Proceedings of Ispat General Hospital- 2013


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Proceedings of Ispat General Hospital- 2013

  1. 1. Proceedings of Ispat General Hospital Editorial Board Editor Reviewers Rabindra N Mohapatra Jaya K Pattanayak Co-Editors Paramananda Rath Premanand 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
  2. 2. Or.Eg.àgmX G.S. PRASAD Chief Executive Officer Message I 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) amCaHo$bm-769 011, Amo{‹S>em, Xÿa^mf : 0661-2510018, ¡$Šg : 0661-2511072, do~gmB©Q> : Rourkela-769011, Odisha, Phone : 0661-2510018, Fax : 0661-2511072, Website : ha {H$gr H$s {OÝXJr go Ow‹S>m hþAm h¡ gob There’s a little bit of SAIL in everybody’s life
  3. 3. Editorial Saroj K Mishra Department of Internal Medicine Ispat General Hospital, Rourkela-769005, India Corresponding author e mail: Ispat General Hospital has grown from a small health centre in 1959 to a fullfledged multi-specialty hospital, and a Post graduate Institute of 2013, and is striding forward. 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 coauthors. 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. 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. 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 I congratulate all the contributors, reviewers and Mr. Ramendra Kumar and his team for the quality publication. I express my appreciation to the Editor-inChief, Dr Rabindranath Mohapatra who is the soul of the Journal and has toiled hard to get the ISSN entry. (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.) 1
  4. 4. Review Article An Overview of Benign Prostatic Hyperplasia Amulya M. Acharya Department of Surgery Ispat General Hospital, Rourkela-769005, India. Corresponding author e 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. 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. 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 stromalepithelial 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. Figure1. Pathophysiology of BPH Symptoms : The symptoms collectively known as lower urinary symptoms are of two typesA) 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 2
  5. 5. pass urine. 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 B) Obstructive or voiding symptoms: weak stream, straining at the time of urination, hesitancy, intermittency, feeling of incomplete emptying, post voids dribbling. 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). 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. 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 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. 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. Figure2.AUA guidelines for management of BPH 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 Symptom assessment and management : Sixth international consensus guideline for management 5α-Reductase Inhibitors (5ARIs) : 5ARIs inhibit the α-reductase isoenzyme and prevent conversion 3
  6. 6. Water induced thermotherapy and transurethral ethanol ablation of prostate are emerging technologies but their efficacy is unproved. 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 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. 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 References : Indications of surgery : 1. Burnett AL, Wein AJ. Benign Prostatic Hyperplasi in primary care:What you need to know? J Urol 2003;170:530-547. 1. Severe bothersome symptoms 2. When medical therapy fails, becomes intolerable due to side effects or too costly and bothersome for the patient. 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. Complications such as acute retention of urine, hematuria, bladder stone, recurrent UTI and deterioration in renal function. 3. C Carson III . Role of dihydro testosterone in Benign Prostatic Hyperplasia. Urology 2003; 61: 2-7 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 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. 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. 7. Roehborn CG. Male Lower Urinary Tract Symptoms (LUTS) and Benign Prostatic Hyperplasia (BPH). Med Clin N Am 2011; 95:87-100. Open prostatectomy is now confined to only large prostate glands and where the minimal invasive surgeries are not available. 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. 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. 4
  7. 7. 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. 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. 11. Roehborn CG, Siami P, Barkin J et al. The effect of combination therapy with dutasteride and tamsulosin Instructions for the Authors 1. Only online submission (or soft copy) is accepted. 2. Letter of submission signed by all the authors. Online submission means all authors have signed the letter of submission. 3. Manuscripts must be submitted in .doc or .docx format. Images may be submitted in .jpg format. 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 5. Figures – Maximum 2 colour photographs per 500 words except case report in images where 4 photographs can be submitted. 6. Title page 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. 7. Abstract (objectives, methods, results, conclusion) along with title, and key words 8. Article proper with reference no. immediately following the description as superscript after punctuation mark. 9. Acknowledgements (separate file). 10. References (Vancouver style). Illustrated below. 11. Each table, figures and diagrams in separate file. 12. Legends in separate file 13. Statement regarding Ethics Committee Approval and informed consent from subjects. 14. CD’s / DVD’s of the article if article is not submitted online. 15. On line submission may be made in e-mail: 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. 5
  8. 8. Original Article Redefining severe anemia in adult patients with malaria Sanghamitra Satpathy, 1Prativa K Behera, 1Aruna M Minz, 2Saroj K Mishra*, Department of Pathology, 2Department of Internal Medicine Ispat General Hospital, Rourkela-769005, India Corresponding 1 1 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. 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 bloodcell 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). 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. 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 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 6
  9. 9. p =0.0001) and death was higher [ p=0.039]. 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). 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 %, 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. 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. 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). 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. 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). 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 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%, 7
  10. 10. anemia, however mild it may be. It needs utmost attention as frequently complications co-exist. 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! 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. 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 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. 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 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. 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. 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. 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. 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 A study from Cameroon 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%. 5 6. Mishra SK, Dietz K, Mohanty S l. Influence of acute renal failure in patients with cerebral malaria - a hospitalbased 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 malariarelated mortality: an analysis of 1103 patients. Ann Trop Med Parasitol 2004 ;98:555-558. 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 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. 8
  11. 11. 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. 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. 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. 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. 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 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. 9
  12. 12. Brief Report Vector borne viral disease surveillance in hospitalized patients (1989-2009) Radhanath Satpathy*, 2Nimain C Nanda, 2Pitabas Mishra, 2Paramananda Rath,3Saroj K Mishra Head, Social Paediatrics and Minority Health, AIPH, Bhubaneswar, 2 Department of Pediatrics, 3Department of Internal Medicine, Ispat General Hospital, Rourkela-769005,India *Corresponding author- e mail: 1 1 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 ecosystem 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. 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. Number of Samples analyzed /year Year Result DF WNF CF 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 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 JE 1989 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 10
  13. 13. 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. 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 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: /LinkFiles /CDS_ vector borne_ diseases_in_India.pdf [Cited 2011 Aug 22]. 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. 2. Focusing on tackling vector borne diseases: ICMR DGTimes 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. To conclude, the industrial city Rourkela is prone to vector borne diseases and is endemic for 11
  14. 14. Short Communication Snake bite : our experience Rajyabardhan Pattnaik*, 1Anita Mohanty, 2Rajlaxmi Panda, 3Sanjib Mohanty Department of Critical Care Medicine, 2Department of Anesthesia, 3Department of Internal Medicine Ispat General Hospital, Rourkela-769005, India *Corresponding Author – e-mail: 1 1 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. 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. 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. 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. 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. 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 Krait bite cases mainly present with pain 12
  15. 15. He was weaned off the ventilator and extubated. He was shifted to ward on 12th day and discharged from the hospital on 20th day. 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. 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. 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 Male per cent Female per cent Ventilated per cent Expired per cent 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. Total 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. 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. 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. 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 13
  16. 16. References : 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. 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. 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. 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 = (B) Deficit = Where sodium distribution = 60%, chloride distribution = 20% and bicarbonate distribution=50% For Potassium (Normal value in meq/l ÷measured value in meq/l) ×electrolyte distribution in body compartment (%) × body weight(kg) Body water = 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. (Normal serum Na+ ÷ Actual serum Na+) × normal Body water Where normal body water =0.6×body weight and normal serum Na+=140meq/l 14
  17. 17. Case Report Bilateral facial nerve palsy (BFNP) following head injury-A case report Pushpa Kumari*, 2Rabindra N Mohapatra Department of Ophthalmology, 2Department of Neurosurgery Ispat General Hospital, Rourkela-769005, India * Corresponding author email: 1 1 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. Figure 1.Face of the patient at the time of presentation shows lack of asymmetry of face. It also shows lack of nasolabial fold and frontal follows. 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. 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. 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). 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. 15
  18. 18. 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 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). 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. 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 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 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 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. 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 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. 16
  19. 19. Case Report Atypical presentation of pulmonary hydatid cyst Megharay Majhi, 1Premanand Panda*, 2Uma Devi, 2Chinnari M Rao, 1Sumitra Ratho Department of Radio Diagnosis, 2Department of Pulmonary Medicine Ispat General Hospital, Rourkela-769005, India. *Corresponding authore mail : 1 1 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 (5570%) followed by the lung (18-35%); the two organs can be affected simultaneously in about 5-13% of cases.7,9 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. Figure1. Chest radiograph on the day of admission revealed non-homogenous opacity in right lower lung zone with obscuration of right costophrenic angle & hemidiaphragm His total leukocyte count was 18000/ Cmmof blood 17
  20. 20. 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 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 neuroimaging 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 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 CONCLUSION: Hydatid disease is not as rare in 18
  21. 21. References : 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. 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. Figure 7. CT scan of thorax in coronal plane of Hydatid cyst showing ecto and endo cyst 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 accurate for practical use for this purpose. At the bed side, the CT slice with the largest area of hemorrhage is identified(reference 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 hemorrhage slice. 19
  22. 22. Case Report Hypocalcemia - a rare cause of childhood congestive heart failure Pitabas Mishra*, Nimain C Nanda, Jayanta Acharya, Paramananda Rath Dept.of Paediatrics, Ispat General Hospital, Rourkela-769005, India *Crrespondening author – e mail: 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. 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. 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. 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, Potassium2.2meq/l, SGPT- 205I.Units, Calcium- 4.0mg%, phosphorous- 2.4meq/l, Magnesium- 1.9mg/dl, 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. Figure1. ECG at the time of admission 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 20
  23. 23. 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). 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. 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) 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. Figure3. X-ray of fore arm showing rarefaction of bones of fore arm 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 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 21
  24. 24. CHF is not improving with conventional anti failure treatment. Careful history taking and clinical evaluation might suggest underlying hypo parathyroid disorder. 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. 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. p19178. 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 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. 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. 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 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. 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. 22
  25. 25. Page - 15, Figure - 1 Page - 2, Figure - 1 Page - 15, Figure - 2 Page - 16, Figure - 4 Page - 3, Figure - 2 Page - 7, Figure - 1 Page - 20, Figure - 1 23
  26. 26. Page - 30, Figure - 4 Page - 27, Figure - 1 Page - 27, Figure - 2 Page - 33, Figure - 1 Page - 34, Figure - 2 Page - 30, Figure - 3 24
  27. 27. Spot the Diagnosis Figure 1A Figure 1B Figure 2 Figure 3 Figure 4 Figure 5 Figure 6 Figure 7 For answers please refer to page 28 25
  28. 28. Down the memory lane 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 26
  29. 29. Case Report Sickle cell disease with recurrent thrombocytopenia secondary to ITP - A rare case report Maya Bose*, 1Nimain C Nanda, 1Jayanta Acharya, 2Sanghamitra Satapathy Department Of Pediatrics and Neonatology 2 Department Of Pathology Ispat General Hospital, Rourkela-769005, India *Corresponding author- 1 1 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) immature forms. The megakaryocytes showed smooth borders without any budding of platelets confirming the diagnosis of ITP (Fig.1&2). Key words : Sickle Cell disease , thrombocytopenia, ITP. Case Report : A 9 years old male child, born of nonconsanguinous 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 nonblanchable pin head size petechiae all over body. There was no bony tenderness, café-au-lait spots, skeletal anomalies or hepatosplenomegaly. 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 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 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 27
  30. 30. 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. 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 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. 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 28
  31. 31. Case Report A rare case of 99 nails in the GI tract!!! 1 Indira Mishra, 2Birendra K Sarkar, 2Jagannath Behera, 3Sanjay K Acharya, 1Saroj K Mishra Departments of Internal Medicine, 2Departments of General Surgery Ispat General Hospital, Rourkela-789005, India Corresponding authore mail: 1 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. 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 cooperative. 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. 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. 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. 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 • GI malignancy is another likely diagnosis due to loss of weight, melena, anaemia and emaciation. 29
  32. 32. 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. 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). 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 Figure3. Nails recovered during surgery. There was no perforation. But the gastric mucosa was congested with multiple ulcerations (Figure 4). 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). 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 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 30
  33. 33. had consumed for three – four months when he experienced pain in the stomach and occasional tarry stool. 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. 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 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. 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. 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. 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. 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 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. 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 31
  34. 34. 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. 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. 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 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 References 6. Anonymous. 1. Aydoğdu S, Arikan C, Cakir M, Baran M, Yüksekkaya HA, Woman has 119 nails in stomach. Updated: 2006-07-02 12:08 Saz UE, Arslan MT. Foreign body ingestion in Turkish 7. h t t p : / / w w w. t h e a g e . c o m . a u / w o r l d / 6 8 0 g - o f - children. Turk J Pediatr. 2009;51:127-32. nails-pulled-from-mans-stomach-20091112-ibj2. 2. Dahshan AH, Kevin Donovan G. Bougienage versus html#ixzz1ul8i9Rfg endoscopy for esophageal coin removal in children. J 8. Clin Gastroenterol. 2007;41:454-56. Nataraj G. Write To Communicate. Foundation Books. 3. Hachimi-Idrissi S, Corne L, Vandenplas Y. Management Page Deccan Herald, Sunday 22 February, 2004. of ingested foreign bodies in childhood: our experience 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 failure, 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 levels (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. 32 61.