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Table of Contents
CASE REPORT
Year : 2022  |  Volume : 10  |  Issue : 1  |  Page : 51-54

Challenges of managing viper envenomation


1 Department of Medicine, INHS, Patanjali, Karnataka, India
2 Department of ENT, INHS, Patanjali, Karnataka, India

Date of Submission24-Aug-2020
Date of Decision28-Aug-2020
Date of Acceptance06-Sep-2020
Date of Web Publication06-Jan-2022

Correspondence Address:
Dr. Purvesh Agrawal
Department of Medicine, INHS Patanjali, Karwar - 581 308, Karnataka
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/ajim.ajim_62_20

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  Abstract 


The signs and symptoms following snakebite envenomation vary according to the type of snake encountered. Typically, Viperidae (vipers) envenomates with a hemotoxin causing coagulopathy and muscle breakdown, while elapids envenomate with a neurotoxin. However, these are not exclusive; the venom from elapids can have a hemotoxic effect and that of the Viperidae can be neurotoxic. We present a case series of viper envenomation presenting to the emergency department at a secondary care Indian Navy Hospital during 2019–2020. These cases highlight the clinical challenges involved in presentation of viper envenomation.

Keywords: Acute kidney injury, acute respiratory distress syndrome, antisnake venom, disseminated intravascular coagulation, twenty-minute whole blood clotting time


How to cite this article:
Agrawal P, Khandelwal N. Challenges of managing viper envenomation. APIK J Int Med 2022;10:51-4

How to cite this URL:
Agrawal P, Khandelwal N. Challenges of managing viper envenomation. APIK J Int Med [serial online] 2022 [cited 2022 Jun 29];10:51-4. Available from: https://www.ajim.in/text.asp?2022/10/1/51/335084




  Case Series Top


Case 1

A 35-year-old serving soldier was found unconscious in his unit noticed during night patrol. After initial first aid, he was transferred to our hospital in gasping condition. The patient had local bite mark over the right great toe and ecchymotic patches over extremities [Figure 1]. There was no active bleeding noted from the site of snake bite. He was hemodynamically unstable. His respiratory rate was 45–50 per minute. Respiratory examination at this point revealed bilateral coarse crepitations, and chest radiograph showed bilateral fluffy opacities [Figure 2]. On admission, his hemoglobin was 13.0 g/dl, total leukocyte count was 17,500/mm3 with 82% neutrophils, and platelet count was 182,000/mm3. Coagulation profile revealed abnormal whole blood clotting test (WBCT), bleeding time of 7 min 30 s, clotting time of 12 min, prothrombin time (PT) of 36 s (control 14 s), and the activated partial thromboplastin time of 52 s (control 23 s). Her serum urea levels were 102 mg/dl, serum creatinine levels were 2.8 mg/dl, serum bilirubin was 0.5 mg%, Aspartate transaminase and alanine transaminase (AST/ALT) was 193/188 IU/l, and urine report showed microscopic hematuria. His serum Creatinine phosphokinase (CPK) levels were 760 IU/l. Arterial blood gas analysis (ABG) showed pH 7.31, PCO2 51 mmHg, PO2 35.6 mmHg, HCO3 28 mmol/l, and SO2 65.3%. Electrocardiogram was suggestive of sinus tachycardia.
Figure 1: Ecchymosis over the right lower limb

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Figure 2: Bilateral fluffy opacities on chest X-ray suggestive of acute respiratory distress syndrome

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On the basis of above findings, a diagnosis of vasculotoxic snake bite with multiorgan dysfunction with noncardiogenic pulmonary edema (acute respiratory distress syndrome [ARDS]) was made. He was put on inotropic support and immediately intubated and put on ventilator support with high Positive end expiratory pressure (PEEP) (10), low tidal volume (350 ml), and high FiO2 (100%).

He was treated with polyvalent antisnake venom (ASV) as 100 cc in 500 ml 5% dextrose over 1 h. WBCT was repeated after initial ASV infusion. It was abnormal, and hence, a second course of 10 vials of ASV was repeated. Along with this, he was given hydrocortisone 100 mg IV q8 h, injection meropenem 1 g IV q8 h, and furosemide 40 mg IV q12 h. He was also transfused with four units of fresh frozen plasma. Strict input and output charting along with central venous pressure monitoring was done along with fluid restriction. A second course of ASV provided only minimal improvement. A further two standard courses of 10 vials ASV were required to overcome his coagulopathy. In total, 40 vials of ASV was required.

Subsequently, over the next 7 days, the patient was carefully monitored for all ventilator parameters. His ventilator requirement of PEEP and FiO2 was significantly reduced, and he was gradually weaned off the ventilator on the 10th day. His chest radiograph was repeated and was within normal limits now [Figure 3]. He tolerated this treatment without obvious adverse effects and was discharged.
Figure 3: Chest X-ray on day 10 with resolution of opacities

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Case 2

A serving soldier, with no relevant medical history, presented to our hospital with acute kidney injury (AKI) after being bitten by a snake on his right lower limb. On arrival to our emergency room, the patient had no lateralizing neurological signs or symptoms. Physical examination revealed moderate pallor, subconjunctival hemorrhages, and chemosis. Jaundice was absent. His vitals were normal, and systemic examination was unremarkable. The right leg and foot were swollen. There was no active bleeding from the fang marks. Laboratory studies disclosed hemoglobin of 9.8 g/dl, hematocrit of 32%, and white blood cell count of 18,000/mm3, with 85% neutrophils and 15% lymphocytes. The platelet count was 16,200/mm3. Blood urea on admission was 110 mg/dl and serum creatinine was 3.6 mg/dl; these rose to 128 mg/dl and 4.2 mg/dl, respectively, the next day. Serum sodium was 132 mEq/l, potassium was 5.4 mEq/l, and bicarbonate was 16 mEq/l. Coagulation studies showed a PT of 18 s with a control of 12 s and a partial thromboplastin time of 62 s with a control of 40 s. The fibrinogen was 200 mg/dl; fibrin degradation products were not detected. A peripheral blood smear showed aniso- and poikilo-cytosis and numerous schistocytes. Urinalysis showed 1+ protein and 10–20 red blood cells (RBCs)/high-power field. Ultrasound revealed normal-sized kidneys with increased echogenicity and maintained corticomedullary differentiation. A provisional diagnosis of AKI was made. ASV was not administered in view of normal 20-min whole blood clotting test (WBCT20) and no apparent bleeding. In the next 24 h, repeat laboratory tests were suggestive of ongoing hemolysis, with hemoglobin falling to <7 g/dl and platelets remaining below 10,000 despite multiple transfusions. Repeated investigations of PT-international normalized ratio (PT-INR), activated partial thromboplastin time, and WBCT20 were always within normal limits. The patient continued to be oliguric but hemodynamically stable. The patient started bleeding through nose and gums and developed malena and bilateral conjunctival effusion. By this time, four units of packed RBCs and 13 units of platelets had been transfused.

In view of ongoing hemolysis, ASV infusion was started. The patient's general condition improved and ongoing bleeding stopped. His platelet count jumped to 50,000/mm3 and hemoglobin stopped falling. He remained oliguric until 10 days after the bite, when he entered a diuretic phase. The serum creatinine returned to 1.0 mg/dl by 16 days after the snake bite, but mild cellulitis and discoloration of the skin of the right leg persisted. He was sent home 21 days after he received the snake bite. Renal function has remained normal on follow-up.


  Discussion Top


Viper venoms contain a number of active substances; some induce clotting, some induce bleeding, and some have other effects. Spontaneous bleeding is caused mainly by direct endothelial damage by a venom component, hemorrhagin, which does not affect coagulation. Hemorrhagin directly damages the blood vessels by loosening the gaps between endothelial cells, thus injuring the basement membrane of the capillaries.[1] In vitro and animal experiments have shown that venoms from Echis carinatus and Russell's viper have a procoagulant effect.[2],[3] In vivo, if the venom dose is large, massive intravascular clotting can stop the circulation and cause rapid death. With smaller doses of venom, such as those typically injected in humans, there is a continuous activation of fibrinogen, producing a fragile fibrin more susceptible to lysis than is ordinary fibrin. The venom thus destroys fibrinogen as quickly as the liver provides it, and as a consequence, the blood either fails to clot or clots poorly. The final coagulation disturbance depends on the balance among the activity of procoagulant, anticoagulant, and fibrinolytic and fibrinogenolytic components of the injected venom. Russell's viper venom selectively activates Factor X. E. carinatus venom, besides activating Factor X, also accelerates conversion of prothrombin to an abnormal thrombin.[4] This abnormal thrombin promotes coagulation, but it simultaneously prevents stabilization of fibrin both by inhibiting Factor XIII activity and by stimulating the plasminogen system. This phenomenon results in a clinical picture similar to that of disseminated intravascular coagulation (DIC), with fibrinolysis and marked consumption of clotting Factor V.[4] In viper bite poisoning, although shock and hemorrhage usually resolve within a week, the coagulation changes can persist for 2 weeks or even longer if specific antivenom is not given. In our first case, ARDS developed probably due to pulmonary vascular endothelial damage caused by direct effect of venom on the vascular endothelium.[5],[6],[7]

Kidneys have high vascularity so are potentially susceptible to venom toxicity. In snake envenomation, the pathogenesis of AKI and renal pathological changes are various, but acute tubular necrosis (ATN) occurs for majority of AKI following snake bite, and most of these cases are self-limiting and resolve completely within 1–8 weeks. In the second case, Acute renal failure (ARF) was primarily caused by the occlusion of renal vessels by microthrombi, ischemia, and shock.[8],[9] Hemoglobinuria and myoglobinuria cause direct nephrotoxicity, leading to ARF.[8],[9] The clinical course was typical of a case of ATN, with renal functions recovering within 3 weeks of injury.

There is a wide variation in hematological abnormalities following a snake bite. The most common coagulopathy associated with snake envenomation is venom-induced consumption coagulopathy (VICC), which results from the activation of coagulation pathway by snake toxins. It causes elevated D-dimer, low fibrinogen, and prolonged PT, all of which are features that overlap with DIC.[10] In the second case, repeated samples of PT-INR and fibrinogen were within normal limits, thereby making a diagnosis of VICC or DIC unlikely. Thrombotic microangiopathy occurs in the subset of patients in snake bite envenomation with or without VICC, although the exact mechanism remains largely unknown.[11]

In the second case, repeated samples of WBCT20 were within normal limits. Hence, ASV was not administered on the day of admission. However, the ongoing hemolysis and continuous fall in platelets prompted us to administer ASV.

Snakebite patients with evidence of coagulopathy, neurotoxicity, or significant systemic effects from envenomation should receive treatment with antivenom. WBCT20 is the most reliable test of coagulation, and if incoagulable blood is found, ASV should be administered.[12] The dose of the antivenom is region-specific, and in the case of India, the initial dose of the polyvalent antivenom (ASV) recommended is 10 vials with further therapy titrated to clinical response, which include improvements in hematological disturbances, halting local tissue effects, and resolution of systemic and neurological effects.[12]

This case series provides a few discussion points. The use of antivenom remains a potent treatment option, even when there is a significant delay from the time of the snakebite to initial care. In a similar fashion to an acute presentation, clinicians faced with a delayed presentation of snakebite envenomation should rely on a complete history, examination, and basic laboratory testing to direct treatment. It is noted, however, that the clinical effects of envenomation are dynamic and recurrence or delayed-onset of significant clinical effects may be seen in up to 50% of cases.[13]

Declaration of patient consent

The authors certify that they have obtained all appropriate patient consent forms. In the form the patient (s) has/have given his/her/their consent for his/her/their images and other clinical information to be reported in the journal. The patients understand that their names and initials will not be published and due efforts will be made to conceal their identity, but anonymity cannot be guaranteed.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.



 
  References Top

1.
Ohsaka A. Hemorrhagic, necrotizing and edema-forming effects of snake venoms. In: Lee CY, editor. Snake Venoms. Berlin: Springer-Verlag; 1979. p. 480-546.  Back to cited text no. 1
    
2.
Chugh KS, Mohanthi D, Pal Y, Dass KC. Coagulation abnormalities induced by Russell's viper venom in the rhesus monkey. Am J Trop Med Hyg 1979;28:763-7.  Back to cited text no. 2
    
3.
Chugh KS, Mohanthy D, Pal Y, Das KC, Ganguly NK, Chakravarty RN. Hemostatic abnormalities following Echis carinatus (saw-scaled viper) envenomation in the rhesus monkey. Am J Trop Med Hyg 1981;30:1116-20.  Back to cited text no. 3
    
4.
Kornalik F, Blombäck B. Prothrombin activation induced by Ecarin - A prothrombin converting enzyme from Echis carinatus venom. Thromb Res 1975;6:57-63.  Back to cited text no. 4
    
5.
Kornalík F, Pudlák P. A prolonged defibrination caused by Echis carinatus venom. Life Sci II 1971;10:309-14.  Back to cited text no. 5
    
6.
Murray JF, Matthay MA, Luce JM, Flick MR. An expanded definition of the adult respiratory distress syndrome. Am Rev Respir Dis 1988;138:720-3.  Back to cited text no. 6
    
7.
Gold BS, Dart RC, Barish RA. Bites of venomous snakes. N Engl J Med 2002;347:347-56.  Back to cited text no. 7
    
8.
Kohli HS, Sakhuja V. Snake bites and acute renal failure. Saudi J Kidney Dis Transpl 2003;14:165-76.  Back to cited text no. 8
[PUBMED]  [Full text]  
9.
Patil TB, Bansod YV. Snake bite-induced acute renal failure: A study of clinical profile and predictors of poor outcome. Ann Trop Med Public Health 2012;5:335-9.  Back to cited text no. 9
  [Full text]  
10.
Dineshkumar T, Dhanapriya J, Sakthirajan R, Thirumalvalavan K, Kurien AA, Balasubramaniyan T, et al. Thrombotic microangiopathy due to Viperidae bite: Two case reports. Indian J Nephrol 2017;27:161-4.  Back to cited text no. 10
[PUBMED]  [Full text]  
11.
Gn YM, Ponnusamy A, Thimma V. Snakebite induced thrombotic microangiopathy leading to renal cortical necrosis. Case Rep Nephrol 2017;2017:1348749.  Back to cited text no. 11
    
12.
Indian National Snakebite Protocols 2007. Indian National Snakebite Protocol Consultation Meeting, Delhi: Neurotoxic Envenomation; August, 2007. p. 10.  Back to cited text no. 12
    
13.
Lavonas EJ, Ruha AM, Banner W, Bebarta V, Bernstein JN, Bush SP, et al. Unified treatment algorithm for the management of crotaline snakebite in the United States: Results of an evidence-informed consensus workshop. BMC Emerg Med 2011;11:2.  Back to cited text no. 13
    


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  [Figure 1], [Figure 2], [Figure 3]



 

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