Proceedings of Ispat General Hospital

Editorial BoardEditor Reviewers

Rabindra N Mohapatra Jaya K Pattanayak

Co-Editors

Paramananda RathPremanand Panda

Executive Editors Nimain C Nanda

Prativa K Behera Prativa K Behera

Rajya B Pattanaik Radha N Satpathy

Sanghamitra Satpathi

International Members Sanjib Mohanty

Lothar Wiese Denmark Saroja K Mishra

Josh Hanson Australia Sudhansu S Pati

Suman Rijal Nepal

National Members

Subhash C Parija Puducherry

Neena Valecha NewDelhi

Subodh Hiran Bhilai

Radha N Satpathy Rourkela

Jaya K Pattanaik Rourkela

Institutional Members Creative consultancy

Jayanta Acharya Sri Ramendra Kumar

Kishore C Mahanta Sri C G Ramalingam

Premananda Panda

Sanjib Mohanty

Saroj K Mishra

Seshadri S Bhattacharyya

Or.Eg.àgmXG.S. PRASAD

Chief Executive Officer MessageI am very happy to learn that ‘Proceedings of Ispat General Hospital’ for the year 2013 is being

published.

Ispat General Hospital, one of the premiere hospitals of the eastern region, has evolved as a Centre

of Excellence over the years. Apart from offering the best medical and health care services, IGH has

also been creating new benchmark in the field of research and medical education. I am happy that the

institution is now attracting post graduate students from all over the country and success rate in this

prestigious examination is at par the national level. Post Graduate Education, Research Work and

Publication in Medical Science go side by side. The section on ‘abstracts of papers published in different

international journals’, epitomizes the high quality research work done in Ispat General Hospital.

Undoubtedly, this has been possible due to excellent laboratories like ‘Anusandhan’ established at IGH

with collaboration of national level laboratories.

I am sure that the ‘Proceedings of Ispat General Hospital’ for the year 2013, will provide a unique

platform for publication of research work as well showcasing of hands-on experience of the doctors of

Ispat General Hospital. At the same time, I hope that the proceedings will provide a good platform for

postgraduate students and young doctors to express themselves. I am also confident that this will find

pride of place amongst other medical journals of repute and reach the medical fraternity not only across

the nation but also beyond its shores.

I extend my hearty congratulations to all the Medical Professionals of Ispat General Hospital who

have contributed to the Proceedings of Ispat General Hospital and wish the publication a grand success.

(GS Prasad)

ha {H$gr H$s {OÝXJr go Ow‹S>m hþAm h¡ gob There’s a little bit of SAIL in everybody’s life

amCaHo$bm-769 011, Amo{‹S>em, Xÿa^mf : 0661-2510018, \¡$Šg : 0661-2511072, do~gmB©Q> : www.sail.co.inRourkela-769011, Odisha, Phone : 0661-2510018, Fax : 0661-2511072, Website : www.sail.co.in

1

Editorial

Ispat General Hospital has grown from a small health centre in 1959 to a full-fledged multi-specialty hospital, and a Post graduate Institute of 2013, and is striding forward.

The hospital became a place of confidence for the patients, the doctors as well as the public. They are our greatest teachers and all of us owe our gratitude to them.

I remember with awe and respect the contributions made by Dr TK Bose in bringing out the initial issues of the Journal- the first of its kind in any steel plant hospital. Under his leadership, the first All India Steel Medical Conference was organized too.

Walking an extra mile, some of the staff became enthusiastic in teaching and research. It has resulted in publications of more than a hundred papers in PUBMED cited journals. Under the guidance of Dr Bhabani S Das, doctors of IGH could go to the height of publishing articles in international journals and being noticed by eminent Professors of Universities of international repute like Oxford and

Cambridge of UK, University of Maryland of the USA, New York University and Universities of France, Germany, the Netherlands, Australia, Thailand etc. I specially mention the name of Dr Jaykrushna Pattnaik (whose article is cited more than 100 times !!!) as our mentors and Dr Sanjib Mohanty, Dr Sudhanshu S Pati, Dr Kishore C Mahanta as my co-authors.

It is a matter of satisfaction and pride that doctors of Ispat General Hospital have contributed in Journals like the Lancet having Impact (I.F.) 39.05, Seminar in Nephrology (I.F.4.5) , Nature, Reviews in Neurology (I.F.15.51), CID (I.F.9.37), JID (I.F.5.85), etc and the WHO- Guidelines for Severe malaria.

I congratulate all the contributors, reviewers and Mr. Ramendra Kumar and his team for the quality publication.

I express my appreciation to the Editor-in-Chief, Dr Rabindranath Mohapatra who is the soul of the Journal and has toiled hard to get the ISSN entry.

Saroj K MishraDepartment of Internal MedicineIspat General Hospital, Rourkela-769005, IndiaCorresponding authore mail: sarojrkl@gmail.com

(Dr S. K. Mishra has 55 PUBMED cited publications to his credit. He initiated the establishment of ‘Anushandhan‘at IGH, a premier research laboratory in collaboration with Department of Biotechnology, Government of India. He is adjunct Professor to the Department of Biotechnology of NIT, Rourkela and a member of ‘Technical Expert group on Management of Severe Malaria’ of WHO, Geneva. While research on Malaria is close to his heart, as an able health administrator he was instrumental in introducing Postgraduate courses in several disciplines in this hospital.)

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Review Article

Introduction : Benign Prostatic Hyperplasia (BPH) seen in elderly men is a complex of three distinct clinical entities of benign prostatic enlargement (BPE), bladder outlet obstruction (BOO) and lower urinary tract symptoms (LUTS).The etiology is poorly understood. The male androgenic steroid dihydrotestosterone (DHT) together with growth factors and other causative factors probably play a major role. Vast literatures are available regarding the pathophysiology, medical therapy, minimal invasive and tissue ablative surgical options for management of BPH. In this article recent literatures are reviewed to present BPH in a comprehensive way for the benefit of surgical residents and practising surgeons.

Key words : Benign prostatic hyperplasia (BPH), Lower urinary tract symptoms (LUTS), α-Blockers, 5α-reductase inhibitors, TURP, Minimally invasive therapy

Incidence : BPH starts after 40 years of age. About 50% prevalence seen by 60 years which rises to 90% by age 85.1 Similarly the bothersome urinary symptoms (LUTS) increase with age.

Pathophysiology : (Fig.1) BPH initiates as proliferation of stromal and glandular cells at the periurethral transitional zone proximal to verumontanum. Although precise cause of BPH not known, androgens, oestrogens stromal-epithelial interactions, growth factors and neurotransmitters may play some role.2

Androgen is required for development of prostate at puberty and aging. Patient castrated before puberty or any genetic disease depriving androgens in men do not develop BPH. In the prostate the enzyme 5α-reductase converts testosterone to DHT which has high affinity towards androgen receptor (AR) protein. This DHT-AR complex initiates cell proliferation by binding to DNA of the nucleus.2 In the elderly though the testosterone level falls due to atrophy of testes, the DHT-AR complex is maintained in high level inside prostatic tissue.

Role of estrogens though not clear in men, in dogs, it is seen to act synergistically to produce experimental BPH.

Growth factors have been suggested to interact with steroid hormones (DHT) altering the balance between cell proliferation and cell death resulting in BPH.3 However the volume of enlargement of prostate does not correlate with the degree of LUTS. The prostatic smooth muscles which contain the α-1A receptors play significant role in increasing the urethral resistance that contributes to LUTS.4

Inflammatory pathways and cytokines have been suggested in causing BPH. Kramer et al published a review of BPH as a potentially auto immune disease.

Figure1. Pathophysiology of BPH

Symptoms : The symptoms collectively known as lower urinary symptoms are of two types-

A) Irritative or Storage Symptoms:

i) Frequency- (>7 times urination a day)

ii) Urgency- Patient has to run for urination

iii) Urge incontinence - urgency followed by leaking of urine before reaching the toilet.

Iv) Nocturia - to get up at night for >1 time to

Amulya M. AcharyaDepartment of SurgeryIspat General Hospital, Rourkela-769005, India.Corresponding authore mail:amulya.acharya@gmail.com

An Overview of Benign Prostatic Hyperplasia

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pass urine.

B) Obstructive or voiding symptoms:

weak stream, straining at the time of urination, hesitancy, intermittency, feeling of incomplete emptying, post voids dribbling.

These symptoms can also be seen in some other non BPH and medical conditions. One has to exclude stricture urethra, detrusor dysfunction of bladder termed as Over Active Bladder(OAB) syndrome, UTI, prostatitis, carcinoma prostate, carcinoma bladder, bladder stones, interstitial cystitis, radiation cystitis, diabetes, Parkinson’s disease, CHF, multiple sclerosis.

Natural History : BPH is a progressive disease and if untreated may lead to complications2 like worsening of symptoms, acute urinary retention(AUR), recurrent UTI, chronic renal insufficiency, bladder stone, incontinence, hematuria.

Figure2.AUA guidelines for management of BPH

Symptom assessment and management : Sixth international consensus guideline for management

of LUTS and the American Urological Association (AUA) guidelines (Fig.2) for management of BPH updated in 2010 are followed for evaluation and management of BPH.5, 6

A detailed medical history is mandatory to rule out causes of LUTS other than BPH. Symptoms are evaluated basing on International Prostate Symptom Score(IPSS) and its impact on quality of life.1 Symptoms are classified into mild (IPSS 0-7), moderate (IPSS 8-19) and severe (IPSS 20-35).

A simple Digital Rectal Examination (DRE) can give information about the prostatic enlargement which can then confirmed by trans-rectal ultrasound. Ultrasound also gives a measurement of Post Void Residual Urine (PVRU) which gives a clue to degree of obstruction to urine flow. In the absence of a large prostate, high PVRU indicates bladder detrussor dysfunction for which additional tests like uroflometry and urodynamic studies may be required to exclude neurogenic bladder.1

Serum PSA : Rise in Sr. Prostate Specific Antigen (PSA) though suggest cancer of prostate, 25% men with BPH may show PSA ≥ 4ng/L. To rule out cancer, free/total PSA ratio, PSA velocity and PSA density should be done.1

Management : 2,6 BPH patients having bothersome symptoms which affect their quality of life need active therapy. Those have mild (IPSS<8) or moderate symptoms (IPSS 8-19) without any bothersome are put on watchful waiting. They can get relief by less fluid intake in night and other life style modification.

Medical Therapy : Medical therapy is required for patients having moderate bothersome urinary symptoms. Single or combined forms of these drugs help in managing these patients.

α-Blockers :4,7 Terazosin, Doxazosin are quite effective but needs dose titration due to vasodilator side effects like postural hypotension, dizziness. Patient should be cautioned while driving or using machinery.

Tamsulosin, Silodosin and Alfuzosin are slow release drugs which are more specific α 1a blockers with less vasodilator side effects. They produce quick symptomatic improvement. However Tamsulosin and Silodosin have higher incidence of retrograde ejaculation which is not seen in Alfuzosin.7

5α-Reductase Inhibitors (5ARIs) : 5ARIs inhibit the α-reductase isoenzyme and prevent conversion

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of testosterone to DHT. This results in reduction in prostate size. Finasterid and Dutasteride are two such drugs available. Dutasteride inhibits both type I and II 5AR isoenzymes producing 90% suppression of DHT as against Finaseride which blocks only type II 5AR resulting in 70% DHT suppression. Both drugs can reduce the prostate size by approximately 25% and reduce PSA to 50% over 3-6 months.8

Anticholinergic (antimuscarinic) drugs :9 These drugs are helpful in controlling the OAB (storage symptoms) associated with BPH and can be added to α-blockers. Available drugs in this group are oxybutinin, tolterodine, darifenacin, solifenacin and trospium.

Combination Therapy : Several Studies including the 5 year MTOPS trial showed that combination of α-blockers and 5ARI are superior to monotheraphy.10 It is further supported by CombAT trial using Tamsulosin and Dutasteride which showed greater improvement in IPSS and Qmax than monotherapy.11

Indications of surgery :

1. Severe bothersome symptoms

2. When medical therapy fails, becomes intolerable due to side effects or too costly and bothersome for the patient.

3. Complications such as acute retention of urine, hematuria, bladder stone, recurrent UTI and deterioration in renal function.

Surgical therapies : Transurethral Resection of Prostate (TURP) is the most thoroughly assessed treatment for BPH and is considered the gold standard treatment. Transurethral Electro Vaporization (TUVP) and Transurethral Incision of Prostate (TUIP) are safe procedures but mostly effective for small prostates. Transurethral Holmiuim Laser Resection or Enunciation and KTP laser prostatectomy are promising alternatives to TURP and effective in large prostates.12

Among newer minimal invasive therapies, Transurethral Microwave Thermotherapy (TUMT) and Transurethral Needle Ablation (TUNA) are less morbid, can be taken up as day care procedure and improve PFR and IPSS. But they are not as effective as TURP. Long term studies are required to prove their efficacy.

Open prostatectomy is now confined to only large prostate glands and where the minimal invasive surgeries are not available.

Water induced thermotherapy and transurethral ethanol ablation of prostate are emerging technologies but their efficacy is unproved.

Summary : BPH is a complex disease producing a host of LUTS .The etiology is poorly understood. The male androgenic steroid DHT together with growth factors, cytokines and other causative factors probably play major role. It is a progressive disease with deterioration of symptoms and affects the quality of life. Patients with mild symptoms require only watchful waiting and others may benefit from medical therapy. α-blockers and 5 α-reductase inhibitors alone or in combination are effective in improving the symptoms. Minimal invasive surgical therapies (MIST) like TUNA and TUMT are superior to medical therapy in long term improvement. Tissue ablative surgeries have definite edge over MIST and medical therapy. Of these, TURP is most thoroughly assessed procedure and taken as gold standard. Laser ablative surgeries are alternative to TURP but are costly.

References :1. Burnett AL, Wein AJ. Benign Prostatic Hyperplasi

in primary care:What you need to know? J Urol 2003;170:530-547.

2. Roehborn CG. Benign prastatic hyperplasia: Etiology,pathophysiology,epidemiology and natural history. In: A J Wein et al.,eds. Campbell - Walsh Urology, 10th edn. Philadelphia: Saunders; 2012.p. 2570 – 2610.

3. C Carson III . Role of dihydro testosterone in Benign Prostatic Hyperplasia. Urology 2003; 61: 2-7

4. Roehborn CG, Schwinn DA. Alfa 1 adren ergic receptors and their inhibitors in lower urinary tract symptoms and Benign Prostatic Hyperplasia. J Urol 2004; 171(3): 1029 - 35.

5. Abraham P, Chapple C, Khoury S et al. Evaluation and treatment of lower urinary tract symptoms in elderly men. J Urol 2009;181 : 1779 – 87.

6. Mc Vary KT, Roehborn CG, Avinis AL, et al. Update on AUA guidelines on management of Benign Prostatic Hyperplasia. J Urol 2011; 185: 1793-803.

7. Roehborn CG. Male Lower Urinary Tract Symptoms (LUTS) and Benign Prostatic Hyperplasia (BPH). Med Clin N Am 2011; 95:87-100.

8. Clark RV, Hermann DJ, Cunningham GR, et al. Marked suppression of Dihydrotestosteron in men with Benign Prostatic Hyperplasia by Dutasteride, a Dual 5 α- Reductase Inhibitor. J Clin Endocrinol Metab 2004; 89: 2179 - 84.

9. Chapple CR,Khullar V, Gabriel Z et al. The effect of anti muscarinic treatment in over active bladder: an update of a systematic review and meta analysis. Eur Urol 2008; 54: 543 - 62.

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10. Mc Conell JD, Roehborn CG, Baustita OM et al. The long term effect of doxazosin, finasteride and combination therapy on the clinical progression of Benign Prostatic Hyperplasia. N Engl J Med 2003; 349: 2387 – 98.

11. Roehborn CG, Siami P, Barkin J et al. The effect of combination therapy with dutasteride and tamsulosin

on clinical outcome in men with symptomatic benign prostatic hyperplasia: 4years results from the CombAT study. Eur Urol 2010; 57: 123 – 31.

12. John M, Fitz Patric. Minimal invasive and endoscopic management of Benign Prostatic Hyperplasia. Campbell – Walsh Urology 10th Edn 2012; vol III: 2655 – 2694.

Instructions for the Authors1. Only online submission (or soft copy) is accepted.

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4. Type of articles - Original article/ Review article -2000 words, Brief reports/view points/case reports- 800 words, guide line of IGH for management of emergency cases 2500 words, article of historical interest -500 words, case reports in Image/ letter to editor -200 words

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Title of manuscript, Full name(s) and department(s), Name, Address, Telephone, and e-mail address of corresponding author (first author), Number of pages, number of figures and number of tables.

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References : 2 most common sources (journal & textbooks) of references are illustrated here.

Journal references

15. Mishra SK, Mohanty S, Satpathy SK, Mohapatra DN. Cerebral malaria in adults - a description of 526 cases admitted to Ispat General Hospital in Rourkela, India. Ann Trop Med Parasitol 2007;101:187-93

16. Singh JK, Bawa M, Kanojia RP, Ghai B, Menon P, Rao KL. Idiopathic simultaneous intussusceptions in a neonate. Pediatr Surg Int 2009;25:445-7.

Book reference

Miyano T, Kobayashi H, Chen SC. Long term results of biliary atresia. In: Gupta DK, editor. Text Book of Neonatal Surgery, 1st edn. New Delhi: Modern Publishers; 2000. p. 288-91.

Citation in the text : In the text, references should be cited as superscript after the punctuation mark.

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Original Article

Abstract : Anaemia occurs frequently among children and pregnant women with Plasmodium falciparum (Pf) malaria. However, the influence of malarial anaemia in adult patients is rarely described. In this study, adult patients with Pf malaria (n=406, M= 265, F= 141) were analyzed. 19 (5%) had severe anaemia (Hb < 5g/dl), 70 (17%) had moderate anaemia (Hb 5 to 8 gm/dl), 184 (45%) had mild anaemia (Hb 8 to 11 g/dl) while 133 (33%) had Hb above 11 gm/dl. Anaemia was frequent among the female patients. 83% female patients and 59% males had Hb < 11 g/dl (p=0.001). Severe anaemia was observed in 9 females and 10 males (p=0.265), moderate anaemia in 34 females and 36 males (p =0.007 ) and mild anaemia in 74 females and 110 males (p=0.034). 41% males and 17% females had Hb > 11gm/dl (p=0.001). 72 had cerebral malaria (GCS≤10), 59 had jaundice (Sr bilirubin > 3mg/dl), 61 had acute kidney injury (Sr creatinine > 3 mg/dl) and 43 died. Mortality was higher among patients with anaemia and Odds ratio of death was 2.32 [95% CI 1.11 - 4.683] at Hb 8 to 11g/dl.

Key words : anemia, death, haemoglobin, malaria, WHO.

Introduction : Several complications may be present in a patient with malaria either alone or in combination.1 These complications also determine the outcome.2 Presentation of malaria differs significantly between adults and children.1,3 While renal failure is seen often in the adults; anemia and seizures occur frequently in the children. Several studies related to cerebral malaria (CM)4, renal involvement,5,6 jaundice or hyperbilirubinemia7 in adults with malaria have been described, but rarely on anaemia.8 Similarly, severe anemia has been studied extensively in children9-11 and pregnant women,12-14 but not on renal failure or jaundice.

Anaemia is one of the common complications in acute Pf malaria. It may be present alone or in association with other complications. The incidence varies from 5 to 15% in different series. In African children, severe anaemia is a life

threatening condition and accounts for most of the deaths along with CM1. But the information regarding anaemia among adult patients and non pregnant women has not received much attention. The incidence/ prevalence of anaemia is not known, nor its influence in the survival been analyzed.

In this study, we report the prevalence of anemia in adult patients with malaria and its influence on mortality.

Materials and Methods: Hospital: Ispat General Hospital, Rourkela is situated in the western part of Odisha, India. This is a referral hospital with 600 beds, facilities like automated blood-cell counter, biochemical auto-analyzer, blood bank, dialysis centre, imaging units like MRI and CT scan, and 11 bed intensive therapy unit. It is a post graduate teaching hospital for eight major specialties at present. It has research collaboration with Universities of USA, UK, Netherlands and Thailand. It is the only hospital in India where a collaborating research laboratory is established with support from NIH, USA and New York University to study Complex malaria in India (CSCMI).

Catchment area : Rourkela is an industrial city of Odisha with approx one million populations. It receives patients from Sundergarh and adjacent districts of Odisha, Jharkhand, Bihar and Chhattisgarh. The catchment areas consist of plain, forested areas, mines and mountainous areas, urban as well as semi-urban and villages. The rain fall is approx 60 to 70” a year. The main transmission time of malaria is July to November and a small peak in February to March.

In the present study all patients (age >14 years) with clinical diagnosis of malaria were admitted to medical wards for further evaluation. Pregnant women and children were excluded from the study. Patients with sickle cell disease, chronic kidney disease & chronic blood loss were also excluded for pre-existing chronic anaemia. The

Redefining severe anemia in adult patients with malaria1Sanghamitra Satpathy, 1Prativa K Behera, 1Aruna M Minz, 2Saroj K Mishra*,1Department of Pathology, 2Department of Internal MedicineIspat General Hospital, Rourkela-769005, IndiaCorresponding author-email:sarojrkl@gmail.com

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patients were evaluated clinically and blood was tested for presence of malaria parasites and hematological & biochemical analysis. Patients with slide positive for Pf malaria or ICT positive were included in the study. Clinical and laboratory data were stored in a computer database. Severity of malaria was defined as per the WHO guideline, viz., in brief, cerebral malaria (GCS < 10), jaundice (Sr bilirubin > 3mg/dl), acute kidney injury (Sr creatinine > 3mg/dl), and severe anaemia (Hb < 5 g/dl).

Statistical analysis : Data was analyzed using Open Epi version2.2.1 (2010) (Emory University, USA). A p value of <0.05 was considered indicative of statistical significance.

Results : We analyzed 406 adult patients with acute Pf malaria to study the influence of malarial anaemia in adult patients. 265 were males with average age 36.53 yrs and 141 female patients with average age 37.96 yrs.

Anaemia : Anaemia was common among the female patients. 83% females and 59% males had Hb < 11 g/dl (p < 0.001). Severe anemia (Hb < 5 g/dl as per WHO criteria) was observed in 6.4 % females and 3.7% males. Mild anaemia (Hb 8 to 11 g/dl) was observed more frequently among the females (52 % vs42 %, p =0.035). Similarly Moderate anaemia (Hb 5 to 8 gm/dl) was noticed in 24% females and 14% males (p=0.007).

Complications : 72 patients had cerebral malaria, 59 had jaundice and 61 had acute kidney injury. There was no difference between males and females in relation to presence of cerebral malaria (p=0.412) and jaundice (p=0.055). But males were more prone for renal failures (p=0.036).

When a patient is anaemic, there is a higher possibility of associated complications and thus increase in the mortality. We compared the patients with different Hb levels, viz., severe anemia, moderate and mild anaemia vis-a-vis complications and mortality.

Severe anemia : We compared all the patients with Hb < 5 (n=19) with those who had Hb > 5 g/dl [n=387]. There were no difference in the two groups, viz., cerebral malaria (p=0.89), Jaundice (p=0.92), acute kidney injury (p=0.87) and even death (p=0.944).

The difference was significant for all patient with Hb < 8 g/dl [n=89] vs Hb > 8g/dl [n=317], viz., cerebral malaria (26 % vs15 %; p=0.023); jaundice (20% vs 13%; p = 0.047), renal failure (31 % vs 10%,

p =0.0001) and death was higher [ p=0.039].

The difference was significant for all patient with Hb < 11 g/dl [n=273] vs Hb > 11g/dl [n=133], viz., cerebral malaria (23 % vs 7 %; p=0.001); jaundice (16.5% vs 11%; p = 0.11), renal failure (19 % vs 6 %,

p =0.001) and death was higher [p=0.033](fig. 1).Figure1. Proportion of patients with complications at various Hb levels

Mortality : Out of 406 patients, 43 expired with overall fatality rate of 10.6%. 5% patients had severe anaemia and they constituted 5% of the deaths; 17% had moderate anaemia and these contributed 30% of the deaths, while 45% had mild aneamia and they contributed 19% deaths. The mortality rate was 6% for patients with Hb above 11 g/dl while it increased steadily to 11% when Hb is between 8 to 11Gm/dl and 19% when it dropped to less than 8G/dl.

The Odds ratio of death for severe anaemia is 0.993 [95% CI 0.150- 3.91], for moderate anaemia 2.32 [95% CI 1.11 – 4.683], and for mild anaemia 1.055 [95% CI 0.554 – 1.998]. It is 0.436 [95% CI 0.184 – 0.941] for Hb above 11g/dl.

In general, associated complications were significantly higher in patients with low Hb. Similarly deaths were proportionately higher in patients with low Hb. We observed that the complications are significantly higher in patients with Hb < 8 gm/dl. The significance does not increase at Hb < 5gm/dl. Rather on the other hand there is no difference in patients having complications or mortality in Hb < and Hb >5gm/dl, thus implying that severe anemia has already influencing before 8gm/dL.

Discussion : Early diagnosis and prompt treatment is the key for the effective management of severe malaria. WHO has defined several complications as components of severe malaria because of the high proportion of fatality, unless utmost attention is given. But it is important to revisit

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the criteria with evidence. Severe anaemia has been historically defined as Hb < 5g/dl. The fatality is high when Hb is very low. The effect of blood transfusion is important in saving lives. But it is not known if blood transfusion at a higher Hb level can save more lives!

There is paucity of data regarding anameia in adult patients with malaria. It is also not known, whether Hb of 5 gm/dl also holds true to this age group.

Anaemia is an important complication of malaria. It is more pronounced in the children and pregnant women, but uncommon in adults and more so among the males. There are very few reports on malaria in adult population.8 The studies from Africa mostly focus on the morbidity and mortality in sub-Saharan Africa. In a recent study from India, it was depicted that children suffer more from anemia and seizures, while adults suffer more from acute renal failure and jaundice.3

Idro et al9 in a study from Uganda reported that the incidence of severe anaemia in children is 19.6%. Rogerson et al13 from Malawi analyzed patients attending an antenatal clinic and found 57.2% of the women were anemic (hemoglobin < 11 g/dl), while 15% had Hb 7.0-8.9 g/dl and 3.2% had Hb<7g/dl. Prevalences of malaria and anemia were highest in the rainy season. Women with moderate/severe anemia had higher parasite prevalences and densities than women with mild/no anemia

Gajida et al14 studied malaria among antenatal clients attending primary health care facilities in Kano state, Nigeria. They observed that anemia, (hemoglobin of <or=11 g/dl) was found in 48.1% (n = 173) patients.

In a report from India, Mishra et al2 have highlighted the importance of anemia in adults where, anemia, renal failure, cerebral malaria and respiratory distress were the four determining factor for survival.

A study from Cameroon5 on adults with malaria mention that of 250 adults examined, the mean haemoglobin level in the study population was 13.16 g/dl±2.21 and the prevalence of anaemia (haemoglobin < 11 g/dl) was 14.80%.

In the present study, we observed that malarial anaemia in not uncommon in adults (both males and females). It occurs in different grades and the morbidity and mortality increase in presence of

anemia, however mild it may be. It needs utmost attention as frequently complications co-exist.

WHO categorizes that severe anemia is considered when Hb is < 5 g/dl. But this study clearly depicts that anemia of any degree is almost always associated with complications. Hb below 8 gm/dl is associated with several other complications and the fatality is high. Malarial anaemia in an adult patient of Hb < 8 gm/dl is as lethal as Hb < 5 in a child or a pregnant woman. All effort should be made to transfuse blood even if Hb is 8 gm/dl.

DECLARATION : All the authors conceptualized the study and collected and analyzed the data. SKM wrote the first draft which was extensively edited and revised by all the authors. The final version is read and approved by all the authors.

Learning points :

a. Malarial Anaemia in not uncommon in adults (both males and females).

b. It is often associated with one or more complications.

c. Prompt attention is needed when Hb < 8 gm in an adult patient with malaria as morality is significantly higher.

Reference :1. WHO, Severe falciparum malaria. Trans. R. Soc. Trop.

Med. Hyg 2000; 94, Supp-1: s/1-s/90.

2. Mishra SK, Panigrahi P, Mishra R, Mohanty S. Prediction of outcome in adults with severe falciparum malaria- a new scoring system. Malaria Journal 2007; 6:24. doi: 10.1186/1475-1875-6-24.

3. Mohanty S, Mishra SK, Pati SS, Pattnaik J, Das BS. Complications and mortality patterns due to Plasmodium falciparum malaria in hospitalized adults and children, Rourkela, Orissa, India. Trans R Soc Trop Med Hyg 2003;97:69-70.

4. Mishra SK, Mohanty S, Satpathy SK, Mohapatra DN. Cerebral malaria in adults - a description of 526 cases admitted to Ispat General Hospital in Rourkela, India. Ann Trop Med Parasitol 2007;101:187-93

5. Mishra SK, Das BS. Malaria and acute kidney injury. Semin Nephrol 2008;28:395-408

6. Mishra SK, Dietz K, Mohanty S l. Influence of acute renal failure in patients with cerebral malaria - a hospital-based study from India. Trop Doct 2007 ;37:103-104.

7. Mishra SK, Pati SS, Satpathy SK, Mohanty S, Mohapatra DN.The influence of hyperbilirubinaemia on malaria-related mortality: an analysis of 1103 patients. Ann Trop Med Parasitol 2004 ;98:555-558.

8. Takem EN, Achidi EA, Ndumbe PM. An update of malaria infection and anaemia in adults in Buea, Cameroon. BMC Res Notes 2010; 30;3:121.

9

9. Idro R, Bitarakwate E, Tumwesigire S, John CC. Clinical manifestations of severe malaria in the highlands of southwestern Uganda. Am J Trop Med Hyg 2005; 72:561-7.

10. Calis JC, Phiri KS, Faragher EB, Brabin BJ, Bates I, Cuevas LE, de Haan RJ, Phiri AI, Malange P, Khoka M: Severe anemia in Malawian children. N Engl J Med 2008, 358:888-899.

11. Nanda NC, Rath P, Acharya J, Mishra P, Mishra SK. Falciparum Malaria in Children-A Brief Report of 305 Patients from Rourkela, Eastern India. Indian J Pediatr. 2011; 78 :475-77

12. Ouma P, van Eijk AM, Hamel MJ, Parise M, Ayisi JG, Otieno K, Kager PA, Slutsker L. Malaria and anaemia among pregnant women at first antenatal clinic visit in Kisumu, western Kenya. Trop Med Int Health 2007 ;12:1515-23.

13. Rogerson SJ, Broek NR van den, Chaluluka E, Qongwane C, Mhango CG, Molyneux ME: Malaria and anemia in antenatal women in Blantyre, Malawi: a twelve-month survey. Am J Trop Med Hyg 2000; 62:335-340.

14. Gajida AU, Iliyasu Z, Zoakah AI. Malaria among antenatal clients attending primary health care facilities in Kano state, Nigeria. Ann Afr Med. 2010; 9:188-93

Editorial Declaration

Copy right of the manuscripts, letters and photographs published in the ‘Proceedings of Ispat General Hospital’ is vested with the contributors of the material. Authors and contributors are free to publish or present their research work anywhere else only under intimation to the editors of this publication.

10

Brief Report

In recent years; vector-borne diseases (VBD) have emerged as a serious public health problem in countries of the South-East Asia Region, including India.1 Nearly half of the world population is infected by vector-borne diseases resulting in high morbidity and mortality. The distribution of the incidence is grossly disproportionate with overwhelming impact in the developing country. Dengue fever (DF), Japanese encephalitis (JE) Chikungunya fever (CF), and West Nile Fever (WNF) are some of the diseases met in clinical practice. Breeding of mosquito, the important vector responsible for the spread of above diseases, are out of proportion due to unplanned urbanization, industrialization and excessive population growth coupled with rural to urban migration. More so, the vector has become resistant to conventional insecticides. Proliferation of engineering projects throughout the country has resulted in eco-system disturbance and enhanced man-mosquito contact. In a recent effort Indian Council of Medical Research (ICMR) wishes to consolidate on tackling vector born viral diseases.2 Diagnosis of viral VBD is relatively difficult in clinical setting and expensive, provision being available at limited places. In the present report we have tried to identify many such suspected cases among hospitalized patients and summarized them for the benefit of the community.

Ispat General Hospital (IGH) under Rourkela Steel Plant, SAIL is a 775 bedded tertiary care general hospital located in the district of Sundargarh. The district is rich in mineral resources and over the last two decades has witnessed rapid industrialization, in particular steel manufacturing. Over a period of 20 years the hospital indoor admission has ranged (declined) from 41452 to 26151. Indoor patients suspected of viral diseases clinically, epidemiologically and by laboratory methods, were subjected to blood and body fluid collection for establishing a diagnosis. Clinical sign symptoms include fever, vomiting, body pain, arthralgia and prostration of acute onset. With these criteria, most of the patients have been selected for test

from medical ward, ICU and pediatric wards. As a result of this varied number of patients has been selected to be tested, ranging from 27 to 146(average 86.2) cases annually.

In all suspected cases blood collection were done in sterile method after due consent and tested for viral diseases in National Institute of Virology, Pune . Results from the testing laboratory were preserved and analyzed. The present reporting is a retrospective analysis of the available results of last 20 years.

YearNumber of Samples

analyzed /yearResult

JE DF WNF CF

1989 42 11 0 0 0

1990 56 2 0 0 0

1991 106 5 0 0 0

1992 27 1 1 0 0

1993 42 11 6 0 0

1994 143 0 6 0 0

1995 48 5 1 0 0

1996 100 1 2 0 0

1998 115 3 21 2 0

1999 53 2 0 0 0

2000 86 2 1 2 0

2001 107 2 0 4 0

2002 74 1 0 0 0

2003 88 4 0 0 0

2004 128 3 3 0 0

2005 135 2 2 0 0

2006 99 0 0 0 0

2007 39 2 0 0 1

2008 146 5 0 0 0

2009 132 3 1 0 0

Total 1766 65 44 8 1

JE=Japanese encephalitis, DF=Dengue Fever, WNF=West Nile Fever, CF= Chikungunya Fever

Table 1. Result of Sample analysis

Over a period of 20 years we have sent for 1766 samples of which 118(6.68%) samples were positive for various diseases such as DF, JE, WNF and CF. These are the vector borne and of public health importance. The distribution shows the

Vector borne viral disease surveillance in hospitalized patients (1989-2009)1Radhanath Satpathy*, 2Nimain C Nanda, 2Pitabas Mishra, 2Paramananda Rath,3Saroj K Mishra1Head, Social Paediatrics and Minority Health, AIPH, Bhubaneswar,2Department of Pediatrics, 3Department of Internal Medicine,Ispat General Hospital, Rourkela-769005,India*Corresponding author- e mail: drsatpathy@rediffmail.com

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endemicity and occurrence of two outbreaks of JE in 1989 and 1993(Table-1). With the help of Public Health Institute, Calcutta necessary community measures were undertaken. Dash et al. reported an incidence of 40% and 17% sera positive for JE and DF respectively from Orissa.3 In the year 1993, 1994 and 1998 the area was affected by DF leading to major morbidity and mortality (Table 1). For the first time DF was reported from Orissa in 1993.4 Cases like encephalitis with serological positive finding for WNF have been reported in 2002 from Maharastra, Rajasthan Goa and Orissa.5 In the present series WNV was in circulation from 1998 to 2001. WNF virus is closely related to JE virus and belongs to same family (Flaviviridiae). WNV produces febrile and menigo-encephalitic illness in human. CF was reported from southern part and western part of Orissa and we had a case during the same year, 2006. Blood samples were collected from different parts of Orissa that showed 40% to 63% positive for CF virus.6

Disease surveillance is the collection, analysis, and interpretation of data to determine disease trends and patterns. Sentinel surveillance is the collection and analysis of data by designated institutions selected for their geographic location, medical specialty, and ability to accurately diagnose and report high quality data. Generally, sentinel surveillance is useful for answering specific epidemiologic questions, but, because sentinel sites may not represent the general population or the general incidence of disease, they may have limited usefulness in analyzing national disease patterns and trends. The present hospital report and trend is by no means being considered as a national trend of such diseases.

To conclude, the industrial city Rourkela is prone to vector borne diseases and is endemic for

Japanese Encephalitis. Fifty percent of the years showed Dengue positive samples. Chikungunya was only found in 2007. West Nile virus was in circulation from 1998 to 2001. The present sentinel surveillance has been able to keep track of them. Such epidemiological surveillance at different geographical areas will help the health authorities to well plan appropriate containment measures.

Funding –None, Conflict of Interest-None

Acknowledgement: Authors gratefully acknowledge the kind cooperation of hospital departments and the permission of Dr SK Mishra, MD, Director I/C, Ispat General Hospital, Rourkela Steel Plant, SAIL Rourkela for publishing this finding.

References :1. WHO. Vector-Borne Diseases in India. Report of a

Brainstorming Session 9 November 2006. Available from:http://www.searo.who.int /LinkFiles /CDS_ vector borne_ diseases_in_India.pdf [Cited 2011 Aug 22].

2. Focusing on tackling vector borne diseases: ICMR DG- Times of India, Bhubaneswar Ed. 25.11.2010- pg 4

3. Dash AP, Chhotray GP, Mahapatra N, Hazara RK. Retrospective analysis of epidemiological investigation of Japanese Encephalitis outbreak occurred in Rourkela, Orissa, India, South Asean J Trop Med Public Health 2001; 32:137-9

4. Satpathy R, RV Iyar, DB Das, NC Nanda, A Lakra, KS Sulochana, KC Pant, A Saha, U Das. Orissa Medical Journal 1995; 16; 14-17

5. JP Thakare, TLG Rao and VS Padbidri. South Asian J Trop Med Pubic Health, Prevalence of West Nile virus infection in India 2002 Dec; 33: 801-5

6. Dwibedi B, Mohapatra N, Beuria MK, Kerketta AS,SabatJ,Kar SK,Rao EV, Hazra RK, Parida SK and Marai N. Vector Borne Zoonotic Dis. Emergence of Chikunguyan Virus Infection in Orissa India 2010;10:347-54.

12

Short Communication

Abstract : Snake bite is one of the most neglected public health issue in poor rural communities living in tropics, mainly during rainy season. Inadequate understanding of management of snake bite often lands up in increased mortality. Even a lack of simple airway management equipment like Ambulatory Manual Breathing Unit (AMBU) and laryngoscope can add to the difficulty in treatment.

One hundred seventy eight cases of snake bite admitted to our hospital from May 2008- October 2011 were analyzed. Out of 178 patients 40 were non poisonous and 138 were poisonous mostly due to Krait. One hundred thirty four patients recovered and four died. All of them received polyvalent anti snake venom and 55 needed ventilator support, due to respiratory insufficiency.

Patients with Krait bites manifest only neuroparalytic symptoms. Early administration of ASV ( Anti Snake Venom) and mechanical ventilation, in patients with respiratory insufficiency, decreases mortality.

Key word : AMBU bag, Laryngoscope, Krait, ASV, Ventilator

Introduction : Snake bite is a common problem in rainy season, that is from last part of May to mid of October. India is the home to more than 230 species of snakes of whom about 50 species are poisonous. Out of them following species are important. 1. Elapidae- Cobra, Krait (neurotoxic), 2. Hydrophilidae- sea snakes (neurotoxic, myotoxic, hyperkalaemia), 3. Viperidae- Russell viper (coagulopathy).1 All poisonous snakes have broad ventral plates extending right across the belly and two fangs on the upper jaw where as in nonpoisonous snakes there are numbers of small teeth instead of fangs and the ventral plate do not extend across the belly.2,3 In this part of Odisha Krait are the most common species of poisonous snake. Their bite results in neuroparalytic symptoms.

Krait bite cases mainly present with pain

abdomen, myalgia or ptosis which is marked early in the morning. Many of them do not have fang marks. Usual history is that many of the patients after a day’s heavy work, take some alcohol to ease their fatigue and after dinner, they sleep on the floor. Many of them go to toilet to open air in the mid night or early morning then go to sleep again. When they wake up they present with severe body ache , pain abdomen, ptosis , difficulty in breathing or combination of all.

Usually most of the tribal people after snake bite go to Quacks, Guni (Tantrik) before coming to hospital. So time of hospitalization in our case varies for 3 hours to 24 hours. One of the reasons of delay in hospitalization is transportation of patient from interior hilly areas.

Material and Method : The majority of the tribal population in and around Rourkela are engaged in farming, so snake bite is a major occupational hazard particularly during rainy season. We prospectively studied all the cases admitted with neurological symptoms like ptosis, generalized muscle weakness and respiratory paralysis through emergency department of Ispat General Hospital. They were all admitted to ICU( Intensive Care Unit) with high suspicion of snake bite even without the presence of fang marks. Detail history was obtained from patients or their relatives and neurological examination done . They were monitored hourly in the ICU. The prospective study was from May 2008- October 2011. Out of 178 cases, 138 were poisonous (krait) and other 40 were non poisonous snake bite.

In rainy season with this clinical history and prevalence of krait in this area, all the patients were treated with Polyvalent anti snake venom (standard cobra 0.60mg, common krait 0.45mg, Russell’s viper 0.60mg, saw scaled viper 0.45mg manufactured by Biological E. limited , Hyderabad India), ranging from 50-250 (median 100) ml in divided doses over period of 24 to 48 hrs. As the toxins fixed to pre-synaptic junctions are not neutralized by ASV, anticholinesterase drugs like neostigmine and glycopyrrolate are administered

Snake bite : our experience1Rajyabardhan Pattnaik*, 1Anita Mohanty, 2Rajlaxmi Panda, 3Sanjib Mohanty 1Department of Critical Care Medicine, 2Department of Anesthesia, 3Department of Internal MedicineIspat General Hospital, Rourkela-769005, India*Corresponding Author –e-mail: rajyapattnaik@yahoo.co.in

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up to 48 hrs.

Result : Yearwise distribution of poisonous snake bite in last 4 years was, 27 in 2008, 38 in 2009, 33 in 2010 and 40 in 2011. Of these, 72 were male and 66 were female. 55 patients needed ventilator support of which 4 expired.

In last four years 55 patients presented with respiratory muscle paralysis at the time of admission. They were treated with ventilator support. All were given pressure control ventilation (PCV) with required pressure to their body surface area and started with FiO2 1 and titrated to 0 .4. They needed ventilation support for 16 to 240 hours (median 36). ICU stay was ranging from 01 to 12 (median 3) days in all these snake bite cases.

Year Ma-le

per cent

Fe-male

per cent

Ven-tilat-ed

per cent

Ex-pir-ed

per cent

To-tal

2008 12 44.4 15 55.5 11 40.7 01 3.7 27

2009 22 57.8 16 42.1 15 39.5 01 2.68 38

2010 17 51.5 16 48.5 14 42.4 02 6.0 33

2011 21 52.5 19 47.4 15 37.5 Nil ---- 40

Total 72 52.17 66 47.8 55 40 04 2.9 138

Table 1. Details of patients treated and result of treatment

One patient aged 8 years, with history of snake bite ( Krait neurotoxic) admitted with respiratory muscle paralysis was treated with ASV(200 ml), injection neostigmine and injection glycopyrrolate. He was ventilated with PCV for 192 hours. He had right sided aspiration pneumonia which responded well to antibiotic. He recovered completely without any residual problem.

A young lady on 3rd trimester pregnancy, admitted with severe body ache and early morning ptosis had woke up once in the previous night and went to toilet. She was hospitalized 16 hours of the incidence with high degree of suspicion of snake bite, was treated with ASV (80 ml ) and recovered next day.

A 16 years old male admitted with H/O snake bite, GCS-3 and ptosis. He was immediately intubated, ventilated (9 days) and treated with ASV. First 4 days there was no improvement of GCS; pupil bilaterally dilated not reacting to light but heamodynamically stable. He was treated with Inj. ASV 250 ml in divided doses over a period of 48 hrs along with anticholinestrase and other supportive therapy. On 5th day his muscle power and general condition gradually improved.

He was weaned off the ventilator and extubated. He was shifted to ward on 12th day and discharged from the hospital on 20th day.

One Krait bite patient expired in 2008 was due to late arrival to hospital with aspiration pneumonia, ventilated for 9 days and treated with antibiotic, but could not be revived. One elderly patient expired within 24 hours of hospitalization in 2009. His previous cardiac status was not known. Two patients expired in 2010. One was elderly male on ventilation. His cardiac status was not known, expired within 48 hrs of hospitalization. Second case was an elderly lady, the previous cardiac status not known, also succumbed after 72 hours.

Discussion : Rourkela is surrounded by hilly areas where common Krait is the most frequently found poisonous snake. Although people in and around Rourkela are engaged in farming, we do not encounter other poisonous snake bites in our study, which is usual presentation in costal belt of Odisha. Our patients with Krait bite presented with pain abdomen, difficulty in deglutition, severe body ache and some of them presented with early morning ptosis4. Many of them were poor and tribal people with a habit of sleeping on the floor and consume alcohol before going to bed. Common kraits (Bungarus caereleus) come out of their holes due to humidity after rain. About 33% of all the cases do not have fang marks.2,3 They usually bite without provocation. Probably because of the small head of the snake and thick skin of tribal people the bite marks were not prominent or visible in many of them.

The toxin of common krait is beta-bungarotoxin. These toxins are of small molecular size which facilitates rapid absorption to the body. They usually block the pre synaptic acetylcholine receptors. They are 16 times more potent neurotoxic than Cobra.2,3 That is why many of krait bite patients need ventilator for respiratory paralysis.

The findings of this review could enable the clinician to emphasize the importance of early hospital reporting, avoidance of bizarre remedies and the risk in sleeping on the floor in the farm yard.

Conclusion : This analysis highlights that the outcome of neurotoxic snakebite (krait bite) is good if managed in time with anti snake venom and

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mechanical ventilation. The outcome worsens in case of delay in treatment and in case the bite is more severe. Most of the victims can be managed well with antisnake venom dose recommended in National guidelines.

Early hospitalization of the patient with history of severe myalgia, ptosis and pain abdomen with or without fang mark in the rainy season and prompt treatment with ASV and anti cholinesterase, with high degree of suspicion, saves life. Support with mechanical ventilation in patients with respiratory paralysis due to Krait bite, definitely decreases the mortality.

References :1. Bambery P. Snake bite and arthropods envenomation.

In: Shah SN .API text book of Medicine, 7th edn.Mumbai:Association of Physicians of India;2003.1279-82,

2. Warrell DA, Looareesuwan S, White NJ, Theakston RD, Warrell MJ, Kosakarn W, et al. Severe neurotoxic envenoming by the Malayan krait Bangarus candidus (Linnaeus) response to antivenom and anticholinesterase. Br Med J 1983; 286: 678-80.

3. Sanmuganathan PS. Mysthenic syndrome of snake of snake envenomation: a clinical and neuro physiological study. Postgrad Med J 1998;74:596-9.

4. Pattnaik RB, Dutt Anil, Satpathy SK, Mishra SK, Mohapatra DN.Early morning ptosis. Indian Journ of Industrial medicine 1997; 43:3; 29-30.

Calculation of electrolyte deficit

(A) For Sodium, chloride and bicarbonate

Deficit = (Normal value in meq/l ÷measured value in meq/l) ×electrolyte distribution in body compartment (%) × body weight(kg)

Where sodium distribution = 60%, chloride distribution = 20% and bicarbonate distribution=50%

(B) For Potassium

Deficit = For every 1.0 mEq/l decrease in the potassium conc. at or above 3.0 m Eq/l toal body deficit is considered as 100 to 200 mEq.

For every 1.0 m Eq/l decrease in the potassium concentration below 3.0 mEq/l, total body deficit is considered as another 300 to 400 mEq.

Body water = (Normal serum Na+ ÷ Actual serum Na+) × normal Body water

Where normal body water =0.6×body weight and normal serum Na+=140meq/l

15

Case Report

Abstract : Bilateral facial nerve palsy (BFNP) is a rare condition. Traumatic BFNP is still rarer. Diagnosis of BFNP is challenging because of lack of asymmetry in this condition and associated impaired cognitive function of the patient due to the severity of head injury associated with this. Early diagnosis and intervention is essential in this condition for good functional recovery. Careful clinical examination even if the patient is not conscious, high resolution imaging and electro physiological tests may help in this regard.

Key words : bilateral facial palsy, traumatic, BFNP.

Introduction : Bilateral traumatic facial palsy is a relatively uncommon condition and its early identification after head injury can be challenging due to lack of facial asymmetry and poor cognitive function of the patient. 1 High degree of clinical suspicion and physical examination can help to make early diagnosis, which is essential for correct management.2 We, here, report a case of a 21 year old male victim of diffuse axonal injury, who presented with difficulties in smiling, speaking and closing his eyes, on becoming consgious. We are reporting the case as the condition is rare and difficult to diagnose. Due to difficulties in making diagnosis of this condition and its rarity, we are reporting this case.

Case Report : A 21 year male engineering student presented with complaints of inability to smile , dryness of mouth and difficulties in speech for the last two months. All these occurred following a severe head injury which he had suffered from a road traffic accident, two months ago. He was unconscious for the initial five days and diagnosed to have diffuse axonal injury. He also had also history of bleeding from both the ears during the initial period. He was of average build, his pulse, blood pressure and other vitals were within normal limit. He was cooperative, and his higher functions were normal. On careful examination, it was found that his facial muscles were weak on both the sides, though there was no facial asymmetry (Fig1).

Figure 1.Face of the patient at the time of presentation shows lack of asymmetry of face. It also shows lack of naso-labial fold and frontal follows.

Figure2. Patient is unable to close eyes completely. Bell’s phenomena is clearly visible

He was unable to close his eyes completely (Fig2), there was dryness in his eyes, he was unable to smile or grin to show his teeth, and there was dryness in his mouth for which he was not able to speak properly. All other cranial nerves were normal. He did not have any other neurological deficit. All other systems were normal.

High resolution CT scan which was performed during the head injury was again reviewed. Air sinuses on both the temporal bones were filled up with blood (Fig 3) and there was longitudinal fracture of the petrous pyramid on both the sides.

Figure3. CT scan shows opacification in both the temporal air sinuses.

Bilateral facial nerve palsy (BFNP) following head injury-A case report1Pushpa Kumari*, 2Rabindra N Mohapatra 1Department of Ophthalmology, 2Department of NeurosurgeryIspat General Hospital, Rourkela-769005, India* Corresponding authoremail: rkl_pushpa@hotmail.com

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The young man was sent for conduction study of both the facial nerves which revealed demyelenation of the axons on both the sides. As the student had already adjusted his life style with the prevailing deficits, conservative management with physiotherapy of facial muscles and artificial tear application was advised to the patient. At the end of three months he was able to express emotion on his facechange his facial though not able to make a wide grin (Fig 4).

Figure4. Expression of smile on the face of patient, though he is not able to grin.

Discussion : BFNP is very rare. Reported incidence is one case per five million population per year,3 while the incidence of unilateral facial palsy is 1000 per five million population per year.4 Traumatic BFNP is still rarer, only 3% being due to temporal bone fracture.3 Fracture of petrous bone, vascular compromise or hematoma and oedema causing pressure on the nerves are the usual causes of traumatic facial paralysis. Our patient had longitudinal fracture of petrous bone on both the sides. Longitudinal fracture of petrous bone accounts for 90% of all the fractures of petrous bone and causes facial nerve injury in 10-25% of cases1. Transverse fracture of petrous bone accounts for 10% of temporal bone fracture and causes facial palsy in 30-50% of cases.5

BFNP usually results from longitudinal petrous pyramid fracture. The mechanism of facial nerve paralysis in temporal bone fracture is well described by de Villiers.6

Due to lack of facial asymmetry BFNP is difficult to diagnose.1,7 when there is no history of trauma, the cause of the condition should be searched thoroughly.3 Bilateral facial palsy usually has some underlying cause, whereas unilateral facial palsy is mostly idiopathic.3 In traumatic BFNP though etiology is obvious, treatment modalities are controversial. Treatment varies from conservative management, surgery to physiotherapy.7,8 Immediate onset of facial palsy with fracture dislocation along fallopian canal is an indication for early surgical intervention.8 Delayed onset of facial paralysis after trauma is

usually thought due to hematoma or oedema, so managed conservatively.9 Surgery varies from decompression, anastomosis or grafting of the nerve. Plastic surgery may be required for cosmetic purposes and to save the eyes.Artificial tear is used if there is dryness in eyes.9 Use of steroid is controversial, though many uses it.2

Localisation of lesion in facial nerve injury can be made clinically, from the presence of facial muscle weakness along with presence or absence of lacrimation, salivation and taste sensation in anterior 2/3rd of tongue or hyperacusis.

In BFNP, though facial symmetry is not lost, careful examination will reveal symmetric facial muscle weakness. In our case, there was bleeding from both the ears from the beginning, indicating basilar skull fracture. On careful testing, our patient was found ro have incomplete closure of both the eyes with Bell’s phenomena (figure1). He was also unable to smile and speak properly due to dryness of mouth.

Electrophysiological test of facial nerves showed demyelination of axon of facial nerve. The patient was managed conservatively as the onset of facial palsy was delayed and patient had well adapted to the deficit.

In trauma, evidence of basilar skull fracture like bleeding from ears, improper eye closure, expressionless face to pain should alert the physician to search for bilateral facial paralysis. Early detection of the lesion helps in correct management of the disease.

Reference :1. Li J, Goldberg G, Munin MC, Wagner A, Zafonte R.

Posttraumatic bilateral facial palsy: A case report and literature review. Brain Inj 2004;18: 315-20

2. Ju Yeon Hwang, Cheol Su Jwa, Kang Hyun Kim, Jae Kyu Kang. Post-traumatic Bilateral Facial Paralysis - A Case Report. J Kor Neurotraumatol Soc 2006;2(2):136-139.

3. George K, Pahor L.Sarcoidosis: A cause for bilateral facial Palsy. Ear, Nose, and Throat Journal 1991;70:492-3.

4. Sherwen PJ, Thong NC. Bilateral facial nerve palsy: A case study and literature review. J Otolaryngol 1987;16:28-33.

5. Harker A, McCabe F. Temporal bone fracture and facial nerve injury. Otol Clin N Am 1991;24: 425-31.

6. de Villiers J. Fracture-dislocation of the petrous temporal bone. J Neurol Neurosurg & Psychiat 1971; 34:104-9.

7. Faiz Uddin Ahmad, Ashish Suri, Ajay Garg, Ashok Kumar Mahapatra, Veer Singh Mehta. Post traumatic bilateral facial palsy causing severe psychosocial impairment. Pan Arab Journal of Neurosurgery 2009;13:125-7.

8. Lee GY, Halcrow S. Petrous to petrous fracture associated with bilateral abducens and facial nerve palsies: A case report.J Trauma 2002;53:583-5.

17

Case Report

Abstract : Presence of uncomplicated hydatid cyst is usually asymptomatic but it becomes symptomatic by pressure affect, rupture or by secondary infection. In more than 75% cases the liver is involved. We report a case of a 50 year old man who had ruptured hydatid cyst of the right lung. The chest radiograph and CT features were suggestive of a ruptured hydatid cyst with detached and collapsed endocyst within the exocyst. Presentation as complicated pneumonia with interesting CT appearance is the reason for this case report.

Introduction : Echinococcosis or hydatid disease, caused by larvae of the tapeworm Echinococcus, is frequently seen in an endemic country like India.1,2 The two main types of hydatid disease are caused by E granulosus and E multilocularis. The vast majority of infestations in humans are caused by E granulosus.3-6 The clinical presentation of hydatid disease is often non-specific and many patients may be asymptomatic.7 The symptoms depend on the size and site of the lesion and the accessibility of the organ involved for clinical examination.7 Infestation by hydatid disease in humans most commonly occurs in the liver (55-70%) followed by the lung (18-35%); the two organs can be affected simultaneously in about 5-13% of cases.7,9

Figure1. Chest radiograph on the day of admission revealed non-homogenous opacity in right lower lung zone with obscuration of right costophrenic angle & hemidiaphragm

Figure2. Chest radiograph on 3rd day of admission revealed cavity with uneven fluid level (folded handkerchief sign) & perilesional air space consolidation in right mid lung zone

Figure3. Ultrasonogram of chest showing multiloculated right basal pleural effusion

CASE REPORT : 50yrs male presented to intensive care unit with chest discomfort, breathlessness, vomiting followed by hematemesis. Patient did not have a history of allergy or self medications. Patient was conscious with respiratory rate 35 per minute(/min). His pulse was 120/min, blood pressure 80/60 of mercury, & oxygen saturation 86%. Respiratory system showed diffuse crepts on both sides.There was coffee ground aspiration from the stomach.

His total leukocyte count was 18000/ Cmmof blood

Atypical presentation of pulmonary hydatid cyst1Megharay Majhi, 1Premanand Panda*, 2Uma Devi, 2Chinnari M Rao, 1Sumitra Ratho1Department of Radio Diagnosis, 2Department of Pulmonary MedicineIspat General Hospital, Rourkela-769005, India. *Corresponding author-e mail : panda.premanand@gmail.com

18

with high neutrophil count. Chest radiograph taken on the day of admission showed non homogenous opacity in right lower zone with obliteration of costophrenic angle & right hemidiaphragm (Fig.1). Arterial blood gas analysis showed hypoxia with normal PH. A provisional diagnosis of pneumonia right lower lobe with parapneumonic effusion & stress GI bleed was made. Patient improved with broad spectrum antibiotics but chest examination revealed persistence of crepitations in the right inter and infra scapular area. Chest radiograph done on 3rd day of admission showed cavity with air-fluid level with consolidation in right mid zone (Fig.2). Ultrasound (US) examination of abdomen & thorax were unremarkable except for right basal multiloculated collection (Fig. 3). Persistence of clinical findings & incongruence of ultrasound & radiographic findings with previous provisional diagnosis, it was decided to repeat the chest radiograph & CT scan of thorax after two days to rule out other possible etiology. Now the radiograph (Fig. 4) revealed well defined thin walled cavity with an air fluid level & wavy linear opacities within. CT features (Fig. 5, 6, &7) suggested ruptured hydatid cyst with detached endocyst. Hydatid scolex was negative in the aspiration & sputum. A final diagnosis of ruptured hydatid cyst in right lower lobe of lung was made.

Figure 4. Radiograph of chest shows well defined thin walled cavity with an air fluid level & wavy linear opacities within (Water lily sign)

Figure 5. CT scan of thorax showing ruptured hydatid cyst with detached endocyst

Figure 6. CT scan of thorax showing ruptured hydatid cyst with detached endocyst (Water lily sign)

DISCUSSION : Hydatid cyst is composed of a parasite, the endocyst, surrounded by a pericystic layer, the exocyst, which is a fibrous layer due to host reaction.7 The endocyst is fluid filled, white, elastic hyaline, cyst and is easily dissectible from the pericyst with slight adhesion between them.7 The exocyst, which is functionally a protective layer against the cyst, consists of compressed lung tissue with its associated inflammatory reaction and fibrosis.7 If the pericyst ruptures, a thin crescent of air will be seen around the periphery of the cyst, producing the meniscus or crescent sign. If the cyst itself ruptures, the contents of the cyst are expelled into the airways, producing an airfluid level. On occasion, the cyst wall may be seen crumpled and floating within an uncollapsed pericyst, producing the pathognomonic sign of the camalote or WATER LILY sign (Fig. 4, 5 & 6).7 Our case reported classically the rupture of hydatid cyst in to the bronchus presenting with acute lung injury, hypoxic respiratory failure & peripheral circulatory failure. Radiological studies play a very important role in detecting and evaluating echinococcal cysts. Plain films will define pulmonary cysts; the cyst appears as a homogeneous spherical opacity with definite edges. Ultrasonography, CT, echocardiography and magnetic resonance imaging (MRI) are of great value in diagnosing and determining the anatomic extent and relationship of the cyst. Specific diagnosis could be made histologically by demonstration of parasite in excised tissue, Sputum examination for scolices or by neuro- imaging studies by demonstrating a cystic lesion with scolex. A Clinical diagnosis can be made by combination of clinical presentation radiographic studies, serological tests and history of exposure.7,8

CONCLUSION: Hydatid disease is not as rare in

19

our part of the world as suggested by the paucity of published reports. The tendency of the disease to remain quiescent over long periods and lack of availability of proper diagnostic facilities on a large scale contributed to the lack of knowledge of incidence of the disease in this area. Hence we have reported an atypical presentation of a common problem of rupture of the cyst into bronchus and classical CT appearance.

Figure 7. CT scan of thorax in coronal plane of Hydatid cyst showing ecto and endo cyst

References :1. Kulpati DD, Hagroo AA, Talukdar CK, Ray D. Hydatid

disease of lung. Indian Chest Dis 1974;16:406-10.

2. Reddy CR, Narasiah IL, Parvathi G, Somsundra RM. Epidemiology of hydatid disease in Kurnool. Indian Med Res 1968;56:1205-20.

3. Pedrosa I, Saíz A, Arrazola J, Ferreirós J, Pedrosa CS. Hydatid Disease: Radiologic and Pathologic Features and Complications. RadioGraphics 2000; 20:795–817.

4. Pumarola A, Rodriguez-Torres A, García-Rodriguez JA, Piédrola-Angulo G. Microbiología y parasitología médica. 2nd ed. Barcelona, Spain: Salvat, 1990.

5. King CH. Cestodes (tapeworms). In: Mandell GL, Bennett JE, Dolin R, editors. Principles and practice of infectious diseases. 4th ed. New York, NY: Churchill Livingstone, 1995; 2544–2553.

6. Beggs I. The radiology of hydatid disease. AJR Am J Roentgenol 1985; 145:639–648.

7. GH Basavana, G Siddesh, BS Jayaraj, MG Krishnan. Case report: Ruptured hydatid cyst of lung. Japi 2007; 55: 141 – 5.

8. Morar R, Feldman C. Pulmonary Echinococcosis. Eur Respir J2003; 21:1069-77.

9. Arora V, Snijjar I, Gill KS, Singh G. Case Report: Primary Hydatid Cyst of Muscle-A Rare Site. Ind J Radiol Image 2006; 16:239-41.

Measuring Intracerebral Hemorrhage Volumes

The formula ABC/2 is used, where A is the greatest hemorrhage diameter by CT, B is the greatest diameter 90° to A, and C is the approximate number of CT slices with hemorrhage multiplied by the slice thickness.

ABC/2 is the simplified formula for the volume of an ellipsoid, and found to be accu-rate for practical use for this purpose.

At the bed side, the CT slice with the largest area of hemorrhage is identified(ref-erence slice). The largest diameter (A) of the hemorrhage on this slice is measured. The scale given on the slice can be used. (B) is the largest diameter 90° to A on the same slice. (C) is the number of slices showing the hemorrhage when taken at 10 mm apart.

If the hemorrhage area in a slice is below 25% of the reference slice, it should not be taken into account. If the hemorrhage area in a slice is in between, 25% to 75% of the reference slice, it should be considered half a hemorrhage slice. Slice having hemorrhage area greater than 75% of reference slice then it is considered one hem-orrhage slice.

20

Case Report

Abstract : Hypocalcemia causing cardiac failure in children having no underlying cardiac illness is rare in literature. Most reported cases are in adult age. We report, a girl of13 years with no significant past illness, presenting with hypocalcaemia and cardiac failure. During investigation it was found that hypoparathyroidism is the cause of hypocalcemia.

Key words : Hypocalcemia, hypoparathyroidism, congestive heart failure (CHF)

Introduction : Parathyroid hormone and vitamin D work hand in hand to maintain the calcium level in blood, which in turn helps in contraction of both cardiac and skeletal muscles.1 Hypocalcaemia can occur due to a variety of causes that results in vitamin D and parathyroid hormone (PTH) deficiency. Hypocalcaemic states are more commonly seen in newborn. In vitamin D deficiency states hypocalcaemia is not severe as body tries to compensate under the influence of PTH. Generally hypocalcaemia is manifested by tingling of limbs, hyperexcitability in form of carpopedal spasms and cardiac rhythm abnormalities.1 But cardiac decompensation leading to congestive cardiac failure is rarely seen though there is a theoretical possibility. Hypoparathyroidism in children occurs very uncommonly due to a group of genetically determined deficiency states, and due to operation, radiation, tumors and autoimmune diseases.

Case Report : A 13-year girl was admitted to the pediatric ward of Ispat General Hospital with progressive breathlessness, pain abdomen and tingling sensation in limbs of two days duration. She had past history of one generalized seizures at the age of three years, which subsided without any medical treatment. She suffered from severe back pain, for which she was treated with calcium and anti tubercular drugs. Her milestones of development were normal and she had not attained her menarche. There was no apparent cause of malnutrition or suggestion of a bone related disease. Family history of seizures was absent.

Her height was 128 cm and weight was 33kg, both of which were less than third percentiles (IAP growth chart)*. She was drowsy, breathless and afebrile at the time of admission. Her heart rate and respiratory rate were 160 and 65 per minute respectively. Blood pressure was 80/60 mm of Hg and carpopedal spasm occurred while BP was recorded. There was central cyanosis, raised jugular venous pressure (JVP), parasternal heave and increase in cardiac dullness. Heart sounds were normal and there was no murmur. Chest auscultation revealed diffuse rales all over the lung fields. Abdomen was distended; liver was enlarged 5 cm. below right costal margin in mid clavicular line, smooth and tender and spleen was palpable just below left costal margin. Her hands and feet were short and broad and wrists were broadened. She had rough skin and had scabies. There were no neurological deficits or neck rigidity.

Her Hb% was 15 gm/dl and there was neutrophilic leukocytosis. Blood biochemistry reports were, RBS-80mg/dl, Urea-23mg%, Creatinine-0.7mg%, Bilirubin-0.5mg%, Sodium- 135meq/l, Potassium-2.2meq/l, SGPT- 205I.Units, Calcium- 4.0mg%, phosphorous- 2.4meq/l, Magnesium- 1.9mg/dl,

Alkline phosphatase- 517 IU. Blood gas analysis showed -pH -7.416, Pa O2 - 46.8, Pa CO2 -34.4, HCO3 -22meq/l, BE- 1.0 and SaO2- 83%. Urine examination was normal. Bedside ECG showed (Fig.1) sinus tachycardia, QRS axis -150, poor

Hypocalcemia - a rare cause of childhood congestive heart failurePitabas Mishra*, Nimain C Nanda, Jayanta Acharya, Paramananda Rath Dept.of Paediatrics, Ispat General Hospital, Rourkela-769005, India*Crrespondening author –e mail: pitabasmishra@yahoo.co.in

Figure1. ECG at the time of admission

21

progression of R-waves, 6mm up sloping ST depression in anterior leads, ST elevation in lead-I and aVL, prominent T-U waves and QT prolongation (QTc0.445).

Chest X-ray showed cardiomegaly (CT index 60%), and features of pulmonary oedema(Fig.2).

Figure 2. X-ray of chest showing features of pulmonary oedema

Skeletal survey showed osteoporotic changes (decreased mineralization) in limb bones (Fig.3), pelvic bones and lumbar spines (Fig.4)

Figure3. X-ray of fore arm showing rarefaction of bones of fore arm

Figure4. X-ray of pelvis shows decreased mineralization

On admission, she was diagnosed as pneumonia with CHF and antibiotics, digoxin, injectable furosemide and oxygen were prescribed. Within first six hours she worsened. After getting

biochemical report of calcium 4mg/dl, calcium gluconate was administered 2mg /kg as infusion. As, X-Ray feature suggested pulmonary oedema and the girl was afebrile, pneumonia was apparently ruled out. Injection furosemide was repeated and 100% oxygen was administered. She continued to be breathless and oxygen saturation was at 60%. She was put on Bi Pap ventilation. Calcium infusion was continued and improvement was noted twelve hours after admission. She could be weaned off from ventilator by 24 hrs. We initially did not think that failure was due to hypocalcemia. The calcium level in serum after 24 hours was 7mg/dl. Re examination after improvement did not show any clinical evidence of cardiac disease. ECG was reverting back to normal pattern. As a part of investigation for hypocalcaemia, we advised for serum Vitamin D3 and parathyroid hormone estimation which was 36ngm/l-(12.5-72) and 05ngm/l (19-60) respectively. The parathyroid hormone level was low and vitamin D3 level was adequate. Thyroid hormones showed normal level. Echo done on seventh day (when child could move) showed no evidence of cardiac disease. There was no dilatation of ventricular cavities.

Since therapeutic response occurred with calcium infusion upon confirmed hypocalcaemia, we considered it a case of hypocalcaemic heart failure. As parathyroid hormone level was low and no secondary causes could be found, we diagnosed it as a case of primary hypoparathyroidism.

Discussion : Hypoparathyroidism is less frequently seen in pediatric population. Often diagnosis is delayed in pediatric age group as components of its clinical features are confused with other clinical syndromes. This results in non-evaluation of the case especially in resource –poor settings and the patient suffers from long-term complication of the disease.

There are well-known effects of electrolytes on cardiac function. Calcium ions are important both for contraction and relaxation of cardiac muscle. It is believed that the membrane depolarisation results in sudden increase in the intracellular availability of calcium ions. The ions interact with the regulatory protein troponin and tropomyosin allowing actin to activate myosin ATPase. ATP hydrolysis occurs at very rapid rate to provide energy for the activation of cross bridges linking adjacent actin and myosin filaments. Hypocalcemia prolongs the duration of phase two of action potential of cardiac muscle, which

22

probably causes prolongation of QT interval.2 Due to hypocalcaemia there can be coronary spasm, which may mimic myocardial infarction. However, cardiac decompensation leading to heart failure due to hypocalcaemia in chronic endocrine diseases is rarely seen in clinical practice.

Bronsky et al (1958) described four cases of heart failure out of fifty cases of idiopathic hypoparathyroidism.3 Three of them were adults. Antebi et al (1966) described cardiomegaly due to hypocalcaemia.4 Aryanpur et al (1974) described one 14-year girl child with features of idiopathic hypoparathyroidism manifesting with congestive heart failure that responded to calcium therapy, very much similar to our case5. There have been reports of hypocalcemic heart failure and ECG changes in adults in medical literatures where patients are known to be suffering from diseases causing hypocalcemia.6, 7 It is rare in pediatric age group except in neonates in whom it can be more commonly noticed. Searching through Indian medical literatures we found two reports in adult population (Gupta RP et al 2007, Jariwala P V et al 2010) who were 24 and 18 years old.8,9 Recently, Gupta P et al. in a retrospective analyses of all cases of cardiac failure, showed five cases with hypocalcaemia in infants more than 3 month of age, out of which only one has hypoparathyroidism.10

Delayed diagnosis in this reported case led to prolonged suffering from primary hyperparathyroidism. It was treated symptomatically till serum calcium level lowered to a critical level causing CHF, even if there was no structural defect in heart or metabolic disease. One should suspect the condition, if

CHF is not improving with conventional anti failure treatment. Careful history taking and clinical evaluation might suggest underlying hypo parathyroid disorder.

References :1. Doyle D A. Disorders of the parathyroid gland. In:

Kliegman R M, Editor. NelsonText Book of Pediatrics, 19th ed. Philadelphia:Elsevier,Saunders; 2012. p1917-8.

2. Joseph L, Peter L, Eugene B. Basic Biology of Cardiovascular System, Cellular basis of Cardiac Contraction. In: Harrison’s Principle of Internal Medicine, 17th Ed.Newyork:2008. p1369-71.

3. Bronsky D, Kushner D S, Dubin A Snapper I, Idiopathic hypoparathyroidism and pseudohypoparathyroidism: Case reports and review of literatures. Medicine 1958;37: 317

4. Antebi L, Bouchard R, Guendeny J, Perles C W J. Cardiomegaly due to chronic hypocalcemia. Pediatrics 1966;38:909.

5. Aryanpur I, Farhoudi A, Zangeneh F. Congestive heart failure secondary to idiopathic hypoparathyroidism. Arch Pediatr Adoless Med 1974;127:738-9.

6. Brenton DP, Gonjales J, Pollard AB. Hypocalcemic cardiac failure. Post Grad Med J 1978; 54:611-615.

7. Lehman G, Deisenhofer I, Ndrepepa G, Schmitt C. ECG changes in a 25 year old woman with hypocalcemia due to hypoparathyroidism: hypocalcemia mimicking acute myocardial infarction.Chest 2000;7:843-52.

8. Gupta RP, Krishnan RA, Kumar S, Beniwal S, Devaraja R, Kochar SK. A rare case of heart failure-Primary Hypoparathyroidism. JAPI 2007; 55:522-24.

9. Jariwala P V, Sudarshan B, Aditya MS, Praveer L, Sarat Chandra K. Hypoparathyroidism – A Cause of Reversible Dilated Cardiomyopathy. JAPI 2010; 5: 500-502.

10. Gupta P, Tomar M, Radhakrishnan S, and Shrivastava S.Hypocalcemic cardiomyopathy presenting as cardiogenic shock. Ann Pediatr Cardiol 2011;152-5.

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Figure 1A

Figure 2

Figure 4

Figure 6

For answers please refer to page 28

Figure 1B

Figure 3

Figure 5

Figure 7

Spot the Diagnosis

26

Swamiji before delivering a spiritual discourse at Ispat General Hospital

A Sister is providing nursing care during physiotherapy session

A Picnic team from IGH in the era of black and white photography

Down the memory lane

27

Case Report

Abstract : Sickle cell disease (drepanocytosis) is an inherited blood disorder characterised by the polymerization of deoxygenated hemoglobin ‘S’ into rigid rodlike polymers causing sickling of erythrocytes .Bleeding diasthesis in sickle cell disease is explained by thrombocytopenia due to hypersplenism and hypercoagulable states. We report here a case of sickle cell disease with recurrent thrombocytopenia. due to immune thrombocytopenic purpura (ITP)

Key words : Sickle Cell disease , thrombocytopenia, ITP.

Case Report : A 9 years old male child, born of non-consanguinous marriage presented with bleeding from nose, blood mixed vomiting and black stools for the previous two days. He was a known case of sickle cell disease. There was no history of any joint pains, dyspnoea, abdominal pain, rash, fever or sorethroat .The child had been admitted with similar complaints of recurrent episodes of epistaxis and thrombocytopenia. He had been put on oral prednisolone on tapering doses, since then. Examination revealed a well looking child with normal growth and development and stable vitals. He had epistaxis, pallor and multiple non-blanchable pin head size petechiae all over body. There was no bony tenderness, café-au-lait spots, skeletal anomalies or hepatosplenomegaly.

The cardiovascular system revealed a soft systolic haemic murmur .The rest of the systemic examination was normal. The hemogram reavealed hemoglobin of 4.8 gm % ,reticulocyte count of 6%, serial low platelet counts in the range of 11000 to 18000 per cmm of blood. Peripheral bloodsmear revealed sickle cells, microcytosis, poikilocytosis and target cells. Platelets were grossly reduced. WBC counts showed reactive leucocytosis. Sickling test was positive. The coagulation profile was normal. The liver function tests, renal function tests and electrolytes were normal . Fundoscopy was normal. Bonemarrow aspiration revealed increased megakaryocytes with both mature and

immature forms. The megakaryocytes showed smooth borders without any budding of platelets confirming the diagnosis of ITP (Fig.1&2).

Figure 1. Bone marrow aspirate with increased number of megakaryocytes showing smooth borders without any budding of platelets (Giemsa :100X)

Figure 2. Bone marrow aspirate with increased number of megakaryocytes showing smooth borders without any budding of platelets(Giemsa :40X)

The patients hemoglobin electrophoresis revealed ASF pattern . He was managed with prednisolone, anti-D and supportive treatment. He was discharged as a case of chronic ITP and sickle cell disease with folic acid and tapering doses of prednisolone.

Discussion : The association of ITP with sickle cell disease has not been reported. Our patient presented with epistaxis, malena, petechiae and purpura which are suggestive of a platelet

Sickle cell disease with recurrent thrombocytopenia secondary to ITP - A rare case report1Maya Bose*, 1Nimain C Nanda, 1Jayanta Acharya, 2Sanghamitra Satapathy1Department Of Pediatrics and Neonatology2Department Of PathologyIspat General Hospital, Rourkela-769005, India*Corresponding author- Email:bosemaya@rediffmail.com

28

disorder. Bleeding episodes in sickle cell disease is explained by microparticle related coagulopathy which are derived from platelets.1 Thrombocytopenia in sickle cell disease is explained by hypersplenism, sequestration crisis and vaso-occlusive crisis.2,3 However in our case serial readings of thrombocytopenia, associated leucocytosis, with bonemarrow megakaryocytosis ruled out pancytopenia and hypersplenism as a cause.The commonly accepted theory of ITP is development of auto anti bodies against platelets causing increased destruction and resultant thrombocytopenia.4 Other entities like auto immune hemolytic anemia, thrombotic thrombocytopenic purpura, Evan’s syndrome, post-transfusion purpura, and HIV were ruled out. All causes of bonemarrow megakaryocytosis with thrombocytopenia were also ruled out. Hence

Answers to spot the Diagnosis

1. Dorsal meningocele

2. ST elevation in ECG

3. Heart block

4. Filarial worm in a Breast lump (FNAC)

5. Peripheral blood smear showing P. Falciparum

6. Free gas under the diaphragm indicating perforation of hollow viscus

7. Pneumothorax

diagnosis of sickle cell trait with ITP based on clinical and laboratory findings was done.Though the association of ITP in sickle cell disease is rare,the possibility should be kept in mind when dealing with a case of sickle cell disease with recurrent thrombocytopenia.

References :1. Westerman MP, Cole ER, Wu k. The effect of spicules

obtained from sickle red cells on clotting activity.Br J Haematolo1984; 56:557-62.

2. Haut MJ, Conar DH, Haris JW. Platelet function & survival in sickle cell diesease. J.Lab Clinmed 1973;82:44-53.

3. Stuart PM, Nagel PR. Sickle cell disease. Lancet 2004; 364:1343-60.

4. Blanchette V, Bolton-Maggs P. Childhood immune thrombocytopenic purpura: Diagnosis & Management. Hematol Oncol Clin North Am. 2010;24:249-73.

29

Case Report

Abstract : A 40 year male was admitted with history of weight loss, black stool and weakness. There was no history of haematemesis, diabetes, hypertension or tuberculosis. He was a chronic alcoholic. At the time of admission, he was severely pale, emaciated and hypotensive. Haemoglobin was 6.2 G/dl. The biochemical investigations were normal. The routine chest X-ray was normal except an artifact looking opacity at the left subphrenic area. The repeat X-ray of chest along with upper abdomen revealed multiple nails in the stomach. During exploratory laparatomy ninety nine 4” nails were discovered from the stomach, duodenum and transverse colon. This is one of the rare case where so many nails (FB) were recovered from the GI tract. Intentional ingestion of foreign bodies has been reported by various authors but ingestion of sharp nails of such numbers and size is not reported in the literature. The history of ingestion of nails was not revealed. After detection of nails, on interrogation, he said that he was in the habit of ingesting nails after the death of his brother to keep his spirit away.

Key words : Foreign body, stomach, 99 nails, adult

Introduction : Foreign body ingestion occurs mostly in the children between the age of 6 months to 5 years, but can occur in adolescents too. It is not an unusual occurrence in clinical practice as they become curious, and try to explore and taste!!! Some may swallow it at times. Thus, foreign body gets impacted in the GI or respiratory tract.1-4 But this is extremely rare among the adults. While children swallow radio-opaque objects, such as coins, pins, screws, button batteries, or toy parts,1 adults usually ingest radiolucent foreign bodies like seeds or foods.

We encountered a young man of 40 years, who was admitted with history of weight loss, pain abdomen and malena. The patient or the relatives did not give any history of ingestion of foreign bodies. During investigations, it was detected by

a chance finding in the radiographic study. We report the case due to rarity of the event.

Case Report : A 40 year unmarried male was admitted to Ispat General Hospital, Rourkela in India with the history of weakness for 20 days, black colored stool for 7 days and weight loss. There was no history of haematemesis, fever, cough or hemoptysis. There was no history of bleeding from other sites. He was not a known diabetic or hypertensive. There was no previous history of GI bleeding. But he used to get pain in the upper abdomen on and off but was not investigated elsewhere.He denied to have taken any analgesics or oral steroids. He was unmarried and stays single. Recently he lost his brother who died due to some chronic illness, the details of which were not available. He was a chronic alcoholic.

On clinical examination, he looked very sick and emaciated. He was conscious, oriented and co-operative. He was communicative, but appears to be withdrawn and responding only in few words. He was severely pale, with bilateral pedal oedema. His blood pressure was 80/ 60 mm of Hg and pulse was 100 / min, and low volume. There was no icterus, lymphadenopathy or purpuric spots.

His heart sounds were normal without any added sounds but breath sound was diminished on right side. The abdomen was scaphoid, soft without any palpable mass. There was no free fluid in the abdomen. But epigastrium was tender. The provisional diagnosis were:

• Chronic alcoholic with bleeding from erosions or ulcer in the stomach or duodenum. Variceal bleeding was unlikely as there was no hematemesis,

• He was emaciated. Hence, the possibility of tuberculosis was also kept in mind due to its high prevalence in India.

• GI malignancy is another likely diagnosis due to loss of weight, melena, anaemia and emaciation.

A rare case of 99 nails in the GI tract!!!1Indira Mishra, 2Birendra K Sarkar, 2Jagannath Behera, 3Sanjay K Acharya, 1Saroj K Mishra1Departments of Internal Medicine, 2Departments of General SurgeryIspat General Hospital, Rourkela-789005, IndiaCorresponding author-e mail: mishraindira_63@yahoo.co.in

30

The investigations were accordingly performed. There was profound anaemia, but coagulation parameters were normal. The renal function and liver function tests were within normal limits. His hemoglobin was 6.2 gm/dl, total leucocyte count 5800 / cmm of blood. Differential counts, coagulation workup and biochemical studies were within normal limit. Tests for HIV and HBsAg were negative.

The chest ski gram showed normal lung fields and cardiac silhouette. There were no hilar shadows, no pericardial effusion or pleural effusion. However, a radio-opaque shadow (Figure 1) was

Figure 1. Artifact (?) in the chest radiograph

observed at the left sub-phrenic area and appeared to be an artifact. Hence, a repeat X’-ray was ordered along with the chest and upper abdomen. It showed multiple nail shadows over the stomach area (Figure 2).

Figure2. X-ray:revealing multiple nails in abdomen

The unusual presence of multiple nails in the stomach was discussed by the physicians and the surgeons. Surgical consultation was solicited

and exploratory laparotomy was planned as endoscopic removal of large number of nails may not be possible. The patient was taken up for surgery under general anesthesia. During the surgery ninety nine rusted nails of 4 inches each were removed from the stomach, duodenum & transverse colon (Figure 3).

Figure3. Nails recovered during surgery.

There was no perforation. But the gastric mucosa was congested with multiple ulcerations (Figure 4).

Figure4. Intraoperative picture

After the discovery of multiple nails in the stomach in the second x-ray, the patient was evaluated by a psychiatrist before and after surgery too. He was having depressive psychosis, delusion of persecution and was withdrawn most of the times. The history of ingestion of nails was not forth-coming. After detection of nails in the second X-ray, it was revealed that the patient had lost his brother a year back. He was afraid of his dead brother’s spirit. So to keep it away, he started keeping a naill under his pillow for six to seven months. But to be confident that the metal stay with him all the time, he started ingesting small nails. Then gradually he felt that he can gulp down a large nail of 4 inch size with a banana. He

31

had consumed for three – four months when he experienced pain in the stomach and occasional tarry stool.

Discussion : Usually children are encountered with foreign body ingestion, and rarely the grownups and adults. In the adolescent and adults, concomitant psychiatric problems, mental disturbances, and risk-taking behaviors may lead to foreign body ingestion. Though it is difficult to know the exact figures, about 125,000 ingestions of foreign bodies by people were reported to American authorities in 2007. A survey of 1500 children revealed that 4% children swallowed a coin. These foreign bodies may be expelled in the stool. But some are retained and may cause mucosal erosion, obstruction, scarring, or even perforation. Systemic reactions may occur, but are rare.1-4

Children of all ages ingest foreign bodies. However, incidence is greatest in children aged 6 months to 4 years. The case reports of adults ingesting FB are extremely rare or rarely reported in the literature.

In the present case, elder brother of the patient had expired an year back. He apprehended that the dead brother’s soul may cause harm to him. So to counter the evil spirit, he started to keep a nail with him under his pillow. It is believed that a metal kept by the side of a sleeping person keeps away the ill effects of evil spirits. He had delusion of persecution. So instead of keeping the nails near his head, he started swallowing it along with a banana.

Clinical presentation in these conditions may be varied. At times, it may be asymptomatic, while in others it can cause severe discomfort. The FB inside the stomach may cause feeling of fullness, distention, or pain. Sharp objects have the tendency to cause erosion, bleeding and perforation. Plain X-ray clinches the diagnosis, as most foreign bodies are radio-opaque. At times, endoscopic visualization along with removal may be possible without subjecting the patient to imaging studies. CT scan or MRI is rarely necessary. Handheld metal detectors may be used for localization of ingested metallic objects.

Endoscopic removal of these can be attempted by experts, as this is the procedure of choice. Other methods include Foley catheter or Bougienage method. The bougienage method is cost-effective than endoscopy. A few FB can be expelled spontaneously, viz, coins. Often, the coin passes through, and a removal procedure can be avoided.

Sharp or pointed objects are often liable to perforate the wall, and should be removed from the stomach or intestine. Large objects which cannot pass through the pyloric sphincter need to be removed surgically or endoscopically.

Round objects need not be removed immediately, as they generally pass through the lower GI tract without difficulty. If not detected from the excreta (stool) repeat X-rays should be done to check for its presence or descent in the intestine.

In an adult, psychiatric consultation should always be done. Similarly in children with repeated FB ingestion a consultation with a psychiatrist is helpful.

Waters et al5 reported an interesting case reports. A 76-year-old female was investigated for weight loss and diarrhea. A flexible sigmoidoscopy revealed severe diverticulosis and a subsequent CT abdomen showed a linear foreign body in the stomach but no other abnormality. The symptoms resolved spontaneously. On interrogation, she recalled that she had unintentionally swallowing a pen 25 years back. A gastroscopy demonstrated a plastic felt-tip pen sitting in the lumen of the stomach without evidence of any gastric damage.

A 43 year woman from Can Tho City of China was admitted with severe stomach ache. The X-ray revealed a stack of strange objects. After surgery, 119 nails of 3 inches long each were removed.6

A 26 year M construction worker from Peru has been eating coins, scrap metal, nails, and copper wire for several months. When it started causing stomach pains, he underwent surgery and removed 1.5 pounds of metal debris from within his stomach in 2009.7

In the present case, the 40year male ingested a big nail of 4” size day after day to repel the evil spirit of his own brother. The history was not

32

revealed to the doctor or nurse. It came to light only after a chance finding of a nail- head in the stomach which led to the full view X-ray of the abdomen.

Intentional ingestion of foreign bodies has been reported by various authors but ingestion of sharp nails of such numbers and size has not yet been reported in the literature.8

References

1. Aydoğdu S, Arikan C, Cakir M, Baran M, Yüksekkaya HA,

Saz UE, Arslan MT. Foreign body ingestion in Turkish

children. Turk J Pediatr. 2009;51:127-32.

2. Dahshan AH, Kevin Donovan G. Bougienage versus

endoscopy for esophageal coin removal in children. J

Clin Gastroenterol. 2007;41:454-56.

3. Hachimi-Idrissi S, Corne L, Vandenplas Y. Management

of ingested foreign bodies in childhood: our experience

and review of the literature. Eur J Emerg Med. 1998

;5:319-23.

4. Yalçin S, Karnak I, Ciftci AO, Senocak ME, Tanyel FC,

Büyükpamukçu N. Foreign body ingestion in children: an

analysis of pediatric surgical practice. Pediatr Surg Int.

2007 ;23:755-61.

5. Waters RW, Daneshmend T, Shirazi T. An incidental

finding of a gastric foreign body 25 years after ingestion.

BMJ Case Reports 2011; doi:10.1136/bcr.10.2011.5001

6. Anonymous. Woman has 119 nails in stomach.

Chinadaily.com.cn Updated: 2006-07-02 12:08

7. h t tp ://www.theage .com.au/wor ld/680g -o f -

nails-pulled-from-mans-stomach-20091112-ibj2.

html#ixzz1ul8i9Rfg

8. Nataraj G. Write To Communicate. Foundation Books.

http://www.foundationbooksindia.com/ Page 61.

Deccan Herald, Sunday 22 February, 2004.

Types of respiratory failure

Respiratory failure is inadequate gas exchange by the respiratory system, with the result that levels of arterial oxygen, carbon dioxide or both cannot be maintained within their normal ranges.

Type 1 respiratory failure is defined as hypoxia without hypercapnia, and the PaCO2 may be normal or low. It is typically caused by a ventilation/perfusion mismatch; the volume of air flowing in and out of the lungs is not matched with the flow of blood to the lungs. This is the most common form of respiratory fail-ure, and it can be associated with virtually all acute diseases of the lung, which generally involve fluid filling or collapse of alveolar units. Some examples of type I respiratory failure are cardiogenic or noncardiogenic pulmonary edema, pneumonia, and pulmonary hemorrhage.

Type 2 respiratory failure is caused by inadequate alveolar ventilation; both oxygen and carbon dioxide are affected. The build up of carbon dioxide lev-els (PaCO2) that has been generated by the body but cannot be eliminated. Common etiologies include drug overdose, neuromuscular disease, chest wall abnormalities, and severe airway disorders.

33

Case Report

Abstract : Primary Non-Hodgkin’s lymphoma of bone (PLB) is a rare type of extra nodal lymphoma that originates in the bone. We report a case of PLB in a 50 years old lady who presented with pain and swelling over the left elbow joint following trauma. Plain radiographs of the left elbow joint revealed areas of lytic lesion and fracture in olecranon process of left ulna. Routine investigations were within normal limit. Provisional diagnosis of pathological fracture due to malignant bone tumour was made. Fine Needle Aspiration Cytology (FNAC) from the medial aspect of the left elbow joint suggests non Hodgkin’s lymphoma (NHL). The diagnosis of diffuse large B- cell lymphoma was established on histopathological and immunohistochemical analysis. Lymph node screening and whole body scan confirmed it to be PLB. This case is being reported for its rarity and clinical importance of recognizing such cases because of excellent prognosis.

Key words : Bone, FNAC, Biopsy, Primary Non-Hodgkin’s Lymphoma.

Introduction : Lymphoma usually originates in the lymph node or any lymphatic sites.

Any organ like thyroid, lung, bone, brain or gonads can be involved either by spread from lymphatic sites or as a manifestation of primary extra nodal disease, PLB means lymphoma arising primarily in the bone in contrast to secondary involvement of bone by primary nodal lymphoma or other extra nodal lymphoma. PLB accounts for less than 2% of all lymphoma in adult,1 3% of all primary bone tumors and 3 to 5% of all extra nodal non-Hodgkin’s lymphoma.2,3 PLB generally presents as solitary extensive destructive bone lesion. Usually age ranges from 2 to 88 yrs and male to female ratio ranges from 1.5 to 2.1.4 A case of PLB is being reported here for its rarity and clinical importance of recognizing such cases

because of its good prognosis compared to other malignant bone tumours and metastasis from nodal or extra nodal lymphoma.

Case report : A 50 yr old lady presented with the complaints of pain and swelling over the left elbow joint since two months following trauma. There was no past history of fever or weight loss or trauma. On examination, there was a single tender large swelling over the medial aspect of the left elbow joint. There was no lymphadenopathy or organomegally. Routine investigations were within normal limit. Plain radiographs of the left elbow joint revealed areas of lytic lesion in the left ulna. Due to presence of lytic lesion, a neoplastic origin was suspected; so search was made for evidence of neoplastic process anywhere else in the body. Accordingly, plain X-ray of chest, spine and lower extremities were taken up which were normal. Ultrasound of the abdomen and pelvis were also normal. M-band was absent on serum protein electrophoresis .FNAC of the involved site revealed sheets of monomorphic population of large lymphoblast (Fig1).

Figure 1: Photomicrograph of cytosmear showing

Monomorphic population of large lymphocytes having one

or more distinct nucleoli (Giemsa X 400)

It was diagnosed as NHL. Histopathology of excisional biopsy from left ulnar lesion revealed predominantly large lymphoblast with non

Primary Non-Hodgkins Lymphoma of bone : A rare case report with literature review1Prativa K Behera*, 1Rabi R Panda, 1Sanghamitra Satpathy, 1Aruna M Minz, 2Megharay Majhi, 3Ranjan K Patra1Department of Pathology, 2Department of Radiology, 3Department of OrthopedicsIspat General Hospital, Rourkela-769005, IndiaCorresponding author, email: pk_rkl@yahoo.in

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cleaved nucleus having prominent nucleoli in a diffused pattern (Fig.2).

Figure 2.Photomicrograph of tissue section of bone showing

diffuse infiltration of monomorphic population of large

lymphocytes (H&E X200)

The diagnosis of NHL (diffuse large cell type) of bone was confirmed. Immunohistochemical analysis using monoclonal antibodies showed that tumor cells were strongly positive for CD20 and CD45 and negative for CD3 and CD5, which confirmed B cell lineage of lymphoma. Thus the diagnosis of diffuse large B-cell lymphoma (WHO classification) of the bone was established. Then CT examination of the chest, abdomen and pelvis were done to exclude primary soft tissue origin or distant disease, and were found to be normal. Bone marrow biopsy from iliac crest revealed no involvement. The diagnosis of PLB was established because of absence of any other lymph node, organ or bone marrow involvement by the tumor cells.

Discussion : Lymphoma usually originates in the lymph node. The term extra nodal lymphoma is used for the lymphomas arising in the tissue other than lymph nodes. PLB is a rare type of extra nodal lymphoma. Most (94%) PLB cases result from non-Hodgkin’s lymphoma . A case of Hodgkin’s type PLB was reported by Gerbert et al in 2004.4 The most common clinical presentation for PLB is pain followed by lump, or both pain and lump followed by fracture.2 The etiology of bone lymphoma is unknown. Viral agents and immune suppression are implicated in some cases. Cytogenetics and molecular abnormalities are involved in pathophysiology of many different lymphomas.5

WHO diagnostic criteria for PLB are:4

1. Primary focus in a single bone

2. Histological confirmation of lymphoma in the bone and

3. No evidence of distant soft tissue or distant lymph nodes involvement at diagnosis.

Regional lymph node involvement at diagnosis is not considered exclusionary using these criteria.

Currently it is recognized that PLB may involve multiple bones as long as the other 2 criteria are met. According to Inwords et al,6 primary lymphoma of bone is diagnosed if no evidence of lymphoma is found elsewhere within six months after the diagnosis.6

PLB tumor produces osteoclast stimulating factors that cause lytic bone lesion. The differential diagnosis are - bone metastasis, Ewing’s sarcoma, multiple myeloma, other round cell tumours.4 When the biopsy of the bone lesion confirmed the diagnosis of lymphoma, whole body CT scan is mandatory to exclude a primary soft tissue origin or a distant disease. Once soft tissue origin and distant diseases are excluded, MRI is the method of choice to evaluate the extent of the disease within the affected bone.4 It is extremely unusual for a low grade or follicular lymphoma to create a mass lesion in the bone.7

Some studies have suggested that the stage of the disease is much more important prognostically in lymphoma of bone than the histologic type.7 We report a rare case of PLB in a middle aged patient for its rarity. Incidence of PLB in our institution is a rarity. It is the first case reported in our hospital in a decade (1997-2007).

Treatment of PLB is combined modality therapy. Combined modality therapy includes a method of local control, usually radiation therapy and a systemic treatment usually combination chemotherapy.8 The 100% 5 years survival and 88% 15 years survival rate are reported with combined modality therapy in Cleveland Clinic.9

Conclusion : Younger age, advanced stage, multiple bone involvement and non large cell histology are associated with decreased survival as compared with elder age, localized disease,

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single bone involvement and large cell histology respectively.10

So the prognosis appears to be good in our patient. Furthermore extra nodal lymphoma follows a more indolent course than nodal lymphoma. PLB has higher survival rate compared to other type of NHL.

References:

1. Dubey P, Ha CS, Besa PC. Localized primary malignant lymphoma of bone. It J Radiat Oncol Biol Phys 1997 ; 37: 1087.

2. Limb D, Dreghorn C, Murphy JK, Mannion R. Primary lymphoma of bone. Int Orthop 1994; 18: 180.

3. Freeman C, Berg Jw, Cutler SJ. Occurrence and prognosis of extra nodal lymphomas. Cancer 1972 ; 29: 252.

4. Mulligan M E. 2007 e-Medicine Lymphoma bone; updated 12 April; www.emedicine.com/radio/topic819.htm

5. Weiss L M, Warnke A.R, Sklar J and Cleary M L. Molecular Analysis of the T(14;18) Chromosomal Translocation in

Malignant Lymphomas. N Engl J Med 1987; 317:1185-89.

6. Gerbert C, Hardes J, Ahrens H .Primary multifocal osseous Hodgkin’s disease: A case report and review of the literature. J Cancer Research Clin Oncol 2004;Dec 15 (Medline).

7. Inwards CY, Unni KK. Bone tumors. In: Mills SE, eds. Sternberg’s diagnostic surgical pathology. Philadelphia: Lippincott Williams & Wilkins, 2004 : 270-1.

8. Ford D R, Wilson D, Sothi S .Primary bone lymphoma treatment and outcome. Clinoncol [Rcoll Radioll] 2007; 19[1]: 50-5 [Medline].

9. Kirsch J, Lastan H, Bauer T W. The incidence of imaging finding and the distribution of skeletal lymphoma in a consecutive patient population seen over five year’s. Skeletal radial. 2006; 35[8]: 590-4 [Medline].

10. Glotzbecker M P, Kersun L S, Choi J K, Wills B P, Schaffer A A, Dormans J P Primary Non-Hodgkin’s lymphoma of bone in children. Am J Bone and joint surgery 2006; 88: 583-594.

Answer to multiple choice questions

1d, 2c, 3b, 4c, 5a, 6c, 7d, 8a, 9a, 10c, 11d, 12d, 13d, 14b, 15b & c, 16b, 17c, 18c, 19a, 20d, 21b, 22b, 23a, 24a, 25c, 26a, 27a, 28c, 29d, 30c, 31a, 32a, 33d, 34a, 35b, 36a, 37c, 38a, 39c, 40b, 41b, 42b, 43a, 44c, 45a, 46a, 47c, 48d, 49b, 50a, 51a, 52b, 53c, 54a.

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Clinical Image

Case report : A female of 56 years was admitted to our hospital with stab injury on her back. She was attacked from behind by her son during an altercation. On admission she was found to be profoundly disturbed due to the incident and was lying on her side as the kitchen knife (Fig1) was protruding from her back. Her clothes were blood stained, her pulse, blood pressure and other vital parameters were within normal limit. The knife was firmly stuck on her lumbo-sacral region on the midline and directed from left to right. Her abdomen was soft with mild tenderness in lower abdomen. Per rectal examination was normal except mild tenderness posteriorly during examination. There was pain during movement of her lower limbs but no neurological deficit could be detected. All other systems were within normal limit. She was immediately started with intravenous fluid, antibiotics and blood was sent for hemogram and biochemical study. Immediate arrangement was made for a CT scan study of her spine as MRI may be harmful for her and ski-gram may not be adequately informative.

After the plain CT scan, contrast CT scan was also taken-up to gather information regarding the proximity of the weapon to the blood vessels. Blood vessels are found to be away from the knife.

The knife was seen passing from left to right (Fig2 & 3) at the lumbo-sacral junction, it’s cutting margin was laterally directed and it had crossed the spine protruding into the pelvis.Thespine has traversed the spinal canal.

As the sharp margin was away from the spinal canal (Fig 4&5) a decision was made to remove the knife in the operation theatre keeping everything ready to proceed for laparatomy if situation demands.

In the OT the knife (Fig6) was removed cautiously avoiding side to side movement to avoid iatrogenic injury.The patient was observed carefully for neurological deficits, CSF leak and infection. At the end of one month,patient was doing well without any complications.

Figure 1. The knife protruding at the lumbo-sacral spine

Figure 2. CT scan showing the knife passing through the spine

Figure3.CT scan showing the presence of knife at the centre of spinal canal

Stab injury of lumbar spine : a case report1Binayak Rath, 2Sanjay K Tiwari, 3Megharay Majh , 4Rabindra N Mohapatra*1Department of GeneralSurgery, 2Department of Orthopedics, 3Department of Radiology, 3Department of NeurosurgeyIspat General Hospital, Rourkela-769005, IndiaCrresponding author-e mail: rkl_neororabi@dataone.in

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Figure 4. 3-D reconstruction of CT scan of L S spine showing the position of knife.

Figure5. 3-D reconstruction of CT scan of L S spine showing the laterally directed sharp margin.

Figure 6.The knife

Discussion : In USA, only 1% of spinal cord injury occur from stab injury of spine.1 Common site of stab injury in spine are cervical, lower dorsal and lumbar.2,3 In absence of neurological deficit surgical intervention is controversial due to the risk of adding iatrogenic deficit.4 In the present case the direction of knife was from medial to lateral the sharp edge remaining away from the spinal canal. Though the knife has traversed the spinal canal, probably, it pushed the neural elements away from its blunt border like the blunt end of Lulmbar puncture needle pushes the nerve roots. Definite surgical exploration is indicated in retained broken fragments of knife, CSF leak, and damage to the neural elements. MRI is usually deferred as the movement of knife can occur in the strong magnetic field of MRI which can lead to further damage to the neural elements.5 Prognosis for the stab injuries is better than the gunshot wounds with recovery being reported in more than 66% of incomplete injuries.6

References:1. Burney RE, Maio RF, Maynard F, Karunas R. Incidence,

characteristics, and outcome of spinal cord injury at trauma centers in North America. Arch Surg 1993;128: 596-609

2. Lipshitz R. Stab wound of the spinal cord. Handbook. Clin Neurol 1976; 25: 197-207.

3. Peacock WJ, Shrosbree RD, Key AG. A review of 450 stab wounds of the spinal cord. S Afr Med J 1977; 51: 961-964 .

4. Li X, Curry EJ, Blais M, Ma R, Sungarian AS. Intraspinal penetrating stab injury to the middle thoracic spinal cord with no neurologic deficit. Orthopedics 2012 ;35(5):e770-3.

5. Kulkarni AV, Bhandari M, Stiver S, Reddy K. Delayed presentation of spinal stab wound: Case report and review of the literature. J Emerg Med 2000; 18:209-13.

6. Velmahos GC, Degiannis E, Hart K, Souter I, Saadia R: Changing profiles in spinal cord injuries and risk factors influencing recovery after penetrating injuries. J Trauma 38: 1995;334-7.

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Residents Section

This practice paper is designed to incite intrusiveness amongst all the doctors and particularly for doctors desirous to take part in different competitive examinatios. Though key to question paper is given elsewhere, all are requested to verify the answers from standard text books.

Please choose the most appropriate answer to each question.

1. In cerebellar disease all of the following can occur except

a. ataxia b. nystagmus c. scanning speech d. weakness of muscles

2. Which of the statement is true for communicating hydrocephalus?

a. it is a type of hydrocephalus where ventricular system is blocked at foramen of morno.

b. it is a type of hydrocephalus where cerebral aqueduct is blocked

c. it is a type of hydrocephalus where flow of csf is obstructed at superior sagital sinus

d. lumbar puncture is harmful in this condition

3. To rule out subarachnoid hemorrhage which of the following investigations should be carried out without delay?

a. MRI of brain b. CT Scan of brain c. Lumbar puncture d. DSA (angiogram)

4. In spinal cord injury which of the following is most important

a. X-ray of spine b. CT scan of the spine c. immobilization of the spine d. administering high dose of steroid

5. Gandhi neuron or Mirror neuron is found abundantly in the CNS of persons with following qualities.

a. empathy b. anger c. telling truth d. simple life style

6. Which is true regarding treatment of severe acute hyponatremia ( dilutional)

a. infuse 3% normal saline rapidly to bring the serum level of sodium to normal within hours

b. normal saline (0.9%) is the fluid of choice to treat the condition

c. hyponatremia can cause headache, seizure, vomiting coma.

d. fluid restriction should be avoided in the treatment of this condition.

7. Which of the following is not an emergency surgical (operative)condition

a. obstructed hernia b. irreducible hernia c. volvulus d. paralytic ileus

8. Rigidity may not be a feature in which of the following condition

a. Paralytic ileus b. Acute cholecystitis c. Acute appendicitis with perforation d. Peptic perforation

9. Immediate surgery is usually not recommended in which of the following condition

a. acute pancreatitis b. acute appendicitis c. strangulated hernia d. volvulus

10. Pad sign is seen in a. stone in gall bladder

Practice PaperContributors : 1Paramananda Rath, 2Prativa Behera, 3Rabindra N Mohapatra1Department of Pediatrics, 2Department of Pathology, 3Department of NeurosurgeryIspat General Hospital, Rourkela - 769005, India

39

b. carcinoma of stomach c. carcinoma of head of pancreas d. volvulus

11. The highest concentration of potassium is in a. plasma b. isotonic saline c. ringer lactate d. darrow’s solution

12. Highest concentration of potassium is seen in

a. duodenum b. jejunum c. ileum d. colon

13. colonic pseudo-obstruction occurs in all except

a. diabetes mellitus b. dermatomyositis c. scleroderma d. hyperthyroidism

14. Commonest site of ischemic colitis a. hepatic flexure b. splenic flexure c. transverse colon d. sigmoid colon

15. Turcot’s syndrome is associated with a. duodenal polyps b. familial adenomatous polyposis c. brain tumors d. villous adenoma e. hyperplastic polyps

16. Colopotomy is done to treat a. ischeorectal abscess b. pelvic abscess c. appendicular abscess d. perianal abscess

17. Ursodeoxycholic acid is a a. urinary stone dissolving drug b. thrombolytic drug c. gallstone dissolving drug d. antifibrinolytic

18. Aspirin sensitive asthma is associated with a. extrinsic asthma

b. urticaria c. nasal polyps d. obesity

19. Most common sign of aspiration pneumonitis is a. tachypnoea b. bronchospasm c. cyanosis d. crepitations

20. A 60 year old man presented to the emergency with breathlessness ,facial swelling and dilated veins on the chest wall the most common cause is

a. thymoma b. lung cancer c. hodgkin’s lymphoma d. superior venacaval obstruction

21. Most common cause of superior venacaval obstruction

a. thrombosis b. extrinsic compression c. mediastinal lymphoma d. teratoma

22. The following are located in the anterior mediastinum except

a. thymoma b. neurofibroma c. neurogenic parasitic cyst d. teratoma

23. In kartagener’s syndrome all are seen except

a. cystic fibrosis b. dextrocardia c. sinusitis d. absence of cilia

24. Electrical alterans is seen in a. cardiac tamponade b. restrictive cardiomyopathy c. left atrial myxoma d. COPD

25. Which one of the following is not an combined injectable contraceptive ?

a. cyclofem b. cycloprovera

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c. depot provera d. mesigyna

26. Mini pill or micro pill contains a. progesterone b. oestrogen c. both progesterone and oestrogen d. gossypol e. non-steroidal and non-estrogenic

components

27. Which one of the following is an example of a second generation IUCD ?

a. NOVA T b. condom c. lippes loop d. LNG 20

e. progestasert

28. Which one of the following method of communication is not a method of mass approach ?

a. internet b. poster c. role play d. exhibition

29. Nosocomial pneumonia is most commonly caused by ?

a. gram negative bacilli b. gram positive bacilli c. gram negative cocci d. mycoplasma

30. Radiofrequency ablation is done for ? a. ventricular tachycardia b. PSVT c. WPW d. atrial tachycardia

31. Megaloblastic anemia should be treated with both folic acid and Vit B12 because –

a. folic acid alone causes improvement in hematological symptoms but worsening of neurological symptoms.

b. it is a co-factor c. it is enzyme d. none of the above

32. Ring sideroblasts are characteristically seen in

a. myelodysplalstic syndrome(mds) b. acute lymphoid leukemia(ALL) c. acute myeloid leukemia(AML) d. anemia of chronic disease.

33. Pancytopenia with cellular marrow is seen in all except

a. megaloblstic anemia. b. myelodysplasia c. PNH d. g6-pd deficiency.

34. Most common blood transfusion reaction is

a. febrile non hemolytic reaction b. hemolysis c. malarial transmission. d. hypothermia.35. Drug of choice for chronic myeloid

leukemia (CML) is a. hydroxyurea b. imatinib c. infliximab d. ifn

36. Which of the following is a non-absorbable suture

a. polypropylene b. vicryl c. catgut d. polydioxanone

37. Which of the following is defined as Penetrating Neck Injury?

a. 2cm depth of wound. b. injury to vital structure c. breach of platysma d. through and through wound

38. Abbe-Estlander Flap is used for a. lip b. tongue c. eyelid d. ears

39. Most common histological type of the thyroid Ca is

a. medullary type b. follicular type c. papillary type

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d. anaplastic type

40. Anal fissure best diagnosed by a. anoscopy b. history and superficial clinical

examination. c. PR examination d. USG

41. Epispadius is associated with a. bifid pubic symphysis b. chordee c. anal atresia d. intestinal obstruction

42. A new born child has not passed meconium for 48hrs. What is the diagnostic procedure of choice ?

a. USG b. contrast enema c. CT d. MRI

43. First sign of puberty in girls is a. breast budding b. growth sport (peak height velocity) c. menarche d. pubic and axillary hair growth

44. Least failure in sterilization occurs with a. falope ring b. bipolar cautery c. unipolar cautery d. hulka clip

45. Virus associated with cancer cervix is a. HPV b. HIV c. EBV d. HTLV

46. All of the following are known causes of recurrent abortion except

a. TOURCH infection b. SLE c. Rh incompatibility d. syphilis

47. Induction at term is indicated in all of the following except

a. hypertension b. diabetes mellitus

c. heart disease d. renal disease

48. All of the following agents are tocolytics except

a. ritodrene b. salbutamol c. isoxsuprine d. misoprostol

49. Which of the following dietary supplements is recommended for a pregnant lady on heparin

a. follic acid b. calcium c. zinc d. copper

50. The most common cause of short stature is a. constitutional b. systemic disease c. hypothyroidism d. growth hormone deficiency.

51. Probiotics have been found beneficial for use in

a. necrotizing enterocolitis b. neonatal sepsis c. candidiasis d. intestinal perforation

52. Which of the following is most commonly associated with coarctation of aorta?

a. PDA b. bicuspid aortic valve c. aortic stenosis d. VSD

53. Commonest types of seizure in newborn- a. clonic b. tonic c. subtle d. myoclonic

54. Auto logous bone graft is commonly taken from

a. iliac crest b. tibial tuberosity c. greater trochanterd d. fibula

For answers please refer to page 35

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Year 20131. Infect Immun. 2013 Oct 14. [Epub ahead of print]

MBL2 variations and malaria susceptibility in Indian populations.

Jha AN, Sundaravadivel P, Singh VK, Pati SS, Patra PK, Kremsner PG, Velavan TP, Singh L,

Thangaraj K.

CSIR - Centre for Cellular and Molecular Biology, Hyderabad, India.

AbstractBackground : Human Mannose-binding lectin (MBL) encoded by the MBL2 gene is a pattern recognition protein and have been associated with many infectious diseases including malaria. We aim to investigate the contribution of functional MBL2 gene variations with P.falciparum malaria in well-defined cases and in matched controls.

Methods : We re-sequenced the 8.7kb of the entire MBL2 gene in 434 clinically classified malaria individuals from malaria endemic regions of India. The study cohort includes 176 patients with severe malaria, 101 with mild malaria and 157 ethnically matched asymptomatic individuals. Additionally, 830 individuals from 32 socially, linguistically and geographically diverse endogamous populations of India were investigated for the distribution of functional MBL2 variants.Results: The MBL2-221C (X) allelic variant is associated with increased risk of malaria (mild malaria OR: 1.9, P =0.0036; severe malaria OR: 1.6, P =0.02). The exon1 variants MBL2*B (severe malaria OR: 2.1, P =0.036; mild vs. severe malaria OR: 2.5, P =0.039) and MBL2*C (mild vs. severe malaria OR: 5.4, P =0.045) increase the odds of malaria. The exon1 MBL2*D/*B/*C variant increases the risk towards severe malaria (OR:3.4, P =0.000045).The frequencies of low MBL haplotypes were significantly higher in severe malaria (14.2%) compared to mild malaria (7.9%) and asymptomatic (3.8%). The MBL2*LYPA haplotypes confers protection whereas MBL2*LXPA

increases the malaria risk.

Conclusions : Our first findings in Indian populations demonstrate that MBL2 functional variants are strongly associated with malaria and infection severity.

PMID: 24126531 [PubMed - as supplied by publisher]

2. Malar J. 2013 Sep 25;12(1):345. [Epub ahead of print]

Variations in ncRNA gene LOC284889 and MIF-794CATT repeats are associated with malaria susceptibility in Indian populations.

Jha AN, Sundaravadivel P, Pati SS, Patra PK, Thangaraj K.

AbstractBackground : There are increasing evidences on the role of non-coding RNA (ncRNA) as key regulator of cellular homeostasis. LOC284889 is an uncharacterized ncRNA gene on reverse strand to MIF mapped to 22q11.23. MIF, a lymphokine, regulates innate immune response by up-regulating the expression of TLR4, suppressing the p53 activity and has been shown to be involved in malaria pathogenesis.

Methods : In this study, the possible effect of MIF variations on malaria susceptibility was investigated by re-sequencing the complete MIF gene along with 1 kb each of 5[prime] and 3[prime] region in 425 individuals from malaria endemic regions of the Orissa and Chhattisgarh states of India. The subjects comprised of 160 cases of severe malaria, 101 of mild malaria and 164 ethnically matched asymptomatic controls. Data were statistically compared between cases and controls for their possible association with Plasmodium falciparum malarial outcome.

Results : It is the first study, which shows that the allele A (rs34383331T > A) in ncRNA is significantly associated with increased risk to P. falciparum malaria [severe: OR = 2.08, p = 0.002 and mild: OR = 2.09, P = 0.005]. In addition, it has been

Abstracts of research papers of IGH published in National and Inter-national Journal

43

observed that the higher MIF-794CATT repeats (>5) increases malaria risk (OR = 1.61, P = 0.01). Further, diplotype (MIF-794CATT and rs34383331T > A) 5 T confers protection to severe malaria (OR = 0.55, P =0.002) while 6A (OR = 3.07, P = 0.001) increases malaria risk.

Conclusions : These findings support the involvement of ncRNA in malarial pathogenesis and further emphasize the complex genetic regulation of malaria outcome. In addition, the study shows that the higher MIF-794CATT repeats (>5) is a risk factor for severe malaria. The study would help in identifying people who are at higher risk to malaria and adapt strategiesfor prevention and treatment.

PMID: 24066864 [PubMed - as supplied by publisher]

3. Infect Genet Evol. 2013 Mar;14:369-74. doi: 10.1016/j.meegid.2012.12.029. Epub 2013 Jan 17.A rare non-synonymous c.102C>G SNP in the IFNB1 gene might be a risk factor for cerebral malaria in Indian populations.

Jha AN, Singh VK, Singh R, Pati SS, Patra PK, Singh L, Thangaraj K.

CSIR-Centre for Cellular and Molecular Biology, Hyderabad, India. adityanjha@ccmb.res.in

AbstractInterferon beta1 (IFNB1) is a type I interferon that is mainly known for its antiviral activity, but it also regulates a number of anti-inflammatory and immunomodulatory functions. Studies on mouse models of cerebral malaria have established that IFNB1 regulates severe malaria pathogenesis and increases overall survival against malaria. It down-regulates proinflammatory cytokines: TNF, IFNG and ICAM-1, resulting in decreased adherence of Plasmodium falciparum parasitized RBC to capillary wall, entry into the brain and delayed onset of death. Therefore, we hypothesized that variations in IFNB1 gene could regulate malarial pathogenesis. We re-sequenced the complete IFNB1 gene along with 900bp of 5’ up-stream and 500bp of 3’-UTR in 437 individuals from malaria endemic regions of the Orissa and Chhattisgarh states of India. The subjects comprised of 173 cases of severe malaria, 101 of mild malaria, and 156 ethnically matched asymptomatic controls.

Data were statistically compared between cases and controls for their possible association with P. falciparum malarial outcome. Two single nucleotide polymorphisms (SNPs): a synonymous c.153C>T (rs1051922) and a non-synonymous substitution c.102C>G (rs139262191, p.Ser34Arg) were identified. The genotype and allele distribution of c.153C>T did not differ significantly between the study groups [mild, χ(2)2=4.10, p-value<0.13 and severe χ(2)2=0.06, p-value<0.97]. Interestingly, the rare non-synonymous SNP (rs139262191) was observed only in malaria patients. The differences between all cases and controls did not reach statistical significance,however, a statistically significant difference was observed between the asymptomatic control group and the cerebral malaria group [OR=20.32, 95% CI=1.08-382.63, p-value=0.044]. Moreover, the genotypes between cerebral malaria positive and negative groups were not significantly different [OR=5.58, 95% CI=0.61-50.97, p-value=0.123]. Our findings suggest that the IFNB1 variant, p.Ser34Arg, might be a risk factor for cerebral malaria in Indian populations.

PMID: 23333334 [PubMed - indexed for MEDLINE]

4. J Vector Borne Dis 50, September 2013, pp. 232–235

Cardiac involvement in malaria: An overlooked important complicationSaroj K. Mishra, Prativa K. Behera & Sanghamitra Satpathi

5. Malaria Journal 2013, 12:348

The reliability of the physical examination to guide fluid therapy in adults with severe falciparum malaria: an observational studyJosh Hanson, Sophia WK Lam, Shamsul Alam, Rajyabardhan Pattnaik, Kishore C Mahanta, Mahatab Uddin Hasan, Sanjib Mohanty, Saroj Mishra, Sophie Cohen, Nicholas Day, Nicholas White and Arjen Dondorp

doi:10.1186/1475-2875-12-348

Abstract (provisional)Background

Adults with severe malaria frequently require intravenous fluid therapy to restore their

44

circulating volume. However, fluid must be delivered judiciously as both under- and over-hydration increase the risk of complications and, potentially, death. As most patients will be cared for in a resource-poor setting, management guidelines necessarily recommend that physical examination should guide fluid resuscitation. However, the reliability of this strategy is uncertain.

MethodsTo determine the ability of physical examination to identify hypovolaemia, volume responsiveness, and pulmonary oedema, clinical signs and invasive measures of volume status were collected independently during an observational study of 28 adults with severe malaria.

ResultsThe physical examination defined volume status poorly. Jugular venous pressure (JVP) did not correlate with intravascular volume as determined by global end diastolic volume index (GEDVI; rs = 0.07, p = 0.19), neither did dry mucous membranes (p = 0.85), or dry axillae (p = 0.09). GEDVI was actually higher in patients with decreased tissue turgor (p < 0.001). Poor capillary return correlated with GEDVI, but was present infrequently (7% of observations) and, therefore, insensitive. Mean arterial pressure (MAP) correlated with GEDVI (rs = 0.16, p = 0.002), but even before resuscitation patients with a low GEDVI had a preserved MAP. Anuria on admission was unrelated to GEDVI and although liberal fluid resuscitation led to a median hourly urine output of 100 ml in 19 patients who were not anuric on admission, four (21%) developed clinical pulmonary oedema subsequently. MAP was unrelated to volume responsiveness (p = 0.71), while a low JVP, dry mucous membranes, dry axillae, increased tissue turgor, prolonged capillary refill, and tachycardia all had a positive predictive value for volume responsiveness of <=50%. Extravascular lung water >=11 ml/kg indicating pulmonary oedema was present on 99 of the 353 times that it was assessed during the study, but was identified on less than half these occasions by tachypnoea, chest auscultation, or an elevated JVP. A clear chest on auscultation and a respiratory rate <30 breaths/minute could exclude pulmonary oedema on 82% and 72% of occasions respectively.

ConclusionsFindings on physical examination correlate poorly with true volume status in adults with severe malaria and must be used with caution to guide fluid therapy.

Regisration - NCT00692627

Year 20124. PLoS One. 2012;7(10):e48136. doi: 10.1371/journal.pone.0048136.Epub 2012 Oct 24.IL-4 haplotype -590T, -34T and intron-3 VNTR R2 is associated with reduced malaria risk among ancestral indian tribal populations.

Jha AN, Singh VK, Kumari N, Singh A, Antony J, van Tong H, Singh S, Pati SS, Patra PK, Singh R,

Toan NL, Song le H, Assaf A, Messias-Reason IJ, Velavan TP, Singh L, Thangaraj K.

Centre for Cellular and Molecular Biology, CSIR, Hyderabad, India.

AbstractBackground : Interleukin 4 (IL-4) is an anti-inflammatory cytokine, which regulates balance between T(H)1 and T(H)2 immune response, immunoglobulin class switching and humoral immunity. Polymorphisms in this gene have been reported to affect the risk of infectious and autoimmune diseases.

Methods : We have analyzed three regulatory IL-4 polymorphisms; -590C>T, -34C>T and 70 bp intron-3 VNTR, in 4216 individuals; including: (1) 430 ethnically matched case-control groups (173 severe malaria, 101 mild malaria and 156 asymptomatic); (2) 3452 individuals from 76 linguistically and geographically distinct endogamous populations of India, and (3) 334 individuals with different ancestry from outside India (84 Brazilian, 104 Syrian, and 146 Vietnamese).

Results : The -590T, -34T and intron-3 VNTR R2 alleles were found to be associated with reduced malaria risk (P<0.001 for -590C>T and -34C>T, and P = 0.003 for VNTR). These three alleles were in strong LD (r²>0.75) and the TTR2 (-590T, -34T and intron-3 VNTR R2) haplotype appeared to be a susceptibility factor for malaria (P = 0.009, OR =

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0.552, 95% CI = 0.356 -0.854). Allele and genotype frequencies differ significantly between caste, nomadic,tribe and ancestral tribal populations (ATP). The distribution of protective haplotype TTR2 was found to be significant (χ²3 = 182.95, p-value <0.001), which is highest in ATP (40.5%); intermediate in tribes (33%); and lowest in caste (17.8%) and nomadic (21.6%).

Conclusions : Our study suggests that the IL-4 polymorphisms regulate host susceptibility to malaria and disease progression. TTR2 haplotype, which gives protection against malaria, is high among ATPs. Since they inhabited in isolation and mainly practice hunter-gatherer lifestyles and exposed to various parasites, IL-4 TTR2 haplotype might be under positive selection.

PMID: 23110190 [PubMed - indexed for MEDLINE] PMCID: PMC3480467

5. Perit Dial Int. 2012 Nov-Dec;32(6):656-9. doi: 10.3747/pdi.2011.00053.Peritoneal dialysis in patients with malaria and acute kidney injury.

Mishra SK, Mahanta KC.

Internal Medicine, Ispat General Hospital Orissa, India. sarojrkl@gmail.com

PMID: 23212861 [PubMed - indexed for MEDLINE] PMCID: PMC3524900

6. Adv Exp Med Biol. 2013;765:101-7. doi: 10.1007/978-1-4614-4989-8_15.Oscillations in cerebral haemodynamics in patients with falciparum malaria.

Kolyva C, Kingston H, Tachtsidis I, Mohanty S, Mishra S, Patnaik R, Maude RJ, Dondorp AM, Elwell CE.

Department of Medical Physics and Bioengineering, University College London, London, UK.

AbstractSpontaneous oscillations in cerebral haemodynamics studied with near-infrared spectroscopy (NIRS), become impaired in several pathological conditions. We assessed the spectral characteristics of these oscillations in 20 patients with falciparum malaria admitted to Ispat General Hospital, Rourkela, India. Monitoring included continuous frontal lobe NIRS recordings

within 24 h of admission (Day 0), together with single measurements of a number of clinical and chemical markers recorded on admission. Seven patients returned for follow-up measurements on recovery (FU). A 2,048 sampling-point segment of oxygenated haemoglobin concentration ([ΔHbO(2)]) data was subjected to Fourier analysis per patient, and power spectral density was derived over the very low frequency (VLF: 0.02-0.04 Hz), low frequency (LF: 0.04-0.15 Hz) and high frequency (HF: 0.15-0.4 Hz) bands. At Day 0, VLF spectral power was 21.1 ± 16.4, LF power 7.2 ± 4.6 and HF power 2.6 ± 5.0, with VLF power being statistically significantly higher than LF and HF (P < 0.005). VLF power tended to decrease in the severely ill patients and correlated negatively with heart rate (r = 0.57, P < 0.01), while LF power correlated positively with aural body temperature (r = 0.49, P < 0.05). In all but one of the patients who returned for FU measurements, VLF power increased after recovery. This may be related to autonomic dysfunction in severe malaria, a topic of little research to date. The present study demonstrated that application of NIRS in a resource-poor setting is feasible and has potential as a research tool.

PMID: 22879021 [PubMed - indexed for MEDLINE]

7. Hematol Rep. 2012 May 10;4(2):e9. doi: 10.4081/hr.2012.e9. Epub 2012 Jun 26.Genotype-phenotype correlation of β-thalassemia spectrum of mutations in an Indian population

Sahu PK, Pati SS, Mishra SK.

Department of Biochemistry and Molecular Biology, Ispat General Hospital, Rourkela, Orissa;

AbstractCoexistence of thalassemia, hemoglobinopathies and malaria has interested geneticists over many decades. The present study represents such a population from the eastern Indian state of Orissa. Children and their siblings (n=38) were genotyped for β-thalassemia mutations and genotype-phenotype correlation was determined. The major genotype was IVS 1.5 mutation: 26% homozygous (n=10) and 37% (n=14) double heterozygous with other mutations or hemoglobinopathies. Sickle hemoglobin was the major associated hemoglobinopathy (n=12,32%).

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Other mutations found were Cd 8/9, HbE and Cd 41/42. The study population did not contain any IVS 1.1 mutations which is the second major Indo-Asian genotype. Genotypephenotypecorrelation revealed that genotypes of IVS 1.5, Cd 8/9 Cd 41/42 alone or in association, exhibit severe, moderate and mild severity of thalassemia, respectively. Identification of the mutation at an early age as a part of new born screening and early intervention may help reduce the thalassemia-related morbidity.

Keywords : HbS, IVS 1.5 associated genotypes, genotype-phenotype correlation, malaria., β-thalassemia mutations

PMID: 22826799 [PubMed] PMCID: PMC3401138

8. Virus GenesDOI 10.1007/s11262-012-0851-5

Optimization of Dengue-3 recombinant NS1 protein expression in E. coli and in vitro refolding for diagnostic applications T. N. Athmaram • Shweta Saraswat • Princi Misra • Saurabh Shrivastava • Anil K. Singh • Shailendra K. Verma • N. Gopalan • Prativa K. Behara • P. V. L. Rao

Defence Research and Development Establishment, Ministry of Defence (Government of India), Gwalior, MP

Abstract :Dengue non-structural protein (NS1) is known to be protective antigen and also has immense application for serodiagnosis. Several serodiagnostic assays availablefor dengue viral infection are dependent on tissue culturegrown viral proteins. This task is unsafe, laborious, moreexpensive that makes it unsuitable for routine large-scale production. Although bacterial expression is relatively simple and easy for recombinant protein expression, it is more challenging to make NS1 protein with

native structuraland immunological features using bacterial expression system. We have successfully developed a method leading to the purification and refolding of recombinant dengue virus type 3 (DENV3) NS1. The gene encoding NS1 was amplified and cloned in pET28a (?) vector. In order to increase the purity of the recombinant NS1, the transgene was engineered to carry 69 Histidine tags at both N and C-terminal ends. The recombinant construct (pETNS1) was transformed into E. coli Rosetta-gami cells and the expression conditions viz IPTG concentration, media type, temperature, and harvest time were optimized. The size of the expressed protein was found to be*45 kDa and the authenticity of the expressed protein was confirmed using anti-His and anti-NS1 monoclonal antibodies. The NS1 protein was purified under denaturing conditions, to attain the native conformation, NS1 protein was in vitro refolded and dialyzed. The refolded NS1 protein was detected by commercial Immuno chromatographic strip and NS1 specific monoclonal antibodies. IgM antibody capture ELISA was performed using refolded recombinant NS1 protein which recognized the IgM antibodies in dengue- positive samples of acute phase of infection. Our result suggests that rNS1 protein has immense diagnostic potential and can be used in developing point of care diagnostic assays.

9.Nat Rev Neurol. 2012 Aug;8(8):415-6. doi: 10.1038/nrneurol.2012.144. Epub 2012 Jul 24.Infectious disease: Pathogenesis of cerebral malaria-a step forward.

Pati SS, Mishra SK.

Department of Internal Medicine and Biochemistry, Ispat General Hospital, Orissa, India.

PMID: 22825704 [PubMed - indexed for MEDLINE]

About the Ispat General Hospital

Shri G S Prasad inaugurating the AC lounge for waiting patients

CEO Shri G S Prasad at APICON, ODISHA 2012

Chairman Shri C S Verma’s visit to IGH

Liquid Oxygen plant nearing completion

Ispat General Hospital is a modern, multidisciplinary,

comprehensive and premier medical centre in

the eastern region equipped with state of art

diagnostic facilities, equipment and a committed

task force of competent professionals, catering

to the health requirements of employees of RSP,

their family members, supporting population and

inhabitants of neighbouring areas of Odisha and its

adjoining states. The rise in ratio of non-entitled

patients itself speaks of the services provided.

Besides providing clinical services the hospital is

recognized by National Board of Examinations for

providing DNB (post-graduate training) & has won

a prominent place on World map for the quality of

research activities and publications.

There have been many renovations and

modifications in the hospital to keep abreast

with the latest trends in health-care globally.

AC lounges havebeen developed in OPD and near

OTs for comfort of patients and attendants.The

project work for oxygen supply through pipelines

in all units of hospital is nearing completion. This

will give a boost to patient care in all units of the

hospital. Work is on in full swing for development of

trauma centre, which will provide comprehensive

treatment to accident victims in the vicinity of

emergency unit.

Slowly but steadily, as per need and trends, newer

facilities are being developed keeping an eye on

the ultimate goal – “excellence in patient care”.

Contents Page number

Editorial 1Review Article l An Overview of Benign Prostatic Hyperplasia 2 Amulya M. Acharya

Instruction to the authors 5

Original Paper l Redefining WHO criteria of “Severe anemia”in adult patients with malaria 6 Saroj K Mishra

Brief Report l Vector borne viral disease surveillance in hospitalized patients (1989-2009) 10 Radhanath Satpathy, Nimain C Nanda, Pitabas Mishra, Paramananda Rath Saroj K Mishra

Short Communication l Snake bite : our experience 12 Rajyabardhan Pattnaik, Anita Mohanty, Rajlaxmi Panda, Sanjib Mohanty

Case Reports l Bilateral facial nerve palsy (BFNP) following head injury-A case report 15 Pushpa Kumari, Rabindra N Mohapatra

l Atypical presentation of pulmonary hydatid cyst 17 Megharay Majhi, Premanand Panda, Uma Devi, Chinnari M Rao, Sumitra Ratho

l Hypocalcemia - a rare cause of childhood congestive heart failure 20 Pitabas Mishra,, Nimain C Nanda, Jayanta Acharya, Paramananda Rath

l Sickle cell disease with recurrent thrombocytopenia secondary to ITP- A rare Case report 27 Maya Bose,1Nimain C Nanda, Jayanta Acharya, Sanghamitra Satapathy

l A rare case of 99 nails in the GI tract!!! 29 Indira Mishra, Birendra K Sarkar, Jagannath Behera, Sanjay K Acharya, Saroj K Mishra

l Primary Non- Hodgkins Lymphoma of bone: A rare case report with literature review 33 Prativa K Behera, Rabi R Panda, Sanghamitra Satpathy, Aruna M Minz, Megharay Majhi, Ranjan K Patra

Clinical Image l Stab injury of lumbar spine: a case report 36 Binayak Rath, Sanjay k Tiwari, Megharay Majh, Rabindra N Mohapatra

Residents Section

l Practice paper 38

Paramananda Rath, Behera, Rabindra N Mohapatra

Abstracts of research papers of IGH published in National and Inter-National Journal 42

About the IGH

Colour Plates 25-28