Tetanus: Debilitating Infection

PATIENT PRESENTATION AND TETANUS TYPES

The CDC describes tetanus as “the acute onset of hypertonia and/or painful muscle contractions (usually of the muscles of the jaw and neck) and generalized muscle spasms without other apparent medical cause.”¹⁵ Clinicians should always consider tetanus in patients with dysphagia and trismus, especially if the patient has a wound, had not received primary vaccination, or has not had a booster in several decades. Tetanus cannot be ruled out based on the lack of a wound, however, since up to 25% of patients who develop tetanus have no obvious site of inoculation.¹⁶ The incubation period ranges from 3 to 21 days, with more severe cases having shorter incubation periods (< 8 days).¹⁰ The closer the site of inoculation is to the CNS, the more serious the disease usually is—and the shorter the incubation period will be.¹

Presentation depends on the time elapsed since inoculation, the severity of illness (determined by the Ablett classification; see Table 1), and the form of tetanus involved. The patient may present early when the infection and toxin are localized to the wound and have not progressed to the CNS (localized tetanus). There may be a wound with signs of infection, including erythema, induration, edema, warmth, tenderness, and drainage. If the injury is on the head or neck, cephalic tetanus may occur, causing the patient to present with painful spasms of the extra-ocular, facial, and/or neck muscles; trismus; dysphagia; or even a Horner-like syndrome. The patient with more advanced, generalized tetanus may have decorticate posturing, abdominal wall rigidity, or opisthotonus.^1,2,5,17

Four types of tetanus have been described: generalized, localized, cephalic, and neonatal.

Generalized tetanus is the most common form, accounting for approximately 80% of cases.¹⁰ It may involve contractions of the masseter muscles, producing trismus; facial muscles, producing risus sardonicus (sardonic smile); neck and shoulder muscles; abdominal wall muscles, mimicking guarding; and back muscles, producing opisthotonus (arching of the back, neck, and head; see Figure 1) and decorticate posturing (flexion and adduction of the arms, clenched fists, and extension of the lower extremities).^1,5,6 Patients with generalized tetanus often exhibit hyperresponsiveness to the environment. As a result, noises and sudden light changes may result in acute spasms. In addition, patients may experience painful spasms when affected muscles are palpated. Affected reflex arcs are usually hyperresponsive to stimuli.¹ Intermittent spasms of the thoracic, pharyngeal, and/or laryngeal muscles may cause periods of apnea. Autonomic effects of tetanus mimic those associated with the catecholamine excess of pheochromocytoma. Patients exhibit restlessness, irritability, diaphoresis, fever, excessive salivation, gastric stasis, hypertension, tachycardia, and arrhythmia. There may be interposed hypotension and bradycardia.^1,5,17

Localized tetanus involves painful spastic contraction of muscles at or near the site of inoculation. It often evolves into generalized tetanus as the toxin spreads further into the CNS.

Cephalic tetanus involves facial and laryngeal muscles. It is rare, accounting for 1% to 3% of tetanus cases.⁶ Patients may initially have flaccid paralysis, mimicking stroke, rather than spasm, because the toxin has not completely migrated up the peripheral nerve into the CNS. As the toxin enters the CNS and induces the typical spasm (trismus), the diagnosis will be more obvious. The presence of trismus or a subacute wound on the head may be used to discriminate tetanus from stroke. Cephalic tetanus often evolves into generalized tetanus, affecting more of the body in a caudal direction.⁵

Neonatal tetanus develops within one week after birth. The neonate with tetanus is usually born to a mother lacking immunization. Typically, the infant sucks and feeds for the first couple of days, then develops inability/refusal to suck/feed, has difficulty opening his/her mouth, becomes weak, and develops muscle spasms.³ The affected child may develop risus sardonicus, clenched hands, dorsiflexion of the feet, and opisthotonus.³

DIFFERENTIAL DIAGNOSIS

The clinician should consider other CNS conditions in the differential diagnosis (see Table 2). Although similar to generalized seizures, tetanus causes painful spasms and does not produce a loss of consciousness.^1,17 Tetanus, intracranial bleed, and meningitis all can cause meningismus; meningitis, however, is more likely to manifest with other symptoms of infection, such as headache and fever. Although the autonomic dysfunction of tetanus can cause pyrexia, fever would usually coincide with other sympathetic symptoms, such as hypertension, tachycardia, and diaphoresis. Intracranial bleeding tends to have a more rapid onset than tetanus and produces headache and mental status changes. Seventh nerve palsy produces muscle flaccidity, not spasm, and is usually painless unless associated with herpetic inflam­mation.^1,5,6,14,17

Poisoning and medication effects should also be considered. Strychnine poisoning manifests similar to tetanus but occurs without a wound.⁵ Blood and urine assays for strychnine can be diagnostic. Dystonic reactions resulting from neuroleptic medications—such as phenothiazines—include torticollis, oropharyngeal muscle spasms, and deviation of the eyes. Unlike tetanus, drug-induced dystonia does not cause reflex spasms and often resolves with benztropine or diphenhydramine administration.¹ Neuroleptic malignant syndrome can also cause muscular rigidity and autonomic instability, but unlike tetanus, it often causes altered mental status; it should be considered in patients who recently received a causative medication.^5,17

Tetanus often manifests with reflexive muscle spasms similar to those seen in electrolyte and acid-base abnormalities. Hypocalcemia may produce a reflexive spasm of the facial muscles when the facial nerve is percussed (Chvostek sign), while alkalemia may produce reflexive spasm of the hand and wrist muscles (Trousseau sign).¹ Lab tests can rule out these diagnoses.^1,5

A patient with an odontogenic abscess may have pain and muscle spasm/trismus, but the infection is usually easily detected on exam. The clinician should be cautious in attributing the trismus solely to the swelling, however, as C tetani has been found in odontogenic abscesses and the patient may have both.^1,17 Peritonsillar abscess will often produce trismus. When abscess is the cause, careful examination of the oropharynx will usually demonstrate tonsillar exudate, hypertrophy, soft tissue erythema, and tenderness, as well as a misplaced uvula.¹