3 

Various previous workers have assumed the 

IV 26-30 22‘ L 5 

- L 2 

difference of at least two vertebrae from the 

V 31-35 40 L 4 

-L 2 normal average level as normal deviation. 

VI 36-38 20 L 4 

– L 1.5 There are different findings on the level of 

VII 39-40 17 L 3.5 

- L 1.5 termination of spinal cord at term viz: the 

Discussion 

The spinal cord occupied the whole length of 

the vertebral column during early development. 

Later on it gradually ascend upwards. Aeby 9 , 

Ballantyne 10 and Bardeen 11 have found a 

spinal cord ascent upwards to its term level 

at the second or third lumbar vertebrae but it 

may end anywhere between twelfth thoracic 

and third lumbar vertebrae 5 , conus medullaris 

leveled at the thirth lumbar vertebra at 

birth 12,13 and betwen second and third lumber 

vertebrae 14 . 

The present study also shows that the spinal 

cord terminate at the level between first and 

thirth lumbar intervertebral disc at term and 

there is no much deviation from the findings 

of other workers from different regions. It is 

also observed that there is a constant change 

of position of the lower limit of the spinal cord 

throughout the period of pregnancy. A rapid 

ascent of the spinal cord is also found during 

the first half of pregnancy. 



References 

1. Lawrence H. Bannister, Martin M. Berry, 

Patricia Collins, Marry Dyson, Julan E. Dussek 

& Mark W.J. Fergusson: Nervous System: 

Spinal Cord: Vertebral levels of spinal cord 

segments.In: Patricia Collins editor, Gray’s 

Anatomy 38 th Ed,Edinbourgh, Churchill 

Livingstone 1995; pp. 1101. 

2. Hamilton w.j. . Spinal cord and meninges 2 th 

ed. , London, Macmillan Press 1976; 521. 

3. Hamilton W.J. , Boyd & H.W.Mossman . 

Human Embryology4 th ed., London, Macmillan 

Press1950; 93-101. 

4. Arey L. B. The Spinal cord: External form. 

In:Leslei Brainerdarey, editor, Developmental 

Anatomy 7th ed., Philadelphia, W. B. 

Saunders 1966; 467-68. 

5. Barson A.J. . The vertabral level of termination 

of the spinal cord during normal and abnormal 

development. Journal of Anatomy 1970;106(3): 

489-97. 

6. K.L. Moore . Central Nervous System : The 

Spinal Cord. In: Keith L. Moore Ph. D. Editor, 

Before we are born 4 th 

Ed.Philadelphia,Saunders 1993; 196-200. 

7. T.W. Sadler : Central Nervous System . Medical 

Embryology, Langman J. 7 th ed., Baltimore, 

William & Wilkins1995; 384. 

8. Rao V.S. . The lower limit of the spinal cord in 

South Indian Fetuses . Journal of Anatomical 

Society of India 1946; 83: 175. 

9. Aeby C.T. . Die Altersverchidenheiten der 

menchilchen Wirbelsavile. Arch.anat. 

Entwagwsh 1879. 

10. Ballantyne. J.W. The spinal column in the 

infant. Edin: Med. J. 1892(37); 913-22. 

11. Bardeen C.R. Studies of the developmentof the 

human skeleton. The curves & the 

proportionnate regional lengthof the spinal 

column during the first three months of 

embryonic development. American Journal of 

Anatomy 1905; 4: 275-78. 

12. J.G. Chusid. Central Nervous System: Spinal 

Cord. In: J.G. Chusid editor, Correlative 

Neuroanatomy & functional Neurology 16 th 

ed. , New york, Lange Med. Publication 1976; 

62. 

13. Snell R.S. . The development of Central Nervous 

System. Clinical Neuroanatomy 6 ed, 

Philadelphia, Lippincott Williams &Wilkins 

1995; 501. 

14. Malcom B. Carpenter . Regional Anatomy of 

the Central Nervous System. Murray L. Barr & 

John A. Kiresan 4 th ed. , Philadelphia, Harper 

& Row Publishers Inc. 1983; 62. 

54 


REVIEW ARTICLE 

Oral changes in diabetics - a review 

1 

Ng. Sanjeeta, 1 W. Robindro, 2 T. Nabachandra Singh 

Introduction 

The countries with the largest number of 

diabetes are India, China and the US, with 

India beginning to be regarded as the diabetic 

capital of the world 1 . The chronic 

hyperglycemia and attendant metabolic 

dysregulation in diabetes mellitus (DM) may 

be associated with secondary damage in 

multiple organ systems, especially the kidneys, 

eyes, nerves and blood vessels 2 . The 

association between DM and changes in the 

oral cavity have been the subject of reports in 

both the medical and dental literatures. A 

number of oral soft tissue abnormalities have 

been associated with DM by various reports, 

with more emphasis being given on its relation 

with periodontal diseases 3 . There are strong 

evidence of both type 1 and type 2 diabetic 

patients having more severe periodontal 

disease than do individuals without 

diabetes 4,5,6,7 . Other specific conditions that 

have been identified include geographic 

tongue, fissured tongue, median rhomboid 

glossitis, hyperplastic gingivitis, lichen planus, 

parotid gland enlargement, candidiasis, 

xerostomia, burning sensations of oral 

mucosa, taste disturbances, increased 

incidence and severity of dental caries, 

traumatic ulcers, etc 3 . “Grinspan syndrome” 

1 

Assistant Professor, 2 Professor & Head, Department 

of Dentistry, Regional Institute of Medical Sciences, 

Imphal 


Dr. Ng. Sanjeeta, Assistant Professor, Department of 

Dentistry, Regional Institute of Medical Sciences, 

Imphal 

is an interesting condition in which there is 

coexistence of DM, lichen planus and 

hypertension in the same individual. 

Pathogenesis 

The underlying cause for increased 

susceptibility to infection, impaired wound 

healing capabilities and vascular injury 

following chronic hyperglycemia in DM can be 

attributed to various underlying mechanisms 2 . 

The underlying mechanisms 2,8 which, in turn, 

affect infections can be associated with 

• Sorbitol- myoinositol osmolarity changes 

• Oxidative- redox stress 

• Non-enzymatic glycation reactions 

(advanced glycation end products- AGEs) 

• Activation of the protein kinase C- 

diacylglycerol pathway. 

The diabetic state impairs the synthesis of 

collagen and glycosaminoglycans in the 

gingiva and enhances crevicular fluid 

collagenolytic activity. It results in the loss of 

periodontal fibres, supporting alveolar bone 

resulting in loosening and exfoliation of the 

teeth 9 . 

Diabetes- induced changes in immune cell 

function produces an inflammatory immunecell 

phenotype (upregulation of 

proinflammatory cytokines from monocytes/ 

polymorph nuclear leukocytes and 

downregulation of growth factors from 

macrophages), predisposing to chronic 

inflammation, progressive tissue breakdown, 



and diminished tissue repair capacity 9 . 

Sialosis 

Sialosis which is defined as an asymptomatic, 

non-inflammatory, non-neoplastic 

enlargement of the salivary glands due to 

metabolic causes has been observed in 24% 

of the diabetic subjects 10 . Sialosis is caused 

by fatty infiltration of the interstitium and 

enlargement of the acinar cells. In diabetics, 

it is characterized by bilateral enlargement of 

the parotid salivary glands though the 

submandibular gland may also be involved. 

Compensatory hyperplasia of the glandular 

parenchyma following a declining plasma 

insulin concentration, and a compensatory 

mechanism to combat xerostomia in diabetics 

has been interpreted by investigators as the 

causes of the glandular enlargement 10 . 

Xerostomia 

Xerostomia is a subjective sensation of the 

dryness of the mouth and has been a feature 

of uncontrolled diabetes. Xerostomia in 

diabetes is traced to decreased salivary 

secretion related to various factors associated 

with diabetes. Microvascular disease, 

autonomic neuropathy, dehydration and loss 

of urinary electrolytes resultant to polyuria are 

considered as causative mechanisms for the 

decreased salivary secretion in diabetics 10 . 

Experimental studies in diabetic rats have 

shown that fatty infiltration and degeneration 

of the parotid gland destroy the secretory 

tissue leading to diminished saliva 

production 10 . However, more than a third of 

diabetic patients report xerostomia in the 

presence of normal production of saliva with 

some studies reporting comparable or 

increase in volumes of salivary secretion. 

Hence, the pathogenesis of this condition still 

remains unclear and may have a 

psychological component 10 . 

Taste impairment 

All the primary taste sensations may be 

blunted as is demonstrated by chemical 

gustometry. Taste threshold may also be 

altered and is demonstrable by 

electrogustometry. Impairment of the sweet 

taste has been most frequently reported and 

may be present at diagnosis. Although taste 

56 

impairment is usually well tolerated, a blunted 

sweet sensation may favour sweet tasting 

food and may exacerbate the hyperglycemia 

in an undiagnosed diabetic patient. The role 

of altered taste sensation in the predilection 

for food containing refined sugar and the 

subsequent poor dietary compliance in some 

diabetics has not been investigated. 

Sulphonylureas, the group of drugs 

commonly used in type 2 diabetes have been 

shown to be associated with altered taste 

sensation 10 . 

Oral lichen planus and lichenoid reaction 

Lichen planus is a mucocutaneous disorder 

of uncertain aetiology. An association between 

oral lichen planus (OLP) and impaired glucose 

tolerance has been reported, but may be 

coincidental as it has not been confirmed by 

various investigators. OLP may either regress 

spontaneously or may respond to local 

treatment unrelated to the glycemic state in 

DM. The triad of OLP, DM and hypertension 

in Grinspan’s syndrome may be a coincidental 

association. What is clinically diagnosed as 

lichen planus could perhaps be a lichenoid 

reaction developing as a side-effect of certain 

oral hypoglycemic or antihypertensive 

10, 11 

drugs. 

Oral candidosis 

Candida species have frequently been 

reported to be more prevalent and have been 

isolated in greater numbers from the oral 

cavity of diabetics compared to non-diabetic 

individuals. Enhanced growth of the yeast may 

be attributed to low salivary secretion and 

presence of a high concentration of salivary 

glucose. Subjects with diabetes were found 

to be at least five times more likely than control 

subjects to have oral soft tissue disease 

attributable to candidiasis. Prerequisites for 

candidal infections like enhanced 

adhesiveness of candida to oral epithelium 

and an impaired immune response due to 

defective neutrophil function is a feature of 

diabetes. 10 

Dental caries 

Saliva and gingival crevicular fluid, in addition 

to constituents of the diet are the source of 



fermentable carbohydrates required for the 

growth of cariogenic bacteria. Significantly 

elevated levels of glucose in saliva and 

crevicular fluid, along with decreased salivation 

as they occur in diabetics may promote the 

increase in the incidence of dental caries. 

Although the total oral intake of refined 

carbohydrates may be reduced in diabetic 

patients, ingestion of food still occurs at 

frequent intervals throughout the day, and 

causes a repeated reduction in the pH of the 

oral cavity which is another factor for the 

increased susceptibility. 10 

Mucormycosis 10 is a rare but serious 

systemic fungal infection that may occur in 

uncontrolled diabetes. 

Tongue changes 

Various studies report increased incidence of 

median rhomboid glossitis, benign migratory 

glossitis, burning mouth syndrome or fissuring 

of the dorsum of the tongue. 

Median rhomboid glossitis which is a painless, 

central, depapillated area on the middle third 

of the dorsum of the tongue has been reported 

in 30% of 175 diabetic patients surveyed 10 . 

There has been a four fold increase in 

incidence of geographic tongue compared to 

non diabetes according to a survey 10 . In nondiabetic 

patients this lesion responds to 

systemic zinc therapy. 

Burning mouth syndrome which particularly 

affects the tongue and reported in subjects 

with undiagnosed diabetes are not related 

primarily to candidal infection and almost 

always resolves when glycemic control is 

instituted. Acute neuritis, chronic neuropathic 

lesion and xerostomia seen in diabetics are 

implicated in the aetiology, highlighting its 

multifactorial origin. 

Fissured tongue was present in 28.0% in a 

survey of 175 diabetics 12 . Majority of them 

showed varying degree of placation with a 

transverse component to the fissures. 

Symmetrical, medially placed, double, 

longitudinal fissures extending from sulcus 

terminalis, meeting centrally to demarcate a 

triangular area of tongue were seen in some 

instances. 

Traumatic ulcers and irritation fibromas 3 

Higher prevalence for oral ulcers and irritation 

fibromas are reported in diabetics. Several 

mechanisms like slower healing time, 

microangiopathy or a defective function of the 

polymorph nuclear leukocytes may be 

responsible. 

Periodontium and DM 

The relationship between periodontal disease 

and DM has been extensively studied and has 

been definitive enough to consider 

periodontitis as the sixth complication of 

DM 13 . In diabetes with poor glycemic control, 

gingival and periodontal inflammations are 

manifested as increase in incidence and 

severity, with deep periodontal pockets, rapid 

bone loss, and frequent periodontal 

abscess 8 . There has also been a correlation 

between the severity of the periodontal 

destruction, the duration of the diabetes and 

the presence of diabetic complications. 

Defective polymorphonuclear leukocyte 

function with resultant susceptibility of 

infection, increased collagenase activity, 

decreased synthesis and maturation of 

collagen and extra cellular matrix are 

postulated as causes of poor periodontal 

health in diabetics 8 . The abnormal state of 

the collagen is attributed to excessive 

formation of advanced glycation end 

products (AGEs) in hyperglycemic states, 

which crosslink the collagen rendering it less 

soluble and hence less likely to be repaired 

or replaced 8 . 

Tendency towards enlarged gingiva, sessile 

or pedunculated gingival polyps, polypoid 

gingival proliferations, abscess formation, 

periodontitis, and loosened teeth are the other 

varieties of periodontal changes described in 

DM. 

CONCLUSION 

The oral changes in diabetes are less likely to 

be seen in well controlled diabetics. The 

changes are not specific or pathognomonic 

for diabetes. The association of specific oral 

diseases and diabetes is not only of 

importance in the detection of undiagnosed 

diabetes, but also in the elucidation of the 

pathogenesis of various oro-facial diseases. 



However, the association of certain oral 

conditions with DM is not definitive and is still 

a matter of debate. In view of the ever 

increasing sedentary lifestyles and poor eating 

habits that have contributed to the escalation 

of DM worldwide, DM-related oral diseases 

deserve adequate recognition and further 

investigation. 

References 

1. Sharma A, Tiwari A. Diabetes mellitus and 

Dental Disease-a review. JIDA 2002; 73: 

116-21. 

2. Alvin C Powers. Diabetes Mellitus. In: 

Fauci AS, Braunwald E, Kasper DL, 

Hauser SL, Longo DL, Jameson JL, 

Loscalzo J, editors. Harrison’s Principles 

of Internal Medicine. 17 th Ed. United States 

of America:McGraw-Hill;2008 (2): 2275 – 

304. 

3. Guggenheimer J, Moore PA, Rossie K, 

Myers D, Mongelluzzo MB, Block HM. 

Insulin-dependent diabetes mellitus and 

oral soft tissue pathologies. I. Prevalence 

and characteristics of non-candidal 

lesions. Oral Surg Oral Med Oral Pathol 

Oral Radiol Endod 2000; 89 (5): 563 –69. 

4. Finestone AJ, Bouriji. Diabetes mellitus 

in periodontal disease. Diabetes1967;10: 

336 – 40. 

5. Cerda J. Periodontal disease in NIDDM. 

The effect of age and time since diagnosis. 

J Periodontol 1995; 65: 991 –95. 

6. Campus G, Salem A, Uzzau S, Baldoni 

E, Tonolo G. Diabetes and periodontal 

disease: A case control study. J 

Periodontol 2005; 76 (3): 418 – 25. 

7. Shlossman M, Knowler WC, Pettit DJ, 

Genco RJ. Type 2 DM and periodontal 

disease. JADA 1990; 121: 532 – 36. 

8. Klokkevold PR, Mealey BL,Carranza FA. 

Influence of Systemic Disease and 

Disorders on the periodontium. In: 

Newman MG, Takei HH, Carranza FA, 

editors. Carranza’s Clinical 

Periodontology. 9 th ed. Philadelphia: 

Saunders; 2003. p 208-11. 

9. Kiran M, Arpak N, Unsal E, Erdogan MF. 

The effect of improved periodontal health 

on metabolic control in type 2 diabetes 

mellitus. J Clin Periodontol 2005; 32 (3): 

266 – 72. 

10. Lamey PJ, Darwazeh AM, Frier BM.Oral 

disorders associated with diabetes 

mellitus. Diabet Med 1992; 9 (5): 410 –1 

6. 

11. Borghelli RF, Pettinari IL, Chuchurru JA, 

Stirparo MA. Oral lichen planus in patients 

with diabetes: An epidemiologic study. 

Oral Surg Oral Med Oral Pathol 1993; 75: 

498 – 500. 

12. Farman AG. Atrophic lesions of the tongue: 

A prevalence study among 175 diabetic 

patients. J Oral Pathol 1976; 5: 255 – 64. 

13. Loe H. Periodontal disease. The sixth 

complication of diabetes mellitus. 

Diabetes care 1993;16: 329-34. 

58 


CASE REPORT 

Synchronous carcinomas of larynx and oesophagus: a case report 

1 

T. Dhaneshor Sharma; 2 Th. Tomcha Singh, 3 S. Thingbaijam; 

A 45-year-old male, heavy smoker and heavy 

alcoholic who never chewed tobacco was 

admitted in our ward with complaints of 

odynophagia to solid food for the last 2 months 

Indirect laryngoscopy showed a growth on left 

aryepiglottic fold without vocal cord fixation 

and pooling of saliva in the left pyriform 

fossa. There were no palpable cervical 

lyphadenopathy. All vital signs were within 

normal limits. His complete haemogram, kidney 

function test, random blood sugar level 

were within normal limits. But, liver function 

test showed raised alk. Phosphate (349.0 IU/ 

L, normal range;30-120 IU/L).General physical 

and systemic examinations revealed no 

abnormality. His CT thorax report was suggestive 

of carcinoma mid oesophagus with 

azygo-oesophageal extension and superior 

segment of right lung lower lobe. Endoscopy 

revealed an infiltrative growth at left ary-epiglottic 

fold and a polypoid mass of 5 cm length 

at mid oesophagus at a distamce of 30 cm 

from incisor. There were healthy and normal 

mucosa of more than 5 cm. between the two 

growths. Biopsies were taken from these 

growths and confirmed squamous cell carcinomas 

were confirmed histopathologically 

from both sites (Fig. I & II).Thus, the synchronous 

carcinomas of supraglottic and 

1. Sr. Registrar; 2. Prof. & Head, Dept. of Radiotherapy; 

3. Assoc. Prof., Dept. of ENT, RIMS, Imphal 

Corresponding Author: 

Dr. T. Dhaneshor Sharma, Sr. Registrar, Department 

of Radiotherapy, RIMS, Imphal Manipur. 

e-mail:dhaneshorsharma@ymail.com 

Fig.I. Biopsy from (L) ary-epiglottic fold showed a tissue 

fragment line by stratified squamous-epithelium 

with features of squamous cell carcinoma well differentiated. 

Fig. II. Biopsy from middle esophagus showed only 

tumour tissue displaying features of squamous cell 

carcinoma-poorly differentiated. 

oesophagus in stage I and III respectively was 

diagnosed. Patient was given 3 cycles of 

cisplatin -based anterior chemotherapy followed 

by radiotherapy and discharged. 

Discussion 

Second primary tumour that occurs 

simultaneously or within 6 months of the first, 

are called synchronous tumours. A second 

synchronous may develop in esophagus, 

head and neck and lungs in 10-40% of patients 


CASE REPORT 

with head and neck squamous cell 

carcinoma 1,2 . In another study 9% of the 

synchronous second cancers are detected 

in oesophagus, 46% in lung, 17% in head and 

neck, 18% outside the aerodigestive tract in 

patients of head and neck carcinomas 3 . 

Synchronous squamous cell carcinomas of 

involving supraglottic and esophagus are very 

rare. Only few cases are reported in the 

literature of synchronous maligancy 1 . This 

case is the first case reported so far in our 

department. 

There is a similar exposure pathway to the 

mucosa from environmental carcinogens 

because of the common conduit connecting 

the oral cavity, lung and esophagus causing 

synchronous or metachronous tumors. 

Genetic analysis has shown that closely 

spaced tumors in the head and neck are often 

derived from the same neoplastic clone but 

most head and neck squamous cell 

carcinomas (HNSCCs) and oesophageal 

squamous cell carcinomas (ESCCs) were 

found to be entirely independent tumors 4 . The 

synchronous tumors in our case may also 

be treated as independent tumors. 

Second primary tumors are a major problem 

in head and neck oncology, because their 

development has a profound impact on longterm 

survival and often fatal. The survival rate 

for head and neck cancers with a second 

cancer at oesophagus is only 3%, whereas 

it is 20% for a second head and neck cancer 

and 2% for a second lung cancer 5 . Therefore, 

management of synchronous malignancies 

are challenging for curative treatment. But, if 

the primary malignancies are diagnosed in 

early stages the survival rates could be 

increased. In addition to curative treatments 

there lies major role of chemoprevention for 

such patients in view of the presence of alter 

clones on mucosa remaining beyond the limits 

of surgical resection and irradiated clinical 

target volume to prevent local recurrences and 

metachronous malignancies. 

As the incidence of head and neck cancers 

are increasing the incidence of the 

synchronous tumors will be increasing and 

there is paramount importance of awareness 

among clinicians about the possibility of 

esophagus being second primary tumor in 

patients of head and neck cancers. The case 

is presented due to its rarity in our centre and 

its clinical importance for early detection, 

treatment decision and prognostication. 

References 

1. Lieciardello J, Spitz M, Hong W. Multiple 

primary cancer in patients with cancer of the 

head and neck: second cancer of the head and 

neck esophagus, and lung. Int. J. Radiat, Oncol, 

Biol. Phys. 17: 467-476, 1989. 

2. Jones A, Morar P, Phillips D, Field J, Husband 

D, Helliwell T. Second primary tumors in 

patients with head and neck squamous cell 

carcinoma. Cancer (Phila), 75:1343-1353, 

1995. 

3. Strobel K, Haerle SK, Stoeckli SJ, Schrank M, 

Soyka JD, Viet-Haibach P, Hany TF: Head and 

neck squamous cell carcinoma (HNSCC)- 

detection of synchronous primaries with (18) 

F-FDG-PET/CT. Eur J Nucl Mol Imaging. 2009: 

Jun; 36(6): 919-27. Epub 2009 Feb 10. 

4. Joseph Califano Paul L. Leong Wayne M. Koch, 

Claus F. Eisenberger David Sidransky and 

William H. Westra: Second esophageal 

tumours in patients with head and neck 

squamous cell carcinoma: An assessment of 

clonal relationships. Clinical Cancer Research 

July 1999; 5: 1862. 

5. Schwartz LH, Ozsahin M, Zhang GN, Touboul 

E, De Vataire F, Andolenko P, Lacau-Saint- 

Guily J, Laugier A, Schlienger M.: Synchronous 

and metachronous head and neck carcinomas. 

Cancer. 1994 Oct 1; 74(7): 1933-8. 

60 


CASE REPORT 

Infection associated hemophagocytic syndrome 

1 

Sharmila Laishram, 2 Rachael Simray, 3 Phurailatpam Madhubala Devi, 4 Durlavchandra Sharma, 

Case report: 

1 yr/male,Hindu from Kakwa, Imphal-west, 

Manipur was admitted in Paediatric Ward, 

RIMS on 4 th Feb ‘ 08 with the chief complaint 

of fever (1 mth), loose motion (15days), 

vomiting (7 days), puffiness of face (4 days), 

decrease micturation(3days). 

No significant past, personal & family 

history,no h/o of consanguineous marriage. 

On general physical examination, patient is 

of average Indian built, conscious, alert but 

irritable. He is febrile, very pale with puffy face. 

On systemic examination the positive findings 

are sternal tenderness & hepatosple 

enomegaly. 

Provisional Diagnosis of PUO with severe 

anaemia was given. 

Investigation profile shows the following: 

Hemogram shows pancytopenia ( TC-320/ 

cumm, Hb%-4.2g%, Pl Ct-22000/cumm) 

(fig-1). 

Pus cell in urine (20-30/HPF), E.Coli in urine 

C/S. LFT shows low protein( T.protein-4.4g/ 

1. MBBS, Demonstrator 2. MBBS, Demonstrator 

3. Associate Professor, 4. Professor & Head, Dept. of 

Pathology, Regional Institute of Medical Sciences, 

Imphal, Manipur. 

Corresponding Author: 

Dr. Sharmila Laishram, Demonstrator, Department 

of Pathology, RIMS, Phone number: 9856135291, 

Email: sharibam@yahoo.co.in 

Legends: 

Figure 1: Peripherial smear showing 

cytopenia(Leishman stain, 40X) 

dl, albumin-2.8g/dl, globulin-1.6g/dl) high 

enzyme level( GOT-460 U/L, GPT-132U/L, alk. 

Phosphatase-337U/ L). 

Figure 2a & 2b: B M smear showing 

hemophagocytosis(Leishman stain, 100X) 

High triglyceride (854mg%), prolonged PT & 

PTT and deep venous thrombosis in rt 

brachiochephalic & rt axillary vein. BM 

aspiration showed marked increased in the 

number of macrophages(60%) , majority of 

them phagocytosing hemopoeitic cells.(fig-2a 

& 2b) 


Discussion 

Hemophagocytic syndrome is a 

clinicopathological condition characterized by 

the uncontrolled activation & proliferation of 

macrophages / histiocytes with prominent 

hemophagocytosis in the bone marrow & other 

reticuloendothelial systems.The proliferating 

macrophages are reactive in most cases & 

rarely a part of a neoplastic clone. There are 

two main types: (1)Primary/Familial 

hemophagocytic lymphohistiocytosis(FHL), 

(2). Secondary/Reactive which includes a) 

Infection associated hemophagocytic 

syndrome (IAHS) due to viruses, bacterias, 

fungal, malaria, leishmaniasis, tsutsugamushi 

disease b) Malignancy associated in 

lymphoma, multiple myeloma, leukemias, 

melanoma, HCC c) autoimmune associated 

d) Miscellaneous due to drugs, Kawasaki 

disease, Chediak-Higashi disease etc 1 . The 

main primary clinical & biochemical 

features of HPS are non-remitting fever, 

hepatosplenomegaly, cytopenia, 

hypertriglyceridemia, hyperferritinemia. 

Diagnostic hallmark is the presence of welldifferentiated 

macrophages phagocytosing 

hemopoietic cells in the bone marrow 2 . It was 

seen in our case also. 

HPS is a rare and severe disease with a high 

mortality rate(50%). The clinical picture of HPS 

is due to increase inflammatory response 

caused by hypersecretion of proinflammatory 

cytokines like IFN-g, TNF-a, IL-6,8,10,12,18, 

M-CSF, MIP-1, by activated T-lymphocytes and 

macrophages 3 .One important phenomenon of 

HPS is the engulfment of blood cells by 

activated macrophages. The phaghocytic 

process is a non-random biologic event which 

involves sophisticated ligand receptor 

interaction 4 . 

References 

1. Shunichi Kumakura. Hemophagocytic 

syndrome. Internal Medicine 44: 278-280, 2005. 

2. Osugi Y, Hara J, Tagawa S, et al. Cytokine 

production regulating Th1 and Th2 cytokines 

in hemophagocytic lymphohistiocytosis. Blood 

89: 4100-4103, 1997. 

3. Menasche G, Feldmann J, Fisher A, de Siant 

Basile G. Primary hemophagocytic syndromes 

point to a direct link between lymphocyte 

cytotoxicity and homeostasis. Immunol Rev 

62 

CASE REPORT 

The diagnostic guidelines for HPS were 

proposed by Henter et al and the FHL study 

group of the Histiocyte society in 1991, which 

included clinical, laboratory and 

histopathological criteria 5 . 8 criterias were 

given , out of which 5 should be present to 

give a diagnosis of HPS. The criterias were – 

fever, hepatosplenomegaly, cytopenias >2 cell 

lines (Hb 

1000 U/l, elevated transaminases & bilirubin 

are other supportive evidences. 

Conclusion : 

Familial & secondary HPS are 

indistinguishable clinically & histologically. 

Proper history regarding the age of the 

patient, consanguineous marriage,any h/o of 

similar illness in the family, associated 

infection, any underlying disease will help in 

distinguishing between the two.Genetic / 

molecular testing is confirmatory for familial 

cases. In our case there is no family history, 

no consanguinity, but there was 

infection, therefore infection associated 

hemophagocytosis was given. 

Lastly for any case of prolonged fever & 

cytopenia a high level of suspicion & vigilance 

helps in early diagnosis & treatment, as HPS 

is a rare & life threatening disease. 

203: 165-179, 2005. 

4. Aderem A, Underhill DM. Mechanisms of 

phagocytosis in macrophages. Annu rev 

Immunol 17: 593-623, 1999. 

5. Chen et al. Hemophagocytic syndrome: a 

review of 18 pediatric cases. J Microbiol 

Immunol Infect 37: 157-163, 2004. 

6. Henter JI, Horne A, Arico M et al.HLH 2004: 

Diagnostic and therapeutic guidelines for 

hemophagocytic lymphohistiocytosis. Peadiatr 

Blood Cancer 2006. 


CASE REPORT 

Bilateral ankyloblepharon filiforme adnatum 

1 

Ibohal Salam, 1 A. Suchitra Devi, 1 M. Satyabhama Devi, 2 R.K. Bhabanisana 

One month old female child was referred from 

the Department of Pediatrics to the EYE OPD, 

RIMS on 30.1.09 with complain of inability to 

open the eyes properly. On examination, there 

was one fine band joining the two eyelids on 

the right side and two fine bands joining the 

left eyelids. The band on the right side was 

located at the junction of lateral one-third and 

medial two-third of the palpebral aperture. On 

the left side, one band was situated between 

medial one-third and lateral two-third and 

another between medial two-third and lateral 

one-third of the palpebral aperture. The bands 

were thin, about 1mm long, 0.3 mm thick and 

quite stretchable. The child was referred to a 

Paediatrician for detailed examination for any 

other associated anomalies, but no apparent 

congenital anomaly could be detected. 

Unfortunately, chromosomal analysis could 

not be done to rule out genetic error like 

Edwards syndrome. Except for the bands 

there was no eyelid structure abnormality. 

Because of the bands there was restriction 

on opening of the eyes. Anterior and posterior 

segments could not be examined properly. No 

similar case had occurred in the family. The 

bands were divided in Operation Theatre 

under topical anaesthesia with 4% Lignocaine. 

The eyelids were retracted by an assistant 

and the bands divided by the tip of conjunctival 

scissors. As the bands were very fine, they 

1. Associate Prof. 2. Fromer Professor, Department of 

Ophthalmology, Department of Pediatrics, RIMS. 


Dr. A. Suchitra Devi, Associate Professor,k Department 

of Ophthalmology, RIMS, Imphal. 

were cut with ease 

and no bleeding 

occurred during 

division of all the 

bands. Antibiotic eye 

drop and eye 

ointment were given 

for a few days postoperatively. 

The child was 

brought for follow-up 

2 months after the 

surgical procedure. 

On examination, 

there were no 

remnants of the 

bands, the eyelids 

appeared completely 

normal, the eyes 

w e r e 

orthophoric, 

o c u l a r 

movements 

were full and free 

with no 

abnormal 

movements. 

Fig 2. Post operative picture 

Anterior segment and posterior segment were 

normal. Fundus was within normal limits and 

developmental milestones were normal. 

Discussion 

Ankyloblepharon filiforme adnatum (AFA) is a 

rare congenital abnormality wherein the lid 

margins are connected by fine bands of 

extensile tissue, which reduce the palpebral 

a 

b 

Fig-1. a, b - Preoperative picture 


CASE REPORT 

fissure by interfering with the movements of 

the lids. It is distinguished from 

ankyloblepharon wherein the lid margins are 

directly fused together. AFA was first described 

by Von Hasner in 1882 and there has been 

sporadic case reporting since. The bands may 

be unilateral, 1 bilateral or multiple. The length 

of the bands has varied from 1 to 10mm, their 

breadth from 0.3 to 5mm and they are 

invariably extensile. The bands expand 

somewhat at their attachments which always 

lie between the cilia and the orifices of the 

tarsal glands. 2 On histological examination, 

the band has been shown to consist of a 

central vascular connective tissue which is 

usually highly cellular and embryonic in 

nature. 

It is now generally accepted that it results from 

(i) A temporary arrest of epithelial growth or 

(ii) An abnormally rapid proliferation of 

mesoderm or (iii) A combination of the two 

which allows union of unepithelised 

mesenchyme at certain points. The 

occasional familial occurrence and the 

presence of associated anomalies suggest 

such an origin. It can occur with cleft lip and 

palate, 3 as part of popliteal pterygia syndrome, 

as part of ankyloblepharon-ectodermal 

dysplasia-clefting syndrome or as part of curlyhair 

ankyloblepharon-nail dysplasia. Other 

reported association include hydrocephalus, 

meningocele, imperforate anus, bilateral 

syndactaly, cardiac problems, such as patent 

ductus arteriosus, ventricular septal defect, 

ectodermal syndrome, Edwards syndrome. 4 

In 1980 Rosenman et al proposed the 

classification of AFA(Table-1) into four 

subgroups to which has been added a fifth. 5 

Table- 1 Classification of AFA 

Group Associated anomalies 

1 None 

2 Cardiac or CNS 

3 Ectodermal dysplasia 

4 Cleft lip and/palate 

5 Chromosomal anomaly 

The major importance of this anomaly is that 

when it occurs, it should alert the physician to 

the possible presence of other congenital 

problems. 

References : 

1. Jain S, Atkinson AJ, Hopkisson B. 

Ankyloblepharon filiforme adnatum. Br. J 

Ophthalmol 1997;81:705. 

2. Duke- Elder S . System of Ophthalmology. Vol 

III. Normal and Abnormal Development. Part 2. 

Congenital Deformities. London: Henry 

Kimpton; 1964.p 869-871. 

3. Modi AJ, Adrianwalla SD. A multiple 

malformation syndrome with ankyloblepharon 

filiforme adnatum, with cleft lip and palate. Indian 

J Ophthalmol 1985;33:129-131. 

4. Clark DI, Patterson A. Ankyloblepharon filiforme 

adnatum in trisomy 18( Edward , s syndrome). 

Br. J. Ophthalmol .1985;69:471-473. 

5. Evans DG, Evans ID, Donnai D, Linderaum RH. 

Ankyloblepharon filiforme adnatum in trisomy 

18 Edwards syndrome. J Med Genet. 

1990;27:720-721. 

64 


CASE REPORT 

Plasmodium vivax cerebral malaria – a report of two cases 

1 

Sunilbala Keithellakpam, 2 Y. Tomba Singh, 3 

Ch. Syamsunder Singh 

Case report 

Case – 1. A 4½ year old girl presented with 

fever, headache, vomiting and pain abdomen 

for 4 days, passing yellowish urine for 3 days 

and two episodes of generalized tonic-clonic 

seizures followed by loss of consciousness 

for the last 24 hours. She hailed from a malaria 

endemic region. She received paracetamol 

syrup, tab. primaquine and liver tonics at 

home. On admission, she was febrile(101ºF), 

comatose (GCS-5), had pallor and icterus; 

RR-60/min, PR–120/min, regular and BP of 

90/50 mmHg; Wt-10kg (54.6%); Ht-102.5cm 

(93.2%) [Grade III PEM]. There was 

hepatomegaly (5cm) and splenomegaly 

(2cm); chest and CVS examinations were 

normal. Initial investigations showed – Hb-9.7 

g/dl,TLC-7000 /mm 3 , DLC – P 56 

L 42 

M 1 

E 1 

ESR 

– 10mm/1 st hr; platelets -1.6 lacs/mm 3 ; 

peripheral smear- normocytic and 

normochromic red cells. Malarial parasite 

(MP) smear showed plenty of P.vivax 

trophozites; blood glucose – 30mg/dl; liver 

function test (LFT)- total s. bilirubin (TSB)-8.8 

(conjugated-6.9); total protein-6.5 (albumin/ 

globulin-2.6/3.9); SGOT/SGPT-1284/1610; 

SAP-533; kidney function tests and serum 

electrolytes were normal. Blood smear 

1. Registrar, 2. Associate Professor, 3. Asst. Professor, 

Department of Pediatrics, Regional Institute of Medical 

Sciences, Imphal 

Corresponding Author : 

Dr. Ch. Shyamsunder Singh, Assistant Professor, 

Department of Pediatrics, Regional Institute of 

Medical Sciences, Imphal-795 004, Manipur, India., 

E-mail - drchssunder@gmail.com 

repeated the next day still showed 

trophozoites of P.vivax. The child was given 

IV fluids, alongwith empirical IV Cefotaxime 

(150mg/kg/d TID), IV Ranitidine (3mg/kg/d) 

and oral paracetamol (through nasogastric 

tube). Seizures were controlled with IV 

phenytoin sodium – 15mg/kg initially followed 

by 5mg/kg maintenance IV which was given 

till discharge. Hypoglycemia was managed 

with 10% dextrose - 5ml/kg bolus initially and 

then started maintenance IV dextrose to 

maintain the blood sugar above 60mg/dl. IV 

Quinine HCl – 20mg/kg loading followed by 

10mg/kg 8 hrly was given for 4 days till the 

child regained consciousness and changed 

to oral quinine sulphate to complete a total 

duration of 7 days. USG abdomen showed 

hepatomegaly with no other gross liver 

abnormalities. HBs Ag and HCV Ab were 

negative. The child was discharged after 8 

days of hospital stay in a clinically stable 

condition with oral primaquine 0.3 mg/kg/day 

for 5 days and negative MP smear, declining 

LFT with no seizure recurrences and normal 

neurological functions. 

Case – 2. A 2 year old boy from a malaria 

endemic area presented with intermittent 

fever for 15 days, dry cough for 10 days and 

generalized tonic-clonic seizures(3 episodes) 

followed by altered sensorium for 1 day. He 

received inj. paracetamol and inj. 

dexamethasone at a PHC before being 

referred. There was no history of febrile 

seizures, head trauma, ear discharge or other 

similarly affected family members. On 


CASE REPORT 

admission, he was afebrile and stuporose 

(GCS-6) There was no pallor and jaundice; 

RR -40/min;PR-92/min;BP-110/70 mmHg; 

chest-bilateral crepitations; abdomen - 

hepatomegaly (4cm) and splenomegaly 

(3cm); CVS was normal. Emergency 

investigations revealed – Hb- 9.8g/dl, rapid test 

for malaria (Optimal Test) for MP- P.vivax 

(+ve) and Widal test– negative; random blood 

sugar– 84mg/dl. The child was initially started 

on IV fluids, inj.Ceftriaxone – 75mg/kg BID, 

inj.Lorazepam -0.1mg/kg/dose SOS. After 

getting the blood MP report, which was 

positive for P.vivax -inj Quinine HCL – loading 

of 20mg/kg followed by maintenance of 10mg/ 

kg 8 hourly was added; later investigations, 

done next day, revealed normal blood RE, but 

smear was negative for MP; LFT,KFT, 

s.electrolytes and blood sugar were normal; 

Fundoscopy- normal; CSF - RE and C/S were 

normal. Blood for MP repeated after 48 hours 

was negative. The child had become afebrile 

on the 5 th day of admission and regained 

consciousness with restoration of oral feeding; 

quinine was changed to oral form and tab. 

Primaquine (0.3 mg/kg OD for 5 days) was 

started after 7 days of total quinine therapy. 

The patient was discharged after 12 days of 

hospital stay in a stable condition with no 

neurological deficits. 

At follow-up after 1 month post-discharge, the 

first child had no clinical icterus and liver 

function tests were normal. In both the 

children, there were no seizure recurrences 

or neurological handicaps. 

Discussion 

Cerebral malaria, usually representing a fatal 

form of severe malaria, is almost always due 

to P. falciparum species, but there are also a 

few reported cases of P.vivax causing 

cerebral malaria, half of them occurring in 

children. 1,2 Though cerebral malaria due to 

P.falciparum have been encountered 

frequently in children in Manipur, a North 

Eastern State of India, cases due to P.vivax 

have never been reported in children. The 

reported severe manifestations caused by P. 

vivax include cerebral malaria, hepatic 

dysfunction, renal dysfunction, severe 

anemia, acute respiratory distress syndrome 

(ARDS), shock, abnormal bleeding, and 

multiple organ involvement. 3 In our patients, 

though P.vivax was identified, as they reside 

in a malaria endemic area recognized for 

P.falciparum infections and due to the 

presenting severe clinical state, parenteral 

quinine therapy was initiated. 

The exact pathogenesis of P.vivax cerebral 

malaria is not clear, but it has been proposed 

that P.vivax can cause both sequestration 

and non-sequestration related complications 

of severe malaria, which are common in 

P.falciparum cerebral malaria. 4 Beg et al 5 

had suggested the central nervous system( 

CNS) malaria could be due to impedence of 

cerebral blood flow resulting from 

cytoadherence of parasitized red blood cells 

(RBCs) to cerebral vascular endothelium, 

which may be compounded by agglutination 

of parasatized RBCs, fibrin microthrombi, 

altered rheologic properties of the 

parasaitzed RBCs and vascular endothelial 

changes. Molecular studies have postulated 

the contributory role of detrimental nitric 

oxide (NO) generation resulting from 

localized and generalized ischaemic hypoxia 

which can enhance cytokine-induced NO 

generation. 6 

Hepatic dysfunction and jaundice (which was 

observed in the first case) are the commonest 

abnormalities encountered in complicated 

P.vivax malaria and is probably due to 

sequestration. 4 Management of such liver 

dysfunction is usually conservative while 

treating the primary pathology. 

Glucose metabolism abnormalities, 

hypoglycemia in particular, is found in both 

adult and pediatric patients (prevalence~ 

10%) 7 and is associated with a poor 

prognosis in children with severe malaria. 

Hypoglycemia in severe malaria is believed 

to be due to impaired glucose production 

caused by disruption of gluconeogenesis 8 and 

also due to direct effects of quinine. In our 

first case, hypoglycemia might have also 

contributed to the seizures and 

encephalopathy. 

66 


Conclusion 

Malaria is still rampant in our part of the 

country. Though severe malaria have 

traditionally been attributed to be due to P. 

falciparum in most cases, P.vivax can also 

CASE REPORT 

cause serious life threatening disease. 

Recognition of such serious disease forms, 

its early diagnosis and initiation of effective 

treatment is of paramount importance to 

reduce morbidity and mortality in children. 

References 

1. White NJ. Malaria In : Cook GC, Zumla AI, eds. 

Manson’s Tropical Diseases. 21 st Edn.. 

London: Elsevier Saunders;2002;1205-1278. 

2. Ozen M, Gungor S, Atambay M, Daldal N. 

Cerebral malaria owing to Plasmodium vivax: 

case report. Ann Trop Paediatr. 2006;26 

(2):141-144. 

3. Kochar DK, Saxena V, Singh N, Kochar SK, 

Kumar SV, Das A. Plasmodium vivax malaria. 

Emerg Infect Dis 2005;11(1):132–134. 

4. Kochar DK, Das A, Kochar SK, Saxena V, 

Sirohi P, Garg S, Kochar A, Khatri MP, Gupta 

V. Severe Plasmodium vivax malaria : A report 

on serial cases from Bikaner in Northwestern 

India. Am J Trop Med Hyg. 2009;80(2):194-198. 

5. Beg MA, Khan R, Baig SM, Gulzar Z, 

Hussain R, Smego RA. Cerebral involvement 

in benign tertian malaria. Am J Trop Med Hyg 

2002; 67: 230–232. 

6. Mohanty D, Ghosh K, Nandwani SK, Shetty 

S, Phillips C, Rizvi S, Parmar BD. Fibrinolysis 

inhibitors of blood coagulation and monocytederived-coagulant 

activity in acute malaria. Am 

J Hematol, 1997;54:23-29. 

7. English M, Wale S, Binns G, Mwangi I, 

Sauerwein H, Marsh K. Hypoglycaemia on and 

after admission in Kenyan children with severe 

malaria. QJM 1998;91(3):191-197. 

8. Jaffar S, Van Hensbroek MB, Palmer A, 

Schneider G, Greenwood B. Predictors of a 

Fatal outcome following childhood cerebral 

malaria. Am J Trop Med Hyg. 1997;57(1):20- 

24. 


CASE REPORT 

The death tell tales 

1 

Th. Bijoy Singh, 2 H.Nabachandra 

Case report 

On 20-9-’98 at about 4.30 a.m. the deceased 

was found dead on her bed by her son and 

rushed to RIMS Hospital and there it was 

declared brought dead. She was an alcoholic 

and had been suffering from bronchial 

asthma. Her sons thought that she might have 

died due to preexisting disease (bronchial 

asthma) and ready for cremation on the same 

day at about 10 am. There was history of 

physical violence about three days back by 

her sons for consuming alcohol and bad 

habits. All of a sudden public raised objections 

before torching the funeral pyre and alleged 

that her sons might have murder the 

deceased. So a case was registered at 

Heingang PS. under FIR No.93 (9) 

98HNGPS.U/S 302/34 IPC. Thus the body 

was taken down from the funeral pyre and 

brought for post mortem examination in the 

Department of Forensic Medicine, RIMS, 

Lamhelpat Imphal. Post mortem examination 

was done on 21-9-98 at 10.40 am at RIMS 

Morgue.The findings are as follows: Eyes and 

mouth were closed, both conjunctivae 

congested, cyanosis present, pupils dilated, 

rigor mortis feebly present in the lower limbs, 

post mortem staining present on back and 

1. Associate professor, 2. Professor and Head of the 

Department, Forensic Medicine, Regional Institute of 

Medical Sciences, Imphal. 


Dr. Th. Bijoy Singh, 

Associate Professor, Department of Forensic 

Medicine, RIMS 

68 

fixed, greenish discoloration on right iliac fossa 

present, black eye on right eye present. 

External injuries: 

I. Healing wound on right side of forehead 

situated 4cms from midline and just above 

eyebrow measuring an area of 3cmx2cm 

with brown scab present. 

II. 

III. 

Contusion on left side of face around the 

angle of mandible dark blue in colour 

measuring an area of 2cmsx 7cms 

present. 

Small bruise on outer aspect of left thigh 

measuring10cmsX3cms in area and 

bluish black in colour present. 

IV. Contusion on right side of face over 

zygoma measuring an area of 4cms X 

3cms and bluish black in colour present. 

Internal findings: 

All viscera were congested. 

Larynx, Trachea, bronchi were congested and 

froth present in the lumens. 

Stomach was congested and mucosal 

erosion with haemorrhages present. 

Yellowish brown fluid with oil steaks having 

kerosene like smells present about 

100cc.Small intestine was congested and 

yellowish brown fluid present having kerosene 

like smell. Large intestine was congested and 

faecal matter present. 

The findings were consistent with poisoning 

and cause of death was given as asphyxia 

resulting from poisoning and suicidal. 


CASE REPORT 

External injuries were ante mortem and about 

3-4 days old. 

* Visceras were preserved for chemical 

analysis. 

Discussion: 

False allegations are often found in our society 

more so with pre existing history of quarrel 

among the family members or the strenuous 

relationship between the blood relatives viz. 

parents and sons or husband and wife or inlaws 

etc. Innocent members of the family 

members are often harassed and put behind 

the bars. The punishment for murder is defined 

under section: 302 of IPC which states that 

whoever commits murder shall be punished 

with death or imprisonment for life and shall 

also be liable to fine and under section 306IPC 

and 309 IPC which deal with abatement of 

suicide and attempt to commit suicide, the 

punishment extend to ten and one year 

respectively 1 . 

In our case, the post mortem findings clearly 

proves that the lady did not died of physical 

violence or due to pre-existing disease and 

died after consumption of poison which is 

towards suicidal and final decision will be given 

by the court. 

Very often false allegations were made against 

the relatives and faced lots of legal problems 

by them. 

Unless a meticulous post mortem examination 

is done to ascertain the exact cause of death 

the problem would not have been solved as 

in this case. It is very important for a forensic 

expert to believe his own post mortem findings 

and not to do the post mortem examination 

guided (misguided) either by I.O. or the 

statements given by the witnesses. Besides 

the witnesses even I.O. may have some 

interests in the case and may misguide the 

autopsy surgeon by giving a cooked history 

of the case. 2 

This case is being reported to establish the 

importance of meticulous post mortem 

examination to ascertain the exact cause of 

death and manner of death in cases of 

suspicious sudden deaths and false 

allegations to their family members and well 

wishers. 

Conclusion: 

The autopsy surgeon should therefore utilize 

his skill in these types of cases and help the 

judiciary in giving the correct final verdict and 

in administration of justice. 

References: 

1. Universal Law publishing Co., The Indian Penal 

Code1860 (Amendment Act 1995) Edn. I, 

1998, 124-127. 

2. K.K.Banerjee. Misrepresented‘ Homicide Jour. 

F. M.and Toxicology, vol20,no-1,Jan-June ’03, 

22-23. 


CASE REPORT 

Autonomic dysreflexia: a case report 

1 

N. Ratan Singh, 1 Laithangbam PKS, 2 S. Sarat Singh 

A 35 year old man paraplegic patient was 

posted for fistulectomy for fistula in ano under 

spinal anaesthesia. The paraplegia developed 

below the 5 th thoracic vertebra following gun 

shot injury to the spine about 12 years ago. 

He had loss of control over his bowel and 

bladder requiring enema and catheterisation 

everyday; however, he had some sensation 

over the anal region. Even though, general 

anaesthesia (GA) was considered suitable for 

the procedure, the patient did not like to 

undergo the procedure under GA. Hence, the 

subarachnoid block (SAB) spinal anaesthesia 

was kept on standby and the procedure was 

taken up after local infiltration of the anal area. 

The patient started screaming and his heart 

rate (HR) fell from 78 to 45 and the blood 

pressure (BP) increased from 136/ 76 mmHg 

to 237/ 138mmHg. The manipulative 

procedure had to be immediately stopped and 

following this, the BP dropped to 197/ 112 

mmHg. However, the BP increased up to 201/ 

120mmHg on resumption of the surgical 

procedure. Hence, to control the 

hemodynamic abnormalities, Inj. Propofol 50 

mg i.v, Inj. Atropine 0.6 mg i.v and Inj. 

Butorphanol 800µg i.v were administered. 

Following these medications, the changes 

were brought to the baseline. The condition 

1. Asst. Professor, and 2. Assoc. Professor 

Department of Anaesthesiology, Regional Institute of 

Medical Sciences, Imphal 


Dr. N. Ratan Singh, Asst. Professor, Department of 

Anaesthesiology, Regional Institute of Medical 

Sciences, Imphal – 795004, 

e-mail: drnratansingh@gmail.com 

70 

was explained to the patient and after obtaining 

a written informed consent for regional 

anaesthesia, the case was rescheduled for 

the next day and surgical procedure was 

performed under SAB under spinal 

anaesthesia. 

Discussion 

First recognized by Anthony Bowlby in 1890, 

autonomic dysreflexia (AD) is a syndrome of 

massive imbalanced reflex sympathetic 

discharge occurring in patients with spinal 

cord injury (SCI) above the splanchnic 

sympathetic outflow (T5-T6) 1 . AD is caused 

by massive sympathetic discharge triggered 

by either noxious or non-noxious stimuli below 

the level of the SCI. It is correlated with 

aberrant sprouting of peptidergic afferent fibres 

into the spinal cord below the injury 2 . It is 

characterised by sudden severe uncontrolled 

hypertension and accompanying bradycardia 

3 

. The onset of autonomic dysreflexia most 

commonly occurs in the reflexic stage of the 

condition, usually between 3 weeks and 12 yr 

after injury, but recent case reports indicate 

an earlier onset (within 7 days) in some 

patients during the flaccid phase 4 . In the 

present case, the autonomic dysreflexia 

developed after a span of more than 12 years. 

The loss of sensation caused by spinal injury 

means that many patients can undergo 

surgery without anaesthesia and without 

feeling pain from the operative site and the 

choice is “Standby anaesthesia” in cases with 

SCI 5 . Spinal anaesthesia has been 

recommended especially for urological 


CASE REPORT 

surgery in such cases 6,7 . However, spinalepidural 

anesthesia has been used 

successfully for the purpose of prevention and 

treatment of autonomic dysreflexia during 

labor and delivery. 8 . However, in spinal 

anaesthesia, it may be impossible to 

determine the level of the block and it is not 

known whether the usual dose/response 

characteristics are seen in these cases. 

It is a known fact that lidocaine block can limit 

the response to susceptible patients 

undergoing ano-rectal surgical procedures. In 

the present case, the AD syndrome developed 

despite the use of lidocaine local infiltration. 

Hence, a prompt intervention along with 

subsequent administration of spinal 

anaesthesia helped in successful 

management of the case. 

Conclusion: 

Hence, anaesthesiologists and surgeons 

dealing with chronic SCI patients must remain 

vigilant and be cautious about the possibility 

of development of AD (Autonomic Dysreflexia) 

in these cases and ever prepared for its 

management. 

References 

1. Campagnolo DI: Autonomic Dysreflexia in Spinal 

Cord Injury; www.emedicine.medscape.com. 

Updated: Jul 2, 2009 

2. Rabchevsky AG. Segmental organization of 

spinal reflexes mediating autonomic dysreflexia 

after spinal cord injury.http://www.mc.uky.edu/ 

scobirc/research/2007. Assessed on 8/9/10. 

3. Shergill IS, Arya M, Hamid R, Khastgir J, Patel 

HRH and Shah PJR. The importance of 

autonomic dysreflexia to the urologist. B J U 

International, Vol. 93 2004: 923–26 

4. Jones NA and Jones SD. Management of lifethreatening 

autonomic hyper-reflexia using 

magnesium sulphate in a patient with a high 

spinal cord injury in the intensive care unit, 

British Journal of Anaesthesia, 2002, Vol. 88, 

No. 3 434-38. 

5. Hambly PR & Martin B. Anaesthesia for chronic 

spinal cord lesions; Anaesthesia, Vol. 53,1998: 

273 -89 

6. Alderson JD. Chronic care of spinal cord injury. 

In: Alderson JD, Frost E, eds. Spinal cord 

injuries. Anaesthetic and associated Care. 

Butterworth: London, 1990; 104-25. 

7. Barker I, Alderson J, Lydon M, Franks CI. 

Cardiovascular effects of spinal subarachnoid 

anaesthesia. Anaesthesia 1985; 40:533-6. 

8. Osgood SL and Kuczkowski KM. Autonomic 

dysreflexia in a parturient with spinal cord injury, 

Acta Anaesth. Belg., 2006, 57, 161-62 


CASE REPORT 

Malignant melanoma of the nose and paranasal sinuses 

- an unusual case report 

1 

Nicola C. Lyngdoh, 2 S. Thingbaijam, 1 R.K. Bedajit 

Case Report 

A 57 year old female patient from Ukhrul District 

was admitted to the Female ENT ward on 14 th 

February 2006 with the complaints of a mass 

in left nasal cavity, nasal obstruction, epistaxis 

off & on and headache for the past 8 months. 

Fig. 1-Gross external deformity of nose. 

On E.N.T. examination, there was gross 

external deformity of left side of the lower part 

of the nose. Anterior rhinoscopy revealed a 

greyish-pink mass coming out through the left 

nostril completely occupying the left nasal 

cavity. The septum was pushed to the 

opposite side but there was no surface 

ulceration. Posterior rhinoscopy revealed a 

pigmented mass in the left choana. The 

nasopharynx was free and the dorsum of soft 

palate was normal. On digital palpation, the 

mass was firm and the palpating finger was 

blood-stained. There was no PNS tenderness, 

no cervical lymphadenopathy, no orbital 

symptoms, no facial pain or numbness and 

no dental problems(Fig-1). 

Routine Investigations for blood were normal. 

A Coronal & Axial C.T. Scan of the Nose & 

Para-nasal sinuses revealed a soft tissue 

mass occupying left nasal cavity eroding the 

left lateral nasal wall and extending to the left 

maxillary antrum. The nasal septum was 

thinned out and pushed to the opposite nasal 

cavity. There was obstruction of the drainage 

pathways of the ethmoid and frontal sinuses. 

However, the cribriform plate and medial orbital 

wall were intact. The patient underwent Nasal 

endoscopy and biopsy of nasal mass under 

local anaesthesia. Endoscopic examination 

revealed a greyish-pink mass anteriorly, but 

as the scope was passed posteriorly, the 

mass was blackish-brown in colour. The 

histopathological examination was suggestive 

of melanocarcinoma(Fig-2). 

1. Assistant Professor, 2. Associate Professor, 

Department of Otorhinolaryngology (ENT), Regional 

Institute of Medical Sciences, Imphal -795004. 


Dr Nicola C. Lyngdoh, 

Department of Otorhinolaryngology, Regional Institute 

of Medical Sciences, Imphal. e-mail address: 

nicolyng@yahoo.com 

Fig. 2-HPE picture of Melanocarcinoma 

72 


Following the histopathological report, the 

patient consented for operation and underwent 

Lateral rhinotomy with Medial maxillectomy 

with septectomy and clearance of the anterior 

ethmoids. The growth appeared black-brown 

in colour and was seen to extend from the 

lateral wall of the nose to the opposite side of 

the nasal cavity. The septum and medial wall 

of the maxilla were eroded. The anterior 

ethmoid air cells showed secondary infection. 

Histopathological examination of the excised 

mass also suggested the same diagnosis, i.e. 

melanocarcinoma. Following the operation, the 

patient was advised a course of radiotherapy 

after 4 weeks of operation. After she was 

discharged from the ward, the patient did not 

even return for a follow-up treatment. The 

patient, however, came back for re-admission 

in September i.e. after six months, this time 

with a bilateral recurrent nasal mass, more 

aggressive than the last time. Due to financial 

constraints, she refused any form of specific 

treatment and was finally lost to follow-up. 

Discussion 

Primary mucosal melanomas of the head and 

neck are extremely rare and accounts for 1 – 

2% of all melanomas. Mucosal melanomas 

of the sino-nasal tract are even rarer and 

account for 0.6 – 0.7% of all sino-nasal 

cancers, It is more aggressive than its 

cutaneous counterpart with a 5-year survival 

rate of less than 30%. 1 

The sites most commonly affected by 

mucosal melanomas in head and neck areas 

are the nose & paranasal sinuses in 40% 

cases, oral cavity in 47%, and the pharynx in 

11% cases. 2 The nasal and paranasal sinus 

involvement as highlighted by Stammberger 

et.al.(1999) showed Maxillary sinus 

involvement in 47%, Ethmoid sinus 

involvement in 18% , Frontal sinus involvement 

in 14%, Sphenoid sinus involvement in 07% 

and Nasal cavity involvement in 14%. 3 

Mucosal melanomas are thought to arise from 

melanocytes in the mucosa of the nose and 

paranasal sinuses and not from a pre-cursor 

naevus. The site of origin is difficult to 

determine as tumours are often multicentric 

and bulky at the time of presentation. There 

is no sex predilection. The peak age of 

incidence is between the 5th and 8th decades 4 

as seen in our case. The commonest 

presenting symptoms are nasal obstruction 

and epistaxis, (all indolent symptoms 

commonly resulting in late presentation.) Pain 

and facial deformity are more frequent in 

advanced cases. The commonest site of 

origin is the lateral nasal wall. 5 These findings 

were similar in our case also. The commonest 

finding is a sessile polypoidal mass which 

bleeds on touch. About 75% are pigmented 

but about 10-20% may be weakly pigmented 

or amelanotic. Mucosal melanomas are 

usually solitary or multi-centric, friable or 

partially necrotic haemorrhagic lesions. 

Conventional staining with Fontana stain 

facilitates diagnosis. Enzyme immunohistochemistry 

melanomas react strongly to 

S-100 protein, a calcium binding protein found 

in neural tissues. It also reacts strongly to 

monoclonal antibody HMB-45, a superb 

diagnostic marker. This antibody reacts with 

oncofetal antigen found in immature 

melanosomes. 4,5 

Since mucosal melanomas are highly 

aggressive & lethal, treatment is challenging 

& equally frustrating as recurrence rates are 

very high (40-80%). Time interval from 

remission to recurrence is in months to years, 

majority occurring within the first three years. 

The five year survival rate at 5 and 10 years is 

17% and 5% respectively. Patients with nasal 

mucosal melanoma have a 31% survival rate, 

whereas sinus melanoma patients fare poorly, 

with 0% rate of survival. Because of their rarity 

and their uniformly low survival rates, 

determination of the ideal treatment is difficult. 

Management is multifactorial and includes 

Surgery, Radiotherapy, Chemotherapy, 

Immunotherapy and Gene therapy 4 . 

CASE REPORT 

Conclusion 

There is no statistical difference in local control 

or survival between patients receiving surgery 

alone and those receiving surgery & 

radiotherapy. The addition of chemotherapy 

as adjuvant therapy has no impact on survival 

rates. However, despite surgical and imaging 

techniques with adjuvant therapeutics, the 

mean survival has not changed over the last 

15 years. 2,5 


CASE REPORT 

REFERENCES 

1. Holdcraft J. & Gallagher X. Malignant 

melanomas of the nasal and paranasal 

mucosa. Ann. Otol Rhinol Laryngol, 1969, 

78: 5 -20. 

2. Conley J.J. Melanomas of mucous 

membrane of head & neck. Laryngoscope. 

1989;99-1248-54 

3. Stammberger H., Anderhuber W., Walch 

C. Possibilities & limitations of endoscopic 

management of nasal & paranasal 

malignancies. A cta Otorhinolaryngol. 

Belg.1999;53-199-205 

4. Spiros Manolidis & Paul J. Donald. 

Malignant melanomas of the head 

and neck – review of literature and report 

of 14 patients. Cancer, 80: 1373 – 1386, 

1997. 

5. Yen-Fu cheng, Chien-Chung Lai, Wing- 

Yin Li, Ching-Zong Lin. Primary Sino-nasal 

mucosal melanoma with unusual longterm 

survival. Tzuchi Med J, 

2005;17(3):177-79. 

74 


CASE REPORT 

A case of neural tube defect – craniorachischisis totalis 

1 

Th. Naranbabu, 2 M. Matum, 3 I. Deven 

Case report: 

A 21week female fetus was collected from 

the Department of O & G, RIMS, Hospital, 

Imphal and examined for the defect presented 

in the fetus. Examination of the fetus revealed 

asbence of cranial vault and the whole brain 

covered by meninges was found protruded. 

Eye ball was protuded due to inadequate bony 

cavity and thorax was prominent. Examination 

of the brain reveal that hypoplastic and 

degenerated cerebrum, agenesis of 

cerebellum and brain stem. The whole spinal 

cord was exposed and appeared as flattened 

tissue. Vertebral arches were found absent. 

Sagital section as well as X-ray film of the 

foetus showed under developed vertebrae in 

the cervical, lumbar and sacral regions. The 

fetus presented all the features of complete 

failure of neural tube closure, the 

Craniorachischisis Totalis(Fig-1 A, B, C). 

A 

C 

B 

Fig.-1 (A, B, C) Craniorachischisis Totalis. 

Discussion: 

1. Professor 2. Assoc. Prof. 3. Demonstrator 

Department of Anatomy, RIMS, Imphal 


Dr. Th. Naranbabu, Professor, Deptt of Anatomy, RIMS, 

Imphal. 

Neural tube is formed from the neuroectoderm 

under the induction of notochord and neural 

tube is closed in the fourth week of gestation. 

Brain and spinal cord are develop from this 

structure. Its derivative, neural crest cells 

developed into structures like dorsal root ganglia 

and mesenchyme of the cranial vault. 

Notochord influences the formation of the ver- 


CASE REPORT 

tebral bodies from sclerotomes, whereas the 

vertebral arch developes under the influence 

of dorsal root ganglia. Therefore, the failure of 

neural tube to close leads to absence of cranial 

vault and vetebral arches 1,2,3 . The patterning 

of the vertebral arches is dependent on 

the interaction between transforming factor 

Sonic hedgehog from the notochord/floor plate 

of neuroectoderm and BMP4 (bone morphogenic 

protein 4) from the roof plate and 

overlying ectoderm. Pax, Hox, MsxI and MsxII 

are some of the genes which influence the 

formation of vertebrae. These factors may 

|explain the abnormalities of vertebrae 

associated with craniorachischisis 1 . 

Anencephaly is the feature presented when 

the rostral end of neural tube failed to close.In 

anencephaly brain matter was degenerated 

and appears as spongy vascular mass due 

to abnormal structure and vascularization 3 . 

Neural tube defects(NTDS) aetiologically can 

be classified as: 1) Chromosomal - trisomy13 

and trisomy18, 2) Syndromal and 3) Isolated. 

The empiric recurence risk to first degree 

relatives vary according to the local population 

incidence and are as high as 4-5% 4 . This 

high incidence may be due to a mother 

harboring both mutation of 5, 10 

methyltetrahydrofolate reductase or of 

methionine synthase reductase homozygous 

mutant genotypes and such a mother has a 

high possibility to bear fetus with NTDS. Many 

factors are implicated in the induction of 

NTDS like: retinoic acid, hyperglycaemia, 

hyperthermia, antiepileptic drug like valproic 

acid and trypan blue 2 . 

NTDS are more common in female fetuses 

than male fetuses. Again, it is more common 

in white than black. Fetuses with 

craniorachischisis lead to spontaneous 

abortion. Fetuses with such lethal 

malformations can’t survive and has poorly 

developed neuroendocrine system 5 . 

References: 

1. Susan Standering. Development of vertebral 

column. In: Patricia Collins, editor. Gray’s 

Anatomy 39 th ed., Edingurgh, Churchill 

Livingstone 2005; 789-97. 

2. William J. Larsen. Human Embryology 3rd 

ed. New york, Churchill Livingstone 2001 ; 79- 

112. 

3. Sadler T.W. Langman’s Medical 

Embryology10th ed., Baltimore, Lippincott 

Williams & Wilkins 2006; 126.. 

4. Robert F. Mueller, Ian D. Young. Emery’s 

Elements of Medical Genetics 11ed., 

Edinburgh,Churchill Livingstone 2001; 223-33. 

5. Kenneth F. Swaiman, Stephel Ashwal and 

Donna M. Ferriero. Congenital Structural 

Defects, In: Joseph G. Gleeson, William B. 

Dobyns et al. editors, Paediatric Neurology, 

Principles & Practice 4 th ed., Philadelphia, 

Mosby 2006; 363-490. 

76 


Instructions to authors 

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78 

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A word count is mandatory and should not exceed 

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6.1.1 

Title page: It should be paginated as page 1 of the 

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Statistical methods: The details of statistical tests 

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If more than one tests are used it is important to 

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6.1.5 Results 

The results should be stated concisely without 

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This section should deal with the interpretation of 

results, rather than recapitulation of them. It is 

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also the weakness or pitfalls in the study. New 

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6.1.7 Conclusion 

Avoid unqualified statements and conclusions not 

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mention. 

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accordance to the “Uniform Requirement for 

Manuscripts Submitted to Biomedical Journals”, 

which can be accessed at http:/ /www.icmje.org/ 

index.html or N Engl J Med 1997;366:309-15. 5.1.10 

Tables 

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whether the given values are mean, median, mean 

.:t. SD or mean .:t. SEM. All significant results 

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Each figure must be numbered and a short caption 

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one of each. The summary should be less than 

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The manuscript should not be divided into 

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simple figure or table. 

6.4. Letters to Editor 

It can have a maximum of 800 words (including a 

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or table. The manuscript should not have 

subsections. 

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It should contain title page. Summary (need not be 

in structured form) and key words. The text proper 

should be written under appropriate subheadings. 

The authors are encouraged to use flowcharts, 

boxes, simple tables and figures for better 

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The authors should revise the manuscript 

immediately after the receipt of the comments from 

JMS. A note mentioning the changes incorporated 

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by point) should be sent. The revised manuscript 

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annotated original paper within 2 weeks. If the 

revised manuscript is received 2 weeks after 

despatch from the Editorial Office, it will be 

considered as anew submission. 

Calling for revision does not guarantee acceptance. 

The revised manuscripts that require major revision 

are likely to be sent to referees for evaluation. If the 

authors have substantial reasons that their 

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request for reconsideration. The correspondence 

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Proofs will be sent to the corresponding author for 

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should be made. 

9. Reprints. 

Reprints must be ordered while returning the 

corrected page proofs. 

80

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