Journal of Forensic and Legal Medicine 42 (2016) 79e81

Contents lists available at ScienceDirect

Journal of Forensic and Legal Medicine

j o u r n a l h o m e p a g e : w w w . e l s e v i e r . c o m / l o c a t e / j fl m

Case report

An eleven year old boy with pain abdomen and early morning
neuroparalytic syndrome
Milap Sharma*, Shaurya Kalia, Seema Sharma
Department of Pediatrics, DRPGMC, Kangra, H.P., India

a r t i c l e i n f o a b s t r a c t

Article history: An 11 year old boy presented with pain abdomen and tenderness all over body when he got up from
Received 10 June 2015 sleep early in the morning and subsequently had one vomiting after 30 min. He had no other significant
Received in revised form past medical history. The child was shifted to nearby health facility where he was managed as a case of
21 December 2015
acute abdomen on the basis of suggestive history and clinical findings. Within 2 h after the onset of
Accepted 4 May 2016
Available online 24 May 2016
clinical features suggestive of acute abdomen the patient went on to develop marked ptosis and flaccid
quadriplegia. The young boy underwent a sequence of clinical tests which were noncontributory. Based
on the clinical picture, a differential diagnosis of hypokalemic paralysis, botulism, Miller Fischer syn-
Keywords:
Elapid
drome and EMNS were considered. Through exclusion, the most probable diagnosis for the symptoms
Envenomation was elapid envenomation hence he was started on anti-snake venom (ASV) with working diagnosis of
Paralysis EMNS. Within 2 h, he began to show improvement. This recovery with ASV suggests the possibility of
Early morning neuroparalytic syndrome elapid envenomation.
EMNS © 2016 Elsevier Ltd and Faculty of Forensic and Legal Medicine. All rights reserved.

An eleven-year-old boy after having dinner with his family at 9
p.m. went to sleep an hour later in the same room as his mother. At
midnight, his sleep was disturbed by itching over left pinna, which
the boy ignored and it was attributed to mosquito bite. His sleep
then remained undisturbed until he woke up at 4 a.m. and com-
plained of non-colicky, continuous and dull aching epigastric pain
which was followed by one episode of nonbilious vomiting con-
taining only food particles. Subsequently the boy complained of
generalized pain and tenderness all over body and developed
weakness which lead to difficulty in getting up from sitting posi-
tion. In next 2 h the boy was not able to sit unsupported. There was
no history of loose motions, hematuria, subcutaneous bleeds,
constipation, malaena, jaundice, burning micturition, convulsions,
rash, any drug intake or similar illness in any other family member.
The child continued to have pain abdomen and was taken to nearby
health institution. The attending physician started the manage-
ment on the lines of acute abdomen. The child didn't show any
improvement and was referred to next center.
The child presented in the triage area of pediatric emergency of
the hospital where he was referred to at 6.45 a.m. on same day. On
* Corresponding author.
E-mail addresses: dr.milapsharma66@gmail.com (M. Sharma), sk.griffinix@
gmail.com (S. Kalia), seema406@rediffmail.com (S. Sharma).
physical examination he was unable to hold his head unsupported,
had marked ptosis (Fig. 1) and quadriparesis with power of 2/5 over
all joints and negative Babinski's sign. His GCS was 10/15 (E2M4V4),
temperature was 98.6  F, pulse was regular at a rate of 100 bpm,
oxygen saturation was more than 97%, blood pressure was 100/
70 mm Hg and respiration was labored and abdomino-thoracic at a
rate of 24 breaths/min. The child was in severe distress secondary
to his epigastric discomfort, altered sensorium and had tenderness
all over body. His lungs were clear to auscultation. There was no
frothing from mouth. His voice was low toned and he made mur-
muring sounds on deep painful stimulus. Both the pupils were
dilated and there was complete external ophthalmoplegia. The
patient's extremities showed no edema and capillary refill time was
less than 2 s. S1 and S2 heart sounds were normal, and no murmurs
were detected.
Routine laboratory tests revealed a normal complete blood
count and normal plasma values for sodium, potassium, chloride,
bicarbonate, and magnesium. Serum amylase level was normal.
Whole blood clotting time (WBCT) was less than 20 min. Pro-
thrombin time and activated partial thromboplastin time were
normal. His cerebrospinal fluid examination was unremarkable and
EEG did not show any epileptiform activity. Renal function test,
liver function test and X-ray chest were also normal.
The condition of the child had deteriorated considerably since
first complaint of epigastric pain. The examination of site of itching

http://dx.doi.org/10.1016/j.jflm.2016.05.002
1752-928X/© 2016 Elsevier Ltd and Faculty of Forensic and Legal Medicine. All rights reserved.
80 M. Sharma et al. / Journal of Forensic and Legal Medicine 42 (2016) 79e81
Fig. 1. Before treatment.
i.e. lobule of left pinna did not reveal any swelling, induration,
ecchymosis or ulceration. However, on very close observation of the
site, two very faint blanchable petechiae could be made out. These
marks could have gone unnoticed, had the history for the same not
been asked specifically. Based on the clinical picture suggestive of
ptosis (Fig. 1), dilated pupils, complete external ophthalmoplegia
and flaccid quadriparesis with bilateral down going plantar
response, a differential diagnosis of hypokalemic paralysis, botu-
lism, Miller Fischer syndrome and early morning neuroparalytic
syndrome (EMNS) were considered. Through exclusion, the most
probable diagnosis for the symptoms was elapid envenomation,
hence he was started on anti-snake venom (ASV) with working
diagnosis of EMNS. Within 2 h, he began to show improvement.
This recovery with ASV suggested the possibility of elapid enven-
omation. The ptosis, ophthalmoplegia and quadriparesis resolved
over the next 24 h (Fig. 2) and the child was discharged after 48 h of
hospitalization. Subsequent follow up showed no signs of focal
neurological deficits.
There are a total of about 2500e3000 species of snakes
distributed worldwide and of which 500 are venomous.1e4 In In-
dia, the common species of snakes seen are the Elapidae which
includes common cobra, king cobra and krait, Viperidae which
includes Russell's viper, pit viper and saw-scaled viper and
Hydrophiidae (the sea snakes).5 Snake-bite envenomation is a
common occurrence in India especially in the rural areas of the
country and is often a neglected problem affecting millions of
people.6 Depending on the offending snake species, the clinical
picture may be dominated by local symptoms at the site of bite, or
by systemic or neurological manifestations. Serious neurological
complications, including stroke and muscle paralysis, are related
Fig. 2. After treatment.
to the toxic effects of the venom, which contains a complex
mixture of toxins affecting the coagulation cascade, the neuro-
muscular transmission, or both. Metalloproteinases, serine pro-
teases, and C-type lentins (common in viper and colubrid venoms)
have anticoagulant or pro-coagulant activity and may be either
agonists or antagonists of platelet aggregation; as a result,
ischemic or hemorrhagic strokes may occur. In contrast, the
venom of elapids is rich in phospholipase A and three-finger
proteins, which are potent neurotoxins affecting the neuromus-
cular transmission at either presynaptic or post-synaptic levels.
Post-synaptic (a) neurotoxins such as a-bungarotoxin and cobro-
toxin, consist of 60e62 or 66e74 amino acids. They bind to
acetylcholine receptors at the motor end plate. Presynaptic (b)
neurotoxins such as b-bungarotoxin, crotoxin, and taipoxin,
contain 120e140 amino acids and a phospholipase A subunit.7
They release acetylcholine at the nerve endings at neuromus-
cular junctions and then damage the endings, preventing further
release of transmitter. Presynaptic-acting neurotoxins (called b-
neurotoxins) inhibit the release of acetylcholine, while post-
synaptic-acting neurotoxins (called a-neurotoxins) cause a
reversible blockage of acetylcholine receptors.2 Following the
immediate pain of mechanical penetration of the skin by the
snake's fangs, there may be increasing local pain (burning,
bursting, throbbing) at the site of the bite, local swelling that
gradually extends proximally up the bitten limb and tender,
painful enlargement of the regional lymph nodes draining the site
of the bite.3 However, bites by kraits, sea snakes and Philippine
cobras may be virtually painless and may cause negligible local
swelling but the muscle paralysis is marked as was noticed in the
case of this child (Fig. 1). Someone who is sleeping may not even
wake up when bitten by a krait and there may be no detectable
fang marks or signs of local envenoming8,9 as in this case. A
fundamental problem throughout much of the Asia-Pacific Region
is that snake-bite treatment has remained in the domain of
traditional, herbal or ayurvedic practitioners, so that the majority
of snake-bite victims are not seen or recorded in western-style
hospitals or dispensaries. Kraits (Bungarus species) are slender,
nocturnal snakes that often enter human dwellings at night in
search of prey. Case fatality rates of krait envenoming reach up to
77%e100% without treatment.10,11
Early morning neuroparalytic syndrome is a rare presentation of
the elapid bite.8 It is commonly seen among farmers and slum
dwellers that sleep out in the open environment and various
studies have shown that 60e70% of the cases of krait bite occurred
when the patients were asleep.9 These patients are brought to the
hospital with a history of ptosis and paralysis with no bite marks on
the body. Paralysis is first detected as bilateral ptosis and external
ophthalmoplegia progressing to involve the muscles of the palate,
jaw, tongue, neck and deglutition. Generalized flaccid paralysis may
result with retained consciousness provided the patient is not in
circulatory failure. Pre-paralytic symptoms include pain abdomen
paresthesia and numbness. The young boy initially presented with
the same symptoms. Neurotoxic effects were completely reversible
in response to anti-venom. A survey conducted in India and
Pakistan showed that many doctors were even unable to recognize
systemic signs of unobserved viperidae envenoming.12 However it
really becomes difficult to diagnose elapidae envenomation
because of painless bite during sleep13 and is true in the above case
as the child was initially being managed as a case of acute abdomen.
Anti-venom is the only specific antidote to snake venom. A most
important decision in the management of a snake-bite victim is
whether or not to administer anti-venom. This was observed in this
case where the boy responded dramatically to the treatment. A
differential diagnosis for an acute onset of flaccid paralysis should
include EMNS in snake-bite endemic areas and ASV should be
 M. Sharma et al. / Journal of Forensic and Legal Medicine 42 (2016) 79e81
started immediately even in the absence of snake-bite marks. Anti-
venom treatment alone cannot be relied upon to save the life of a
patient with bulbar and respiratory paralysis.14 Patients continue to
die of asphyxiation because some doctors believe that anti-venom
alone is sufficient treatment, though this patient did not require
assisted ventilation. Increased collaboration between clinicians,
epidemiologists, and laboratory toxicologists should enhance the
understanding and treatment of envenoming following snake-bite.
Conflict of interest statement
We wish to confirm that there are no known conflicts of interest
associated with this publication and there has been no significant
financial support for this work that could have influenced its
outcome.
We confirm that the manuscript has been read and approved by
all named authors and that there are no other persons who satisfied
the criteria for authorship but are not listed. We further confirm
that the order of authors listed in the manuscript has been
approved by all of us.
We confirm that we have given due consideration to the pro-
tection of intellectual property associated with this work and that
there are no impediments to publication, including the timing of
publication, with respect to intellectual property. In so doing we
confirm that we have followed the regulations of our institutions
concerning intellectual property.
We further confirm that any aspect of the work covered in this
manuscript that has involved or human patients has been con-
ducted with the ethical approval of all relevant bodies.
We understand that the Corresponding Author is the sole con-
tact for the Editorial process (including Editorial Manager and
direct communications with the office). He/she is responsible for
81
communicating with the other authors about progress, sub-
missions of revisions and final approval of proofs. We confirm that
we have provided a current, correct email address which is acces-
sible by the Corresponding Author.
References
1. Kasturiratne A, Wickremasinghe AR, de Silva N, et al. The global burden of
snakebite: a literature analysis and modelling based on regional estimates of
envenoming and deaths. PLoS Med. 2008;5:e218.
2. Gold BS, Dart RC, Barish RA. Bites of venomous snakes. N Engl J Med. 2002;347:
347e356.
3. Warrell DA. Clinical toxicology of snake bites in Asia. In: White MA, ed.
Handbook of Clinical Toxicology of Animal Venoms and Poisons. CRC Press; 1995:
493e588.
4. Ahuja ML, Singh G. Snake bite in India. Indian J Med Res. 1954;42:661e686.
5. Stephen MP. Biochemistry and pharmacology of colubrid snake venoms.
J Toxicol Toxin Rev. 2002;21:43e83.
6. Simpson ID, Norris RL. Snakes of medical importance in India: is the concept of
the “Big 4” still relevant and useful? Wilderness Environ Med. 2007;18:2e9.
7. Del Brutto OH, Del Brutto VJ. Neurological complications of venomous snake
bites: a review. Acta Neurol Scand. Jun 2012;125(6):363e372. http://dx.doi.org/
10.1111/j.1600e0404.2011.01593.x.
8. Haneef M, George DE, Babu AS. Early morning neuroparalytic syndrome. Indian
J Pediatr. 2009;76:1072.
9. Saini RK, Singh S, Sharma S, et al. Snake bite poisoning presenting as early
morning neuroparalytic syndrome in jhuggi dwellers. J Assoc Physicians India.
1986;34:415e417.
10. Kularatna SAM. Common krait in Anuradhapura, Sri Lanka: a prospective
clinical study, 1996e98. Postgrad Med J. 2002;78:276e280.
11. Lewis RL, Gutmann L. Snake venoms and the neuromuscular junction. Semin
Neurol. 2004;24:175e179.
12. Simpson ID. A study of the current knowledge base in treating snake bite
amongst doctors in the high-risk countries of India and Pakistan: does snake
bite treatment training reflect local requirements? Trans R Soc Trop Med Hyg.
2008;102:1108e1114.
13. Gautam P, Sharma N, Sharma M, et al. Clinical and demographic profile of
snake envenomation in Himachal Pradesh, India. Indian Pediatr. 2014;51:
934e935.
14. Warrell DA. Snake bite. Lancet. 2010 Jan 2;375:77e88.