| Article Access Statistics|
| Viewed||3882 |
| Printed||54 |
| Emailed||0 |
| PDF Downloaded||12 |
| Comments ||[Add] |
| Cited by others ||2 |
Click on image for details.
|Year : 2013 | Volume
| Issue : 3 | Page : 235-236
A patient of Russell's viper envenomation presenting with cortical venous thrombosis: An extremely uncommon presentation
SK Das1, S Khaskil1, S Mukhopadhyay1, S Chakrabarti2
1 Department of Medicine, R. G. Kar Medical College and Hospital, Kolkata, West Bengal, India
2 ESIC Hospital, Joka, Kolkata, West Bengal, India
|Date of Web Publication||12-Sep-2013|
S K Das
Department of Medicine, R. G. Kar Medical College and Hospital, Kolkata, West Bengal
Source of Support: None, Conflict of Interest: None
|How to cite this article:|
Das S K, Khaskil S, Mukhopadhyay S, Chakrabarti S. A patient of Russell's viper envenomation presenting with cortical venous thrombosis: An extremely uncommon presentation. J Postgrad Med 2013;59:235-6
|How to cite this URL:|
Das S K, Khaskil S, Mukhopadhyay S, Chakrabarti S. A patient of Russell's viper envenomation presenting with cortical venous thrombosis: An extremely uncommon presentation. J Postgrad Med [serial online] 2013 [cited 2020 Oct 27];59:235-6. Available from: https://www.jpgmonline.com/text.asp?2013/59/3/235/118051
A patient bit by a hemotoxic snake presents with an uncommon mode of presentation.
A 27-year-old healthy female presented with bilateral ptosis and passage of coffee-colored urine for the last 4 hours following snake bite on her left foot 10 hours before admission. The killed snake was identified as Russell's viper. Examination showed edematous, red, hot, and tender left foot with two fang marks [Figure 1], and presence of bilateral ptosis. Twenty minute whole blood clotting time (20 minute WBCT) was markedly raised to (45 minutes). Polyvalent antisnake venom was administered along with an intravenous injection of neostigmine (0.5 mg) and atropine (0.6 mg) in a ratio of 3:2, intermittently. Her ptosis improved.
|Figure 1: Snake bitten right foot showing two fang marks (black arrow) along with local edema and redness|
Click here to view
Routine investigations were normal. Bleeding time (BT) (8 minutes, normal <7.1 minutes), prothrombin time (PT) (50 seconds, control 12 seconds), and activated partial thromboplastin time (aPTT) (65 seconds, control 34 seconds) were raised. Urine examination showed hematuria and gross proteinuria. Initial blood D-dimer, fibrinogen, and fibrin degradation product were normal. Subsequently, she developed dysarthric speech, acalculia, finger anomia, right-left disorientation (suggestive of Gerstmann's syndrome) and right-sided hemiparesis. Other systemic examinations were normal.
Subsequent laboratory investigations revealed persistent hematuria, raised BT, PT and aPTT which were normalized on fifth admission day. Magnetic resonance imaging (MRI) of brain revealed wide area of acute infarction involving left parietofrontal region [Figure 2]. Magnetic resonance (MR) angiography of brain was normal. MR venography of brain showed left lateral sinus thrombosis [Figure 3]. With further enquiry, she had no history of any fever, severe dehydration, offending medication, including OCP intake, hereditary coagulopathies, systemic diseases, or trauma. Carotid and vertebral artery Doppler study was normal. Computed tomography scan of thorax, ultrasonogram of abdomen and echocardiography were normal.
|Figure 2: MRI (axial diffusion weighted imaging) brain showing acute left parietofrontal infarct (white arrow)|
Click here to view
|Figure 3: Coronal image from time‑of‑flight MR venography of brain showing left lateral sinus thrombosis (white arrow)|
Click here to view
On seventh admission day, all coagulation parameters were normalized and hematuria disappeared. Anticoagulant therapy was then started and continued for 3 months. Serum homocysteine, lipoprotein a (Lpa), antinuclear antibody human epithelioid cells (ANA HEp 2), anticardiolipin antibody (IgM, IgG), and anti-ί 2 -glycoprotein I (GPI) antibody, protein C, protein S, antithrombin III, and factor V Leiden mutation were within normal range.
Russell's viper bite is the most common hematotoxic snake bite in India, and most of the patients are referred from rural areas.  Common clinical manifestations are coagulopathy, hemolysis, renal failure, rhabdomyolysis, and neurotoxicity.  Bleeding is the usual presentation of Russell's viper bite. Initially, our patient presented with complication of disseminated intravascular coagulation as evidenced by hematuria, raised BT, PT, aPTT, D-dimer, and low fibrinogen level, which were normalized subsequently. Some patients present with some neuromuscular blockade symptoms. Stroke is an unusual presentation of Russell's viper bite, more so ischemic ones. 
In our case, ischemic stroke was found to be due to lateral cortical sinus thrombosis as a result of Russell's viper bite. Moreover, all the inherent as well as acquired prothrombotic conditions for cortical venous thrombosis were excluded. Follow-up MR venography of brain after 3 months revealed normal study.
The exact pathophysiology of lateral sinus thrombosis due to Russell's viper bite is still unknown. Activation of clotting factors, especially factors V, X and prothrombin by procoagulant enzymes such as arginine, esterase, and hydrolase present in the Russell's viper venom, are the leading cause of vascular thrombosis. Moreover, venom containing protease inhibitors, hemorrhagins, several enzymes and phospholipase A 2 cause toxic vasculitis, vasospasm, endothelial injury, and disseminated intravascular coagulation, which may also play an important role. 
Presence of vascular thrombosis instead of bleeding, remote site of involvement (Vascular thrombosis usually occurs in vessels adjacent to the site of envenomation), and cortical venous thrombosis are an extremely uncommon presentations of Russell's viper envenomation.
| :: References|| |
|1.||David AW. Guidelines for the clinical management of snake-bites in the south-east Asia region. New Delhi: World Health Organization, Regional Office for South East Asia; 2005. p. 1-67. |
|2.||Mosquera A, Idrovo LA, Tafur A, Del Brutto OH. Stroke following Bothrops spp. snakebite. Neurology 2003;60:1577-80. |
|3.||Seneviratne U, Dissanayake S. Neurological manifestations of snake bite in Sri Lanka. J Postgrad Med 2002;48:275-8. |
|4.||Simpson ID. Snakebite management in India, the first few hours: A guide for primary care physicians. J Indian Med Assoc 2007;105:324-8. |
[Figure 1], [Figure 2], [Figure 3]
|This article has been cited by|
||Varalaxmi, B., Ram, R., Sandeep, P., Siva Kumar, V.
| ||Posterior reversible encephalopathy syndrome in a patient of snake bite |
| ||Journal of Postgraduate Medicine. 2014; 60(1): 89-90 |
||Viper envenomation and cerebral venous thrombosis
| ||Senthilkumaran, S. and Balamurugan, N. and Thirumalaikolandusubramanian, P. |
| ||Journal of Postgraduate Medicine. 2013; 59(3): 171-172 |