Snakebite is a common medical emergency and an important occupational hazard in many parts of India, where agriculture remains a major source of employment. Farmers, plantation workers, and rural laborers are particularly vulnerable due to frequent exposure to snake habitats. In 2009, snakebite was included in the World Health Organization’s list of neglected tropical diseases, confirming its significant public health impact in tropical regions. Snakebite accounts for tens of thousands of deaths annually and results in considerable morbidity, including chronic physical disability. Extensive research has identified the venomous snake species responsible for envenomation, the biochemical nature of their venoms, and the clinical effects observed in human victims.¹ Globally, up to five million snakebites occur each year, resulting in an estimated 2.4 million envenomations and approximately 94,000–125,000 deaths annually. Limited access to healthcare facilities, delays in treatment, and scarcity of antivenom significantly increase the severity of envenomation and worsen outcomes.² The Indian subcontinent accounts for more than 40% of global snakebite-related mortality,³ largely due to ignorance, persistence of harmful traditional practices, and lack of adequate medical facilities in remote areas. Various studies estimate that 15,000–25,000 deaths occur annually in India due to snake envenomation,⁵ whereas global mortality is estimated at 30,000–40,000 deaths per year. Snakebite contributes to 2.8–5.3% of total hospital mortality in different Indian states, compared to approximately 20 deaths per year in the United States and an even lower mortality rate in Europe. The high mortality in India is attributed to climatic factors, rural predominance of the population, and heavy dependence on agriculture. For these reasons, India is often referred to as the “land of exotic snakebites.”⁵ Snakebite is frequently encountered in the Andhra Pradesh region. Among the toxic effects of envenomation, bleeding diathesis due to haematotoxic venom is the most common and clinically significant manifestation. Snakebite is an environmental, occupational, and climatic hazard in rural areas, and community education regarding preventive measures may substantially reduce the incidence of bites. Awareness of local snake species, their habitats, seasonal and diurnal activity patterns, and environmental conditions associated with increased snake activity is essential. While some species such as kraits are predominantly nocturnal, others are mainly diurnal. India is home to approximately 216 species of snakes, of which about 52 are venomous. However, only a few species are commonly responsible for clinically significant envenomation.4,5 These include: 1. Russell’s viper (Daboia russelii) 2. Cobra (Naja naja) 3. Krait (Bungarus caeruleus) 4. Saw-scaled viper (Echis carinatus) and pit vipers Considering the high incidence of snakebite and the predominance of haematotoxic manifestations in this region, the present study was undertaken to evaluate the clinical spectrum of snakebite envenomation, with particular emphasis on coagulation disorders, as bleeding diathesis represents the most common and serious manifestation. The study also aims to analyze both haematotoxic and neurotoxic clinical presentations following snakebite. AIMS AND OBJECTIVES To study the various clinical manifestations following snakebite and to evaluate coagulation abnormalities following haematotoxic snakebite. Prognostic factors assessed include: 1. Time interval between snakebite and hospital admission 2. History of first-aid measures received 3. Presence of systemic involvement 4. Site of the bite

Study Design and Source of Data This cross-sectional observational study was conducted in the Emergency medical ward of Katuri Medical College, Chinnakondrupadu, Guntur, Andhra Pradesh. A total of 100 patients presenting with definite evidence of snakebite were included during the study period from July 2017 to October 2022. All patients were evaluated at the time of admission, before and after administration of antisnake venom (ASV), and were managed according to standard treatment protocols. Patients were followed up during their hospital stay until recovery or death. Patients who reported a history of snakebite but lacked definite clinical features or evidence of envenomation were excluded. Bites due to other animals or non-poisonous snakes were also excluded. Previous studies have shown that haemorrhagic manifestations are among the most common and significant clinical features following snakebite. In this study, patients were evaluated for coagulation disorders after screening with bedside clotting time (CT) and bleeding time (BT), even when these values were initially normal, if there was evidence of systemic envenomation. Methods of Data Collection Patients admitted with symptoms, signs, and definite evidence of snakebite were enrolled. The following were considered definitive evidence of snakebite: 1. Presence of fang marks 2. The snake responsible for the bite being identified and brought by the patient or attendants 3. Reliable and unequivocal history of the snake being seen biting the patient by the victim or attendants Initial laboratory evaluation included bedside assessment of bleeding time (BT) and clotting time (CT). Prolongation of either test was considered evidence of envenomation with coagulation abnormality. Evidence of envenomation was also established by observing local reactions such as pain, swelling, rapid progression of edema, or cellulitis extending beyond one joint. One healthy volunteer matched for age and sex was selected as a control for comparison. Clinical features were analyzed even in patients with initially normal BT and CT, as venom toxicity may manifest as haematotoxicity, neurotoxicity, or a combination of both. Inclusion Criteria 1.History of snakebite 2.Presence of fang marks 3. Prolonged bleeding time or clotting time on bedside testing 4. Presence of one or more clinical manifestations of snakebite, including: oLocal swelling oHaemorrhages oBlister formation oVomiting oAbdominal pain oRegional lymphadenopathy Exclusion Criteria 1.Bites due to causes other than snakebite 2.Known bleeding disorders 3.Chronic alcoholism 4.Acute or chronic liver disease 5 Pregnant women 6. Patients receiving anticoagulant therapy Sampling Procedure All patients admitted to the emergency ward with definite evidence of poisonous snakebite were assessed through detailed clinical examination based on inclusion criteria. Clinical features and coagulation parameters were recorded in a pre-designed proforma that included all possible manifestations of snakebite envenomation. Data from cases were compared with controls and subjected to statistical analysis. Laboratory Parameters • Bleeding Time (BT): Normal range 2–7 minutes • Clotting Time (CT): Normal range 30–36 seconds • Prothrombin Time (PT): Normal range 11–18 seconds Tourniquet Test (Capillary Resistance Test of Hess) The tourniquet test was performed to assess capillary fragility associated with thrombocytopenia. A sphygmomanometer cuff was applied to the upper arm and inflated to 100 mmHg for 5–7 minutes. If systolic blood pressure was less than 100 mmHg, the cuff was inflated to a pressure midway between systolic and diastolic values. Two to three minutes after deflation, once congestion subsided, petechiae were counted in a 3-cm diameter area located 1 cm below the cubital fossa. In normal individuals, up to 10 petechiae may be present, though up to 20 can be considered normal. More than 20 petechiae was considered abnormal. In severe thrombocytopenia, petechial counts may exceed 100. The test is positive in most cases of significant thrombocytopenia but may be negative in mild or moderate cases. In patients with widespread purpura, the test was considered unnecessary and inappropriate. Statistical Analysis Continuous variables were expressed as mean ± standard deviation (SD), and categorical variables were expressed as percentages. Differences between study and control groups were analyzed using the Chi-square test. A p-value<0.005 was considered statistically significant.

A total of 100 patients with snakebite were analyzed. Males constituted 65% and females 35% of cases. Most patients were farmers from rural areas, indicating snakebite as an occupational hazard. The majority belonged to the 18–45 year age group. Temporal and Circumstantial Distribution Fifty-five percent of bites occurred between May and September, corresponding to the rainy season. Most bites (69%) occurred during daytime (6 am–6 pm). Eighty-two percent of patients presented within 6 hours of the bite, 15% within 6–24 hours, and 3% after 24 hours, often with severe bleeding manifestations. First Aid Measures Some patients received first aid such as tight tourniquet application or local incision before admission, while most received tetanus toxoid at nearby primary health centers. Patients who received tourniquets or incisions had increased local swelling; however, there was no significant difference in systemic envenomation or haemorrhagic complications between those who received first aid and those who did not. Confirmation and Site of Bite Fang marks were observed in 87 patients. The snake species was identified in 37 cases (35 viper, 2 cobra). The majority of bites involved the lower limbs (feet and toes), followed by upper limbs (hands and fingers). Severity of Envenomation Fifteen patients had severe systemic envenomation, 84 had moderate, and one had mild envenomation. Neurotoxicity was observed in 5 patients, with 2 showing combined neurotoxic and haematotoxic features, suggesting predominance of viper bites in this region. Local and Haemorrhagic Manifestations Local swelling was the most common finding. Bleeding manifestations were seen in 82 patients, most commonly bleeding from the bite site (73%), followed by bleeding from injection sites. Ecchymosis was noted in 5 patients. Haematuria occurred in 4 patients and gum bleeding in 2 patients. Severe bleeding required blood transfusion and resolved following ASV therapy. Neurological and Systemic Manifestations Five patients developed neurological symptoms, including ptosis, dysphagia, and respiratory paralysis. Two patients required mechanical ventilation and recovered within three days; the remaining responded to ASV and anticholinesterase therapy. Vomiting occurred in 57 patients and was ASV-related in 16 cases. Cardiovascular symptoms such as palpitations, chest pain, and breathlessness were attributed to anxiety, as examinations and ECGs were normal. Renal and Other Complications Fourteen patients developed acute renal failure; 10 improved with conservative management, while 4 required hemodialysis, with complete recovery. Other complications included blister formation (48%), local infection (38%), fever (12%), confusion (8%), shock (2%), deep vein thrombosis (1%), and transient limb weakness (2%). ASV Reactions and Mortality Adverse reactions to ASV occurred in 10 patients: 6 mild and 4 severe, all managed successfully with appropriate treatment. No cases of tetanus or gas gangrene were observed. The overall mortality was 2%, with both deaths occurring in patients presenting with severe haemorrhagic shock and non-clotting blood. Table 1. Analysis of the coagulation tests GROUPS Total Test control PLATELET COUNT <1lakh Count 3 1 4 % within GROUPS 3.0% 1.0% 2.0% >1lakh Count 97 99 196 % within GROUPS 97.0% 99.0% 98.0% Clotting Time Abnormal Count 15 0 15 % within GROUPS 15% 0% 7.5% Normal Count 85 100 85 %within groups 85% 100% 92.5% Prothrombin Time Normal Count 77 100 177 % within GROUPS 77.0% 100.0% 88.5% Ab Normal Count 23 0 23 % within GROUPS 23.0% .0% 11.5% APTT Normal Count 85 100 185 % within GROUPS 85.0% 100.0% 92.5% Ab Normal Count 15 0 15 % within GROUPS 15.0% .0% 7.5% TABLE 2: Complications, haemoglobin levels Frequency Valid Percent Cumulative e Percent Valid Minor complications 83 83.0 83.0 ARF 14 14.0 97.0 DVT 1 1.0 98.0 Death 2 2.0 100. Hb<10 Count 15 14 29 % within groups 15.0 14.0 14.5 Hb>10 Count 85 86 171 % within groups 85.0 86.0 85.5 TABLE 3: Laboratory parameters in the study Frequency PLATELET COUNT LESS THAN ONE LAKH 3% HEMOGLOBINLESS THAN 10 GM 15% % PROTHROMBIN TIME PROLONGED 23% % APTT PROLONGED AFTER SNAKEBITE 15% BLEEDINGTIME Prolonged 2 CLOTTINGTIME Prolonged 15 PLATELETCOUNT<1 lakh 3 PROTHROMBINTIME Prolonged 23 APTT Prolonged 15 Table 4. Statistical analysis of haematological and coagulation tests Mean Std. Minimum Maximum P value BT Tes 93.1300 61.12888 66.00 600.00 .444 Ctrl 87.7900 33.47011 66.00 235.00 CT Tes 245.737 103.88039 .00 310.00 .869 Ctrl 243.280 106.23559 .00 310.00 PT Tes 18.7216 5.43281 14.00 38.00 .855 Ctrl 18.8660 5.54457 14.00 38.00 APTT Tes 31.9583 21.60503 20.00 222.00 .997 Ctrl 31.9688 21.60431 20.00 222.00 PLT Tes 1.6581 .46551 .16 2.50 .330 Ctrl 1.9901 3.36664 .16 35.00 P <0.005 is highly significant

The incidence of the snake bite in males in present study (100 patients) is 65% and females is 35%, ratio of male to female is 1.8:1. As males were involved in farming the incidence is also higher. This study is in accordance with Shubham Agarwal et al 60 (53 patients) who also saw the same incidence in males and females with male to female ratio of 1.7:1. Age of the patients ranged from 17-85 years in Shubham Agarwal et al 6 but in our study age group ranged from 18-45 years (74%). The maximum incidence of snakebites in summer months in tropical and sub-tropical climates appear to be universal. In present study most of snakebite occurred during day 69% which is different from N Sharma et al. 60.6% occurred at night and in Bhalla et al also maximum bites were in the night (72.66%), Sharma et al., studied 142 cases of snake bite, of which 52 were viper bites . In our study 35 cases were due to viper bite and 16 viper bites in Krishnappa et al.7-11 Fang marks are presented in 87 patients out of 100 cases in present study but Harshavardhana et al 12., reported in 33 (66%) patients had fang marks. In our study there was essentially no difference in the clinical picture of the patients bitten by Russel’s Viper and of those bitten by Echis carinatus. This result is similar to that of the study reported by Bhat RN from Jammu in 1973.13 In Viperine bite local swelling has been emphasized as the most valuable sign of venom dose. The presence of local swelling in all the 51 patients who received local treatment and only in 49 patients who had no local treatment, with no appreciable difference in the grade of systemic poisoning in the two groups, would indicate that local treatment only aggravates the local swelling without any benefit to the patient. In view of this result we strongly advocate, not to give any local treatment following snakebite. This results is similar to that of observed by Bhat in 1973. We observed that the study of time period between the snakebite and the onset of coagulation disorder varied from person to person between one to several hour depending upon the amount of venom injected and type of snake. In his study Bhat reported that only 3% of his patients developed bleeding within the 1st 6 hours after the bite while the majority of the patients (83%) developed haemorrhages between 7 and 48 hours and 13% developed haemorrhages even after 48hour. Arterial thrombosis has been described as a local complication of bites by some vipers, but would seem to be an unlikely complication in patient with incoagulable blood. Yet one of Bhat’s patients developed gangrene of left arm after being bitten on the right foot, by E,carinatus. Ameratunga found clinical and angiographic evidence of middle cerebral artery occlusion in a patient with viper russelii bite. In Patil et al.,14 one patient developed myocardial infarction and cortical venous sinus thrombosis but in our study none of them developed these complications. We recommend to search for these unusual complications. Most common bleeding manifestation we have observed is bleeding form site of bite (48 patients i.e.,48% ). In Chaudhari et al.15 66 (85.7%) had bleeding from bite site, and in K Saravu et al., 23 (41.07%), suggesting bleeding from site of bite is most common. Ecchymosis was present in 2 (4.75%) patients in the Bhalla et al. but in present study 5 (5%) patients had ecchymosis. In Bhalla study 18 (42.85%) patients had hematuria but in our study 4 (4%) patients had Hematuria. Patil et al., observed 9 (10.22%) patients and Krishnappa et al had noted hematuria in( 6.7% ).This finding differed from Bhat RN and Reid 16 et al. Haematuria was profuse. Haemoptysis was actually mild with only blood stained sputum. As |Bhat RN6, we have not found it advisable to elicit this symptoms by asking the patient to cough hard, as has been recommended by Reid25. Violent coughing can precipitate a severe haemoptysis in a patient with no clotting blood. None of our patients developed subarachnoid haemorrhage while Bhat reported three patients with subarachnoid haemorrhage. Following his study Bhat suggested that it is important to keep a patient in bed rest as long as coagulation defect persist to prevent SAH. We strongly advocate this practice because SAH, once developed is dangerous, life threatening condition. Bleeding from the gums developed in 2 patients out of 100 patients in present study, in Patil et al 7 patients and 20 patients out of 50 patients in Harshavardhana’s study. In Bhalla et al.,3(7.14%) patients had gum bleeding. This could be early sign of DIC which should be watched for the purpose of early intervention. The other symptoms which needed prompt attention was fear of death due to Ophidian myths the patient had. We took help of all the house surgeons working in the ward for reassuring the patients and their attenders. Electrolyte disturbances both hyperkalemia and hypokalemia developed in studies of Patil et al55 and Kavitha saravu et al, no such potassium disturbances were there in present study. As both hyperkalemia and hyopkalemia leads to cardiac membrane instability which leads to rhythm disturbances,electrolytes should be monitored regularly. Patil et al., noted 9 (8.73%) patients had vomiting but we observed 57(57%) patients had vomiting. In Chaudhari et al 53., reported 155(59.6%) had vomitimg. It is an important feature of severe systemic envenomation, has not received much attention in clinical practice. However, vomiting is not a specific sign of severe envenoming, and may be induced by fear or use of herbal medicines or alcohol after a snake bite, may be a feature of early anaphylactoid reaction to ASV, uraemia or autonomic disturbances. Thus, whether vomiting is a surrogate marker of severity of snake bite requires more research. Bhalla et al. had 47.61 % acute kidney injury (AKI) developed following snake bite but present study and Patil study had the same incidence of AKI. Rest of the studies i.e., K Saravu et al.,and N Sharma et al.,had similar percentage of AKI following snake bite. Hypotension , shock and direct vasculotoxic effects of snake envenomation are the causes of development of acute renal failure. Uremic features develops 5- 7 days after snake bite, so these features should be recognized early and treated to prevent acute renal failure and mortality. Out of 20 patients with AKI in Bhalla study, eleven patients were treated conservatively with diuretics, renal diet, and fluid restriction. Seven patients needed hemodialysis. In our study out of 14 patients with AKI, 10 patients improved with conservative management and 4 patients required hemodialysis. Neuroparalytic features are the hallmark of cobra and krait bites and hemostatic abnormalities due to viper bites. Both hemostatic and neuroparalytic abnormalities can be developed in snake bite due to combination of toxins in venom. Both K Saravu et al.,(5.3%) and Shubham Agarwal et al.,(5.66%) had similar results which differed from present study(2%). No such combined complications were reported from N Sharma et al. Respiratory paralysis developed in 13 (86.66%) patients of Patil et al and 3.3% of Krishnappa et al. In our study we noted 2 (2%) patients which required ventilator support. In present study 5% developed neuroparalysis following snake bite, K Saravu et al., noted 25%, Patil et al., noted 14.6% and Dharod et al17., observed 27.04% neuroparalytic patients in snake bite. Patil et al., reported 13 (86.66%) patients and 8.3% of Krishnappa et al., had ptosis but we observed 1 (1%) patient had ptosis which the most common manifestation of neuroparalysis. None of our patient developed tetanus. Majority of the patient were given inj. Tetanus toxoid. We have not come across the snakebite in a pregnant woman, we couldn’t analyse the effect of snake venom on pregnancy. All 3 pregnant patients in Bhat’s study aborted and had severe bleeding needing blood transfusion. Shock developed in 29(11.2%) patients in Chaudhari et al., Shock in two(2%) patients were post haemorrhagic in present study. Delay in treatment and haemorrhage are liable to precipitate post haemorrhagic peripheral circulatory failure. One patient developed shock within first 2 hr after the bite and died while undergoing treatment may be due to arrhythmias. In this regard we don’t agree with Bhat’s finding shock does not seem to be a direct result of envenomation. No patient was seen in Bhat’s study whose blood after remaining normal for 24hours, developed clotting defect later. He concluded that – • If the clotting defect does not develop within the first 24hr after the bite, systemic poisoning can be ruled out. • There is no correlation between the time of onset of clotting defect and the time of onset of haemorrhagic syndrome. • The onset of haemorrhagic syndrome may be delayed upto 72 hour. • The delayed onset of haemorrhagic syndrome seems to be related to trauma and physical exertion after snakebite before the clotting defect is reversed. • Physical activity after snake bite seems to increases the incidence and severity of bleeding. Since our observation were similar to his conclusion even we advised complete bed rest and immobilization. The only effective and relevant treatment of snakebite poisoning to be advocated in a hospital, is the administration of anti snake venom. As signs of systemic poisoning are not always clinically evident and as a patient with a non- clotting blood is potentially in danger of developing haemorrhagic syndrome, its not our practice to delay the administration of ASV as has been suggested by Reid. We agree with Bhat’s this conclusion in administering ASV. Immediately after admission when systemic poisoning is detected by finding defective coagulation ASV should be administered. Delay in the administration of ASV will delay the reversal of coagulation defect and is liable to endanger a patient’s life by otherwise preventable haemorrhage. In present study, it is clearly evident that the longer the treatment with ASV was delayed, the more persistent was the coagulation defect, more was the quantity of ASV necessary to reverse the defect. In all patients, whose bleeding continued in spite of ASV beyond 24hours, blood transfusion and fresh frozen plasma was given in addition. Besides replacing the blood lost, it shortens the duration of bleeding. In the absence of ASV, blood transfusion by itself can stop the bleeding but the coagulation defect may be reversed only temporarily. In our study we observed that most of the patient (82%) came to hospital within six hour and received treatment, this is similar to Patil et al,who reported that 78.64% presented within 6 hours of snake bite. We observed very less complication compared to other studies with long duration between bite and admission to hospital. On the contrary, in one study they observed that there was no association of bite to hospital time with development of AKI. Chaudhari et al 53. also found that prolonged bite to hospital time i.e., delayed arrival to hospital was associated with mortality. Sharma et al had found that median bite to hospital time in their study group was 9 hours, which was quite different from our study. The bite to hospital time varies depending on the availability of medical facilities and the settings in which the study has been done. We strongly recommend to create public awareness regarding treatment of snakebite to reduce the complication. Overall mortality due to venomous snake bites was 19.57%, with a significantly higher mortality in victims who developed AKI in Bhalla study. We had 2% mortality in our study. In Patil et al., also had 2.27% mortality. Hemoglobin less than 10 gm in 15% patients of present study but Harshavardhana54 reported 26%. Prothrombin time prolonged in 28(56%) patients of Harshavardhana study but in present study PT prolonged in 23 (23%) patients. APTT prolonged in 31(62%) patients of Harshavardhana study but present study we observed 15(15%) patients had abnormal APTT.

Snakebite remains a common occupational hazard in rural populations. Although awareness regarding first aid, early hospitalization, and the role of anti-snake venom (ASV) is improving—as reflected by 82% of patients presenting within six hours—further efforts are needed. Protective measures for commonly affected body parts and adequate lighting at night can help reduce the incidence of bites. Simple tests such as bleeding time and clotting time are useful indicators of haematotoxicity, while more sensitive investigations may be used where available. ASV remains the cornerstone of management, with dosage tailored to the severity of envenomation and continued until clinical control is achieved. Adverse reactions to ASV are uncommon and manageable. Supportive care, including blood transfusion, dialysis for renal failure, antibiotics, tetanus prophylaxis, and anti-inflammatory therapy, is essential. Prevention through protective measures is preferable to killing snakes, which disrupts ecological balance.

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