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]

[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]

[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 in severe tetanus — continuous ECG and intra-arterial BP with telemetry for arrhythmias; SpO2 and, if ventilated, capnography and serial blood gases; serum magnesium every 6 to 12 hours during magnesium infusion (target 2 to 4 mmol/L) with knee reflexes before each dose; urea and electrolytes, creatinine, CK (for rhabdomyolysis and AKI), glucose, lactate, and blood cultures if line sepsis is suspected; plus DVT prophylaxis, pressure-area care and nutrition.[5]

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]

[2] [3]

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]

[5]

Pillar 1 — Neutralise unbound toxin: HTIG

HTIG (human tetanus immune globulin) provides passive immunity by binding and neutralising circulating, unbound tetanospasmin. It does not reverse toxin already bound to nerve tissue — which is why it limits progression but cannot abolish existing symptoms. Give it early, give it intramuscularly, and give it before you manipulate the wound.[3][6]

• Dose and route — 500 IU IM as soon as the diagnosis is made (some authorities use 3000 to 6000 IU; no strong evidence favours higher doses, and 500 IU is the WHO-supported practical dose). Infiltrate a portion around the wound before debridement; give the rest IM at a site distant from the toxoid vaccination site, so the immunoglobulin does not blunt the active immune response.
• Timing — ideally before wound debridement, so that toxin released by surgical manipulation is neutralised.
• Equine antitoxin — used where HTIG is unavailable (10,000 to 20,000 units IV or IM after a test dose), but it carries a real risk of serum sickness and anaphylaxis; HTIG is preferred wherever it can be obtained.[6]

Pillar 2 — Eradicate the organism and remove its anaerobic source

• Metronidazole is the antibiotic of choice — IV metronidazole 500 mg every 8 hours for 7 to 10 days (or oral 400 mg every 12 hours where appropriate) eradicates the bacillus.[3]
• Avoid high-dose penicillin G. Penicillin is bactericidal against C. tetani but is structurally a GABA antagonist; high doses can worsen spasms. Metronidazole avoids this and is at least as effective. Where neither is available, macrolides (erythromycin) or doxycycline are alternatives.
• Surgical wound debridement — remove all necrotic tissue, foreign bodies and sealed-over scabs that recreate the anaerobic environment, ideally after HTIG has been given so that toxin released by manipulation is neutralised. Even a trivial-appearing wound should be opened and cleaned.[2]

The classic trap: reaching for the penicillin that worked for the cellulitis next door. In tetanus it worsens the spasms; metronidazole is the standard.[3]

Pillar 3 — Control spasms and support vital functions

Benzodiazepines are the cornerstone — they bind the GABA-A receptor and enhance inhibitory tone, partially countering the loss of GABA and glycine. Diazepam has been traditional (large doses, e.g. 10 to 40 mg IV repeated, or 100 to 300 mg per 24 hours by infusion); midazolam is preferred for continuous infusion because of its shorter half-life and predictable kinetics (e.g. 0.05 to 0.2 mg/kg/h).[3]

Magnesium sulphate — in severe (grade III or IV) tetanus — inhibits presynaptic catecholamine release and competes with calcium at the neuromuscular junction, controlling both spasms and autonomic storms and reducing the need for sedation and ventilation. The Thwaites 2006 randomised controlled trial established its role.[5]

[5]

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 is treated with a morphine infusion (0.05 to 0.2 mg/kg/h, blunting sympathetic surges), magnesium (above), short-acting beta-blockers (esmolol or labetalol for hypertension and tachycardia — avoid long-acting propranolol, which can precipitate sudden cardiac death from unopposed vagal surges), and vasopressors or inotropes for hypotensive episodes. Swings of BP and heart rate can be extreme; titrate carefully.[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]

[3]

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.
• Worsening spasms from high-dose penicillin G given instead of metronidazole.
• 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

Recognise early (day 5 to 14, poor feeding, rigidity, spasms); treat as severe tetanus with HTIG 50 to 200 IU/kg IM, benzodiazepines and meticulous ICU support. The decisive intervention is maternal vaccination.[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 — the CDC/ACIP table (reproduced verbatim)

Every wound in every patient should trigger a check of the immunisation history. The decision to give toxoid alone versus toxoid plus immunoglobulin depends on the wound type and the number of prior toxoid doses.[7]

[7]

Tetanus-prone wounds include those contaminated with dirt, soil, faeces or saliva; puncture wounds; wounds containing necrotic or devitalised tissue; burns, frostbite, crush and avulsion injuries; wounds from missiles; and wounds delayed over 6 hours before treatment. HTIG prophylaxis dose: 250 IU IM (some references use 250 to 500 IU), given at a site separate from the toxoid.[7]

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. The optimum dose of HTIG (500 versus 3000 to 6000 IU) is uncertain; the choice of autonomic agent (labetalol versus esmolol versus morphine versus magnesium) is largely empirical; the role of intrathecal antitoxin is now not supported; and there are no high-quality trials of early elective intubation versus delayed intubation, although expert consensus favours early airway control in grade III or IV disease.[3][6]

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)

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 (Ablett III) — a clinical diagnosis; no test will help. Move him to a dark, quiet, undisturbed room, give IV diazepam 10 mg titrated to spasm control, place suction and intubation equipment at the bedside and have a low threshold to intubate. Establish IV access and prepare labetalol, morphine, magnesium and vasopressors. Then deliver the four pillars: HTIG 500 IU IM (a portion infiltrated around the healed thorn site, the rest IM distant from the planned vaccination site), IV metronidazole 500 mg every 8 hours, wound debridement after HTIG, and — before discharge — the first dose of a full tetanus toxoid primary course, because the disease does not immunise. Admit to ICU; plan for a tracheostomy if paralysis and ventilation are needed.[3]

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

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 — generalised tetanus from umbilical-stump infection with C. tetani in an infant of an unvaccinated mother. Treat as severe tetanus: HTIG 50 to 200 IU/kg IM, benzodiazepines, meticulous ICU support, and a quiet environment. The decisive preventive intervention is maternal tetanus toxoid vaccination during pregnancy — two doses four weeks apart, the second at least two weeks before delivery — combined with clean delivery and cord care. This is how neonatal tetanus is eliminated, and how India reached validation in 2015.[4]

Stem 3 — the mimics in casualty (answer)

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]

References

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, Binh ND, Truong AH, 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