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LETTER
Year : 2014  |  Volume : 60  |  Issue : 1  |  Page : 89-90

Posterior reversible encephalopathy syndrome in a patient of snake bite


Department of Nephrology, Sri Venkateswara Institute of Medical Sciences, Tirupati, Andhra Pradesh, India

Date of Web Publication14-Mar-2014

Correspondence Address:
R Ram
Department of Nephrology, Sri Venkateswara Institute of Medical Sciences, Tirupati, Andhra Pradesh
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/0022-3859.128830

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How to cite this article:
Varalaxmi B, Ram R, Sandeep P, Kumar V S. Posterior reversible encephalopathy syndrome in a patient of snake bite. J Postgrad Med 2014;60:89-90

How to cite this URL:
Varalaxmi B, Ram R, Sandeep P, Kumar V S. Posterior reversible encephalopathy syndrome in a patient of snake bite. J Postgrad Med [serial online] 2014 [cited 2019 Nov 13];60:89-90. Available from: http://www.jpgmonline.com/text.asp?2014/60/1/89/128830


Sir,

We read the article of Das et al., [1] on cortical vein thrombosis following snake bite. We present another rare manifestation of snake bite.

A 45-year-old gentleman, nondiabetic and not a hypertensive has presented with history of snake bite. The snake was killed and identified to be a pit viper. The snake bite was on left foot and there was only pain on the 1 st day. Patient did not seek medical aid, till he noticed swelling of left leg, worsening of pain, and fever on day 3 after the snake bite. A day later he noticed anuria and was brought to our institute. On examination there was warmth, redness, and tenderness of left lower limb till mid-thigh; he was not anemic; there were no bleeding manifestations and no jaundice. Blood pressure was 130/80 mmHg and pulse was 96 bpm. The examination of cardiovascular, respiratory, and central nervous system was unremarkable. Investigations revealed, blood urea: 120 mg/dL, serum creatinine: 10.8 mg/dL, serum sodium: 144 mEq/L, serum potassium: 5.8 mEq/L, and hemoglobin: 13.8 g/dL. He was initiated on hemodialysis via right jugular vein catheter. Anti-snake venom was not given. On the 2 nd day after hospital stay, patient complained sudden loss of vision and headache. Examination revealed neither perception of light nor response to projection of rays and normal fundus in both the eyes. Blood pressure was 140/90 mmHg. A computed tomography (CT) of brain showed cortical hypodensity in bilateral occipital regions and magnetic resonance imaging (MRI) revealed cortical hyperintensity in bilateral, parietal, and occipital and subcortical white matter [Figure 1]. The diagnosis of posterior reversible encephalopathy syndrome (PRES) was made. He was given a session of hemodialysis and was monitored for blood pressure rise. About 12 h later there was gradual improvement in vision. The vision returned to normal in 24 h. Patient received 16 sessions of hemodialysis before his urine output improved.
Figure 1: Magnetic resonance imaging (MRI) brain, fluid-attenuated inversion recovery (FLAIR) sequence, axial sections showing cortical hyperintensity in bilateral parietal and occipital and subcortical white matter

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PRES was initially recognized in association with immunosuppressive therapy after transplantation, eclampsia, and acute hypertensive encephalopathy associated with renal disease. [2] The CT and/or MRI of the brain reveals focal regions of symmetric hemispheric edema. [3] The edema of brain predominates in the parietal and occipital regions. [3] There are two theories to explain pathophysiology of PRES. Severe hypertension with failed autoregulation, injury to the capillary bed, and hyperperfusion remains the most popular theory for the brain edema that develops in PRES. [4] The earlier original theory was vasoconstriction due to evolving hypertension leading to hypoperfusion and ischemia and subsequent vasogenic edema. [4] However, in 20-30% of patients who develop PRES, blood pressure is essentially normal. [4] The 'systemic process' may establish a state of neurotoxicity that leads to the PRES imaging pattern. [4]

Our patient neither had sudden increase in blood pressure nor did he receive anti-snake venom, which is not entirely free from central nervous system adverse effects. In the only reported patient of PRES associated with the snake bite, [5] the patient received polyvalent anti-snake venom. In that report the blood pressure of the patient remained lower than 140/90 mmHg and there was no renal failure. Our patient had acute renal failure which by itself is a risk factor for PRES and neurotoxicity of venom might be another cause for PRES.

 
 :: References Top

1.Das SK, 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.  Back to cited text no. 1
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2.Hinchey J, Chaves C, Appignani B, Breen J, Pao L, Wang A, et al. A reversible posterior leukoencephalopathy syndrome. N Engl J Med 1996;334:494-500.  Back to cited text no. 2
    
3.Bartynski WS. Posterior reversible encephalopathy syndrome, part 1: Fundamental imaging and clinical features. AJNR Am J Neuroradiol 2008;29:1036-42.   Back to cited text no. 3
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4.Bartynski WS. Posterior reversible encephalopathy syn-drome, part II: Controversies surrounding pathophysiology of vasogenic edema. AJNR Am J Neuroradiol 2008;29:1043-9.  Back to cited text no. 4
[PUBMED]    
5.Delgado ME, Del Brutto OH. Case Report: Reversible posterior leukoencephalopathy in a venomous snake (Bothrops asper) bite victim. Am J Trop Med Hyg 2012;86:496-8.  Back to cited text no. 5
    


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