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Saudi Journal of Kidney Diseases and Transplantation
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Year : 1998  |  Volume : 9  |  Issue : 3  |  Page : 285-289
Acute Renal Failure Due to Snake-Bite: Clinical Aspects

Associate Professor of Medicine, King Saud University, College of Medicine, Abha, Saudi Arabia

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How to cite this article:
Al-Homrany MA. Acute Renal Failure Due to Snake-Bite: Clinical Aspects. Saudi J Kidney Dis Transpl 1998;9:285-9

How to cite this URL:
Al-Homrany MA. Acute Renal Failure Due to Snake-Bite: Clinical Aspects. Saudi J Kidney Dis Transpl [serial online] 1998 [cited 2022 Jan 18];9:285-9. Available from: https://www.sjkdt.org/text.asp?1998/9/3/285/39271

   Introduction Top

Snake-bite poisoning constitute a significant health hazard in the tropics. The estimated annual world mortality from snake-bite is 30,000 to 40,000 of which 15,000 deaths occur in the Indian subcontinent [1],[2] . Of the 2,500 -3,000 species of snakes, only 500 are considered venomous [3] . These species belong to four families: Hydrophidae, which is conventionally characterized as myotoxic; the Elapidae, which is neurotoxic; the Viperidae, which is vasculotoxic and the Atractaspididae, which has mixed chara­cteristics [4] . Hemostatic, vascular and renal complications following snake-bite are well known [5] . This review will highlight the clinical aspects of renal failure due to snake-bite.

   Incidence Top

Renal involvement is a rare complication of severe envenoming by almost any species of snakes [4] , however, it is a common event following bites by Russell's vipers, Echis car hiatus and sea snakes [6],[7],[8] . By far the most important of all renal syndromes is acute renal failure (ARF), which has been reported with varying frequency in different studies. The precise incidence in different geographical regions is lacking but obviously varies with the distribution of the snakes. The incidence of ARF following snake-bite is reported to be as high as 13 - 32% in India [6],[7],[8],[9] , 11% in Nigeria [7] , 6.2% in Middle East [10] , 5% in Thailand [11] and 27% in Ceylon [12] . Although, snake-bite is a common health problem in some areas of Saudi Arabia, the true incidence of ARF following snake-bite is not known and only few case reports were published [13],[14] . This variation in the incidence of ARF is not likely to be due to any genetic predisposition among different ethnic groups but to the venom constituents of different subspecies of snake [15] .

   Mechanism of Envenomation and Renal Involvement Top

Snake's venom contains approximately 20 different enzymes, smaller proteins and peptides [16] . Many of the non-enzymatic proteins are essential for the breakdown of the endothelium. Following a bite, the breakdown of endothelium results in significant loss of fluid in the third space, hypotension and, possibly, cardiovascular collapse [17] . Phospholipase A2, which is one of the components of venom, causes changes in ceil membrane permeability that results in red cell ghost, hemoglobin deposition and liberation of creatine phospho­kinase from muscle cells [18] .

Also snake venom can cause hemostatic defect in a number of different ways: venom procoagulants activates intravascular coagu­lation and produce consumption coagulopathy leading to incoagulable blood. Venom from Russell's viper for instance, selectively activates factor X. Echis carinatus venom activates factor X and accelerates the conversion of prothrombin to abnormal thrombin [19] . This abnormal thrombin promotes coagulation and, at the same time, it prevents stabilization of fibrin both by inhibiting factor XIII activity and stimulating the plasminogen system [15] . These disturbances result in a clinical picture similar to that of disseminated intravascular coagulation (DIC). Elipid and some colubrid venoms activate complement via the alternative pathway, whereas some viperid venoms activate the classical pathway. The role of complement activation in the pathogenesis of envenoming is unclear, but there are many possible interactions with the clotting system and other humoral mediators [20],[21] .

Due to all of these complications several mechanisms have been postulated as possible causes of renal failure. These mecha­nisms include: hemorrhage, hypotension, intravascular hemolysis and hemoglobinuria, rhabdomyolysis, DIC as well as the direct effect of the venom or reaction to the antivenomous protein [22] .

   Presentations and Renal Manifestations Top

The signs of envenomation are well recognized. Initially, severe pain and burning may be noted. These symptoms may be followed by increasing edema, echymosis, nausea, vomiting, hypotension, disseminated intravascular coagulopathy, hemolysis and vesicle and bleb formation [18] . Renal involvement presents with oliguria in 52%, anuria in 9%, and hematuria and proteinuria in 20-80% of the cases [8],[23] . Oliguria or anuria may develop within a few hours, as late as 96 hours after the bite [6],[24],[25] . The pathological changes found by kidney biopsies in patients bitten by snakes are variable. Acute tubular necrosis, interstitial inflammation and edema, hemorrhage, glomerular swelling, aneurysmal dilatation of glomerular capi­llaries and cortical necrosis are common findings [8],[23],[24] . Glomerular lesions are uncommon. However, there are documented cases of proliferative and crescentic glome­rulonephritis [26],[27],[28] . Recently, a review by Mittal revealed that glomerular lesions were observed in a significant number of their series. These lesions were in the form of: mesangiolysis, ballooning of glomerular capillaries, endothelial swelling and splitting of the glomerular basement membrane [29] . Findings related to immunofluorescence and electron microscopic studies are scanty. Golmerular deposits of C3 without immuno­globulins in the glomerular mesangium and arterial wall as well as electron dense mesangial deposits were reported [30],[31] .

   Management First Aid Therapy Top

The general management of a patient bitten by a poisonous snake should begin in the field where the envenomation occurred. This includes calm reassurance, immobility of the affected part, achieved with splint, inactivity and placement of the bitten appendage below heart level. Immediate transfer to the nearest hospital is essential [18] . Incision and suction often result in increased morbidity and disfigurement and are not recommended. Cryotherapy is contra­indicated, since it further compromises blood flow and may result in loss of the bitten appendage [32] .

   Hospital Management Top

Patients should be examined carefully for signs of systemic involvement. Two large­bore intravenous lines should be placed for cardiovascular support and administration of anti-venom, if indicated. Initial laboratory tests should include a complete blood count (CBC), prothrombin time (PT), partial thromboplastin time (PTT), fibrin split products and bleeding time, serum electrolytes, blood urea nitrogen (BUN), serum creatinine, creatine phosphokinase, arterial blood gases, urinalysis and peripheral blood smears. Chest radiographs and electrocardiographs should be obtained in patients with preexisting pulmonary, cardiac disease or with moderate to severe envenomation [18] . Blood tests should be repeated at four to six hour intervals until abnormal parameters stabilize. Patients should be well hydrated using normal saline until blood products can be administered. Platelets should be infused until initial bleeding parameters normalize. In addition, blood should be typed and cross-matched and administered as rapidly as possible, until the patient is hemodynamically stable. Ten to 20 units of fresh-frozen plasma should be infused in the presence of prolonged PT and PTT [33] . Vasopressors for the treatment of hypotension should be withheld until intravascular volume has been restored. Administration of tetanus toxoid and effective treatment of pyogenic infection with appropriate antibiotics is essential. Adequate hydration and alkalization of the urine is recommended in the presence of intravascular hemolysis or rhabdomyolysis.

Once ARF is established, careful monitoring of fluid balance is required. Acid-base and electrolyte disturbances should be corrected using conservative measures and initiation of dialysis whenever indicated. There are reports of successful treatment of ARF by both hemodialysis and peritoneal dialysis [13],[23],[30],[34] . Patients with ARF due to snake-bite, therefore, should be continued on dialysis until irreversibility of the underlying lesion have been proved beyond doubt [24] .

   Prognosis Top

Several factors have been found to influence the severity of ARF. These factors include: the venom dose, the severity of bleeding, hypotension, hemostatic abnormalities and the degree of myoglobinuria [15] . In addition, the prognosis of renal failure was found to directly vary with the severity of renal histopathological changes [8],[15] . Severe renal involvement with diffuse or patchy cortical necrosis is associated with poor prognosis and longer hospitalization [8],[15] . Early hospitalization and effective treatment with maximal dose of antivenom can reduce morbidity and mortality [15],[35],[36],[37] .

   Acknowledgment Top

I would like to thank Mr. Syed Rashid Sami for his excellent secretarial assistance.

   References Top

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2.Chatterjee SC. Management of snake-bite cases. J Indian Med Assoc 1965;45:654-9.  Back to cited text no. 2  [PUBMED]  
3.Reid H. Animal poisons. In: Manson B (ed). Manson's Tropical Disease, London. Balliever Tindall 1982:544-66.  Back to cited text no. 3    
4.Warrell D. Animal toxins. In: Goodon C. Cook. Manson's Tropical Disease, W.B. Sunder Company Ltd 1996:468-515.  Back to cited text no. 4    
5.Mymt-Lwm, Warrell DA, Phillips RE, Tin-Nu-Swe, Tun-Pe, Maung-Maung-Lay. Bites by Russell's viper (Vipera Russelli Siamensis) in Burma: haemostatic, vascular and renal disturbances and response to treatment. Lancet 1985;2:1259-64.  Back to cited text no. 5    
6.Chugh KS, Pal Y, Chakravarty RN, et al. Acute renal failure following poisonous snake-bite. Am J Kidney Dis 1984;4:30-8.  Back to cited text no. 6  [PUBMED]  
7.Warrell DA, Davidson NM, Greenwood BM, et al. Poisoning by bites of the saw scaled or carpet viper (Echis carinatus) in Nigeria. Q J Med 1977;46:33-62.  Back to cited text no. 7    
8.Sarangi A, Patnaik BC, Das GC, et al. Renal involvement in viperine snakebite. Indian J Med Res 1980;71:918-23.  Back to cited text no. 8  [PUBMED]  
9.Chugh KS, Singhal PC, Nath IV, et al. Spectrum of acute renal failure in North India. J Assoc Physicians India 1978:26:147-54.  Back to cited text no. 9    
10.Efrati P, Reif L. Clinical and pathological observation on 65 cases of viper bite in Israel. Am J Trop Med Hyg 1953;2:1085 - 1108.  Back to cited text no. 10  [PUBMED]  [FULLTEXT]
11.Sitprija V, Boonpucknavig V. In Snake venomous and nephrotoxicity (ed): Lee CY. Berlin, Springier-Verlag 1979;997:1018.  Back to cited text no. 11    
12.Visuvaratnam M, Vinayagamoorthy C, Bala Knshnan S. Venomous snake-bite in North Ceylon: a study of 15 cases. J Trop Med Hyg 1970:73:9-14."  Back to cited text no. 12    
13.Al-Homrany M. Acute renal failure following snakebite: case report and review. Saudi J Kidney Dis Transplant 1996:7(3): 309-12.  Back to cited text no. 13    
14.Tilbury C, Madkour M, Saltissi D, Suleiman M. Acute renal failure following the bite of Burton's carpet viper Echis coloratus Gunther in Saudi Arabia: case report and review. Saudi Med J 1987;8:87­-95.  Back to cited text no. 14    
15.Chugh KS. Snake-bite-mduced acute renal failure in India. Kidney hit 1989:35:891­-907.  Back to cited text no. 15    
16.Wingert WA. Chan L. Rattlesnakebites in Southern California and rationale for recommended treatment. West J Med 1988:148:37-44.  Back to cited text no. 16    
17.Garfin SR Mubarak SJ, Davidson TM. Rattlesnakebites: current concepts. Clin Orthop 1979; 140:50-7.  Back to cited text no. 17    
18.Fork TP. Evaluation and treatment of poisonous snakebites. Am Fam Physician 1994;50:123-30,135.  Back to cited text no. 18    
19.Kornalik F, Blomback B. Prothrombin activation induced by ecavin - a prothrombin converting enzyme from Echis carinatus venom. Thromb Res 1975:6:57-63.  Back to cited text no. 19    
20.Warrell DA, Greenwood BM, Davidson MM, Ormerod LD, Prentice CR. Necrosis, hemorrhage and complement depletion following bites by the spitting cobra (Naja nigricollis). Q J Med 1976;45:l-22.  Back to cited text no. 20    
21.Chugh KS, PalY, Ganguly NK. Complement depletion following envenomation by Russell's viper and Echis carinatus (saw scaled viper) in the rhesus monkey. Am J Trop Med Hyg 1977;26:1039-43.  Back to cited text no. 21    
22.Grace TG, Omer GE. The management of upper extremity pit viper wounds. J Hand SurgAm 1980;5:168-77.  Back to cited text no. 22    
23.Shastry JC, Date A, Carman RH, Johny KV. Renal failure following snakebite. A clinicopathological study of nineteen patients. Am J Trop Med Hyg 1977;26:1032-8.  Back to cited text no. 23    
24.Chugh KS, Aikat BK, Sharma BK, Dash SC, Mathew MT, Das KC. Acute renal failure following snakebite. Am J Trop Med Hyg 1975;24:692-7.  Back to cited text no. 24  [PUBMED]  [FULLTEXT]
25.Reid H. Myoglobinuria and sea snakebite poisoning. Br Med J 1961;1:1284-9.  Back to cited text no. 25    
26.Steinback A. Nephrotic syndrome developing after snakebite. Med J Aust 1960; 1:543-5.  Back to cited text no. 26    
27.Seedea YK, Reddy J, Edington DA. Acute renal failure due to proliferative nephritis from snakebite poisoning. Nephron 1974; 13: 455-63.  Back to cited text no. 27    
28.Sitprija V, Boonpucknavig V. Extracapillary proliferative glomerulo­nephritis in Russell's Viper bite. Br Med J 1980;280:1417.  Back to cited text no. 28    
29.Mittal BV. Acute renal failure following poisonous snakebite. J Postgrad Med 1994; 40(3): 123-6.  Back to cited text no. 29    
30.Sitprija V, Benyajati C, Boonpucknavig V. Further observations of renal insufficiency in snakebite. Nephron 1974; 13:396-403.  Back to cited text no. 30  [PUBMED]  
31.Date A, Shastry JC. Renal ultra structure in acute tubular necrosis following Russell's viper envenomation. J Pathol 1982;137:225-41.  Back to cited text no. 31  [PUBMED]  
32.Wingert WA, Wainschel J. Diagnosis and management of envenomation by poisonous snakes. South Med J 1975;68:1015-26.  Back to cited text no. 32  [PUBMED]  [FULLTEXT]
33.Davidson TM. Intravenous rattle snake envenomation. West J Med 1988; 148:45-­7.  Back to cited text no. 33  [PUBMED]  [FULLTEXT]
34.Sitprija V, Sribhibhadh R, Benyajati C. Hemodialysis in poisoning by sea snake venom. Br Med J 1971;3:218-9.  Back to cited text no. 34  [PUBMED]  [FULLTEXT]
35.Malik GM. Snakebites in adult from the Asir region of Southern Saudi Arabia. Am J Trop Med Hyg 1995;52(4):314-7.  Back to cited text no. 35    
36.Annobil SH. Complications of Echis colorata snakebites in the Asir region of Saudi Arabia. Ann Trop Pediatr 1993;13:39-44.  Back to cited text no. 36    
37.Gilon D, Shalev O, Benbassat J. Treatment of envenomation by Echis coloratus (mid­east saw scaled viper): a decision tree. Toxicon 1989;27:1105-12.  Back to cited text no. 37  [PUBMED]  

Correspondence Address:
Mohammed A Al-Homrany
Associate Professor of Medicine, King Saud University, P.O. Box 641, Abha
Saudi Arabia
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