Rikin Raj
BACKGROUND
On the Indian subcontinent, almost all snakebite deaths have traditionally been attributed to the big four consisting of the Russell's viper, Indian cobra, saw-scaled viper and the common krait. In India, the incidence of acute kidney injury following Russell’s viper( E. carinatus) bite is 13 to 32%. As many of the cases are not reported and many cases are falsely believed due to some other underlying factors, the actual figure may actually be upto 40%.1 Tubular necrosis and cortical necrosis are the main causes of AKI.
The aim of the study is to-
1. Evaluate all patients with snakebite both clinically and by investigations.
2. Assess the risk factors and the prognostic factors in snakebite-induced Acute Kidney Injury (AKI).
3. Determine the in-hospital outcome of snakebite patients with AKI.
MATERIALS AND METHODS
Observational Study (A Descriptive and Prospective Type of Study)-
Period of Data Collection- December 2013 to November 2014 (total duration of 1 year).
Inclusion Criteria- All patients coming to emergency department with a definitive history of snakebite. A clinical history taking and a complete physical examination was done in each case. It was followed by laboratory investigations.
RESULTS
Out of 113 patients, 35 patients developed acute kidney injury. Primarily, symptoms complained by the patients were pain at local bite site (74.3%), local bite site swelling (38.1%), vomiting (37.2%), decreased urine output (30.1%), bleeding from any site (24.8%), black or brown urine (20.4%), giddiness (16.8%), limb weakness (15.0%), ptosis (12.4%), altered sensorium (6.2%) and abdominal pain (6.2%). Neurotoxicity was present in 36 (31.9%) patients. Haemotoxicity was present in 36 (31.9%) patients. Local toxicity was present in 42 (37.2%) patients. Primary renal toxicity was present in only 1 (0.8%) patient. IV haemolysis was observed in 12 patients in AKI group, which was seen in only 11 out of 78 patients in non-AKI group, which was statistically significant (p=0.013). All 6 AKI patients who expired had snakebite over lower limb, while 13 of 29 patients who survived had lower limb bite. It was significant statistically (p=0.013). All 6 patients with AKI who expired were observed to have intravascular haemolysis, while only 6 out of 29 AKI patients who survived had intravascular haemolysis. Statistically significant (p=0.002). 5 out of 6 patients with AKI who expired had hypotension on admission, while only 8 out of 29 AKI patients who survived had hypotension on admission. It was statistically significant (p=0.01). All 6 expired AKI patients were observed to have uraemic encephalopathy during their hospital stay, while only 7 out of 29 AKI patients who survived had uraemic encephalopathy. It was statistically significant (p=0.005). All 6 patients with AKI who expired had local toxicity. It was significant statistically (p=0.038). 2 out of 6 patients with AKI who expired had haematotoxicity. Not statistically significant (p=0.83). 2 out of 6 expired AKI patients had undergone haemodialysis, while 7 out of 29 AKI patients who survived received haemodialysis. Not statistically significant (p=0.63). 3 out of 6 patients with AKI who expired had neurotoxicity. Not statistically significant (p=0.93).
CONCLUSION
Overall mortality due to snakebite was 9.7%. Incidence of AKI in snakebite was 30.9%. Lack of education, lapse of time in seeking proper healthcare, visit to any traditional healer/quack therapy prior to hospitalisation, local toxicity (cellulitis, local sepsis, etc.), intravascular haemolysis (in form of black/brown urination), hypotension at presentation, prolonged hospitalisation after neurotoxicity and requirement of ASV on admission were significantly associated with occurrence of AKI and so they were predictors of AKI. Mortality in snakebite-induced AKI patients was 17.1%.
