2. 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

3. 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> : www.sail.co.in
Rourkela-769011, Odisha, Phone : 0661-2510018, Fax : 0661-2511072, Website : www.sail.co.in
ha {H$gr H$s {OÝXJr go Ow‹S>m hþAm h¡ gob
There’s a little bit of SAIL in everybody’s life

5. Editorial
Saroj K Mishra
Department of Internal Medicine
Ispat General Hospital, Rourkela-769005, India
Corresponding author
e mail: sarojrkl@gmail.com
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

6. Review Article
An Overview of Benign Prostatic Hyperplasia
Amulya M. Acharya
Department of Surgery
Ispat General Hospital, Rourkela-769005, India.
Corresponding author
e mail:amulya.acharya@gmail.com
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

7. 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

8. 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

9. 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
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References : 2 most common sources (journal & textbooks) of references are illustrated here.
Journal references
15. Mishra SK, Mohanty S, Satpathy SK, Mohapatra DN. Cerebral malaria in adults - a description of 526
cases admitted to Ispat General Hospital in Rourkela, India. Ann Trop Med Parasitol 2007;101:187-93
16. Singh JK, Bawa M, Kanojia RP, Ghai B, Menon P, Rao KL. Idiopathic simultaneous intussusceptions in
a neonate. Pediatr Surg Int 2009;25:445-7.
Book reference
Miyano T, Kobayashi H, Chen SC. Long term results of biliary atresia. In: Gupta DK, editor. Text Book of
Neonatal Surgery, 1st edn. New Delhi: Modern Publishers; 2000. p. 288-91.
Citation in the text : In the text, references should be cited as superscript after the punctuation mark.
5

10. 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 author-email:sarojrkl@gmail.com
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

11. 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

12. 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

13. 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

14. 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: drsatpathy@rediffmail.com
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

15. 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:http://www.searo.who.int
/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

16. 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: rajyapattnaik@yahoo.co.in
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

17. 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

18. 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

19. 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: rkl_pushpa@hotmail.com
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

20. 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

21. 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 : panda.premanand@gmail.com
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

22. 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

23. 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

24. 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: pitabasmishra@yahoo.co.in
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

25. 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

26. 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

27. 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

28. 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

29. 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

30. 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

31. 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- Email:bosemaya@rediffmail.com
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

32. 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

33. 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: mishraindira_63@yahoo.co.in
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

34. 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

35. 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

36. 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
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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.