TETANUS

INTRODUCTION
Tetanus is an infectious disease caused by Clostridium tetani, an anaerobic, gram positive
and spore forming rod which is found in soil-most frequently in cultivated soil. The organism
produces two exotoxins; hemolysin and tetanospasmin, the later is a neurotoxin that is
responsible for the clinical manifestation of tetanus disease. Tetanus may be categorized into
the following four clinical types such as generalized tetanus, localized tetanus, cephalic
tetanus and neonatal tetanus. The most common type is generalized tetanus which is
responsible for 80% of cases. It results from the haematogenous spread of the toxin.
1,2

The global incidence of tetanus is still estimated at one million cases annually, with a case
fatality ratio ranging from 6% to 72% depending on the availability of well equipped
intensive care unit. The incidence of tetanus in the developed world is markedly low and is
no longer responsible for significant mortality, this has been attributed to high level of health
awareness in terms of vaccination and availability of human and material resources to
manage the disease. Meanwhile in developing countries tetanus is common in the young due
to lack of effective immunization program and appropriate treatment of injuries. In Indonesia
tetanus incidence rate in urban areas is around 6-7/1000 live births, while the rate in rural
areas is around 11-23/1000 live births by the number of deaths of approximately 60,000
babies each year. The most likely reason is because of the difference in the ease of reaching
health care facilities, the level of knowledge, and awareness to quickly refer the child to the
clinic, as well as the geographical difficulties between urban and rural.
2,3

C. tetani usually enters the body through a wound. In the presence of anaerobic (low
oxygen) conditions, the spores germinate. Tetanospasmin which is an extremely potent
neurotoxin is produced and disseminated via blood and lymphatics. Tetanospasmin 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. The incubation period ranges from 3 to 21 days, usually about 8 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.
4,6
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. 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. During prolonged spasms, severe hypoventilation and
life-threatening apnoea may occur. Laryngeal spasms also occur resulting in sudden airway
obstruction and respiratory arrest.
6

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.
6

No specific laboratory tests exist for determining the diagnosis of tetanus. The diagnosis
is clinically based on the presence of trismus, dysphagia, generalized muscular rigidity,
spasm, or combinations thereof. Blood counts and blood chemical findings are unremarkable.
Laboratory studies may demonstrate a moderate peripheral leukocytosis. The spatula test is a
simple diagnostic bedside test that involves touching the oropharynx with a spatula or tongue
blade. In normal circumstances, it elicits a gag reflex, and the patient tries to expel the spatula
(ie, a negative test result). If tetanus is present, patients develop a reflex spasm of the
masseters and bite the spatula (ie, a positive test result).
5,9

The goals of treatment in patients with tetanus include the following:
Initiating supportive therapy
Debriding the wound to eradicate spores and alter conditions for germination
Stopping the production of toxin within the wound
Neutralizing unbound toxin
Controlling disease manifestations
Managing complications
Patients should be admitted to an intensive care unit (ICU). The most important early
aspects of treatment, after airway protection, is passive immunotherapy with human tetanus
immunoglobulin to eliminate as much of the toxin burden as possible. The source of toxin
should be eradicated by debridement. Although the disease is caused by the toxin and not
active infection, the use of antibiotics may be of help, particularly when there is
osteomyelitis. Penicillins are the most frequently used antibiotics although metronidazole
may be useful. Administration of antispasticity agents is the major element of treatment to
compensate for the failure of central nervous system inhibition. These drugs are GABA-A
agonists, thereby functioning as indirect antagonists of the effect of the toxin on inhibitory
systems. Diazepam is used most commonly in managing tetanus in children. Lorazepam may
be preferable because of its longer duration of action.
7,10

Finally, supportive care until recovery occurs by the formation of new synapses is
essential to minimize the risk of precipitating spasms. The patient's room should be as quiet
and dark as possible. Active immunization should be initiated prior to hospital discharge.
7,8,