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An Official Organ of North Bengal Medical College, Sirajganj

Contents

Editorial 1

Original Articles

Clinicopathological Study on Lichen Planus in Rajshahi Medical College Hospital Samia Naz, Md. Fazlur Rahman, SM Badruddoza, Afsar Siddique

4

Outcome of Primary Postpartum Haemorrhage in North Bengal Medical College Hospital Monowara Khatun, Kh Mohammad Ali, Sharmin Akhtar

10

Pattern of dermatophyte at Shaheed Ziaur Rahman Medical College Hospital, Bogra, Bangladesh Muhsina Alam Shaheed, Shah Alam, Taslima Yasmin, Ziaul Ahsan, Syed Mohammad Monowar Ali

18

Review Article

Effectiveness of Oral Examination as an Assessment Method in Medical Education

S M Akram Hossain, S M Mosaddeq Hossain 24

Case Reports

Syringomyelia with Unusual Presentation Tapashi Rahman Khan, Md. Faruk Hossen, Md. Rafiqul Islam,

Md. Abdul Hamid, Shamim Adom

30

Rheumatoid Vasculitis Syed Mohammad Monowar Ali, Md Shahidul Islam Talukder,

Md Azizul Haque, Md Abul Kalam Azad

35

Instructions for the Authors

40

NORTH BENGAL MEDICAL COLLEGE JOURNAL

Vol 4 No 1 January 2018


NORTH BENGAL MEDICAL COLLEGE JOURNAL Vol 4 No 1 January 2018 The North Bengal Medical College Journal (NBMCJ) is a peer-reviewed journal published biannually. It is the official organ of North Bengal Medical College, Sirajganj, Bangladesh.

EDITORIAL BOARD

CHAIRPERSON Professor Dr. M A Muqueet EDITOR IN CHIEF Professor Dr. S M Akram Hossain

EXECUTIVE EDITOR Dr. Md. Abul Kasem Khan

ASSOCIATE EDITORS Dr. A.T.M. Fakhrul Islam Dr. Md. Saber Ali

ASSISTANT EDITOR Dr. Md. Sultan-E-Monzur

MEMBERS Professor Dr. Gopal Chandra Sarkar Professor Dr. Md. Shamim Adom Professor Dr. Rafiqul Alam Professor Dr. M A Awal Professor Dr. Md. Rafiqul Islam Professor Dr. Mahbub Hafiz Professor Dr. Ali Mohammad Rashid Professor Dr. Md. Kausar Alam Dr. Chaklader Md. Kamal Jinnah Dr. Shaheen Akhter Dr. Taslima Yasmin Dr. Dilrose Hussain Dr. Chowdhury Mokbul-E-Khoda Dr. Md. Israil Hossain Dr. Zillur Rahman Dr. Md. Shamsul Alom Dr. Md. Kamrul Rasel Khan Dr. Md. Shafiqul Islam Dr. Samsoon Nahar Joly Dr. Md. Nayem Ullah Dr. Md. Faisal Aziz Chowdhury Dr. Md. Zahurul Haque Raza

ADVISORY BOARD

Professor Dr. Md. Jawadul Haque Professor Dr. Md. Anwar Habib Dr. Md. Ashraful Alam Dr. Md. Mofazzal Sharif

Address of Correspondence: Editor in Chief North Bengal Medical College Journal North Bengal Medical College Dhanbandhi, Sirajganj. Email: [email protected]

Copyright No part of the materials published in this journal may be reproduced, stored or transmitted by any means in any form for any purpose without the prior written consent of the Editorial Board of the journal. Annual subscription

Taka 300/= for local subscribers USD 20 for overseas subscribers


EDITORIAL

The Gene Gun: Current Genetic Revolutionary Engineering Technique

ARTICLE INFO Article history:

Received: 04 June 2017 Accepted: 08 August 2017

Online: www.nbmc.ac.bd

he advancement in genetics and molecular biology research has generated an increased interest in the field of gene

therapy among medical scientists. Several clinical applications have been recently attempted and many others appear to be on the horizon. Originally, gene therapy was introduced as a mechanism to replace absent or defective gene in heritable disorders. In fact many heritable disorders have well-characterized genetic defects, making them favourable targets for gene therapy. The gene therapy has evolved to include genetic vaccination, suicidal genes for cancer therapy, immunomodulation, genetic pharma-cology, and others.1-5

Gene gun is a biolistic technique of genetic engineering which is commonly used to transfer the genetic material inserts into the cells by the particles coated onto small DNA sequences. The gun is fired at the cluster of the cells and the DNA sequences enter the desired cell. The method of gene gun is used in the laboratory and for the research purposes. The gene gun was introduced around 1987 when the researchers wanted to insert the genetic material into the organism.6 The method was first developed for the plant cells but it is also applied in human and animals studies. With time, modifications are made in this method to make it more useful to perform its

functions efficiently. With the many new innovations to the original device, the gene gun has evolved in terms of applications and efficiency. From a device that revolutionized plant breeding and engineering to one that is slowly moving towards revolutionizing medical treatments for a variety of significant diseases.

This technique has been revolutionized the science of genetic engineering which involves manipulating genes on microscopic gold or titanium particles (bullets) into living tissues. The high velocity acceleration of particle using gene gun may be provided by compressed gas, centripetal force (external force to move a body along a curved path), electric discharge, or firing explosives.7 Acceleration provides the necessary force to puncture the cell membrane and deliver the materials into cells of living tissues. These cells become genetically modified and can be used for various purposes. When the genetic material is inserted into the cells, a genetic marker is also inserted with the bullet so that it can show that the genetic material has entered the cells successfully. Gene gun is conducted using two main methods such as microprojectile gun method involves the use of a gas driven gene gun that launches high velocity microprojectiles or microparticles, which are small particles composed of metals such as tungsten or gold.8

T

NORTH BENGAL MEDICAL COLLEGE JOURNAL [2018], VOL., 4, No. 1 : 1-4


The DNA is first coated on microparticles and then delivered into tissues using gene gun. Currently, hand-held instruments has been developed to utilize the ballistic particle-mediated delivery system, commercially these devices are available such as the Helios gene gun (Bio-Red, Hercules, California) (Figure 1). This gene gun is convenient to use to allow rapid transfer of genes into various targets in living tissues. The major advantage of this technique is very easy to transfer genetic material in different traits in a single experiment.9

The gene gun method has potential to be used for a wide spectrum of clinical applications both in vivo and in vitro. However currently it is being used mainly for DNA vaccination and gene therapy for replacing defective gene that can cause disease or preventing illness and immunomodulation, treatment of cancer disease. Sometimes the cell does not produce the desired protein, for this reason the researcher use this method to force the cell to produce the specific protein.

The gene gun has brought molecular biological techniques to the forefront of medical study. The gene gun has played an increasingly significant

role most prominently in cancer research and potential tumor elimination techniques. It has also aided in the growth of the burgeoning field of gene therapy by providing an efficient delivery method for transmitting therapeutic genes into the bodies of patients. With the development of the new modifications of gene gun design, and its safety and efficiency have become exciting for us and for the next few years, it is likely that gene guns could become one of the most common treatment tools in fields ranging from common vaccination to cancer therapy.

The gene gun has proven to be useful and potential in gene therapy research and clinical applications gene replacement, vaccines, immunomodulation and cancer therapy. The ability of gene gun to deliver genes to a variety of cell type offers distinctive advantages over other delivery systems. That’s why the gene gun will likely remain a standard gene delivery technique in future gene therapy applications.

M. A. Kasem Khan Associate Professor, Department of Dermatology, North Bengal Medical College, Sirajganj [email protected]

REFERENCES 1. Cesco-Gaspere M, Zentilin L, Giacca M.

Boosting anti-idiotype immune response with recombinant AAV enhances tumour protection induced by gene gun vaccination. Scand J Immunol. 2008; 68(1): 58-66.

2. Golden JW, Josleyn MD, Hooper JW. Targeting the vaccinia virus L1 protein to the cell surface enhances production of neutralizing antibodies. Vaccine. 2008; 26(27-28): 3507-3515.

3. Denman CJ, McCracken J, Hariharan V, Klarquist J, Oyarbide-Valencia K, et al. HSP70i Accelerates Depigmentation in a Mouse Model of Autoimmune Vitiligo. J Invest Dermatol. 2008; 128(8): 2041-2048.

Figure 1: Gene gun technology with the Helios gene gun (Bio-Red, Hercules, California)


4. Smahel M, Poláková I, Pokorná D, Ludvíková V, Dusková M, Vlasák J. Enhancement of T cell-mediated and humoral immunity of beta-glucuronidase-based DNA vaccines against HPV16 E7 oncoprotein. Int J Oncol. 2008; 33(1): 93-101.

5. Webster RG, Robinson HL. DNA vaccines: a review of developments. Bio Drugs. 1997; 8(4): 273-292.

6. Klein T.M, Wolf ED, Wu R, Sanford JC. High-velocity microprojectiles for delivering nucleic acids into living cells. Nature. 1987; 327: 70–73.

7. Jolly D. Viral vector systems for gene therapy. Cancer Gene Ther. 1994; 1: 51-64.

8. Williams RS, Johnston SA, Riedy M, DeVit MJ, McElligott SG, Sanford JC. Introduction of foreign genes into tissues of living mice by DNA-coated microprojectiles. Proc Natl Acad Sci U S A. 1991; 88 (7): 2726-2730.

9. Michael TS, Leena P, Jouni U, Kyonggeun Y. The gene gun: current applications in cutaneous gene therapy. 2000; 39: 161–170.


ORIGINAL ARTICLE

Clinicopathological Study on Lichen Planus in Rajshahi

Medical College Hospital

*Samia Naz,1 Md. Fazlur Rahman,2 SM Badruddoza,3Afsar Siddique4


Received: 26 October 2016 Accepted: 12 January 2017 Online: www.nbmc.ac.bd Keywords: Lichen planus, Lichenoid skin lesion, Papulosquamous, Oral lichen planus, Dermatoses.

ABSTRACT Introduction: This study was carried out to confirm the clinically diagnosed cases of lichen planus in patients presented with lichenoid skin lesions by histopathology. Methods: Total of 94 skin biopsies were taken from the site of lichenoid skin lesions and histopathological study was done. Results: Among 94 cases of lichenoid skin lesion, 39 (41.48%) were histopathologically diagnosed as lichen planus, of them 22 (56.41%) were male and 17 (43.59%) were female. Males were predominant. Conclusion: In most cases, clinical study alone is not sufficient for the diagnosis. So, both clinical examination and histopathological study are needed for appropriate diagnosis and management of lichen planus patients.

1. Assistant Professor, Department of Pathology, Rajshahi Medical College, Rajshahi 2. Professor, Department of Pathology, Anwer Khan Modern Medical College, Dhaka 3. Professor, Department of Pathology, Rajshahi Medical College, Rajshahi 4. Assistant Professor, Department of Dermatology and Venereal Diseases, Rajshahi Medical College, Rajshahi

*Corresponding author: [email protected]

INTRODUCTION

ichen planus (LP) is a common subacute or chronic inflammatory papulosquamous disorder of unknown aetiology. It

affects skin, mucous membrane, nails and hair follicles. It is characterized by erythematous to violaceous, flat-topped, polygonal papules. Both genetic and environmental components such as drugs or infections may interact to elicit this disease. Cell-mediated immunity plays the major role in triggering the clinical expression of the disease.1,8,9 Recent studies provide evidence that auto reactive cytotoxic T lymphocytes are the effector cells which cause degeneration and destruction of keratin-ocytes.9,12,14 LP are of several varieties such as

classic, atrophic, hypertrophic, linear, annular, bullous, ulcerative, oral, actinic etc.1 It is a chronic, usually self-limited benign dermatosis. Malignant transformation is extremely rare. The severe and prolonged chronic inflammation due to persistence of hypertrophic LP leads to development of squamous cell carcinoma.2,8 The papulosquamous disorders are complex to diagnose, as they may resemble a similar disorder of the group. Histomorphological diagnosis is important for separation of these disorders because the treatment and prognosis for each tends to be disease specific.13 Hence, the study was done to correlate the clinical diagnosis of LP with histopathological findings.

L



METHODS

This cross-sectional descriptive type of study was carried out in the Department of Pathology, and Dermatology and Venereal Diseases of Rajshahi Medical College, Rajshahi,

during the period of July 2005 to June 2007. A total of 94 patients of both sexes aged between 5-75 years were included in this study. Biopsies of skin and mucous membrane were taken from those patients with licheniod skin lesions. A full thickness of elliptical incisional biopsy was taken from the lesions with proper aseptic precaution under local anaesthesia (2% lignocaine) after taking a valid consent. Then the sites of incision were closed by sutures. The biopsy materials were preserved in 10% formalin. Then paraffin block was prepared for histological section and Haematoxyline and Eosin staining was done. During

histopathological examina-tion following features were carefully noted such as hyperkeratosis, focal hypergranulosis, acanthosis with saw-toothing rete ridges, band-like inflammatory infiltrate at dermo-epidermal junction and civette bodies. All the histopathological features were correlated with the clinical findings.

RESULTS

Lichenoid skin lesions were diagnosed as lichen planus (LP) by histopathological study. Out of 94 lichenoid skin lesion cases, 39 (41.48%) were histopathologically diagnosed as LP. Among them 22 (56.41%) were male and 17 (43.59%) were female respectively. Male and female ratio was 1.3 : 1. The age was from 5 years to 75 years with a mean age of 30.6 years. Maximum number of patients (11, 28.21%) was in age group 21- 30 years (Table I).

Table I: Age and sex distribution of lichen planus cases

Age groups (years) Male % ( n-22) Female % ( n-17) Total % (n- 39)

0-10 01(33.33) 02(66.67) 03(7.69)

11-20 06(85.71) 01(14.29) 07(17.95) 21-30 04(36.36) 07(63.64) 11(28.21) 31-40 03 (60.00) 02 (40.00) 05(12.82) 41-50 07 (70.00) 03 (30.00) 10(25.64) 51-60 01 (50.00) 01 (50.00) 02(5.13)

>61 -- 01 (100) 01(2.56) Total 22 (56.41) 17 (43.59) 39 (100)

Number of lichen planus cases and duration of lesions are shown in Figure- 1.

Figure 1: Duration of skin lesions of lichen planus

Papules and plaques with scales were mainly confined to the extremities and trunk. They were distributed as follows: 20 (51.28%) in

limbs and trunk, 7 (17.95%) in both upper and lower limbs. But 1 (2.56%) in oral mucosa, 1 (2.56%) in lower limbs, 2 (5.13%) in upper limbs and 7 (17.95%) were generalised (Table II).


Table II: Distribution of skin lesion in different parts of the body

Site of lesion Number (n- 39)

( % )

Limbs & trunk 20 51.28 Both upper & lower limbs 07 17.95 Oral mucosa 01 2.56 Lower limb 01 2.56 Upper limb 02 5.13 Generalised 07 17.95

Total 39 100 Different varieties of lichenoid dermatoses among 94 cases of lichenoid skin lesions were

categorized by histopathological examination, are shown in Table lll.

Table III: Histopathological diagnosis of 94 cases of lichenoid skin lesion

Serial No.

Histopathological diagnosis Number of patients (%)

1. Lichen planus 39 41.49 2. Chronic non-specific dermatitis 35 37.23

3. Lichen simplex chronicus 07 7.45

4. Benign lichenoid keratosis 05 5.32

5. Prurigonodularis 01 1.06

6. Prurigo simplex 01 1.06 7. Inflammatory linear verrucous epidermal

nevus 01 1.06

8. Pityriasis lichenoides et varioliformis acuta

01 1.06

9. Psoriasis vulgaris 01 1.06

10. Lupus vulgaris 01 1.06 11. Lepromatous leprosy 01 1.06

12. Squamous cell carcinoma with features of lichenoid reaction

01 1.06

Total 94 100

Among the several variants of lichen planus (LP) cases (n-39), classical, oral, hypertrophic and atrophic type were observed in this study are

shown in Table III. Almost all of cases (36, 92.32%) were classical variant of LP.

Table III: Distribution of several variants of lichen planus cases

Varients of lichen planus Number of cases (n- 39) (%)

Classical 36 92.32

Oral 01 2.56

Hypertrophic 01 2.56

Atrophic 01 2.56

Total 39 100


Histologically, mild degree of hyperkeratosis was observed in 4 (10.26%), moderate degree in 34(87.18%) and marked degree in1 (2.56%) cases. Similarly, mild degree of hypergranulosis was observed in 2 (5.13%) and marked degree in 37 (97.87%) cases. Acanthosis of the epidermis in mild degree was observed in 1 (2.56%), moderate degree in 37 (97.87%) and marked degree in 1 (2.56%). Focal degeneration of basal layer was observed in 16 (41.03%)

cases and diffuses infiltration in 23 (58.97%) cases. Band-like infiltration of chronic inflammatory cells along the dermo-epidermal junction was observed in 26 (66.67%) cases and civette bodies in 17 (3.59%) cases. One case was clinically diagnosed as ulcerated oral lichen planus but histopathologically it was diagnosed as squamous cell carcinoma with lichenoid reaction within the adjacent mucosa (Table IV).

Table IV : Important histological features of lichen planus Histological features Mild Moderate Marked Total

Hyperkeratosis 4 (10.26%) 34 (87.18%) 1 (2.56%) 39 (100%) Hypergranulosis 2 ( 5.13%) _ 37 (97.87%) 39 (100%) Acanthosis 1 (2.56%) 37 (97.87%) 1 (2.56%) 39 (100%) Focal degeneration of basal layer

16 (41.03%) _ 23 (58.97%)

39 (100%)

Band-like infiltrate along dermoepidermal junction

_ 3 (7.69% ) 26 (66.67%) 39 (100%)

Figure 2: Photograph of lichenoid skin lesion in lower extremities

The clinical diagnosis showed concordance with histopathological diagnosis in 39 (41.49%) cases of lichen planus.

Figure 4 : Photomicrograph of Hypertr-ophic lichen planus showing hyper-keratosis ( H & E stain, 10X)

Figure 3 : Photomicrograph of lichen pla-nus showing band-like infiltrate of lymphocytes along the dermoepi-dermal junction (H & E stain, 10X)


DISCUSSION

In the present study, Lichen Planus (LP) is

common among patients clinically presented with lichenoid skin lesions. There were no significant sex difference and most of the patients were within 21–30 yrs. The skin lesions were violaceous papules and plaques with scales involving preferentially the flexural surfaces of the limbs and trunks. In few cases, it was also found in oral mucosa. Pruritus were moderate to severe. Our study is similar with Boyed and Neldner where they found the skin involvement tends to occur at a younger age, most of the patients were in third decade.1 The cutaneous lesions tend to involve the flexor surface of arm and wrist is the classic characteristic site. The arms and legs were the most common sites, although, the thigh, lower back, trunk and neck were also involved.9,10

The papules were faintly erythematous to violaceous, flat-topped and occasionally polygonal form. LP tends to be intensely

pruritic.9 The age group, sites of involvement and types of lesion correlates well with the present study.

An Egyptian scientist stated in a clinical and epidemiological study of LP, the age range of patients were 10-65 years, and male to female ratio were 1.3:1.7 The majority of the patients in the present study fall in 21-30 years of age. Presentations include classic, hypertrophic, oral and atrophic. Pruritus was the chief complaints and limbs were the initial site of onset. The histologic picture of LP showed hyperkeratosis, hypergranulosis, irregular acanthosis, focal degeneration of basal layer and band-like

infiltrates of lymphocytes along the dermo-epidermal junction. Civette bodies were also seen in few cases which is similar with the study of Ellis.3 The present study is also showed similar histological findings with Bhuiyan.11,13

Among the morphologic variants of LP, classic type, hypertrophic LP, Oral LP (OLP) and

atrophic LP were found in this study. Patients develop hypertrophic lesion if persists for longer time period. The absence of hyperkeratosis was seen in atrophic LP.11,,13

One case diagnosed as squamous cell carcinoma (SCC) with lichenoid reaction was presented with plaque-like lesions in buccal mucosa with ulcerated growth and erythematous areas. Particularly the erosive and plaque-like forms of OLP had the possibility of transformation to carcinoma.4 A feared complication of OLP was the development of oral SCC.5 The frequency of malignant transformation ranges from 0.4% to more than 5% with the highest rate noted in erosive lesions. Chronic irritation by sharp teeth, dentures or tobacco were suggested as the precipitating factor for malignant transform-ation of OLP.2 In the present study, one of the patients was female of 55 years who had lesion for 18 months and had history of chewing betel nut. So, there may be association of OLP with chronic irritation for the development of SCC as stated in the above studies.

The present study showed 42.55% concordance and 57.45% discordance between the clinical and histopathological diagnosis among the 94 cases of licheniod skin lesions. So, clinical evaluation alone is not sufficient for the diagnosis of lichenoid skin lesions, rather a subsequent histopathological examination would enable us to reach a correct diagnosis and proper management of the patients.10,12

CONCLUSION

It may be concluded from the present study that all clinically diagnosed lichenoid skin lesions were not lichen planus, a few of them were different types of chronic dermatitis. Clinical evaluation alone is not sufficient for the diagnosis. So, all lichenoid skin lesions require biopsy and histopathological examination for proper diagnosis and management of patients.


Conflicts of Interest There is no conflict of interest.

REFERENCES

1. Boyed AS, Neldner KH. Lichen planus. J Am Acad Dermatol. 1991; 25: 593-619.

2. Kronenberg K, Fretzin D, Potter B. Malignant degeneration of Lichen planus. Arch Dermatol. 1971; 104: 304-307.

3. Ellis FA. Histopathology of lichen planus based on analysis of one hundred biopsy specimens. Journal of Investigative Dermatology. 1967; 48(2): 143-148.

4. Lodi G, Scully C, Carrozzo M, Griffith M, Sugerman PB, Thongprason K. Current controversies in oral Lichen planus: Report of an international consensus meeting. Part 2. Clinical management and malignant transformation. Oral Surg Oral Med Oral Path Oral Radiol Endod. 2005; 100: 164-178.

5. Eisen D. The clinical features, malignant potential and systemic association of oral lichen planus: A study of 723 patients. J Am Acad Dermatol. 2002; 46: 207-214.

6. Tilly JJ, Drolet BA, Easterly NB. Lichenoid eruptions in children. J Am Acad Dermatol. 2004; 151 (4): 606-624.

7. Anber T, Barakat M, Ghannam SF. A clinical and epidemiological study of lichen planus among Egyptians of Al- Minya Province. Dermatology online Journal. 2003; 11(2): 1-11.

8. Lakshmipriya G, Uma S. Clinicopatho-logical study of Lichen planus in a tertiary care center. Int J Sc study. 2016; 4(1): 244-247.

9. Parihar A, Sharma S, Bhattacharya SN, Singh UR. A clinicopathological study of cutan-eous lichen planus. Journal of Dermatology & Dermatologic Surgery. 2015; 19: 21-26.

10. Karumbaiah KP, ArshiyaAnjum, Mallika-rjun M. A histopathologic study of papulo-squamous lesions of skin. Indian Journal of Pathology: Research and Practice. 2017; 6(2): 404-409.

11. Gargi R, Maheshwari, Hita H. Mehta, Vivek Nikam. Clinocopathological correla-tion for diagnosis of licheniod interface dermatoses. Journal of Dermatology & Dermatologic Surgery. 2016; 20: 115-124.

12. Richard D, Southeimer. Lichenoid tissue reaction/Interface dermatitis: Clinical and Histologic perspectives. J Invest Dermatol. 2009; 129: 1088-1099.

13. Chavan SD, Mahajan SV, Vankundre AJ. A descriptive study on papulosquamous lesions at Tertiary care Institute. MPV Journal of Medical Sciences. 2014; 1(1): 30-35.


ORIGINAL ARTICLE

Outcome of Primary Postpartum Haemorrhage in North Bengal Medical College Hospital

*Monowara Khatun,1 Kh Mohammad Ali,2 Sharmin Akhtar3


Received: 10 December 2016 Accepted: 28 March 2017 Online: www.nbmc.ac.bd Keywords: Primary postpartum Haemorrhage, Oxytocin, Atonic uterus .

ABSTRACT Introduction: Postpartum haemorrhage (PPH) is a major cause of maternal morbidity and mortality worldwide. Rapid recognition of clients at risk of PPH and early diagnosis is essential for successful management and favorable outcome of labour. The study was conducted to determine the predisposing factors for primary PPH. Methods: This is a descriptive type of cross-sectional study conducted at the Obstetrics and Gynaecology Department of North Bengal Medical College Hospital (NBMCH), Sirajganj, among 88 pregnant women who developed primary PPH after delivery. Data were abstracted from the medical and delivery records. All cases with primary PPH were included. All study subjects were interviewed of socio-demographic risk factors, medical and obstetric histories, antenatal events, labour and delivery outcomes. Results: Among the total 88 patients, 42 (47.73%) belonged to 26-30 years age group. Most of the responders 60 (68.18%) were housewife and completed their primary level of education 56 (63.64%). Primary PPH occurred mostly after vaginal delivery 73 (82.95%) and rest were after caesarean section 15 (17.05%). Common causes of primary PPH were atonic uterus 54 (61.36%), retained bits of placenta 12 (13.64%), cervical tear 10 (11.36%) and remaining were vaginal tear, inverted uterus, ruptured uterus. PET/Eclampsia (12), multiple pregnancy (11), polyhydramnios (10), macrosomia (06) and instrumental delivery (05) were the common risk factors. The majority 61 (71%) were treated conservatively in which fundal massage was done in 32 (52.11%) cases. Regarding surgical management, majority of the patients (10, 47.62%) were managed by repair of cervical and vaginal tear. Other managements include manual removal of placenta (6, 28.57%) and subtotal hysterectomy (2, 9.52%). A small number of patients was managed by B-lynch suture (1, 4.76%), repair of ruptured uterus (1, 4.76%) and ligation of uterine arteries (1, 4.76%). Among the patients (22, 25%), had developed complications due to shock. Other cases of complications were puerperal sepsis (10, 11.36%) and acute renal failure (1, 1.14%). Death occurred in five patients, due to shock in two patients (40%), one patient each due to sepsis, ARF and DIC. Conclusion: Efforts to reduce the incidence of PPH should be taken for proper management of labour about the mentioned risk factors.

1. Assistant Professor, Department of Obstetrics and Gynaecology, North Bengal Medical College, Sirajganj 2. Assistant Professor, Department of Community Medicine, Shaheed M Mosur Ali Medical College,

Sirajganj 3. Lecturer, Department of Community Medicine, Shaheed M Mosur Ali Medical College, Sirajganj




INTRODUCTION

ost partum haemorrhage (PPH) is an obstetrical emergency that can follow vaginal or caesarean delivery. Primary

PPH is blood loss greater than 500 ml from the

genital tract within the first 24 hours following delivery.1 This compares with greater than 1000 ml of blood loss for caesarean section. The mean blood loss reported after vaginal and caesarean deliveries were approximately 500 ml and 1000 ml respectively.2 Worldwide the average maternal mortality from PPH is 25%.3 In Bangladesh about 31% of maternal death occurs due to PPH.4

PPH is best diagnosed clinically as excessive bleeding that makes the patient symptomatic with pallor, weakness, palpitation, restlessness, confusion, syncope and result in sign of hypovolemia (e.g., hypotension, tachycardia, oliguria, low oxygen saturation). A timely, accurate diagnosis of PPH is important to initiate intervention and improve outcome.5 Atonicity of the uterus is the commonest (90%) cause of immediate PPH.6 Other causes include trauma (cervical, vaginal, perineal), retained or adherent placental tissue, clotting disorder, inverted uterus, ruptured uterus.6

Factors thought to increase the risk for PPH are over distension (multiple pregnancy, macro-somia/polyhydramnios), prolonged labour, induced or augmented labour, grand multiparity (more than 4), instrumental

delivery, pre-eclampsia, problems with placenta (e.g., retained placenta, placenta previa), previous PPH, maternal bleeding disorder.7 Complications from PPH includes hypovolemic shock and anaemia, blood transfusion may be necessary and carries associated risks. In severe cases, haemorrhagic shock may lead to anterior pituitary ischaemia with delay or failure of lactation (i.e. postpartum pituitary necrosis).8 Acute renal

failure, DIC and death may also occur.9

Prevention of uterine atony is the key for reducing the incidence of PPH. Preventive measure includes active management of 3rd stage of labour which involves- administration of uterotonic agents within one minute after the birth of baby, controlled cord traction, uterine massage after the delivery of placenta.10 Oxytocin, ergometrine, and mis-oprostol are different medical preparations used as uterotonics for prophylaxis and therapeutic management of PPH.11

When there is uterine atonicity, conventional managements like bimanual compression, balloon catheterization is prescribed. When all these measures fail, exploration of the uterine cavity should be done quickly to remove any placental beats or blood clots to make the effective contraction of uterus. In most of the cases, the above mentioned measures will control the bleeding but when proved inadequate and unsatisfactory, various surgical measures like ligation of the uterine artery, bilateral ligation of the internal iliac artery, ligation of the ovarian artery , sometimes B-Lynch suture can be tried. Hysterectomy is used as a last measure to save the life of the patient. Women with a prior PPH have as much as a 10% risk of recurrence in subsequent pregnancy. Thus, it is important to set up a regular protocol and profile for the risk of primary PPH to reduce maternal morbidity and mortality. So, this study gives an insight to the obstetrician about the post partum obstetric care in Bangladesh.

METHODS

This was a descriptive type of cross-sectional study. The study was carried out at North Bengal Medical College Hospital, Sirajganj between January,2014 to December,2015. There were 88 women (69 patients were booked and 19 patients were unbooked)

P


admitted in the hospital during the period with the clinical diagnosis of primary PPH and included those delivered both in the hospital and outside the hospital. These included women managed primarily in the hospital and those referred to the hospital without PPH having delivered at home or other maternity centers. Informed consent was obtained from all patients.

All patients with primary postpartum haemorrhage in the Department of Obstetrics and Gynaecololgy, North Bengal Medical College Hospital after vaginal delivery/ caesarean section were included. Excluded from the study were women with congenital bleeding disorder, patients on heparin/ warfarine Postpartum blood loss in the hospital was based on measurement from a basin, plus a visual estimate of blood on linens and used swabs. The amount was noted on the maternity record at the time of delivery, with the estimate incorporating both measured and estimated amount.

The hospital uses a standardized maternity record from antenatal care, delivery and postnatal care. Data were collected from the maternity record forms of the cases and

controls and entered into a standard data collection form specifically designed for the study. Additional information was obtained individually from the patients when the records were incomplete or when there was the need to confirm the accuracy of the entries. Information was obtained on socio-demographic risk factors, medical and obstetric history, antenatal events, labour and delivery outcomes. The test statistics used were descriptive statistics as appropriate. Ethical permission from ethical committee and appropriate authority was taken.

RESULTS

There were 88 women with primary PPH. Selected sociodemographic characteristics are shown in Table I. Most of the patients belong to 26-30 years of age (42, 47.73%) followed by 21-25 year which is (29, 32.95%). Considering level of education, maximum were primary (56, 63.64%) followed by higher secondary (10, 11.36%) and (9, 10.23%) were illiterate (Table I). Most of the patients were house wife (60, 68.18).

Table I: Socio-demographic characteristics of the patients with PPH

Variables Number Percentage (%)

Age in years

≤20 8 9.09

21-25 29 32.95

26-30 42 47.73 >30 9 10.23 Mean±SD 26.07±4.3 Educational status Illiterate 9 10.23 Primary 56 63.64 Secondary 8 9.09 Higher secondary 10 11.36 Graduate 5 5.68 Occupational status House wife 60 68.18 Service holder 28 31.82


PPH were found to occur mainly in multigravida (42, 47.72%). Some (22,25.0%) of the cases were unbooked and received antenatal care outside the hospital and others (66, 75.0%) of cases had regular antenatal checkup. The

prolonged labour (24, 27.27%) and grand multiparity (20, 22.73%) were the two major risk factors for developing PPH found in this study (Table II).

Table II: Pregnancy and antenatal events


Parity Primi gravid 31 35.23 Multigravida (2-4) 42 47.72 Grand multi (more than 4) 15 17.05 Antenatal booking Booked 66 75.0 Unbooked 22 25.0 Risk Factors Prolonged labour 24 27.27

Grand multiparity 20 22.73

PET/Eclampsia 12 13.64

Multiple pregnancy 11 12.50 Polyhydramnios 10 11.36 Macrosomia 6 6.82

Instrumental delivery 5 5.68

Table III : Mode of delivery

Mode of delivery Number Percentage (%)

Normal vaginal delivery 73 82.95

Instrumental delivery 15 17.05

The majority (73, 82.95%) of the cases were managed by vaginal delivery and remaining (15, 17.05%) were by caesarean section (Table III).

Table IV: Source of haemorrhage in women with primary PPH Variables Number Percentage (%)

Atonic uterus 54 61.36 Retained bits of placenta 12 13.64 Cervical tear 10 11.36 Vaginal tear 7 7.95 Inverted uterus 4 4.54 Ruptured uterus 1 1.14


Table-IV outlines the causes of hemorrhage among the cases. Uterine atony (54,61.36%) was the commonest identifiable cause of PPH. Trauma to the genital tract caused by cervical tear (10,11.36%), vaginal tear (7,7.95%), inverted uterus (4,4.54%) and ruptured uterus (1,1.14%) accounted for nearly quarter of cases.

In this study, most of the patients (67, 76.14%) were managed medically by using medicine and

by giving fundal massage and bimanual compression. Table V shows that (8, 11.94%) of the cases were managed by using only Oxytocin, (28,41.79%) by using Oxytocin+ Ergometrine, (11, 16.42%) by Oxytocin+ Misoprostol and (20,29.85%) by Oxytocin+ Ergometrine Misoprostol.

Table V: Management of PPH patients (n-88)


Medical management (n-67) Only oxytocin 8 11.94 Oxytocin +Ergometrine 28 41.79 Oxytocin +Misoprostol 11 16.42 Oxytocin +Ergometrine+Misoprostol 20 29.85 Surgical management (n-21) Repair of cervical and vaginal tear 10 47.62 Manual removal of placenta 6 28.57 Subtotal hysterectomy 2 9.52 B-Lynch suture 1 4.76 Repair of ruptured uterus 1 4.76 Uterine arteries ligation 1 4.76

Table V shows that maximum of the patients (10,47.62%) were managed by repairing the cervical and vaginal tears. Some (6,28.57%)

patients needed manual removal of placenta and (2,9.52%) patients required subtotal hysterectomy.

Table VI: Outcome of Patients


Maternal complication (n- 88) No complication 50 56.82

Shock 22 25.00 Puerperal sepsis 10 11.36 Acute renal failure 1 1.14 Maternal Death 5 5.86 Cause of maternal death (n-5) Shock 2 40.00 Sepsis 1 20.00 ARF 1 20.00 DIC 1 20.00 Total 5 100.0


Table VI shows (50, 56.82%) patients had no maternal complication but 43.2% had different complications. This study mentioned maternal death in 5 patients among them two was due to shock, and one of each for sepsis, ARF and DIC.

DISCUSSION

Primary postpartum hemorrhage (PPH) is defined as excessive bleeding from the vaginal tract after delivery of a child of more than 500 milliliters within the first 24 hours.12 This is the most common cause of maternal mortality and accounts for 25% of all maternal deaths worldwide. Majority of these deaths 88% occur within first 4 hours of delivery due to events in 3rd stage of labour.13

The demographic profiles of the patients with PPH showed that subjects had a lower age profile with a mean age of 26.07±4.30 years with the highest number of cases 47.73% falling in the 26-30 years of age group. In a study, Naz et al.14 mentioned that most of the cases were over 35 years. But in another study Naz and Hasan15 showed that the highest number of cases fell 43.90% in the 31-40 years age of group. The reason for this young age is the relative increased gravidity and parity at a younger age in our society.

This study showed 35.23% were primipara,

47.72% were multipara and 17.05% were grand

multipara. In another study Rasheed et al.16

found primiparas were 10.97%, 31.70% were

multipara, 34.75% were grandmultipara and

22.56% were more than para 9. Multiparity,

particularly grand-multiparity, has been

specified as a factor predisposing to increased

frequency of PPH by different studies17,18 and

this is supported by this study also. Other

studies reported multiparity has been cited in

many previous studies as an important risk

factor19 and it has been used as an important

clinical marker for PPH by practitioners.

This study showed 82.95% cases of PPH occurred after vaginal delivery. Caesarean section was carried out in 17.05% cases which were performed at different hospitals and clinics. Another study Naz and Hasan15 found 64.63% cases of PPH occurred after vaginal delivery of which (52.83%). Instrumental delivery was 23.17% and caesarean section occurred in 12.20% cases.

Like other studies20 this study also reported uterine atony as the commonest cause of PPH and accounted for 61.36% of the cases. These results are comparable with the study of a researcher who reported a twofold increased risk of postpartum haemorrhage due to uterine atony.21 Another study conducted at Hyderabad Medical Complex in which grand multiparity and obstructed labour were found to be main risk factors for uterine atony playing their role in 50% of the cases.22 Retained placenta (13.64%) was the second most common cause seen in this study. Reason for this observation was that majority of cases seen had their delivery outside the hospitals at home where the third stage was poorly managed.

Uterine atony was the most common cause of PPH in other countries also, the figures varying from 50% to 76%.23 Studies in Pakistan have also mentioned uterine atony as the main cause of PPH, the figure in different studies being 65%, 58% and 34%.17, 21

Naz and Hassan15 in another study also reported that retained placenta accounted for 14.63% cases of PPH. Thirteen (7.93%) cases of PPH occurred following Antepartum Haemorr-hage (APH). PPH due to coagulation disorders was seen in 1.83% cases, 2 due to hepatitis with jaundice, and 1 case due to thrombocytopenia.

This study showed that prolonged labour (27.27%) and grand multiparity (22.73%) were the important risk factors for this study


population. In previously published studies, these risk factors have been reported to be associated with PPH.24 However; other risk factors were PET/Eclampsia, multiple pregnan-cies, polyhydramnios, macrosomia and instru-mental delivery. In another study Sosa et al.21 found risk factors were retained placenta (33.3%), multiple pregnancy (20.9%), macro-somia (18.6%), episiotomy (16.2%), and need for perineal suture (15.0%).

In this study, maximum of the patients (47.62%) were managed by repairing cervical and vaginal tears. Some 28.57% patients needed manual removal of placenta, 9.52% patients’ required subtotal hysterectomy, 4.76% patients treated by repair of ruptured uterus and 4.76% patients needed ligation of uterine arteries. This finding is consistent with other researchers.25, 26 This may be due to the fact that the other studies were carried out at tertiary care hospitals and the majority of the patients were treated with misoprostol. In those cases, they conducted the delivery of the placenta by controlled cord traction rather than doing manual placental removal which may contribute to an insignificant different result.

In this study, maternal death was five and this result was probably due to the prompt and appropriate intervention was taken for the patients in order to prevent mortality due to haemorrhage in a tertiary setting with ready availability of emergency obstetric services. Apart from the mortality, PPH was found associated with maternal morbidities such as increased need of blood transfusion with its accompanying complications, renal failure due to hypovolaemia, disseminated intravascular

coagulopathy, failure of lactation and infertility.

Maternal mortality has been used as a measure of the quality of care. Recently, maternal morbidity has also been taken into account to assess the burden of the diseases. It has been

estimated that PPH increases the risk of morbidity 50 times, and has nearly 5 times higher morbidity than mortality.15, 27

CONCLUSION

This study explored that the common causes of PPH were atonic uterus followed by retained bits of placenta and cervical tear. Therefore, preventive efforts for PPH should be made keeping in mind the above mentioned risk factors.


REFERENCES

1. Michael S. Rogers, Alan M.Z. Chang. Post partum hemorrhage and other problems of the third stage. High Risk pregnancy management options. 3rd ed. Elsevier: 2006: 1560-1565.

2. Stafford I Dildy GA, Clark SL, Belfort MA. Visually estimated and calculated blood loss in vaginal and cesarean delivery. Am J Obstet Gynecol. 2008; 199: 519. e1.

3. Callaghan WM, Kuklina EV, Berg CJ. Trends in postpartum hemorrhage: United States, 1994-2006 Am J Obstet Gynecol. 2010; 202: 353. e1

4. Bangladesh Maternal Mortality Survey 2010, Maternal and Child Health Situation in Bangladesh.

5. Prata N, Gerdts C. Measurement of postpartum blood loss. BMJ. 2010; 340: c555.

6. Koh E, Devendra K, Tan L K. B-Lynch suture for the treatment of uterine atony. Singapore Med J. 2009; 50(7): 693-697.

7. Magann EF, Evans S, Chauhan SP, Lanneau G, Fisk AD, Morrison JC. The length of the third stage of labor and the risk of postpartum haemorrhage. Obstet Gyne-col. 2005; 105: 290-293.

8. Sert M, Tetiker T, Kirim S, Kocak M. Clinical report of 28 patients with Sheehan’s syndrome. Endocr J. 2003; 50: 297-301.


9. Reyal F, Deffarges J, Luton D, Blot P, Oury JF, Sibony O. Severe post-partum hemorrhage: descriptive study at the Robert-Debre Hospital maternity ward [French]. J Gynecol Obstet Biol Reprod (Paris). 2002; 31: 358-364.

10. Lalonde A, Daviss BA, Acosta A, Herschderfer K. Postpartum hemorrhage today: ICM/FIGO initiative 2004-2006. Int J Gynaecol Obstet. 2006; 94: 243-253.

11. Elbourne DR, Prendiville WJ, Carroli G, Wood J, McDonald S. Prophylactic use of oxytocin in the third stage of labour. In: The Cochran Database of Systemic Reviews 2001, Issue 4.

12. Tripop L, Jarunee L, Wiboolphan T. Primary Postpartum Hemorrhage in Siriraj Hospital. Siriraj Med J. 2012; 72: 395-398.

13. Bibi S, Danish N, Fawad A, Jami M. An audit of primary post partum haemo-rrhage. J Ayub Med Coll. 2012; 19(4): 365-369.

14. Naz H, Sarwar I, Fawad A, Nisa AU. Maternal morbidity and mortality and mortality due to primary PPH-Experience at Ayub Teaching Hospital Abbott Abad. J Ayub Med Coll. Abbottabad 2008; 20(2): 59-65.

15. Naz T, Hassan L. Primary postpartum hemorrhage; profile at a Tertiary Care Hospital. J Med Sci. 2010; 18(1): 49-53.

16. Rasheed N, Nasim N, Malik MA. Primary

postpartum haemorrhage; Comparison of effectiveness of misoprostol and synto-cinon in the prophylaxis. Professional Med J. 2010; 17(2): 308-313.

17. Malik S, Naz F. Grandmultiparity- A Continuing Obstetric Risk in Pakistan. J Surg Pakistan. 2001; 6: 29-31.

18. Hazra S, Chilaka VN, Rajendran S, Konje JC. Massive postpartum hemorrhage as a cause of maternal morbidity in a large tertiary hospital. J Obstet Gynaecol. 2004; 24: 519-428.

19. Tsu VD. Postpartum haemorrhage in Zimbabwe: a risk factor analysis. Br J Obstet Gynaecol. 1993; 100: 327–333.

20. Soriano D, Dulitzki M, Schiff E.A prospective cohort study of oxytocin plus ergometrine compared with oxytocin alone for prevention of postpartum haemorrhage’. Br J Obstet Gynaecol. 1996; 103(11): 1068-1073.

21. Shaheen B, Hassan L. Postpartum haemorrhage: A preventable cause of maternal mortality. J Coll Physicians Surg Pak. 2007; 17: 607-610.

22. Feerasta SH, Motiei A, Motiwala S, Zuberi NF. Uterine atony at a tertiary care hospital in Pakistan: a risk factor analysis. J Pak Med Assoc. 2000; 50: 132-136.

23. Japaraj RP, Raman S. Segstakeu Blakemore tube to control massive postpartum hemorrhage. Med J Malaysia 2003; 58: 604-607.

24. Bais JM, Eskes M, Pel M, Bonsel GJ, Bleker OP. Postpartum haemorrhage in nulliparous women: incidence and risk factors in low and high risk women. A Dutch population-based cohort study on moderate (> or = 500 ml) and severe (> or = 1000 ml) postpartum haemorrhage. Eur J Obstet GynecolReprod Biol. 2004; 115: 166–172.

25. Nasreen HE, Nahar S, Mamun MA, Afsana K, Byass P. Oral misoprostol for preventing postpartum haemorrhage in home births in rural Bangladesh: how effective is it?’, Global Health Action. 2011; 4: 70-77.

26. Nisa MU, Zahida, Sadia, Misbah, Nawaz R, Shazia. Prophylaxis of atonic postpartum hemorrhage with misoprostol in underd-eveloped countries. Annals of KEMU 2009; 15: 185-189.

27. Kaul V, Bagga R, Jain V, Gopalan S. The impact of primary postpartum hemorrhage in “near-miss” morbidity and mortality in a tertiary care hospital in north India. Indian J Med Sci. 2006; 60(6). 233-240.


ORIGINAL ARTICLE

Pattern of dermatophyte at Shaheed Ziaur Rahman Medical College Hospital, Bogra, Bangladesh

Muhsina Alam Shaheed,1 Shah Alam,2 Taslima Yasmin,3 Ziaul Ahsan,4 Syed Mohammad Monowar Ali5


Received: 04 February 2017 Accepted: 20 May 2017 Online: www.nbmc.ac.bd Keywards: Dermatophytes, Tinea unguium, Microsporum

ABSTRACT

Introduction: The dermatophytes are a group of fungi that invade and grow in the dead keratin of skin, hair and nails. Dermatophytes are by far, the most prevalent of the 3 major classes of superficial infections.Our aim was to determine the prevalence of superficial cutaneous fungal infections especially dermatophytosis at ShahidZiaur Rahman Medical College Hospital, Bogra, Bangladesh. Methods: A total of 270 specimens were collected from clinically suspected tinea corporis, tinea cruris, tinea capitis, tinea faciei, tinea pedis, tinea manuum, finger and toe onychomycosis and examined by microscopy using 20% KOH and culture on Sabouraud dextrose agar medium. Results: Direct microscopy revealed fungal infections in 150 (55.55%) cases whereas 128 (47.45%) were positive in culture. Commonest age groups were between 21-30 years 93 (34.07%). Incidence amongst male were 152 (56.3%) which is higher than female 118 (43.7%) and male to female ratio being (1:1.29). Majority cases were from low socioeconomic status. Conclusion: This study identifies the epidemiologic trends and the predominant organisms causing dermatophytosis in Bogra, Bangladesh. These data can be used to ascertain the past and present trends in incidence predict the adequacy of our current pharmacologic repertoire and provide insight into future development

1. Assistant Professor, Department of Microbiology, Shaheed Ziaur Rahman Medical College, Bogra 2. Professor Shah Alam, Department of Microbiology, Rajshahi Medical College, Rajshahi 3. Associate Professor, Department of Microbiology, North Bengal Medical College, Sirajganj 4. Associate Professor, Department of ENT, TMSS Medical College, Bogra 5. Associate Professor, Department of Medicine, Shaheed M Monsur Ali Medical College, Sirajganj

Corresponding author: [email protected]. INTRODUCTION

ermatophytosis, also known as ringworm, is a fungal infection of the skin.1 Typically it results in a red, itchy,

scaly, circular rash.2 Hair loss may occur in the area affected.3 Symptoms begin four to fourteen days after exposure.1 Multiple areas can be affected at a given time.4 Dermatophytes are by far the most significant fungi because of their

D



widespread involvement of population at large and their prevalence all over the world.5 The dermatophytes are a group of closely related fungi that have the capacity to invade the keratinized tissue (skin, hair and nails) of humans and other animals to produce an infection, dermatophytosis, commonly referred to as ringworm.2 Infections are generally restricted to the skin and they do not penetrate the deeper tissue or organs of immunocompetent hosts.6

Although the fungi are worldwide today over 200,000 fungal species have been described. Approximately 100 of which are able to cause human mycoses and out of them 41 are dermatophytes.7 Dermatophytosis is an infection of most commonly the Trichophyton genus and less commonly of the Microsporum or Epidermophyton genera.2 Tinea capitis, tinea pedis, and onychomycosis are common dermatologic diseases that may result from such an infection.8 Surveillance for fungal infections is important to define their burden and trends, to provide the infrastructure needed to perform various epidemiological and laboratory studies, and to evaluate interventions. Surveillance systems require the following basic elements: a clear case definition, a defined population, mechanisms for reporting, analyzing and disseminating the data and incentives to conduct surveillance. For fungal diseases, each one of these elements presents distinct challenges.9

Accurate diagnosis of fungal infection is based on clinical findings, microscopic examination and mycological culture. Present study was undertaken to find out the clinical pattern of dermatophytosis and isolation of the most common dermatophyte species and to compare the clinical diagnosis with KOH smear positivity and culture positivity in this part of our country.

METHODS

This is a retrospective study over a period of 1 year from January 2016- December 2016, attending in the outpatient department of Shahid Ziaur Rahman Medical College Hospital, Bogra, Bangladesh. The collections of infected materials were done from a total 270 suspected cases of dermatophytosis patient, age between 1-70 years. Data regarding age and sex duration, types of lesion, socio-economic status of the patient were examined and grouped in different clinical types depending upon the site of involvement. Collection and processing of the sample: Samples were collected from affected lesions. Whenever the patients presented with lesions at clinically different sites, samples were collected from all those sites and each of these were processed and examined individually. Collection of samples from skin: The affected area was swabbed with 70% ethyl alcohol and the active edge of lesion scrape sterilized blunt scalpel. The scrapings were collected from active margin of lesion without injuring the skin surfaces and collected in black paper packet to prevent contamination. Skin Scraping: It was taken by applying a water proof vinyl adhesive tape to affected skin lesion and then this was carried to laboratory by adhering to glass slide in black paper packets. From the nails: The affected nails were swabbed with 70% ethyl alcohol after which the nails were scraped deeply enough to obtain recently affected nail tissue. Nail clippings were also collected in addition to nail scrapings from the lesions whenever it is feasible. From the scalp (hair): The same procedure as mentioned for skin scrapings was followed, in addition few affected hairs were also epilated and collected with the help of scissors, collect the basal portion of hair (hair stub) as the fungus was usually found in this area. The nail clippings and hair samples were cut into small fragments of


1mm in size. Out of the material collected, part of it was used for direct KOH examination and remaining part was used to inoculate onto Sabouraud dextrose agar media with chloramphenicol and cycloheximide, Dermato-phyte test medium (DTM) with supplement to isolate the causative dermatophytes. These three culture media used in our mycology laboratory were obtained as dehydrated media (manufac-turer HiMedia Laboratories, Mumbai) and prepared in-house following stringent quality control measures. DTM is a selective medium recommended for the isolation and cultivation of pathogenic dermatophytic fungi. It is a modific-ation of a commercial formulation made by Taplin et al.10, 11

KOH examination Skin and hair specimens were treated with 20% KOH solution. The preparation was kept at room temperature for 30 mins. Subsequently examination was done under high power objective (40x) of the microscope for branching and septate hyphae.

Culture Skin, hair and nail samples were inoculated after reducing the size of the samples to approximately to 1-2 mm as it was mentioned earlier. Inoculations were done at four sites at well spaced interval onto Sabouraud dextrose agar slants with chloramphenicol (0.05mg/ml) and cyclohexamide (0.5mg/ml).10,12 Inoculations of specimens were also done on Dermatophyte test medium (DTM) slopes for isolating dermato-phytes where mixed pathogens were suspected. The tubes were incubated in incubator at 250c and also at room temperature to achieve good growth of some dermatophytes, which prefer a little higher temperature. The tubes were examined at regular intervals for evidence of fungal growth and were discarded after four

weeks of incubation. Any visible growth on SDA was examined for colony morphology, texture, urea production pigmentation on surface. Microscopic examination of colony was done by doing a lactophenol cotton blue mount to examine the hyphal structure, different vegetative structures formed by hyphae, microconidia, macroconidia and chlamydoco-nidia.13 RESULTS

During 1 year period of study, a total of 270 populations were included irrespective of age and sex. Figure 1 shows male preponderance, which was 152/270 (56.3%). Table I shows the most commonly involved age group in years was 21-30, followed by 31-50 years which were 93 (34.07%) and 56 (20.74%) respectively. Table II shows most common age group for Tinea corporis was 21-30 (60) years and next common age group for Tinea unguium 31-40 (24) years. Table III shows 150 (55.56%) dermatophytes were positive by microscopy. Table IV shows most common isolated dermatophytes was Trichophyton rubram 92 (71.9%).

Figure 1: Gender distribution of cases

160140120100

80604020

0

Num

ber o

f Cas

es

Male Female

Gender of Cases


Table I: Age distribution of dermatophyte infection in the study group

Completed age in years Number of cases (%)

1-10 20 (7.4)

11-20 50 (18.5)

21-30 93 (34.07)

31-40 56 (20.74)

41-50 31 (11.48)

51-60 14 (5.19)

>60 years 06 (2.22)

Total 270 (100)

Table II: Age distribution of different clinical types of dermatophytes

Distribution of patients in different age group in years Clinical types 1-10 11-20 21-30 31-40 41-50 51-60 >60

Tinea corporis

14 29 60 14 20 8 2

Tinea cruris - 7 13 9 4 3 -

Tinea unguium

- 8 12 24 5 3 3

Tinea capitis

4 3 - - - - -

Tinea pedis - 3 5 5 - - 1

Tinea facci - - 3 3 2 2 -

Tinea manum

2 - 1 1 - - -

Total 20 50 93 56 31 14 6

Table III: Comparisons between microscopy and culture positive for dermatophyte

Test Name Microscopy Culture

Positive 150(55.56%) 128(47.4%)

Negative 120 (44.44%) 142(52.59%)

Total 270 (100%) 270 (100%)

Table IV: Isolated species of dermatophytes by culture

Species of Dermatophytes Number (n-128) %

Trichophyton rubram 92 (71.9)

Trichophyton

mentagrophytes

24 (18.8)

Microsporum gypseum 02 (1.6)

Epidermophyton

floccosum

10 (7.8)

Total 128 (100)


DISCUSSION

Dermatophytosis is an infection of keratinized tissue (skin, hair and claws) by one of the three genera of fungi collectively called dermato-phytes-Epidermophyton, Microsporum and Tric-hophyton. Most superficial fungal infections are easily diagnosed and readily amenable to treatment.14 The prevalence of dermatophytosis among male 56.3% was higher than the female 48.7% (Figure 1) and male female ratio was 1.29:1, which was similar to Rumana et al.15

Males are more likely to be infected compared to females. The probable factors may be increased sweating in outdoor physical activities but our study shows the ratio of male and female was slightly lower than previous study.16 It may be due to involvement of the outdoor activities of the females. All age groups were suspected for dermatophytes but in this study more involvement were found among 21-30 years which was 37.7%, followed by 31-40 years 20.74%. Tinea corporis 54.44% was commonest clinical type encountered in age group of 21-30 years, which was more common in male. Tinea unguium was the second most common clinical type mainly age group 31-40 years and was most common in female as they were engaged mostly with household activities like washing, cleaning, cooking etc. Tinea capitis was more in 1-10 years which was more than other studies.9 It may be due to less secretion of sebum that has antifungal activity. Tinea pedis was seen in 5.19% cases both in of 21-30 years and 31-40 years age group but in other studies the incidence was 7.5%.17 Direct microscopic examination of hairs or skin scrapings may enhance clinical suspicion by demonstrating characteristic hyphae or arthrospores in the specimen.9 In this study, 150 (55.6%) cases were positive by microscopy, which is higher than another studies,18 where it ranged from 32.8%-37.5% but lower than some studies

where it ranged from 76-85%.18 Culture positivity rate was 47.4% which compared to the rate varying from 30.3%-53.05% in other studies.9,19 An ELISA for the sero diagnosis of canine dermatophytosis had been researched. The sensitivity and specificity is high and similar to that of fungal culture with DTM, but positive results can be seen after elimination of the dermatophyte infection.20 These different reports may be due to difference of climate, personal hygiene, food habit and standard of living. CONCLUSION

Further investigation over the course of several years will be needed to determine whether these changes reflect a continuing trend. Limitation: In this study, sample size is relatively small size and period of time may be extended to get the actual picture of dermatophytosis. Acknowledgements: The authors are thankful to the department of Microbiology, Shaheed Ziaur Rahman Medical College, Bogra, Bangladesh.

Conflicts of Interest There is no conflict of

interest.

REFERENCES

1. Rippon JW. Medical Mycology, 3rd ed. Philadelphia. London: Lea and Febiger; 1992

2. Weitzman I. Summerbell RC. The dermatophytes. Clin.Microbiol. Rev. 1995; 8(2): 240-259.

3. Aste N, Pau M, Aste N, Biggo P. Tinea pedis observed in Cagliari, Italy, between 1996 and 2000. Mycoses.2003; 46: 38-41.

4. Hiruma M, Shiraki Y, Nihei N, Hirose N, Suganami M. Questionnaire investigation of incidence of Trichophyton tonsurans infection in dermatology clinics in the Kanto area. Jpn J Med Mycol. 2005; 46: 93-95.


5. Pierard GE, Arrese JE, Pierard-Franchimont C. Treatment and prophylaxis of tinea infections. Drugs. 1996; 52(2): 209-224.

6. Sohnle PG. Dermatophytosis, fungal infection and immune response in Immunology of the fungal diseases. In: Cox RA, Boca Raton FL, CRC press; 1989: p. 27-47.

7. Liz J. Dermatophytes-The skin eaters. Mycologist.2003;17(4): 147 149.

8. Gupta AK, Ryder JE, Chow M, Cooper EA. Dermatophytosis: the management of fungal infections. Skin med. 2005; 4(5): 305-310.

9. Foster KW, Ghannoum MA, Elewiki BE. Epidemiologic surveillance of cutaneous fungal infection in United States from 1999 to 2002. J Am Acad Dermatol. 2004; 50: 748-752.

10. Madhavi S, Rama MV, Jyothsna K. Mycological study of dermatophytosis in rural population. Ann. Biol Res. 2011; 2(3): 88 -93.

11. Taplin D, Zaias G, Rebell H. Superficial noninflammatory lesions of the feet: Demonstration in sections of a fungus of the genus Actinomyces . Dermatol. 1969; 9: 203- 209.

12. Emmons CW, Bindford CH, Utz JP, Kwon-Chung KL. Dermatophytoses, In: Medical Mycology, 3rd ed. Philadelphia: Lea & Febiger; 1977: p. 117–167.

13. Cheesbrough M. “District laboratory practice in tropical countries.” Part 2. UK: Cambridge University Press; 2006: p. 137-150.

14. Clayton YM. Clinical and mycological diagnostic aspects of onychomycoses and dermatomycoses.ClinExpDermatol. 1992; 17: 37-40.

15. Mochizuki T, Tanabe H, Kawasaki M, Anzawa K, Ishizaki H. Survey of Trichophyton tonsurans infection in the Hokuriku and Kinki regions of Japan. Jpn J Med Mycol. 2005; 46:99-101.

16. Rahim MR, Saleh AA, Miah MRA, Anwar S, Rahman MM. Pattern of dermatophyte in Bangabandhu Sheikh Mujib Medical University. Bangladesh J Med Microbiol. 2012; 06(02): 11-17.

17. Rashidul M, Rahman S, Awal AA, Sadik MH, Rahman MA, Shukur A. A Study on Pattern of Dermatophytosis at Shahid Ziaur Rahman Medical College and Mohammad Ali Hospital, Bogra. J Shahid Ziaur Rahman Med Coll. 2004; 8 (1): 31-33.

18. Siddique MA, Alam S, Ahmed AA, Haque JA, Yusuf MA, Naz S, et al. Diagnosis Of Dermatomycoses by Microscopy and Culture. J Shahid Ziaur Rahman Med Coll. 2010; 15 (1):6-9.

19. Walke HR, Gaikwad AA and Palekar SS. Clinico-mycological profile of dermato-phytosis in patients attending dermatology OPD in Tertiary Care Hospital, India. Int J Curr Microbiol App Sci. 2014; 3(10): 432-440.

20. Jahromi SB, Khaksar AA. Aetiological agents of tinea capitis in Tehran (Iran). Mycoses. 2006; 49: 65-67.


REVIEW ARTICLE

Effectiveness of Oral Examination as an Assessment Method in Medical Education

*S M Akram Hossain,1 S M Mosaddeq Hossain2

ARTICLE INFO Article history: Received: 19 September 2017 Accepted: 08 November 2017 Online: www.nbmc.ac.bd Keywords: Assessment methods, Medical education, Oral exam

ABSTRACT An oral Examination is a form of assessment where a set of stimulus questions are developed that address critical areas of knowledge or sets of abilities related to a competency or set of competencies. Students are expected to respond verbally in their own words, which allow an assessment of student’s depth of comprehension, and capacity to apply knowledge and insights to different situations. Responses to the questions are assessed using a rating scale or scoring system. In practice, oral exams were used not as a substitute, but as a complement to written exams. They are a way to ask what is not feasible through the written format. Traditional oral examination has been changed to structured form to ensure greater reliability. Even then, teachers are not yet building up to conduct oral exam in such a structured way. Examiners differ in their personality, style and level of experience with variation of questioning and scoring from student to students. Weakness of reliability on oral examination still exists. Students also feel very stressful during the oral examinations. Two concepts are important to appreciate about the methods used for assessment. It must be valid, namely that what is measured truly reflects the trainee’s ability. Second, a method should be reliable so that if repeated multiple times with the same resident the results are consistent. Worlds’ leading medical schools now-a-days used oral examination only for borderline and distinction students. Substantial work, however, is needed to develop the prevailing oral exam into a ‘best practical oral’ format appropriate for medical education.

1. Professor, Department of Anatomy, North Bengal Medical College, Sirajganj 2. Resident, Department of Pathology, Rajshahi Medical College, Rajshahi


INTRODUCTION

n assessment is defined as to include all activities that students undertake in the classroom that can be used to modify

students’ learning. It also include observation of students made by teachers in the classroom discussions, analysis of work done by students in classroom, homework tasks and tests.1

Competence in medical science is defined as “the

habitual and judicious use of communications, knowledge, technical skills, clinical reasoning, emotions, values, and reflection in daily practice for the benefit of the individuals and communities being served”.2,3 Competence is not an achievement but rather a habit of lifelong learning3 and it is contextual, reflecting the relationship between person’s abilities and the tasks he or she required to perform in a particular

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situation in the real world.4 Medical educators around the world have successfully used many methods of assessing learners, both written and oral.5 The oral method of assessment was defined by Joughin as an “assessment in which a student’s response to the assessment task is verbal, in the sense of being expressed or conveyed by speech instead of writing”.6 He also pointed out that oral examinations enable two qualities to be measured: student command of the oral medium, and a student’s command of content.6 Teaching and learning are mutual procedures that influence each other and assessment determines both students and teachers efforts.7 The purpose of assessment is to meet the public expectation about the quality graduates, to give feedback to the educational stakeholders about the curriculum, to differentiate the students practical ability according to their efficiency and to monitor their own learning. Assessment also provides a high degree of fairness and objectivity in testing and produces data to enable continuous quality improvement.8 The welfare and indeed the future health of people depend on the quality of medical graduates and the quality of medical graduates depends on effectual medical education. Educationists believe that, simply by changing the assessment style for the learners can affect the way of engagement of students with the subject contents.9 Assessment drives learning and learning drives practices. This review aimed to highlight the prevailing oral assessment pattern and to suggest further changes in its system in order to produce competent medical practitioners to meet the health needs of the community.

Assessment tools

Assessment tools comprise a wide range of instruments and methodologies designed to gather this information for feedback, diagnostic purposes, and identifying successful attainment of competence. The utility or usefulness of an assessment has been defined as a product of its validity, reliability, cost-effectiveness, accepta-bility and educational impact.10

Validity

Validity “is the degree to which a test ‘truly’ measures what it is intended to measure”. Validity is the “first priority of any assessment”.11

Validity essentially deals with the design aspect of an assessment. An assessment should fulfill the objective for which it is designed. The objective of the assessment is to facilitate a student’s capacity to demonstrate the knowledge, skills and they acquire in relation to the subject being assessed.

Types of validity

Content validity

It measures the extent to which the content of the test matches the instructional objectives. For example, if the final exam includes content covered only during last six weeks, it is not a valid measure of the course’s overall objectives, that is, it has a very low content validity.10, 11

Criterion validity

It determines the extent to which scores on the test are in agreement with (concurrent validity) or predict (predictive validity) an external criterion. For example, if the end-of-year final exams in a university correlate highly with the national competitive exam, they would have concurrent validity.10, 11

Construct validity

It determines the extent to which an assessment corresponds to other variables, as predicted by some rationale or theory. If you can correctly hypothesize that English for speakers of other languages (ESOL) students will perform differently on a reading test than English-speaking students (because of theory), the assessment may have construct validity.10, 11

Reliability

Reliability relates to consistency in measurement, that is, scores derived from a reliable assessment tool are similar across assessment events.


Reliability is of central importance in assessment because trainees, assessors, regulatory bodies and the public alike want to be reassured that assessments used to ensure that students are competent enough and would reach the same conclusions if it were possible to administer same test again on the same student in the same circumstances. Reliability is typically reported as value ranging from 0.0 to 1.0. Reliabilities above 0.90 are considered to be excellent, Reliabilities below 0.70 are considered suspect, and results from such an assessment tool should be interpreted with caution.10

Types of reliability

Inter-rater or inter-observer reliability

It is used to assess the degree to which different raters/observers give consistent estimates of the same phenomenon. It can be calculated by measuring the percent of agreement between the raters, or calculating the correlation between the ratings of the two observers.13

Test-retest reliability

It is used to assess the consistency of a measure from one time to another, given same assessment twice, separated by days, weeks, or months. Reliability is stated as the correlation between scores at Time 1 and Time 2.13

Parallel-forms reliability

It is used to assess the consistency of the results of the two tests constructed in the same way from the same content domain. To measure, create two forms of the same test (vary the items slightly). Reliability is stated as correlation between the scores Test 1 and Test 2.13

Internal consistency (Alpha,a)

It assesses the consistency of the results across items within a test. Compare one half of the test to the other half. Or, use methods such as Kuder-Richardson Formula 20 (KR20) or Cronbach’s Alpha. Coefficient alpha and KR-20 both represent the average of all possible split-half

estimates. The difference between the two arises when they would be used to assess reliability.13

Relationship between reliability and validity If a test is unreliable, it cannot be valid. For a test to be valid, it must be reliable. However, because a test is reliable does not mean it will be valid. Hence, reliability does not imply validity. In terms of accuracy and precision, reliability is analogous to precision, while validity is analogous to accuracy.5,6,10,11,13

Effectiveness of oral Exams

The oral exam format enables instructors to test the students on all five cognitive domains of Bloom’s taxonomy (Figure 1).14

Figure 1: Cognitive Domains of Bloom’s Taxonomy

Oral exams thus cover several cognitive domains and also the psychomotor skill of oral expression. In practice, oral exams are used not as substitute, but as a complement to written exams. Oral Examination enables interactive dialogue between candidate and assessor, allowing the examinee to demonstrate strengths between superficial and real knowledge via in-depth questioning and also the ability to modify the questions asked to the needs of each individual candidate.15 This form of assessment is well suited for the evaluation of reflective and critical thinking competencies along with problem-solving abilities and analytic abilities. Oral exams also have the potential to measure the student’s


achievement in course outcomes not restricted to knowledge, but related to individual’s professionalism, ethics, interpersonal compe-tence and qualities.16

Recommendations for increasing the effecti-veness of oral exams

Orient the students

The candidates should be informed about the examination process in advance. The recommended preparatory techniques such as guidance from the supervisor, clearly defined guidelines, and mock oral exams can reduce students’ stress levels.17

Train the examiners

Examiner performance can be enhanced by appropriate guidelines and instructions and training of new examiners. It may produce more uniform delivery of questions and evaluation of performance. Formal training programs can be adopted to increase both validity and reliability of oral examinations. Despite concerns about the subjectivity of oral exams, a longitudinal study of oral practice examination within medical programs revealed substantial internal consis-tency and reliability of orals, identifying a positive correlation to in-training examination scores and evaluation scores.18, 19

Use multiple assessors

Norman suggested that the oral examination must sample more broadly across cases and examiners to enhance reliability and scope of feedback.20

Assess on multiple occasions

Use a number of orals to enhance reliability and perceptions of fairness and accuracy

Questions should be straightforward and clear

Questions should be capable of being asked in a few sentences which are clear, unambiguous, uncomplicated, and without repetition.

Use simple grading system or rubrics

Criteria for answers can provide clear guidelines on what is not an acceptable answer to the

examiner’s questions. Checklists have been suggested as mechanism to reduce the variability in content of questions and grading. It may be that: “the more rigid the structure of oral the higher the reliability”.21 Examiners ratings of each student can be summated to give a score out of 60, which can then be converted to a percentage contribution reflecting his or her performance for this assessment component.22

Structure the oral on clinical scenarios

Structured oral examination (SOE) based on a clinical case with well-defined goals can often give great insight into a candidate’s knowledge, interpretive ability, problem solving and attitudes thereby improving the inter-rater reliability results. Most authors agree that SOE has better validity and reliability, with less susceptibility to gender or cultural bias than unstructured examinations.23

Establish quality assurance standards

It is highly recommended to implement stand-ards, benchmarks, performance indicators for effective oral examinations.24

CONCLUSION

Single assessment does not fulfill all aspects of assessment and there is a need for an evaluation system with multiple ways of assessment. Examiners differ in their personality, style and level of experience with variation of questioning and scoring from student to students. So, weakness of reliability on the oral examination still exists. Now-a-days worlds’ leading medical schools used oral examination only for borderline and distinction students. Considering all these challenges, current assessment practices would be enhanced if the following principles summarized below were implemented:

The content, format, and frequency of assessment, as well as the timing and format of feedback, should follow the specific goals of the medical education program.

Proper orientation and faculty developmental activities are essential.


The various domains of competence should be assessed in an integrated, consistent and longitudinal fashion with the use of multiple methods and provision of frequent constructive feedback.

Educators should be mindful of the impact of assessment on learning, the potential unintentional effects of assessment, the limitations of each method (including cost), and prevailing traditions of the program or institution in which the assessment is occurring.

Multiple methods of assessment imple-mented longitudinally can provide the data that are needed to assess trainees’ learning need and to identify and remediate suboptimal performance by clinicians.

The consistency and comparability of assessments methods should be maximized through a quality assurance system.

Educators also face the challenge of developing tools for the assessment of qualities such as professionalism, teamwork, and expertise that have been difficult to define.


REFERENCES

1. Black P and Williams D. “assessment and classroom learning.”Assessment in Education. 1998; 5(1): 7-74.

2. Epstein RM and Hundert EM. Defining and assessing professional competence. JAMA. 2002; 287: 226-235.

3. Leach DC. Competence is a habit. JAMA. 2002; 287: 243-244.

4. Klass D. Reevaluation of clinical competency. Amm J Phys Med Rehabil. 2000; 79: 481-486.

5. Epstein RM. Assessment in medical education. N Engl J Med. 2007; 356: 387-396.

6. Joughin G. Dimensions of oral assessment. Asses Eval High Educ. 1998; 23: 367-387

7. Kellough RD and Kellough NG. Secondary School Teaching: A Guide to Methods and Resources; Planning for Competence. 1999. Prentice Hill, Upper Saddle River, New Jersey.

8. Amin Z. Purposeful assessment. Medical Education. 2012; 46: 3-12. http://dx.doi.org/10. 1111/j. 1365-2923. 2011. 04170. x PMid: 22150188.

9. Salam A, Rabeya Y, and Mahmood CB. Assessment in Medical Education. JCMCTA; 15 (1&2): 15-18.

10. Van der Vleuten C. The assessment of professional competence: Developments, research and practical implications. Adv Health Sci Educ. 1996; 1: 41-67.

11. Newbel DA. Handbook for Medical Teachers. In: Norwell, 2nd ed. Boston, Massachusetts: MTP Press: 1987.

12. Memon MAG, Joughin and Memon B. “Oral assessment and postgraduate medical: establishing conditions for validity, reliability and fairness”. Advances in Health Sciences Education. 2008.

13. Rousson V, gasser T and Seifer B. Assessing intrarater, interrater and test-retest reliability of continuous measurements. Stat Med. 2002; 21: 3431-3446.

14. Bloom BS. Taxonomy of Educational Objectives, Handbook I: The Cognitive Domain. New York: David McKay Co Inc; 1956.

15. Gibbs H, Habeshaw S and Habeshaw T. Interesting Ways to Teach: 53 Interesting Ways to assess your students. Bristol: Technical and Educational Services; 1988.

16. Harden RM. Developments in outcome based education. Med Teach. 2002; 24: 117-120.

17. Tinkler P and Jackson C. In the dark? Preparing for the PhD viva. Qual Assur Educ. 2002; 10: 86-97.

18. Birley H. The Society of Apothecaries Diploma Examination in Genitourinary Medicine: death of the viva voce? Sex Transm Infect. 2001; 77: 223-224.


19. Iqbal IZ, Naqvi S, Abeysundara L and Narula AA. The value of Oral Assessments: A Review. Bull R Coll Surg Engl. 2010; 92: 1-6.

20. Norman G. Examining the examination: Canadian versus US radiology certification exam. Can Assoc Radiol J. 2000; 51: 208-209.

21. Muzzin LJ and Hart L. Oral examinations. In: Neufeld RV, editor. Assessing Clinical Competence. New York: Springer Publishing Co; 1985.

22. Pearce G and Lee G. Viva voce (oral examination) as an assessment method insight from marketing students. J Mark Educ. 2009; 31: 120-130.

23. Simpson RG and Ballard KD. What is being assessed in the MRCGP oral examination? A qualitative study. Br J Gen Pract. 2005; 55: 430-436.

24. Morley L, Leonard D, and David M. Quality and equality in British PhD assessment. Qual Assur Educ. 2003; 11: 64-72.


CASE REPORT

Syringomyelia with Unusual Presentation

*Tapashi Rahman Khan,1 Md. Faruk Hossen,2 Md. Rafiqul Islam,3

Md. Abdul Hamid,4 Shamim Adom5


Received: 08 September 2017 Accepted: 14 October 2017 Online: www.nbmc.ac.bd Keywords: Syrigomyelia, Syrinx, Arachnoid cyst, Arnold-Chiari.

ABSTRACT Patients with syringomyelia may have diverse aetiology and experience a variety of symptoms, the commonest presentation is dissociated sensory loss affecting pain and temperature sparing touch and vibration sensation which is suspended over the nape of the neck, shoulders, and upper arms. This report describes two cases of syringomyelia with different profiles in that they presented with dominant motor deficits.

1. Assistant Professor, Department of Radiology and Imaging, Dhaka Community Medical College, Mogbazar, Dhaka

2. Registrar, Department of Medicine, Shaheed Ziaur Rahman Medical College Hospital, Bogra 3. Professor, Department of Medicine, North Bengal Medical College, Sirajganj 4. Registrar, Department of Medicine, North Bengal Medical College Hospital, Sirajganj 5. Professor, Department of Orthopaedics, North Bengal Medical College, Sirajganj


INTRODUCTION

yringomyelia is a rare neurological disorder characterized by slowly developing central fluid-filled areas (cyst or syrinx) that usually

involve the cervical spinal cord and expand as well as extend downwards causing progressive damage to the spinal tracts. Classic presentation is a central cord syndrome with dissociated sensory loss showing loss of pain and temperature sensation sparing touch and vibration suspended over the nape of the neck, shoulders, and upper arms in a cape distribution or is in the hands. Muscle wasting in the lower

neck, shoulders, arms, and hands with asymmetric or absent reflexes reflects extension of the syrinx to the anterior horns.1-4 More than half of all cases are associated with Arnold-Chiari type I malformations in which the cerebellar tonsil protrudes through the foramen magnum and into the cervical spinal canal.5-7 Syringomyelia has a prevalence of 3.3 to 8.5/100,000 people with some ethnic variability.1-4 In the United States, syringomyelia is more common in African-Americans than in Caucasians.8 It occurs more frequently in men than in women and usually manifests in the third or fourth decade of life. Rarely, syringomyelia may develop in childhood

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or late adulthood. Loss of pain sensation is the most common early neurological manifestation in syringomyelia with Chiari-1 malformation.9

The presenting two cases are unusual in that, they had pain and temperature sensations intact rather with features of dorsal column and pyramidal tract lesions which could otherwise suggest a diagnosis of slowly developing compressive spinal myelopathy.

Case 1

An 18-year-old male, a university student, came to medicine outpatient department of Dhaka Community Medical College Hospital with limb weakness and gait disturbance for 3 months. In suspicion of cervical myelopathy, spinal X-ray was done and found normal.He was advised for neuroimaging. He is a resident of Sariakandi, Bogra and was later admitted in the department of Medicine, Shaheed Ziaur Rahman Medical College Hospital for the same complaints. He had no complaints of headache, visual disturbance, bladder or bowel dysfunction, fever or joint pain or history of neck trauma. His milestones of physical and mental developments were seemingly normal.

On examination, the patient was ill looking, with normal higher psychic function and speech. Cranial nerves were intact with normal optic fundi. Bulk of the muscle was reduced in both upper limbs with diminished tone, power (4 of 5) and jerks. In both lower limbs, muscle bulk was normal with hypertonia, grade 4 of 5 power and exaggerated deep tendon reflexes, extensor planter response and sustained clonus. Dorsal column sensations (sense of position and vibration) were reduced but pain and temperature sensations were intact in all 4 limbs. Romberg test was positive. Tests for cerebellar functions were normal. There was no spinal deformity. Other systemic examination revealed no abnormality.

Figure 1: MR images showing a large syrinx extending from C2 to D2

Investigations revealed haemoglobin-12 gm/dl, total leucocyte count-8000/mm3 with normal differential counts and erythrocyte sedimen-tation rate-15 mm in 1st hour.Urinalysis, fasting blood glucose level, renal and liver function tests and serum vitamin B12 level were normal. MRI of cervical and dorsal spine (Figure 1) revealed a large syrinx extending from cervico-medullary junction to second dorsal spine without herniation of cerebellar tonsil. With these findings, the case was diagnosed as syringomyelia with unusual presentation.

Case 2

A 35-year-old male, married, normotensive, non-diabetic, farmer hailing from Jamua, Sirajgang, presented with progressive weakness of both upper limbs as well as wasting of muscles in his upper back region for two years. There was no history of bladder or bowel dysfunction. There was no disturbance of sensation. He gave no history of tuberculosis or trauma to the head or spine. There was no history of such illness among other members of his family.

On examination, the patient was conscious and well oriented. Higher psychic functions were normal. There was no abnormality in speech. Cranial nerves were intact. Bulk of the muscle


was reduced in both upperlimbs and upper back of the trunk, which was marked around the shoulder girdle (Figure 2). There was no fasciculation. In both upper limbs, muscle tone was diminished, muscle power was grade3 of 5 and deep tendon reflexes were reduced. In the

lower limbs, muscle tone, power and reflexes were normal.

Figure 2: Photographs (a & b) showing muscle wasting of the shoulder girdle with winging of scapula

Plantar response was flexor in both sides. All modalities of sensations were intact. There were no signs of cerebellar lesion.

Routine investigations and biochemical values viz.urinalysis, complete blood counts, erythrocyte sedimentation rate, fasting blood glucose and serum creatinine, T3, T4 and TSH were all within the normal limits. Plain radiograph of spine was normal. MRI of cervical and dorsal spine (Figure 3) revealed a large syrinx extending from cervical to upper dorsal region.

Figure 3: MR images showing a large cervico dorsal syrinx

DISCUSSION

Syringomyelia is a developmental cavity (syrinx) of the cervical cord that is prone to enlarge and produce progressive myelopathy. Symptoms begin insidiously in adolescence or early adulthood, progress irregularly, and may undergo spontaneous arrest for several years. A number of pathological conditions can cause an obstruction of the normal cerebrospinal fluid (CSF) spaces. These include Chiari malfor-mation, spinal arachnoiditis (post infectious, inflamma-tory, post-irradiation or blood in subarachnoid space), scoliosis, spinal vertebrae misalignment, pathological masses (arachnoid cysts, rheumatoid arthritis pannus, occipital encephalocoele, tumours), spina bifida and others.10,11 The reasons that cause blockage of the CSF space within the subarachnoid space can result in syrinx formation are not known. Moreover, it is unclear if syrinx fluid originates from bulk movement of CSF into the spinal cord, from bulk transmural movement of blood fluids through the spinal vasculature into the syrinx, or from a combination of both. Many young patients acquire a cervical-thoracic scoliosis. More than half of all cases are associated with Chiari type 1


malformations in which the cerebellar tonsils protrude through the foramen magnum and into the cervical spinal canal blocking the flow of CSF. Acquired cavitations of the cord in areas of necrosis are also termed syrinx cavities; these follow trauma, myelitis, necrotic spinal cord tumors, and chronic arachnoiditis due to tuberculosis and other etiologies.

The presentation is a central cord syndrome with dissociated sensory loss in cape distribution or in the hand and areflexic weakness in the upper limbs. Most cases begin asymmetrically with unilateral sensory loss in the hands that leads to injuries and burns that are not appreciated by the patient. Muscle wasting in the lower neck, shoulders, arms, and hands with asymmetric or absent reflexes in the arms reflects expansion of the cavity into the gray matter of the cord. As the cavity enlarges and further compresses the long tracts, spasticity and weakness of the legs, bladder and bowel dysfunction, and Horner's syndrome appear. Some patients develop facial numbness and sensory loss from damage to the descending tract of the trigeminal nerve (C2 level or above). In cases with Chiari malformations, cough-induced headache and neck, arm, or facial pain are reported. Extension of the syrinx into the medulla or syringobulbia causes palatal or vocal cord paralysis, dysarthria, horizontal or vertical nystagmus, episodic dizziness or vertigo, and tongue weakness with atrophy.12

MR imaging accurately identifies developmental and acquired syrinx cavities and their associated spinal cord enlargement. MRI images of the brain and the entire spinal cord should be obtained to delineate the full longitudinal extent of the syrinx, to assess posterior fossa structures for the Chiari malformation, and to determine whether hydrocephalus is present.13

Treatment of syringomyelia is not fully satisfactory. The Chiari tonsillar herniation is usually decompressed, usually by suboccipital craniectomy, upper cervical laminectomy, and placement of a dural graft. Obstruction of fourth ventricular outflow is reestablished by this procedure. If the syrinx cavity is large, some surgeons recommend direct decompression or drainage by one of a number of methods, but the added benefit of these procedures are uncertain, and morbidity is common. With Chiari malformations, shunting of hydrocephalus should generally precede any attempt to correct the syrinx. Surgery may stabilize the neurologic deficit, and some patients improve. Syringomyelia secondary to trauma or infection is treated with a decompression and drainage procedure in which a small shunt is inserted between the syrinx cavity and the subarachnoid space. Alternatively, the cavity can be fenestrated. Cases due to intramedullary spinal cord tumor are generally managed by resection of the tumor. Assessing treatment results is difficult because of the rarity of syringomyelia, variability of presentation and natural history, and the relatively short follow-up in most studies. In one study, half of cases were in clinically stable condition for several years.14 Although an older study had suggested that 20% of patients died at an average of 47 years, mortality rates are likely lower in today's patients as a result of surgical interventions and better treatment of complications.

Conflicts of interest: None

REFERENCES

1. Brewis M, Poskanzer DC, Rolland C, Miller H. Neurological disease in an English city. Acta Neurol Scand. 1966; 42(24): 21-89.

2. Brickell KL, Anderson NE, Charleston AJ, Hope JK, Bok AP, Barber PA. Ethnic differences in syringomyelia in New Zealand. J Neurol Neurosurg Psychiatry. 2006; 77(8): 989-991.


3. Gudmundsson KR. The prevalence of some neurological diseases in Iceland. Acta Neurol Scand. 1968; 44(1): 57-69.

4. Kurland LT. Descriptive epidemiology of selected neurologic and myopathic disorders with particular reference to a survey in Rochester, Minnesota. J Chronic Dis. 1958; 8(4): 378-418.

5. Barnett HJM, Foster JB, Hudgson P. Syringomyelia. Major Probl Neurol. 1973; 1: 13-18.

6. Sotaniemi KA, Pyhtinen J, Myllyla VV. Computed tomography in the diagnosis of syringomyelia. Acta Neurol Scand. 1983; 68: 121-127.

7. Netsky MG. Syringomyelia. A clinical and pathological study. Arch Neurol Psychiat. 1953; 70: 741-777.

8. Tipton AC, Jr., Haerer AF. Syringomyelia in Mississippi. J Miss State Med Assoc. 1970; 11(10): 533-537.

9. Kaneko K, Kawal S, Fuchigami Y, Morita H, Ofuji A. Cutaneous silent period in syringomyelia. Muscle and Nerve. 1997; 20: 884-886

10. Gelabert-Gonzalez M. Intracranial arachnoid cysts. Rev Neurol. 2 004; 39(12): 1161-1166.

11. Ergun T, Lakadamyali H. Multiple extradural spinal arachnoid cysts causing diffuse myelomalacia of the spinal cord. Neurologist. 2009; 15(6): 347-350.

12. Allen CMC, Lueck CJ and Dennis M. Neurological disease. In: Boon NA, Colledge NR, Walker BR. eds. Davidson`s Principles and Practice of Medicine. 20thed. USA: Elsevier Publishing. 2006: p. 1245-1246.

13. Brant WE, Helms CA. Fundamentals of diagnostic radiology, 3rd ed. USA: Lippincott Williams and Wilkins, 2007: p. 626-627

14. Sudo K, Miyazaki Y, Tajima Y. Spontaneous resolution of idiopathic syringomyelia. Neurology. 2002; 58(10): 1576-1577.


CASE REPORT

Rheumatoid Vasculitis

*Syed Mohammad Monowar Ali,1 Md Shahidul Islam Talukder,2

Md Azizul Haque,3 Md Abul Kalam Azad 4

ARTICLE INFO Article history: Received: 08 September 2017 Accepted: 14 October 2017 Online: www.nbmc.ac.bd

Keywords: Rheumatoid arthritis, Rheumatoid vasculitis, Coronary vasculitis

ABSTRACT

Rheumatoid vasculitis (RV) is a protean, destructive inflammatory process that is centered on the blood vessel wall and is associated with substantial morbidity. Diverse and severe manifestation of this rare condition is a big diagnostic and management challenge indeed. This report describes a 47-year-old male who presented with digital gangrene, myocardial infarction and peripheral neuropathy (diagnosed as a case of rheumatoid arthritis with rheumatoid vasculitis admitted into the department of rheumatology BSMMU, January 2013). Patient is now under regular follow up, is being treated with methotrexate and doing well. Studying this case may help to develop insight into rheumatoid vasculitis

1. Associate Professor, Department of Medicine, Shaheed M Monsur Ali Medical College, Sirajganj 2. Assistant Professor, Department of Medicine, Shaheed M Monsur Ali Medical College, Sirajganj 3. Associate Professor, Department of Endocrinology, Shaheed Ziaur Rahman Medical College, Bogra 4. Assistant Professor, Department of Dermatology, Shaheed M Monsur Ali Medical College, Sirajganj *Corresponding author: [email protected]

INTRODUCTION

ystemic vasculitis has been a diagnostic challenge in the areas of clinical medicine and rheumatology for many years. Among

these is rheumatoid vasculitis, a rare and serious complication of rheumatoid arthritis (with an annual incidence of 3.4/million),1 characterized by inflammation of mid-size arteries and capillaries, is associated with a particularly dire outcome, 2-3 with up to 40% of patients dying within 5 years due to organ damage from vasculitis and/or consequences of immuno-suppressive therapy.4,5 RV can be clinically

heterogeneous and can simultaneously affect multiple vascular beds. Clinical manifestations may include deep cutaneous ulcers, peripheral gangrene, vasculitic neuropathy, inflammatory eye disease and visceral infarction, all associated with poor outcomes. Long-standing RA, male sex, smoking, rheumatoid nodules have been associated with an increased risk of RV.6-8

The present case is different in that, the patient had shorter duration of disease (5 years) and even rarer presentation of coronary vasculitis (high lateral MI).9

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The Case Mr A Bari, a 47- year-old farmer from Royganj, Sirajganj, got himself admitted into the department of rheumatology Bangabandhu Sheikh Mujib Medical University (BSMMU), January 2013. He had symmetrical polyarthritis involving small hand and feet joints (for 5 years) with deformity. Presenting complaints were aggravation of joint pain, low grade fever and digital gangrene with severe pain involving 2nd to 5th digits (bilateral) for about 2 months. Few days prior to admission in BSMMU he experienced severe retrosternal chest pain and was diagnosed as a case of acute myocardial infarction (high lateral MI) in National Institute of Cardiovascular Disease (NICVD) and was treated accordingly in that institute, from where he was referred to BSMMU. It may be mentioned that he had no other risk factors for coronary arterial disease except for a, 10 pack year smoking history (and of course, he is a male). He was normotensive, non-diabetic with normal lipid profile and had no family history of premature coronary arterial disease.

On examination, peripheral pulses were okay, dry gangrene with demarcation line on the aforementioned digits were present. Neurological examination revealed mild distal sensory neuropathy with bilateral carpal tunnel syndrome. Examination of other systems revealed no abnormality. Clinical disease activity index (CDAI) score was 52 (very high disease activity, his weight was 53 kg.

Investigations revealed, total count of WBC 16000/mm,3 Neutrophil 70%, ESR 90 mm in 1st hour, liver function test and renal function test were normal. ECG recent MI (high lateral), Echocardiography normal, rheumatoid factor, anti-cylic citrullinated peptide strongly (Anti-CCP) positive, anti-neuclear antibody(ANA)

negative, anti -double stranded (ds) DNA negative, Anti phospholipid antibody negative, perineuclear and cytoplasmic antinutriphil cytoplasmic antibody (P & CANCA) negative.

Referral and opinion from orthopedic department was sought, digital amputation along with head the proximal phalanges under local anaesthesia was done, on four different occasions (last on 19.02.13). Histopathology report was consistent with vasculitis with no immunoglobulin deposits on direct immunofluorescence (DIF).

Among the drugs prescribed, was clopidogrel, aspirin, ramipril, atorvastatin, antibiotics and after wound healing, oral cyclophosphamide (2mg/kg/day), with plenty of water intake, prednisolone (1mg/kg), cotrimoxazole (960 mg) 3 tabs /week, calcium + vitamin D, non-steroidal anti-inflammatory drugs (NSAIDS) and omeprazole. Rituximab (anti CD-20 monoclonal antibody) was not considered, as patient could not afford its cost.

Vaccination against Influenza virus and pneumococcal pneumonia was administered. Patient was under regular follow up, at vasculitis clinic BSMMU. He took cyclophophosphamide for 18 months, gangrene did not appear or recur, neither was there any infection.

Patient is now under regular follow up at rheumatology clinic Shaheed M Monsur Ali Medical College Sirajganj. He had exacerbation of his primary disease (rheumatoid arthritis) and is on methotrexate (MTX), NSAID along with other medication now. He quitted smoking just after diagnosis of the disease. Last visit was a couple of months ago, when was doing well (with CDAI 12) (Figure 1 and 2).


Figure 1: Palmar aspect with a closer look of the gangrenous digits

Figure 2: After digital amputation look of the gangrenous digits

DISCUSSION

Rheumatoid arthritis (RA) is a relatively common chronic inflammatory autoimmune disease that affects men and women of all ages, with worldwide presence. It affects 0.3–2.1% of the world population.10 In addition to joint manifestations, several organs and specific systems can be affected in RA, enabling the onset of various extra-articular manifestations.11 These manifestations are usually observed in individuals with high titres of rheumatoid factor and anti-CCP.12 Rheumatoid vasculitis is one of the most important as well as grave manifestation of RA. The clinical presentation of RV continues to

remain heterogeneous and rare, similar to that reported in older case series.13-15

Rheumatoid vasculitis typically affects small and medium-sized vessels, with associated sensory peripheral neuropathy (often motor), deep cutaneous ulcers, digital gangrene, nail bed infarcts and palpable purpura. CNS vasculitis, mesenteric vasculitis, scleritis/episcleritis, pulmonary angitis, necrotizing glomerulonephritis are rare presentation. The most common manifestation of RV is cutaneous vasculitis (as much as 90%), followed by neurologic (peripheral neuropathy, around 40%).8-9 Mononeuritis multi-plex may also occur. Mononeuritis multiplex has three clinical hallmarks: asymmetry, asynchrony, and a predilection for distal nerves. Motor mononeuritis multiplex may cause a devastating loss of function of the hands and feet, requiring assisted devices for feeding and leg braces (ankle-foot orthoses) for ambulation. Although cases of coronary vasculitis are well-documented in the medical literature, myocardial infarctions that are the direct result of coronary arteritis in RV are rare.16-18 All except superficial cutaneous lesions are associated with poor outcome.

RV typically occurs in patients with longstanding, joint-destructive RA. In one study, the mean duration between the diagnosis of RA and the onset of vasculitic symptoms was 13.6 years.9

Presentations of RV within five years of the RA diagnosis are very unusual. Patients with RV nearly always have rheumatoid nodules and are typically strongly positive for rheumatoid factor.19 RV usually develops at a time when the inflammatory arthritis is “burned out”. Treatment of RV depends on the extent and the type of organ involved. Isolated nail fold vasculitis has a low risk for progression to systemic vasculitis and may be treated symptomatically without resorting to immunosuppressive therapy. Opportunistic infection should be excluded in RA


patients who appear to have developed RV before the initiation of more intensive immune suppression. Disseminated herpes zoster has been described as a mimic of RV in immune suppressed RA patients.

Systemic RV has a poor prognosis, should be treated with immunosuppressive therapy. Rituximab (375 mg/m 2 weekly times four doses) plus high-dose glucocorticoids (1-1.5 mg/kg body weight) are recommended first line treatment option for severe RV. This treatment is appropriate for patients with severe visceral involvement, including deep cutaneous ulcers, vasculitic neuropathy, scleritis, digital ischemia, and other significant manifestations of RV. Combination of daily oral cyclophosphamide (up to 2 mg/kg per day, assuming normal renal function) and high-dose glucocorticoids, can be suitable alternative to rituximab. Azathioprine can be used as maintenance therapy after remission induction with rituximab or cyclophosphamide. Prophylactic therapy against Pneumocystis pneumonia (trimethoprimsulph-amethoxazole) should be provided when patient is on cyclophosphamide and glucoco-rticoids in combination.

The strong encouragement of smoking cessation is important because of the well-established synergy of the risk factor with anti-CCP antibodies in contributing to severe RA.

Conflicts of interest: None.

REFERENCES

1. Ntatsaki E, Mooney J, Scott DGI, Watts RA. Systemic rheumatoid vasculitis in the era of modern immunosuppressive therapy. Rheu-matology (Oxford). 2014; 53: 145–152

2. Erhardt CC, Mumford PA, Venables PJ, Maini RN. Factors predicting a poor life prognosis in rheumatoid arthritis: an eight year prospective study. Ann Rheum Dis. 1989; 48: 713.

3. Turesson C, O’Fallon WM, Crowson CS, Gabriel SE, Matteson EL . Occurrence of extra-articular disease manifestations is associated with excess mortality in a community based cohort of patients with rheumatoid arthritis. J Rheumatol. 2002; 29 (1): 62-67.

4. Puechal X, Said G, Hilliquin P, Coste J, Job-Deslandre C, Lacroix C, et al. Peripheral neuropathy with necrotizing vasculitis in rheumatoid arthritis. A clinicopathologic and prognostic study of thirty-two patients. Arthritis Rheum. 1995; 38 (11): 1618-1629.

5. Voskuyl AE, Zwinderman AH, Westedt ML ,Vandenbroucke JP, Breedveld FC, Hazes. JMW. The mortality of rheumatoid vasculitis compared with rheumatoid arthritis. Arthritis Rheum. 1996; 39: 266-271.

6. Turesson C, Matteson EL. Vasculitis in rheumatoid arthritis. Curr Opin Rheumatol. 2009; 21 (1): 35-40.

7. Turesson C, O’Fallon WM, Crowson CS, Gabriel SE, Matteson EL. Extraarticular disease manifestations in rheumatoid arthritis: incidence trends and risk factors over 46 years. Ann Rheum Dis. 2003; 62: 722-727.

8. Watts RA, Carruthers DM, Symmons DP, Scott DG. The incidence of rheumatoid vasculitis in the Norwich Health Authority. Br J Rheu-matol. 1994; 33: 832-833.

9. Scott DG, Bacon PA, Tribe CR. Systemic rheumatoid vasculitis: a clinical and laboratory study of 50 cases. Medicine.1981; 60: 288-297.

10. Fauci AS, Braunwald E, Kasper DL, Hauser SL, Longo DL, Jameson JL, et al. Harrison’s principles of internal medicine. 17thed. New York: McGraw-Hill; 2008.

11. Mclnnes IB, Schett G. The pathogenesis of rheumatoid arthritis. N Engl J Med. 2011; 365: 2205–2219.

12. Mongan ES, Cass RM, Jacox RF, Vaughen JH. A study of the relation of seronegative and seropositive rheumatoid arthritis to each other and to necrotizing vasculitis. Am J Med (Rochester, NY). 1969; 47:23–35

13. Bywaters EG, Scott JT. The natural history of vascular lesions in rheumatoid arthritis. J Chronic Dis. 1963; 16: 905-914.


14. Schmid FR, Cooper NS, Ziff M, McEWEN C. Arteritis in rheumatoid arthritis. Am J Med. 1961; 30: 56-83.

15. Wilkinson M, Torrance WN. Clinical background of rheumatoid vascular disease. Ann Rheum Dis. 1967; 26: 475-480.

16. Sokoloffl. The heart in rheumatoid arthritis. Am Heart J. 1953; 45: 635.

17. Cruickshank B. The arteritis of rheumatoid arthritis. Ann Rheum Dis. 1954; 13: 136.

18. Van Albada-Kuipers GA, Bruijn JA, Westedt ML, Breedveld FC, Eulderink F. Coronary arteritis complicating rheumatoid arthritis. Ann Rheum Dis. 1986; 45: 96.

19. Voskuyl AE, Zwinderman AH, Westedt ML, Mieke HJ. Factors associated with the development of vasculitis in rheumatoid arthritis: results of a case-control study. Ann Rheum Dis. 1996; 55: 190.


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1. World Health Organization (WHO). WHO Recommendations: Low Birth Weight: preventing and managing the Global Epidemic. Geneva, Switzerland: WHO, 2000 (Technical Report Series no.894)

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