Anti-snake venoms are immunoglobulins raised by immunising horses with the venom of poisonous snakes, and they remain the only effective antidote for snakebite envenoming [1]. In India a polyvalent preparation is used, containing antibody against the cobra, Russell's viper, common krait and saw-scaled viper, because in the absence of a dead specimen there is no objective means of identifying the offending species and therefore no rational basis for selecting a monovalent product [2]. Antivenom reverses systemic envenoming, and while it is sensible to continue treatment for as long as evidence of coagulopathy persists, the overriding principle is that it should be administered as early as possible [1]. The optimal dose, however, remains genuinely unsettled. National standard treatment guidelines recommend 10 vials as a stat infusion for neuroparalytic envenoming, repeated after one hour, and for vasculotoxic bites permit either low-dose infusion or high-dose intermittent bolus regimens, the two having been shown to be of comparable efficacy [2]. Published series report widely differing mean requirements — from 11.5 vials for upper-limb bites to over 21 for lower-limb bites in one Nepalese cohort [3], and 15.6 vials in a Kerala series [4] — and some studies have found no significant association between the dose administered and clinical cure [5]. Since each vial carries both cost and a risk of anaphylactic, pyrogenic and serum-sickness reactions, quantifying the dose actually required in relation to the envenomation syndrome is of practical importance. Complications account for much of the morbidity of envenoming. Local necrosis and secondary bacterial infection may progress to cellulitis, abscess formation and, in severe cases, the need for debridement [6]. Acute renal failure follows chiefly Russell's viper and saw-scaled viper envenoming and is a major contributor to both morbidity and mortality [7]. Venom-induced consumption coagulopathy may culminate in disseminated intravascular coagulation requiring fresh frozen plasma [8]. In elapid envenoming, the hallmark is a progressive descending paralysis that, once it reaches the diaphragm and intercostal muscles, causes death by respiratory failure unless ventilation is instituted [1]. Anticipating respiratory failure is therefore central to the management of neuroparalytic bites. The single breath count — the number a patient can count aloud in a single exhalation — has been proposed as a simple, equipment-free bedside measure of ventilatory reserve, and national guidance regards a count above 30 as normal, with a declining count and pooling of saliva serving as predictors of descending paralysis [2,9]. Kumar et al. described the test as a reliable clinical sign of impending respiratory distress in a large Kerala series [10], yet the threshold at which intervention becomes necessary has been variously reported and requires validation across settings. Reported case fatality varies strikingly between Indian centres, from under 3% to more than 13% [4,11,12], differences that reflect species mix, delay to antivenom, and the availability of intensive care rather than any single biological factor. The present study was therefore undertaken to define antivenom requirement in relation to envenomation syndrome, to evaluate the single breath count as a predictor of ventilatory need, and to document the complications and outcome of snakebite in a North Karnataka teaching hospital.

This hospital-based prospective observational study was carried out in the Department of General Medicine, Koppal Institute of Medical Sciences, Koppal, Karnataka, a tertiary care teaching hospital with intensive care and ventilatory facilities serving a rural agrarian district. Study period and sample: One hundred consecutive patients admitted with snake bite between 1 August 2022 and 30 May 2024 who met the eligibility criteria were enrolled. Ethical considerations: Institutional Ethics Committee approval was obtained before commencement. Written informed consent was taken from each participant, or from an accompanying relative where conscious level precluded personal consent. Participants were told that the investigations and treatment provided were those routinely indicated for snakebite and would be unaffected by participation, and that they were free to withdraw at any time. Eligibility: Patients were included if they gave a history of snake bite together with one or more clinical manifestations of envenomation — fang marks, local swelling, haemorrhage, blister formation, vomiting, abdominal pain, regional lymphadenopathy or neurotoxicity. Patients bitten by creatures other than snakes, and those with non-poisonous bites showing no manifestation of envenomation, were excluded. Clinical assessment and classification: Vital parameters — systolic and diastolic blood pressure, pulse rate, respiratory rate and peripheral oxygen saturation — were recorded on admission. Blood pressure was categorised as normal, raised or hypotensive, and pulse rate as bradycardia, normal or tachycardia. A full systemic examination was performed, with the single breath count and neck-holding test used to assess neuromuscular reserve; the single breath count was recorded as 30 or below, above 30, or not assessable. Each patient was assigned an envenomation syndrome on clinical and laboratory grounds: local, haemotoxic, neurotoxic, or combined neurotoxic and haemotoxic. Investigations: Complete blood count, renal function tests, liver function tests, coagulation profile including prothrombin time with international normalised ratio and activated partial thromboplastin time, bleeding and clotting time, serum electrolytes, urine routine and microscopy, and the 20-minute whole blood clotting test were performed in all patients. Electrocardiography and chest radiography were obtained as indicated. Anaemia was defined as haemoglobin below 10 g/dL, leucocytosis by an elevated total leucocyte count, and thrombocytopenia as a platelet count below 100,000/mm³. Anti-snake venom protocol: Polyvalent anti-snake venom was reconstituted and administered as 10 vials in 500 mL of normal saline infused over one hour. Clinical assessment together with repeat prothrombin time with international normalised ratio and the 20-minute whole blood clotting test was performed thereafter to determine the requirement for further doses. Additional 10-vial increments were given as indicated, to a maximum of 30 vials. The total number of vials administered was recorded for each patient and cross-tabulated against the envenomation syndrome. Supportive care and outcome measures: The need for ventilatory support was assessed continuously, and duration of ventilation recorded as under 24 hours, 24 to 48 hours, or beyond 48 hours. The requirement for dialysis and for transfusion of blood or blood products, including fresh frozen plasma, was assessed and acted upon as clinically indicated. Complications were documented as cellulitis, acute kidney injury, respiratory failure, disseminated intravascular coagulation, or none. The primary outcome was survival to discharge versus death, with the cause of death recorded. Statistical analysis: Data were analysed using SPSS version 21 and Microsoft Excel. Categorical variables are presented as frequencies and percentages, and continuous variables as mean ± standard deviation and median with minimum and maximum values. Mean antivenom requirement per envenomation category was derived from the vial-by-syndrome cross-tabulation.

One hundred patients admitted with venomous snake bite were followed to discharge or death. Table 1. Baseline characteristics of the cohort (n = 100) Characteristic Value Mean age (years) 35.98 ± 13.55 Male, n (%) 70 (70.0) Female, n (%) 30 (30.0) Mean bite-to-hospital interval (hours) 4.17 ± 2.05 Presented within 6 hours, n (%) 91 (91.0) Fang marks visible, n (%) 93 (93.0) Local envenomation, n (%) 52 (52.0) Haemotoxic envenomation, n (%) 30 (30.0) Neurotoxic envenomation, n (%) 16 (16.0) Neurotoxic + haemotoxic, n (%) 2 (2.0) The cohort comprised young adults, predominantly male, presenting early — 91% within six hours of the bite. Systemic envenomation of some type was present in 48 patients (48%), with local envenomation alone in the remaining 52 (52%). These four syndrome categories form the basis of the antivenom analysis that follows. Table 2. Vital parameters on admission (n = 100) Parameter Value Systolic blood pressure (mmHg), mean ± SD 119.9 ± 16.9 Diastolic blood pressure (mmHg), mean ± SD 75.87 ± 10.12 — Normal blood pressure, n 71 — Raised (≥140/90 mmHg), n 27 — Hypotension (<90 mmHg systolic), n 2 Pulse rate (per minute), mean ± SD 100.3 ± 10.3 — Tachycardia (>100/min), n 50 — Normal, n 38 — Bradycardia (<60/min), n 12 Oxygen saturation (%), mean ± SD 96.51 ± 2.71 Mean vital parameters lay within normal limits, but the aggregate figures conceal meaningful variation. Half the cohort (50%) was tachycardic on admission and 27% hypertensive — findings consistent with the sympathetic activation, pain and anxiety that accompany envenoming, and with the hypertension and tachycardia described in neuroparalytic bites. Only 2 patients (2%) were hypotensive, indicating that cardiovascular collapse was rare in this series. Bradycardia in 12 patients (12%) is a less expected finding and may reflect vagal responses or the effect of prior first-aid measures. Mean oxygen saturation of 96.51 ± 2.71% was preserved, consistent with the small proportion who developed respiratory compromise. Table 3. Haematological and biochemical parameters (n = 100) Parameter Mean ± SD Abnormality n (%) Haemoglobin (g/dL) 12.91 ± 1.77 <10 g/dL 5 (5.0) Total leucocyte count (/mm³) 10,769 ± 4,766 Leucocytosis 10 (10.0) Platelet count (×10³/mm³) 257.98 ± 78.03 <100 ×10³/mm³ 1 (1.0) International normalised ratio 1.84 ± 1.27 — — Blood urea (mg/dL) 31.75 ± 10.9 Within normal limits in all 0 (0.0) Serum creatinine (mg/dL) 0.981 ± 0.428 1.8–3.0 mg/dL 11 (11.0) Mean values for all parameters fell within reference limits, reflecting the predominance of local envenomation in the cohort. Individual derangements were nonetheless informative. Anaemia below 10 g/dL affected 5 patients (5%) and leucocytosis 10 (10%), the latter recognised as an early marker of systemic envenoming. Thrombocytopenia was distinctly uncommon, occurring in a single patient. The mean international normalised ratio of 1.84 ± 1.27, with a standard deviation nearly as large as the excess over unity, indicates a bimodal distribution — normal coagulation in most patients with marked prolongation in the coagulopathic minority, consistent with the 33% who had a non-clotting 20-minute whole blood clotting test. Eleven patients (11%) had serum creatinine between 1.8 and 3.0 mg/dL, yet none required dialysis, indicating renal impairment that was real but of modest degree and reversible with antivenom and supportive care. Table 4. Anti-snake venom requirement by envenomation syndrome (n = 100) ASV vials Local (n=52) Haemotoxic (n=30) Neurotoxic (n=16) Neuro + haemo (n=2) Total n (%) 10 vials 40 (76.9%) 7 (23.3%) 0 (0.0%) 0 (0.0%) 47 (47.0) 20 vials 10 (19.2%) 13 (43.3%) 12 (75.0%) 1 (50.0%) 36 (36.0) 30 vials 2 (3.8%) 10 (33.3%) 4 (25.0%) 1 (50.0%) 17 (17.0) Total 52 (100%) 30 (100%) 16 (100%) 2 (100%) 100 (100) Mean vials 12.7 21.0 22.5 25.0 17.0 Percentages within each syndrome column. A formal test of association was not performed. This table is the core analysis of the study, and the pattern is unambiguous. Antivenom requirement rose in direct proportion to the presence and complexity of systemic envenoming. Patients with purely local envenomation were overwhelmingly managed on the initial 10 vials alone (76.9%), with a mean requirement of 12.7 vials. Haemotoxic envenoming required a mean of 21.0 vials, with only 23.3% controlled on 10 vials and a third needing the full 30. Most striking is the neurotoxic group: not a single one of these 16 patients was controlled on 10 vials, three-quarters required 20 and a quarter required 30, giving a mean of 22.5 vials. The two patients with combined neurotoxic and haemotoxic envenoming needed the most of all, averaging 25.0 vials. Aggregating the three systemic categories gives a mean of 21.7 vials against 12.7 for local envenoming — a difference of some nine vials per patient with direct implications for antivenom stocking. Table 5. Single breath count and requirement for ventilatory support (n = 100) Variable Category n (%) Single breath count ≤30 26 (26.0) >30 68 (68.0) Not assessed 6 (6.0) Ventilatory support Required 6 (6.0) Not required 94 (94.0) Duration of ventilation <24 hours 2 24–48 hours 3 >48 hours (96 hours) 1 Sixty-eight patients (68%) had a single breath count above 30, the accepted normal threshold, while 26 (26%) counted 30 or fewer and the test could not be performed in 6 (6%). All six patients who subsequently required mechanical ventilation were drawn from the group counting 30 or below — that is, the test showed complete sensitivity for identifying eventual ventilatory need in this cohort. Its specificity was however low, since only 6 of the 26 patients with a reduced count (23.1%) actually progressed to ventilation. The single breath count therefore functions well as a screening tool: a count above 30 was reassuring in every case, whereas a reduced count identified a high-risk group warranting close observation rather than mandating immediate intubation. Ventilation was mostly short, three patients requiring 24 to 48 hours and two under 24 hours, with a single patient ventilated for 96 hours. Table 6. Complications and outcome (n = 100) Category Finding n (%) Complications Cellulitis 52 (52.0) Respiratory failure 6 (6.0) Acute kidney injury 5 (5.0) Disseminated intravascular coagulation 2 (2.0) No complication 35 (35.0) Interventions Ventilatory support 6 (6.0) Fresh frozen plasma transfusion 2 (2.0) Dialysis 0 (0.0) Outcome Survived 99 (99.0) Died 1 (1.0) Thirty-five patients (35%) recovered without any complication. Cellulitis was by far the commonest, affecting 52 patients (52%) — a figure exactly matching the number with local envenomation, indicating that local tissue injury proceeded to secondary infection in essentially all such cases. Respiratory failure occurred in 6 patients (6%), acute kidney injury in 5 (5%) and disseminated intravascular coagulation in 2 (2%), the latter two receiving fresh frozen plasma. Notably, although 11 patients had raised serum creatinine, only 5 met criteria for acute kidney injury and none required dialysis. Ninety-nine patients (99%) survived to discharge. The solitary death resulted from neuroparalysis complicated by respiratory failure, underlining that elapid envenoming remains the principal threat to life even where the majority of bites produce only local effects.

The overall mean antivenom requirement of 17.0 vials in this series sits within the range reported from comparable Indian centres. Harshvardhan et al. described means of 16.8 vials among patients who developed acute renal failure and 12.8 among those who did not [13], while Chandrakumar et al. reported 15.6 vials from Kerala [4]. Devkota, working in Nepal, found requirement to differ by bite site, averaging 21.7 vials for lower-limb and 11.5 for upper-limb bites [3]. The exact dose to be administered in envenomation remains a matter of discussion, with some studies showing no significant association between cure and the quantity of antivenom given [5]. The present data, however, demonstrate a clear gradient by envenomation syndrome that merits emphasis. Mean requirement rose from 12.7 vials for purely local envenoming to 21.0 for haemotoxic, 22.5 for neurotoxic and 25.0 for combined syndromes, and no patient with neurotoxic envenoming was controlled on the initial 10-vial dose. This pattern is physiologically coherent, since systemic envenoming implies a larger venom load requiring correspondingly greater neutralising capacity, and it is consistent with national guidance recommending an immediate second 10-vial dose in neuroparalytic bites [2]. It should be noted that no formal test of association was applied, and the finding should be regarded as descriptive. Laboratory derangements were modest, reflecting the predominance of local envenoming. Kumar et al. found leucocyte count, international normalised ratio, urea and creatinine significantly higher among non-survivors [11], and Raju et al. reported similar associations for leucocytosis, thrombocytopenia and prolonged clotting time [14]. With one death here, such associations could not be examined. The single breath count identified all six patients who required ventilation, every one of whom counted 30 or below. This supports the national standard treatment guideline position that a count above 30 is normal and that a declining count, together with pooling of saliva, predicts descending paralysis [2]. Bhandari et al., in a systematic review, concluded that the count is useful in assessing neurotoxic outcome [9], while Kumar et al. treated a threshold below 20 as indicating respiratory distress, reporting counts below 20 in 27% of common krait and 37.7% of cobra bites [10]. The low specificity observed here suggests the count is best used to define a group requiring intensive observation rather than as an absolute trigger for intubation. Cellulitis at 52% closely matches the 50% reported by Kumar et al. and the 44% of Mathur et al. [11,15]. Acute kidney injury at 5%, with no patient requiring dialysis, compares favourably with the 25% and 27% reported in those series, where 18.3% and 2.6% respectively required dialysis, and with the 7.7% renal failure of Chandrakumar et al. [4]. Early presentation is the most plausible explanation. Survival of 99% is among the highest reported: mortality elsewhere ranges from 2.9% [4] through 4% [12] and 6.3% [14] to 13.3% [16] and 13% [11]. The favourable outcome here reflects the tertiary setting with advanced life support, together with the finding that 91% presented within six hours. Limitations: The offending species could not be identified in any case, so antivenom requirement could not be related to snake type. The single death precluded analysis of predictors of mortality, and formal statistical testing of the antivenom-syndrome relationship was not undertaken.

In this prospective study of 100 patients with venomous snake bite, anti-snake venom requirement was closely related to the type of envenomation. Mean requirement was 12.7 vials for purely local envenoming, rising to 21.0 vials for haemotoxic, 22.5 for neurotoxic and 25.0 for combined neurotoxic-haemotoxic envenoming, against an overall mean of 17.0 vials. No patient with neurotoxic envenoming was controlled on the initial 10-vial dose, and 76.9% of those with local envenoming required no more than that dose. Antivenom stocking and initial dosing decisions can therefore reasonably be guided by the clinical syndrome identified at presentation. The single breath count proved a valuable bedside screening tool: all six patients who eventually required mechanical ventilation had a count of 30 or below, though only 23.1% of those with a reduced count progressed to ventilation. A count above 30 was reassuring in every instance, making the test well suited to triage in settings without ready access to blood gas analysis or spirometry. Cellulitis was the commonest complication, affecting 52% and corresponding exactly to the group with local envenomation, which argues for early attention to wound care and monitoring for secondary infection. Acute kidney injury occurred in 5% and disseminated intravascular coagulation in 2%, and notably no patient required dialysis despite 11% showing raised serum creatinine. Survival was 99%, the single death resulting from neuroparalysis with respiratory failure. These outcomes — among the most favourable reported from Indian centres — are attributable to a combination of early presentation, with 91% reaching hospital within six hours, prompt antivenom administration and the availability of tertiary-level supportive care including ventilation. They reinforce that reducing delay to antivenom, rather than escalating its dose, is the most powerful determinant of outcome in snakebite envenoming. Prospective studies incorporating species identification are needed to refine syndrome-specific dosing further.

1. Warrell DA. The clinical management of snake bites in the Southeast Asian region. Southeast Asian J Trop Med Public Health. 1999;30(Suppl 1):1–85. 2. Standard treatment guidelines — snakebite. New Delhi: Directorate General of Health Services, Ministry of Health and Family Welfare, Government of India; 2016. 3. Devkota G. Factors associated with treatment outcomes in anti-snake venom (ASV) administered snakebite patients. J Patan Acad Health Sci. 2020;7(3):129–35. 4. Chandrakumar A, Suriyaprakash TNK, Mohan PL, Thomas L, Vikas PV. Evaluation of demographic and clinical profile of snakebite casualties presented at a tertiary care hospital in Kerala. Clin Epidemiol Glob Health. 2016;4(3):140–5. 5. Açikalin A, Gökel Y, Kuvandik G, Duru M, Köseoğlu Z, Satar S. The efficacy of low-dose antivenom therapy on morbidity and mortality in snakebite cases. Am J Emerg Med. 2008;26(4):402–7. 6. Blaylock RS. Antibiotic use and infection in snakebite victims. S Afr Med J. 1999;89(8):874–6. 7. Chugh KS. Snake-bite-induced acute renal failure in India. Kidney Int. 1989;35(3):891–907. 8. White J. Snake venoms and coagulopathy. Toxicon. 2005;45(8):951–67. 9. Bhandari SK, Bist A, Ghimire A. Single breath count test and its applications in clinical practice: a systematic review. Ann Med Surg (Lond). 2024;86(4):2130–6. 10. Kumar SKG, Narayanan S, Udayabhaskaran V, Thulaseedharan NK. Clinical and epidemiologic profile and predictors of outcome of poisonous snake bites — an analysis of 1,500 cases from a tertiary care center in Malabar, North Kerala, India. Int J Gen Med. 2018;11:209–16. 11. Kumar A, Dungdung A, Kumar A, Shashank, Kumar R, Pandey V, et al. A cross-sectional study of various clinical and laboratory parameters in snakebite and their association with mortality at a tertiary care centre in Jharkhand. J Family Med Prim Care. 2022;11(11):7089–94. 12. Harshavardhana HS, Pasha I, Prabhu NCS, Amira, Ravi P. Snake bite induced coagulopathy: a study of clinical profile and predictors of poor outcome. Int J Sci Stud. 2014;2(1):2–5. 13. Harshvardhan L, Lokesh AJ, Tejeshwari HL, Halesha BR, Metri SS. A study on the acute kidney injury in snakebite victims in a tertiary care centre. J Clin Diagn Res. 2013;7(5):853–6. 14. Raju R, Biju A, Mathew A, Ramasami P. The profile and outcome of snakebite envenomation in patients admitted to a rural tertiary care hospital in South India. Int J Contemp Med Res. 2020;7(1):E1–6. 15. Mathur H, Aharda RS, Singh DP, Singh Y, Jain A. A study of clinical profile and outcome of snakebite at tertiary care centre in South Rajasthan. J Med Sci Clin Res. 2019;7(1):893–7. 16. Hariprasad S, Sukhani N. Assessment of clinical parameters among patients with snake poison induced coagulopathy. Int J Adv Med. 2018;5(6):1374–9.