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Acute, often fatal disease caused by exotoxins produced by Clostridia tetani. Characterised by generalized muscle rigidity, autonomic stability, and sometimes convulsions.


  • tetanus only occurs when spores of C. tetani gain access into tissues
  • usual mode of entry is through puncture wound or laceration. Injury itself is often trivial and in 20% of cases there is no evidence of wound
  • spores germinate from wound and toxin tetanospasmin is released into blood stream. It is then taken up into motor nerve endings and transported into CNS

Clinical presentation

  • incubation period 2-60 days, but usually <15
  • period of onset (time from first symptom to first spasm) also variable
  • presenting symptoms pain and stiffness
  • subsequently develop rigidity. Initially this is localised (lockjaw) but later becomes generalized
  • spasms are caused by external stimuli eg noise. As disease progresses even minor stimuli may trigger severe spasms
  • laryngeal spasm may occur and is life threatening

Autonomic dysfunction

- occurs in severe cases
- begins a few days after muscle spasms (toxin has further to diffuse to reach lateral horns of spinal cord)
- increased basal sympathetic tone: tachycardia, bowel and bladder dysfunction
- episodes of marked sympathetic overactivity involving both alpha and beta receptors. Vascular resistance, CVP and CO (usually) are increased. Manifestations include:

  • labile hypertension
  • pyrexia
  • sweating
  • pallor
  • cyanosis of digits

- episodes usually of short duration. May occur without provocation
- due to reduced inhibition of post-synaptic sympathetic fibres in intermediolateral cell column
- other postulated causes: loss of inhibition of adrenal medulla; direct inhibition by tetanospasm of release of endogenous opiates; increased release of thyroid hormone
- role of parasympathetic system unclear. Episodes of bradycardia, low TPR, low CVP and profound hypotension are seen. Frequently pre-terminal. Sudden and repeated cardiac arrests occur, especially in IV drug abusers. Have been attributed to total withdrawal of sympathetic tone as atropine has no effect. Alternative mechanisms: catecholamine-induced myocardial damage or direct brainstem damage

Differential diagnosis

- dystonic reaction to tricyclics
- strychnine poisoning
- local temporomandibular diseae
- local oral disease
- convulsions
- tetany
- intracranial infections or haemorrhage
- psychiatric disorders


Passive immunisation

- human antitetanus toxin: 3000-6000 U IV
- neutralizes only circulating toxin at best
- no prospective evidence of benefit
- meta-analysis suggests that intrathecal antitetanus toxin is ineffective and suitable intrathecal preparations are not available
- adverse effects of antitetanus toxin include: fever, shivering, chest/back pain, tachycardia and hypotension
- equine antitetanus serum can be used after testing and desensitization if human antitoxin not available

Eradication of organism

- through cleaning of wound and extensive debridement of necrotic tissue after antitoxin has been given
- antibiotics to destroy spores:

  • metronidazole 500mg IV 8 hrly for 10 days. More effective than penicillin
  • penicillin G 1-3 MU IV qds for 10 days. Penicillin is a central GABA antagonist and may aggravate spasms
  • erythromycin has been used but should not be routinely used

Suppression of effects of tetanospasmin

- ETT or tracheostomy if muscle spasms present
- ventilate if respiratory muscles involved
- muscle relaxants or deep sedation may be necessary to allow effective ventilation
- deep sedation not only may prevent spasms but may improve autonomic dysfunction
- traditionally combination of alpha and beta blockade used to treat sympathetic overactivity
- alpha blockade: phenoxybenzamine, phentolamine, bethanidine or chlorpromazine have been used
- unopposed beta blockade has resulted in death from acute CCF. Removal of beta mediated vasodilatation in limb muscles causes a rise in SVR which beta blocked myocardium may not be able to cope with
- esmolol can be used to control sympathetic crises but catecholamine levels remain high with continuing risk of myocardial damage
- catecholamine output can be decreased with benzodiazepines and opiates. Former increase affinity and efficacy of GABA while latter probably act by replacing deficient endogenous opiates. Very large doses may be required and are well tolerated
- magnesium has been used as an adjunct to sedation: aim for concentration of 2.5-4 mmol/L. Decreases SVR and HR with small decrease in CO. In animals decreases catecholamine secretion and decreases receptor sensitivity. Has additional advantage of neuromuscular blocking properties. Must be used with sedatives and calcium supplements may be required
- clonidine has been used to produce sedation and control of autonomic dysfunction
- intrathecal baclofen produces same result but causes significant respiratory depression in 1/3


- hypoxia
- complications of mechanical ventilation
- myoglobinuria and attendant problems
- sepsis, particularly pneumonia
- fluid and electrolyte problems (including SIADH)
- DVT and PE
- bed sores
- fractures: especially of mid-thoracic vertebrae (no clinical importance: no neurological complications, no pain and heal spontaneously without deformity)

Neonatal tetanus

- usually follows infection of the umbilical stump
- most often presents on day 7 of life with a short history of failure to feed
- spasms may be misdiagnosed as convulsions of another aetiology
- also vomiting (due to increased intra-abdominal pressure) and dehydration (because of inability to swallow) often result in meningitis and sepsis being considered first

Local tetanus

- uncommon mild form with mortality of 1%
- clinical features confined to a limb or muscle
- may be due to immunization
- Cephalic tetanus also rare. Results from injuries to head and neck, eye infections or otitis media. Cranial nerves, especially VII commonly involved. Prognosis poor. May progress to more generalized form.

Further reading

Lipman J, Oh TE. Tetanus. In Oh TE (ed), Intensive Care Manual, 4th ed. 1997 Butterworth Heinemann, Oxford, pp 423-7

© Charles Gomersall November 1999


©Charles Gomersall, April, 2014 unless otherwise stated. The author, editor and The Chinese University of Hong Kong take no responsibility for any adverse event resulting from the use of this webpage.
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