Volume 01 Number 01 January 2012

BIMSMEDICAL JOURNAL

Peer Reviewed Medical Journal ofBelgaum Institute of Medical Sciences,

Belgaum-590001, Karnataka.

BIMS MEDICAL JOURNALPeer Reviewed Medical Journal of

Belgaum Institute of Medical Sciences,Belgaum-590 001. Karnataka.

Volume-01 Number-01 January 2012

Publisher : Dr. S. T. Ved Bhushan, Editor.

Proprietor : Director,Belgaum Institute of Medical Sciences,Dr. B. R. Ambedkar Road, Belgaum-590 001.

Publication : Bi-annuallyJanuary and July

Journal Office : BIMS Journal Office,III Floor, Belgaum Institute of Medical Sciences,Dr. B. R. Ambedkar Road, Belgaum-590 001.Phone : 0831-2491360

Printed at : Killeprint,659, Door Darshan Nagar,Belgaum-590 001.

BIMS MEDICAL JOURNALPeer Reviewed Medical Journal of

Belgaum Institute of Medical Sciences,Belgaum-590 001. Karnataka.

Patron

Dr. M. R. ChandrashekharDirector,

Belgaum Institute of Medical Sciences, Belgaum.

Editor

Dr. S. T. Ved Bhushan

Editorial Advisory Board

Dr. P. R. Malur Dr. P. A. Patil(KLE University, Belgaum) (KLE University, Belgaum)

Dr. (Lt. Col) Halli Vijayanand Dr. S. T. Kalsad

Dr. Aruna Bhushan Dr. Vidyadhar Kinhal, (VIMS Bellary)

Dr. Shobha Karikatti Dr. Rajshekhar Kaujalgi, (BRIMS Bidar)

Dr. Ashok Kumar Shetty Dr. Kaza Moiduddin,

Sunanda Halaki, (Statistician)Shadan Medical Institute, Hydrabad.

Editorial

Belgaum Institution of Medical Sciences, Popularly known as BIMS is one of six medical collegesstarted by an ordinance in March 2006. These institutions are Autonomous Government Medical Colleges.BIMS has grown surely and steadily over the years. First batch of MBBS students are doing their internship.We are happy that pre-clinical and Para clinical post graduate courses are started since 2010 and MCIinspection is over for clinical post graduate courses this year (2012). Dr. M.R. Chandrashekhar the director,has been encouraging and stressing the importance of academic excellence. BIMS Medical Journal is thefirst medical journal of its kind among the government medical colleges. BIMS medical journal shall bepublished biannually once in January and in July every year.

PUBLISHING ARTICLES IS NEED OF THE HOUR:

Medical teaching faculty all over the world more in the western world and now even in theAsian sub-continent is increasingly aware of this necessity. Frequent publication is one of thefew methods at a scholars disposal to demonstrate their academic capabilities. Successfulpublications lead scholars and their sponsoring institutions to progress in their respective field.

Medical faculty who publish infrequently or focus on activities such as teaching under graduatesmay find it difficult to progress into higher academic grade (1). It has been said that some medicaluniversities desire their faculty to publish at least 3 articles per annum-

In our country even the regulating bodies such as MCI (Medical Council of India) desires the facultyto publish articles in the national and indexed Journals at every level of grade in promotions(2).

We hope to bring the journal regularly and in due course of time it will be an indexed journal. Firstissue of BIMS medical journal will have original articles and case reports, most of which are contributed byBIMS faculty. We have an editorial committee which reviews all the articles for their content and style ofwriting. I am happy the editorial committee has done a commendable job.

1. Fanelli D, Scalas, Enrico. ed. Do pressures to publish increase scientists. Bias? Anempirical support from USA states data. PMID 20422014 (2010).

2. Medical Council of India Bulletin – MCI website 2011.

Wishing you all a very Happy New Year and Makara Sankranti

Dr. S. T. VED BHUSHAN, M.S., FAISAssociate Professor of General SurgeryBIMS. Belgaum.

January 2012.

Original Article

Microbiological quality of water and Dialysateat a Haemodialysis unit in India

Chandrashekar M. R., *Asha B. Patil, **Krishna B. V. S.Dean, Department of Microbiology, Belgaum Institute of Medical Sciences, Belgaum- 590 001, Karnataka.

ABSTRACTThe microbiological contamination of water and the dialysis fluid has recently gained great actuality. It must be

assured that the dialysis fluid is free of bacterial contamination, so as to guarantee the absence of endo-toxins (1). Inthe present study the main water supply source was contaminated 92.86% of times sampled, the dialysate and thewater after reverse osmosis (RO) were contaminated in 14.28% of samples. The results reveal the need to improvethe disinfection procedures and to ensure the removal of bio-film in the overhead tank which is probably responsiblefor the high contamination rates in the water source.

BIMS Med. J. 2012, 01 : 2-4

INTRODUCTIONThe contamination of dialysate fluid by bacteria

and pyrogens is currently a serious problem ofhaemodialysis (1). Much of this contamination has beendue to Gram negative water bacteria and nontuberculous mycobacteria (2). These bacteria canpersist and actively multiply in the aqueous environmentsassociated with the haemodialysis equipment, resultingin massive levels of Gram negative bacteria, which candirectly or indirectly affect the patients by septicaemiaor endotoxemia (3). Gram negative water bacteriaand their associated lipopolysaccharides and nontuberculous mycobacteria ultimately come from thecommunity water supply and levels of these bacteria canbe amplified depending on the treatment systems,dialysate distribution systems, type of dialysis machineand method of disinfection (2). Monitoring the bacterialcontamination of water and dialysate therefore becomesessential and is recommended to be done as a routineat regular intervals.

A new fully fledged modern haemodialysis unitwas established at Karnataka Institute of MedicalSciences, (KIMS) Hospital, Hubli, India in June 2001 andit became completely operational by November 2001.This article presents the analysis of the bacteriologicalquality of water at the haemodialysis unit of our hospitaland attempts to identify the factors contributing to thecontamination of treated water and dialysate.

MATERIAL AND METHODSThe haemodialysis unit KIMS Hospital, Hubli has

7 haemodialysis machines which are of Nikkiso DBB-26 (Japan) make, each incorporating an ultrafilter. Thesource of community water used at the dialysis center isfrom both surface and ground water. This water treatedby reverse osmosis is distributed to individual

*Associate Professor, Department of Microbiology, Karnataka Institute of Medical Sciences, Hubli-580 022.**University Hospital of North Staffordshire, NHS Trust U. K.

freestanding dialysis stations. At each station, the wateris mixed with dialysate concentrate by 2 stepcontinuous dilution system by automatic proportioning.All the haemodialysis systems are of the single passtype. The disinfection of the dialysis machines arecarried out after each session of dialysis using sodiumhypochlorite as disinfectant. The dialysers arereprocessed for reuse in the same patient.

The bacteriological analysis of the water and dialysatefluid used at the haemodialysis unit is ordinarilypreformed at monthly intervals, and whenever needed,more frequently. In this article the results of thebacteriological analysis performed from January 2002to December 2002 are evaluated. Two more sampleswere taken apart from the monthly samples.

The following samples were routinely collected;Main water supply, water used to prepare the dialysate(after reverse osmosis) just before entering thedialysate proportioning units, dialysis fluid samplescollected proximal to the dialyser from each of the 7haemodialysis units collected at the end of dialysis andthe bicarbonate dialysate.

Disinfection procedure was initiated including theoverhead water tank, reverse osmosis unit, distributionsystem and dialysis machines. When these samplesshowed unacceptable levels of bacterial count, routinedisinfection of all the components from the water tank tothe distribution system is carried out using formaldehydeon a bimonthly basis.

The samples for bacteriological analysis werecollected by using sterile precautions. Water/dialysatewas allowed to run freely and after rejecting the first fewmilliliters, a volume of about 10 ml was collected into asterile wide mouthed container. The samples were then

2012; Vol : 1 BIMS Medical Journal 3

immediately transported to the microbiology laboratoryand processed as per standard methods (3). The totalviable bacterial count was performed by spread platetechnique on trypticase soy agar (Himedia, Mumbai,India) and incubated at 370 C for 48 hours. TheAmerican Association of Medical Instrumentation (AAMI)recommends standards for treated water and dialysatequality. According to these standards the limitsregarding the total bacterial counts are 200 colonyforming units/ml (cfu/ml) for treated water and 2000 cfu/ml for dialysate. The microorganisms were identified bystandard methods.

RESULTSThe results of the bacteriological analysis of

water used to prepare the dialysis fluid and thedialysate are detailed in the table. All the isolatesobtained consisted of non fermenting Gram negativewater bacteria. Pathogenic bacteria or faecal coliformsor faecal streptococci were not isolated from any of thesamples. It is important to note that the dialysate hadbacterial counts of >2000 cfu/ml during 14.28 % of totalsamples obtained. The dialysate concentrate water fromthe overhead tank and water immediately after reverseosmosis were sampled 14 times during the study periodbecause one or more of the routine samples tested hadsignificant bacterial counts. The overhead tank water wascontaminated 13(92.86%) of the times. Water after ROjust before entering the dialysate proportioning units wascontaminated in 14.28% samples. Haemodialysis fluidfrom individual machines also showed contamination,33% in all the machines, 25% times in single machineand 42% of times in more than 2 machines.

Table 1 : Results of sterility testing

Sample Total times tested Contamination

Dialysate 14 02 (14.28%)

Water from tank 14 13 (92.86%)

Water after RO 14 02 (14.28%)

DISCUSSIONHaemodialysis is being increasingly used for

chronic renal conditions and patients undergoinglong-term dialysis have a compromised immune systemand other disorders that can make them moresusceptibility to infectious disease(4). Because of themore frequent use of high-flux dialysis membranes, therole of endotoxin and in particular, endotoxin fragmentsin the water used for dialysis or the dialysate has beenreassessed during recent years. The origin of themicrobiological contamination has to be identified to itssuccessful implementation. The water, the bicarbonateconcentrate, and the fluid distribution system can bemajor contributors of bacterial contamination in the

system (5). The distribution system should be designedto prevent stagnation of water during non-use like bends,rough joints and dead arms and other recontaminationsites.

Measures needed to maintain the bacterial countat a low level have 2 targets: one is to maintain theultrapurity of the water feeding the haemodialysismachine by means of frequent disinfection of watertreatment system, destruction of biofilm by chemicalagents, change of filters and disposal tubings at regularintervals and by permanent recirculation of ultra purewater in the distribution system (hydraulic loop); the otheris to prevent recontamination and bacterial proliferationin the haemodialysis machine by means of frequentdisinfection, use of sterile liquid concentrates/powder andperiodic change of ultrafilters (5).

The contamination of the dialysate in 14.28%samples in this study indicates a serious problem in thehaemodialysis unit. This contamination is notwithstanding the presence of an ultrafilter in thehaemodailysis machines. Although the waterimmediately after reverse osmosis was sterile in 12samples collected (it was <50 cfu/ml and 51-199 cfu/mlin 2 samples respectively), water used to prepare thedialysate had high counts on many occasions. Thereverse osmosis plant is situated away from thehaemodialysis unit and the distribution system has bentloops at many places with a potential for waterstagnation. Theses could be the niches wherein thebacterial growth can occur in the form of biofilms. These4 times reverse osmosis water showed growth was justbefore the routine bimonthly disinfection of the systemwas due.

Reverse osmosis treated water is designed toprovide ultrapure water with very low level of bacterialand endotoxin contamination (0.1 cfu/ml, endotoxins <0.25 endotoxin units/ml with Limulus amoebocyte lysateassay) along with high chemical purity. Canaud et al,recommend performing disinfection of the watertreatment system weekly using peracetic acidbased solution, having a dual bactericidal andcleansing activity and alternate it with heat or steamdisinfection. Microfilter with depyrogenating capacity(positively charged) has also been suggested to beplaced at the head of the recirculation loop to ensurethe final sterility of the treated water. The disinfection ofwater treatment systems in our setup is clearlyinadequate and needs to be performed more frequently.Moreover peracetic acid based agents may give betterresults. Initially when the unit was under trial run, thehypochlorite used as the disinfecting agent was foundto be wanting and was changed to formaldehyde.

Regular periodic change of the ultrafilters of the

water treatment system and the dialysis machines arebeing carried out in our centre.The ultrafilter in thehaemodialysis machine has been shown to be highlyeffective in preventing bacteria. So, the onlyexplanation for the contamination in the dialysate is theinefficient disinfection of the haemodialysis machine.Again we noted that our unit uses sodium hypochloritefor machine disinfection whereas, use of peracetic acidis recommended.

The community water source stored in theoverhead tank was most of the times (98.86%)contaminated. Chlorine treated community watersupplies are rarely of high bacteriological purity in mostparts of the world. But storage of water in the overheadtank in itself, as opposed to a continuous supply canenhance the growth of water bacteria forming a biofilmwhich will render the disinfection process ineffective,unless the tank and the pipelines are scrubbedthoroughly prior to disinfection.

Pyrogenic reactions and Gram negative sepsisare the most common complications associated with highlevels of Gram negative bacterial contamination ofdialysis fluid.2 The contamination of the dialysate hasrecently gained much attention and this is because ofthe extensive use of bicarbonate as dialysate buffer,which favours bacterial proliferation implicated inpyrogenic reactions. The other reason being, thepresence of endotoxin in the dialysis fluid which isassociated with production of pro-inflammatory cytokinesimplicated in the dialysis-related pathology of long term

disease patients.

Although endotoxin assays were not performedin ourinstitution due to lack of facilities, they arevaluable in ensuring safety of the dialysate.

ACKNOWLEDGEMENTSThe authors are grateful to the staff of the

Haemodialysis unit, KIMS, Hubli for their cooperationduring the study.

REFERENCES

1. Perez-Garcia R, Rodriguez-Benitez PO. Why and howto monitor bacterial contamination of dialysate? NephrolDial Transplant 2000; 15(6):760-4.

2. M Arvanigidou, S Spaia, C Katsinas P Pangidis, TConstantinidis, V Katsouyannopoulos G Vayonas.Microbiological quality of water and dialysate in allhaemodialysis centers Greece. Nephrol Dial Transplant1998; 13(4):949-54.

3. Favero MS, Alter MJ, Bland LA Nosocomial infectionsassociated with hemodialysis. In: Mayhall GC (ed).Hospital epidemiology and infection control. 1996 Edn.Publisher place 693-714.

4. Ledebo I, Nystrand R. Defining the microbiologicalquality of dialysis fluid. Artif Organs 1999; 23(1):37-43.

5. B. Canaud, J. Y. Bose, H Leray and F. Stec.Microbiological purity of dialysate for on-line substitutionfluid preparation. Nephrol Dial Transplant 2000;15: 21-30.

4 Quality of water and dialysate Chandrashekar M. R. et al

Original Article

Prospective comparative clinical study of Adenoid Size in HIVand non HIV patients : A Pilot Study

Shalini Huddar, *Vijayanand Halli, **Satish Bagewadi, ***Irranna Palled, ****Umadevi AngadiSenior Resident, Department of ENT, Belgaum Institute of Medical Sciences, Belgaum-590 001.

ABSTRACTHIV infection causes various head and neck manifestations. Adenoid hypertrophy has been reported in adult

patients but, in pediatric patients very few studies are reported. In our study we are aiming to find whether HIV infectionaffects the size of adenoids in pediatric patients with features of adenoiditis.

Keywords : adenoid hypertrophy, HIV infection, adenoid-nasopharyngeal ratio.BIMS Med. J. 2012, 01 : 5-7

INTRODUCTIONThe adenoid forms the part of Waldeyers ring of

lymphoid tissue at the portal of the upper respiratorytract. In early childhood this is the first site ofimmunological contact for inhaled antigens.The adenoidcan be identified by MRI by the age of 4months in 18%of children. By the age of 5months, adenoid could beidentified in all children.Growth continues rapidlyduring infancy and childhood. The adenoid appears tobe at its largest in the 7yr age group. Regression occursrapidly after 15yrs of age (1).

Adenoid hypertrophy has been reported in46-69% of HIV positive adult patients. In pediatricpatients very few studies are reported. D. Balsom (1995)reported 9 out of 18 children studied, had abnormallysmall adenoids (2). S. A. Hickey (1990) reported a caseof symptomatic recurrent adenoidal hypertrophy in HIVpositive haemophilic 8 yr old boy(3). There is noconclusive data available with respect to adenoid sizein pediatric patients with HIV infection.

Objective of the studyTo find out whether HIV infection affects the size

of adenoids, in HIV positive pediatric patients withfeatures of adenoiditis.

MATERIALS AND METHODSA prospective comparative clinical study (pilot)

was conducted from 2010 to 2011 at BIMS hospital,Belgaum. In our study, 20 HIV and 20 non HIV patientsattending ART centre and ENT OPD, with clinicalfeatures of adenoiditis were included in the study.

Inclusion criteria1. Patients between age group 3-12 yrs2. Patients with features of adenoiditis

*Prof. and HOD, Dept. of ENT, Belgaum Institute of Medical Sciences, Belgaum-590 001.

**Asso. Prof., Dept. of ENT, Belgaum Institute of Medical Sciences, Belgaum-590 001.***Asst. Prof., Dept. of Radiology, Belgaum Institute of Medical Sciences, Belgaum-590 001.

****Asst. Prof., Dept. of ENT, Belgaum Institute of Medical Sciences, Belgaum-590 001.

Fig. 1 : Adenoidal measurement.

Fig. 2 : The nasopharyngeal space measurement.

Fig. 3 : Lateral radiograph of nasopharynx showingmeasurement of A and N.

Exclusion criteria1. Patients below 3 yrs and above 12 yrs.2. Patients with cleft palate.3. Post-adenoidectomy patients

Lateral radiographs of nasopharynx were usedto assess the size of adenoids. Adenoidal-nasopharyngeal ratios were calculated according toFujioka’s method (4).

Adenoidal measurement-A (fig 1) representsdistance from A1, point of maximal convexity along theinferior of adenoid shadow to line B, drawn along straightpart of anterior margin of basiocciput. A1 is measuredalong a line perpendicular from point A1 to itsintersection with B.

Nasopharyngeal measurement-N (fig 2) is thedistance between C1, postero-superior edge of hardpalate, and D1 antero-inferior edge of spheno-basioccipital synchondrosis.

The Adenoidal-Nasopharyngeal Ratio (AN ratio)is obtained by dividing the measurement for A by thevalue for N (fig 3).

RESULTSThe study included 20 non HIV and 20 HIV

patients with features of adenoiditis. The age and sexdistribution is shown in table-1 and table-2 respectively.

In non HIV patients Mean AN ratio was 0.525and Mean AN ratio was 0.335 in HIV patients (Table 3).Other associated findings in non HIV patients were acutesuppurative otitis media-1 (5%), chronic suppurative otitis

Table 1 : Age distribution of the patients

Age Non-HIV Patients HIV Patients

3-7 4 (20%) 5 (25%)

8-12 16 (80%) 15 (75%)

Table 2 : Sex distribution of the patients

Sex Non-HIV patients HIV

Male 12(60%) 11(55%)

Female 8(40%) 9(45%)

Table 3 : Adenoidal-Nasopharyngeal Ratios (AN Ratio)in non HIV and HIV children

Non HIV patients HIV patientsMaximum AN ratio 0.914 0.468

Minimum AN ratio 0.307 0.115

Total No n1=20 n2= 20

Mean AN ratio 0.525 0.335

Unpaired t test, p<0.001,

media-2 (10%), otitis media with effusion-2 (10%).

Other associated findings in HIV patients were,chronic suppurative otitis media -7 (35%), acutesuppurative otitis media-1 (5%), otitis media witheffusion–2 (10%), Parotid enlargement-2 (10%),Cervical lymphadenopathy -2 (10%).

DISCUSSIONAdenoid hypertrophy has been reported in

46-69% of HIV positive adult patients by various authors.Williams (1989) reported in small series the head andneck manifestations in PAIDS. These include acute,chronic and serous otitis media, muco -cutaneouscandidiasis, cervical adenopathy and parotidenlargement (5). S. A. Hickey (1990) reported a case ofsymptomatic recurrent adenoidal hypertrophy in HIVpositive haemophilic 8 yr old boy (3). D. Balsom (1995)reported 9 out of 18 children studied had abnormallysmall adenoids(2). According to the study, HIVinfection is in the spectrum of immunodeficiencydiseases associated with an abnormally emptynasopharynx . In our study the AN ratios of two groupswere compared using unpaired t test. The difference inthe mean AN ratios in two groups was statistically highlysignificant (p<0.001).

CONCLUSIONSAccording to our study it appears that pediatric

patients with HIV infection have smaller adenoids ascompared to non HIV patients. However conclusioncannot be drawn because of small sample size. Furtherstudy with larger sample size is recommended.

6 Adenoid size in HIV and non HIV patients Shalini Huddar et al

REFERENCES1. Peter J Robb. The adenoid and adenoidectomy. Scott –

Brown’s Otorhinolaryngology, Head and Neck Surgery,7th Edition (Volume-1) London; Edward Arnold Ltd 2008: 1094.

2. Balsom D, Kanth N, Balbi H. Abnormally small adenoidsin HIV-infected children.Pediatric Radiol 1995; 25: 74-76.

3. Hickey SA, Buckley JG, Macartney JC et al. Adenoidal

hypertrophy as the presenting feature of HIV infection.J Laryngol Otol 1990;104: 58-59 .

4. Fuijioka M ,Young LW,Girdany BR Radiographicevaluation of adenoid size in children: adenoidal-nasopharyngeal ratio AJR 1979;133: 401-404.

5. Williams MA. Head and neck findings in pediatricimmune deficiency syndrome Laryngoscope 1987; 97:713-716.

2012; Vol : 1 BIMS Medical Journal 7

Original Article

Breastfeeding practices among the infants living inRural Area - A Longitudinal Study

Praveena Gunagi, *Vijaya A. Naik, **Mallapur M. D.Assistant Professor, Department of Community Medicine, Belgaum Institute of Medical Sciences, Belgaum-590 001.

ABSTRACTBackground and objectives

Breast feeding is an unequalled way of providing ideal food for the healthy growth and development of infantand has unique biological and emotional influence on the health of both mother and child. This study was aimed todescribe the breastfeeding practices prevalent in rural areas.

MethodologyThe present longitudinal study was conducted in one of the randomly selected subcentre of PHC Vantamuri

attached to the Department of Community Medicine, J. N. Medical College, Belgaum during the period of November2005 to October 2006. The sample size included was 60. All the mothers in the study were visited independently oncea month to known the breast feeding practices.

ResultsIn the present study the administration of prelacteal feeds was 63.3%, 50% of babies did not receive colostrum

and Initiation of breastfeeding within one hour was 31.67%. Only 36.6% did exclusive breastfeeding until 6 months.Initiation of top feeds before 6 months was 46.7%. There was no significant association between socio-demographicfactors and exclusive breast feeding.

ConclusionThis study emphasizes the need for breastfeeding intervention programs especially for the mother during

antenatal and postnatal check-ups and practices like discarding the colostrum and early/ late weaning are still widelyprevalent and need to be addressed.

Keywords : Exclusive Breastfeeding, pre-lacteal feeds, rural areas.BIMS Med. J. 2012, 01 : 8-11

INTRODUCTIONBreast feeding is an unequalled way of

providing ideal food for the healthy growth anddevelopment of infant. It has unique biological andemotional influence on the health of both mother andchild. Breast feeding alone is estimated to save anadditional one to two million lives if breast feedingpractices were improved. “Breast feeding was the best,is the best and will remain the best” as far as infantfeeding is concerned.

Breast feeding is an important crosscuttingcomponent of child survival and maternal healthprograms. During the first two years of life it cansignificantly reduce mortality and morbidity. It providesthe best health benefits when started immediately afteran infant’s birth and continued exclusively for the firstsix months of life and then continued along with suitablecomplementary feeding through age two or longer.

During the first six months of life, infants who

*Professor and Head, Department of Community Medicine, J. N. Medical College, Belgaum- 590 010.**Lecturer in Statistics, Department of Community Medicine, J. N. Medical College, Belgaum-590 010.

are exclusively breast fed have one fifth to one sixth thediarrheal mortality and one third to one half therespiratory disease mortality than infants who receiveno breast milk (1,2).

Data from demographic health surveys andreproductive health surveys shows that most of thechildren are breastfed. Yet only minorities of infants arebreast fed in optimal ways. In most of the countries lessthan 50% of infants are breastfed within one hour of birth,less than half are exclusively breastfed (3, 4). InKarnataka only 35.6% of the children are breast fed withinone hour after birth, 58% are exclusively breast fed (5).Most studies assessing breastfeeding practices in Indiaare cross-sectional in nature (6, 7, 8).

OBJECTIVESi. To study the prevalence of exclusive breast

feeding and patterns of breast feeding.ii. To identify the socio-demographic factors

associated with exclusive breast feeding.

2012; Vol : 1 BIMS Medical Journal 9

Table 2: Association between socio-demographicfactors and exclusive breastfeeding

Socio Study groupdemographic

factors No EBF Percentag

Age of the mother

15-19 12 04 33.33

20-24 24 08 33.33

25-29 20 09 45.00

> 30 04 01 25.00

Total 60 22 36.67

P value x2 = 0.770, df = 3, p = 0.857

Educational status

Illiterate 29 10 34.48

Primary 12 04 33.33

Secondary 15 07 46.67

P. S. 02 01 50.00

Graduate 02 00 00.00

Total 60 22 36.67

P value x2 = 0.481, df = 3, p = 0.923

Socio economic status

Class I 00 00 00.00

Class II 02 01 50.00

Class III 05 00 00.00

Class IV 35 13 37.14

Class V 8 18 44.44

Total 60 22 36.67

P value x2 = 1.374 df = 3, p = 0.723

METHODOLOGYThe present longitudinal study was conducted in

one of the randomly selected subcentre Bhutramatti ofPHC Vantamuri attached to the Department of com-munity medicine, J. N. Medical College, Belgaum duringthe period from November 2005 to October 2006.All the Pregnant Women who had completed 32 weeksof gestation and who had agreed to stay in the area forat least 6 months after delivery were enrolled from Nov.2005 to April 2006 and followed up for 6 months atscheduled intervals. Totally 60 mothers were enrolledduring this period. Mothers having babies with birthweight<1500 grams, gestational age <32 weeks,admitted in intensive care unit for >48 hours or havingcontraindications for breastfeeding were excluded.After obtaining informed written consent, first twointerviews were conducted one day after delivery;Subsequent interviews were conducted every month upto 6 months. Data was collected by interview methodusing predesigned pre structured questionnaire.Questionnaire included socio demographic data, detailson the initiation, administration of pre-lacteal feeds,discarding of colostrum and duration of breastfeeding.Analysis was done using percentages and chi squaretest.

RESULTSSocio-demographic profile

Out of the 60 mothers interviewed 20(33.3%)were in the age group of 25-29 years and mean agewas 23.5 years, 29(48.3%) were illiterate and 35(58.3%)belonged to class IV according to modified BG Prasadclassification.25 (43.3%) of the mothers wereprimigravidae 43(71.7%) were hospital deliveries.

Initiation of breast feeding.Out of the 38 (63.3%) mothers who administered

prelacteal feeds 27(45%) gave sugar water, 10(16.6%)gave both sugar water and honey and one baby wasgiven (1.67%) cow’s milk, 28(68.2%) mothers said thatsince there was no milk secretion they started with

Table 1 : Distribution of newborns based on the breastfeeding practices

Breastfeeding Breastfeedingincorrect practices No. % correct practices No. % P Value

Prelacteal feeds given 38 63.3 Prelacteal feeds not given 22 36.7 P < 0.05

Discarding of colostrum 30 50 Colostrum given 30 50 P > 0.05

Breast feeding 41 68.3 Breastfeeding initiation 19 31.67 P < 0.01initiation> one hour within one hour

Top feeds given 28 46.66 EBF till 6 months 22 36.7 P < 0.05before 6 months

Complementary 10 16.7feeds <6 months

n = 60

prelacteal feeds and other reasons were familyrestriction 4(9.76%) and certain medical causes likecaesarean section, difficulty in sucking and mother wasill. 55(91.7%) pregnant women delivered normally and5(8.3%) by caesarean section and those who deliveredby caesarean section started feeding after 3-4 hours.

Exclusive breast feedingOnly 36.6% did exclusive breastfeeding until 6

10 Breastfeeding practices Praveena Gunagi et al

months. A total of 46.7% had given top feeds like cow’smilk 25(41.67%) followed by commercial milk, 16.7% ofthe mothers started premature complementary feeding.The most common reason for starting top feeds andcomplementary feeds was insufficient milk. Nosignificant association was found between sociodemographic factors, obstetric factors and breastfeeding.

DISCUSSIONIn our study we found that though breastfeeding

was universal but the breastfeeding practices were farfrom optimal. Out of the 60 newborns 63.3% receivedprelacteal feeds. According to NFHS 3 report (2005-2006) 57% newborns received prelacteal feeds(5).Similar results were found in a study conducted atRajasthan which showed that 65.2% of mothers gavejaggery water as a prelacteal feed (6). Ideally nothing

should be given to infant up to 6 months, but wrongbeliefs and culture lead people to think that prelactealfeed is good for newborn. According to IYCF (2006)guidelines, breastfeeding initiation should be done withinone hour of birth (9). In our study it is only 31.6%.Common reasons for late initiation were no milksecretion and family restrictions. In Central Karnataka inIndia, a community-based study was conducted whichshowed that Only 3 infants (0.3%) were offeredbreastfeeding within 1 hour after delivery (7). 50% of themothers discarded colostrum. Our findings were similarto the NFHS report and study by Bharadwaj et al inUttarpradesh (5,8). As colostrum is thick secretion it wasconsidered unhealthy. This shows their lack ofknowledge regarding physiology of milk secretion. Sothere is a need for proper counseling of motherregarding the same. Various studies have reporteddifferent results regarding discarding of colostrums likea study by Banapurmath C.R et al (7) wherein 28.6% ofmothers discarded the colostrum and 77% discardedcolostrum in a study by Singh M B, at Rajasthan (6).

Exclusive breastfeeding should be done for 6months. But in our study only 36.7% were doing. Reststarted either with top feeds and some withcomplementary feeds. Main reason was insufficient milk.Many studies have shown similar results (6, 7, 8, 10).About 16.7% of the mothers started prematurecomplementary feeding. A study done at Rajasthanshowed that 9.1% of mothers introducedsupplementary foods before 3 months of age, 15.6% ofmothers introduced these foods at 3-6 months of age(6). Other socio-demographic factors like age of themother, type of the family socio-economic status,parity, place of delivery seem to have not made anydifference on the exclusive breast feeding practices inthe present study. Our study findings did not match withthe results from a study done in Gujarat which revealedthat maternal & paternal education, socioeconomicstatus and type of family revealed a significantassociation with newborn’s exclusive breastfeeding (11).

The influence of mother in-law and selfassumption about lack of milk for the baby are sited asmajor reasons for non exclusive breast feeding. Thuscounseling by peer counselors and development ofcounseling skills among doctors might help inconveying the right message to mothers about breastfeeding.

CONCLUSIONSThis study emphasizes the need for

breastfeeding intervention programmes especially for themother during antenatal and postnatal checkups.Behavior change strategies are the basis of breastfeedingpromotion programs. Although many mothers are aware

Table 3 : Association between obstetric factors andexclusive breastfeeding

Obstetric Study groupfactors

No EBF Percentage

Parity

Primiparous 25 8 32

Multiparous 35 14 40

Total 60 22 36.67

P value x2 = 0.18, df = 1, p >0.5

No of antenatal visits

< 3 9 3 33.33

> 3 51 19 37.25

Total 60 22 36.67

P value x2 = 0.031, df = 1, p >0.5

Place of delivery

Home 17 7 41.17

Dist 04 04 100

Pvt 34 10 29.41

PHC 02 01 50.00

Total 60 22 36.67

P value x2 = 1.02 df = 3, p >0.5

of importance of Breastfeeding, they are often reluctantor unable to do it effectively.

Use of peer groups that provide social andemotional support will help mothers to overcomeobstacles to breastfeeding. Supports from householddecision makers have direct influence on infant feedingdecision & practices.

REFERENCES1. United States Agency for International Development,

Bureau for Global Health: PVO Child survival and Healthgrants programs: Technical reference materials. USAID/GH/HIDN; Nutrition 2004.

2. Tiwari SK, Chaturvedi P. IMS Act 1992; Need for moreamendments and publicity. Indian Paediatrics 2003; 40:743-6.

3. Population reports: Breast feeding gains and goals.Issues in World Health Series L, 2006;14.

4. WHO Community based strategies for breast feedingpromotion and support in developing countries. 2003.

5. Ministry of Health and Family Welfare, Government ofIndia. National Family Health Survey of India – 3, 2006

Available from: URL: www.nfhsindia.org/pnfhs3.html

6. Singh M B, Haldiya KR, Infant feeding and weaningpractices in some semi-arid rural areas of Rajasthan. JIndian Med Assoc.1997;95(11):576-8, 590.

7. Banapurmath CR, Nagaraj MC, Banapurmath S, KesareeN Breastfeeding practices in villages of centralKarnataka.Indian Pediatr. 1996 ; 33(6):477

8. Bhardwaj, N.; Hasan, Badrul S.; Zaheer, Mohammad.:Breast-Feeding and Weaning Practices - A Rural Studyin Uttar Pradesh. The Journal of Family Welfare. 1991.39(1): 23-29.

9. National guidelines on infant and young child feeding2006. Available from: URL:

10. Madhu K, Chowdary S, Masthi R. Breast feedingpractices and newborn care in rural areas: A descriptivecross-sectional study. Indian J Community Med2009;34:243-6.

11. Chudasama R.K., Patel P.C. & Kavishwar A.B.:Breastfeeding initiation practice and factors affectingbreastfeeding in South Gujarat region of India. TheInternet Journal of Family Practice. 2009;7 (2) Availablefrom: URL www.ispub.com

2012; Vol : 1 BIMS Medical Journal 11

Original Article

Assessment of Nutritional Status among Undergraduate MedicalStudents - A Cross Sectional Study

Karikatti S.S., *Radhika M. M., **Spurthi U. C., ***Sunanda Halki, ****Hallappanavar A. B.Associate Professor, Department of Community Medicine, Belgaum Institute of Medical Sciences, Belgaum-590 001,

ABSTRACTBackground

Obesity is a complex condition, with serious social and psychological dimensions, affecting virtually all agesand social groups. The Medical students and young professional are exposed to the environmental stress and thechange in life style patterns like status or high economic profile, habits like alcohol consumption, new diet patterns etc,due to peer pressure which, tends to affect nutritional status. Hence, the study was undertaken to assess thenutritional status of medical students.

MethodologyA cross-sectional study was carried out among undergraduate medical students with a purposive sample of 78

students. Socio demographic variables like age, sex, education, family history of obesity etc, were collected.Anthropometric readings like height, weight, waist circumference were taken and BMI was calculated and overweightand obesity were assessed. The proportions and percentages were calculated and chi square test was used forstatistical analysis and relative risk of associate factors was calculated.

ResultsThe study comprised of 47(60%) girls and 29(40%) boys. The prevalence of overweight and obesity was

11(14.47%) and 4(5.26 %) among boys and girls respectively. Overall, 28/76 (36.84%) students were physicallyinactive and family history of obesity was one of risk factor which showed almost two times risk of being obese.

Keywords : Overweight, Obesity, Risk factors, Non communicable diseases, Medical students, Urban.

BIMS Med. J. 2012, 01 : 12-15

INTRODUCTIONMalnutrition conditions of young children in

India have received much attention recently, but adultsare also experiencing a variety of nutritional problemsespecially, obesity. Obesity is a complex condition, withserious social and psychological dimensions, affectingvirtually all ages and socioeconomic groups and hasbegun to replace under nutrition and infectious diseasesas the most significant contributor to ill-health. This hasbeen attributed to nutritional transition in India,characterized by a shift in the diet content towards ahigh fat and high sugar diet. It is a polygenic,multi-factorial disease occurring by the interaction ofgenes and environmental factors and associated withmany diseases.

Approximately 1.2 billion people in the worldare overweight and at least 300 million of them are obese(1). Many studies have shown that the prevalence ofoverweight among adolescents varies between 10 and

30% (2). A phenomenal rise has been observed evenamong Indian youth (3). Prevalence varies within thecountry and within various groups because of differencesin the lifestyle, mainly in the dietary patterns andphysical activity.

The newly rich urban, middle, and high incomepopulations suffer from an emerging problem of obesitydue to changing lifestyles and diet (4). Medical studentsare young professional who are exposed to theenvironmental stress and change in life style patternslike status or high economic profile, habits like tobacco,alcohol consumption etc. due to peer pressure. Thisnecessitates, assessing and identifying young adults whoare at risk of becoming obese or obese and subsequentlyrequiring appropriate intervention. Hence, the study isundertaken for early detection of risk factors related toobesity, risk behaviour and lifestyle especially, amongmedical students which, is essential considering theirrole as future physicians and role model in public health

*MBBS III / I Phase, Belgaum Institute of Medical Sciences, Belgaum-590 001.

**MBBS III / I Phase, Belgaum Institute of Medical Sciences,, Belgaum-590 001.

***Lecturer in Statistics, Department of Community Medicine, Belgaum Institute of Medical Sciences, Belgaum-590 001.****Professor, Department of Community Medicine, Belgaum Institute of Medical Sciences, Belgaum-590 001.

2012; Vol : 1 BIMS Medical Journal 13

and their own heath status.

The main aim of undertaking this study was toassess the nutritional status of medical students, todetermine the prevalence of some nutritional problemsamong them and to assess the risk factors of obesityamong medical students.

Objectives1. To assess the prevalence of obesity among

under graduate medical students.2. To assess the prevalence of under weight

among under graduate medical students.3. To assess the factors associated with nutritional

status.

MethodologyA cross-sectional study was carried out among

undergraduate medical students of Belgaum Institute ofMedical Sciences, from July 2011 to August 2011. Apurposive sample was taken with total sample size of88 students. Out of 88 students, 76 students respondedand were included in the study. A self administratedquestionnaire was used to collect data which includedsocio demographic data (name, age, sex, education, totalfamily members, income and occupation), family historyof obesity and physical activity during leisure time andconsumption of alcohol or tobacco. List of physicalactivities were included in each category and hencestudents were classified as physically inactive andphysically active (mild, moderate and heavy activity).Students with mild or no physical activity wereconsidered physically inactive. Anthropometric readingswere taken which included height (Height was read tothe nearest of 0.5 cm), weight (Weight was measured tothe nearest of 100 grams) and waist circumference (WC)(Waist circumference was measured with a measuringtape to the nearest 1 mm) (5). Body Mass Index (BMI)was derived using the following equation: weight (kg) /height (mt)2 and obesity,overweight, underweight weredefined if BMI >27.5>23 and <18.5 respectively(6). Theproportions and percentages were calculated and chisquare test was used for statistical analysis and relativeratio of risk factors was calculated.

RESULTSOut of 88 students 76 students participated in

the study. The students belonged to 20 years to 22 yearsand of that 50 (65.8%) belong to the age group of 21 yrs.The study comprised of 47 (60%) girls and 29(40%) boys.The age and sex wise distribution is as shown in thefigure.

The nutritional status of students was assessedaccording to body mass index and the results were as intable 1. In the study 11(14.47%) boys and 4(5.26 %)girls were having overweight including obesity.

Fig. 1: Age and sex wise distribution of students

The Central Obesity was assessed as per waistcircumference and 8/29(27.59%) boys and 3/47(6.38%)girls were having central obesity and rest had normalwaist circumference. The overall prevalence of centralobesity was 14.77%. The risk factors for obesity wereassessed and the results revealed that, 14(18.42%)students had a family history of obesity among anyparents.

Among boys 7/29 (24.14%) were physicallyinactive and 21/47(44.68%) girls were inactive. Overall28/76 (36.84%) students were physically inactive andnone of the girl was involved in heavy physical activity.According to a history of alcohol consumption 6/

n = 76

Table 1 : Nutritional status of students according tobody mass index

Nutritional status Boys Girls Total

Underweight 6 (20%) 14 (27.65%) 20 (26.3%)

Normal 12 (41.3%) 29 (61.7%) 41 (53.94%)

Overweight 8 (27.59%) 3 (6.38%) 11 (14.47%)

Obese 3 (10.35%) 1(2.13%) 4 (5.26%)

Total 29(100) 47(100%) 76 (100%)

n = 76

Table 2 : Family history of obesity amongparents of students.

F/H/O Total Obesity Obesity Relative

Obesity Present Absent Ratio

Only mothers Yes 6 2 4

No 70 13 57 1.79

Only father Yes 7 2 5

No 69 13 56 1.52

Either parents Yes 12 4 8

No 64 11 53 1.94

n = 76

29(20.68%) boys used to consume alcoholoccasionally and 3/47(6.4%) girls had attempted thealcohol consumption. The alcohol consumption rateincreased with body mass index,

DISCUSSION AND CONCLUSIONIndians are at increased risk to get diabetes or

heart problems due to obesity compared to Caucasiansof same weight, height and age. The obesity causes anapproximately threefold increase in CHD risk. Beingoverweight is an important contributor to risk ofmorbidity in younger people, particularly to CHD.

In the present study the prevalence of overweightand obesity among boys and girls was 14.47% and 5.26% respectively. Among students 27.59% boys and 6.38%girls were having central obesity. More boys were obesecompared to girls. The under nutrit ion was alsoprevalent among medical students as 20% boys and27.65% girls were underweight. Overall 26.3% studentswere having underweight. The nutritional status wascomparatively better among boys than girls. The studyconducted for assessment of cardiac risk factors inmedical students of Tehran University revealed that, theprevalence of obesity (body mass index = 27) was 40.3%in boys and none of girls were obese, the overallprevalence of obesity was 32.9 among medical studentsand abdominal obesity was 10.2%. In the same studythe main risk factors found were physical inactivity(43.5%), low high-density lipoprotein cholesterol (26.2%),smoking (10.3%), obesity in 23.4% etc. Whereas, in thepresent study the prevalence of obesity was 15.7% andcentral obesity was 14.47%. And 36.84% students were

physically inactive and 18.42% students had familyhistory of obesity. The prevalence of obesity and riskfactors were comparatively higher among Tehranmedical students. The life style and dietary factors maybe the precipitating factors as it is totally different fromthe Indian culture or may the increased rate of physicalinactivity among Tehran students have lead to obesity (7).

Being overweight is an important contributor torisk of morbidity in younger people, which need to bemodified. It is well established that at all BMI,individuals with visceral obesity (excess deepabdominal fat as indicated by waist circumference) areat highest risk of cardiovascular disease and otherchronic diseases. Surprisingly, in the present study theprevalence of central obesity (14.47%) among medicalstudents was higher than Tehran students (10.2%).Hence, it is advisable within the normal range of BMI itis better to be leaner and have the optimal BMI.

The risk factors like, family history of obesity,physical inactivity were assessed; 15.7% students hada family history of obesity and 36.84% students werephysically inactive and none of the girls were involvedin heavy physical activity. The difference betweenvarious grades of physical activity was not statisticallysignificant; whereas, prevalence of physical activity andinactivity were statistically significant. The life style trendsshowed that, alcohol consumption rate was 20.68%among boys and 6.4% girls had attempted the alcohol.The alcohol consumption rate increased with body massindex.

Another study, from South India revealed that,the prevalence of overweight (BMI: 25-29.9 kg/m2) waspresent in 33.26% (males 34.2%, females 32.44%),Obesity (BMI 30-35 kg/m2) was present in 26.5% (males24.5%, females 28.24%) and high WC in 33.4% (males39.9%, females 59.15%) of young population. Theobesity among South Indian adults was almost doubleof that of young professionals (8). However, the obesityappears to be an emerging problem of young Indians,that too, among medical students. The study also showsthat development of obesity and central obesity isassociated with simultaneous increase in manybiological risk factors such as changes in bloodpressure levels and glucose and lipid abnormalities.

Similar study, done in Karachi, to determine theprevalence of major risk factors of CVD, includingdietary modification, Body Mass Index (14%) andphysical inactivity (37.9%) in medical students ofgovernment teaching hospitals of Karachi showed sameprevalence rates and low consumption rate of alcoholamong Karachi students which, may be attributed toreligious taboos of the society (9). In a survey inUniversity of Crete, medical students, 27.6% were

Table 3 : Sexwise and gradewise distribution ofphysical activity among students.

S t u d e n t s A c t i v e I n a c t i v e

Mild Moderate Heavy Active Inactive

Total Total

Boys 10(34.48) 10(34.48) 2(6.90) 22(75.86) 7(24.14)

Girls 13(27.66) 13(27.66) 0 26(55.32) 21(44.68)

Total 23(30.26) 23(30.26) 2(2.63) 48(63.16) 28(36.84)

X² = 2.4 P > 0.05 X² = 4.49 P < 0.05

n = 76

Table 4 : Nutritional status and history ofalcohol consumption

Alcohol Non alcohol Total

Underweight 1 (5.00%) 19 (95.00%) 20

Normal 3 (7.69%) 36 (92.30%) 39

Pre Obese/Obese 3(17.64%) 14(82.35%) 17

n = 76

14 Obesity Karikatti S. S. et al

overweight and 4.3% were obese (10). Many studies, inSlovakia (16% of male but only 2% of female medicalstudents had overweight) (11), a study in US (malemedical students, 30% were overweight with BMI22.8–24.7 kg/m2) (12) were having the similar problem;In Louisiana State University, 37% of males and 9% offemales were overweight (13). A study conducted among154 medical students in South Africa reported, rates ofoverweight and obesity were 8.9% and 2.5%respectively for Indian and 19.7% and 4.6% for blackstudents (14).

Although, the range of definitions complicatescomparisons with other studies of young adults ormedical students, they reveal the facts that, theoverweight / obesity among young adults includingmedical students are towards increasing trends, whichis an alarming factor in promotion of health for all andoverall development of national health status. A studydone to know the prevalence of obesity among clinicalstudents in a Malaysian medical school, in which, BMIwas assessed based on the Asian cut-off showed that,combined prevalence of overweight and obesity amongstudents was 30.0%; In this study Malays and Indianswere more obese than the Chinese (15). Like in our study,in most of the studies, males had higher proportion ofoverweight and obesity.

The study concludes that, overweight/obesityand its risk factors are prevalent among medicalstudents and more so among boys than girls. Thealcohol consumption rate was high among overweightboy. Similarly, one third of medical students areunderweight.

The proportions of physical activity andinactivity were significantly varied among students. Thelifestyle and environmental factors appears to be thedeterminants of overweight/obesity and are moreprevalent among medical students.

The limitation of the study is that, the detaileddietary history on the types and quantities of foodconsumed by the students, any missing of meals,consumption of junk food etc were not collected hence,the study was unable to determine the impact ofnutrition intake on the weight of the students. Further,studies can be conducted to assess dietary factorsassociated with obesity. The intervention measures toprevent & control overweight and obesity among thiseducated group is need of hour though it is achallenging task and to establish an ongoing and inbuiltprogram for students can be recommended to theinstitute.

REFERENCES1. Power C, Lake JK, Cole TJ. Measurement and long-term health

risks of child and Adolescent fatness.International

Journal of Obesity 1997; 21: 507-26. 

2. Kotian MS, Ganesh Kumar S, Kotian SS. Prevalence anddeterminants of overweight and obesity amongadolescent school children of South Karnataka, India.2010; 35: (1) 176 – 78.

3. Kapil U, Singh P, Pathak P, Dwivedi SN, Bhasin S:Prevalence of Obesity amongst affluent adolescentschool children in Delhi. Indian Paediatrics 2002; 39:449-52.  

4. Kapil U. The problem of overweight and obesity.Proceedings of the UGC sponsored national seminaron obesity: A well fed undernourished syndrome,Ernakulam, Kerala, India, 2004: 7-18.

5. Cole TJ, Bellizi MC, Flegal KM, Dietz WH. Establishing astandard definition for hild overweight and obesityworldwide: An international survey. Br Med J 2000;320:1240-43.

6. Kaneria Y, Singh P, Sharma DC., Prevalence of over-weight andobesity in relation to socio economic con-ditions in two different groups of school age children ofUdaipur city (Rajastan). Indian J Community Med 2006;7: 133-5.

7. Mahmoudi MJ, Nematipour U, Moradmand S, GharouniS, Mahmoudi M, Rezaei N, Ahmadvand A R and KarimiN., Assessment of cardiac risk factors in medicalstudents of Tehran University. Acta Medica Iranica. 2004;42(6): 402-10.

8. Desigamani K , Priya K , Rita MA., Age, gender relatedprevalence of cardiovascular risk factors in overweightand obese south Indian adults Int J Biol Med Res. 2011;2(2): 513- 22.

9. Sajjad R, Muhammad A S, Muhammad Fawwad A H,Saad E S, Rabia M, Sina A,et al, Dietary modification,Body Mass Index (BMI), Blood Pressure (BP) andcardiovascular risk in medical students of a governmentmedical college of Karachi. J Pak Med Assoc 2010;60(11): 970-74.s

10. George B, Ioannis M, Manolis L, Anthony K,.Overweightand obesity in relation to cardiovascular diseaserisk factors among medical Students in Crete, Greece.BMC Public Health 2003, 3:3 .available from: http://www.biomedcentral.com/1471-2458/3/3.

11. Baska T, Straka S and Mad’ ar R Smoking and some life-style changes in medical students – Slovakia, 1995–1999.Cent Eur J Public Health 2001, 9:147-49.

12. Gelber C, Hochberg C, Mead A, Wang N-Y, Wigley Mand Klag J Body mass index in young men and the riskof subsequent knee and hip osteoarthritis. Am J Med1999, 107:542-48.

13. Farris R, Strada R, Wolf T and Suskind R Nutrient intakeand cardiovascular risk factors of first-year medicalstudents. J Vasc Med Biol 1994, 5:138-43.

14. Morar N, Seedat YK, Naidoo DP and Desai DKAmbulatory blood pressure and risk factors for coronaryheart disease in black and Indian medical students. JCardiovasc Risk 1998, 5:313-38.

15. Boo N Y, Chia GJQ, Wong L C, Chew R M, Chong W, LooRC The prevalence of Obesity among clinical studentsin a Malaysian Medical School. Singapore Med J 2010;51(2): 126-32.

15 Obesity Karikatti S. S. et al

Original Article

Biochemical screening tests of urine in mentally retarded childrenIndira Bhaskar, *Aruna Bhushan, **Narasimha Rao S.

Assistant Professor, Department of Biochemistry, KPC Medical College, Kolkata.

ABSTRACTMentally retarded children pose a great difficulty in the investigations and management. Most of the tests that

are commonly done are complex and need sophisticated equipment. We have done simple screening tests of urineshowing reducing substances such as mucopolysaccharides, Ketoacids and phenylketonuria. Major biochemicaldisorders identified were mucopolysaccharidosis, G-6-P dehydrogenase deficiency and metachromaticleukodystrophy.

Keywords : Biochemical Screening, Mental retardation, Mucopolysaccharidosis.

BIMS Med. J. 2012, 01 : 16-18

INTRODUCTIONMental retardation specifies an I.Q less than 70

resulting from a patho-physiological process affectingthe cerebrum during the developmental period (1).Inborn errors of metabolism (IEM) are heterogeneousgroup of disorders caused by a single gene defect.This may manifest immediately after birth or after fewweeks after birth (2).

Most of these defects are due to the abnormalactivity of key enzymes in their metabolic pathwaysleading to accumulations of compounds which followalternate pathways of metabolism producing toxicmetabolites and deficiency of biologically importantcompounds (3).

Older mothers tend to have babies with Down’ssyndrome than the young mothers. Among the mentallyretarded it was reported that 5.75% of them were due toinherited metabolic disorders (4). And abnormalmetabolites such as phenylketonuria (PKU),mucopolysaccharidosis (MPS) and galactosemia areassociated with mental retardation. These abnormalmetabolites can be estimated by urine examination inthe clinical laboratories. In our institution this study wasthus conducted.

*Associate Professor, Department of Pharmacology, B.I.M.S., Belgaum-590 001.**Director of Laboraties, UMC, Mangalore.

Aim of the studyTo screen the abnormal metabolites in the urine

of mentally retarded children with different geneticdisorders.

MATERIALS AND METHODSThe present study was conducted in two special

schools (mentally retarded) in Mangalore. All 190children of age 5 years and above belonging to bothsexes were included in the study. Institutional ethicalclearance was obtained for the study and informedconsent was taken from the guardian of the child.

The detailed history with general history,milestones, vaccination, treatment taken for any illnessesand other relevant information about each child waselicited. Even parental consanguinity, sibling deaths, birthhistory and postnatal development was recorded inspecially designed proforma.

The urine samples were collected in sterile plasticcontainers in the morning hours. The co-operation of theauthorities of the schools and children in particular helpedus in evaluation of our data in a systematic way. Thesimple screening tests for abnormal metabolites in urinesample done are tabulated in table 1.

Table 1 : Simple screening tests

Procedure Inference

The test is reckoned positive if a purple coloration developsindicative of presence of mucopolysaccharides in the urine sample.

Test for PKU:- Ferric Chloride Test (6).5-10 drops of 10% ferric chloride solution is added to 5ml of urinein a test tube.

Phenylpyruvic acid gives a green to olive green colour. (The colouris transient and fades rapidly due to oxidation within fewseconds.)

Test for MPS:- Toluidine Blue Spot Test (5).Apply 1 drop of normal and 1 drop of pathological urine to twoseparate Whatman No 1 filter paper strips and wait till the sampleare completely dry at room temperature. Immerse the paper stripsin the toluidine blue solution. Wait for 1 minute, transfer the paperstrips to acetic acid solution and wash thoroughly to removeexcess dye.

2012; Vol : 1 BIMS Medical Journal 17

Test for Ketoacids:- DNPH Test (7).

Mix equal quantities of filtered urine and 2,4 DNPH solution 0.4gm/dl in HCl,1mol/L.

Yellow to yellow – white precipitate formed in less than 5minindicates a large quantity of ketoacids.

Test for Reducing Substances:- Benedict’s Test (8).

Add 8 drops of urine to 5 ml of Benedict’s reagent. Boil for 2 min.

Depending on the amount of reducing substances present inurine, the precipitate forms greenish- yellowish to reddish brownprecipitate.

RESULTSThe study comprised of 190 mentally retarded childrenwho were diagnosed with following abnormalities asshown in Table 2.

Table 2 : Children with abnormalities

Abnormalities Number

Down’s Syndrome 9

Cerebral Palsy 5

Other Mentally Retarded children 176

Urine samples of these children were tested forinborn errors of metabolism.

Among the cases screened males werepredominant. All children were immunized none hadprevious family history, but they had delayed milestonesand 6 children of consanguineous marriage were noted.

In our study, based on preliminary test in inbornerror metabolism Of 9 Down’s syndrome children, 6samples gave positive Benedict’s test. 4 were positivefor Toluidine blue test for MPS, and 3 were negative forketoacid and reducing substances. These findingsindicated biochemical disturbance.

In 5 case of Cerebral Palsy, 4 children showedpositive toluidine blue and Benedict’s test. 1 child showednegative results for both these tests.

Other 176 mentally retarded children whenurinary screening tests were performed, none of themshowed any significant alterations.

Positive biochemical f indings and theirdistribution sex-wise are shown in Table 3.

Table 3 : Sexwise distribution of children with positivebiochemical findings

Test Positive in

Boys Girls TotalToluidine blue 23 15 38

Ferric chloride 1 - 1

DNPH 5 - 5

Benedict’s 27 12 39

DISCUSSIONCongenital and genetic disorders are the second mostcommon cause of death in infancy and childhood (9). It’s

reported that amongst 24 million annual births 20,800had metabolic disorders (10). And it is summarized that60-65% of the population will suffer from a geneticallydetermined disorder during their lifetime (11, 12).Earlier investigation was limited to family history andphysical examination.

Berry and Spinanger introduced simple spot test,toluidine blue test (13). He tested 20,000 urine samplesof high risk infants and children, 45 samples gavepositive tests which were subsequently confirmed byquantitative measurements (14). In our study 38 samplesshowed positive out of 190 urine sample collected.

A case of PKU was first reported by Folling in1934 (15). Levy reported that in European populationsthe abnormality is present in about 1 in 15,000 newborninfants (16). Sridhara Rama rao et al reported higherincidence of PKU in karnataka (17). Jaikhani R et al alsoreported a one year old child of PKU by urinechromatography (18). Our finding is in contradiction toabove reports that ferric chloride test is significant onlyin newborns. As in our series of urine sample tested atwelve year old boy showed positive for ferric test. Butfurther confirmation should be done by bloodphenylalanine levels using Tandem mass spectrometry.

DNPH test was performed as per Tietz (7). It israpid test useful in field surveys. But positive test shouldbe confirmed by specific & sensitive technique.

And metabolic screening test for geneticdiseases of carbohydrate metabolism includesBenedict’s test. 39 children were tested positive in mostof the cases it was indicative of trace presence. Nonewere known diabetics. Each test was repeated toconfirm the results obtained. However, results obtainedin this study need not be indicative of alteredcarbohydrate metabolism. They only suggest a moredetailed study in each of these mentally retardedchildren.

CONCLUSION

It is not always possible to refer susceptiblepersons, to established centers in India forstandardization and diagnosis of various metabolicdisorders. So with this in mind, we had undertaken this

simple qualitative biochemical tests with urine samplesto initiate the study. As early diagnosis by various simplepreliminary laboratory tests is essential, in order toprevent complications. Data obtained from the field workis expected to be useful in evaluating the need for adetailed study.

REFERENCES

1. Forfar JD. Forfar and Arniel’s. Text book of pediatrics 8thedition. Edinburgh: Churchill Livingstone 1992.

2. Choudhuri T and Sengupta S. Inborn error ofmetabolism an Indian perspective. Int J Human Genet2006; 6: 89-91.

3. Childs B, Valle D, Jimenez-Sanchez. The inborn errorand biochemical variability. In: Scriver CR, Beaudet AL,Sly WS, Valle D. The metabolic and molecular basis ofinherited disease. 8th ed New York: Mc-Graw Hill. 2001:155-66.

4. ICMR Collaborating centers and central Co-coordinating unit Multicentric study on genetic causes ofmental retardation on India. India J. Med Res (B) 1991;94: 161-69.

5. Pesece Kaplan. Methods in clinical chemistry 1987: 194.

6. Tocci P. Screening for metabolic diseases in, W L Nyhan(ed) Amino acid metabolism and genetic variation, NewYork: MC-Graw Hill 1968: 461.

7. Norbert W. Tietz. Aminoacids. Fundamentals of clinicalchemistry. 5th ed 2006: 123.

8. Harold varley. Practical clinical biochemistry. Tests forglucose and other reducing substance in urine. 4 th

edition 2002: 123.

9. Community approaches to the control of hereditarydiseases. (Report of a WHO advisory group ofhereditary diseases) 1985.

10. Verma IC. Burden of genetic diseases in India. Indian JPediat 2000; 67: 893-98.

11. Bard PA. Genetic disorders in children and young adults;a population study. Am. J. Human Genetics 1988; 42:677-93.

12. Czeizel A, Shankar Narayanan K. The load of geneticand partially genetic disorders in man. Mutation research1984; 128(1): 73-103.

13. Berry, H. K. and Spinanger J. A paper spot test useful instudy of Hurlers Syndrome. J. Lab Clin Med 1960; 55:136-38.

14. Berry H. K. Screening for metabolic disorder among highrisk infants and Children. Health Lab Sci 1977; 14:183-93.

15. Folling. The principles of Human Biochemical genetics3rd edition 1980: 201.

16. Levy HL. Genetic screening advances in humangenetics 24th edition. Plenum press. New York 1973.

17. Sridhara Rama Rao BS, Jayasimha N, Subhash MN.Biochemical screening in mental retardation. Indian JPaediat 1981; 48: 229-34.

18. Jaikhani R. Patil VS, Laxman H. B. et al. Selectivescreening for inborn error of metabolism in children.Single Centre Experience from Karnataka J. Clin andDiagnositic Research 2008; 2: 952-58.

18 Mentally retarded children Indira Bhaskar et al

Medical Education

Need based medical educationProf. Dr. B. M. Hegde, MD. FRCP, Former Vice-Chancellor MAHE.

BIMS Med. J. 2012, 01 : 19-21

This is an attempt to look at our present daymedical education from within, after nearly five decadesif, I hope, fecund involvement. Modern medicaleducation in India goes back to the year 1857, when theEast India company started three medical colleges inMadras, Bombay, and Calcutta. The initial syllabus wasbrought from the London University. It has, of course,changed a bit here and there, but there has never beenan attempt to really do some introspection for nearly onecentury and a half. There has never been an attempt tosee if our hoary past, with its wonderful medicalknowledge, could, at least, be amalgamated with thewestern thoughts brought from outside, with benefit tothe suffering humanity.

Most of us inside the system have a holier-than-thou attitude towards anything Indian that has not beencertified to be scientific by the West. I think time hascome now to think of all that, as the West itself is lookingto the East for inspiration in this field with the top heavy,hi-tech western medicine having become prohibitivelyexpensive.The London Royal College of Physiciansrecently brought out a manual, following a symposiumon The Science of Alternative Medicine, highlighting thepositive aspects of the latter and also bringing out a lotof good scientific material in them. It is time now for usto take a fresh look.

What is wrong with the present system?

On the surface everything looks good. Manywould want to know that if it was good enough for us whynot continue it for the next generation. How good is good?Modern hi-tech medicine, sold all over as very scientifichas a very shaky foundation. David Eddy, a formerassociate professor of cardiovascular surgery at theStanford, after very extensive research and doing hisPhD in mathematics, wrote that 85% of what doctors dois based on very soft data, while only 15% is based onhard unequivocal data. He has now invented a newcomputer model ARCHIMEDES that shows most of ourinterventions in very poor light.

The recent UNIDO report showed that about 80%of the world’s population today does not have thebenefit of modern medicine. Many studies have veryclearly shown that the most important risk factor for alldiseases, from common cold to cancer, is poverty.

Poverty and ignorance begin to have their ill

effects on the future man right from the first trimester ofpregnancy inside his mother’s womb and bothers himchasing him to the tomb! Studies in the West have shownthat whereas the diseases are in plenty in the far-flungvillages, surplus of doctors are in the cities andmetropolises. This inverse-care law, propounded by afamily doctor, Tudor Edward Hart, working in a Welshmining village, speaks volumes about what happens inthe third world countries.

The art of medicine, that which makes thepatient’s day, is not being taught enough in the medicalschools. Even when passing remarks are made by someteachers about the art of medicine, most of it getsdrowned in the sea of awe-inspiring technology. There isa lot we could do in this field, as shown very well by anOxford professor, David Weatherall, in his book TheScience of Medicine and its Quiet Art, and by Shervin B.Nuland, Stanford professor of clinical surgery, in hisbook Wisdom of the body. This has been proved by ascientific study by a group of professors of medicine inEngland published in the BMJ. Professor Calnan’s booktalking with patients brings out the anguish of a thinkingteacher at the Hammersmith hospital, London. Too muchof technology and teaching subtleties to undergraduateswere shown to be counter-productive in a study by threegenerations of teachers in the department of cardiologyat the Andrews University, Dundee.

The student gets lost in memorizing data for thesake of the examination and thus loses sight of the woodswhile counting the trees. Bereavement is an integral partof a doctor’s life! Very little input is given in this directionto students to cope with it. Memorizing the subject hasanother dangerous consequence in that the student justbefore the examination, and if he passes theexamination for ever after, deludes himself with the ideathat he knows everything that is to be know. This feelingof “Knowing” is suicidal in this field. One should aimat making the student realize genuinely that he does notknow! That is where curiosity starts and wisdom begins.Another very important reason why medical educationhas become irrelevant to the present day needs is thecraze for trying to do good to the apparently healthy insociety in the name of health screening and predictingthe unpredictable.

Predicting the future of any organism in thisdynamic universe needs the knowledge of the total

Re-printed with permission

initial state of the organism, which is impossible todaysince we have no clue about the genotype of man andhis consciousness! In addition, the linear thinking that ifone were to change the initial states from abnormal tonormal there is no guarantee that this change holds goodas time evolves. Time evolution in a dynamic system doesnot follow this rule. Long term studies have shown thefutility of this kind of exercise. Doctors have beenpredicting the unpredictable was the judgement of aphysicist, professor Firth, in his enlightening article inthe BMJ in 1991.

What could be done to rectify this?

Content and Methodology :-

The syllabus is already overburdened. Itcannot and should not be expanded; instead it could beprofitably cut short, without affecting the quality-nay evenenhancing the quality of education. Problem basedlearning, where the student and the tutor are bothcurious to learn, would be a better method. More timeshould be given to the students to think for themselves,in place of all the didactic teaching of facts. Facts keepchanging every day, what with the new informationpouring in at a phenomenal pace seven per cent permonth. The correct method of obtaining the data frommany sources today is to be taught in place of teachingfacts.

Didactic lectures could be cut to the bareminimum, replaced by small group tutorials. Studies haveshown that an unprepared mind absorbs less than fiveper cent of what is told in a lecture class. Clinicalclerkships must take more of the student’s time. Thereagain the ritualistic bedside clinics should give place tocollective effort between the teacher and the taught toarrive at the diagnosis and management strategies forevery patient under their charge. Then and then onlydoes the student realize the most important lesson inmedicine that diagnoses and management are basicallyfull of uncertainty. The gray zone in medicine isexpanding every day and the student should be awareof that as much as the teacher.

Medical education should be a collective effortat learning between the two parties, the teacher and thetaught. The conventional teaching by humiliation shouldgive place to learning with pleasure with a footing ofequality. On the bedside the student learns byobserving the teacher, in all its ramifications, viz,manners, ready wit, compassion, understanding, humandignity, patient leeway, frustrations, anxieties, and whathave you. This would give the student the courage tokeep learning. To know that the emperor also could bewithout his robes is a very good stimulus to learn.

Specialists Vs Generalists :

There was craze for specialization in the westfor more than two decades now. There were somany specialties and subspecialties that they have nowrealized the bad effects of these both on the recipient,the patient, and also on the system. This kind offragmentation is doomed to fail as per the 1st Law ofThermodynamics! Medical specialties grew directlyproportionate to the growth of technology. The result isthat technology has become top heavy and thehospitals have become prohibitively expensive even forthe middle class Americans.

The University of Minneapolis has started thesystem of having three major specialities: generalsurgery, general medicine and midwifery. Only when thereis a definite indication for any type of intervention doesthe patient get referred to the particular specialist.Similar trend is coming to the UK also of course, weIndian believe in the dictum that we have to make themistakes ourselves before, we learn from them. We arewise enough not to learn other’s mistakes. We are whereAmericans were twenty years ago, starting more andmore specialties and corporate hospitals.

A large country like ours, where more than 80%of patients are spread over the 5,75,000 odd villages,we would have to, per force, have more generalists. Inaddition, our present day medical training for a graduateis not conducive to send him to a village to manage alone.He would be a fish out of water there, as the groundrealities in the community incidence of illnesses is notrepresented in the teaching hospitals. This is one of themain reasons why doctors do not want to go to thevillage. New doctors are not comfortable with theirclinical abilities sans the hi-tech that they are used to intheir medical school hospital. Our graduates are goodfor working as junior doctors in larger corporatehospitals to order all the tests for everyone who comesthere for the boss to review or to work in junior postsabroad. Left alone in a village he would be helpless.

Evaluation: This is the real pain in the neck forboth teachers and students alike. I know of no fool proofmethod of evaluation. The present system that wefollow, which has been followed since the beginning ofmedical education in India, is far from satisfactory. Eventhough the best is yet to be thought off we could try andmake it more effective. The end term, one timeexamination should be replaced by continuous on thejob evaluation. This could be split into teacher evaluationand peer evaluation. The latter could bring out theweaknesses and strengths of a candidate much morecandidly. The teacher evaluation should be a long drawnobservation in place of the short, anxiety generatingincomplete assessment.

20 BIMS Medical Journal 2012; Vol : 1

The debate about the type of theoryexamination is a never-ending one. The West went intothe multiple choice objective theory test, only to go backnow to the time-tested essay type examination.However, both of them test the memory power of theexaminee and not his total ability. In their place a novelcreative type of theory examination could be held. Thestudent is posed a real life problem and is given enoughtime to write a critical answer on the lines of his futurework outside. A critical appraisal of the problem shouldbe able to give the candidate the capacity to learn thecommunication skills also in later life.

Practical and clinical examinations should mimicthe real life situation. They should aim to assess thecandidate’s ability to listen to his patient, hiscompassion and human understanding, his knowledgeof the clinical methods of eliciting the signs of disease,his interpersonal relations, his ability to get on withcolleagues, his temperament as a doctor, and hismastery of the diagnostic skills and managementstrategies. Viva-Voce examination is an opportunity tocheck the student’s thinking capacity, instead of onceagain assessing his memory recall. This could beutilized to find out what kind of a doctor he would makein real life, his interest in furthering his skills andknowledge, his capacity to look at the same thing fromdifferent angles and also to fathom his reasoning power.

Examination should have also a check on them.All the markings should be in the close-marking method.The positive and negative aspects of the student’sabilities should be noted down for the future guidance ofthe candidate should she/he fail to make the grade. Theexaminers performance should be computerized toassess them as examiners. Erring people should beblacklisted and their names sent to all the examiningbodies with valid explanations. They could be reassessedafter the lapse of a particular number of years!

Beyond the Four Walls of the Class Room:

Doctoring needs more skills than all that iswritten above. There are important areas not covered bythe conventional teaching methods. One area that needswider knowledge of human affairs is the capacity of thedoctor to handle the only certain thing in life that is death.

One of the questions asked is “why” did a patient get aparticular disease or why did he die? These twoquestions could never be answered in biology. One needsto know a bit of teleology and also philosophy. Positivesciences answer the question “how” or “how much”, butnot the question “why”. One needs special skills ofcompassion and understanding to manage bereavementand separation.

The bane of modern medicine today is its cost.Every doctor must have an exposure to pharmaco-economics. It is one thing to read a book and write themedicine or order an operation, but the crux of thematter is if the recipient is able to afford that and if notwhat are the alternatives. That leaves the much-harriedpatient in a worse state. The mind of man is known to bethe most important part of the whole gamut of healthand disease and the modern doctor should be able tounravel the depths of human mind, with a reasonableknowledge of human psychology, local customs, taboo,fears, anxieties and even superstitious beliefs. Anassessment of the patient’s surroundings, his worries,his anxieties, his near and dear ones, and his social tieswould all have to be taken care of in some specialsituations.

Knowledge advances by refuting false dogmas.Genuine research demands that doctors keep an openmind on all aspects of their learning and try and get thefalse dogmas demolished to the extent possible. Thisrequires the capacity to keep meticulous records of allour dealings with patients sincerely and honestly.Documentation should be taught to students from dayone in their routine work as well. Research is notrepeating others work in your laboratory. Clinicalmedical research is “having a question on the bedsideand trying to go as far away from the bed as one could toget an answer.” We urgently need a uniform nationalstandard for our postgraduate degrees to be recognizedall over the world.

In short, medical education is an education forlife. The right kind of education would bring out best inevery doctor who becomes patient friendly and wouldbe able to most good to most people most of the time.He is ideally one who knows not but, knows he knowsnot. May his tribe increase!

2012; Vol : 1 BIMS Medical Journal 21

Lighting up the way

GENIUS REMEMBERDED Louis Braille, along with his friend Gabriel Gauthier, made the first Braillewriting board. It was a boon for the blind, their passport into the world of reading and writing

If I were to ask you to shut your eyes and read a book, you would consider the demand both silly andimpossible. Yet this precisely was the sad situation for the blind for countless years. The genius of one man broughtabout a radical change. His name was Louise Braille. He was born in 1809, in Coupvray, a village near Paris, France.His father was a saddle-maker and had a workshop that was filled with leather, mallets, sharp knives and pointed awls.While his father worked, three-year-old Louise was allowed to play. One day he took a sharp-pointed tool and tried toimitate his father. It slipped and cut into his eye. His parents quickly bandaged the eye and took him to an old womanwho was considered a healer. She applied lily-water on the wound. But it only succeeded in infecting the eye. Worse,it damaged the good eye as well. Within a few days, Louise became blind.

His father made him a cane. When he walked, he had to count the number of steps he took, so that he couldwalk back again. He now became more aware of sounds, smells and the shape and feel of things, but his world hadturned into a dark and lonely one. Jacques Palley, a priest, decided to help him. He became Louis’s first teacher. Hetaught him the Bible and also to recognise animals by their sound, and flowers by their feel and scent. Then his fatherwas struck by a new idea. He hammered round-tipped upholstery nails into a board to form letters. Louis felt the headsand learned the alphabet. His father now taught him how to combine letters and form words. Louis joined school,something rather unusual for those times. His teacher was kind and Louis, being a smart child with a good memory,was able to make progress.

In 1819, Louis went to Paris to live and study at the National Institute for Blind Children. It was the word’s firstschool for the blind. There were books there for Louis to read.

They had raised letters that he could feel, but the books were very big and heavy. The process was slowbecause he would have to distinguish between a P and an R, an E and an F. In 1821, Louis was taught sonography ornight writing. It was a code of raised dots and dashes and had been invented by Charles Barbier, a captain in theFrench army. It enabled soldiers to read messages in the dark without lighting lamps.This method had Louis greatlyexcited. It helped him a great deal in reading and writing. But there was a drawback. It required as many as 12 dots torepresent one symbol. In the same year Barbier visited the Institute and Louis was able to identify the major failing inthe code. It was based on sounds and therefore unwieldy. It was not possible for the human finger to encompass thewhole symbols without moving. As a result proceeding quickly from one symbol to another was difficult and turnedreading into a slow process. Louis devised symbols that instead represented the letters of the alphabet.

He was thus able to reduce each symbol to a 6-dot cell. This was a much simpler code and could represent anyletter of the alphabet within the space of a fingertip. What is more, words, scientific symbols, mathematical notationsand capitalisation were all possible. Students could also take notes and write essays by punching dots into paper witha pointed instrument.

By 1825, Louis Braille along with his friend Gabriel Gauthier was able to make the first Braille writing board. Itwas a boon for the blind, their passport into the world of reading and writing.

Late in 1851, Louis became seriously ill with tuberculosis. “I am convinced my mission on earth is completed,”he told his friend. He died on January 6, 1852. Helen Keller, who was blind and deaf, called Louis Braille a genius. Herrich tribute to him echoes down the years, “He built a large, firm stairway for millions of sense-crippled human beings toclimb from hopeless darkness to the Mind Eternal.”

Leela Ramswamy DH 4/11/2011

22 BIMS Medical Journal 2012; Vol : 1

Case Report

Massive Colonic DilatationVed Bhushan S. T.,*Uppin V. M., **Santosh Patil, ***Biju Chandran

Associate Professor, Department of Surgery, Belgaum Institute of Medical Sciences, Belgaum-590 001, Karnataka.

ABSTRACTMassive colonic dilatation is seen in cases of mega colon. Mega colon is a condition in which there is dilatation

of the colon either a part or whole. Mega colon can be congenital as it is in Hirschsprung’s disease. Acquired megacolon is seen in conditions such as chronic constipation, post-operative colonic surgeries and pseudo-obstructions ofthe colon in which there is no mechanical obstruction.

In some cases colonic dilation is secondary to sepsis and in ICU settings which are called Toxic mega colon.

Mega colon can also be secondary to neoplastic strictures and malignant tumours as it was seen in our case.

Keywords : Mega colon, Massive colonic dilatation, Colonic resection, Colonic diversion.

BIMS Med. J. 2012, 01 : 23-25

INTRODUCTIONMassive colonic dilatation resulting in mega

colon needs surgical intervention.

Toxic mega colon needs aggressiveresuscitation and total colectomy in fit patients withileostomy (1).

Colonic dilatation secondary to malignanttumour or stricture requires timely surgical interventionsuch as colonic resection with colonic diversion.(Hartmanns procedure).

CASE REPORT82 years old man was admitted with complaints

of acute pain and distension of the abdomen since 2days. Pain was colicky and present all over theabdomen. Distension of the abdomen was increasingsteadily over the last 24 hours. All these complaintspreceded by abdominal discomfort, distention andconstipation over the last 6 months. There was a stronghistory of incomplete evacuation of stools requiringfrequent use of laxatives from medical practioners.Patient also gives history of loss of appetite and loss ofweight of more than 5 kgs in the last few months.

On examination the patient was an elderly mantall, well built but poorly nourished, sick looking,conscious, co-operative and well oriented.

All the vital signs were within normal limits.Abdominal examination revealed distended, tenseabdomen with eversion of the umbilicus, moving lesswith respiration. A tense, tender mass of 10 cms x 8cms was palpable in the left iliac and lumbar regions.

*Professor of Surgery, J. N. Medical College, Belgaum-590 010.

**Assistant professor, J. N. Medical College, Belgaum-590 010.

***P.G. in Surgery, J. N. Medical College, Belgaum-590 010.

Bowel sounds were sluggish and soft stool was presentin the rectum.

Intestinal obstruction of large bowel wasdiagnosed and the patient was aggressively resuscitatedwith IV fluids, nasogastric aspiration, urinarycatheterization ensuing adequate hydration and urineoutput.

All routine investigation of blood and urine wasdone which were within normal limits. Blood wasarranged. Patient was taken up for exploratorylaparotomy under general anesthesia.

The findings were massively dilated colon fromcaecum to rectosigmoid junction. Fig (1). Volvulus of thesigmoid colon, and a tumour was noticed at 5 cms fromrectosigmoid junction. Careful mobilization of the leftcolon was done after derotation. Open decompressionof the colon done just above the tumour and evacuated5 kidney trays of well formed stool Fig (2). The tumourwas excised with healthy margins. Distal end was closedand the proximal end was brought out as an endcolostomy (HARTMAN’S PROCEDURE). Abdomen wasclosed in layers with a drain.

Histopathological report of the specimen wasinfiltrating adeno-carcinoma of the sigmoid colon.Surgical margins were free and lymphoid nodes werefree of metastasis. Post-operative period wasuneventful and the patient has received 6 cycles ofchemotherapy.

DISCUSSIONMassive colonic dilatation is seen in conditions

of mega colon. Mega colon could be congenital as inHirschsprung’s disease (2) or acquired in pseudo-obstruction of colon. There is acute colonic pseudo-obstruction in which there is no mechanical obstructionattributed to autonomic motor motility dysfunction (3).

Massive mega colon also is seen in ICU

Figure 1 : Intra-operative-obstructed recto sigmoid junction

Figure 2 : Intra-operative-open decompression

Figure 3 : Laporotomy-closure with end colostomy

settings both in medical and surgical patients withunderlying sepsis and respiratory failure (4).

Massive colonic dilatation may be encounteredin post-operative period after colonic surgery such aspost polypectomy (5).

After a thorough literature search to our bestknowledge. We were able to find just one case ofmassive mega colon needing open decompression,evacuating about 12 kg of stools after ileostomy forhabitual mega colon (6).

Massive colonic dilatation of the entire colon hasbeen recorded as a result of primary mesenteric venousthrombosis.(7)

Chronic lifelong constipation in a 25 year old manpresented to the emergency department with acuteabdomen. He underwent emergency laparotomy,subtotal colectomy with ileostomy for feculentperitonitis with mega colon of rectum and sigmoidcolon.(8)

In a study of 50 cases of obstructive colitis, theauthors found, obstructive colit is is anulcero-inflammatory and necrotizing condition thatoccurs in the colon proximal to being or malignantstenosing lesions. It is the result of ischemia due toimpairment of blood supply secondary to elevation ofendoluminal pressure,distension of the colonic wall andother factors which impair adequate perfusion.Obstruction was most common in the recto sigmoidjunction. Half the patients had adenocarcinoma. 24patients had benign obstruction and 15 had diverticulardisease. Type, extent and depth of ischemic lesions werehighly variable and comprised early mucosalhemorrhage and edema, in 16 patients massivedilatation with stretching and thinning of the bowel wall,associated with a blow-out type of perforation or withtransmural necrosis.(9)

We are publishing this, as it is only the secondcase in mega colon which needed open decompression.

REFERENCES

1. Marvin L Colman Ed. Colon and Rectal Surgery. LippincotWilliams Wilikins 5th Edi 2005; 482.

2. Oravar Swenson. Early history of therapy ofHirschsprung’s disease. J. Paed Surg Aug 1996: (31) 8

3. Saunders MD and MB Kimmey. Systemic review: acutecolonic pseudo-obstruction. Alimentary pharmacologyand therapeutics. 2005; (22)10: 917-925

4. Saunders MD. Acute colonic pseudo-obstruction. Currgastroenterol Rep 2004;6: 410-416

5. M Atiq, Aduli F, Refai W, Orden KW. Post polypectomyacute colonic pseudo-obstruction (ogilvie’s syndrome)Endoscopy 2008; 40: E 163 DOI 10-1055/s-2007-995770.

24 Masive colonic dilatation Ved Bhushan S. T. et al

6. Ingo Menkenburg, Markus lcibig, Christoy weber et al.Recurrent severe gastro intestinal bleeding and malabsorption due to extensive habitual mega colon. WorldJ. of G.E. 2005;11.48 PP 7686-87.

7. Roman RJ, Loeb PM. Massive colonic dilatation asinitial presentation of mesenteric vein thrombosis. DigDis Sci 1987; 32(3): 323-6.

8. Lundy JB, Gadacz TR. Massive fecal impactionpresenting with mega rectum and perforation of astercoral ulcer at the recto sigmoid junction. South MedJ. 2006;99 (5):525-7.

9. Gratama S, Smedts F, Whitehead R. Obstructive colitis:an analysis of 50 cases and a review of the literature.Pathology. 1995(10);27(4):324-9.

2012; Vol : 1 BIMS Medical Journal 25

Case Report

Hereditary Spastic ParaparesisKalasad S. T., *Archana Dambal, **Krishna R. Malagi, ***Krutika A. M.

Professor & Head, Department of Medicine, Belgaum Institute of Medical Sciences, Belgaum-590 001.

ABSTRACTSpastic Paraparesis is a condition in which there is hypertonia of lower limbs associated with bilateral lower

limb weakness.

Hereditary Spastic Paraparesis is a heterogenous group of genetic disorders characterized by progressivelyworsening spasticity of lower extremities with variable degrees of weakness due to pyramidal tract dysfunction. It isrelatively a rare condition. The estimated prevalence is 0.5 to 11.9 per 1, 00,000 population (1). History of similarsymptoms and signs in one or more family members is very much essential for the diagnosis of Hereditary SpasticParaparesis.

It is transmitted either as an autosomal dominant, autosomal recessive or X-linked inheritance. Most casespresent from second to fourth decade of life.

Key Words : Spastic Paraparesis, consanguineous marriage, spastin, pyramidal tract.

BIMS Med. J. 2012, 01 : 26-28

INTRODUCTIONHereditary Spastic Para paresis is a

progressive degenerative condition of the nervoussystem involving the terminal portions of the longestcortico-spinal tracts and to a lesser degree, theposterior columns and manifests as spastic weaknessof lower limbs with hyper-reflexia, often accompaniedby mildly impaired vibration sensation in distal lowerextremities and hypertonic urinary bladder with evidenceof similar features among other members of family.

CASE REPORTA 26 year old young man, presented to the

medicine outpatient department, in the month of August2011 with a history of weakness in both lower limbs andintermittent muscle spasms since 14 years, difficulty inwalking since 1 year and difficulty in passing urine sincepast 6 months. The weakness was insidious to start withand progressive over these years, equally affecting bothlower limbs and distal muscle weakness being more thanproximal.

The lower limb weakness was associated withintermittent muscle spasms which started almostsimultaneously. The spasms first experienced in the calfmuscles, progressed to involve the muscles of thigh,abdomen and the back. They were intermittent,unpredictable, appearing spontaneously without anyspecific triggering stimulus and lasting for about 5 to 10seconds. He attributed his difficulty in walking to the lower

limb weakness and his foot deformity. Patient also haddifficulty in passing urine and adductor spasms. He hadslurred speech since childhood.

There was no history of fall or trauma precedingthe symptoms. There was no history of neck pain,weakness in the upper limbs, tingling or numbness inhands or feet, convulsions, involuntary movements orbowel disturbances. There was no history suggestive ofaltered sensation, extreme emotional disturbances,cognitive impairment or cranial nerve weakness. Hecould appreciate temperature while bathing.

There was no history suggestive of perinatalasphyxia, he is not a known case of tuberculosis or AIDS,and there was no history suggestive of high riskbehavior or syphilis or consumption of khesari dhal for along time.

He is vegetarian and his appetite is good, sleepadequate, used to chew gutka for 3 years. No history ofalcohol intake, smoking or drug abuse.

He was born to a couple of Grade IIconsanguineous marriage. His younger brother hadsimilar complaints of weakness in his both lower limbsand muscle spasms since 6 months. There was nohistory of similar complaints in his younger sister oramong any other family member. His father died in aroad traffic accident 10 years ago.

*Assistant Professor, Department of Medicine, Belgaum Institute of Medical Sciences, Belgaum-590 001.

**Intern, Belgaum Institute of Medical Sciences, Belgaum-590 001.***Intern, Belgaum Institute of Medical Sciences, Belgaum-590 001.

2012; Vol : 1 BIMS Medical Journal 27

On examination, patient was conscious,co-operative and well oriented to time, place andperson. He is right handed.

His higher mental functions were normal,except for the dysarthria. He had spastic gait withscissoring of lower limbs. Cranial nerve examinationrevealed lingual muscle weakness. Examination ofmotor system revealed wasting of small muscles of bothhands. There was clasp knife spasticity in both upper limbs(grade I-II) and lower limbs (grade II-III). Power in upperlimbs was grade III to grade IV while in the lower limbsgrade II to grade III with distal muscle weakness beingmore than proximal muscle weakness. Foot drop waspresent. Co-ordination was normal. No involuntary move-ment noted. Superficial reflexes were present with bilat-eral extensor plantar reflexes. Deep tendon reflexes were2+ in upper limbs and 3+ (brisk) in both lower limbs. Therewas no ankle clonus or patellar clonus noted. Jaw jerkwas absent. Sensations were intact to fine and crudetouch, pain and temperature. Posterior columnsensations were intact. Skull and spine were normal. Noneuro-cutaneous markers seen. No carotid bruit heard.

Respiratory system, cardio-vascular system andper-abdomen examination was normal.

INVESTIGATIONSBlood count was within normal limits. Urine

routine and microscopy was normal, Glucose random andrenal function tests were within normal limits MRI scan ofbrain and spine, both plain and with contrast revealed noplaques, mass lesions, artero-venous malformations orvertebral column pathology.

Patient’s brother was also examined.

Examination revealed similar signs as that of his elderbrother, hypertonia in both the lower limbs withexaggerated reflexes, bilateral extensor plantar reflexesand grade II to grade III power in both lower limbs. Adiagnosis of Hereditary Spastic Paraparesis was madein both the brothers taking into account, the presentingfeatures, history of consanguineous marriage inparents and the familial presentation.

The patient and his brother were treated withoral baclofen and physiotherapy. He and his familymembers were well counselled regarding the nature ofthe disease and its progression, chances of itsinheritance and its implications. The patient was askedfor follow up after one month. The muscle spasms hadreduced both in frequency and severity and theweakness in the lower limbs due to spasticity hadimproved.

DISCUSSIONHereditary Spastic Paraparesis (HSP) also

known as Familial Spastic Paraparesis orStrumpell-Lorrain disease is a relatively rare condition.First described by Adolph-Strumpell and later explainedin detail by Maurice-Lorrain, it is a heterogeneous groupof genetic disorders which is characterized byprogressively worsening spasticity of thelowerextremities with variable degrees of weakness dueto pyramidal tract dysfunction.

HSP is classified as “uncomplicated” or “pure” ifneurologic impairment is limited to progressivelower-extremity spastic weakness, hypertonic urinarybladder disturbance, mild diminution of lower-extremityvibration sensation and, occasionally, joint position

Family Tree

Consanguineous Marriage

Patient Patient Patient26 years brother sister

21 years 19 years

Affected

Dead

Male

Female

28 Hereditary Spastic Paraparesis Kalsad S. T. et al

sensation. Uncomplicated HSP begins at any age, fromearly childhood through late adulthood, and progressesslowly over many years without exacerbations,remissions, or periods of abrupt worsening. Affectedindividuals experience progressive difficulty walking andoften require canes, walkers, or wheelchairs. Urinaryurgency and lower-extremity paresthesia may occur.Individuals with uncomplicated HSP typically retainnormal strength and dexterity of the upper extremitiesand have no involvement of speech, chewing, orswallowing. HSP is classified as “complicated”(“complex”) if the impairment present in uncomplicatedHSP is accompanied by other system involvement orother neurologic findings such as optic neuropathy,deafness, ataxia, icthyosis, peripheral neuropathy,dementia, extra-pyramidal dysfunction, mentalretardation or seizures. The underlying pathology in HSPis the defective genes resulting from mutations leadingto abnormal amino acid protein called Spastin. More than130 mutations have been identified that affect this gene(2). Disturbance in the interaction of abnormal Spastinwith cellular protein Tubulin leads to disruption of axonaltransport leading to axonal degeneration. These affectmainly the terminal portions of longest cortico-spinal tractand to a lesser degree the posterior columns. At least 35different genes/loci are associated with HSP. Otherdefective proteins coded include atlastin, paraplegin andalsin.

Diagnosis of HSP is largely based on evidenceof family history in the setting of progressive lower limbweakness, with evidence of corticospinal tract deficitsaffecting both lower extremities (spastic weakness,hyperreflexia, typically associated with bilateralextensor plantar responses); often accompanied by mildlyimpaired vibration sensation in the distal lowerextremities and hypertonic urinary bladder. Laboratorytesting includes Genetic testing targeted towards knowngenetic mutations. Magnetic resonance imaging (MRI)of the brain and spinal cord are usually normal. In somecases MRI may show decrease in cervical and thoracicspinal cord diameters. Prominent thinning ofcorpus-callosum may be seen in some patients (3).

Sensory evoked potential may be abnormal evenin the absence of clinically evident sensory loss.Magnetic stimulation usually shows abnormality ofcentral motor conduction, responses are either absentor delayed. MRI can also be helpful to rule out otherconditions such as Multiple sclerosis and other causesof spastic paraplegia. CSF examination is not diagnostic(5).

Differential diagnosis of HSP includedegenerative/inflammatory conditions(Multiple sclerosis,

Amyotropic Lateral Sclerosis, Leukodystrophy),infections(Syphilis, HIV/AIDS, Lyme disease, HTLVI-Tropical spastic paraplegia, HTLV II) metabolicdiseases (vitamin B12 deficiency, subacute combineddegeneration of spinalcord), toxins (Neuro-lathyrism–kesari dhal/BOAA toxin,Konzo-cassava roots/thiocyanates) familial (HSP, Friedrich’s ataxia, MotorNeuron disease) para-neoplastic syndromes andVascular (Artero-venous malformations).

There is no specific treatment to prevent, slow/reverse the disease. Management is mainlysymptomatic. Physical rehabilitative measures aim atminimizing the disability resulting from spasticity andweakness. These include range of motion andstretching exercises, locomotor training, vibration therapy(increases pre synaptic spinal inhibition), gait training andco-ordination training. Drugs that can be helpful inreducing the intermittent spasms and spasticity areBaclofen, Tizanidine, Gabapentin, Diazepam andclonazepam, Dantrolene etc. Nerve block proceduressuch as injecting botulinum toxin for local spasticity,intrathecal baclofen pump can be helpful in severe cases(4).Orthopaedic procedures such as Tendon releaseprocedures, tendon transfer, osteotomy and arthrodesiscan be helpful in long standing contractures andcorrecting deformities.

CONCLUSIONHSP is a progressive disease causing

considerable physical disability leading to impairment inday to day activit ies and psychological stress.Patients with HSP need effective rehabilitative measuressuch as physical, emotional, psycho-social andoccupational support to help them lead a near normallife.

REFERENCES

1. Brian Murray and Hiroshi Mitsumoto. Disorders of Uppermotor neurons-Hereditary Spastic paraplegia. Neurologyin clinical practice.5th edn. 2008; (2):2187.

2. McDermott C J. clinical features of Hereditary Spasticparaplegia due to spastin mutation. Neurology 2006;67:45-51.

3. Sperfeld A D, Baum Gartner and Kassubek. MagneticResonance investigation of upper spinal cord in pure andcomplicated Hereditary Spastic paraplegia. Eur Neurol2005; 54: 181-85.

4. McLean B N. Intrathecal Baclofen in severe jointspasticity. Br J Hosp Med 1993; 49:262-67.

5. Lewis P Roland and Paul Gordon. Spinal cord diseases-Hereditary spastic paraplegia. Merritt’s. Neurology 11th

edn. 2005: 856.

Case Report

Urinary tract infection : A very rare presentation of geotrichumcandidum infection

Rupali Shinde, *Walvekar R. R., **Jnaneshwara K. B., ***Mantur B. G.Assistant Professor, Department of Microbiology, Belgaum Institute of Medical sciences, Belgaum-590 001.

ABSTRACTGeotrichum candidum, a fungus from the class fungi imperfecta is found saphrophtically in nature and as a

commensal in the mouth, bronchi, lungs, gastrointestinal and genitourinary tract. The pathogenecity of the fungusgeotrichum candidum has not been clearly defined. We describe a patient of perforative peritonitis who developedurinary tract infection (UTI) secondary to catheterization. Urine sample isolated geotrichum candidum with significantcolony count & also repeated isolation yielded same organism. Though it is yeast of low virulence, it is an emergingpathogen associated with infections in immunocompromised & debilitated individuals.

Keywords : Geotrichum candidum, UTI, Urinary geotrichosis.

BIMS Med. J. 2012, 01 : 29-30

INTRODUCTIONGeotrichum, a fungus from the class fungi

imperfecta is found saprophytically in nature and alsoas a commensal in mouth, bronchi, lungs andgastrointestinal and genitourinary tract (1).

Though previously considered non pathogenicit can cause opportunistic infection in immuno-compromised patient (2, 3). Infections vary frombronchial, oral, intestinal, cutaneous and evendisseminated infection (3, 4, 5). To the best of ourknowledge urinary tract infection (UTI) caused bygeotrichum is not reported till now. We report a case ofgeotrichum as a significant pathogen of UTI insepticemic patient.

CASE HISTORYA 20 year old female was admitted in BIMS

hospital with complaints of giddiness, breathlessness,abdominal pain and generalized weakness since oneday. Patient underwent tubectomy in private nursinghome two days prior. Patient was P2L2A0.patient haddelivered a male child one month prior by normaldelivery. On examination patient had pallor, fever(>100degree F), blood pressure of 100/70 mmHg, andrespiratory rate of 34/min. Per abdominal examinationrevealed distended abdomen, bloody discharge atsuture site with gaping wound. Peristaltic sounds weresluggish with abdominal rigidity. Patient was diagnosedas a case of perforative peritonitis. Patient was startedon broad spectrum antibiotics. On emergencylaparotomy ileal perforation was detected probablysecondary to injury during tubectomy. Post operativelypatient developed hypostatic pneumonia of left side andwas put on ventilator.

She had hemoglobin of 7.3gm%, total leucocyte

*Assistant Professor, Dept. of Medicine, BIMS, Belgaum. **Assistant Professor, Dept. of Microbiology, BMC, Bangalore.***Professor & Head, Dept. of Microbiology,BIMS, Belgaum.

count of 15650, with 69% neutrophils, 27% lymphocytesand 4% eosinophils. Pus sample from wound isolatedklebsiella pneumoniae. Patient developed urinary tractinfection on 4th day of catheterization with obviousheamaturia. Urine sample was collected by asepticprecaution and sent to microbiology laboratory. Urinesample was streaked on blood agar and MacConkeyagar by T method on 2 consecutive days that is day 4and 5 of admission. Urine examination showed 6-8 puscells/high power field (hpf), 4-5 RBC’s /hpf, with hyphalstructures. Gram stain showed pus cells with hyphalstructures rectangular in shape measuring 4-8 µm withcharacteristic hockey stick appearance (fig 1), Urineculture isolated growths of geotrichum candidum in pureculture with significant colony count. Colonies were dry,white to cream with hairy appearance (fig 2). Patient

Figure 1 : Gram stain showing rectangular hyphalstructures with characteristic hockey stick

appearance (arrow).

condition deteriorated on day 5 and patient succumbedto illness after 6 days of admission.

DISCUSSIONGeotrichum candidum, a fungus is found

saprophytically in nature and as commensal in the mouth,bronchi, lungs, gastrointestinal and genitourinary tract.Although rare, it can cause opportunistic infection inimmunocompromised individuals like leukemia, renaltransplant and neutropenia (2,3). Bronchialgeotrichosis is the most common form of presentationfollowed by skin, gastrointestinal tract, oral anddisseminated infection (3, 4, 5). Urinary tract infection isvery rarely encountered and to the best of ourknowledge no case is reported till now in the worldliterature. In our case patient developed urinary tractinfection following catheterization. Indwelling cathetersserve as a nidus for bacterial and fungal growth and actsas a source for urinary tract infection. Geotrichumbeing the commensal in genitourinary tract must havecaused UTI in the particular case because of thedebilitating status of the patient. Repeated isolation ofthe G. candidum with characteristic arthropores and

Figure 2 : showing growth of geotrichum on MacConkeyagar from urine sample.

hyphae in fresh urine sample both by direct microscopyand culture confirm diagnosis of geotrichosis. Alsoabsence of other urinary tract pathogen adds toconfirmation of urinary geotrichosis. Geotrichumcandidum was considered as significant pathogen forUTI in our case because of repeated isolation withsignificant colony count and also isolation on all theculture media inoculated. Also patient had clear signs ofUTI. Microscopy showed etiological agent along withinflammatory cells.

Geotrichum candidum infection rate isunderreported since it can be misidentif iedhistopathologically as candida sp. Aspergillus sp. ortrichosporon sp. (3). This possibility of misidentificationillustrates the importance of obtaining fungal cultures inaddition to histopathological studies. Better awarenessof its pathogenicity could delineate its true incidence,patterns of clinical disease and response to therapy.

REFERENCES

1. Rippon, J.W. Medical Mycology. The pathogenic fungiand the pathogenic actinomycetes. 3rd ed. W.B.Saunders, Philadelphia, 1988: 714-718.

2. S Varghese, P Ravichandran. Geotrichum candiduminfection in a renal transplant recipient. Indian J Nephrol2003; 13: 72-74

3. Hassanali kassamali, Elias anaissie, Jae ro et al.Disseminated geotrichum candidum infection. J. of clinmicro 1987; 25(9): 1782-1783.

4. Ramani R, Rao PV, Kumari GR, Shivananda PG.Pulmonary geotrichosis. Postgrad med j 1992; 68(796):150

5. Bonifaz A, Vázquez-González D, Macías B, Paredes-Farrera F, Hernández MA, Araiza J, Ponce RM. Oralgeotrichosis: report of 12 cases. J oral sci 2010; 52 (3):477-83.

30 Urinary tract infection Rupali Shinde et al

Case Report

Primary splenic cyst-A rare entityAruna S, *Jadhav M. N., **Kittur S. K.

Associate Professor, Department of Pathology, Belgaum Institute of Medical Sciences, Belgaum.590 001.

ABSTRACTCystic lesions of spleen are very rare and comprise of less than 1% of splenectomy specimen. Fewer than

1000 cases have been reported in the literature. Based on presence or absence of lining epithelium splenic cysts areclassified into primary (true) cysts and secondary (false) cysts. In primary cysts lining epithelium may be columnar,cuboidal (mesothelial-like) or squamous epithelium. Here we are presenting one such case. A 25years old malepresented with abdominal pain in the left hypochondrial region of 8 months duration. Ultrasonography revealed cysticlesion measuring 4cms in diameter in the lower pole of the spleen. The other abdominal organs were unremarkable.Splenectomy specimen showed cyst measuring 4.5 cms in diameter and cut surface revealed unilocular cyst with thickwall filled with amber coloured fluid. Internal surface was roughened and trabeculated. Microscopy showed thickfibrous wall lined by low cuboidal mesothelial –like epithelium and adjacent spleen showed features of congestion.Hence a final diagnosis of primary splenic cyst was offered. The case is presented because of its rarity

Keywords : Spleen, Primary cyst, Mesothelial.

BIMS Med. J. 2012, 01 : 31-32

*Associate Professor, Department of Pathology, Belgaum Institute of Medical Sciences, Belgaum.590 001.**Professor, Department of Pathology, Belgaum Institute of Medical Sciences, Belgaum.590 001.

INTRODUCTIONSplenic cysts are rare entities found in less than

1% of splenectomy specimens (1). Fewer than 1000cases have been reported in the literature. Cysticlesions of spleen comprise of parasitic and non-parasitic cysts. Non-parasitic cysts are classified asprimary (true) cysts and secondary (false) cysts basedon presence or absence of lining epithelium (1, 3). Inprimary cysts the lining epithelium may be cuboidal(mesothelial–like), columnar or squamous epithelium (2).Various authors suggest that, the epithelial cysts of thespleen are derived from embryonic inclusion ofepithelial cells of adjacent structures (2, 5). We reportone such case in a 25years old male patient.

CASE REPORTA 25years old male patient admitted to our

hospital with dull aching abdominal pain in the lefthypochondrial region, radiating to left shoulder of 8months duration. His general physical and systemicexamination findings were unremarkable.Routinehaematological and biochemical investigations werewithin normal limits.

The abdominal ultrasonography revealed acystic lesion measuring 4cms in diameter in the lowerpole of the spleen. The other abdominal organs wereunremarkable. Splenectomy was done and sent forhistopathological examination.

PATHOLOGICAL FINDINGS :Gross: Splenectomy specimen was measuring15x8x5cms and showed a cystic lesion measuring 4.5

cms in diameter in the lower pole of the spleen (Fig 1).

Fig 1 : Gross specimen showing cyst with glisteningsurface in the lower pole of the spleen.

in diameter in the lower pole of speen (Fig 1).

Cut surface revealed a unilocular cyst filled with38ml of amber coloured fluid. The inner surface of cystwas roughened and showed marked trabeculations (treeroot like appearance) (Fig 2).

Microscopy :Multiple sections were taken and showed cyst

wall made up of thick fibrocollagenous tissue and linedby low cuboidal (mesothelial–like) epithelium (Fig 3).

The adjacent spleen showed features ofcongestion.

Figure 2 : Shows cut surface of the cyst

Figure 3 : Photomicrograph showing lining epithelium ofcyst and adjacent spleen is congested.(H&E).

(Inset-mesothelial-like ephthelium)

With all the above gross and microscopicfindings case was diagnosed as primary splenic cyst.

DISCUSSIONThe splenic cyst is a rare clinicopathological

entity, was first described by Andral in 1829 at autopsy.The primary (true) splenic cyst as previously classifiedhas lining epithelium which may be mesothelial,cuboidal, columnar or squamous type of epithelium. YonDo Ough et al described that the true splenic cysts arethose cysts with an epithelial lining and several uniquecharacteristics (1, 2, 5). Clinically, these are seenpredominantly in children and young adults and areusually asymptomatic (1, 5,) or clinical manifestationsdepends on size of the cyst and present with abdominalpain radiating to the left shoulder (3). In the present studyalso patient was young adult and presented with

abdominal pain in the left hypochondrial region andradiating to left shoulder. In one large series, theaverage size of the cyst was 10cms (1). Riazi H, et alsuggested that majority of the cysts are located in thelower pole of the spleen (3). Grossly the cysts areusually unilocular and filled with sanguineous fluid. Theinternal surface has roughened and tree root liketrabeculations (1, 2, 3, 5). In the present study also thecyst was centered in the lower pole of the spleen andunilocular with marked trabeculations in the innersurface of the cyst.

Microscopically, cyst wall composed of thickfibrocollagenous tissue and lining epithelium may becolumnar, cuboidal (mesothelial-like) or squamousepithelium (1, 2, 4). Cysts lined by squamousepithelium are termed as epidermoid cysts but, Yon DoOugh et al concluded that mesothelial cyst withsquamous metaplasia is more accurate than epidermoidcyst or metaplastic mesothelial cyst (3, 4, 5,). In our studythe lining epithelium was low cuboidal (mesothelial -like)epithelium. There was no squamous metaplasticchanges. Surgery is the treatment of choice.The patientunderwent splenectomy and doing well.

CONCLUSIONPrimary splenic cysts are rare lesions and should

refer to those lesions with gross features oftrabeculation. Internal surface and microscopically cystswith an epithelial lining which may be mesothelial,columnar, cuboidal or squamous epithelium.

REFERENCES

1. Karen L. Chang, Daniel A. Arber, Karl K. Gaal. LawrenceM. Weiss: Lymphnodes and spleen In: steven G.Silverbery editor: Silverberg’s Principles and practiceofsurgical pathology and lytopathology. 4th edition. ChirchillLivengstone: 2006; P. 507-608.

2. Juam Rasai spleen in : Rosi and Ackerman editor Rasaiand Akerman’s surgical pathology. Vol-2, 9th edition. MOSby-2004; P. 2019-46.

3. Riazi H, Kohsari MR,Hoda S.Splenic epithelial(epidermoid) cyst. Saudi J Gastroenterol 2003; 9: 20-2.

4. Burrig KF. Epithelial (true) splenic cysts. Pathogenesis ofthe mesothelial and so-called epidermoid cyst of thespleen. Am J Surg Pathol 1988; 12(4): 275-81.

5. Yon Do.Ough,Nash HR,Wood DA. Mesothelial cysts ofthe spleen with squamous metaplasia. Am J Clin Pathol1981; 76:666-69. Now the patient is under close follow up.

32 Splenic cyst Aruna S. et al

Case Report

Retroperitoneal inflammatory pseudocystEshwar B. Kalburgi, *Suresh I. Basarkod, **Yamanur P. Lamani, ***Chethan V. N.

Professor & HOD, Department of General Surgery, S. Nijalingappa Medical College & HSK Hospital & RC, Bagalkot-587 102.

ABSTRACTRetroperitoneal inflammatory pseudocysts are uncommon. Only a few cases are reported in the literature. We

report a case of, 18 years old boy presenting with a mass in the right lumbar region. He underwent partial excision ofthe cyst and marsupilization after tumor was confirmed by computerized tomography. Histopathology report revealedas retroperitoneal inflammatory pseudocyst.

Keywords : Retroperitoneal tumors, retroperitoneal cyst.

BIMS Med. J. 2012, 01 : 33-35

INTRODUCTIONRetroperitoneal cysts (RPCs) are uncommon with

an estimated incidence of 1/5750 to 1/250000, approxi-mately 1/3rd of patients with retroperitoneal cysts areasymptomatic & the cyst is found incidentally (1). Retro-peritoneal cystic masses arise within retroperi-toneal space but outside the major organs. They attain avery large size and can cause pressure on ureterscausing hydronephrosis. The inflammatory cysts arefirmly adherent to surrounding vital structures like me-sentery and small bowel anteriorly, caecum and as-cending colon to lateral wall of the cyst, inferior vena

* Associate Professor, Department of General surgery, S.N.M.C & HSKH & RC, Bagalkot-587 102.

** Assistant Professor of General surgery, S.N.M.C & HSKH & RC, Bagalkot-587 102.*** PG in General Surgery, S.N.M.C & HSKH & RC, Bagalkot-587 102..

cava and aorta posteriorly. Hence total excision of thecyst is not possible. Drainage of the cyst, partialexcision and marsupilization of the cyst is recommended.Retroperitoneal cysts that have no epithelial lining in thewall are called retroperitoneal pseudocysts. Opensurgical excision either through transperitoneal approachor extraperitoneal approach is the mainstay of treatmentfor these lesions, though laparoscopic approach hasbeen described.

CASE REPORT18 years old male presented with mass in the

right lumbar region since 20 days. There was no history

Figure 1 : CT showing Retroperitonel Cyst

34 Retroperitoneal Inflammatory Psuedocyst Eshwar B . Kalburgi et al

of pain & fever. There were no associated bowel andbladder symptoms. General examination was noncontributory. Abdominal examination revealed a 15 x15cm mass in the right Lumbar region. It was nontender, soft and cystic in consistency, located inretroperitoneum. Right renal angle was free. It wasbimanually palpable. Ultrasonography of abdomenshowed large complex cystic lesion measuring 10.7 x7.5 x 14.1cm with thick septation within. Lesion wasseparate from right kidney. Contrast enhancedcomputerized tomography (CECT) of the abdomen andpelvis revealed a large well defined water density lesionwith thick enhancing wall in right Lumbar regionmeasuring 113 x 77 x 151 mm. The lesion was relatedposteriorly to right Kidney & psoas muscle, anteriorly tosmall bowel loops, transverse colon and anteriorabdominal wall, medially to aorta and inferior vena cava,laterally to liver. Fat planes between lesion andsurrounding structures were maintained. There was mildto moderate hydronephrosis in right Kidney withhydropelvis due to extrinsic compression by cyst lesion.Relevant hematological & biochemical investigationswere normal.

He was diagnosed as a case of retroperitonealcyst & surgical excision was planned under spinalanesthesia. Patient was placed in supine position; midmidline incision was used to expose the mass. The masswas about 15 x 15 cm in the retroperitoneum,mesentery & small bowel, caecum & ascending colonwere densely adherent to the anterior wall of the cystwhich was thick walled, brownish yellow in colour. About20ml of brown colored fluid was aspirated from the cyst.Cyst was opened & drained. Free part of the wall of thecyst was excised, posterior wall of the cyst was found todensely adherent to the inferior vena cava & aorta. Thesmall part of the cyst wall was left behind wasmarsupilised.

The incision was closed in layers.Postoperative recovery was uneventful.Histopathological report confirmed the diagnosis ofretroperitoneal inflammatory pseudocyst.

DISCUSSIONRetroperitoneal cysts are classified into 1.

Urogenital, 2.Mesocolic, 3.Cyst arising in cell inclusions,4.Parasitic, 5.Lymphatic cysts (1, 2).

Urogenital cysts are bluish & thin walled & areflabby with no visible vessels in their wall, they have nopedicles & no connections apart from areolar tissue withthe surrounding structures. They are single & notmultilocular & they contain clear serous fluid of lowspecific gravity. Lymphatic cysts are chylous cysts &lymphangiomas. These cysts are unilocular ormultilocular, contain clear or milky fluid & lined with singlelayer of flattened epithelium. Cysts arising in cellinclusions such as dermoid cysts have thick walls &usually filled with sebaceous material & hair (2).Traumatic blood cysts may be due to hematomaresulting from an injury, or due to ruptured abdominalaneurysm, anticoagulation therapy or blood dyscrasias& they usually present as an emergency (2,3). Hydatidcysts are not infrequent in the retroperitoneal space.Adrenal pseudocysts are known to occur and have beenreported in the literature. These cysts may be unilocularor multilocular and need to be distinguished fromhydronephrosis or giant ovarian cyst.

There are no pathognomic signs ofretroperitoneal cyst. The presentation is mass perabdomen. Abdominal pain & distension are present in50% of cases (4). They may occasionally present withacute abdominal pain (5). CT is ideal for theassessment of retroperitoneal disease because itprovides sectional images of the organs &retroperitoneal compartments. Treatment of choice iscomplete excision of the cyst. They can be excised byusing transperitoneal f lank approach or anextraperitoneal approach (6). But complete excision isnot possible in all cases. Laparoscopic excision thoughtedious, is definitely beneficial for the patient aslaparotomy usually require large incision to remove thecyst. Laparoscopic excision entails small incisions,better cosmesis, less pain and early recovery (7). Inthis case partial excision & marsupilization was donedue to thick inflammatory adhesions to surrounding vitalstructures.

REFERENCES1. Guile M, Fagan M, Simopolous A, Ellerkman M.

Retroperitoneal cyst of Mullerian origin: A case reportand review of literature. J of pelvic medicine andsurgery. 2007; 13: 149-152. doi:10.1097/SPV.0b013e3180622272. (Cross Ref).Figure 2 : Intra-Operative showing Cyst. Excision

2. Handfield-Jones R. Retroperitoneal cysts: Theirpathology, diagnosis and treatment. BJS. 1942; 119-134.

3. Yang D, Jung D, Kim H, Kang H, Kim S, Kim J, Hwang H.Retroperitoneal cystic masses: CT, Clinical andPathological Findings and Literature Review. RG.2004;25: 1353-1365.

4. Kurtz RJ, Heimann TM, Beckar et al. Mesenteric andretroperitoneal cysts. Ann Surg 1986; 203: 109-12.

5. Mohanty SK, Bal RK, Maudar KK. Mesenteric cyst - anunusual presentation. J Pediatric surg 1999;33(5): 792-3.

6. Tsukada O, Kawabe K. A case of retroperitonealpseudocyst filled with necrotic material. Nippon HinyokikaGakkai Zasshi 1978; 69: 1667-1670.

7. Chinnusamy Palanivelu, Muthukumaran Rangarajan etal. Laparoscopic Excision of an Infected “Egg-shelled”Retroperitoneal Pseudocyst. J Gastrointestin Liver Dis.December 2008;(17) 4: 465-468.

2012; Vol : 1 BIMS Medical Journal 35

Case Report

Multiple myeloma an unusal presentationArif Maldar, *Srinivas B., **Salil Patkar,

Asst. Professor, Department of Medicine. J. N. Medical College, KLE University, Belgaum-590 010.

ABSTRACTMultiple Myeloma is a malignant plasma cell disorder, presenting at a mean age of 60 years, usually

accompanied by a serum or urine paraprotiens or both. Clinical manifestations may include hypercalcemia, anaemia,lytic bone lesions with bone pain and acute renal failure. Presenting a case of multiple myeloma a very rarepresentation in a young adult male.

Keywords : Bony pain, Plasma cells, Electrophoresis, Bence Jones proteins.

BIMS Med. J. 2012, 01 : 36-38

*Professor, Department of Medicine. J. N. Medical College, KLE University, Belgaum-590 010.

**PG, Department of Medicine, J. N. Medical College, KLE University, Belgaum-590 010.

INTRODUCTION

Multiple myeloma (MM) is a debilitatingmalignancy that is part of a spectrum of diseasesranging from monoclonal gammopathy of unknownsignificance (MGUS) to plasma cell leukemia. Firstdescribed in 1848, it is characterized by a proliferationof malignant plasma cells and a subsequentoverabundance of monoclonal paraprotein (M protein).An intriguing feature is that the antibody-forming cells(ie, plasma cells) are malignant and, therefore, maycause unusual manifestations.

The proliferation of plasma cells may interferewith the normal production of blood cells, resulting inleukopenia, anemia, and thrombocytopenia. The cellsmay cause soft-tissue masses (plasmacytomas) or lyticlesions in the skeleton causing bone pain,hypercalcemia, and spinal cord compression.

The aberrant antibodies that are produced leadto impaired humoral immunity, and patients have a highprevalence of infection, especially with encapsulatedorganisms such as Pneumococcus. The overproductionof these antibodies may lead to hyperviscosity,amyloidosis, and renal failure.

The presentation can range from asymptomaticto severely symptomatic with complications requiringemergency treatment. Although patients benefit fromtreatment (ie, longer life, less pain, fewer complications),currently no cure exists. Recent advances in therapyhave helped to lessen the occurrence and severity ofadverse effects of MM.

CASE REPORT

Patient aged of 37 yr old, was a farmer hailingfrom a rural district (Bijapur, Karnataka) was admitted to

KLES Dr. Prabhalar Kore Hospital and Medical ResearchCentre, Belgaum with presenting complaints ofgeneralised itching since three years, generalisedweakness since 2 years, Fever and cough since threemonths and swelling of both lower limbs since 15 days.

Patient presented with complains of generalizeditching from 3 years, not associated with rashes.

Patient complained of fever from 4 months,initially high grade for 5 days and decreased in intensityfollowing medication, and is presently low grade,intermittent not associated with chills and rigors. Nohistory of night sweats.

Patient also complained of dry cough from last 4months, insidious in onset, gradually progressive. Nohistory of change in voice, breathlessness or chest pain.

Patient took medications from local doctor forsimilar complaints in the form of intravenous fluids,following which patient developed hematoma andabscess at the intravenous catheter site, whichdecreased on treatment after 15 days.

Patients also gives history of swelling of bothlower limbs from 15 days, gradual in onset, progressiveand associated with facial puffiness from one week. Nohistory of abdominal distention or decreased urineoutput.

On taking detailed history, the patient informedthat there were multiple swellings in left axilla from onemonth, gradually increasing in size, not associated withpain or any discharge.

History of polyarthalgia, right sided headacheone month back which decreased on treatment after 10days. There is history of loss of appetite and loss of

weight. No history of jaundice or any other swelling inthe body. No history of altered bowel or bladder habits.The patient is a non-smoker, and non-alcoholic.

Past History : History of swelling of left lower limbfollowing trauma and formation of multiple pustules about3 years back which decreased after 15 days oftreatment.

There is no history of DM, Hypertension orTuberculosis.

General Physical Examination revealed pallor,bilateral pitt ing pedal edema up to knees andgeneralized hyperpigmentation of skin. Axillarylymphadenopathy was present (3 in number), non-tender, mobile, firm in consistency with no signs ofinflammation.

Per-abdominal examination revealed moderatesplenomegaly, non-tender, smooth surface, firm. Othersystemic examination was normal.

Investigations : Showed haemoglobin of 4 gm%, totalleucocyte count of 7700/mm3, and differential countrevealed eosinophilia (33%). Peripheral smear showeddimorphic anaemia with eosinophilia. ESR was raisedat 112 mm/1st hr. Renal function tests were impairedwith a blood urea of 33mg/dl and serum creatinine of 2.4mg/dl. Liver function tests were within normal limits.Serum calcium was elevated at 11.5 mg/dl, UrinaryBence Jones Proteins were absent.

Bone marrow examination showed hypercellularmarrow with megaloblastic reaction and increase inplasma cells (25%) with few plasmoblasts.

Serum electrophoresis showed increase in BetaGlobulin (20.5%), Gamma Globulin (28.6%) and Alpha

Bone Marrow Biopsy

2 Globulin (12.5%) and a decrease in Albumin (35%).No M band was seen.

DISCUSSIONMultiple myeloma, also known as plasma cell

myeloma or Kahler’s disease, is a cancer of plasma cells(1). The disease develops in 1–4 per 100,000 peopleper year, and is more common in men. The median ageof patients with MM is 68 years for men and 70 years forwomen. Only 18% of patients are younger than 50 yearsand 3% of patients are younger than 40 years (2).

Many organs can be affected by myeloma, thesymptoms and signs vary greatly. A mnemonicsometimes used to remember the common tetrad (fourparts) of multiple myeloma is CRAB (3):

C=Calcium (elevated): The breakdown of bonealso leads to release of calcium into the blood, leadingto hypercalcemia and its associated symptoms.

R = Renal failure: Renal failure may develop bothacutely and chronically in multiple myeloma. It iscommonly due to hypercalcemia. It may also be due totubular damage from excretion of Bence Jones proteins.

A = Anaemia: usually normocytic andnormochromic. It results from the replacement ofnormal bone marrow by infiltrating tumor cells andinhibition of normal hematopoiesis by cytokines.

B = Bone lesions: Severe bone pain usuallyinvolving the spine and ribs, which worsens with activity.The bone lesions are lytic in nature which appears as“punched-out” resorptive lesions (including the “pepperpot” appearance of the skull on radiography).

Multiple myeloma is also associated withincreased risk of developing various infections. The mostcommon infections are pneumonias (commonly S.pneumoniae, S. aureus, and K. pneumoniae) andpyelonephritis (commonly by E. coli and other gram-negative organisms) (4).

Diagnostic criteriaSymptomatic myeloma : Clonal plasma cells >10% onbone marrow biopsy or (in any quantity) in a biopsy fromother tissues (plasmacytoma)

A monoclonal protein (paraprotein) in eitherserum or urine (except in cases of true non-secretorymyeloma)

Evidence of end-organ damage felt related tothe plasma cell disorder (related organ or tissueimpairment, ROTI, commonly referred to by theacronym “CRAB”):Hyper calcemia (corrected calcium >2.75 mmol/L)

2012; Vol : 1 BIMS Medical Journal 37

Renal insufficiency attributable to myelomaAnaemia (hemoglobin <10 g/dL)Bone lesions (lytic lesions or osteoporosis withcompression fractures)

Asymptomatic myeloma :Serum paraprotein >30 g/L and/or Clonal plasma

cells >10% on bone marrow (5).

Workup : The presence of unexplained anaemia,kidney dysfunction, a high erythrocyte sedimentation rate(ESR) and high serum protein (especially raisedimmunoglobulin) may prompt further testing. Protein elec-trophoresis of the blood shows the presence of a para-protein (monoclonal protein, or M protein) band, with orwithout reduction of the other (normal) immu-noglobulins (known as immune paresis). In theory, mul-tiple myeloma can produce all classes of immunoglobu-lin, but IgG paraproteins are most common, followedby IgA and IgM. IgD and IgE myeloma are very rare.

A bone marrow biopsy is usually performed toestimate the percentage of bone marrow occupied byplasma cells. This percentage is used in the diagnosticcriteria for myeloma. Immuno histochemistry: myelomacells are typically CD56, CD38, CD138 positive and CD19and CD45 negative.

Beta 2-microglobulin can be assayed whichprovides prognostic information.

The prognosis of myeloma varies widelydepending upon various risk factors. Patients withdeletion of chromosome 13 or hypodiploidy byconventional cytogenetics, t(4;14), t(14;16) or 17p- bymolecular genetic studies, or with a high plasma cell la-beling index (3% or more) are considered to have high-risk myeloma (6).

TreatmentTreatment for multiple myeloma is focused on

disease containment and suppression. Forasymptomatic disease, treatment may be deferred.

Initial therapy- High-dose chemotherapy with hematopoietic

stem-cell transplantation for patients under the ageof 65. Prior to stem-cell transplantation. The mostcommon induction regimens used arethalidomide–dexamethasone, bortezomib basedregimens, and lenalidomide–dexamethasone (6).

- Patients over age 65 and patients with significant

concurrent illness often cannot tolerate stem cell trans-plantation. For these patients, the standard of carehas been chemotherapy with melphalan and pred-nisone (7).

Maintenance therapySometimes after the initial treatment an ongoing

maintenance therapy is offered. A 2009 review ofmaintenance therapy concluded in younger patients,post-stem cell transplant maintenance therapy withthalidomide appears to increase tumor burdenreduction further, which translates into prolongedprogression free survival.

Relapse

- Re-treatment with the original agent,

- Use of other agents (such as melphalan,cyclophosphamide, thalidomide or dexamethasone,alone or in combination), and

- a second autologous stem cell transplant.Bisphosphonates, erythropoietin analogoues,dialysis etc may be required to treat the associatedconditions.

REFERENCES

1. Raab MS, Podar K, Breitkreutz I, Richardson PG,Anderson KC. “Multiple myeloma”. Lancet 2009; 374(9686): 324–39.

2. Detailed Guide: Multiple Myeloma What Are the KeyStatistics About Multiple Myeloma? American CancerSociety. Available at http://bit.ly/dMwLDk. Accessed May28, 2009.

3. International Myeloma Working Group. “Criteria for theclassification of monoclonal gammopathies, multiplemyeloma and related disorders: a report of theInternational Myeloma Working Group”. Br. J. Haematol2003; 121 (5): 749–57.

4. Hargreaves RM, Lea JR, Griffiths H, et al.“Immunological factors and risk of infection in plateauphase myeloma (stable phase)”. J. Clin. Pathol 1995;48 (3): 260–6.

5. Kyle RA, Rajkumar SV “Criteria for diagnosis, staging,risk stratification and response assessment of multiplemyeloma”. Leukemia 2009; 23 (1): 3–9.

6. Kyle, R.A., Rajkumar, S.V. “Multiple myeloma”. Blood2008; 111 (6): 2962–2972.

7. Harousseau J.L. “Maintenance therapy in multiplemyeloma.” Rene Guaducheau Cancer Center, Nantes/St. Herblain Cedex, France. Licensee PAGE Press, Italy,Hematology reports 2009; 1 doi:4081/hr.2009.e12.

38 Multiple Myeloma Arif Maldar et al

BIMS MEDICAL JOURNALInstructions to Authors

BIMS Medical Journal is the official publication of Belgaum Institute of Medical Sciences. The journalconsiders for publication ,original articles dealing with different branches of Medical Sciences. Only papers that make asignificant contribution to the existing state of knowledge in a particular field will be published. The journal publishesoriginal articles, review articles, special articles, case reports, technical communications, medical intelligence articles,radiology forum, book review and letters to the editor. BIMS medical journal shall be published bi-annually, in Januaryand in July.

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(A) Review Articles and (B) Educational ForumReviews are written by researchers of considerable experience in the field concerned. The authors should

review the recent trends or advances in that field in the light of their own work. However, when an author has not doneenough original work on a topic but wants to share the knowledge on recent advances/trends which may be useful forpost-graduate students or junior members of faculty, one may do so by writing for Educational Forum.

The major portion of the above articles should deal with the up-to-date developments in the field in the last3-5 years.

These articles should contain a covering letter, title page, abstract (need not be structured) and key words.They should be written under appropriate sub-headings. The authors are encouraged to use flowcharts, boxes, tablesand figures for better presentation. Some of the other details are given below.(C) Original Research Articles

These may either be a full length research article or a short communication. These papers should be arrangedinto the following sections:

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Acknowledgment References Tables Figures

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It should be paginated as page 1 of the paper. It should include the title, authors’ names and affiliations, runningtitle, address for correspondence including e-mail address and also the total number of pages, figures and tables. Title : Must be informative, specific and short. And cryptic titles are to be avoided.Authors and affiliations : The names of authors and their affiliations should be given. It should be made clear whichaddress relates to which author.Running title : It is a short title printed in the journal at the right top corner of right hand page of the article. (Except thelead page). It should be not more than 50 characters in length.Address for correspondence :

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It should start on a new page. Essentially this section must introduce the subject and briefly say how the idea forresearch originated. Give a concise background of the study. Do not review literature extensively but provide the mostrecent work that has a direct bearing on the subject. Justification for research aims and objectives must be clearlymentioned without any ambiguity. The purpose of the study should be stated at the end. Only 3-4 pertinent referencefor case reports, 10-12 for original articles and review articles may be given.5) Materials and Methods

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40 BIMS Medical Journal 2012; Vol : 1

are to be clearly stated. If necessary brand names may be mentioned in brackets.Ethics :

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And these should be numbered consecutively in the order in which they are first mentioned in the text.Identifyreferences in text, tables, and legends by Arabic numerals in parentheses. References cited only in tables or figurelegends should be numbered in accordance with the sequence established by the first identification in the text of theparticular table or figure. Reference indicated in Round Brackets and should be quoted in ‘Vancouver style’. The titlesof journals should be abbreviated according to the study used in Index Medicus. Consult the List of journals indexed inIndex Medicus, published annually as a separate publication by the library and as a list in the January issue of IndexMedicus The list can also be obtained through the library’s web site (http://www/nlm.nih.gov). The reference must beverified by the author(s) against the original document. Unpublished work should not be parenthetically within the text.List all the authors when there are six or fewer; but when there are seven or more, list the first six, then add ‘et al’.Examples of correct form of references are given here:

2012; Vol : 1 BIMS Medical Journal 41

Articles in Journals1. Standard Journals articles : Nagaraj LV, Fangman W, White WL, Woosley

JT, Prose N, Selim MA, et al. Self-healing juvenile cutaneous mucinosis:Cases highlighting subcutanoues/fascial involvement.J Am Acad Dermatol 2006; 55:1036-43.

2. More than six authors: Werth VP, Fivenson D, Pandya AG, Chen D, RicoMJ, Albrecht J, et al. Multicenter randomized, double-blind, placebo-controlled, clinical trial of dapsone as a glucocorticoid-sparing agent inmaintenance-phase pemphigus vulgaris. Arch Dermatol 2008; 144: 25-32.

3. Books and other Monographs :(a) Personal author(s) : Behera D, Text Book of Pulmonary Medicine. Second Edn

(in two volumes), New Delhi, Japee Brothers. 2010.(b) Editor(s), Complier as authors:Shankar PS. (Ed) Respiratory Futurology, Mumbai,

Academy of Respiratory Medicine, 2010.(c) Chapters in a book : Secli JR, Sandford K. Molecular mechanisms of disease in Boon

NA, Colledge NR, Walker BR, Hunter JAA (eds) Davidson’sPrinciples and Practice of Medicine,20th edn, Edinburgh,Churchill Livingstine, 2006:1141-57.

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42 BIMS Medical Journal 2012; Vol : 1

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BIMS MEDICAL JOURNALAuthorship Responsibility & Copyright Transfer Agreement

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2012; Vol : 1 BIMS Medical Journal 43

BIMS MEDICAL JOURNALCONTENTS

Volume-01 Number-01 January 2012

Editorial 1

Original articles

1. Microbiological quality of water and dialysate at a haemodialysis unit in India. 2- Chandrashekar M. R., Patil A.B., Krishna B.V.S.

2. Prospective comparative clinical study of adenoid size in HIV and non HIV patients. 5- Shalini Huddar, Vijayanand Halli, Satish Bagewadi, Irrana Palled, Angadi U.

3. Breast feeding practices among the infants living in rural area –A longitudinal study. 8- Gunagi P.R, Mallapur M.D, Naik V.A.

4. Assessment of nutritional status among undergraduate medical students – A cross sectional study. 12- Karikatti S.S., Radika M., Spurthi C., Halki S., Hallappanavar A.B.

5. Biochemical screening tests of urine in mentally retarded children. 16- Indira Bhaskar, Aruna Bhushan, Narasimha Rao S.

Medical Education

6. Need based medical education 19- Hegde B. M.

Lighting of the way 22

Case Reports

6. Massive colonic dilatation 23- Ved Bhushan S. T., Uppin V. M., Patil S., Chandran B.

7. Hereditary spastic paraparesis 26- Kalsad S.T, Archana Dambal, Malagi K.R, Pattanshetti M.

8. Urinary tract infection : A very rare presentation of geotrichum candidum infection 29- Rupali Shinde, Walvekar R.R., Jnaneshwara K. B., Mantur B. G.

9. Primary splenic cyst – A rare entity. 31- Aruna S., Jhadhav M. N., Kittur S. K.

10. Retroperitoneal inflammatory pseudocyst 33- Kalburgi E. B., Basarkod S. I., Lamani Y. P., Chethan V. N.

11. Multiple myeloma an unusal presentation 36- Arif Maldar, Srinivas B., Salil Patkar

Instructions to Authors 39