328
Short Communication
Cerebral Infarction in a Young Female
Following Snake Bite
RlFAAT BASHIR, M . D . , AND JOHN JlNKINS, M . D . *
SUMMARY We present a normal 13-year old female who developed left cerebral infarction following
envenomation by the carpet viper (Echis car inat us). We have read of only one other case of cerebral
infarction following viper envenomation (Viperi russelli). Possible mechanisms for cerebral infarction in
these circumstances are discussed. It is believed that this complication may be more common than is
reported in the literature.
Stroke Vol 16, No 2, 1985
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ECHIS CARINATUS, the saw-scaled viper, occurs
throughout the Middle East and there have been sightings in many areas of Saudi Arabia.1 Envenomation by
this snake causes local swelling and severe tissue necrosis. Systemic complications are primarily related to
bleeding due to blood depleted of fibrinogen and factors V, VII, II and XIII. This is manifested as hemorrhage in different parts of the body including the gums,
nasopharynx, gastrointestinal tract, urinary tract and
central nervous system.2 The neurological symptoms
include drowsiness, confusion and convulsions. Subarachnoid hemorrhage was seen in three of 115 patients reported from Nigeria, two of whom died.2
Arterial thrombotic complications in vessels near
the site of some viper bites have been well described,3
but arterial thromboses at distant sites are quite rare.
We are aware of only two such instances reported in
the literature.4-5 In this communication, a Saudi Arabian patient who had cerebral infarction after a bite from
Echis carinatus is described, and possible mechanisms
for this phenomenon are discussed.
Case History
A 13-year old right-handed Saudi Arabian female
was clearing the ground for her sheep when she was
bitten on her hand by a snake. She described the snake
as being 50 centimetres long. When we showed her
colored pictures of different snakes, she consistently
pointed out Echis carinatus. A few minutes after the
bite the patient developed severe pain and swelling in
the right arm. She was taken to a nearby infirmary
where she was given three 10 ml intravenous injections
of polyvalent anti-snake serum (Behringwerke). She
showed no immediate reaction to the antivenom and
was subsequently transferred to a local hospital. On
examination, the vital signs were stable. Two deep
fang marks were seen on the right middle finger and
the right arm was markedly swollen. A neurological
examination was normal. Four hours after admission
From the Departments of Medicine, and Radiology,* King Faisal
Specialist Hospital and Research Centre.
Address correspondence to: Dr. Rifaat Bashir, Department of Medicine, King Faisal Specialist Hospital and Research Centre, Riyadh
11211, Saudi, Arabia.
Received August 14, 1984; accepted September 25, 1984.
(ten hours after envenomation), she developed right
hemiplegia with aphasia which evolved over one to
two hours. Complete blood count including platelets,
bleeding studies and prothrombin time, were normal.
She received two more 10 ml injections of polyvalent
anti-snake serum with no change in condition.
Seventeen days later she was transferred to the King
Faisal Specialist Hospital for investigation. The fang
marks on the right middle finger were visible and healing, and there was mild swelling of the right arm. She
had non-fluent aphasia with difficulty in expression
and understanding. She also had right spastic hemiparesis involving the face and the arm, and to a lesser
degree the leg.
A pre- and post-contrast computed tomographic cranial scan performed three weeks after the snake bite
demonstrated areas of low density in the left parietal
region (fig. la, lb) which enhanced irregularly following contrast administration with a serpiginous pattern
(fig. lc, Id). This is compatible with an enhancing
insult to this region and most consistent with infarct. A
digital subtraction angiogram performed subsequently
demonstrated non-filling of the left supraclinoid internal carotid artery and delayed flow within the multiple
left middle cerebral artery branches as compared with
the normal right side (fig. 2). This suggests thrombosis
of the supraclinoid internal carotid artery with attendant slowed flow in the left middle cerebral artery as
collateral flow perfuses the left hemisphere.
Hemoglobin, white blood cell and platelet counts
demonstrated no abnormality, neither did the prothrombin time, partial thromboplastin time and bleeding time. Fibrinogen degradation products, antinuclear
antibody test and antithrombin III activity were all
within the normal range. Platelet aggregability studies
were normal, as were chest X-ray, electrocardiogram
and echocardiogram.
The patient underwent physical therapy and was
seen a few months later, at which time she showed
only moderate improvement.
Discussion
The clinical and radiological presentation of our patient strongly suggests a vascular thrombosis as a cause
for her deficit. The occurrence of vascular thromboses
CEREBRAL INFARCTION FOLLOWING SNAKE B\TE/Bashir and Jinkins
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FIGURES la and lb.
region.
329
Precontrast computerized tomography: demonstrates an ill-defined area of low density in the left parietal
in vessels adjacent to the site of envenomation by some
vipers has been well described;3 however, it is extremely rare for thromboses to occur in distant vessels.2 No clinical thrombosis was seen in 115 patients
reported from Nigeria and only one out of 300 patients
reported from India developed a remote thrombosis. 2 ' 4
That patient was bitten on a leg by Echis carinatus and
developed gangrene of an arm. 4 Another patient, reported from Ceylon, was bitten on the leg by Viper a
russelli and developed thrombosis of the middle cerebral artery, demonstrated by angiography. That patient
did not receive snake anti-venom injections, and the
stroke developed three to four hours after she had been
bitten.5
The rarity of thrombotic events in distant vessels
following Echis carinatus bites is not surprising. The
venom contains endopeptidases that deplete the circulation of fibrinogen, factors V, VII, II and XIII leading
to a state of hypocaogulability. 67 Ancrod, a purified
protein from the venom of the Malayan pit viper (Agkistroden rhodostoma), produces defibrination in vivo
by converting plasma fibrinogen into a soluble, noncross-linked form of fibrin.8'9 Because of this property
Ancrod has been used in clinical trials for the treatment
of thrombotic stroke.10
As a result of defibrination, high titres of fibrinogen
degradation products are seen in some patients.2 There
is evidence mat thrombin formed when Echis carinatus procoagulant acts on prothrombin is unlike physiological thrombin.2 This observation may explain why
thrombocytopenia and microangiopathic hemolysis
are seen in only a few of the more seriously envenomated patients: 10 out of 115 cases in WarreH's study.2
FIGURES lc and Id. Post intravenous contrast computerized tomography: demonstrates irregular, serpiginous areas of high
density corresponding to the low density areas seen on the precontrast computerized tomography compatible with enhancing
infarct.
330
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FIGURE 2.
STROKE
Digital subtraction angiogram: frontal view dem-
onstrates non-filling of the left supraclinoid internal carotid
artery (lower arrow), and delayed flow in multiple left middle
cerebral branches (upper arrow) as compared with the opposite
normal right side.
VOL 16, No 2, MARCH-APRIL 1985
tension could possibly lead to cerebral infarction,13 but
the distribution of the infarct in our patient is not the
typical watershed infarct seen in hypotension.13 Furthermore, as far as could be determined from the treating physician, the patient was not hypotensive before
or after the catastrophe.
The cause of this rare incident of cerebral infarction
is intriguing. It could be related to the vessel damaging
toxin in the snake's venom possibly acting on a preexisting abnormality in a blood vessel wall; or it could
be due to a low grade disseminated intravascular coagulopathy. An episode of hypotension that was unnoticed after the anti-venom injection might have contributed to the patient's problem. Most envenomations
from Echis carinatus occur in the third world,'•2 and so
the possible introduction of computed tomography into
these countries may lead to more reports of cerebral
infarction following snake bite. A contributing factor
to this apparent rarity may also be inefficient or inaccurate reporting of snake bites and their complications in
areas of high incidence. Therefore, with advanced diagnostic equipment and more careful reporting in the
future, the true frequency of this particular sequel to
snake bite may be realized.
References
This diffuse intravascular consumptive coagulopathy
could lead to small, and possibly large, occlusions,"
explaining cerebral infarction in the absence of heart
disease in our patients. However, the bleeding studies
and platelet count being normal the day our patient had
an infarct contravenes this possibility. Studies done at
this hospital 17 days later showed no evidence of disseminated intravascular coagulopathy or pre-existing
coagulopathy. Heart disease was also excluded.
The venom of Echis carinatus contains a vessel
damaging factor "hemorrhagin" which is complement
dependent and can cause leakage across endothelial
cells of cerebral capillaries.2 This factor could have
contributed to our patient's catastrophe but the fact that
the insult was only in one hemisphere argues against
this hypothesis unless there was a pre-existing vascular
problem on that side. Digital substraction angiography
did not show an arteriovenous malformation or other
gross vascular lesion in the cerebral circulation, however this technique cannot rule out the presence of
subtle lesions.
Our patient received three 10 ml injections of snake
anti-venom at a local infirmary immediately after being bitten. About 13 percent of recipients have an
immediate reaction to the Behringwerke antivenom
which includes fever, urticaria, coughing, sneezing,
itching, vomiting and hypotension.12 Profound hypo-
1. Kingston ME: Management of snake bite in Saudi Arabia. King
Faisal Specialist Hospital Medical Journal 1: 87-94, 1981
2. Warrell DA, Davidson NMcD, Greenwood BM et al: Poisoning by
bites of the saw-scaled or carpet viper (Echis carinatus) in Nigeria.
Q J Med 46: 33-62, 1977
3. Warrell DA, Ormerod LDL, Davidson NMcD: Bites by puff-adder
(Bilis arietans) in Nigeria, and value of antivenom. Brit Med J 4:
697-704, 1975
4. Bhat RN: Viperine snake bite poisoning in Jammu. J Indian Med
Assoc 63: 383-392, 1974
5. Ameratunga B: Middle cerebral occlusion following Russell's viper bite. J Trop Med Hyg 75: 95-97, 1972
6. Chugh KS, Mohanthy D, Pel Y et al: Hemostatic abnormalities
following Echis carinatus (saw-scaled viper) envenomation in the
Rhesus monkey. Am J Trop Med Hyg 30: 1116-1120, 1981
7. Koranlik F, Blomback B: Prothrombin activation induced by
Ecarin — a prothrombin converting enzyme from Echis carinatus.
Thrombosis Res 6: 53-63, 1975
8 Bell WR, Bolton G, Pitney WR: The effect of Arvin on blood
coagulation factors. Br J Haematol 15: 589-602, 1968
Pitney WR, Bell WR, Bolton G: Blood fibrinolytic activity during
Arvin therapy. Br J Haematol 16: 165-171, 1969
10. Hossmann V, Hewiss W, Bervermeyer H, Wiedmann G: Controlled trial of Ancrod in ischemic stroke. Arch Neurol 40: 803808, 1983
11 Schwartzman RJ, Hill JB: Neurologic complications of disseminated intravascular coagulation. Neurology (Ny) 32: 791-797, 1982
12 Warrell DA, Warrell MJ, Edgar W et al: Comparison of Pasteur
and Behringwerke antivenoms in envenoming by the carpet viper
(Echis carinatus). Brit Med J 1: 607-609, 1980
13 Adams JH, Brierley JB, Connor RCJ, Treig C: The effects of
systemic hypotension upon the human brain. Clinical and neuropathological observations in 11 cases. Brain 89: 235-268, 1966
Cerebral infarction in a young female following snake bite.
R Bashir and J Jinkins
Stroke. 1985;16:328-330
doi: 10.1161/01.STR.16.2.328
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