Paediatrics chapters

Tetanus including neonatal tetanus

Tetanus in children and newborns: Clostridium tetani and tetanospasmin, how the toxin causes rigidity and spasms, neonatal tetanus from the umbilical stump, wound care and tetanus prophylaxis, antitoxin, sedation and nursing, and prevention by maternal and infant vaccination.

UHS PGET syllabus: Infectious diseases (10 MCQs), Tetanus: organism and pathophysiology; clinical features; wound care, immunisation and antitoxin; managementUpdated November 2026
In 30 seconds
  • Tetanus is caused by the toxin tetanospasmin of Clostridium tetani, an anaerobic, spore-forming Gram-positive rod from soil and animal faeces that enters through wounds or, in newborns, the umbilical stump; the toxin travels up motor nerves and blocks inhibitory neurones, giving rigidity and painful spasms with a clear mind.
  • Features: trismus (lockjaw), risus sardonicus, opisthotonos, spasms set off by touch, noise or light, autonomic instability; neonatal tetanus begins about day 3-10 (often day 7) with failure to suck, then trismus and spasms.
  • Treat with human tetanus immunoglobulin (or ATS), wound cleaning, penicillin or metronidazole, diazepam and other relaxants, a quiet dark room, tube feeding and airway care; disease gives no immunity, so vaccinate afterwards; prevent with EPI vaccination, Td for pregnant women and clean delivery and cord care.
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Overview

Tetanus is an acute, often fatal disease caused by a neurotoxin, not by spreading infection. Spores of Clostridium tetani enter a wound, germinate in low-oxygen tissue, and release tetanospasmin, which causes muscle rigidity and violent, painful spasms while the patient stays fully conscious. Neonatal tetanus, from an unclean umbilical stump, kills most affected babies and is entirely preventable by vaccinating mothers and clean delivery. Tetanus is not communicable from person to person.

Organism

  • Clostridium tetani: Gram-positive, anaerobic, spore-forming rod; terminal spores give a drumstick shape.
  • Spores survive for years in soil, dust and the faeces of animals (and humans); they resist boiling and many disinfectants and are best destroyed by autoclaving.
  • Vegetative bacilli are killed by heat and disinfectants and are sensitive to penicillin and metronidazole.
  • The organism is not invasive: it stays in the wound and acts only through its toxin.

Pathophysiology

  1. Spores enter a wound: deep punctures, dirty or crush wounds, thorn pricks, burns, ear piercing, otitis media, injections with dirty needles; in the newborn, the umbilical stump cut with an unclean instrument or dressed with soil, ash or dung.
  2. In anaerobic tissue (dead tissue, foreign body) spores germinate and bacilli release two toxins:
    • Tetanospasmin: the neurotoxin that causes disease.
    • Tetanolysin: enhances the effect.
  3. Tetanospasmin binds at motor nerve endings and travels backwards up the axon to the spinal cord and brainstem.
  4. There it blocks the release of inhibitory transmitters (glycine and GABA) from inhibitory interneurones, so motor neurones fire unchecked: rigidity with superimposed spasms of opposing muscle groups.
  5. The sympathetic system is also disinhibited: tachycardia, labile hypertension, sweating, arrhythmias.
  6. Consciousness and sensation are not affected.
High-yield

Once toxin is bound to neurones it cannot be neutralised. Antitoxin only mops up circulating toxin, so it must be given early; recovery needs new nerve terminals to grow, which takes weeks.

High-yield

The amount of toxin that causes tetanus is too small to produce immunity. Recovery from tetanus does not protect: the child must be fully immunised afterwards.

  • Incubation: usually 2-14 days (Akbar), as short as a day or as long as weeks; Park gives 6-10 days usually.
  • A shorter incubation, and a short gap between first symptom and generalised spasms, mean more severe disease.

Clinical features

Forms

FormFeatures
GeneralisedCommonest form in children and newborns; described below
LocalisedRigidity and spasm near the wound; rare in children; usually resolves without sequelae
CephalicAfter head or face injury or otitis media; short incubation (1-2 days); cranial nerve palsies are characteristic
Neonatal (tetanus neonatorum)Generalised tetanus in the newborn from the umbilical stump

Generalised tetanus

  • Trismus (lockjaw): spasm of the masseters, difficulty opening the mouth; the presenting feature in about half.
  • Risus sardonicus: a fixed grin from spasm of facial muscles.
  • Neck stiffness, difficulty swallowing, rigid abdomen.
  • Opisthotonos: arching of the back, sometimes so severe that only head and heels touch the bed.
  • Spasms are triggered by touch, noise, light, swallowing or handling, and are extremely painful.
  • Laryngeal and respiratory muscle spasm: airway obstruction, apnoea, asphyxia.
  • Autonomic dysfunction: tachycardia, arrhythmias, labile blood pressure, sweating, vasoconstriction, urinary retention.
  • Mind clear throughout; fever may be absent or due to spasms or secondary infection.

Neonatal tetanus

  • Usually a baby born at home to an unimmunised mother, with unclean cord care.
  • Starts 3-10 days after birth, typically around day 7 (Park notes the local name "8th day disease").
  • First sign: failure to suck, then inability to open the mouth (trismus).
  • Excessive crying, irritability; then risus sardonicus.
  • Within a day, generalised spasms: arms flexed and adducted, fists clenched, legs extended, opisthotonos.
  • Spasms set off by touch, noise or light; the baby is conscious.
  • Spasms of glottis and respiratory muscles cause apnoea, cyanosis; septic umbilicus, fever and jaundice may be present.
  • Symptoms worsen over 3-7 days, plateau in the second week, and subside over 2-6 weeks in survivors.
Exam trap

A newborn with spasms but a clear sensorium, trismus and a dirty cord has tetanus, not neonatal sepsis with meningitis or hypocalcaemic fits. The key early clue is a baby who sucked well and then stopped.

Memory hook

"Sucks, stops, spasms": the newborn feeds normally for several days, stops sucking, then develops spasms.

Differential diagnosis

Meningitis or encephalitis (altered consciousness, abnormal CSF), hypocalcaemic tetany, neonatal seizures, dental abscess or peritonsillar abscess (local trismus), drug reactions (phenothiazine dystonia), rabies, strychnine poisoning.

Diagnosis

  • Clinical: history of a wound or unclean delivery, non-immunisation, trismus, spasms and a clear mind.
  • Investigations are mostly normal: blood count (occasional leucocytosis from infection or stress), CSF normal, calcium and glucose normal, EEG normal.
  • Wound Gram stain or culture is positive in only about a third and is not needed for diagnosis.

Management

Aims (Akbar)

  1. Remove the source of toxin (wound care, antibiotics).
  2. Neutralise circulating toxin before it binds.
  3. Control spasms and support the child until the toxin's effect wears off.

1. Antitoxin

ProductNotes (Akbar)
Human tetanus immunoglobulin (TIG)Treatment of choice: 3,000-6,000 units IM as a single dose; minimum about 500 units in newborns; half-life about 30 days; no serum sickness
Equine anti-tetanus serum (ATS)If TIG unavailable: 50,000-100,000 units (half IM, half IV), at least 10,000 units in newborns; sensitivity test first; serum sickness in about 15%

Injecting TIG directly into the wound is unnecessary (Akbar).

2. Wound care and antibiotics

  • Clean and debride the wound, remove foreign bodies and dead tissue (removes the anaerobic site). Do not excise the umbilical stump in neonatal tetanus; clean it.
  • Crystalline (benzyl) penicillin: 200,000 units/kg/day in four doses for 10-14 days (Akbar).
  • Metronidazole is equally effective; erythromycin or (over 8 years) tetracycline for penicillin allergy.

3. Control of spasms

  • Diazepam IV 0.1-0.2 mg/kg every 3-6 hours (Akbar), titrated to stop spasms.
  • Other options: magnesium sulphate, other benzodiazepines, chlorpromazine, phenobarbitone, baclofen, dantrolene; severe cases need neuromuscular paralysis and ventilation.
  • Aim: a child who breathes normally and has only occasional spasms. Over-sedation shows as shallow breathing and loss of tone.

4. Supportive and nursing care

  • Quiet, dark room; minimal handling; group procedures together.
  • Airway: frequent suction, oxygen, intubation or tracheostomy for laryngeal spasm, ventilation if needed.
  • Cardiorespiratory monitoring for apnoea and autonomic storms.
  • Nasogastric feeding (expressed breast milk in newborns) once spasms are controlled; IV fluids early.
  • Change posture regularly; care of mouth, skin, bladder and bowel.

5. Immunise

Start tetanus toxoid before discharge: the disease leaves no immunity.

Complications

  • Aspiration pneumonia and respiratory failure (main causes of death).
  • Laryngospasm, apnoea, asphyxia.
  • Fractures of vertebrae, tongue and lip lacerations during spasms.
  • Autonomic instability: arrhythmias, hypertension, cardiac arrest.
  • Pressure sores, malnutrition, hospital infections.

Prognosis

  • Akbar: mortality 60% or more in tetanus neonatorum and 20-50% in older children; most deaths in the first week.
  • Park quotes up to 80-90% case fatality in neonatal tetanus even with treatment.
  • Better prognosis (Akbar): incubation of 8-10 days or more, slow progression (over 60 hours to generalised spasms), absence of fever, localised disease.
  • Worse prognosis: incubation under 7 days, less than 3 days from trismus to generalised spasms, high fever, neonatal age.

Wound care and prophylaxis after injury

Principles

  • Clean every wound thoroughly with soap and water; remove dirt, foreign bodies and dead tissue.
  • Decide on toxoid and TIG from the number of previous doses and the type of wound (Nelson, Table 94-1):
Previous tetanus dosesClean minor woundAll other wounds (dirt, soil, faeces, saliva; punctures, crush, burns, bites, missiles)
Unknown or fewer than 3Toxoid; no TIGToxoid + TIG
3 or moreToxoid only if 10 years or more since last doseToxoid only if 5 years or more since last dose; no TIG
  • Akbar's local advice is more cautious: give a toxoid booster if none in the last 5 years, or the last 3 years for a heavily contaminated wound.
  • When toxoid and immunoglobulin are given together, use separate syringes and different sites.
  • For an unimmunised child, complete the primary course afterwards.
  • Park: TIG 250 units IM is the usual prophylactic dose (no serum reactions); antibiotics alone do not replace immunisation.
Worked example: which prophylaxis?

Child, 6 years, fully vaccinated (3 primary doses + booster at 4 years)
Deep puncture wound from a rusty nail in soil
Years since last toxoid = 6 - 4 = 2 → less than 5 years
Action: clean and debride; no toxoid needed (Nelson table); no TIG
Same wound, unvaccinated child → toxoid now + TIG, then complete the course

Exam trap

A tetanus-prone wound in an unimmunised child needs both toxoid and TIG; toxoid alone is too slow to protect.

Prevention

Childhood vaccination

  • Tetanus toxoid in DPT, given in Pakistan's EPI as pentavalent vaccine at 6, 10 and 14 weeks; later boosters with DT or Td as per the current national schedule (Federal Directorate of Immunization, EPI Pakistan, checked 8 Nov 2026).
  • Tetanus is the one vaccine-preventable disease where herd immunity gives no protection: spores are everywhere in soil, so every individual must be vaccinated.

Neonatal tetanus

  • Immunise women: an unimmunised pregnant woman needs two doses of tetanus toxoid (now Td) at least 4 weeks apart, the second at least 3-4 weeks before delivery (Park says 3, Akbar 4); a previously immunised woman needs one booster. Maternal IgG crosses the placenta and protects the baby.
  • Never miss a chance: give at least one dose even if the woman is seen late in pregnancy (Park).
  • Clean delivery: deliveries in health facilities and trained birth attendants.
  • The "three cleans" (Park): clean hands, clean delivery surface, clean cord care (clean blade, clean tie, nothing applied to the stump).
  • Report every case of neonatal tetanus; WHO counts elimination as fewer than 1 case per 1,000 live births in every district (WHO tetanus fact sheet, checked 8 Nov 2026).
High-yield

The two pillars of neonatal tetanus prevention are maternal tetanus toxoid (Td) and clean delivery and cord care.

Exam focus

Expect: C. tetani as an anaerobic spore-forming Gram-positive rod from soil and dung; tetanospasmin travelling up motor nerves and blocking inhibitory neurones; trismus, risus sardonicus, opisthotonos and stimulus-induced spasms with a clear mind; neonatal tetanus from the umbilical stump presenting around day 7 with failure to suck; diagnosis is clinical with normal CSF, calcium and glucose; TIG as the antitoxin of choice, penicillin or metronidazole, diazepam, a quiet room, airway and tube feeding; no immunity after disease; wound prophylaxis by vaccine history and wound type; maternal Td, clean delivery and the three cleans; poor prognosis with short incubation and rapid progression.

Quick revision

  • C. tetani: anaerobic, spore-forming, Gram-positive drumstick rod; soil and dung; not communicable.
  • Tetanospasmin: retrograde axonal transport; blocks inhibitory transmitters; rigidity and spasms; mind clear.
  • Trismus, risus sardonicus, opisthotonos; spasms on stimuli; autonomic instability.
  • Neonatal: home birth, unimmunised mother, dirty cord; day 3-10; stops sucking, then spasms.
  • Investigations normal; diagnosis clinical.
  • TIG 3,000-6,000 units IM (or ATS); clean wound; penicillin 10-14 days or metronidazole.
  • Diazepam, quiet dark room, suction, NG feeds, ventilation when needed; vaccinate after recovery.
  • Prevention: EPI pentavalent, maternal Td, three cleans; wound prophylaxis by doses and wound type.

Written by The House Job from standard references (Basis of Paediatrics by Pervez Akbar; Nelson Essentials of Paediatrics; Park's Preventive and Social Medicine).

FAQ

Why does a child with tetanus stay conscious during spasms?

The toxin acts on inhibitory neurones in the spinal cord and brainstem that control muscle tone; it does not affect the cortex, so consciousness and sensation remain normal and the spasms are painful.

Why must a child who survives tetanus still be vaccinated?

The tiny amount of toxin that causes disease is not enough to stimulate antibody, so there is no lasting immunity after recovery.

Why is human immunoglobulin preferred to horse serum?

Human TIG lasts longer in the body (about 30 days), does not need a sensitivity test and does not cause serum sickness or anaphylaxis to horse protein.

How does vaccinating the mother protect the newborn?

Antitoxin (IgG) made by the mother after tetanus toxoid crosses the placenta, so the baby is born protected during the period when the cord stump can be contaminated.