Tetanus is a rare disease in the United States, with only about 40–50 cases reported each year. Tetanus is caused by an exotoxin produced by Clostridium tetani, an anaerobic, spore-forming, gram-positive rod found widely in soil and in the GI tract. Tetanus typically is seen in older persons (especially older women), recent immigrants, and IV drug users who have not maintained adequate tetanus immunization.
Mechanism of toxicity. The growth of C tetani in a wound under anaerobic conditions produces the toxin tetanospasmin. The toxin enters the myoneural junction of alpha motor neurons and travels by retrograde axonal transport to the synapse. There, it blocks the release of the presynaptic inhibitory neurotransmitters gamma-aminobutyric acid (GABA) and glycine, causing intense muscular spasms.
Toxic dose. Tetanospasmin is an extremely potent toxin. Fatal tetanus can result from a minor puncture wound in a susceptible individual.
Clinical presentation. The incubation period between the initial wound and the development of symptoms averages 1–2 weeks (range, 2–56 days). The wound is not apparent in about 5% of cases. Wound cultures are positive for C tetani only about one-third of the time.
The most common initial complaint is pain and stiffness of the jaw, progressing to trismus, risus sardonicus (“sardonic grin”), and opisthotonus over several days. Uncontrollable and painful reflex spasms involving all muscle groups are precipitated by minimal stimuli and can result in fractures, rhabdomyolysis, hyperpyrexia, and asphyxia. The patient remains awake during the spasms. In survivors, the spasms may persist for days or weeks.
A syndrome of sympathetic hyperactivity often accompanies the muscular manifestations, with hypertension, tachycardia, arrhythmias, and diaphoresis that in some reports alternate with hypotension and bradycardia.
Neonatal tetanus occurs frequently in developing countries as a result of inadequate maternal immunity and poor hygiene, especially around the necrotic umbilical stump. Localized tetanus has been reported, involving rigidity and spasm only in the affected limb. Cephalic tetanus is uncommonly associated with head wounds and involves primarily the cranial nerves.
Diagnosis is based on the finding of characteristic muscle spasms in an awake person with a wound and an inadequate immunization history. Strychnine poisoning (See Strychnine) produces identical muscle spasms and should be considered in the differential diagnosis. Other considerations include hypocalcemia and dystonic reactions.
Specific levels. There are no specific toxin assays. A serum antibody level of 0.01 IU/mL or greater suggests prior immunity and makes the diagnosis less likely.
Other useful laboratory studies include electrolytes, glucose, calcium, BUN, creatinine, creatine kinase (CK), arterial blood gases, and urine dipstick for occult blood (positive with myoglobinuria).
Emergency and supportive measures
Maintain an open airway and assist ventilation if necessary (See Airway and Breathing).
Treat hyperthermia (See Hyperthermia), arrhythmias (See QRS interval prolongation, Tachycardia, and Ventricular dysrhythmias), metabolic acidosis (See Anion gap metabolic acidosis), and rhabdomyolysis (See Rhabdomyolysis) if they occur.
Limit external stimuli such as noise, light, and touch.
Treat muscle spasms aggressively.
(See Benzodiazepines (Diazepam, Lorazepam, and Midazolam...