IM21.1-9 | Envenomation — Practice Quiz

Correct. Russell's viper (Daboia russelii) is identified by its stout body, dark oval blotches with pale borders arranged in three rows, and is the most common cause of venom-induced consumption coagulopathy (VICC) plus acute kidney injury in India. The non-clotting 20WBCT confirms haematotoxic envenomation consistent with Russell's viper.

The big four Indian snakes: Russell's viper (stout, dark oval blotches with pale borders, haematotoxic — VICC + AKI); saw-scaled viper (small, keeled rough scales, rasping sound when coiled, haematotoxic); cobra (spectacle mark on hood, neurotoxic + local necrosis); common krait (shiny black with thin white crossbands, nocturnal, purely neurotoxic, minimal local signs).

The description — stout body with dark oval blotches with pale borders, haematotoxic picture with VICC, local swelling — points to Russell's viper. Cobra and krait cause neurotoxic envenomation; saw-scaled viper also causes coagulopathy but the description and regional predominance favour Russell's viper here.

Correct. Tourniquets are contraindicated in snakebite first aid. Venom enters the lymphatic system within minutes of injection and has already disseminated before a tourniquet can be applied. Tourniquets cause compartment syndrome, increase local tissue necrosis, and may precipitate ischaemia of the limb — without providing any benefit.

Correct snakebite first aid: immobilise the limb below heart level, apply a pressure immobilisation bandage ONLY for neurotoxic (cobra/krait) bites — NOT for haematotoxic bites where it worsens local necrosis. NEVER apply tourniquet, incise, suck, or apply electric shock. Remove jewellery. Transport rapidly to hospital.

The most dangerous first-aid error is applying a tourniquet. Venom is absorbed via the lymphatics almost immediately; tourniquets do not prevent systemic envenomation but do cause compartment syndrome and worsen local necrosis. The correct approach is immobilisation (pressure immobilisation bandage for neurotoxic bites only), calm reassurance, and rapid transport.

Correct. In neurotoxic envenomation with falling SpO2 and descending paralysis, airway and ventilatory support is the MOST critical immediate step — the patient may need intubation and mechanical ventilation. While ASV is also needed, failure to secure the airway will cause death before antivenom can work. The ABCDE approach always prioritises airway.

Hospital stabilisation of snakebite follows ABCDE: Airway (intubate if descending paralysis, failing SpO2) → Breathing (supplemental O2, ventilatory support) → Circulation → Disability (GCS, pupillary signs) → Exposure. In neurotoxic snakebite, respiratory failure is the cause of death — ASV and neostigmine are important but secondary to airway management.

The most immediate threat to life in this patient is respiratory failure from neuromuscular paralysis. Airway and ventilatory support must come first. ASV is also indicated (neurotoxic envenomation = systemic envenomation), and neostigmine/atropine may help post-synaptic paralysis, but none of these matters if the airway is not secured.

Correct. The common krait (Bungarus caeruleus) is nocturnal and typically bites sleeping persons. Its bite is painless or mildly uncomfortable, so victims often do not wake; they present in the morning or hours later with descending paralysis (ptosis, diplopia) and minimal to no local swelling. This is a classic krait presentation.

Common krait history clues: nocturnal, bites sleeping persons on the floor, painless bite, no local swelling, pure neurotoxic (ptosis, diplopia, descending paralysis). The 7-domain history in snakebite: time/circumstances, species ID features, local evolution, haematotoxic symptoms (gum bleed, haematuria, VICC), neurotoxic symptoms (ptosis, diplopia, dysphagia, paralysis), pre-hospital interventions, background history.

The key features pointing to krait are: nocturnal bite on a sleeping person, painless bite site, no local swelling, and pure neurotoxic signs (ptosis, descending paralysis). Cobra also causes neurotoxicity but has prominent local pain and necrosis. Russell's and saw-scaled vipers are haematotoxic.

Correct. Ptosis is the earliest and most reliable sign of neurotoxic envenomation. It results from weakness of the levator palpebrae superioris (innervated by CN III, with contribution from sympathetic innervation of the superior tarsal muscle). It typically appears within 1–4 hours of a neurotoxic bite and precedes external ophthalmoplegia, diplopia, dysphagia, and ultimately respiratory paralysis.

Neurotoxic examination sequence: PTOSIS is the sentinel sign — look for it actively by asking the patient to open eyes wide and observing upper eyelid position. Descending paralysis follows: CN III (ptosis, diplopia) → CN IX/X (dysphagia, nasal voice) → neck flexors → respiratory muscles. Regular ptosis checks every 30 minutes are mandatory in any neurotoxic snakebite.

Ptosis is the earliest clinical sign of neurotoxic snakebite envenomation and must be actively looked for. The neurological examination proceeds cranially to caudally: ptosis → external ophthalmoplegia → diplopia → facial weakness → dysphagia → neck weakness → limb paralysis → respiratory failure. Respiratory failure is the latest and most dangerous sign.

Correct. The 20WBCT is the cornerstone bedside test for haematotoxic snakebite. Place 2-3 mL of fresh venous blood in a clean, dry GLASS tube and leave undisturbed for 20 minutes. Non-clotted blood = venom-induced consumption coagulopathy (VICC) = ASV indication. The test requires no equipment, no electricity, and works in the most resource-limited setting.

20WBCT technique: clean, DRY, GLASS tube (plastic tubes do not allow contact activation of the coagulation cascade — result is unreliable); 2-3 mL fresh venous blood; leave undisturbed at room temperature for exactly 20 minutes; tilt gently — does not clot = positive (VICC). Repeat 6-hourly to monitor response to ASV. Normal clotting time is 4-9 minutes in glass.

The 20WBCT is the most important first investigation: place fresh blood in a clean dry GLASS tube (not plastic — glass contact activation is essential) and wait 20 minutes. Non-clotting = VICC = antivenom indication. This test can be performed anywhere with any clean glass container and costs nothing.

Correct. Non-clotting 20WBCT is an absolute indication for ASV — it confirms VICC, which is systemic haematotoxic envenomation. ASV indications are signs of SYSTEMIC envenomation: coagulopathy (20WBCT non-clot, spontaneous bleeding), neurotoxicity (ptosis, paralysis), cardiovascular effects, AKI, or haemoglobinuria. Local swelling alone, even if extensive, is NOT an indication for ASV.

ASV indications — systemic envenomation: Haematotoxic: non-clotting 20WBCT, spontaneous bleeding (gum bleed, haematuria, haemoptysis), rising creatinine (AKI). Neurotoxic: ptosis, diplopia, dysphagia, descending paralysis. Cardiovascular: shock, ECG changes. Haemoglobinuria/myoglobinuria. LOCAL signs alone (swelling, pain, local necrosis without systemic features) do NOT indicate ASV. ASV does NOT treat local tissue damage.

The key rule: ASV is indicated for SYSTEMIC envenomation only — not for local signs alone. A non-clotting 20WBCT proves VICC (venom-induced consumption coagulopathy) and is an absolute ASV indication. Local swelling, pain, or fang marks alone are not sufficient. Bite from a venomous species without evidence of systemic envenomation does not justify ASV — it is a biological product with real risks.

Correct. This is anaphylaxis to ASV. The immediate action is: STOP the infusion AND give IM adrenaline 0.5 mg (0.5 mL of 1:1000) into the anterolateral thigh. Adrenaline is the only life-saving drug in anaphylaxis — it reverses bronchospasm and hypotension. IV hydrocortisone and antihistamines are adjuncts administered AFTER adrenaline. Have adrenaline drawn up BEFORE starting any ASV infusion.

ASV anaphylaxis management sequence: 1) STOP infusion immediately; 2) IM adrenaline 0.5 mg (1:1000) anterolateral thigh; 3) IV fluids for hypotension; 4) IV chlorphenamine 10 mg + hydrocortisone 200 mg (adjuncts, after adrenaline); 5) Consider salbutamol nebulisation if bronchospasm persists; 6) Once reaction controlled and patient stable, resume ASV at slower rate with cover. Pre-emptive prophylaxis with adrenaline/antihistamine/steroid before ASV is controversial and not routinely recommended.

Anaphylaxis treatment: STOP the trigger (ASV infusion) + IM adrenaline 0.5 mg (1:1000) into the anterolateral thigh — this is the only life-saving drug. Antihistamines and steroids are slow-acting adjuncts and do not reverse anaphylaxis. The golden rule: draw up adrenaline BEFORE starting ASV — the window between onset of severe reaction and cardiovascular collapse can be minutes.

Correct. This is Grade II scorpion envenomation (systemic features: hypertension, tachycardia, diaphoresis, priapism) due to Mesobuthus tamulus (Indian red scorpion). The specific treatment is prazosin — an alpha-1 adrenoreceptor blocker that counters the massive catecholamine surge. Beta-blockers (propranolol) are CONTRAINDICATED because blocking beta-2 vasodilation while alpha-1 vasoconstriction is unopposed causes severe hypertension and cardiovascular collapse.

Scorpion envenomation grading: Grade I = local pain/swelling only; Grade II = systemic autonomic features (hypertension, tachycardia, diaphoresis, cold extremities, priapism, hypersalivation, priapism); Grade III = pulmonary oedema, cardiogenic shock. Prazosin dose: 250 mcg for <5 years or 500 mcg for >5 years, repeat every 3 hours if features persist. Beta-blockers CONTRAINDICATED. Calcium channel blockers and sedatives may precipitate shock.

This is Grade II scorpion envenomation (Indian red scorpion — autonomic storm with hypertension, diaphoresis, priapism — no urticaria/wheeze to suggest anaphylaxis). Prazosin is the specific treatment — alpha-1 blocker counters the catecholamine surge. Beta-blockers are absolutely contraindicated: they unmask unopposed alpha-1 vasoconstriction, causing dangerous hypertension.

Correct. Massive bee envenomation (>50 stings) causes DIRECT TOXIC envenomation, not anaphylaxis. Bee venom phospholipase A2, melittin, and other toxins directly lyse red blood cells (haemolysis) and skeletal muscle cells (rhabdomyolysis), releasing haemoglobin and myoglobin into urine. This causes pigment nephropathy (AKI) — dark brown urine is haemoglobinuria/myoglobinuria. There is NO urticaria or wheeze because this is NOT IgE-mediated.

Bee sting — two syndromes to distinguish: (1) ANAPHYLAXIS (single sting, sensitised): urticaria + wheeze + hypotension → IM adrenaline 0.5 mg FIRST; (2) TOXIC MASSIVE ENVENOMATION (>50 stings, unsensitised): dark urine + AKI + haemolysis, no urticaria/wheeze → IV fluids + urine alkalinisation + renal monitoring — NOT adrenaline. Confusing the two syndromes is a potentially fatal clinical error.

The absence of urticaria/wheeze distinguishes direct toxic envenomation from anaphylaxis. Massive bee stings cause direct haemolysis + rhabdomyolysis via phospholipase A2 and melittin → haemoglobinuria + myoglobinuria → AKI (pigment nephropathy). Management: aggressive IV fluids + urine alkalinisation + monitor renal function — NOT adrenaline.