Tetanus

Tetanus toxin produces spasticity by blocking the release of the inhibitory neurotransmitters, glycine and glutamic acid decarboxylase (GAD), from presynaptic nerve terminals that synapse on alpha motor neurons in the spinal cord and brainstem. With the loss of inhibitory input, the uninhibited lower motor neuron increases resting muscle tone, producing rigidity. Tetanus is divided into four clinical forms: localized, generalized, cephalic, and neonatal. The incubation period is defined as the time from inoculation with C. tetani spores to the appearance of the first symptom. The incubation period is followed by the period of onset of tetanus, which is defined as the interval from the first symptom to the first reflex spasm. Localized tetanus is limited to the extremity in which there is a contaminated wound, blister, or burn. The patient’s initial complaint is stiffness of the muscles in the extremity with voluntary movement. This is followed by the development of a continuous spasm or rigidity in the group of muscles in close proximity to the wound. Local tetanus may remain restricted to the limb or may become generalized. In generalized tetanus, the usual manifesting sign is trismus (lockjaw), which is a rigidity of the masseter muscles, causing an inability to open the mouth to speak or to chew. Another early sign is risus sardonicus due to increased tone in the orbicularis oris, causing a sneering grin. The generalized spasm consists of opisthotonic posturing with flexion and adduction of the arms, clenching of the fists, and extension of the lower extremities. The spasms are often precipitated by external stimuli and are extremely painful. Sudden spasms of the muscles of respiration may stop respiration for 10 to 20 seconds, and laryngeal or pharyngeal spasms may obstruct the airway, compromising respiration. Cephalic tetanus involves the muscles supplied by one or more cranial nerves and almost always follows a head wound. The facial nerve is affected most often. Neonatal tetanus typically develops as a result of infection of the umbilical stump, and the usual manifesting symptom is poor feeding. The infant cannot suck, and when a finger is put into its mouth its jaw clamps tightly. This is followed by involvement of the muscles of facial expression, risus sardonicus, and then opisthotonos.

Tetanus is a clinical diagnosis. When tetanus is suspected, a careful immunization history should be obtained because tetanus is unlikely if the patient has received a complete primary series of toxoid injections with booster doses every 10 years. Diagnosis is dependent on ruling out the diseases that have an appearance similar to tetanus, including strychnine poisoning, a dystonic reaction secondary to a neuroleptic agent or a dopamine-blocking agent, and rabies. Dystonic reactions are quickly reversed with intravenous benztropine or diphenhydramine.

There are three goals of treatment in tetanus: (1) securing the airway and treating generalized spasms with benzodiazepines, (2) stopping production of the toxin by surgical debridement of the wound and antimicrobial therapy (the most frequently recommended antibiotic is metronidazole), and (3) passive immunization with human tetanus immunoglobulin (HTIG).

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