178 Tetanus
Key Points• Puncture wounds pose the highest risk for tetanus. Tetanus also occurs following clean, minor wounds, abscesses, and cellulitis.
• Keep current the tetanus immunization status of patients with any injury, even minor, clean wounds.
• Give tetanus immune globulin to patients with wounds, other than clean, simple wounds, who have never completed a primary tetanus immunization series.
• Tetanus is a clinical diagnosis. Begin treatment when the diagnosis is suspected in any patient with unexplained rigidity.
• Tetanus treatment consists of tetanus immune globulin, antibiotics, and local wound care.
Epidemiology
Tetanus is a rare disease in the United States, with only 20 cases reported in 2003. In 1990 to 2000, the average number of cases in the United States was 50 per year. The average annual incidence from 1995 to 2000 was approximately 0.16 cases per million population.1,2 Tetanus is more common among people 60 years old or older (0.35 cases per million population), patients 60 years old or older who have diabetes (0.70 cases per million population), and Hispanic persons (0.37 cases per million population). Injecting drug users are at unique risk for tetanus and accounted for 15% of cases of tetanus from 1998 to 2000.1 Most (74%) injecting drug users who developed tetanus reported injecting heroin, and 100% reported “skin popping” rather than intravenous injection.3
Tetanus morbidity and mortality remain high, even with appropriate treatment. Current vaccination status decreases the severity of the disease and the likelihood of death from tetanus. In 1998 to 2000, 18% of patients with tetanus died. Of fatal cases, 75% occurred in patients who were 60 years old or older. No patients with an up-to-date vaccination status died of tetanus.1
Perspective
In addition to recognizing the clinical presentation of tetanus, EPs play a vital role in the prevention of the disease. Primary pediatric vaccination and regular decennial booster vaccination are the mainstays of disease prevention and severity modulation.4 Herd immunity does not occur with tetanus. Therefore, only people who receive the vaccination benefit from immunization. In the United States, the prevalence of tetanus immunity decreases by age, after 40 years of age. At 40 years of age, 80% of the population is immune to tetanus. By the age of 80 years, only 30% of the population remains immune. This decrease is most striking in women and Mexican Americans.5 Only 36% of persons age 65 years old or older report receiving tetanus vaccination in the past 10 years.6,7 Most cases of tetanus and fatalities resulting from tetanus are in patients who either have never been vaccinated or have not had a booster in the past 10 years.8 EPs have the opportunity to provide booster vaccination at times of minor to severe injury and skin infection. In light of pertussis epidemics, providers should also consider a patient’s pertussis immunization status when choosing the tetanus vaccine.
From Centers for Disease Control, September 2005. Available at http://www.cdc.gov/mmwr/preview/mmwrhtml/00041645.htm
Facts and Formulas
Tetanus Booster Based on Age
| Infant to 7 years | DTap (diphtheria, tetanus, acellular pertussis) |
| DT (pediatric diphtheria, tetanus preparation), if pertussis is contraindicated | |
| Age 7 to 10 years | dT |
| Tdap, if not previously given once in primary series | |
| Age 11 to 18 years | Tdap (tetanus, diphtheria, acellular pertussis) preferred |
| Td (tetanus, diphtheria) acceptable | |
| Adult | Td |
| In people aged 11 to 64 years, if primary series not completed, can substitute Tdap for one Td; substitution should be done in people aged 11 to 18 years who have not completed a primary series |
Anatomy
Most cases of tetanus are associated with acute trauma (Table 178.1), but many cases are associated with abscesses, cellulitis, chronic ulcers, dental infections, frostbite, and gangrene. In one study of injecting drug users with tetanus, 69% had an abscess at the injection site.3 Tetanus affects postpartum women, with an increased risk after unsanitary birth or abortion practices.1
| MOST THREATENING | MOST COMMON | |
|---|---|---|
| Location of injury | Face | Lower extremity Upper extremity Head and trunk |
| Type of injury | Puncture wound Crush injury Burn Chronic ulcer |
Puncture wound Laceration Chronic wound Abrasion |
| Patients | Diabetic patients Age > 60 yr Neonates No prior tetanus immunization |
Intravenous drug users Age > 60 yr Hispanic ethnicity Diabetic patients No prior tetanus immunization Last immunization >10 yr ago |
Puncture wounds are the most frequent type of acute trauma associated with tetanus. Puncture wounds include nail injuries to the foot, splinters, barbed wire injuries, tattoos, drug injection, penetrating eye injuries, and spider bites. Crush injuries, burns, and eye injuries are also portals of tetanus infection. In patients with tetanus, approximately 50% of injuries are located on the lower extremity, 36% on the upper extremity, 10% on the head or trunk, and 5% on other areas.1
The occurrence of tetanus following minor or trivial wounds is well documented in the literature. Tetanus results from minor wounds and abrasions when proper wound care is not administered.2,9–12 Nearly half of the wounds that resulted in tetanus in 1998 to 2000 occurred indoors.1
Red FlagsC. tetani enters the body through a wound and produces two exotoxins: tetanolysin and tetanospasmin. Tetanolysin causes local cell death and creates an anaerobic environment in the wound site.13 Tetanospasmin interferes with the transmission of inhibitory impulses in the central nervous system. It creates a presynaptic blockage of the inhibitory Renshaw cells and Ia fibers of alpha motoneurons that transmit gamma-aminobutyric acid (GABA) and glycine. Renshaw cells that transmit acetylcholine are not affected as strongly. Tetanospasmin binding prevents inhibitory signals in the central nervous system.
Tetanus becomes a systemic disease as the toxin spreads through the body. Tetanospasmin binds to nerve terminals, is internalized, and travels in retrograde fashion to the cell synapse. The toxin travels at 75 to 250 mm/day, and it affects synapses of shorter nerves before synapses of longer nerves.14 The toxin also travels by lymphatic and blood flow to remote nerves. The toxin exhibits local effects first and then spinal motor effects. The autonomic system is the last to be affected because of the length of the nerves. Tetanospasmin also inhibits acetylcholine release, a process that leads to flaccid paralysis between episodes of spasticity.15
The result of the general loss of inhibitory signals is rigidity with periods of spasticity. The reflex inhibition of antagonizing muscles is lost, thus allowing agonist and antagonist muscle groups to contract simultaneously. Autonomic disinhibition occurs late in the disease. Toxin binding appears to be irreversible; the growth of new nerve terminals is required to overcome the effects.16
Clinical Presentation
The average incubation period from time of injury to the onset of symptoms is 7 to 10 days, with a range of 1 to 60 days. Shorter incubation times are associated with more severe clinical presentation and a poor prognosis.8,16 Tetanus is usually an afebrile disease until autonomic instability occurs late in the disease. Fever suggests coinfection of the wound or other infectious causes. Generalized tetanus, or tetanus affecting the whole body, is the most common form of tetanus.
Before modern mechanical ventilation, death resulted from respiratory failure or aspiration.17 With modern mechanical ventilation, death is more commonly caused by autonomic events.18,19
