Tetanus is an acute illness caused
by an exotoxin produced by the vegetative form of Clostridium
tetani. The tetanus bacillus is an anaerobic, gram-positive,
spore-forming organism. It is widely distributed in the soil in most
parts of the world. Clostridium tetani is normally
present in the intestines of horses, cattle, and other herbivora,
and is found in 2% to 30% of normal human fecal
flora. The highest number of colonized persons occurs in agricultural
communities. The tetanus organism is a wound contaminant and does
not cause tissue destruction or inflammation.
Tetanus in children is rare in the United States, with fewer
than 20% of cases in persons less than 20 years of age.
Although it has been largely eliminated from the United States, neonatal
tetanus causes more than 400,000 deaths annually worldwide because
of the practice of applying animal excreta to the umbilical stump
for hemostasis. Neonatal tetanus is the cause of 23% to
73% of neonatal deaths and 25% to 30% of
deaths in the first year of life in developing countries. The increasing
use of prophylaxis in the care of wounds of all kinds, and the widespread
use of active immunization have greatly reduced the incidence in
Contamination of wounds by spores of the tetanus bacillus occurs
without clinical signs of infection. Anaerobic conditions in the wound allow
conversion of spores to the vegetative form and the subsequent production
of a plasmid-encoded exotoxin, tetanospasmin, that acts at the myoneural
junction of skeletal muscles and on neuronal membranes in the spinal cord,
to block inhibitory pulses to motor neurons, producing spasms of
muscles. This requires a low oxidation-reduction potential, which
is achieved in deep puncture wounds, crushing injuries, and burns.
Contamination with dirt, soil, or manure provides a heavy inoculum
of organisms; however, C tetani spores are ubiquitous,
and any wound has the potential to become contaminated.
Although some toxin diffuses into the surrounding muscles, most
toxin is distributed hematogenously to neural tissues. Some evidence
suggests that tetanus toxin also travels along axis cylinders to
reach the spinal cord and medulla. The exotoxin tetanospasmin consists
of binding and toxin components. Tetanospasmin binding occurs to
gangliosides at the myoneural junction and toxin interferes with
neuromuscular transmission by inhibition of acetylcholine release. The
toxin’s action in the central nervous system lowers the threshold
of reflexes in which the lower motor neurons are involved, and induces
susceptibility to reflex spasms and convulsions. The toxin combines
with high affinity to neural tissue and binding is essentially irreversible by
antitoxin. Thus, only toxin circulating in the blood can be neutralized
by antitoxin. Tetanospasmin also affects the sympathetic nervous
system, resulting in labile hypertension, tachycardia, profuse sweating,
and increased urinary excretion of catecholamines.
Two clinical forms of tetanus are observed: generalized and local. The
generalized form is the result of widespread distribution of toxin; the
local form is caused by distribution of toxin in the vicinity of
the portal of entry. The two forms may occur simultaneously. In
children, local tetanus is rare, presenting with stiffness in a
single group of muscles, such as those of the jaw, the muscles of
deglutition, or muscles in other parts of the body. The generalized form
is more common, especially in the developing world.
Tetanus produces no characteristic pathologic changes in muscle.
Various lesions may result from the violent spasms, such as hemorrhage
in muscles, or even rupture of skeletal muscles and compression
fractures of vertebral bodies.
Mean incubation period is 5 to 12 days after infection. Short
incubation periods (eg, ⩾ 5 days) are associated with higher mortality rates, whereas
long incubation periods (eg, ⩾ 10 days) are associated with the
lowest mortality rates. The local wound is often unremarkable and
appears to be trivial. The onset is insidious, with gradually increasing
stiffness of muscles, particularly those of the neck, jaw, and the
large muscles of the back and lower extremities. Within 24 hours
of the onset of first symptoms, the disease is generally fully evident
with marked stiffness or spasms of the jaw and neck (trismus). Swallowing
may be difficult, and other parts of the body musculature progressively
become involved. Certain spasms are quite characteristic of tetanus.
Cutaneous, auditory, or visual stimulation and attempts at voluntary
motion initiate paroxysmal contraction of the muscles of the body
as a whole that lasts for 5 or 10 seconds. During the spasm, the
entire body becomes rigid; the head is retracted, the back is arched in
opisthotonos, the legs and feet are extended, and the arms are outstretched,
with fists clenched and thumbs adducted. The jaws are immobile,
and the face assumes a tonic expression known as risus sardonicus. The
eyebrows are raised, the palpebral fissures narrowed, the angles
of the mouth drawn downward and outward, and the upper lip is pressed
firmly against the teeth. Consciousness is not lost, and the patient
is usually very apprehensive.
At first, spasms are infrequent, with complete relaxation between
episodes and only mild discomfort. With progression, spasms become
more numerous, more prolonged, and painful. Relaxation between the
seizures is then only partial, and a considerable degree of rigidity
persists. The paroxysms may affect the respiratory muscles or those
of the larynx, with fatal results. Partial or complete relaxation
occurs during sleep or with anesthesia, and sedatives may afford
some relief. Spasm of the sphincters with retention of urine is common.
Sweating is sometimes marked but fever is usually absent. The duration
of tetanus in fatal infections is seldom more than 3 or 4 days,
and may be less than 24 hours. Death usually results from respiratory
failure, and body temperature sometimes shows an abrupt terminal
rise. Patients who recover seldom have much fever; after several
days the paroxysms gradually decrease in frequency and the muscular
rigidity diminishes, although several weeks may elapse before they
disappear entirely. Trismus is often the last symptom to disappear.
Tetanus neonatorum usually follows introduction of C
tetani into the umbilical cord. The illness usually starts
between the third and tenth day of life and is manifested by excessive
crying and unwillingness or inability to suck. These symptoms are
rapidly followed by trismus, sustained tonic contractions, spasms, and
convulsions.1 Anoxia, exhaustion, and caloric deprivation
result in death.
Tetanus must be diagnosed clinically. The causative organism, C
tetani, may not be demonstrable, but finding the organisms
alone cannot confirm the diagnosis. There are few diseases with
which tetanus is apt to be confused. The history of a wound, the
onset with trismus, the facial expression, and the spasm accentuated
by external stimuli are quite characteristic. Meningitis may be
difficult to rule out without lumbar puncture. The differentiation
from rabies is discussed in Chapter 321. Muscle
spasms resulting from a dystonic reaction are easily confused with
tetanus but its causes are likely to be elicited in the medical history.
Local tetanus should be considered when stiffness of muscles
and irritability to local mechanical stimuli develop in the neighborhood
of a wound, particularly a compound fracture.
Laboratory studies are rarely specific. Cerebrospinal fluid findings
are normal; leukocytosis may be present. Wounds should be débrided
and cultured for C tetani.
The management of tetanus includes careful supportive measures,
control of spasms and seizures, prevention of complications, administration
of antitoxin to prevent the binding of additional toxin, and surgical
debridement where needed. Noise and unnecessary disturbance should
be minimized to decrease the frequency of spasms. Maintenance of
oxygenation is of prime importance. Some experts recommend routine
intubation or tracheotomy and the use of assisted ventilation to
reduce the risk of respiratory arrest, anoxia, and aspiration. Management
of the airway includes suctioning of secretions accumulating in
the pharynx and the tracheobronchial tree. Support of fluid, electrolyte,
and caloric balance may be accomplished through an indwelling nasogastric
tube or total parenteral nutrition.
Several classes of drugs have been used in the symptomatic management
of this disease to control pain and to treat severe anxiety, seizures,
spasms, and secretions. Diazepam (Valium), barbiturates, and meprobamate,
in high doses given by continuous or intermittent intravenous (IV)
administration, are useful. Most centers now manage tetanus with
continuously administered neurologic blocking agents or general
anesthesia with complete support of ventilation, fluids, and nutrition.
Tetanus antitoxin in sufficient quantity may prevent unbound
toxin from reaching the central nervous system but does not displace
bound toxin. The dose of antitoxin should be gauged by the severity
of the disease, not by the size of the patient. Human tetanus immunoglobulin
in doses of 3000 to 6000 U, given intramuscularly, is recommended.
If equine or bovine antitoxin must be used, the dose is 50,000 to
100,000 U. Highly purified antitoxin should be used with appropriate
testing for sensitivity. In mild disease, the intramuscular route
is the safest. In severe disease, one third of the antitoxin may
be given intravenously and the rest intramuscularly.
It is essential that injuries receive proper surgical care, but
extensive operative intervention is neither necessary nor indicated.
Although penicillin and other antibiotics will not neutralize tetanus
toxin, the eradication of the toxin-producing organism from the wound
is achieved with antibiotic treatment. Recent data indicate that
treatment with metronidazole instead of penicillin G (doses of metronidazole
are 30 mg/kg/day administered in four doses intravenously
and given for 10 to 14 days) improves survival and decreases disease
The most common and severe complications are vertebral compression
fractures resulting from convulsions. Anoxia as a result of spasm
of the intervertebral muscles may be a common mechanism of death.
Aspiration may occur during tetanic spasms or seizures.
The mortality of tetanus ranges between 30% and 50%,
in spite of all therapeutic measures. Age is the single most important
factor in determining outcome. The very young and the very old fare
poorly. Most patients who survive 10 days of symptoms eventually
recover completely. The disease leaves no sequelae.
Every patient with clinical tetanus should have roentgenography
of the spine to detect thoracic or lumbar vertebrae compression fractures.
Following recovery from clinical tetanus, the patient must be actively
immunized against tetanus because tetanus disease does not induce
All age groups are susceptible to tetanus. Protection is afforded
only by active or passive immunization. Recommendations for active immunization
are summarized in Chapter 244. Following immunization,
an antitoxin level of 0.01 IU/mL is considered protective.3 If
an individual has completed a primary series of tetanus immunization,
a booster of Td (or at least one dose of Tdap when appropriate)
will only be needed at the time of injury for clean, minor wounds
if it has been more than 10 years since the last booster. For wounds
that are dirty or neglected, or where the blood supply is severely
compromised, a booster of Td (or Tdap, when appropriate) will be
needed at the time of injury if it has been more than 5 years since the
Passive immunization is needed in addition to toxoid only if
the primary series was never completed or if more than 10 years
have elapsed since the previous booster. If passive immunization
is needed, the product of choice is human tetanus immune globulin
(TIG) 250 U intramuscularly. The human preparation provides longer protection
and causes fewer adverse reactions than antitoxin of animal origin.
The latter should be used only if TIG is not available and only
after suitable sensitivity testing. The dose of TIG is 3000 to 5000
U intramuscularly. Td (or Tdap) should always be given as a booster
when TIG is given to a child older than age 7 years, whereas DTaP
or DT should be given at the beginning of a series to unimmunized
children younger than age 7 years. If Td and TIG are given concurrently,
separate syringes and sites should be used and only adsorbed toxoid
is recommended in this situation.
Wound cleansing and debridement is an additional essential step
in preventing tetanus. Recommendations for tetanus prophylaxis in
routine wound management are shown in Table 289-1.4
Table 289-1. Summary
Guide to Tetanus Prophylaxis in Routine Wound Management ||Download (.pdf)
Table 289-1. Summary
Guide to Tetanus Prophylaxis in Routine Wound Management
|History of Adsorbed Tetanus Toxoid||Clean Minor Wounds||All Other Woundsa|
|Td b||TIG||Td c||TIG|
|Unknown or < 3 doses||Yes||No||Yes||Yes|
|⩾ 3 dosesc||Nod||No||Noe||No|