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Tetanus

Overview

Tetanus is a toxin-mediated disease characterized by severe, uncontrolled skeletal muscle spasms. It is caused by Clostridium tetani, an organism whose powerful neurotoxin disrupts inhibitory neurotransmission throughout the nervous system.

Microbiology & Pathophysiology

The organism:
  • C. tetani is a motile, non-encapsulated, obligate anaerobic, gram-positive spore-forming rod
  • Spores are ubiquitous in soil, animal feces, and contaminated surfaces — they survive for years
  • It is non-invasive; disease requires tissue conditions that reduce oxygen tension (devitalized tissue, foreign bodies, infection) to allow spore germination into the toxin-producing vegetative form
Two exotoxins are produced:
  1. Tetanolysin — facilitates bacterial growth
  2. Tetanospasmin — the powerful neurotoxin responsible for all clinical manifestations
Mechanism of tetanospasmin:
  • Produced at the wound site → binds motor nerve endings → travels by retrograde axonal transport to the CNS
  • Does not cross the blood-brain barrier directly
  • In the CNS, it blocks presynaptic release of inhibitory neurotransmitters — primarily glycine and GABA — at inhibitory interneurons afferent to alpha motor neurons
  • Result: loss of inhibitory control → sustained excitatory discharge → characteristic muscle spasms
  • May also affect preganglionic sympathetic neurons and parasympathetic centers → autonomic dysfunction
  • Binding is irreversible; recovery requires regrowth of new axonal terminals

Epidemiology

  • Worldwide: ~100,000 cases/year; mortality 35–40%
  • In the US: >95% decline since 1947 due to vaccination; ~197 cases reported 2009–2015 with 16 deaths
  • Highest incidence: adults >65 years (immunity waning); up to 50% of US cases in injection drug users
  • Case fatality rate: ~8–18% overall; approaches 50% in patients >70 years
  • Neonatal tetanus: ~34,000 deaths/year globally (WHO) from unsterile umbilical stump practices
  • Risk factors: inadequate primary immunization, waning immunity (only 31% of Americans >70 have adequate immunity), injection drug use, diabetes, deep puncture wounds

Portals of Entry

  • Puncture wounds, lacerations, abrasions (most common, >70% of cases)
  • Chronic skin ulcers, abscesses
  • Otitis media, dental procedures
  • Childbirth (umbilical stump in neonates)
  • Surgical procedures (intestinal, abortion)
  • No apparent wound in ~10–30% of patients

Clinical Forms

1. Generalized Tetanus (~80% of cases)

  • Most common and most severe form
  • Trismus ("lockjaw") — masseter spasm — classic presenting symptom (50–75% of patients)
  • Risus sardonicus — characteristic sardonic smile from facial muscle involvement
  • Progression: facial muscles → neck → trunk → extremities (descending pattern)
  • Reflex spasms and tonic contractions cause: dysphagia, opisthotonos (decorticate-like posturing), clenched fists, extended lower extremities
  • Spasms can cause vertebral/long bone fractures and tendon rupture
  • Laryngospasm and respiratory muscle spasm → ventilatory failure → death
  • Autonomic dysfunction (typically 2nd week): tachycardia, labile hypertension, hyperpyrexia, cardiac dysrhythmias, profuse sweating, elevated catecholamines — the major cause of death in patients surviving the acute phase
  • Mental status is normal throughout (key diagnostic point) unless respiratory compromise develops
  • Illness progresses over ~2 weeks; recovery takes ≥4 weeks

2. Localized Tetanus

  • Persistent spasm confined to muscles near the wound site
  • Usually resolves over weeks–months; may progress to generalized form
  • ~1% fatality

3. Cephalic Tetanus

  • Follows head/neck injury or otitis media
  • Cranial nerve dysfunction — most commonly CN VII
  • Poor prognosis; may precede generalized form

4. Neonatal Tetanus

  • A form of generalized tetanus in infants born to inadequately immunized mothers
  • Infection through umbilical stump
  • Presents in 2nd week of life: weakness, irritability, inability to suck
  • High mortality

Diagnosis

Tetanus is a purely clinical diagnosis — no confirmatory lab test exists.
  • Wound cultures: positive in only 1/3 of cases; not reliable
  • Serum calcium: rule out hypocalcemia
  • CT brain: exclude intracranial disease
  • LP: to exclude meningitis (especially in neonates)
  • EMG: may help in cephalic or localized tetanus
The Spatula Test (bedside):
  • Touch the posterior pharynx with a tongue blade
  • Positive (tetanus): reflex masseter spasm → patient bites the spatula
  • Negative (no tetanus): gag reflex, expels blade
  • Sensitivity 94%, specificity 100%

Differential Diagnosis

ConditionDistinguishing Feature
Strychnine poisoningMost similar mimic; also blocks glycine but not GABA; check serum/urine levels
Dystonic reactionMedication history; relieved by benztropine or diphenhydramine
Hypocalcemic tetanyLow serum calcium
RabiesBrainstem dysfunction, hydrophobia, animal exposure; no trismus
Stiff-person syndromeCentrally mediated; proximal lower limbs/lumbar muscles
Meningitis/EncephalitisAltered mental status; CSF abnormalities
Peritonsillar abscessIntra-oral infection on exam
Malignant neuroleptic syndrome / Serotonin syndromeMedication history

Management

Four strategies undertaken simultaneously:

1. Supportive Care — Control Muscle Spasms

  • Minimize sensory stimuli: quiet, darkened room (light/noise trigger spasms)
  • Benzodiazepines (diazepam, midazolam): first-line for spasm control — enhance GABA activity
  • Intrathecal baclofen: GABA-B agonist; effective for refractory spasms
  • Neuromuscular blocking agents (vecuronium, pancuronium) + mechanical ventilation: for severe, uncontrolled spasms
  • Magnesium sulfate: attenuates autonomic instability (reduces catecholamine release)
  • Autonomic dysfunction: morphine, labetalol, clonidine, or magnesium to blunt swings
  • Tracheostomy often required for prolonged mechanical ventilation

2. Eliminate Unbound Toxin

  • Human Tetanus Immunoglobulin (HTIG) — neutralizes circulating tetanospasmin before it enters neurons
    • 500 units IM (some sources recommend 3,000–6,000 units)
    • Infiltrate around wound if possible
    • Does not reverse toxin already bound to nerve tissue

3. Prevent Further Toxin Production

  • Wound debridement — remove devitalized tissue and foreign bodies
  • Metronidazole (drug of choice): 500 mg IV/PO q6h × 7–10 days (kills vegetative C. tetani)
    • Pediatric dosing varies by weight/age
  • Penicillin G: alternative (historically used but a GABA antagonist — metronidazole preferred)

4. Active Immunization

  • Tetanus toxoid must be given — clinical tetanus does not confer immunity (toxin levels too low to stimulate immune response)
  • Administer at a different site from HTIG

Prophylaxis (Wound Management)

Immunization HistoryClean Minor WoundTetanus-Prone Wound*
<3 doses or unknownTdap/Td + HTIGTdap/Td + HTIG
≥3 doses, last dose <5 yearsNothingNothing
≥3 doses, last dose 5–10 yearsNothingTdap/Td
≥3 doses, last dose >10 yearsTdap/TdTdap/Td
*Tetanus-prone wounds: >6 hours old, >1 cm deep, contaminated with soil/feces, puncture/crush injuries, devitalized tissue, burns, frostbite
  • HTIG dose: 250 units IM (separate injection site from toxoid)
  • Children <7 years: DTaP (or DT if pertussis contraindicated)
  • ≥7 years and adults: Tdap preferred (one lifetime dose); subsequent boosters with Td every 10 years
Vaccination:
  • 3-dose primary series → immunity in nearly 100%
  • Immunity wanes 5–10 years after series
  • Tdap single booster replaces one Td dose for adolescents/adults
  • Not contraindicated in pregnancy

Complications

  • Respiratory failure (laryngospasm, respiratory muscle spasm)
  • Aspiration pneumonia (50–70% of autopsy cases)
  • Rhabdomyolysis
  • Long-bone and vertebral fractures (from violent contractions)
  • Cardiac dysrhythmias
  • Death (primarily from autonomic instability in survivors of the acute phase)

Prognosis

  • Shorter incubation period → worse prognosis
  • Age >70: case fatality ~50%
  • Recovery depends on regrowth of axonal nerve terminals (weeks to months)
  • Fully vaccinated patients: no reported deaths

Sources: Rosen's Emergency Medicine, 9e — Ch. 118; Tintinalli's Emergency Medicine, 9e — Ch. 157
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