MBBS viva · Infectious Diseases
Tetanus — clinical recognition and management viva
A final-prof viva on recognising generalised tetanus, explaining its mechanism, defending the four-pillar management with drug/dose/route, and articulating prevention. Examiner expects mechanism and dose-level detail, not labels.
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Interpretation
The examiner presents a clinical vignette: a farmer with progressive jaw stiffness, a grimacing facial expression, board-like abdominal rigidity and painful whole-body spasms on noise, fully alert, two weeks after a soil-contaminated puncture wound, never vaccinated — and asks: "What is the diagnosis, explain the mechanism, and outline the management."
- Diagnosis: generalised tetanus — trismus, risus sardonicus, opisthotonos/board-like abdomen, stimulus-triggered reflex spasms, preserved sensorium with a contaminated wound and absent vaccination. The diagnosis is clinical; no test confirms or excludes it.[3][1]
Key points
The examiner will probe each of these; be ready to defend them at viva depth:
- Mechanism (the centrepiece). Tetanospasmin is a zinc-endopeptidase neurotoxin released by germinating C. tetani in an anaerobic wound. It binds the motor nerve ending, undergoes retrograde axonal transport to the spinal cord, crosses to inhibitory interneurons, and cleaves synaptobrevin (VAMP) — preventing vesicle fusion and blocking release of glycine and GABA. Loss of inhibition → sustained muscle contraction, reflex spasms, autonomic storms, with consciousness and sensation preserved (sensory pathways and cortex are not the target).[3]
- Tetanus vs botulism. Both are SNARE-cleaving neurotoxins; botulinum toxin stays at the NMJ and blocks acetylcholine → descending flaccid paralysis with early cranial nerve palsies; tetanospasmin travels centrally and blocks glycine/GABA → rigidity.[3]
- The four pillars of management — with drug/dose/route. (i) HTIG ~500 IU IM before debridement (neutralises unbound toxin only). (ii) IV metronidazole 500 mg q8h for 7-10 days + wound debridement (avoid high-dose penicillin G — GABA antagonist). (iii) Benzodiazepines (diazepam or midazolam infusion) + IV magnesium (load 40 mg/kg, infusion 1-3 g/h, target Mg 2-4 mmol/L) + paralysis/ventilation for grade IV + ICU in a dark quiet room. (iv) Active vaccination of the survivor (disease does not immunise).[3][5]
- Why magnesium? Thwaites 2006 RCT — reduced the need for ventilation and verapamil but did not reduce mortality; it is an adjunct, not a replacement for ICU. Monitor the knee jerk (loss = first sign of toxicity) and serum magnesium.[5]
- Prognostic markers. Incubation under 7 days, onset-to-spasm under 48 h, Ablett III/IV, autonomic instability, cephalic/neonatal forms predict high mortality.[3]
- Prevention. DTaP/Tdap primary series + booster every 10 years; wound prophylaxis per CDC/ACIP (toxoid ± HTIG by wound type and prior doses); maternal tetanus toxoid to eliminate neonatal tetanus (WHO 2017 position paper; India validated MNTE elimination in 2015).[7]
References
- Bhatia R, et al. Tetanus. Neurology India 2002.[1]
- Yen LM, Thwaites CL. Tetanus. Lancet 2019.[3]
- Thwaites CL, et al. Magnesium sulphate for severe tetanus. Lancet 2006.[5]
- WHO. Tetanus vaccines: WHO position paper, February 2017.[7]
References4ShowHide
- [1]Bhatia R, Prabhakar S, Grover VK. Tetanus. Neurology India, 2002.PMID 12577086
- [3]Yen LM, Thwaites CL. Tetanus. Lancet, 2019.PMID 30935736
- [5]Thwaites CL, Yen LM, Loan HT, et al. Magnesium sulphate for treatment of severe tetanus: a randomised controlled trial. Lancet, 2006.PMID 17055945
- [7]World Health Organization. Tetanus vaccines: WHO position paper - February 2017. Weekly Epidemiological Record, 2017.PMID 28185446