INFECTIOUS DISEASE■ Puncture wounds
■ Wounds with crushed/devitalized tissue
■ Inadequate immunization
■ Produces tetanospasmin
■ Neurotoxin blocks inhibitory nerves
■ Causes overstimulation of
■ Skeletal muscle motor endplates
■ Autonomic nervous system
■ CNS
SYMPTOMS/EXAM
■ Traumatic injury (~30% do not report a specific event)
■ Incubation period: 1 day to >1 month (shorter =more severe)
■ Types:
■ Generalized (#1)
■ Trismus due to masseter spasm (“lockjaw”)
■ Muscle rigidity/spasms
■ Shortest nerves affected first
■ Progresses from head to feet
■ Hydrophobia/drooling
■ Leads to
■ Respiratory failure
■ Autonomic instability
■ Starts in second week
■ Generally hypersympathetic (ie, tachycardia, HTN, diaphoresis)
■ Localized
■ Persistent muscle spasms near site of injury
■ Spontaneously resolves in weeks to months
■ Normally no permanent sequelae
■ Cephalic
■ After head wound or otitis media
■ Cranial nerve dysfunction (most common =CN VII)
■ Neonatal
■ Inadequately immunized mother
■ Unsterile handling of umbilical stump
■ Irritability and poor feeding in first week of life
■ Close to 100% case fatality rate
DIFFERENTIAL
Strychnine poisoning, dystonic reaction, hypocalcemia, encephalitis, menin-
gitis, rabies
DIAGNOSIS
Clinical
TREATMENT
Symptomatic:
■ Aggressive supportive care
■ Benzodiazepines are mainstay for muscle relaxation.
■ Magnesium sulfate will improve spasm control.
■ Labetalol indicated for sympathetic hyperactivity.
■ Avoid isolated β-blockade.
A significant portion of
patients with tetanus do not
report specific trauma.Strychnine acts by blocking an
inhibitory glycine receptor,
rapidly causes convulsions
and death, and is treated with
benzos and dantrolene.