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Year : 2013  |  Volume : 6  |  Issue : 2  |  Page : 197-199  

Vasculotoxic snake bite presenting with sepsis, acute renal failure, disseminated intravascular coagulation, and acute respiratory distress syndrome

Department of Medicine, Padmashree Dr. D. Y. Patil Medical College, Hospital and Research Centre, Dr. D. Y. Patil Vidyapeeth, Pimpri, Pune, India

Date of Web Publication10-Apr-2013

Correspondence Address:
Vikram Bhausaheb Vikhe
Department of Medicine, Padmashree Dr. D. Y. Patil Medical College, Hospital and Research Centre, Sant Tukaram Nagar, Pimpri, Pune, Maharashtra
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/0975-2870.110314

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Vasculotoxic snake bites are well known to cause local complications like necrosis and cellulitis and systemic complications such as coagulopathy, acute renal failure (ARF), and hemolysis. We report a case of young female patient who was bitten by a viper. She developed cellulitis, sepsis, ARF, and Disseminated Intravascular Coagulation. She was treated for the above complications and all her renal and hematological parameters returned to normal on seventh day. After this, on the same day, patient developed Acute Respiratory Distress Syndrome probably due to the direct toxic effect of venom on pulmonary vascular endothelium which has been reported as a late complication of snake venom. With close monitoring and proper management of complications, the patient recovered and walked out of the hospital on the twenty first day without any complications.

Keywords: Acute renal failure, Acute Respiratory Distress Syndrome, disseminated intravascular coagulation, sepsis, vasculotoxic snake bite

How to cite this article:
Vikhe VB, Gupta A, Shende P, Jain J. Vasculotoxic snake bite presenting with sepsis, acute renal failure, disseminated intravascular coagulation, and acute respiratory distress syndrome. Med J DY Patil Univ 2013;6:197-9

How to cite this URL:
Vikhe VB, Gupta A, Shende P, Jain J. Vasculotoxic snake bite presenting with sepsis, acute renal failure, disseminated intravascular coagulation, and acute respiratory distress syndrome. Med J DY Patil Univ [serial online] 2013 [cited 2018 Jan 21];6:197-9. Available from: http://www.mjdrdypu.org/text.asp?2013/6/2/197/110314

  Introduction Top

The incidence of snake bites in India is estimated to be about 14 45 900 per year, of which around 45 900 are reported to be fatal. [1] The highest prevalence is in rural area and the maximum number of cases have been reported in the monsoon season. [1] Viper envenomation results in serious local symptoms as well as potentially fatal systemic manifestations chiefly related to coagulation derangement. [2] These manifestations include local cellulitis, necrosis, acute renal failure, and systemic hemorrhagic manifestations. [3] In our case, the patient had both serious local as well as systemic manifestations in the form of early and late complications. [4]

  Case Report Top

An 18-year-old female was admitted with the history of snake bite over the dorsal surface of left hand. The snake in this case was identified as a viper [Figure 1]. After sometime, she developed pain and swelling over the left hand which progressed to involve whole of the left arm. She then developed nausea, vomiting, pain in abdomen, and breathlessness. She developed cellulitis over her left arm within one day. There was no active bleeding noted from the site of snake bite. Her vitals were stable on admission and respiratory rate was 20 cycles per minute. She did not have any neurological manifestations and all her other systems were unremarkable. On admission, her hemoglobin was 13.5 g/dl, total leukocyte count was 36 000/mm 3 with 73% neutrophils, and platelet count was 42 000/mm 3 . Coagulation profile revealed bleeding time of 7 min. 30 sec., clotting time of 12 min., prothrombin time of 50 sec. (control 14 sec.), and the activated partial thromboplastin time of 60 sec. (control 23 sec.). Her serum urea levels were 120 mg/dl, serum creatinine levels were 3.6 mg/dl, and urine report showed microscopic hematuria. Her serum electrolytes, liver function tests, arterial blood gas (ABG) analysis, chest radiograph, and electrocardiogram were within normal limits. She was immediately treated with polyvalent Anti Snake Venom (ASV) as 150 cc in 500 ml 5% dextrose over 1 hr and 100 cc in 500 ml 5% dextrose q8h. Along with this, she was given hydrocortisone 100 mg IV q8h, ceftazidime 2 g IV q12h, clindamycin 600 mg IV q8h, metronidazole 500 mg IV q8h, and frusemide 60 mg IV q8h. She was also transfused with four units of fresh frozen plasma and four units of platelet concentrate. Strict input and output charting along with central venous pressure monitoring was done along with fluid restriction. On second day, in spite of this treatment, she continued to have breathlessness, decreased urine output, evidence of hemolysis, deranged blood urea and creatinine levels. Her chest radiograph now showed bilateral pulmonary edema suggesting fluid overload [Figure 2]. Due to this, she was urgently taken for hemodialysis along with blood transfusion. She also developed subconjunctival hemorrhages [Figure 3]a and ecchymotic patches all over her body [Figure 3]b on the second day. This management was continued till sixth day. Now, her renal functions improved and all other blood parameters and coagulation profile along with chest radiograph returned to normal. On seventh day, suddenly she became breathless again and developed one episode of generalized tonic-clonic seizures. Her respiratory rate was 45-50 per minute and ABG showed pH 7.359, PCO 2 51 mm Hg, PO 2 35.6 mm Hg, HCO 3 28 mmol/l, SO 2 65.3%. Respiratory examination at this point revealed bilateral coarse crepitations and chest radiograph showed bilateral fluffy opacities [Figure 4]. Her Murray Lung Injury Score was calculated as chest radiograph findings: 4, Hypoxemia score: 3, Respiratory system compliance score: 2, PEEP: 2. According to these values, her final Murray Lung Injury Score was 2.75, which was indicative of severe lung injury. [5] On the basis of above findings, a diagnosis of non-cardiogenic pulmonary edema (Acute Respiratory Distress Syndrome, ARDS) was made and she was immediately intubated and put on volume control mode of ventilator with high PEEP (10), low tidal volume (350 ml), and high FiO 2 (100%). Subsequently, over the next seven days, patient was carefully monitored for all ventilator parameters. Her ventilator requirement of PEEP and FiO 2 was significantly reduced and she was gradually weaned off the ventilator on tenth day. Her chest radiograph was repeated and was within normal limits now [Figure 5].
Figure 1: In our case, snake was identified as viper, as it had a triangular head, covered by numerous diamond-shaped scales all over the body on ventral aspect

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Figure 2: Radiograph of chest shows bilateral pulmonary edema suggesting fluid overload

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Figure 3: Patient developed subconjunctival hemorrhages (a) and ecchymotic patches, (b) on Day 2

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Figure 4: Radiograph of chest shows bilateral fluffy opacities

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Figure 5: Chest radiograph done was within normal limits

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  Discussion Top

The clinical manifestations following viper bites depend upon the severity of envenomation. Vasculotoxic snake bite is generally caused by two Viperoid species: Russell's viper and Saw-scaled viper (Echis carinatus). [4],[6] Our patient presented with local and multiple systemic manifestations which were early as well as late. [4] The early manifestations include local pain, swelling, bleeding from bite site, local necrosis, and cellulitis. [3] The systemic bleeding manifestations include Disseminated Intravascular Coagulation which occurs primarily due to direct endothelial damage by venom and secondarily due to procoagulant activity and prolonged defibrination. [3] This can occur within minutes or after several hours to days. [4] In such patients, ARF can develop as early as within 24 hours and as late as after one week. ARF was primarily caused by occlusion of renal vessels by microthrombi, ischemia, and shock. [7],[8] Hemoglobinuria and myoglobinuria cause direct nephrotoxicity, leading to ARF. [7],[8] Late shock occurs due to hypovolumia caused by loss of plasma and blood in extravascular compartment and pulmonary intravascular clotting. [9] Echarin is a prothrombin activator from the venom of Echis carinatus which activates clotting at specific sites in the coagulation cascade. There occurs fibrinolysis and damage to the vascular endothelium, causing spontaneous bleeding due to the presence of activators of factors V, X, IX, and XIII, platelets, protein C, and hemorrhagins in the viper venom. There is also hypotension due to the direct effects of the viper venom on heart and by vasodilation which causes increase in vascular permeability (leading to hypovolemia). [4],[9]

Vomiting, neurotoxicity, and serum creatinine can help clinicians assess prognosis of their patients more accurately and parsimoniously. They also serve as useful sign posts for clinical decision-making and are significant predictors of mortality among inpatients with snake bite. [10] Later on, ARDS developed probably due to pulmonary vascular endothelial damage caused by direct effect of venom on vascular endothelium. [3],[5],[6]

  Conclusions Top

Despite early administration of ASV and antibiotics, our patient developed significant late manifestations in the form of sepsis, ARF, DIC, and ARDS. [11] In cases of viper bite, systemic complications may develop very late, secondary to prolonged defibrination. In such cases, mortality rate has been reported to be very high. Such patients can be managed by close monitoring and proper management of complications like sepsis, DIC, ARF, and proper ventilator management for ARDS to reduce the mortality and morbidity.

  References Top

1.Mohapatra B, Warrell DA, Suraweera W, Bhatia P, Dhingra N, Jotkar RM, et al. Snakebite mortality in India: A nationally representative mortality survey. PLo S Negl Trop Dis 2011;5:e1018.  Back to cited text no. 1
2.Auerbach PS, Norris RL. Disorders caused by reptile bites and marine animal exposures. In: Fauci A, Braunwald E, Kasper D, Hauser S, Longo D, Jameson J, et al., editors. Harrison's principles of internal medicine. New York: McGraw-Hill; 2008. p. 2741-4.  Back to cited text no. 2
3.Kornalík F, Pudlák P. A prolonged defibrination caused by Echis carinatum venom. Life Sci II 1971;10:309-14.  Back to cited text no. 3
4.Warrell DA. Venomous and poisonous animals. In: Cook GC, Zumla AI, editors. Manson's tropical diseases. Philadelphia: Saunders Elsevier; 2009. p. 557-99.  Back to cited text no. 4
5.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. 5
6.Gold BS, Dart RC, Barish RA. Bites of venomous snakes. N Engl J Med 2002;347:347-56.  Back to cited text no. 6
7.Kohli HS, Sakhuja V. Snake bites and acute renal failure. Saudi J Kidney Dis Transpl 2003;14:165-76.  Back to cited text no. 7
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8.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. 8
  Medknow Journal  
9.Warrell DA. Snake bite. Lancet 2010;375:77-88.  Back to cited text no. 9
10.Kalantri S, Singh A, Joshi R, Malamba S, Ho C, Ezoua J, et al. Clinical predictors of in-hospital mortality in patients with snake bite: A retrospective study from a rural hospital in central India. Trop Med Int Health 2006;11:22-30.  Back to cited text no. 10
11.Kularatne SA, Kumarasiri PV, Pushpakumara SK, Dissanayaka WP, Ariyasena H, Gawarammana IB, et al. Routine antibiotic therapy in the management of the local inflammatory swelling in venomous snakebites: Results of a placebo-controlled study. Ceylon Med J 2005;50:151-5.  Back to cited text no. 11


  [Figure 1], [Figure 2], [Figure 3], [Figure 4], [Figure 5]


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