IM21.1-9 | Envenomation — Glossary

A bedside test where 2–3 mL of venous blood is placed in a clean, dry glass tube and left undisturbed for 20 minutes; failure to form a clot at 20 minutes indicates VICC and is an indication for antivenom; the single most important bedside test in snakebite.

The standard endpoint for assessing antivenom response in haematotoxic envenomation: perform 20WBCT at 6 hours after antivenom infusion completes; clot formation = adequate neutralisation; no clot = still-circulating venom = repeat 10 vials antivenom indicated.

5% acetic acid (household vinegar) applied to the jellyfish sting site for 30 minutes; deactivates remaining nematocysts by acidifying the discharge mechanism; the specific topical first aid for jellyfish envenomation; not to be confused with fresh water (contraindicated).

A major complication of Russell's viper envenomation caused by direct tubular nephrotoxicity, haemoglobin cast formation from haemolysis, and myoglobinuria from myonecrosis; requires IV hydration, urinary alkalinisation if myoglobinuric, and possibly dialysis.

The only proven life-saving treatment for anaphylaxis; dose 0.5 mg IM (1:1000 solution, 0.5 mL) into the anterolateral thigh; must be given first before antihistamines or steroids; acts via alpha-1 (reverses vasodilation), beta-2 (reverses bronchospasm), and beta-1 (supports cardiac output).

First-line and only life-saving treatment for anaphylaxis; dose 0.5 mg IM into the anterolateral thigh (1:1000 solution, 0.5 mL); acts via alpha-1 (reverses vasodilation) and beta-2 (reverses bronchospasm) receptors; must be drawn up and ready BEFORE antivenom infusion is started.

A drug class that blocks noradrenaline binding at alpha-1 receptors on vascular smooth muscle, preventing vasoconstriction and reducing peripheral vascular resistance (afterload); prazosin is the prototype; mechanism of action in scorpion envenomation.

A severe, life-threatening systemic type I IgE-mediated hypersensitivity reaction; bee sting is one of the most common triggers; characterised by rapid onset of urticaria, angioedema, bronchospasm, and cardiovascular collapse; treated immediately with adrenaline 0.5 mg IM anterolateral thigh.

Severe immediate hypersensitivity reaction (wheeze, urticaria, hypotension) to equine antivenom; most reactions are anaphylactoid (complement-mediated) rather than true IgE-mediated; managed by stopping the infusion and administering adrenaline 0.5 mg IM anterolateral thigh as the first action.

A rare but specific late complication of Russell's viper envenomation caused by haemorrhagic infarction of the anterior pituitary gland; presents as Sheehan-like hypopituitarism weeks to months post-bite; should be considered in any patient with unexplained adrenal insufficiency, hypothyroidism, or growth failure after snakebite.

Clinical criteria for antivenom in snakebite: positive 20WBCT, spontaneous systemic bleeding from any site, any neurotoxic sign (ptosis or worse), haemodynamic instability, or AKI attributable to envenomation. Local swelling alone is NOT an indication.

A pre-loaded, single-use device delivering 0.3 mg adrenaline IM for self-administration in anaphylaxis emergencies; prescribed to individuals with confirmed bee venom allergy after a first anaphylactic episode; the EpiPen delivers adrenaline through the anterolateral thigh even through clothing.

Massive simultaneous sympathetic and parasympathetic activation caused by scorpion venom's prolongation of voltage-gated Na+ channels in autonomic nerve terminals; produces hypertension, tachycardia, profuse sweating, excessive secretions, and vomiting; the Grade II syndrome.

Beta-blockers are specifically contraindicated in scorpion envenomation because blocking beta-1 cardiac receptors removes the compensatory cardiac drive against already-elevated alpha-1-mediated afterload, precipitating cardiovascular collapse; only alpha-1 blockade (prazosin) is appropriate.

The four snake species responsible for the majority of medically significant snakebite in India: Russell's viper (Daboia russelii), saw-scaled viper (Echis carinatus), Indian cobra (Naja naja), and common krait (Bungarus caeruleus).

Recurrence of anaphylaxis 1–8 hours after apparent recovery from the initial reaction, without re-exposure to the allergen; occurs in approximately 5–20% of anaphylaxis cases; justifies a minimum 4–6 hour observation period after bee sting anaphylaxis treatment.

Weakness of muscles innervated by cranial nerves IX, X, XI and XII causing nasal voice, dysphagia, dysphonia, and tongue weakness; an advanced sign of neurotoxic envenomation indicating significant brainstem level (or neuromuscular) involvement with risk of aspiration.

A state of inadequate cardiac output causing tissue hypoperfusion; in scorpion envenomation caused by acute LV failure from catecholamine myotoxicity plus high afterload; features: hypotension, cold peripheries, pulmonary oedema, falling SpO2.

Acute reversible myocardial dysfunction caused by direct toxicity of massively elevated circulating catecholamines (noradrenaline and adrenaline) in scorpion envenomation; manifests as reduced LVEF, cardiogenic shock, and pulmonary oedema; recovers with supportive care over days.

H1 antihistamine given IV (10 mg) as an adjunct in antivenom hypersensitivity reactions; reduces urticaria and mild cutaneous reactions; not adequate as sole treatment for anaphylaxis — adrenaline is always first.

The nocturnal, shiny blue-black snake with white crossbands; pre-synaptic beta-bungarotoxin irreversibly destroys the presynaptic terminal vesicle apparatus; bites sleeping victims painlessly; paralysis is difficult to reverse pharmacologically.

Bedside respiratory function test in neurotoxic envenomation: patient takes one deep breath and counts aloud to 20 in a single exhalation; inability to reach 20 indicates reduced vital capacity from respiratory muscle weakness and is a warning sign of impending respiratory failure.

Enzyme released from damaged muscle cells; markedly elevated (often >10,000 IU/L) in myonecrosis from viper venom phospholipase A2; used to quantify rhabdomyolysis severity and guide intensity of IV fluid hydration.

A pattern of progressive motor weakness beginning with ptosis (eyelid drooping), then ophthalmoplegia, bulbar palsy, and finally respiratory muscle paralysis; the hallmark of neurotoxic (elapid) envenomation.

Synthetic catecholamine acting primarily on beta-1 receptors to increase cardiac contractility and heart rate; used as an inotrope in Grade III scorpion envenomation with cardiogenic shock; dose 5–10 micrograms/kg/min IV.

A bite from a venomous snake in which no venom is injected; estimated to occur in 20–50% of bites; characterised by local wound without progressive swelling, no systemic signs, and negative 20WBCT after 6 hours of observation.

Horse-derived immunoglobulin G; the active antitoxin component of antivenom; as a foreign protein it activates complement and can trigger anaphylactoid reactions; half-life approximately 5–7 days in human circulation.

The plasma protein substrate for thrombin that is converted to fibrin during coagulation; the most sensitive laboratory marker of VICC — levels fall rapidly as fibrinogen is consumed by viper venom prothrombin activators; levels < 1 g/L indicate severe defibrination.

A drop in blood pressure with the first dose of prazosin, particularly in patients who are already haemodynamically compromised; requires blood pressure monitoring every 15–30 minutes after the first dose and established IV access before administration.

Blood product containing all clotting factors; used as an adjunct in refractory VICC after antivenom has been given; must NOT be given before antivenom — transfused factors will be consumed by still-circulating viper venom enzymes. Dose: 10–15 mL/kg.

Local envenomation only — severe pain, paresthesia, local sweating at the sting site; no systemic autonomic features; managed with analgesics and 4–6 hours of observation.

Systemic autonomic storm — hypertension, tachycardia, profuse sweating, vomiting, agitation, cold extremities; no pulmonary oedema; specific treatment is prazosin 30 mcg/kg orally.

Cardiovascular failure — acute LV failure with pulmonary oedema, cardiogenic shock, severe hypotension, possible arrhythmias; requires ICU, dobutamine, oxygen/ventilation, prazosin (with caution), antivenom if available.

Envenomation syndrome caused by viper venoms (Russell's viper, saw-scaled viper), characterised by venom-induced consumption coagulopathy, spontaneous systemic bleeding, local tissue necrosis, and often acute kidney injury.

IV corticosteroid (200 mg) given as adjunct in antivenom anaphylaxis to prevent biphasic reactions; delayed onset of action (4–6 hours) means it does not treat the acute reaction; never replaces adrenaline as first-line.

The insect order containing bees, wasps, and hornets; all capable of causing anaphylaxis in sensitised individuals (IgE-mediated, single sting) or toxic massive envenomation (direct, multiple stings); management principle is identical across all Hymenoptera species.

The iconic hooded elapid of South Asia; post-synaptic alpha-neurotoxin blocks nicotinic acetylcholine receptors at the motor end-plate; causes descending paralysis and significant local cytotoxic tissue necrosis.

Clinical criteria indicating the need for immediate endotracheal intubation: SpO2 < 95%, count test < 10, neck flexion power grade ≤ 3/5, or any evidence of aspiration. Elective intubation before respiratory arrest is far safer than emergency intubation; the count test allows prediction of the critical window.

Correct sequence: do NOT rub; remove tentacles with tweezers or card-edge; flush with seawater (NOT fresh water — fresh water triggers nematocyst discharge); apply 5% acetic acid (vinegar) for 30 minutes; analgesia. Two critical avoidances: rubbing and fresh water.

Systemic envenomation syndrome from black widow spider (Latrodectus species) bite; alpha-latrotoxin triggers massive neurotransmitter release causing severe abdominal cramps, diffuse muscle rigidity, diaphoresis, hypertension, and tachycardia; mimics acute abdomen; managed with opioids, benzodiazepines, and antihypertensives.

Oedema at the snakebite site caused by locally deposited venom enzymes already in tissue; circulating antivenom cannot reach tissue-bound venom and therefore has no effect on local swelling; antivenom given for this indication alone exposes the patient to anaphylaxis risk without benefit.

The principal toxic component of bee venom; a membrane-disrupting peptide that causes direct haemolysis, myonecrosis, and mast cell degranulation; responsible for the burning pain of a sting and contributes to the direct organ toxicity of massive envenomation.

The Indian red scorpion; the medically most important scorpion in India; found predominantly in Maharashtra, AP, Telangana, Tamil Nadu, Rajasthan, and Gujarat; venom causes autonomic storm via catecholamine release leading to hypertension, cardiac failure, and pulmonary oedema.

Presence of myoglobin in urine from rhabdomyolysis (myonecrosis); appears as red-brown urine with blood positive on dipstick but no red blood cells on microscopy; indicates risk of pigment nephropathy and AKI; treated with aggressive IV fluid hydration.

Microscopic pressurised coiled tubule on jellyfish tentacles that discharges on contact with skin, injecting venom; triggered by touch including rubbing or fresh water contact; deactivated by 5% acetic acid (vinegar) application; forms the physical basis of jellyfish envenomation.

Anticholinesterase trial for post-synaptic neurotoxic envenomation: neostigmine 1.5 mg IV with atropine 0.6 mg IV (always together to prevent muscarinic side effects); may partially reverse cobra (post-synaptic) paralysis; ineffective for krait (pre-synaptic) envenomation.

Empirical trial of neostigmine 1.5 mg IV plus atropine 0.6 mg IV in a patient with post-synaptic neurotoxic (cobra) envenomation; partial improvement of ptosis within 15–30 minutes suggests post-synaptic blockade; no improvement is consistent with pre-synaptic (krait) blockade or irreversible damage.

Envenomation syndrome caused by elapid venoms (cobra, krait), characterised by descending flaccid paralysis — ptosis, ophthalmoplegia, bulbar palsy, and respiratory muscle paralysis — due to blockade of the neuromuscular junction.

Paralysis of extraocular muscles causing restricted eye movements and diplopia; an intermediate sign of neurotoxic envenomation appearing after ptosis and before bulbar palsy in the descending paralysis pattern.

An enzyme present in viper venoms that disrupts cell membrane phospholipids, causing direct tissue necrosis at the bite site, haemolysis, and myonecrosis; contributes to the local destructive effects and systemic toxicity of viper envenomation.

The major allergen in bee venom that causes both IgE-mediated sensitisation (leading to anaphylaxis on re-exposure) and direct haemolysis and myocyte membrane disruption in massive envenomation; same enzyme class as found in viper venoms.

Acute kidney injury caused by haemoglobin or myoglobin cast deposition in renal tubules; complication of haemolysis (haemoglobinuria) or rhabdomyolysis (myoglobinuria); presents as dark urine with blood on dipstick but no red cells on microscopy; prevented by aggressive IV fluid hydration.

Equine-derived biological product containing IgG antibodies against venoms of all four Indian big four snakes (Russell's viper, saw-scaled viper, cobra, krait); the standard antivenom in India; neutralises circulating venom by antibody-antigen complex formation.

A toxin that binds to the nicotinic acetylcholine receptor on the motor end-plate, blocking acetylcholine binding; example: alpha-cobratoxin from cobra venom; partial reversal with neostigmine + atropine may be attempted.

Selective alpha-1 adrenoceptor antagonist; the specific treatment for Grade II and III scorpion envenomation; dose 30 micrograms/kg orally (max 1 mg in children); reduces peripheral vasoconstriction (afterload), corrects the catecholamine-mediated pathophysiology; must NOT be given with beta-blockers.

A toxin that acts on the presynaptic terminal of the neuromuscular junction to prevent acetylcholine release; example: beta-bungarotoxin from krait venom; blockade cannot be reversed by anticholinesterase drugs.

Subcutaneous adrenaline 0.25 mg given before antivenom infusion to reduce incidence of early reactions; evidence from Sri Lankan RCT (Premawardhena, 1999); recommended in settings with limited monitoring capacity; not universally adopted in India but noted in WHO guidelines.

A firm, even crepe bandage applied from the bite site distally upward to impede lymphatic spread of neurotoxic elapid venom; combined with splinting; recommended for cobra and krait bites only — contraindicated for viper (haematotoxic) bites.

Sustained penile erection caused by autonomic nerve stimulation in scorpion envenomation; a specific clinical sign indicating significant systemic autonomic toxicity, particularly in children; indicates Grade II or III envenomation.

Drooping of the upper eyelid due to weakness of the levator palpebrae muscle; the earliest and most sensitive clinical sign of neurotoxic snakebite envenomation; its appearance mandates close respiratory monitoring and urgent antivenom.

Breakdown of skeletal muscle releasing myoglobin, CK, and other intracellular contents into the circulation; caused by viper venom phospholipase A2; complications include myoglobinuria, pigment nephropathy, and acute kidney injury.

The heavy-bodied viper responsible for the most snakebite deaths in India; identified by three rows of dark oval blotches with pale borders on a brownish body; venom is haematotoxic causing VICC, AKI, and sometimes pituitary haemorrhage.

The smallest of India's big four; characterised by rough keeled scales that produce a rasping sound when the snake rubs its coils; venom is haematotoxic causing coagulopathy and thrombocytopenia; found in dry stony habitats.

Envenomation by the Indian giant centipede via modified front legs (forcipules); causes immediate intense local pain, erythema, and oedema; systemic features (headache, nausea, autonomic effects) are rare; managed with analgesia, ice, wound care, and tetanus prophylaxis; no antivenom available.

Equine-derived antivenom raised against Mesobuthus tamulus venom; available at some centres in Maharashtra and Gujarat; early administration within 1–2 hours of sting may attenuate the autonomic storm; not universally stocked and used in addition to, not instead of, prazosin.

Type III hypersensitivity reaction (immune complex deposition) occurring 5–14 days after antivenom; presents with fever, urticaria, arthralgia, and lymphadenopathy; treated with oral prednisolone 1 mg/kg/day for 5–7 days; more common with higher total antivenom doses.

A device that constricts blood flow; contraindicated in snakebite first aid because venom is already in the lymphatics within seconds and the tourniquet does not prevent systemic envenomation but reliably causes ischaemia, compartment syndrome, and potential limb loss.

Direct toxic syndrome from >50–100 simultaneous bee stings regardless of prior sensitisation; causes haemolysis, rhabdomyolysis, hepatotoxicity, and AKI from haemoglobinuria and myoglobinuria (pigment nephropathy); managed with aggressive IV fluid hydration targeting urine output ≥200 mL/hour; no role for adrenaline.

A state of defibrination caused by viper venom's prothrombin activators triggering uncontrolled coagulation cascade activation, consuming fibrinogen and clotting factors and resulting in inability to form clots; manifests as spontaneous bleeding from multiple sites.

The class of scorpion peptide neurotoxins that prolong the open state of voltage-gated Na+ channels in autonomic nerve terminals and the adrenal medulla, causing repetitive firing and massive catecholamine release; the molecular mechanism underlying the autonomic storm.