Pathogenesis and Pathophysiology. Tetanus is caused by a powerful exotoxin, Clostridium tetani, which produces spores. The spores can remain dormant in the soil or in animal excrement for many years until they enter the body and produce a toxin. In patients with tetanus toxicity, both the CNS and the PNS as well as the musculature are involved. y The major CNS effect occurs through disinhibition on gray matter gangliosides and through presynaptic antagonism of GABA. At high concentrations, tetanus toxin acts like botulism toxin in that it inhibits the release of acetylcholine at cholinergic synapses. The nervous system is infected by tetanus through retrograde axonal transport from the site of infection. The incubation period may range from 5 to 25 days but can be only a few hours. Early in the illness, pathological changes include changes in the nerve cells of the cortex and brain stem. If the illness lasts for more than 5 days, demyelination and gliosis may occur, and in the most severe cases, hemorrhages can occur.

Epidemiology and Risk Factors. In Third World countries, tetanus is still an important cause of morbidity and mortality. The bacteria can be transmitted in the anaerobic conditions of wounds, through soil-contaminated injuries, and, less commonly, by unclean needles used by drug abusers. Tetanus is seen only in adults who have not been immunized. About 50 to 100 cases are reported in the United States each year, and 60 percent of those cases occur in adults over the age of 60.

Clinical Features and Associated Findings. The clinical course consists of early symptoms of chills, headache, restlessness, and pain at the site of injury. Tightness in the jaw and mild stiffness and soreness in the neck are usually noticed within a few hours. As symptoms develop, the jaw becomes stiff and tight (lockjaw). Muscular involvement then progresses to the throat and facial muscles. Muscular rigidity may then become generalized and may include the trunk and extremities. Rigidity in the abdominal muscles can result in a forward arching at the back. The tetanic contractions occur periodically and can cause severe pain. In the most severe cases, convulsions and marked dyspnea with cyanosis can occur, terminating in asphyxia and sudden death. Mental status remains intact. However, the patient suffers from anxiety and mental and physical agony.

Differential Diagnosis and Evaluation. A diagnosis of tetanus can be made by a positive history of a prior wound, a high titer of serum antibody to tetanus, a history of partial immunization, and clinical symptoms as just outlined. Tetanus must be differentiated from the stiff-person syndrome and the Moersch-Woltman syndrome. Trismus is not typical of stiff-person syndrome.

Management. Patients should be hospitalized and external stimuli kept to a minimum. The infected wound should be debrided. Muscle relaxation can be initiated by the use of barbiturates or diazepam. Although antiserum does not neutralize the toxins fixed in the nervous system, human tetanus immunoglobulin (TIG) should be given.

One dose of 3000 to 6000 units given intramuscularly into three sites simultaneously is recommended. If human antitoxin is unavailable, equine antiserum can be given. Tetanus is prevented by immunization. Children should be immunized at 2 months to 6 years of age. In adults, tetanus boosters last approximately 10 years.

Prognosis and Future Perspectives. The prognosis is poor. The fatality rate is approximately 65 percent. Death generally occurs rapidly between the third and fifth day of illness and is due to exhaustion, medullary failure, asphyxia resulting from spasm, or circulatory failure resulting from exertion on the heart. Occasionally, tetanus antitoxin produces an adverse reaction involving primarily the PNS. After 6 months, recovery is usually complete.

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