Tetanus

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178 Tetanus

Lisa D. Mills

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

Although clinical cases are rare, emergency physicians (EPs) often are the first, and sometimes only, point of contact for patients. As a result, physicians must maintain an awareness of the clinical presentation of the disease. The diagnosis can be suspected but not confirmed in the emergency department (ED).

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

Table 178.1 Tetanus Wound Characteristics and Risks

	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

Pathophysiology

Clinical tetanus is caused by two exotoxins produced by Clostridium tetani, a gram-positive, anaerobic rod. The bacterium produces spores that are heat resistant, surviving autoclaving at 250° F for 10 to 15 minutes, and resistant to treatment with phenols and common chemical agents. The bacterium dies with heat or oxygen exposure. The bacterium and spores are widely disseminated in soil, intestines of farm animals and pets, and feces. Spores exist on human skin and contaminated heroin. In anaerobic conditions, such as puncture wounds and crush injuries, spores germinate.

Red Flags

Wounds at Increased Risk of Tetanus
Puncture wounds Crush injuries Partial-thickness or full-thickness burns Chronic ulcers Wounds contaminated with soil, feces, saliva Avascular or gangrenous wounds Frostbite Penetrating eye injuries Avulsions

Wounds at Low Risk of Tetanus

Minor abrasions

Clean, minor wounds

C. 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.

In the first week of illness, the patient presents with rigidity and muscle spasms. Tetanus most commonly affects the cranial nerves first. The most common first symptoms and signs are trismus, neck stiffness, and dysphagia. Muscle spasm progresses diffusely to involve the facial muscles, thus causing the classic facial grimace risus sardonicus. Disinhibition of the neck muscles causes neck extension. Truncal rigidity follows head and neck involvement.

The general increased tone is interrupted by acute spastic events that can involve any muscle groups. These spastic events can be spontaneous or caused by tactile, visual, or auditory stimuli. Agonist and antagonist muscle groups can simultaneously contract. The contractions are painful and can be strong enough to break long bones and avulse tendons. Opisthotonos is a classic spastic event in tetanus. Abdominal rigidity can mimic an acute abdomen. Spasticity of the trunk and diaphragm can interfere with respiration. Laryngeal spasm interferes with the gag reflex or can occlude the airway.

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

The second week of illness involves autonomic instability in addition to the muscle spasms. The sympathetic nervous system is more strongly affected. Sudden increased autonomic tone, with elevated circulating catecholamine levels, increased vascular tone, hypertension, and tachycardia alternate with profound hypotension, bradycardia, and even cardiac arrest. Cardiac dysrhythmias occur, and the patient may develop hyperpyrexia at this point.²⁰^–²³

Recovery begins in the third or fourth week. Muscle spasms decrease, but rigidity may persist. The duration of recovery, in those who survive, ranges from 2 to 4 months, as new axon terminals grow. Most patients return to their baseline with no residual deficit.⁸

Variations

Local tetanus is an uncommon presentation of the disease in which only focal symptoms occur. Muscle spasticity is limited to the area adjacent to the wound. Local tetanus can progress to generalized tetanus, and the disease is generally milder. The exception is in cases of cephalic tetanus.

Cephalic tetanus is another rare form of disease. Cephalic tetanus follows a head or facial wound or, rarely, otitis media. The cranial nerves are initially affected. Spasticity or flaccid paralysis may be the presentation. Cephalic tetanus generally progresses rapidly to generalized tetanus and is associated with a severe course.²⁴

Neonatal tetanus is generalized tetanus of the neonate. It occurs in infants born to mothers who are inadequately immunized. The port of entry is usually the umbilicus, with increased risk if the umbilicus is cut with a nonsterile instrument or is packed with contaminated material, such as soil, dung, or clay. Symptoms manifest on day 3 to 9 of life.²⁵

The initial presentation is failure to feed in a child who previously fed normally. Neonatal tetanus progresses to generalized tetanus as described previously. The mortality rate of neonatal tetanus, when treated, is 25% to 90%.²⁶ Thirteen cases of neonatal tetanus were diagnosed in the United States from 1992 to 2000. In these cases, 85% of the neonates had not been vaccinated because of parental religious or philosophic objections.²⁷

Because tetanus is a rare disease in the United States, it is difficult to suspect and diagnose (Box 178.1). Tetanus should be considered in the differential diagnosis of patients with rigidity or spasticity. The disease can be found in the setting of a minor or trivial injury that may not be remembered by the patient or family.^2,⁹^–¹¹ Tetanus is more common in patients without vaccination or without booster in the last 10 years. Unusually, from 1998 to 2000, 6% of tetanus cases occurred in patients who reported being up to date on tetanus vaccination.¹

Older patients and patients with chronic illness may have a decreased immune response to vaccination and therefore may lack protective antibody levels to tetanus in spite of appropriate vaccination. This situation is increasingly true in patients aged 65 years or older.^28,²⁹

Diagnostic Testing

The diagnosis of tetanus is clinical. The Vaccine-Preventable Diseases Surveillance Manual defines tetanus as “the acute onset of hypertonia or by painful muscular contraction (usually, initially of the jaw and neck) and generalized muscle spasms without other apparent medical cause.”²⁷ No laboratory tests confirm or refute the diagnosis of tetanus. The organism is rarely recovered from wounds and can be cultured from patients without clinical tetanus. Serologic testing to detect anti-etanus antibody levels plays a small role in the diagnosis of the disease. Patients can develop tetanus with “protective” levels of antibody.²⁷ The aim of testing is to rule out other causes of rigidity and spasticity. If tetanus is suspected, begin treatment immediately. Do not delay treatment, because no confirmatory test exists.

Documentation

History

Document the history of onset of symptoms and symptom progression and the history of trauma, even minor, healed wounds, including the location of the wound. Involve witnesses, especially if the patient is having difficulty with speech or breathing. Obtain an immunization history in as much detail as possible. Ascertain allergies or reactions to medications and immunizations.

Physical Examination

Conduct a detailed neurologic examination. Evaluate the cranial nerves with motor function. Test for inducible spasticity (spatula test or other stimuli). Assess for compromise of respiration, ventilation, or airway protective reflexes.

Studies

Document review of any studies, even if results are normal. Exclusion of other disease is an important aspect of the diagnosis of tetanus.

Medical Decision Making

Document reasoning for excluding other, more common diagnoses or the reason for continued consideration of multiple diagnoses while concurrently treating the patient. Note findings in favor of tetanus.

Document the choice of medications for spasticity, including those for deep sedation or muscle relaxation.

Document the indications for intubation or assessment of adequate airway reflexes, ventilation, and respiration.

Procedures

Document wound care, including copious irrigation, incision and drainage, and débridement. Document rapid-sequence induction and intubation, the timing of consultation with the surgeon for extensive wounds, and the timing of the order for tetanus immune globulin.

Hospital Course

Document the patient’s response to treatment.

Document the timing of interventions, including antibiotics, tetanus immune globulin, and intensive care consultation.

Document the indications for change in care, including intubation, deeper sedation, and additional medications.

Check the patient’s electrolytes, primarily to evaluate for hypocalcemia. Order a strychnine level determination if concern exists about exposure to strychnine, with the understanding that illegally imported pesticides contain strychnine.³⁰^–³² Ask patients about pesticide exposure, and consider accidental ingestion in children.^33,³⁴

Obtain a computed tomography scan of the head if an acute intracranial event is considered. A lumbar puncture is necessary only if meningitis or encephalitis is included in the differential diagnosis. Examination of cerebrospinal fluid is noncontributory in tetanus, except to rule out other disorders. Because of unpredictable muscle spasms, performance of lumbar puncture on a patient with generalized tetanus may require intubation and deep sedation or muscle relaxation.

The spatula test has been used to distinguish tetanus from other forms of spasticity. In this test, a blunt instrument such as a tongue blade is used to touch the oropharynx. A patient without tetanus gags and attempts to expel the instrument. In a patient with tetanus, the stimulus triggers masseter spasm, resulting in a reflex bite of the blade.³⁵ Although this test is reported to have a sensitivity of 94% and a specificity of 100%, the results may not be applicable to the United States, where tetanus is rare.

Management

Management of tetanus has two aspects: prevention and treatment. Each time an EP sees a patient with a wound, the opportunity for prevention exists. Treatment of tetanus is multifaceted and includes systemic treatment of the toxin, supportive treatment of the muscle spasms, and wound care.

Priority Actions

Suspect tetanus in patients with rigidity.

• Control airway and ventilation.

• Administer tetanus immune globulin.

• Administer antibiotics.

• Aggressively treat spasticity.

• Débride wounds and incise abscesses.

Prevention

Prevention through vaccination and proper wound care remains the mainstay of therapy for tetanus. Update the patient’s tetanus immunization, and administer tetanus immune globulin according to Centers for Disease Control and Prevention guidelines (Fig. 178.1). Maintain the patient’s current tetanus immunization status in cases of cellulitis, abscesses, eye injuries, chronic ulcers, burns, injecting drugs, minor abrasions, acute lacerations, punctures, and crush injuries (Figs. 178.2 to 178.4). Clean wounds to remove any contaminants.

Fig. 178.1 Approach to tetanus prevention.

CDC, Centers for Disease Control and Prevention; TIG, tetanus immune globulin.

Fig. 178.2 Chronic ulcers, especially in diabetic patients, pose an increased risk for tetanus.

Fig. 178.3 Even subtle abrasions and puncture wounds present an increased risk for tetanus.

Fig. 178.4 A puncture wound to the hand from this organic material introduces a significant tetanus inoculum.

Some patients have decrease in tetanus titers earlier than 10 years. For this reason, patients with wounds that are not clean or are more than minor should receive a tetanus booster at 5 years after the last booster.²⁷ Clinical tetanus does not confer immunity. Therefore, survivors of tetanus require immunization when they are clinically stable. Pregnant women can receive tetanus prophylaxis, if indicated.³⁶^–³⁸ No confirmed risk to the fetus has been determined from tetanus-diphtheria or tetanus immune globulin.³⁶

Treatment

Tips and Tricks

Type of Wounds	Wound Care Tips
Puncture	Copiously irrigate. Remove foreign bodies as indicated.
Simple laceration	Copiously irrigate.
Complex laceration	Copiously irrigate. Débride nonviable tissue.
Abscess	Incise and drain. Débride avascular tissue.
Cellulitis	Débride any necrotic tissue.
Crush	Copiously irrigate. Débride avascular tissue.
Abrasion	Copiously irrigate.
Avulsion	Copiously irrigate. Débride nonviable tissue.