Tetanus
(Lockjaw)
Tetanus is acute poisoning from a neurotoxin produced
by Clostridium tetani. Symptoms are intermittent tonic spasms of
voluntary muscles. Spasm of the masseters accounts for the name lockjaw.
Diagnosis is clinical. Treatment is with human tetanus immune globulin and
intensive support.
Tetanus bacilli form durable spores that occur in soil and
animal feces and remain viable for years.
Worldwide, tetanus is estimated to cause over 200,000 deaths annually, mostly in neonates and young children, but the disease is so rarely reported that all figures are only rough estimates. In the US, 264 cases of tetanus and 19 deaths were reported from 2009 to 2017. Age distribution for cases was 23% in people ≥ 65 years, 64% in people aged 20 to 64 years, and 13% in people < 20 years, including 3 cases of tetanus neonatorum; all tetanus-related deaths occurred in people > 55 years
Disease incidence is directly related to the immunization
level in a population, attesting to the effectiveness of preventive efforts. In
the US, immunity levels tend to be lower in older age groups.
Patients with burns, surgical wounds, or a history of injection drug abuse are especially prone to developing tetanus. However, tetanus may follow trivial or even inapparent wounds. Infection may also develop postpartum in the uterus (maternal tetanus) and in a neonate's umbilicus (tetanus neonatorum) as a result of unsanitary delivery and umbilical cord care practices. Diabetes and a history of immunosuppression may be risk factors for tetanus. read more...
Pathophysiology of Tetanus
C. tetani spores usually enter through
contaminated wounds. Manifestations of tetanus are caused by an exotoxin
(tetanospasmin) produced when bacteria lyse. The toxin enters peripheral nerve
endings, binds there irreversibly, then travels retrograde along the axons and
synapses, and ultimately enters the central nervous system (CNS). As a result,
release of inhibitory transmitters from nerve terminals is blocked, thereby
causing unopposed muscle stimulation by acetylcholine and generalized tonic
spasticity, usually with superimposed intermittent tonic seizures.
Disinhibition of autonomic neurons and loss of control of adrenal catecholamine
release cause autonomic instability and a hypersympathetic state. Once bound,
the toxin cannot be neutralized.
Most often, tetanus is generalized, affecting skeletal
muscles throughout the body. However, tetanus is sometimes localized to muscles
near an entry wound.
Pearls & Pitfalls
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Symptoms and Signs of Tetanus
The incubation period ranges from 2 to 50 days (average, 5
to 10 days). Symptoms of tetanus include
- Jaw stiffness (most frequent)
- Difficulty swallowing
- Restlessness
- Irritability
- Stiff neck, arms, or legs
- Arching of the back (opisthotonos)
- Headache
- Sore throat
- Tonic spasmsLater, patients have difficulty opening their jaw (trismus).
Spasms
Facial muscle spasm produces a characteristic expression
with a fixed smile and elevated eyebrows (risus sardonicus). Rigidity or spasm
of abdominal, neck, and back muscles and sometimes opisthotonos (generalized
rigidity of the body with arching of the back and neck) may occur. Sphincter
spasm causes urinary retention or constipation. Dysphagia may interfere with
nutrition.
Characteristic painful, generalized tonic spasms with
profuse sweating are precipitated by minor disturbances such as a draft, noise,
or movement. Mental status is usually clear, but coma may follow repeated
spasms. During generalized spasms, patients are unable to speak or cry out
because of chest wall rigidity or glottal spasm. Rarely, fractures result from
sustained spasms.
Spasms also interfere with respiration, causing cyanosis or
fatal asphyxia.
Autonomic instability
Temperature is only moderately elevated unless a
complicating infection, such as pneumonia, is present. Respiratory and pulse
rates are increased. Reflexes are often exaggerated. Protracted tetanus may
manifest as a very labile and overactive sympathetic nervous system, including
periods of hypertension, tachycardia, and myocardial irritability.
Causes of death
Respiratory failure is the most common cause of death. Laryngeal
spasm and rigidity and spasms of the abdominal wall, diaphragm, and chest wall
muscles cause asphyxiation. Hypoxemia can also induce cardiac arrest, and
pharyngeal spasm leads to aspiration of oral secretions with subsequent
pneumonia, contributing to a hypoxemic death. Pulmonary embolism is also
possible. However, the immediate cause of death may not be apparent.
Localized tetanus
In localized tetanus, there is spasticity of muscles near
the entry wound but no trismus; spasticity may persist for weeks.
Cephalic tetanus is a form of localized tetanus
that affects the cranial nerves. It is more common among children; in them, it
may occur with chronic otitis media or may follow a head wound. Incidence is
highest in Africa and India. All cranial nerves can be involved, especially the
7th. Cephalic tetanus may become generalized.
Tetanus neonatorum
Tetanus in neonates is usually generalized and frequently
fatal. It often begins in an inadequately cleansed umbilical stump in children
born of inadequately immunized mothers. Onset during the first 2 weeks of life
is characterized by rigidity, spasms, and poor feeding. Bilateral deafness may
occur in surviving children.
Neonatal Tetanus
Neonatal tetanus most commonly affects infants born to nonimmune mothers. Exotoxin produced by Clostridium tetani gains entry to the circulation when the infant's umbilical cord is cut or the umbilical stump is cleaned in a nonsterile fashion. Generalized rigidity and spasm affect the child in the first 2 weeks of life and may be fatal.
Diagnosis of Tetanus
- Clinical
evaluation
Tetanus should be considered when patients have sudden,
unexplained muscle stiffness or spasms, particularly if they have a history of
a recent wound or risk factors for tetanus.
Tetanus can be confused with meningoencephalitis of
bacterial or viral origin, but the following combination suggests tetanus:
- An
intact sensorium
- Normal
cerebrospinal fluid
- Muscle
spasms
Trismus must be distinguished from peritonsillar or
retropharyngeal abscess or another local cause. Phenothiazines can induce
tetanus-like rigidity (eg, dystonic reaction, neuroleptic malignant syndrome).
C. tetani can sometimes be cultured from the
wound, but culture is not sensitive; only 30% of patients with tetanus have
positive cultures. Also, false-positive cultures can occur in patients without
tetanus.
Prognosis for Tetanus
Tetanus has a mortality rate of
- Worldwide:
50%
- In
untreated adults: 15 to 60%
- In
neonates, even if treated: 80 to 90%
Mortality is highest at the extremes of age and in drug
abusers.
The prognosis is poorer if the incubation period is short
and symptoms progress rapidly or if treatment is delayed. The course tends to
be milder when there is no demonstrable focus of infection.
With use of modern supportive care, most patients recover.
Treatment of Tetanus
- Supportive care, particularly respiratory support
- Wound debridement
- Tetanus antitoxin
- Benzodiazepines for muscle spasms
- Metronidazole or penicillin
- Sometimes drugs for autonomic dysfunctionTreatment of tetanus requires maintaining adequate ventilation. Additional interventions include early and adequate use of human tetanus immune globulin (TIG) to neutralize nonfixed toxin; prevention of further toxin production; sedation; control of muscle spasm, hypertonicity, fluid balance, and intercurrent infection; and continuous nursing care. IV immune globulin (IVIG), which contains tetanus antitoxin, may be used if TIG is not available.
General principles
The patient should be kept in a quiet room. Several
principles should guide all therapeutic interventions:
- Prevent
further toxin release by debriding the wound and giving an antibiotic
- Neutralize
unbound toxin outside the CNS with human tetanus immune globulin
- Immunize
using tetanus toxoid, taking care to inject it into a different body site
than the antitoxin
- Minimize
the effect of toxin already in the CNS
Wound care
Because dirt and dead tissue promote C. tetani growth,
prompt, thorough debridement, especially of deep puncture wounds, is essential.
Antibiotics are not substitutes for adequate debridement and immunization but
typically are given.
Antitoxin and toxoid
The benefit of human-derived antitoxin depends on how much
tetanospasmin is already bound to the synaptic membranes—only free toxin is
neutralized. For adults, human TIG 3000 to 6000 units IM is given once; this large
volume may be split and given at separate sites around the wound. Dose can
range from 500 to 6000 units, depending on wound severity, but some authorities
feel that 500 units are adequate.
Supportive care
In moderate or severe cases, patients should be intubated.
Mechanical ventilation is essential when neuromuscular blockade is required to
control muscle spasms that impair respirations.
IV hyperalimentation avoids the hazard of aspiration
secondary to gastric tube feeding. Because constipation is usual, stools should
be kept soft. A rectal tube may control distention. Bladder catheterization is
required if urinary retention occurs.
Chest physiotherapy, frequent turning, and forced coughing
are essential to prevent pneumonia. Analgesia with opioids is often needed.
Prevention of Tetanus
A primary series of tetanus vaccinations followed by regular
boosters is required. Children < 7 years require 5 primary vaccinations, and
unimmunized patients > 7 years require 3. The vaccine may be tetanus toxoid
alone (TT), but toxoid is typically combined with diphtheria and/or pertussis.
Children's vaccines have higher doses of the diphtheria and pertussis
components (DTaP, DT) than adults' vaccines (Tdap, Td).
Children are given DTaP at ages 2 months, 4
months, 6 months, 15 to 18 months, and 4 to 6 years; they should get a Tdap
booster at age 11 to 12 years, and Td every 10 years thereafter
Unimmunized adults are given Tdap initially, then
Td 4 weeks and 6 to 12 months later, and Td every 10 years thereafter. Adults
who have not had a vaccine that contains pertussis should be given a single
dose of Tdap instead of one of the Td boosters. Adults ≥ 65 who anticipate
close contact with an infant < 12 months and who have not previously
received Tdap should be given a single dose of Tdap.
Pregnant women should be given Tdap during each pregnancy,
preferably at 27 to 36 weeks gestation, regardless of when they were last
vaccinated; the fetus can develop passive immunity from vaccines given at this
time.
For routine diphtheria, tetanus, and pertussis immunization
and booster recommendations, see Diphtheria-Tetanus-Pertussis Vaccine and Tetanus-Diphtheria
Vaccine.
After injury, tetanus vaccination is given depending on
wound type and vaccination history; tetanus immune globulin may also
be indicated (see table Tetanus Prophylaxis in Routine Wound Management).
Patients not previously vaccinated are given a 2nd and 3rd dose of toxoid at
monthly intervals.
Because tetanus infection does not confer immunity, patients
who have recovered from clinical tetanus should be vaccinated unless they have
completed a full primary series.
Tetanus Prophylaxis in Routine Wound Management
History of Adsorbed Tetanus
Toxoid |
Clean, Minor Wounds |
All Other Wounds* |
||
Td† |
TIG‡ |
Td† |
TIG‡ |
|
Unknown or < 3 doses |
Yes |
No |
Yes |
Yes |
≥ 3 doses |
Yes if > 10 years since last dose |
No |
Yes if > 5 years since last dose |
No |
* Such as (but not limited to) wounds contaminated with
dirt, feces, soil, or saliva; puncture wounds; crush injuries; avulsions; and
wounds resulting from missiles, burns, or frostbite. |
||||
† For patients ≥ 10 years who have not previously received
a dose of Tdap, a single dose of Tdap should be given instead of one Td
booster. Children < 7 years should be given DTaP or, if pertussis vaccine
is contraindicated, DT. Children aged 7–9 years should be given Td. |
||||
‡ TIG 250–500 units IM. People with HIV infection or
severe immunodeficiency who have contaminated wounds (including minor wounds)
should also receive TIG, regardless of their history of tetanus
immunizations. |
||||
DT = diphtheria and tetanus toxoids (for children); DTaP =
diphtheria and tetanus toxoids, acellular pertussis (for children); Td = tetanus
and diphtheria toxoids adsorbed (for adults); Tdap = tetanus and diphtheria
toxoids, acellular pertussis (for adults); TIG = tetanus immune
globulin (human). |
Key Points
- Tetanus
is caused by a toxin produced by Clostridium tetani in
contaminated wounds.
- Tetanus
toxin blocks release of inhibitory neurotransmitters, causing generalized
muscle stiffness with intermittent spasms; seizures and autonomic
instability may occur.
- Mortality
is 15 to 60% in untreated adults and 80 to 90% in neonates even if
treated.
- Prevent
further toxin release by debriding the wound and giving an antibiotic (eg,
penicillin, doxycycline), and neutralize unbound toxin with human
tetanus immune globulin.
- Give
IV benzodiazepines for muscle spasm, and use neuromuscular blockade and
mechanical ventilation as needed for respiratory insufficiency due to
muscle spasm.
- Prevent
tetanus by following routine immunization recommendations.
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