Tetanus

Meet the patient

A 55-year-old farmer from a village walks in unable to open his mouth. For three days he has had a stiff jaw, a sore throat he blames on the weather, and a vague dread he cannot name. Eight days ago he trod on a thorn in the manure-rich soil behind his shed; the wound was small and has already healed over. Now the slightest noise sends his whole body into a rigid arch, the back off the bed, heels and head pressed down, jaw clamped, grinning grimace he cannot control — and his eyes are wide open and terrified.^[3]

The two questions this man forces you to answer in the next five minutes are the two that decide every tetanus case: is this tetanus? (the bedside picture answers yes the moment you see opisthotonos in an awake patient) and can I keep him breathing through the spasms and the autonomic storms? (the ICU answers that over the next four weeks). Hold those two questions and every section below slots into place.^[3]

One toxin, one disease — why the whole illness is the poison

Tetanus is not an infection in any meaningful sense; it is a poisoning. The bacillus sits in the wound, never invades, and may even have healed over by the time the patient arrives — but the exotoxin it has already released is doing all the damage. That single fact explains everything that follows: why a tiny wound can be fatal, why the diagnosis is clinical, why treatment must begin before any test returns, and why a survivor gets no immunity and must still be vaccinated.^[3]

Clostridium tetani is a Gram-positive, anaerobic, spore-forming drumstick bacillus (the terminal spore gives it the drumstick shape). Its spores are ubiquitous in soil, dust and animal — especially horse — manure worldwide; they survive boiling for short periods and shrug off most disinfectants. Spores germinate only in anaerobic, necrotic, low-redox tissue — a sealed puncture, a crush injury, necrotic skin, a retained foreign body, an umbilical stump dressed with ash. The bacilli multiply locally, release tetanospasmin (TeNT), and the toxin does the rest.^[3]

Etymology for viva gold: the word tetanus comes from the Greek tetanos, "to stretch" or "to be taut" — a description of the rigidity so accurate that 2,400 years of medicine have not improved it. Risus sardonicus, the grimace, is the "sardonic laugh" of ancient Sardinia, where elders were allegedly given a neurotoxic ranunculus flower that produced exactly this stiff grin before death. The names outlived their origin stories because the signs are unmistakable.^[1]

The toxin's journey — why consciousness is preserved and the damage is irreversible

The toxin's path is the single most examinable mechanism in the topic, because it explains the four features examiners probe: the descending pattern, the preserved consciousness, the long incubation, and the irreversibility.^[3]

The cascade runs in six steps:^[3]

1. Inoculation and germination — spores enter a wound and germinate only under anaerobic, low-redox conditions; the bacillus rarely invades, and the wound may look trivial or have healed.
2. Toxin production and uptake — germinating bacilli release tetanospasmin (TeNT), a 150-kDa zinc-endopeptidase neurotoxin (the same family as botulinum toxin). Its heavy chain binds GD1b and GT1b gangliosides on the presynaptic membrane of the motor neurone at the neuromuscular junction, triggering endocytosis.
3. Retrograde axonal transport — the endocytosed toxin climbs the motor axon to the cell body in the anterior horn (or the cranial-nerve nucleus), then crosses to inhibitory interneurons — the Renshaw cells and the glycinergic and GABAergic terminals. This long climb is the incubation period; the longer the nerve, the longer the incubation, and the shorter the incubation the heavier the toxin load and the worse the disease.
4. SNARE cleavage — the toxin's light chain, a zinc-dependent endopeptidase, cleaves synaptobrevin (VAMP), the SNARE protein required for synaptic-vesicle fusion. Vesicles can no longer dock; the neurone cannot release its transmitter.
5. Loss of glycine and GABA — the transmitters silenced are exactly the inhibitory amino acids glycine (Renshaw-cell recurrent inhibition) and GABA. Recurrent and reciprocal inhibition of motor neurones and autonomic centres is removed.
6. Irreversibility and recovery — once synaptobrevin is clipped, the block cannot be undone; recovery requires new synaptobrevin and new synaptic terminals, which takes 4 to 6 weeks. This is why the disease runs its full course even after the toxin is neutralised and the organism eradicated.^[3]

The clinical translation is the punchline every viva candidate must land: loss of inhibition produces sustained muscle contraction (rigidity) in a descending pattern — trismus, risus sardonicus, opisthotonos, board-like abdomen — plus reflex spasms triggered by any stimulus, autonomic instability from loss of sympathetic inhibition, and preserved consciousness and sensation because the toxin spares sensory pathways and the cortex. The patient is awake, aware, and in agony throughout — the single feature that separates tetanus from almost every mimic.^[3]

The classic trap: examiners love to ask why the patient stays conscious when the body is rigid. The answer is the whole mechanism in one breath — tetanospasmin acts on inhibitory motor interneurons and autonomic centres, not on sensory pathways or the cortex, so sensation and awareness are intact. A patient who is drowsy between spasms does not have tetanus; look for meningitis, encephalitis, or status epilepticus.^[3]

Tetanospasmin versus botulinum — the mirror image (the examiner's favourite comparison)

Both are zinc-endopeptidase neurotoxins that cleave SNARE proteins and block neurotransmitter release; they differ only in where they act, and the difference produces the opposite clinical picture.^[3]

^[3]

The one-line discriminator: tetanus is the disease of lost brakes (rigidity, preserved mind); botulism is the disease of lost signal (flaccidity, drooping eyes). Same toxin family, opposite poles.^[3]

The four faces — clinical forms and the Ablett grade

Tetanus is classified by its clinical form (where the toxin lands) and then by its severity (the Ablett grade that decides whether the patient goes to ICU). Both decisions are made at the bedside.^[3]

^{[3] [4]}

Severity grading is the second bedside decision and it sets disposition. The Ablett classification (1967, four grades) stratifies by the intensity of spasms, the presence of autonomic disturbance, and the need for ventilation:^[5]

^[5]

Everyone forgets: a patient can cross from Ablett II to Ablett IV over hours. Re-grade at every contact; grade III or IV means ICU for airway protection, paralysis and autonomic control, not "admit and see".^[5]

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^[3]

Who gets it, and why the wound matters

Tetanus is now rare wherever immunisation is robust, but it has not been eradicated — it remains a disease of the unvaccinated and the under-vaccinated in every country. The bacillus is everywhere; only immunity stands between a soil-contaminated wound and the disease.^[1][3]

The host and the wound that should make you reach for the prophylaxis table:^[1][3]

• Host at risk — never vaccinated or incomplete primary series; lapsed boosters (over 10 years since the last dose, or over 5 years for a tetanus-prone wound); the elderly (waning immunity, lapsed boosters); neonates of unvaccinated mothers; intravenous drug users (skin abscesses, contaminated heroin); people in remote or rural areas with poor vaccine access.
• Wound at risk — puncture wounds (nail, splinter, thorn); contamination with soil, manure, or rust; necrotic or avascular tissue, deep wounds, retained foreign body; burns, frostbite, crush and avulsion injuries; the umbilical stump in a neonate when instrument or cord care is unclean; surgical wounds, dental sepsis, otitis media, chronic ulcers (the diabetic foot), intramuscular injections in drug users; tattooing or piercing with unsterile technique.^[1][3]

The classic trap: a tetanus-prone wound is common; the missing piece in the casualty note is the vaccination history. Every wound in every patient must trigger a check of the immunisation record, not just a dressing — the prophylaxis decision (toxoid alone versus toxoid plus immunoglobulin) depends on both.^[7]

Neonatal tetanus was once a major cause of neonatal death and is now eliminated (fewer than 1 case per 1000 live births in every district) across most of the world through maternal tetanus toxoid vaccination and clean delivery and cord care — the achievement of the WHO maternal and neonatal tetanus elimination (MNTE) initiative. It persists only where mothers remain unvaccinated.^[4]

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^[3]

The classic picture — trismus, risus sardonicus, opisthotonos

The clinical picture is a descending sequence of increasing rigidity and spasm in a patient who is fully alert. Recognise the triad and you have made the diagnosis before any test.^[3][1]

Onset — trismus (lockjaw). The first symptom in about 50 to 75 percent of patients is trismus — painful spasm of the masseters that prevents the patient opening the mouth. It is also the first sign to be misattributed, to dental abscess, tonsillitis, or temporomandibular dysfunction, and that misattribution is the recurring trainee error that delays treatment. Trismus is followed within hours to days by dysphagia, neck stiffness and a diffuse apprehension.^[2]

Established disease — the classic triad:^[3]

• Risus sardonicus — sustained spasm of the facial muscles producing the characteristic grinning grimace (eyebrows raised, corners of the mouth drawn back and up).
• Opisthotonos — extreme spasm of the paraspinal muscles arching the back so that the head and heels approach the bed and the body rests on the occiput and heels.
• Board-like abdominal rigidity — sustained contraction of the abdominal wall that can mimic an acute abdomen and, tragically, prompt a laparotomy that the patient does not need.^[3]

Reflex spasms. Once rigidity is established, any stimulus — a sudden noise, a light switched on, a touch, an airway suction catheter, even the patient's own cough — triggers a violent, painful, sustained spasm lasting seconds to minutes. Laryngospasm during a spasm is immediately life-threatening (sudden apnoea, hypoxic arrest); spasms of the respiratory muscles cause respiratory failure. This is why the patient must be in a dark, quiet, undisturbed room — the single highest-yield nursing intervention in the disease.^[3]

Autonomic instability (severe disease, second week). Loss of inhibition in autonomic centres produces labile hypertension alternating with hypotension, tachycardia (occasionally bradycardia from vagal storms), arrhythmias, profuse sweating, salivation, and pyrexia, typically peaking in the second week. Autonomic failure is the leading cause of death in patients who survive the early spasms — the patient who clears the spasms can still die of an arrhythmia a week later.^[5]

Sensorium is preserved. The patient is awake, terrified and in severe pain throughout. This single feature distinguishes tetanus from meningitis, encephalitis and status epilepticus, in which consciousness is impaired. A drowsy, rigid patient is not a tetanus case you have under-treated; he is a different diagnosis.^[3]

^{[3] [4]}

The mimics that cost lives — exclude the strychnine, the dystonia, the calcium

The combination of trismus, rigidity, stimulus-triggered spasms and a clear sensorium with a relevant wound is essentially diagnostic. The difficulty is the early case (isolated trismus) or the atypical case, and the cost of guessing wrong is high.^[2][3]

^{[2] [3]}

The one-line discriminator: strychnine is the only mimic that shares the mechanism — and it is the one where the muscles go FLACCID between spasms. Tetanus rigidity never relaxes; that is the bedside line.^[2]

The bedside round — confirm, grade, find the portal

A focused examination has three goals: confirm the clinical diagnosis, grade severity (Ablett), and identify the portal of entry.^[3]

Confirming the diagnosis at the bedside:^[3]

• Trismus and the spatula test — touch a spatula against the posterior pharyngeal wall. A positive test is reflex spasm of the masseters biting down on the spatula rather than the normal gag; highly suggestive of tetanus in the right context.
• Risus sardonicus and opisthotonos together are pathognomonic.
• Board-like abdominal rigidity is present even between spasms and must not be mistaken for a surgical abdomen.^[3]

Grading severity (Ablett) — re-applied through the illness, because a patient can deteriorate from grade II to grade IV over hours (see the table above). Grade III or IV mandates ICU for airway protection, paralysis or ventilation, and autonomic control.^[5]

Identifying the portal. Examine every skin break: punctures, lacerations, burns, ulcers (including the diabetic foot), the umbilicus in a neonate, recent injection sites in an IV drug user, otitis media, dental sepsis. And remember the recurring sting — in 15 to 25 percent of cases no portal is found, so a normal-looking wound (or no wound at all) does not exclude tetanus.^[3]

Monitoring in established disease — continuous ECG, SpO2 and intra-arterial BP (in severe disease), spasm frequency, temperature, urine output, and — when magnesium is used — serum magnesium levels and the deep tendon reflexes (loss of the patellar reflex is the first sign of magnesium toxicity).^[5]

There is no test — investigations only exclude mimics

There is no diagnostic laboratory test for tetanus. The diagnosis is clinical; investigations exist to exclude mimics and to support the critically ill patient, never to confirm or exclude the disease.^[3][1]

The tests that earn their place:^[1]

• Serum calcium and albumin (corrected or ionised) — exclude hypocalcaemic tetany.
• Serum creatine kinase — may be elevated from sustained spasm and may progress to rhabdomyolysis with acute kidney injury; non-specific.
• Toxicology screen — strychnine, theophylline, antipsychotics (for dystonia).
• CSF analysis — in meningitis or encephalitis the CSF is abnormal; in tetanus it is normal.
• Neuroimaging (CT or MRI brain) — exclude a space-occupying lesion or stroke where the picture is unclear.
• EEG — distinguish status epilepticus.^[1]

Wound cultures for C. tetani are insensitive and slow; the organism is fastidious and may be gone by presentation. They should never delay treatment.^[1]

ICU monitoring and supportive care in severe tetanus — treatment aims to control spasms and reduce cardiovascular instability, and patients require several weeks of hospitalisation while remaining vulnerable to secondary problems such as hospital-acquired infections.^[3][9] Continuous cardiorespiratory monitoring and meticulous supportive care are the core of intensive management; where a magnesium infusion is running, the rate is titrated to spasm control while retaining the patellar tendon reflex, which is a valid guide against overdose.^[8]

The first fifteen minutes — quiet room, benzo, airway

Tetanus is a time-critical medical emergency. The resuscitation bundle runs concurrently with the diagnostic assessment and is aimed at preventing death from airway obstruction, respiratory failure and a violent spasm.^[3][2]

^{[1] [3] [5]}

The recurring mistake: nursing a tetanus patient in a bright, busy bay because no side-room is free. Any stimulus — a monitor alarm, a door slamming, a nurse's cough — can trigger a fatal spasm. The dark, quiet room is not a comfort measure; it is the first treatment.^[2]

The four pillars — neutralise, eradicate, control, vaccinate

Definitive treatment rests on four pillars: neutralise unbound toxin, eradicate the organism and remove its anaerobic source, control spasms with intensive support, and — the non-negotiable fourth — actively vaccinate the survivor, because the toxin dose that produces disease is too small to induce immunity.^[3]

^{[1] [5] [6]}

Pillar 1 — Neutralise unbound toxin: HTIG

HTIG (human tetanus immune globulin) provides passive immunity by neutralising circulating, unbound tetanospasmin. It does not reverse toxin already bound to nerve tissue — peripherally administered antitoxin penetrates the CNS poorly, which is why it limits progression but cannot abolish existing symptoms. Give it early and by the intramuscular route, alongside the other components of treatment.^[3][6]

• Dose and route — intramuscular antitoxin, as part of initial treatment. In the largest factorial randomised trial the regimens were 3000 IU human or 21,000 U equine intramuscular antitoxin, and the two performed equally; shortages and high costs, not efficacy, now drive the choice between them.^[6][9]
• Timing — antitoxin is given alongside the other components of treatment (wound debridement, antibiotics, spasm control) at the earliest opportunity once the clinical diagnosis is made.^[3]
• Intrathecal antitoxin adds nothing — 500 IU intrathecal human antitoxin was safe but provided no overall benefit in addition to intramuscular antitoxin, so the intramuscular route is standard.^[6]

Pillar 2 — Eradicate the organism and remove its anaerobic source

• Antibiotics plus debridement form the eradication arm — metronidazole may be the preferred antibiotic, although penicillin is still used frequently; adequate wound debridement is necessary to prevent spore germination.^[1][3]
• The choice of antibiotic is not settled dogma — older reviews still describe frequent penicillin use alongside metronidazole preference, and the eradication pillars are antibiotics plus debridement, never antibiotics alone.^[1]
• Debridement targets the anaerobic source — removing necrotic tissue and foreign material prevents spore germination; it sits beside antitoxin (neutralise the toxin) and antibiotics (eradicate the organism) in the combined approach.^[1][3]

The classic trap: assuming any antibiotic will do. Metronidazole may be the preferred antibiotic although penicillin is still used frequently — and antibiotics never work alone: debridement of the anaerobic source is necessary to prevent spore germination.^[1]

Pillar 3 — Control spasms and support vital functions

Benzodiazepines are the standard sedatives for spasm control. Spasms are usually managed by sedatives like diazepam and neuromuscular blocking agents; in the severe-tetanus randomised trial, midazolam was the sedative titrated to spasm control, with pipecuronium where paralysis was needed.^[1][5] Magnesium allowed real sedation-sparing: patients on magnesium required a median of 1.4 mg/kg per day of midazolam versus 7.1 mg/kg per day on placebo, for the same spasm control.^[5]

Magnesium sulphate — in severe tetanus — controls both muscle spasms and autonomic instability while reducing the requirement for other drugs (sedatives, neuromuscular blockers, verapamil). The Thwaites 2006 randomised controlled trial established this role; note that it did not reduce the need for mechanical ventilation.^[5]

^{[5] [8]}

Neuromuscular blockade and mechanical ventilation are required when spasms cannot be controlled, when there is recurrent laryngospasm, or in grade IV disease with autonomic storms. Vecuronium or rocuronium infusion with propofol, midazolam and fentanyl sedation and lung-protective ventilation gives complete spasm control. A tracheostomy is performed early in the ventilated course because the duration of paralysis is usually weeks.^[3]

Autonomic instability — in ventilated patients, tetanus-associated autonomic dysfunction is the commonest cause of death — is managed with a combination of benzodiazepines, morphine, magnesium sulphate and adrenergic blockers.^[1][5] The magnesium evidence is direct: patients on magnesium were 4.7 times less likely to require verapamil to treat cardiovascular instability than placebo-treated patients.^[5]

General supportive care — nasogastric or parenteral nutrition (the metabolic demand of constant muscle activity is high), DVT prophylaxis, pressure-area care, stress-ulcer prophylaxis, careful fluid and electrolyte balance, and prevention of nosocomial infection. The course is long — weeks of ICU — and complications are the rule, not the exception.^[3]

Pillar 4 — Active vaccination of the survivor

Survivors of tetanus must be actively vaccinated. The quantity of toxin that causes clinical disease is too small to provoke a protective antibody response, so a single episode of tetanus confers no immunity. Give a full primary course of tetanus toxoid (3 doses) or, if previously partially vaccinated, complete the series, and reinforce every 10 years. Plan the first dose before or at discharge.^[3][7]

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^{[1] [3] [5]}

The subtypes that change the plan

Neonatal tetanus is generalised tetanus in the neonate, almost always from infection of the umbilical stump (unclean instrument or cord care, application of animal dung or ash) in an infant of a mother without protective antitoxin antibody. Onset is between day 5 and day 14 of life with poor sucking, irritability and excessive crying, progressing to generalised rigidity, opisthotonos and spasms on handling or feeding, then apnoea. Case-fatality is high (50 to 90 percent) without ICU, and elimination (fewer than 1 case per 1000 live births in every district) is achieved by maternal tetanus toxoid immunisation and clean delivery and cord care.^[4]

Cephalic tetanus is rare and follows otitis media, head, face or scalp lacerations, or dental infection. The toxin acts on the cranial-nerve nuclei, producing a lower-motor-neurone cranial-nerve palsy (most often CN VII) together with trismus. It may progress to generalised tetanus and carries a poor prognosis.^[3]

Special exposures that should sharpen suspicion:^[3]

• IV drug users — skin abscesses and contaminated heroin (which may contain C. tetani spores); often unvaccinated.
• Diabetic foot ulcers and chronic wounds — a portal in the elderly with waning immunity.
• Post-surgical, post-partum, intra-abdominal — rare, often severe, sometimes with no obvious wound; tetanus has been described after abdominal surgery and septic abortion.
• Immunisation omission — a survivor of an incomplete primary series remains at risk of a further episode.^[3]

When tetanus kills you — the preventable list

Complications fall into four groups, and the timing of each is the examinable single fact.^[3][5]

^{[3] [5]}

How tetanus patients come to harm — the preventable list:^[3]

• Death from a spasm-related laryngospasm in a patient nursed in a bright, noisy bay — the preventable death of nursing error.
• Death from arrhythmia in the second week in a patient whose autonomic instability was underestimated and not monitored.
• Antibiotic and debridement complacency — metronidazole may be preferred, yet penicillin is still frequently used and the wound's anaerobic source is left undrained.
• A second episode of tetanus in a survivor who was never vaccinated — the disease does not immunise.
• A missed diagnosis of early tetanus attributed to a dental abscess, delaying HTIG by a day.^[3]

Prognosis, disposition, and the numbers that set both

Mortality is set by severity grade, tempo of onset, access to ICU, age and comorbidity.^[3][5]

^[3]

Adverse prognostic factors — incubation period under 7 days; onset-to-spasm interval under 48 hours; severe (Ablett III or IV) presentation; autonomic instability; cephalic tetanus; neonatal tetanus; IV drug use; extremes of age; delayed presentation; and lack of access to ICU, HTIG and mechanical ventilation.^[3]

Recovery and rehabilitation. Because toxin-nerve binding is irreversible, recovery requires regeneration of new synapses over 4 to 6 weeks; rigidity and spasms gradually subside. Rehabilitation addresses deconditioning, contractures, swallowing and the psychological sequelae of weeks of conscious paralysis. Survivors must complete active vaccination.^[3]

Disposition. Grade I or II may be managed on a quiet ward or HDU; grade III or IV, autonomic instability, recurrent laryngospasm or respiratory compromise mandate ICU. Isolate the patient from stimuli; plan a tracheostomy for the prolonged ventilated course; arrange vaccination before discharge.^[5]

Special populations — pregnancy, the neonate, the elderly, the immunocompromised

Pregnancy — preventing neonatal tetanus

Maternal vaccination is the cornerstone of neonatal-tetanus elimination. Protective antitoxin antibody is transferred transplacentally and protects the neonate at birth and through umbilical healing. The WHO 5-dose schedule of tetanus toxoid (TT) or tetanus-diphtheria (Td) in women of childbearing age and during pregnancy eliminates neonatal tetanus in the community.^[4][7]

^[4]

In India, the schedule is part of the universal immunisation programme — 2 doses of tetanus toxoid in pregnancy (Tdap or Td), 4 weeks apart, for primigravidae; a single booster in subsequent pregnancies within 5 years.^[4]

Neonate

Treat neonatal tetanus as severe tetanus with full intensive supportive care — case fatality remains high and treatment is limited by scarcity of resources and effective drug treatments. The decisive intervention is prevention: maternal vaccination and clean birth practices.^[4]

Elderly

Waning immunity and lapsed boosters; a lower threshold for prophylaxis and a higher mortality if disease strikes. Atypical early symptoms — stiffness, dysphagia, falls — must not be dismissed as "old age" before classic trismus appears.^[1]

Immunocompromised and HIV

Vaccinate with toxoid (it is a toxoid, not a live vaccine, and is safe); antibody response may be blunted, so check titres and boost as needed after severe immunosuppression.^[7]

Wound prophylaxis — general principles

Tetanus prophylaxis in wound management — for incompletely immunised individuals presenting with dirty wounds, human tetanus immunoglobulin is considered essential, together with tetanus toxoid vaccination; WHO recommends the five-dose childhood immunisation regimen plus an additional sixth dose after approximately 10 years for long-lasting immunity.^[10]

^[10]

Prophylaxis in practice — tetanus follows contamination of a wound with Clostridium tetani spores: for incompletely immunised individuals presenting with dirty wounds, human tetanus immunoglobulin is considered essential, together with tetanus toxoid vaccination. Identifying who is incompletely immunised is the practical bottleneck — a rapid, point-of-care immunoassay of tetanus immune status can help target prophylaxis instead of over-immunising.^[10]

The trials that changed practice

The 2017 WHO position paper is the global standard, and two randomised trials set the modern drug and antitoxin choices.^[7]

^{[5] [6]}

Where the evidence is weak. Human versus equine antitoxin — the factorial trial found no advantage of human over equine intramuscular antitoxin, yet shortages and high costs persist, so the choice of preparation is a supply question, not an efficacy one. Intrathecal antitoxin is not supported — it was safe but provided no overall benefit in addition to intramuscular antitoxin. Autonomic management remains largely empirical — the randomised-trial evidence covers magnesium (less verapamil required), while other agents rest on practice rather than trials. Key questions about prevention, diagnosis and management remain unanswered.^[6][9]

Regional deltas — the diagnostic and management framework (clinical diagnosis, four pillars, wound prophylaxis, maternal vaccination) is globally consistent; resource-dependent choices differ:^[7]

The mantra, and the mnemonic

^[3]

The mantra: quiet the room, calm the spasms, neutralise the toxin, kill the bug, vaccinate the survivor — and never trust the wound.^[3][7]

Ward-round test — three stems, thirty seconds each

Stem 1 — the man from the top of the topic (answer)ShowHide

The 55-year-old farmer with a healed thorn wound eight days ago now presents with trismus, opisthotonos and stimulus-triggered spasms, fully conscious. What do you do in the first fifteen minutes? Model: This is generalised tetanus — a clinical diagnosis; no test will help. Immediate care: control spasms with a benzodiazepine sedative (diazepam), keep airway equipment and ventilatory support at hand (without mechanical ventilation, mortality remains high), and give antitoxin, antibiotics and wound debridement — metronidazole may be the preferred antibiotic. Admit to ICU: expect several weeks of care, watch for autonomic instability and hospital-acquired infections, and use IV magnesium to reduce the requirement for other spasm- and autonomic-controlling drugs. Before discharge, start active tetanus immunisation — immunisation is the key to prevention.^[1][3][5]

Stem 2 — the neonate who stopped feeding on day 7 (answer)ShowHide

A day-7 neonate of an unvaccinated village mother has stopped sucking, clenches his fists, and goes into opisthotonos when handled. The umbilical stump was dressed with ash. What is this, and what is the single most important preventive intervention? Model: This is neonatal tetanus — tetanus following umbilical-stump contamination in an infant whose mother was not protected by vaccination. Treat as severe tetanus with full intensive supportive care, knowing case fatality is high and effective drug treatments are scarce. The decisive preventive intervention is maternal tetanus toxoid vaccination during pregnancy combined with clean delivery and cord care — the strategy of the Maternal and Neonatal Tetanus Elimination Initiative, which continues to cut incidence through vaccination coverage and birth hygiene.^[4]

Stem 3 — the mimics in casualty (answer)ShowHide

A young man presents with acute trismus and neck torticollis two hours after a prochlorperazine injection for migraine. A second patient, a farmer, has trismus, opisthotonos, a stiff grin and rigidity that does not relaxate between spasms, with a healed thorn wound. A third has trismus, perioral tingling and carpopedal spasm. Name the three diagnoses and the one discriminator each. Model: (1) Drug-induced dystonia — acute trismus after a dopamine antagonist; discriminator is rapid resolution with IV benztropine or diphenhydramine, a diagnostic-and-therapeutic test in one. (2) Tetanus — trismus, opisthotonos, risus sardonicus, stimulus-triggered spasms with rigidity that never relaxes between spasms, a contaminated wound, and a preserved sensorium; treat with the four pillars. (3) Hypocalcaemic tetany — perioral tingling, carpopedal spasm, Trousseau and Chvostek signs; discriminator is low serum ionised calcium and resolution with IV calcium gluconate. The closest mimic of all — strychnine — shares the mechanism but has muscles flaccid between spasms.^[2][3]

References10ShowHide

1. [1]Bhatia R, Prabhakar S, Grover VK. Tetanus. Neurology India, 2002.PMID 12577086
2. [2]Fields B, Guerin CS, Justice SB. Don't Be a Stiff: A Review Article on the Management of Tetanus. Advances in Emergency Nursing Journal, 2021.PMID 33952870
3. [3]Yen LM, Thwaites CL. Tetanus. Lancet, 2019.PMID 30935736
4. [4]Thwaites CL, Beeching NJ, Newton CR. Maternal and neonatal tetanus. Lancet, 2015.PMID 25149223
5. [5]Thwaites CL, Yen LM, Loan HT, et al. Magnesium sulphate for treatment of severe tetanus: a randomised controlled trial. Lancet, 2006.PMID 17055945
6. [6]Van Hao N, Loan HT, Yen LM, et al. Human versus equine intramuscular antitoxin, with or without human intrathecal antitoxin, in tetanus: a factorial, randomised, controlled trial. Lancet Global Health, 2022.PMID 35561721
7. [7]World Health Organization. Tetanus vaccines: WHO position paper - February 2017. Weekly Epidemiological Record, 2017.PMID 28185446
8. [8]Attygalle D, Rodrigo N. Magnesium sulphate for control of spasms in severe tetanus. Can we avoid sedation and artificial ventilation? Anaesthesia, 1997.PMID 9370837
9. [9]Ergönül Ö, Kolsuz S, Figueroa JP. Tetanus. Lancet, 2026.PMID 41544646
10. [10]Cooke MW. Are current UK tetanus prophylaxis procedures for wound management optimal? Emergency Medicine Journal, 2009.PMID 19934122