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Clinical Characteristics

The clinical picture of tetanus is entirely due to the action of the toxin on the central nervous system and not on the peripheral nerves or muscles: the toxin spreads along the nerves or via the blood and abolishes synaptic inhibition. Because reciprocal inhibition is lost, the result is muscle rigidity and spasm, with agonists and antagonists contracting simultaneously. The characteristic signs of the disease, therefore, are rigidity and reflex spasms, and rigidity is usually the first to appear. This may be first seen in the facial muscles, altering the expression considerably to produce a sneer when the patient attempts to smile (trismus, risus sardonicus, or lockjaw). Neck stiffness, abdominal rigidity, and back stiffness all occur and may give rise to opisthotonos. It is often difficult to obtain an adequate history because the patient may be unable to respond. This is certainly in part due to the stiffness of the facial muscles, but probably also to some alteration in consciousness (fortunately many patients who recover have poor memories of their illness).

There are two main patterns of infection: local tetanus and generalized disease. Local tetanus occurs when the rigidity affects a limb or only the head and neck. One variety has been called "cephalic tetanus;' which has a rapid, 3-day onset and affects the cranial nerves. With otitis media, there is often seventh cranial nerve palsy, and there is a high, 15%-30%, mortality. This local reaction probably results from spread of the toxin along the specific nerves rather than through the blood vessels and lymphatics. Tetanus may commence locally and then spread and become generalized, which has a poor prognosis. The use of passive immunization after injury may also permit local tetanus, because the blood-borne toxins are neutralized and only the nerve-borne toxins remain unaffected. This is sometimes known as "modified tetanus." There is considerable variation in the prognosis depending upon the rapidity with which the disease progresses from the first symptom to the establishment of frequent and severe reflex spasms. This "march" of the disease is important in the clinical assessment of the patient. Tetanus has been classified as mild if there are no spasms seen or initiated on admission, moderate when spasms are precipitated by a disturbance or clinical examination, and severe when spasms occur spontaneously.

There are few systemic symptoms, although restlessness, irritability, and headache have been described. In particular, it is important to note that there are no local complaints related to the site of entry of the infection and toxin, because the wound is often a trivial one. In some cases, no wound or injury can be detected. (In one series, 21% of patients showed no evidence of the source of infection.)

If spasms occur rapidly, the prognosis is worse. Spasms usually occur within 48 hours of the onset of muscle stiffness, and then occur with increasing frequency and without apparent stimulus. Because of difficulty in swallowing, babies cannot suckle and at all ages breathing and pulmonary secretions are a major problem and aspiration may result in pulmonary atelectasis. If the spasms are severe, cyanosis may become obvious and respiration may stop. During this time, the patient can remain conscious, and the disease is a painful and traumatic experience.

The major complications are respiratory, including pulmonary emboli, but myocardial damage has occurred: arrhythmia or persistent tachycardia is a significant finding. There is a very considerable fluctuation in the blood pressure and, when the infection is severe, hypotension and circulatory collapse occur. These are probably due to a gram-negative secondary infection rather than to a direct action of the toxin.

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Copyright: Palmer and Reeder