Tetanus - UpToDate

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Tetanus
Author: Daniel J Sexton, MD
Section Editor: John G Bartlett, MD
Deputy Editor: Meg Sullivan, MD
All topics are updated as new evidence becomes available and our peer review process is complete.
Literature review current through: Feb 2020. | This topic last updated: Aug 03, 2018.
INTRODUCTION
Tetanus is a nervous system disorder characterized by muscle spasms that is caused by the toxin-
producing anaerobe Clostridium tetani, which is found in the soil. The clinical features of tetanus and
its relationship to traumatic injuries were well known among the ancient Greeks and Egyptians and to
many clinicians before the introduction of vaccination with tetanus toxoid in the 1940s. The term
"lockjaw" (now called trismus) lives in modern parlance as a reminder of one of the cardinal features
of tetanus: intense, painful spasms of the masseter muscles.
Tetanus can present in one of four clinical patterns:
● Generalized
● Local
● Cephalic
● Neonatal
Although tetanus is now rare in resource-rich settings, the disease remains a threat to all
unvaccinated people, particularly in resource-limited countries. Since C. tetani spores cannot be
eliminated from the environment, immunization and proper treatment of wounds and traumatic injuries
are crucial for tetanus prevention. The epidemiology, pathogenesis, clinical features, diagnosis, and
management of tetanus will be reviewed here. The principles of prevention of tetanus and
management of tetanus-prone wounds are discussed separately. (See "Tetanus-diphtheria toxoid
vaccination in adults" and "Diphtheria, tetanus, and pertussis immunization in children 6 weeks
through 6 years of age" and "Diphtheria, tetanus, and pertussis immunization in children 7 through 18
https://www.uptodate.com/contents/tetanus/print?search=tetanus&source=search_result&selectedTitle=1~150&usage_type=default&display_rank=1 1/22
years of age" and "Infectious complications of puncture wounds" and "Animal bites (dogs, cats, and
other animals): Evaluation and management".)
EPIDEMIOLOGY
Resource-rich countries — Because of almost universal vaccination of children with tetanus toxoid
in resource-rich countries, the incidence of tetanus in these regions has dropped dramatically and
steadily since 1940. During the period between 2001 and 2008, the United States Centers for Disease
Control and Prevention (CDC) reported that there were 233 cases of tetanus in the United States,
with an annual incidence of 0.10 cases/million population overall and 0.23 cases/million among
individuals ≥65 years of age [1]. The case-fatality rate was 13.2 percent overall but was 31.3 percent
among individuals ≥65 years of age. In 2009, 19 cases of tetanus and 2 deaths were reported in the
United States through the national tetanus surveillance system [2].
Most patients with tetanus lack a history of receipt of a full series of tetanus toxoid immunization and
receive inadequate prophylaxis following a wound [1,3,4]. Approximately three-fourths of patients who
acquired tetanus in the United States between 2001 and 2008 recalled an acute injury prior to the
onset of their symptoms, but approximately two-thirds of these individuals did not seek medical care
[1]. Among 51 patients who sought care for an acute wound and had a sufficiently thorough
surveillance report to allow evaluation, 49 (96 percent) did not receive adequate tetanus toxoid
prophylaxis or tetanus toxoid prophylaxis plus tetanus immune globulin [1]. However, occasional
patients with preexisting antitetanus antibodies (as measured by guinea pig or mouse protection
assays) have developed tetanus [5]. (See "Tetanus-diphtheria toxoid vaccination in adults" and
"Diphtheria, tetanus, and pertussis immunization in children 6 weeks through 6 years of age", section
on 'Schedules' and "Diphtheria, tetanus, and pertussis immunization in children 7 through 18 years of
age", section on 'Indications'.)
Unlike in resource-limited nations, neonatal tetanus is extremely rare in the United States. Only one
case of neonatal tetanus was reported between 2001 and 2008; this case occurred in an infant whose
mother had not been vaccinated [6]. Fifteen percent of patients with tetanus had diabetes mellitus,
which is three times the estimated prevalence of diabetes in the United States. Another 15 percent of
patients were injection drug users.
The annual incidence of tetanus in other resource-rich countries is also low and declining due to
vaccination programs. In England and Wales, for example, the annual incidence was 0.2 cases/million
population, with the highest incidence in patients above the age of 64 years [7]. Italy reported the
highest number of cases among the countries of Europe, but the annual incidence decreased from
0.5 to 0.2 per 100,000 from the 1970s to the 1990s [8]. The case-fatality ratio decreased from 68 to
39 percent over that same period; women >64 years of age were disproportionately affected.
Despite the low rate of clinical disease in resource-rich countries, many adults are inadequately
vaccinated against tetanus. In the serologic survey cited above in the United States between 1988
and 1994, protective levels of antitetanus antibody (>0.15 international units/mL) were present in 72
percent of individuals ≥6 years of age but only 31 percent of adults over the age of 70 [9]. Not
surprisingly, protective antibody levels are more likely in adults with a history of military service, higher
levels of education, and higher incomes [10].
Resource-limited countries — In contrast with resource-rich nations where tetanus is rare, tetanus
remains endemic in resource-limited settings, and the incidence often increases following natural
disasters such as earthquakes and tsunamis [11]. Approximately one million cases of tetanus are
estimated to occur worldwide each year, with 300,000 to 500,000 deaths [11]. In 2002, tetanus caused
an estimated 180,000 deaths worldwide [12]. Among patients admitted for neurologic conditions to
one hospital in Nigeria, tetanus was the second most common cause (14 percent) after stroke [13].
Case-fatality rates in resource-limited settings remain high and have not changed significantly in the
past several decades. The pooled fatality rate of 3043 adult African patients reported in 27 studies
was 43 percent (95% CI 37 to 50 percent) [14]. The high fatality rate likely reflects the fact that
mechanical ventilation is often not available in African medical facilities. Longer incubation periods
were associated with lower fatality rates.
Neonatal tetanus, which the World Health Organization targeted for elimination by 1995, accounted
for approximately 59,000 deaths in 2008 [15]. While this represents a decrease in mortality of 92
percent compared with 1988 [15], as of 2014, 24 countries had still not eliminated maternal and
neonatal tetanus [16]. (See 'Neonatal tetanus' below.)
PATHOGENESIS
Tetanus occurs when spores of Clostridium tetani, an obligate anaerobe normally present in the gut of
mammals and widely found in soil, gains access to damaged human tissue. After inoculation, C. tetani
transforms into a vegetative rod-shaped bacterium and produces the metalloprotease tetanospasmin
(also known as tetanus toxin).
After reaching the spinal cord and brainstem via retrograde axonal transport within the motor neuron,
tetanus toxin is secreted and enters adjacent inhibitory interneurons, where it blocks
neurotransmission by its cleaving action on the membrane proteins involved in neuroexocytosis [17-
20]. The net effect is inactivation of inhibitory neurotransmission that normally modulates anterior horn
cells and muscle contraction. This loss of inhibition (ie, disinhibition) of anterior horn cells and
autonomic neurons results in increased muscle tone, painful spasms, and widespread autonomic
instability.
Muscular rigidity in tetanus occurs though a complex mechanism that involves an increase in the
resting firing rate of disinhibited motor neurons and lack of inhibition of reflex motor responses to
afferent sensory stimuli [21]. Lack of neural control of adrenal release of catecholamines induced by
tetanus toxin produces a hypersympathetic state that manifests as sweating, tachycardia, and
hypertension. (See 'Generalized tetanus' below.)
Tetanus toxin-induced effects on anterior horns cells, the brainstem, and autonomic neurons are long
lasting because recovery requires the growth of new axonal nerve terminals. (See 'Duration of illness'
below.)
The mechanisms of binding to and inhibition of neural cells are related to specific portions of the
tetanospasmin (tetanus toxin) molecule. Tetanus toxin is produced initially as an inactive polypeptide
chain by actively growing organisms. This synthesis is controlled by genes located in an intracellular
plasmid.
After death of the clostridial bacterium, the toxin is released and then activated by bacterial or tissue
proteases into its active form, which contains a heavy chain necessary for binding and entry into
neurons and a light chain responsible for its toxic properties [16,20-22]. Heavy chains are further
cleaved by pepsins into specific fragments, which individually mediate binding to specific types of
neural cells. Presynaptic inhibition of neurotransmitter release is mediated via light chains.
Tetanolysin is another toxin produced by C. tetani during its early growth phase. It has hemolytic
properties and causes membrane damage in other cells, but its role in clinical tetanus is uncertain.
Predisposing factors — Because C. tetani will not grow in healthy tissues, a convergence of factors
must be present in order for tetanus toxin to be elaborated in the human host. This combination of
factors usually includes absence of antibodies (ie, from inadequate vaccination) plus two or more of
the following:
● A penetrating injury resulting in the inoculation of C. tetani spores

● Coinfection with other bacteria
● Devitalized tissue
● A foreign body
● Localized ischemia
The above factors explain why tetanus-prone injuries include splinters and other puncture wounds,
gunshot wounds, compound fractures, burns, and unsterile intramuscular or subcutaneous injections
(that often occur in injection drug users). These predisposing factors can also explain why tetanus can
develop in unusual clinical settings such as in:
● Neonates (due to infection of the umbilical stump)

● Obstetric patients (after septic abortions)
● Postsurgical patients (with necrotic infections involving bowel flora)
● Adolescents and adults undergoing male circumcision in sub-Saharan Africa [23]
● Patients with dental infections
● Diabetic patients with infected extremity ulcers
● Patients who inject illicit and/or contaminated drugs [24]
Tetanus in patients without an identifiable cause — An identifiable antecedent cause for tetanus is
obvious in more than 90 percent of patients presenting with tetanus, but no cause can be identified in
a small percentage of patients with classic signs and symptoms of tetanus. Presumably, minor
unnoticed abrasions or skin injuries are responsible for most or all of these "cryptogenic" cases.
Tetanus has occurred rarely in patients who have received a timely and correct series of tetanus
immunizations [25].
CLINICAL FEATURES
Incubation period — The incubation period of tetanus is approximately 8 days but ranges from 3 to
21 days [26]. The incubation period is typically shorter in neonatal tetanus than in non-neonatal
tetanus [16]. (See 'Neonatal tetanus' below.)
Inoculation of spores in body locations distant from the central nervous system (eg, the hands or feet)
results in a longer incubation period than inoculation close to the central nervous system (eg, the
head or neck).
Generalized tetanus — The most common and severe clinical form of tetanus is generalized tetanus.
The presenting symptom in more than half of such patients is trismus (lockjaw), although patients with
generalized tetanus sometimes present with cephalic or localized tetanus. Patients with generalized
tetanus typically have symptoms of autonomic overactivity that may manifest in the early phases as
irritability, restlessness, sweating, and tachycardia. In later phases of illness, profuse sweating,
cardiac arrhythmias, labile hypertension or hypotension, and fever are often present.
Patients with tetanus may develop reflex spasms of their masseter muscles rather than a (normal)
gag response when their posterior pharynx is touched with a tongue blade or spatula (the spatula
test). In one study of 400 consecutive patients with suspected tetanus, the sensitivity and specificity of
this maneuver were high (94 and 100 percent, respectively) [27]. This test may even be useful in
infants, but it is not useful when patients have severe trismus.
Patients with generalized tetanus characteristically have tonic contraction of their skeletal muscles
and intermittent intense muscular spasms. Since patients with tetanus have no impairment of
consciousness or awareness, both the tonic contractions and spasms are intensely painful. Tetanic
spasms may be triggered by loud noises or other sensory stimuli such as physical contact or light.
Tonic and periodic spastic muscular contractions are responsible for most of the classic clinical
findings of tetanus such as:
● Stiff neck
● Opisthotonus
● Risus sardonicus (sardonic smile)
● A board-like rigid abdomen
● Periods of apnea and/or upper airway obstruction due to vise-like contraction of the thoracic
muscles and/or glottal or pharyngeal muscle contraction, respectively
● Dysphagia
During generalized tetanic spasms, patients characteristically clench their fists, arch their back, and
flex and abduct their arms while extending their legs, often becoming apneic during these dramatic
postures.
Local tetanus — Rarely, tetanus presents with tonic and spastic muscle contractions in one extremity
or body region. Local tetanus often but not invariably evolves into generalized tetanus. Diagnosis in
local tetanus can be difficult. For example, rarely patients with early tetanus may develop board-like
abdominal rigidity that mimics an acute surgical abdomen.
Cephalic tetanus — Patients with injuries to the head or neck may present with cephalic tetanus,
involving initially only cranial nerves. Like other forms of local tetanus, patients with cephalic tetanus
often subsequently develop generalized tetanus. Prior to the appearance of the typical features of
generalized tetanus, patients with cephalic tetanus may manifest confusing clinical findings including
dysphagia, trismus, and focal cranial neuropathies that can lead to a misdiagnosis of stroke [28]. The
facial nerve is most commonly in cephalic tetanus [29], but involvement of cranial nerves VI, III, IV,
and XII may also occur either alone or in combination with others.
Neonatal tetanus — Neonatal tetanus occurs as a result of the failure to use aseptic techniques in
managing the umbilical stump in offspring of mothers who are poorly immunized. The application of
unconventional substances to the umbilical stump (eg, ghee or clarified butter, juices, and cow dung)
have been implicated as common cultural practices that contribute to neonatal tetanus [30]. Neonatal
tetanus can also result from unclean hands and instruments or contamination by dirt, straw, or other
nonsterile materials in the delivery field.
Neonatal tetanus typically occurs in infants 5 to 7 days following birth (range 3 to 24 days) [16]. The
onset of illness is typically more rapid in neonatal tetanus than in older individuals and may progress
over hours rather than days, probably because axonal length is proportionately shorter in infants [31].
Neonatal tetanus presents with refusal to feed and difficulty opening the mouth due to trismus [16].
Sucking then stops and facial muscles spasm, which may result in risus sardonicus (sardonic smile).
The hands are often clenched, the feet become dorsiflexed, and muscle tone increases. As the
disease progresses, neonates become rigid and opisthotonus (spasm of spinal extensors) develops.
Severity of illness — The severity and frequency of the clinical features of tetanus may vary from
case to case, depending upon the amount of tetanus toxin that reaches the central nervous system.
Symptoms and signs may progress for up to two weeks after the disease onset. The severity is
related to the incubation period of the illness and the interval from the onset of symptoms to the
appearance of spasms [21]; the longer the interval, the milder the clinical features of tetanus. In
addition, illness may be milder in patients with preexisting but nonprotective levels of antitetanus
antibodies. In one study of 64 patients with tetanus, serum obtained prior to the institution of treatment
contained detectable levels of antibody in 35 percent of patients, and the severity of tetanus in these
patients appeared to be inversely related to the level of pretreatment antitetanus toxin antibody [32].
Duration of illness — Tetanus toxin-induced effects are long lasting because recovery requires the
growth of new axonal nerve terminals. The usual duration of clinical tetanus is four to six weeks.
DIAGNOSIS
The diagnosis of tetanus is usually obvious and can generally be made based upon typical clinical
findings outlined above. Tetanus should especially be suspected when there is a history of an
antecedent tetanus-prone injury and a history of inadequate immunization for tetanus. However,
tetanus can sometimes be confused with other processes, as discussed in the following section.
DIFFERENTIAL DIAGNOSIS
Tetanus can sometimes be confused with the following mimics.
Drug-induced dystonias such as those due to phenothiazines — Drug-induced dystonias often

produce pronounced deviation of the eyes, writhing movements of the head and neck, and an
absence of tonic muscular contraction between spasms. By contrast, tetanus does not produce eye
deviations, and the muscles are characteristic tonically contracted between spasms. Finally,
administration of an anticholinergic agent such as benztropine mesylate will usually immediately
reverse the spasms seen in drug-induced dystonias. Such therapy has no effect on patients with
tetanus.
Trismus due to dental infection — Dental infections may produce trismus that may rarely be
confused with cephalic forms of tetanus. However, the presence of an obvious dental abscess and the
lack of progression or superimposed spasms usually make the distinction between the two diseases
apparent after initial evaluation and/or a period of observation. (See "Deep neck space infections in
adults" and "Complications, diagnosis, and treatment of odontogenic infections".)
Strychnine poisoning due to ingestion of rat poison — Accidental or intentional strychnine

poisoning may produce a clinical syndrome similar to tetanus. Supportive care for both conditions is
critical; thus, the initial treatment of both conditions is identical. Assays of blood, urine, and tissue for
strychnine can be performed in special reference laboratories. Such tests should be obtained when
there is any suspicion of accidental or intentional poisoning or when a typical history of an antecedent
injury or infection for tetanus is lacking or the patient has been adequately immunized for tetanus.
(See "Strychnine poisoning".)
Malignant neuroleptic syndrome — Patients with malignant neuroleptic syndrome can present with
striking symptoms of autonomic instability and muscular rigidity. However, the presence of fever,
altered mental status, and recent receipt of an agent with a propensity to cause this complication
usually makes the distinction from tetanus relatively easy. (See "Neuroleptic malignant syndrome".)
Stiff-person syndrome — Stiff-person syndrome (SPS) is a rare neurologic disorder characterized

by severe muscle rigidity. Spasms of the trunk and limbs may be precipitated by voluntary movements
or auditory, tactile, or emotional stimulation, all of which can also occur in tetanus. The absence of
trismus or facial spasms and rapid response to diazepam distinguish SPS from true tetanic spasms
[33]. In addition, SPS is associated with autoantibodies against glutamic acid decarboxylase. (See
"Stiff-person syndrome".)
TREATMENT
Treatment of tetanus is best performed in the intensive care unit in consultation with an
anesthesiologist or critical care specialist trained in the management of the complications of this
disease, including early and aggressive airway management. Unfortunately, little evidence exists to
support any particular therapeutic intervention in tetanus. There are only nine randomized trials
reported in the literature over the past 30 years [34]. The goals of treatment include:
● Halting the toxin production

● Neutralization of the unbound toxin
● Airway management
● Control of muscle spasms
● Management of dysautonomia
● General supportive management
Halting toxin production
Wound management — All patients with tetanus should undergo wound debridement to eradicate
spores and necrotic tissue, which could lead to conditions ideal for germination.
Antimicrobial therapy — Although antibiotics probably play a relatively minor role in the
management of tetanus, they are universally recommended. However, it is important to emphasize
that appropriate antimicrobial therapy may fail to eradicate C. tetani unless adequate wound
debridement is performed. This was illustrated by one study in which 45 isolates of C. tetani were
obtained at the time of wound debridement from 84 Vietnamese patients with severe tetanus [35]. All
45 isolates were susceptible by disc diffusion and E-test to penicillin and metronidazole, and all were
resistant to trimethoprim-sulfamethoxazole. However, C. tetani was isolated from the wounds of two
patients who underwent debridement after more than two weeks of high doses of penicillin.
Metronidazole (500 mg intravenously [IV] every six to eight hours) is the preferred treatment for
tetanus, but penicillin G (2 to 4 million units IV every four to six hours) is a safe and effective
alternative [11]. We suggest a treatment duration of 7 to 10 days.
The first study to compare penicillin and metronidazole found a greater reduction in mortality in the
metronidazole group (7 versus 24 percent) [36]. However, in two subsequent studies, there was no
difference in mortality in patients treated with penicillin and those treated with metronidazole [6,37]. In
one of the former studies, patients receiving metronidazole required fewer muscle relaxants and
sedatives [6]. It is possible that the observed difference in outcomes may not be due to differences in
the antimicrobial activity of the two agents but rather may be explained by the GABA antagonist effect
of penicillins and third-generation cephalosporins, which may lead to central nervous system (CNS)
excitability.
If a mixed infection is suspected, a first-, second-, or third-generation cephalosporin such as cefazolin

(1 to 2 g IV every 8 hours), cefuroxime (2 g IV every 6 hours), or ceftriaxone (1 to 2 g IV every 24
hours) can be used.
An alternative agent is doxycycline (100 mg every 12 hours); other agents with activity against C.
tetani are macrolides, clindamycin, vancomycin, and chloramphenicol [11,38]. The efficacy of these
agents has not been evaluated but, based upon in vitro susceptibility data, it is likely that they are
effective.
Neutralization of unbound toxin — Since tetanus toxin is irreversibly bound to tissues, only
unbound toxin is available for neutralization. Unbound toxin has been demonstrated in 10 percent of
serum samples and 4 percent of cerebrospinal fluid (CSF) samples of cases upon presentation [39].
The use of passive immunization to neutralize unbound toxin is associated with improved survival,
and it is considered to be standard treatment.
In the United States, human tetanus immune globulin (HTIG) should be readily available and is the
preparation of choice. A dose of 3000 to 6000 units intramuscularly should be given as soon as the
diagnosis of tetanus is considered, with part of the dose infiltrated around the wound [40]. HTIG
should be administered at different sites than tetanus toxoid.
Intrathecal administration of tetanus immune globulin is of unproven benefit. A randomized trial from
Brazil compared intramuscular plus intrathecal administration of immunoglobulin (n = 58) with
intramuscular therapy alone (n = 62) [41]. The patients receiving intrathecal therapy had a shorter
duration of spasms, shorter hospital stay, and a decreased requirement for respiratory assistance.
Mortality was not significantly affected.
However, a number of methodologic issues might have affected this study. The mortality rate for
tetanus patients fell during the study period from 35 percent in historical controls to 12 percent among
control patients in this study. While tetanus cases were graded upon admission, these grades were
not reported, and the only note of more patients with grade III and IV disease among the controls
compared with those receiving intrathecal immunoglobulin implies that these differences arose during
the course of therapy. The investigators refer to tetanus hyperimmune globulin but merely list a
lyophilized human immunoglobulin in the methods section.
In countries in which HTIG is not readily available, equine antitoxin is used intramuscularly or
intravenously. When equine antitoxin is used, an intradermal test dose of 0.1 mL in a 1:10 dilution
should be administered prior to giving the full dose in order to evaluate for hypersensitivity reactions
[11]. In contrast, antecedent skin testing is not needed if a human preparation is to be used.
Infiltration of antitoxin, either human or equine, into the wound has sometimes been advocated but is
of unproven value. The use of pooled intravenous immune globulin (IVIG) has been proposed as a
possible alternative to HTIG [40].
Active immunization — Since tetanus is one of the few bacterial diseases that does not confer
immunity following recovery from acute illness, all patients with tetanus should receive active
immunization with a full series (eg, three doses in adults and children >7 years old) of tetanus and
diphtheria toxoid-containing vaccines, commencing immediately upon diagnosis. Such vaccines

should be administered at a different site than tetanus immune globulin. Specific recommendations on
vaccine formulations and vaccination schedules are discussed in detail separately:
● (See "Tetanus-diphtheria toxoid vaccination in adults", section on 'Routine adult immunization'.)

● (See "Immunizations during pregnancy", section on 'Tetanus, diphtheria, and pertussis
vaccination'.)
● (See "Diphtheria, tetanus, and pertussis immunization in children 6 weeks through 6 years of
age", section on 'Schedules'.)
● (See "Diphtheria, tetanus, and pertussis immunization in children 7 through 18 years of age",
section on 'Schedule'.)
Subsequent tetanus doses, in the form of Td, are recommended at 10-year intervals throughout
adulthood [42]. Tetanus toxoid alone should be given only to those patients with documented allergy
or untoward reactions to diphtheria toxoid. (See "Tetanus-diphtheria toxoid vaccination in adults".)
Control of muscle spasms — Generalized muscle spasms are life threatening since they can cause
respiratory failure, lead to aspiration, and induce generalized exhaustion in the patient. Several drugs
may be used to control these spasms. Attention to placement of the patient and control of light or
noise in the room in an effort to avoid provoking muscle spasms was an important component of care
for patients with tetanus in the past before the availability of drugs to prevent spasms. These
measures are still vital in regions where the availability of neuromuscular blocking agents may be
limited [11].
Benzodiazepines and other sedatives — Benzodiazepines have been used traditionally and are
generally effective in controlling the rigidity and spasms associated with tetanus [11]. They also
provide a sedative effect. Diazepam has been used most frequently, but other benzodiazepines are as
effective as diazepam.
For tetanus, the usual starting dose of diazepam for an adult is 10 to 30 mg IV and repeated as
needed every 1 to 4 hours; total daily doses as high as 500 mg may be required for an adult.
Ventilatory assistance is imperative at these higher doses. When higher doses of the IV formulation of
diazepam are used, the vehicle, propylene glycol, may produce hyperosmolarity and an anion gap
metabolic (lactic) acidosis [43]. These abnormalities are often accompanied by acute kidney injury
and can progress to multisystem organ failure. To avoid these problems when high doses of a
benzodiazepine are required, a continuous infusion of IV midazolam can be given as it does not
contain propylene glycol. For patients who are absorbing drugs well by the enteral route, diazepam
can be given enterally via a feeding tube. Patients with tetanus often show tolerance to the sedating
effects of benzodiazepines and may remain awake and alert after receiving doses that would sedate
or cause anesthesia in other patients [25].
Since these drugs may be required for a prolonged period of time (often weeks), they should be
tapered gradually to avoid withdrawal reactions.
The properties, usual dosing regimens for sedation, and adverse effects of benzodiazepines are
discussed in greater detail separately. (See "Sedative-analgesic medications in critically ill adults:
Properties, dosage regimens, and adverse effects", section on 'Benzodiazepines' and "Sedative-
analgesic medications in critically ill adults: Properties, dosage regimens, and adverse effects",
section on 'Dosage regimens' and "Sedative-analgesic medications in critically ill adults: Properties,
dosage regimens, and adverse effects", section on 'Propylene glycol toxicity'.)
Infusion of the anesthetic propofol may also control spasms and rigidity. Its prolonged use has been
associated with lactic acidosis, hypertriglyceridemia, and pancreatic dysfunction.
Neuromuscular blocking agents — Neuromuscular blocking agents are used when sedation
alone is inadequate. Pancuronium, a long-acting agent, has been traditionally used. However, it may
worsen autonomic instability because it is an inhibitor of catecholamine reuptake. Vecuronium can
also be administered and is less likely to cause autonomic problems, but since it is short acting, it
must be given as continuous infusion to provide adequate effects. Monitoring of patients on these
drugs is extremely important to avoid or recognize complications, and these drugs should be stopped
at least once a day in order to assess the patient's status.
Baclofen, which stimulates postsynaptic GABA beta receptors, has been used in a few small studies.
The preferred route is intrathecal, and it may be given either in a bolus of 1000 mcg or by continuous
intrathecal infusion [44]. Intrathecal baclofen given as an initial bolus in a dose ranging from 40 to 200
mcg followed by a continuous infusion of 20 mcg/hour was found to control spasms and rigidity in 21
out of 22 patients with grade III tetanus in a retrospective outcome study from a single medical center
in Portugal. One of 22 patients developed meningitis secondary to infection of the intrathecal catheter
despite the fact that most patients required such therapy for at least three weeks (range 8 to 30 days)
[45]. In some cases, baclofen has been used without the need for artificial ventilation [46].
Phenothiazines and barbiturates were used in the past to control spasms but have largely been
displaced by neuromuscular blocking agents.
Management of autonomic dysfunction — Several drugs have been used to produce adrenergic
blockade and suppress autonomic hyperactivity; only treatment with magnesium sulfate has been
studied in a randomized clinical trial in tetanus [47] because of its use in clinical series for the
management of autonomic dysfunction and as adjunctive treatment for controlling spasms [47-50].
Magnesium sulfate — Magnesium sulfate acts as a presynaptic neuromuscular blocker, blocks

catecholamine release from nerves, and reduces receptor responsiveness to catecholamines [51]. It
has the advantage of worldwide experience in the treatment of eclampsia.
In a randomized, double blind trial in 256 hospitalized patients with severe tetanus in Vietnam,
magnesium sulfate infusion compared with placebo controlled autonomic dysfunction [47]. The
patients were randomly assigned to magnesium sulfate (loading dose 40 mg/kg over 30 minutes,
followed by continuous infusion of either 2 g per hour for patients over 45 kg or 1.5 g per hour for
patients ≤45 kg) versus placebo (5 percent glucose in water) infusion. The primary outcomes were
requirement for mechanical ventilation and drugs to control muscle spasms and autonomic
dysfunction. Magnesium infusion significantly reduced the requirement for other drugs to control
muscle spasms, and patients treated with magnesium were 4.7 times (95% CI 1.4-15.9) less likely to
require verapamil to treat cardiovascular instability than those in the placebo group. Magnesium
sulfate infusion did not reduce the need for mechanical ventilation.
Beta blockade — Labetalol (0.25 to 1 mg/min) has frequently been administered because of its
dual alpha- and beta-blocking properties. Beta blockade alone with propranolol, for example, should
be avoided because of reports of sudden death [52]. Morphine sulfate (0.5 to 1 mg/kg per hour by
continuous intravenous infusion) is commonly used to control autonomic dysfunction as well as to
induce sedation.
Other drugs — Other drugs for the treatment of various autonomic events, which have been
reported to be useful, are atropine, clonidine, and epidural bupivacaine.
Airway management and other supportive measures — Since tetanus toxin cannot be displaced
from the nervous system once bound to neurons, supportive care is the main treatment for tetanus. In
patients with severe tetanus, prolonged immobility in the intensive care unit is common, much of
which is on mechanical ventilation and may last for weeks. Such patients are predisposed to
nosocomial infections, decubitus ulcers, tracheal stenosis, gastrointestinal hemorrhage, and
thromboembolic disease.
Endotracheal intubation is justified initially, but early tracheostomy is frequently indicated because of
the likelihood of prolonged mechanical ventilation. The latter allows better tracheal suctioning and
pulmonary toilet.
Energy demands in tetanus may be extremely high, so early nutritional support is mandatory. Enteral
feeding is preferred if enough calories can be administered by this route. Placement of percutaneous
endoscopic gastrostomy (PEG) tubes is commonplace, since this route may prevent
gastroesophageal reflux, which may be induced by nasogastric tubes. Prophylactic treatment with
sucralfate or acid blockers may be used to prevent gastroesophageal hemorrhage from stress
ulceration.
Prophylaxis of thromboembolism with heparin, low molecular weight heparin, or other anticoagulants
should be administered early.
Physical therapy should be started as soon as spasms have ceased, since tetanus patients often are
left with disability from prolonged drug-induced paralysis and immobilization.
Considerations in resource-limited settings — Critical care services are often unavailable or

rudimentary in many resource-limited countries [11]. When intensive care units (ICUs) are not
available, acute respiratory failure is a leading cause of death from tetanus. In the absence of an ICU,
a separate ward or room should be designated for patients with tetanus, and sensory stimuli should
be kept to a minimum since loud noises, physical contact, and light can trigger tetanic spasms [11].
Nondepolarizing paralytic agents, such as vecuronium and pancuronium, are not safe to use in the
absence of ventilatory support. However, benzodiazepines and baclofen can be used in such
situations if doses are carefully titrated to avoid respiratory depression. Magnesium sulfate may be
used to manage autonomic dysfunction. (See 'Control of muscle spasms' above and 'Magnesium
sulfate' above.)
PROPHYLAXIS
Tetanus prophylaxis following a puncture wound is discussed in detail separately. The following table
summarizes the approach to tetanus prophylaxis (table 1). (See "Infectious complications of puncture
wounds", section on 'Tetanus immunization'.)
Immunization of women who are pregnant or of childbearing age reduces neonatal tetanus mortality
by approximately 94 percent [16]. Improving hygiene during home births in resource-limited settings is
also likely to play an important role in preventing neonatal tetanus.
PROGNOSIS
Case-fatality rates for non-neonatal tetanus in resource-limited countries range from 8 to 50 percent
[16,31], whereas the majority of patients with tetanus recover when modern supportive care is
available [53].
Neonatal tetanus, once nearly always fatal, now has mortality rates of 3 to 88 percent [16]. Patients
with shorter incubation periods (eg, ≤7 days) have increased disease severity and mortality [16,54].
Among neonatal infections, survivors may recover fully or have varying degrees of neurologic damage
ranging from minor intellectual deficits to cerebral palsy [55]. The prognosis appears excellent
(mortality 2 percent in a study from India) with infections not associated with spasms [54].
SOCIETY GUIDELINE LINKS
Links to society and government-sponsored guidelines from selected countries and regions around
the world are provided separately. (See "Society guideline links: Tetanus infection".)
INFORMATION FOR PATIENTS
UpToDate offers two types of patient education materials, "The Basics" and "Beyond the Basics." The
Basics patient education pieces are written in plain language, at the 5th to 6th grade reading level, and
they answer the four or five key questions a patient might have about a given condition. These articles
are best for patients who want a general overview and who prefer short, easy-to-read materials.
Beyond the Basics patient education pieces are longer, more sophisticated, and more detailed. These
articles are written at the 10th to 12th grade reading level and are best for patients who want in-depth
information and are comfortable with some medical jargon.
Here are the patient education articles that are relevant to this topic. We encourage you to print or e-
mail these topics to your patients. (You can also locate patient education articles on a variety of
subjects by searching on "patient info" and the keyword(s) of interest.)
● Basics topic (see "Patient education: Tetanus (The Basics)")
SUMMARY AND RECOMMENDATIONS
● Although tetanus is now rare in resource-rich settings, the disease remains a threat to all
unvaccinated people, particularly in resource-limited countries. Since Clostridium tetani spores
cannot be eliminated from the environment, immunization and proper treatment of wounds and
traumatic injuries are crucial for tetanus prevention. (See 'Introduction' above.)
● Tetanus is a clinical diagnosis and must be considered in patients with muscle spasms and an
inadequate vaccination history. (See 'Clinical features' above and 'Diagnosis' above.)
● Supportive care is the mainstay of management to avoid complications such as respiratory

failure, nosocomial infections, and thromboembolism. (See 'Treatment' above.)
● Since the disease is mediated by a toxin, a crucial aspect of therapy is to eliminate ongoing toxin
production, neutralize unbound toxin usually with human tetanus immune globulin, and immunize
against tetanus since natural disease does not confer immunity. (See 'Treatment' above.)
● Antimicrobials play an adjunctive role in the therapy of tetanus. We recommend metronidazole

(500 mg intravenously every six to eight hours) for the treatment of tetanus. We suggest a
treatment duration of 7 to 10 days. (See 'Antimicrobial therapy' above.)
● Muscle spasms are controlled with sedation (usually benzodiazepines) or neuromuscular

blockade. (See 'Control of muscle spasms' above.)
● Autonomic hyperactivity can be treated with labetalol or morphine sulfate. Beta blockade without
concomitant alpha blockade should be avoided. The use of magnesium sulfate for both
autonomic dysfunction and additional control of muscle spasms has generated considerable
interest. This drug is readily available and is used worldwide for the treatment of eclampsia. (See
'Management of autonomic dysfunction' above.)
● Patients with shorter incubation periods have increased disease severity and mortality. (See
'Prognosis' above.)
● Tetanus prophylaxis following a puncture wound is discussed in detail separately. The following
table summarizes the approach to tetanus prophylaxis (table 1). (See "Infectious complications of
puncture wounds", section on 'Tetanus immunization'.)
● Immunization of women who are pregnant or of childbearing age dramatically reduces neonatal
tetanus mortality. Improving hygiene during home births in resource-limited settings is also likely
to play an important role in preventing neonatal tetanus. (See 'Prophylaxis' above.)
Use of UpToDate is subject to the Subscription and License Agreement.
REFERENCES
1. Centers for Disease Control and Prevention (CDC). Tetanus surveillance --- United States,
2001-2008. MMWR Morb Mortal Wkly Rep 2011; 60:365.
2. Tejpratap SP, Tiwari MD. Tetanus. In: Manual for the Surveillance of Vaccine-Preventable Diseas
es, 6th ed, Roush SW, Baldy LM (Eds), Centers for Disease Control and Prevention, Atlanta, G
A 2008. http://www.cdc.gov/vaccines/pubs/surv-manual/chpt16-tetanus.html (Accessed on April
22, 2016).
3. Yen C, Murray E, Zipprich J, et al. Missed opportunities for tetanus postexposure prophylaxis--
California, January 2008-March 2014. MMWR Morb Mortal Wkly Rep 2015; 64:243.
4. Yaffee AQ, Day DL, Bastin G, et al. Notes from the Field: Obstetric Tetanus in an Unvaccinated
Woman After a Home Birth Delivery - Kentucky, 2016. MMWR Morb Mortal Wkly Rep 2017;
66:307.
5. Berger SA, Cherubin CE, Nelson S, Levine L. Tetanus despite preexisting antitetanus antibody.
JAMA 1978; 240:769.
6. Yen LM, Dao LM, Day NPJ. Management of tetanus: a comparison of penicillin and metronidazo
le. Symposium of antimicrobial resistance in southern Viet Nam, 1997.
7. Rushdy AA, White JM, Ramsay ME, Crowcroft NS. Tetanus in England and Wales, 1984-2000.
Epidemiol Infect 2003; 130:71.
8. Pedalino B, Cotter B, Ciofi degli Atti M, et al. Epidemiology of tetanus in Italy in years 1971-
2000. Euro Surveill 2002; 7:103.
9. McQuillan GM, Kruszon-Moran D, Deforest A, et al. Serologic immunity to diphtheria and

tetanus in the United States. Ann Intern Med 2002; 136:660.
10. Gergen PJ, McQuillan GM, Kiely M, et al. A population-based serologic survey of immunity to
tetanus in the United States. N Engl J Med 1995; 332:761.
11. Afshar M, Raju M, Ansell D, Bleck TP. Narrative review: tetanus-a health threat after natural
disasters in developing countries. Ann Intern Med 2011; 154:329.
12. Validation of neonatal tetanus elimination in Andhra Pradesh, India. Wkly Epidemiol Rec 2004;
79:292.
13. Talabi OA. A 3-year review of neurologic admissions in University College Hospital Ibadan,
Nigeria. West Afr J Med 2003; 22:150.
14. Woldeamanuel YW, Andemeskel AT, Kyei K, et al. Case fatality of adult tetanus in Africa:
Systematic review and meta-analysis. J Neurol Sci 2016; 368:292.
15. World Health Organization. Immunization surveillance, assessment and monitoring. Maternal an
d Neonatal Tetanus (MNT) elimination. http://www.who.int/immunization_monitoring/diseases/M
NTE_initiative/en/index.html (Accessed on March 14, 2011).
16. Thwaites CL, Beeching NJ, Newton CR. Maternal and neonatal tetanus. Lancet 2015; 385:362.
17. Lalli G, Bohnert S, Deinhardt K, et al. The journey of tetanus and botulinum neurotoxins in
neurons. Trends Microbiol 2003; 11:431.
18. Deinhardt K, Berninghausen O, Willison HJ, et al. Tetanus toxin is internalized by a sequential
clathrin-dependent mechanism initiated within lipid microdomains and independent of epsin1. J
Cell Biol 2006; 174:459.
19. Schiavo G, Benfenati F, Poulain B, et al. Tetanus and botulinum-B neurotoxins block
neurotransmitter release by proteolytic cleavage of synaptobrevin. Nature 1992; 359:832.
20. Caccin P, Rossetto O, Rigoni M, et al. VAMP/synaptobrevin cleavage by tetanus and botulinum
neurotoxins is strongly enhanced by acidic liposomes. FEBS Lett 2003; 542:132.
21. Farrar JJ, Yen LM, Cook T, et al. Tetanus. J Neurol Neurosurg Psychiatry 2000; 69:292.
22. Rummel A, Bade S, Alves J, et al. Two carbohydrate binding sites in the H(CC)-domain of
tetanus neurotoxin are required for toxicity. J Mol Biol 2003; 326:835.
23. Grund JM, Toledo C, Davis SM, et al. Notes from the Field: Tetanus Cases After Voluntary
Medical Male Circumcision for HIV Prevention--Eastern and Southern Africa, 2012-2015.
MMWR Morb Mortal Wkly Rep 2016; 65:36.
24. Gonzales y Tucker RD, Frazee B. View from the front lines: an emergency medicine perspective
on clostridial infections in injection drug users. Anaerobe 2014; 30:108.
25. Ergonul O, Egeli D, Kahyaoglu B, et al. An unexpected tetanus case. Lancet Infect Dis 2016;
16:746.
26. Centers for Disease Control and Prevention. Epidemiology and Prevention of Vaccine-Preventa
ble Diseases. Tetanus. https://www.cdc.gov/vaccines/pubs/pinkbook/tetanus.html (Accessed on
September 06, 2017).
27. Apte NM, Karnad DR. Short report: the spatula test: a simple bedside test to diagnose tetanus.
Am J Trop Med Hyg 1995; 53:386.
28. Doshi A, Warrell C, Dahdaleh D, Kullmann D. Just a graze? Cephalic tetanus presenting as a
stroke mimic. Pract Neurol 2014; 14:39.
29. Weinstein L. Tetanus. N Engl J Med 1973; 289:1293.
30. Idema CD, Harris BN, Ogunbanjo GA, Dürrheim DN. Neonatal tetanus elimination in
Mpumalanga Province, South Africa. Trop Med Int Health 2002; 7:622.
31. Roper MH, Vandelaer JH, Gasse FL. Maternal and neonatal tetanus. Lancet 2007; 370:1947.
32. Goulon M, Girard O, Grosbuis S, et al. [Antitetanus antibodies. Assay before anatoxinotherapy
in 64 tetanus patients]. Nouv Presse Med 1972; 1:3049.
33. Andreadou E, Kattoulas E, Sfagos C, Vassilopoulos D. Stiff person syndrome: avoiding

misdiagnosis. Neurol Sci 2007; 28:35.
34. Thwaites CL, Farrar JJ. Preventing and treating tetanus. BMJ 2003; 326:117.
35. Campbell JI, Lam TM, Huynh TL, et al. Microbiologic characterization and antimicrobial
susceptibility of Clostridium tetani isolated from wounds of patients with clinically diagnosed
tetanus. Am J Trop Med Hyg 2009; 80:827.
36. Ahmadsyah I, Salim A. Treatment of tetanus: an open study to compare the efficacy of procaine
penicillin and metronidazole. Br Med J (Clin Res Ed) 1985; 291:648.
37. Saltoglu N, Tasova Y, Midikli D, et al. Prognostic factors affecting deaths from adult tetanus. Clin
Microbiol Infect 2004; 10:229.
38. Johnson EA, Summanen P, Finegold SM. Clostridium. In: Manual of Clinical Microbiology, 9th ed
ition, Murray PR, Baron EJ, Jorgensen JH, et al (Eds), ASM Press, Washington DC 2007. Vol 1,
p.889.
39. Veronose R. Tetanus: Important new concepts. Excerpta Medica 1981; 183.
40. American Academy of Pediatrics. Tetanus (lockjaw). In: Red Book: 2009 Report of the Committe
e on Infectious Diseases, 28th, American Academy of Pediatrics, Elk Grove Village, IL 2009. p.6
55.
41. Miranda-Filho Dde B, Ximenes RA, Barone AA, et al. Randomised controlled trial of tetanus
treatment with antitetanus immunoglobulin by the intrathecal or intramuscular route. BMJ 2004;
328:615.
42. Liang JL, Tiwari T, Moro P, et al. Prevention of Pertussis, Tetanus, and Diphtheria with Vaccines
in the United States: Recommendations of the Advisory Committee on Immunization Practices
(ACIP). MMWR Recomm Rep 2018; 67:1.
43. Kapoor W, Carey P, Karpf M. Induction of lactic acidosis with intravenous diazepam in a patient
with tetanus. Arch Intern Med 1981; 141:944.
44. Engrand N, Guerot E, Rouamba A, Vilain G. The efficacy of intrathecal baclofen in severe
tetanus. Anesthesiology 1999; 90:1773.
45. Santos ML, Mota-Miranda A, Alves-Pereira A, et al. Intrathecal baclofen for the treatment of
tetanus. Clin Infect Dis 2004; 38:321.
46. Engrand N, Vilain G, Rouamba A, Benhamou D. [Value of intrathecal baclofen in the treatment
of severe tetanus in the tropical milieu]. Med Trop (Mars) 2000; 60:385.
47. Thwaites CL, Yen LM, Loan HT, et al. Magnesium sulphate for treatment of severe tetanus: a
randomised controlled trial. Lancet 2006; 368:1436.
48. Attygalle D, Rodrigo N. Magnesium as first line therapy in the management of tetanus: a
prospective study of 40 patients. Anaesthesia 2002; 57:811.
49. James MF, Manson ED. The use of magnesium sulphate infusions in the management of very
severe tetanus. Intensive Care Med 1985; 11:5.
50. Ceneviva GD, Thomas NJ, Kees-Folts D. Magnesium sulfate for control of muscle rigidity and
spasms and avoidance of mechanical ventilation in pediatric tetanus. Pediatr Crit Care Med
2003; 4:480.
51. Lipman J, James MF, Erskine J, et al. Autonomic dysfunction in severe tetanus: magnesium
sulfate as an adjunct to deep sedation. Crit Care Med 1987; 15:987.
52. Buchanan N, Smit L, Cane RD, De Andrade M. Sympathetic overactivity in tetanus: fatality
associated with propranolol. Br Med J 1978; 2:254.
53. Trujillo MH, Castillo A, España J, et al. Impact of intensive care management on the prognosis
of tetanus. Analysis of 641 cases. Chest 1987; 92:63.
54. Patel JC, Mehta BC. Tetanus: study of 8,697 cases. Indian J Med Sci 1999; 53:393.
55. Barlow JL, Mung'Ala-Odera V, Gona J, Newton CR. Brain damage after neonatal tetanus in a
rural Kenyan hospital. Trop Med Int Health 2001; 6:305.
Topic 5525 Version 34.0
GRAPHICS
Wound management and tetanus prophylaxis
Clean and minor wound All other wounds ¶

Previous doses
of tetanus Tetanus toxoid-
Human tetanus
Tetanus toxoid-
Human tetanus
toxoid* containing containing
immune globulin immune globulin ◊
vaccine Δ vaccine Δ
<3 doses or unknown Yes § No Yes § Yes
≥3 doses Only if last dose given No Only if last dose given No

≥10 years ago ≥5 years ago ¥
Appropriate tetanus prophylaxis should be administered as soon as possible following a wound but should be given
even to patients who present late for medical attention. This is because the incubation period is quite variable; most
cases occur within 8 days, but the incubation period can be as short as 3 days or as long as 21 days. For patients who
have been vaccinated against tetanus previously but who are not up to date, there is likely to be little benefit in
administering human tetanus immune globulin more than 1 week or so after the injury. However, for patients thought
to be completely unvaccinated, human tetanus immune globulin should be given up to 21 days following the injury; Td
or Tdap should be given concurrently to such patients.
DT: diphtheria-tetanus toxoids adsorbed; DTP/DTwP: diphtheria-tetanus whole-cell pertussis; DTaP: diphtheria-tetanus-
acellular pertussis; Td: tetanus-diphtheria toxoids absorbed; Tdap: booster tetanus toxoid-reduced diphtheria toxoid-acellular
pertussis; TT: tetanus toxoid.
* Tetanus toxoid may have been administered as DT, DTP/DTwP (no longer available in the United States), DTaP, Td, Tdap, or
TT (no longer available in the United States).
¶ Such as, but not limited to, wounds contaminated with dirt, feces, soil, or saliva; puncture wounds; avulsions; or wounds
resulting from missiles, crushing, burns, or frostbite.
Δ The preferred vaccine preparation depends upon the age and vaccination history of the patient:
<7 years: DTaP.
Underimmunized children ≥7 and <11 years who have not received Tdap previously: Tdap. Children who receive Tdap at
age 7 through 9 years should receive another dose of Tdap at age 11 through 12 years.
≥11 years: A single dose of Tdap is preferred to Td for all individuals in this age group who have not previously received
Tdap; otherwise, Td or Tdap can be administered without preference. Pregnant women should receive Tdap during each
pregnancy.
◊ 250 units intramuscularly at a different site than tetanus toxoid; intravenous immune globulin should be administered if
human tetanus immune globulin is not available. Persons with HIV infection or severe immunodeficiency who have
contaminated wounds should also receive human tetanus immune globulin, regardless of their history of tetanus
immunization.
§ The vaccine series should be continued through completion as necessary.
¥ Booster doses given more frequently than every 5 years are not needed and can increase adverse effects.
References:
1. Liang JL, Tiwari T, Moro P, et al. Prevention of Pertussis, Tetanus, and Diphtheria with Vaccines in the United States:
Recommendations of the Advisory Committee on Immunization Practices (ACIP). MMWR Recomm Rep 2018; 67:1.
2. Havers FP, Moro PL, Hunter P, et al. Use of tetanus toxoid, reduced diphtheria toxoid, and acellular pertussis vaccines:
Updated recommendations of the Advisory Committee on Immunization Practices - United States, 2019. MMWR Morb
Mortal Wkly Rep 2020; 69:77.
Graphic 61087 Version 34.0
Contributor Disclosures
Daniel J Sexton, MD Grant/Research/Clinical Trial Support: Centers for Disease Control and Prevention;
National Institutes of Health [Healthcare epidemiology]. Consultant/Advisory Boards: Magnolia Medical
Technologies [Medical diagnostics]; National Football League [Infection prevention]; Johnson & Johnson [Mesh-
related infections]. Equity Ownership/Stock Options: Magnolia Medical Technologies [Medical
diagnostics]. John G Bartlett, MD Nothing to disclose Meg Sullivan, MD Grant/Research/Clinical Trial
Support: Gilead Sciences [Pre-exposure prophylaxis for contraception (Tenofovir)]. Consultant/Advisory Boards:
Gilead Sciences [Pre-exposure prophylaxis for contraception (Tenofovir)].
Contributor disclosures are reviewed for conﬂicts of interest by the editorial group. When found, these are
addressed by vetting through a multi-level review process, and through requirements for references to be
provided to support the content. Appropriately referenced content is required of all authors and must conform to
UpToDate standards of evidence.
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Tetanus can present in one of four clinical patterns:

● A penetrating injury resulting in the inoculation of C. tetani spores

● Neonates (due to infection of the umbilical stump)

Tetanus can sometimes be confused with the following mimics.

Drug-induced dystonias such as those due to phenothiazines — Drug-induced dystonias often

Strychnine poisoning due to ingestion of rat poison — Accidental or intentional strychnine

Stiff-person syndrome — Stiff-person syndrome (SPS) is a rare neurologic disorder characterized

● Halting the toxin production

Halting toxin production

If a mixed infection is suspected, a first-, second-, or third-generation cephalosporin such as cefazolin

diphtheria toxoid-containing vaccines, commencing immediately upon diagnosis. Such vaccines

● (See "Tetanus-diphtheria toxoid vaccination in adults", section on 'Routine adult immunization'.)

Magnesium sulfate — Magnesium sulfate acts as a presynaptic neuromuscular blocker, blocks

Considerations in resource-limited settings — Critical care services are often unavailable or

SOCIETY GUIDELINE LINKS

INFORMATION FOR PATIENTS

● Basics topic (see "Patient education: Tetanus (The Basics)")

SUMMARY AND RECOMMENDATIONS

● Supportive care is the mainstay of management to avoid complications such as respiratory

● Antimicrobials play an adjunctive role in the therapy of tetanus. We recommend metronidazole

● Muscle spasms are controlled with sedation (usually benzodiazepines) or neuromuscular

Use of UpToDate is subject to the Subscription and License Agreement.

9. McQuillan GM, Kruszon-Moran D, Deforest A, et al. Serologic immunity to diphtheria and

29. Weinstein L. Tetanus. N Engl J Med 1973; 289:1293.

33. Andreadou E, Kattoulas E, Sfagos C, Vassilopoulos D. Stiff person syndrome: avoiding

Topic 5525 Version 34.0

Wound management and tetanus prophylaxis

Clean and minor wound All other wounds ¶

<3 doses or unknown Yes § No Yes § Yes

≥3 doses Only if last dose given No Only if last dose given No

Graphic 61087 Version 34.0

Conﬂict of interest policy

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