Sunday, October 16, 2016

A Case OF Tetanus



A 26-year-old male presented to the Accident and Emergency Department with a stiff jaw and being unable to open his mouth. Three days previously he was immunized with tetanus toxin after lacerating his finger at work.  On examination, he had evidence of ‘lock jaw’. His injured finger was swollen, painful and exuding pus.

What is the immediate management?
a. Debridement and cleansing of the wound.
b. Injection of tetanus antitoxin into the wound.
c. Oral penicillin V.
d. Intramuscular human tetanus immunoglobulin.
e. Intravenous pancuronium.

Answer:
d. Intramuscular human tetanus immunoglobulin

Discussion: Tetanus is caused by the anaerobic, Gram-positive bacillus Clostridium tetani. The organism produces spores that are commonly found in soil and faeces of domestic animals. Soil is the natural habitat for C. tetani. The organism gains entry into the body through traumatic wounds, where it multiplies under anaerobic conditions and produces tetanospasmin, a potent
neurotoxin. The toxin reaches the spinal cord via the blood or by retrograde axon transport and increases excitability in motor neurones by interfering with the function of inhibitory neurones. The toxin may also produce overactivity of the sympathetic nervous system.

The incubation period after injury is less than 14 days and can be as early as 2 days.

The dominant features of tetanus are rigidity and reflex spasms. Rigidity may affect any muscle, including the jaw muscles, so the mouth cannot be fully opened, as in this case. This is known as ‘trismus’ or ‘lock jaw’. Stiffness may affect the facial muscles, altering facial appearance. Risus sardonicus (pursing of the lips with retraction of the angles of the mouth) is a characteristic feature of this phenomenon. Pharyngeal involvement may produce dysphagia early in the disease. Rigidity of the muscles of the back causes the body to curve back excessively with the head fully retracted (ophisthotonus). Reflex spasms are a sudden exacerbation of underlying rigidity which last 1–2 seconds. The time of onset of spasms from the first symptoms of rigidity is known as the ‘period time’. This is usually within 72 hours. The shorter the period time, the worse the prognosis. Large
groups of muscles are affected at any one time. Relaxation may take a few seconds, which is particularly hazardous when thoracic muscles are involved because respiration is impeded until relaxation of the muscles occurs. Laryngeal spasm is probably the most dangerous event in tetanus.
Autonomic overactivity has effects on the cardiovascular system. Tachycardia, massive swings in
blood pressure and cardiac arrhythmias are recognized complications. Haemodynamic instability may produce hypoperfusion of vital organs leading to multi-system failure and death. Most deaths are from respiratory failure, either due to laryngeal spasms, respiratory muscle fatigue and paralysis or pulmonary aspiration.

The mainstay of treatment in an affected individual is to give intramuscular human immunoglobulin immediately. Human immunoglobulin will remove circulating tetanospasmin from the blood. Fixed neurotoxin has to be removed from the wound by aggressive cleansing and, if necessary, by surgical debridement of the wound. Despite such measures the organism may not be entirely removed
from the wound and added protection with intravenous penicillin is mandatory. Diazepam is useful in controlling spasms. In severe cases total paralysis with curarization (using intravenous pancuronium) and artificial ventilatory support are necessary to reduce mortality from respiratory failure.

Prevention is by active immunization and meticulous wound cleansing as soon as possible after trauma.

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