WHAT IS TETANUS?

Tetanus is an acute, toxin-mediated disease caused by Clostridium tetani. Under favourable

anaerobic conditions, such as in dirty, necrotic wounds, this ubiquitous bacillus may produce
tetanospasmin, an extremely potent neurotoxin. Tetanus toxin blocks inhibitory
neurotransmitters in the central nervous system, resulting in muscular stiffness and spasms that
are typical of tetanus.

It is characterized by an acute onset of hypertonia, painful muscular contractions (usually of the
muscles of the jaw and neck), generalized muscle spasms without other apparent medical causes
and more ominously difficulty in breathing or opisthotonus

Tetanus is commonly known as lockjaw.

It is currently responsible for 1.2 million deaths in the developing world.

WHAT IS ITS CAUSATIVE AGENT?
Clostridium tetani or the tetanus bacillus is a slender, gram-positive, anaerobic rod that may
develop a terminal spore, giving it a drumstick appearance. The organism is sensitive to heat and
cannot survive in the presence of oxygen. The spores, in contrast, are very resistant to heat and
the usual antiseptics. They can survive autoclaving at 249.8F (121C) for 1015 minutes. The
spores are also relatively resistant to phenol and other chemical agents.

The spores are widely distributed in soil and in the intestines and feces of horses, sheep, cattle,
dogs, cats, rats, guinea pigs, and chickens. Manure-treated soil may contain large numbers of
spores. In agricultural areas, a significant number of human adults may harbor the organism. The
spores can also be found on skin surfaces and in contaminated heroin.

C. tetani produces two exotoxins, tetanolysin and tetanospasmin. The function of tetanolysin is
not known with certainty. Tetanospasmin is a neurotoxin and causes the clinical manifestations
of tetanus. On the basis of weight, tetanospasmin is one of the most potent toxins known. The
estimated minimum human lethal dose is 2.5 nanograms per kilogram of body weight (a
nanogram is one billionth of a gram), or 175 nanograms for a 70-kg (154lb) human.

HOW IS IT TRANSMITTED?
Tetanus is not directly transmitted from person to person. Tetanus occurs when the bacterium in
soil or dust is introduced into the body through a puncture wound, abrasion, laceration, burn or
contaminated injected recreational drugs. Tetanus may follow elective surgery, burns, deep
puncture wounds, crush wounds, otitis media, dental infection, animal bites, abortion, and
pregnancy. The presence of necrotic tissue and/or foreign bodies favors growth of the anaerobe
that produces the neurotoxin.

WHAT IS THE PATHOPHYSIOLOGY OF TETANUS?
C. tetani usually enters the body through a wound. In the presence of anaerobic (low oxygen)
conditions, the spores germinate. Toxins are produced and disseminated via blood and
lymphatics. Toxins act at several sites within the central nervous system, including peripheral
motor end plates, spinal cord, and brain, and in the sympathetic nervous system. The typical
clinical manifestations of tetanus are caused when tetanus toxin interferes with release of
neurotransmitters, blocking inhibitor impulses. This leads to unopposed muscle contraction and
spasm. Seizures may occur, and the autonomic nervous system may also be affected.
WHEN IS ITS INCUBATION PERIOD?
The incubation period varies from 321 days, with an average of eight days. In general the
further the injury site is from the central nervous system, the longer the incubation period. The
shorter the incubation period, the higher the chance of death will be. In neonatal tetanus,
symptoms usually appear from 4 to 14 days after birth, averaging about 7 days. Shorter
incubation periods (<7 days) along with delays in seeking treatment are associated with fatal
outcomes.

WHAT ARE THE SIGNS AND SYMPTOMS?

Tetanus is a clinical diagnosis characterized by a triad of muscle rigidity, muscle spasms and
autonomic instability. Early symptoms of tetanus include neck stiffness, sore throat, dysphagia
and trismus (lockjaw). Muscle spasms are extremely painful. They occur spontaneously but are
also provoked by touch, visual, auditory or emotional stimuli. Muscle spasms can be so intense
that they cause tendon rupture, joint dislocation and bone fractures. Spasm extending to the facial
muscles causes the typical facial expression, risus sardonicus. Truncal spasm causes
opisthotonus (rigid somatic muscles that lead to an arched-back posture). During prolonged
spasms, severe hypoventilation and life-threatening apnea may occur. Laryngeal spasms also
occur resulting in sudden airway obstruction and respiratory arrest.

Severe tetanus is associated with profound autonomic instability. This usually starts a few days
after the spasms and lasts 12 weeks. Increased sympathetic tone causes vasoconstriction,
tachycardia and hypertension. Autonomic storms are associated with raised catecholamine
levels. These alternate with episodes of sudden hypotension, bradycardia and asystole. Other
features of autonomic disturbance include salivation, sweating, increased bronchial secretions,
hyperpyrexia, gastric stasis and ileus.

On the basis of clinical findings, three different forms of tetanus have been described.
Local tetanus is an uncommon form of the disease, in which patients have persistent contraction
of muscles in the same anatomic area as the injury. These contractions may persist for many
weeks before gradually subsiding. Local tetanus may precede the onset of generalized tetanus but
is generally milder. Only about 1% of cases are fatal.

Cephalic tetanus is a rare form of the disease, occasionally occurring with otitis media (ear
infections) in which C. tetani is present in the flora of the middle ear, or following injuries to the
head. There is involvement of the cranial nerves, especially in the facial area.
The most common type (about 80%) of reported tetanus is generalized tetanus. The disease
usually presents with a descending pattern. The first sign is trismus or lockjaw, followed by
stiffness of the neck, difficulty in swallowing, and rigidity of abdominal muscles. Other
symptoms include elevated temperature, sweating, elevated blood pressure, and episodic rapid
heart rate. Spasms may occur frequently and last for several minutes. Spasms continue for 34
weeks. Complete recovery may take months.

Neonatal tetanus is a form of generalized tetanus that occurs in newborn infants. Neonatal
tetanus occurs in infants born without protective passive immunity, because the mother is not
immune. It usually occurs through infection of the unhealed umbilical stump, particularly when
the stump is cut with an unsterile instrument.


HOW IS IT DIAGNOSED?

There are currently no blood tests that can be used to diagnose tetanus. The diagnosis is based on
the presentation of tetanus symptoms and does not depend upon isolation of the bacteria, which
is recovered from the wound in only 30% of cases and can be isolated from patients without
tetanus. Laboratory identification of C. tetani can be demonstrated only by production of
tetanospasmin in mice.

The "spatula test" is a clinical test for tetanus that involves touching
the posterior pharyngeal wall with a sterile, soft-tipped instrument, and observing the effect. A
positive test result is the involuntary contraction of the jaw (biting down on the "spatula"), and a
negative test result would normally be a gag reflex attempting to expel the foreign object. A
short report in The American Journal of Tropical Medicine and Hygiene states that, in a patient
research study, the spatula test had a high specificity (zero false-positive test results) and a high
sensitivity (94% of infected patients produced a positive test result)

WHAT IS THE DRUG OF CHOICE?

Tetanus immune globulin (TIG) is recommended for persons with tetanus. TIG can only help
remove unbound tetanus toxin. It cannot affect toxin bound to nerve endings. A single
intramuscular dose of 3,000 to 5,000 units is generally recommended for children and adults,
with part of the dose infiltrated around the wound if it can be identified. Intravenous immune
globulin (IVIG) contains tetanus antitoxin and may be used if TIG is not available.

Because of the extreme potency of the toxin, tetanus disease does not result in tetanus immunity.
Active immunization with tetanus toxoid should begin or continue as soon as the persons
condition has stabilized.

Persons with wounds that are neither clean nor minor, and who have had 02 prior doses of
tetanus toxoid or have an uncertain history of prior doses should receive TIG as well as Td or
Tdap. This is because early doses of toxoid may not induce immunity, but only prime the
immune system. The TIG provides temporary immunity by directly providing antitoxin. This
ensures that protective levels of antitoxin are achieved even if an immune response has not yet
occurred.

Immunotherapy: if available, administer human TIG 500 units by intramuscular injection or
intravenously (depending on the available preparation) as soon as possible; in addition,
administer age-appropriate TT-containing vaccine, 0.5 cc by intramuscular injection at a separate
site. [Tetanus disease does not induce immunity; patients without a history of primary TT
vaccination should receive a second dose 12 months after the first dose and a third dose 612
months later.]

Antibiotic treatment: metronidazole is preferred (500 mg every six hours intravenously or by
mouth); Penicillin G (100,000200,000 IU/kg/day intravenously, given in 24 divided doses).
Tetracyclines, macrolides, clindamycin, cephalosporins and chloramphenicol are also effective.

Muscle spasm control: benzodiazepines are preferred. For adults, intravenous diazepam can be
given in increments of 5 mg, or lorazepam in 2 mg increments, titrating to achieve spasm control
without excessive sedation and hypoventilation (for children, start with doses of 0.10.2 mg/kg
every 26 hours, titrating upward as needed). Large amounts may be required (up to 600
mg/day). Oral preparations could be used but must be accompanied by careful monitoring to
avoid respiratory depression or arrest.

Magnesium sulphate can be used alone or in combination with benzodiazepines to control spasm
and autonomic dysfunction: 5 gm (or 75mg/kg) intravenous loading dose, then 23 grams per
hour until spasm control is achieved. To avoid overdose, monitor patellar reflex as areflexia
(absence of patellar reflex) occurs at the upper end of the therapeutic range (4mmol/L). If
areflexia develops, dose should be decreased.

Other agents used for spasm control include baclofen, dantrolene (12 mg/kg intravenous or by
mouth every 4 hours), barbiturates, preferably short-acting (100150 mg every 14 hours in
adults; 610 mg/kg in children; by any route), and chlorpromazine (50150 mg by intramuscular
injection every 48 hours in adults; 412 mg every by intramuscular injection every 48 hours in
children).

Autonomic dysfunction control: magnesium sulphate as above; or morphine. Note: -blockers
such as propranolol were used in the past but can cause hypotension and sudden death; only
esmalol is currently recommended.

NURSING CARE

To prevent tetanus, within 3 days of a puncture wound, patients with no
previoustetanus immunization require tetanus immune globulin or tetanus antitoxin for
temporary protection. Active immunization with tetanus toxoid is also provided. If the patient
had a previous immunization more than 5 years before the injury, a booster injection
of tetanus toxoid is warranted at the time of injury. Goals of treatment include neutralizing the
toxin, preventing complications, and eliminating the source of the toxin. Human tetanus immune
globulin is administered immediately. One-half of the dose is administered by infiltrating the
wound, and the remaining half is administered intramuscularly into three limbs. Active immunity
is given by administering tetanustoxoid at a site remote from the globulin injections. The
affected wound is thoroughly dbrided after the antitoxin has been administered. Cultures of the
wound may be obtained at that time. Parenteral antibiotics (penicillin in particular if the patient
has no allergies to the drug) are administered for 10 days.

Nursing care focuses on maintaining a patent airway, regular breathing, and adequate circulation
and on providing comfort management, protection from injury, and psychosocial support of the
patient and family. If muscle spasms or seizure activity places the patient at risk for airway
compromise, use the chin lift or jaw thrust to maintain an open airway if possible. Insert an oral
or nasal airway before seizures, but if the patient has lockjaw do not attempt to force an airway
in place because you may injure the patient and worsen the airway patency. Have intubation and
suction equipment immediately available at the bedside should the patient require it. Anchor the
endotracheal tube firmly, and document the lip level of the endotracheal tube in the progress
notes for continuity.

Institute seizure precautions as soon as the patient is admitted to the unit. Pad the side rails of the
bed, and provide immediate access to oxygen, suction, intubation equipment, artificial airways,
and a resuscitation bag. Place the patient in a quiet, dark room to reduce environmental stimuli.
Position the patient who is unconscious or paralyzed from pharmacologic agents in a side-lying
position and turn the patient every 2 hours.

Provide clarification of information about the patients diagnosis, prognosis, and treatment to the
patient and family. Make sure that the family has adequate time for expression of their feelings
each day. Support effective coping mechanisms and provide appropriate referrals to the chaplain,
clinical nurse specialist, or counselor if the patient or family demonstrates ineffective coping
behaviors.

Nursing care plan discharge and home health care guidelines
Teach the patient and family that tetanus is a preventable disease. Inform them of the appropriate
immunization and booster schedule, and encourage them to follow it. Note that the patient may
experience pain, tenderness, redness, and muscle stiffness in the limb in which
the tetanus injection(s) is (are) given. Explain that the convalescent period following tetanus may
be prolonged. The patient may need multidisciplinary rehabilitation and home nursing.