79. Tetanus

Question 1

A 47-year-old farmer presents with dysphagia, malaise and muscle
pains, following a minor accident at work 6 days earlier.

Tell me some causes of dysphagia

Answer 1

It is useful to have some form of sieve for an answer like this that you may not
have directly thought about before. You will know most of the causes, but
delivering them in a structured format will impress.

Mechanical
Benign internal stricture, e.g. oesophageal web
Malignant internal stricture, e.g. oesophageal/gastric cancer
Extrinsic pressure, e.g. lung cancer, retrosternal goitre
Pharyngeal pouch

Motility problems Bulbar palsy
Pseudobulbar palsy
Achalasia
Systemic sclerosis
Myasthenia gravis
Rare infective causes, e.g. tetanus, Chagas’ disease

Others Oesophagitis

Question 2

What is the likely diagnosis in this farmer?

Answer 2

The most likely diagnosis from the history is tetanus

Question 3

What is the causative organism?

Answer 3

The disease is caused by exotoxins produced by Clostridium tetani, an obligate
anaerobic, spore-bearing, Gram-positive bacillus.

The spores exist in the soil and in the gastrointestinal tract of humans and animals.

The organism is non-invasive, but the spores can gain entry through wounds, ulcers etc. where they can proliferate and produce the toxins tetanospasmin (an extremely
potent protein) and tetanolysin.

In 20% no entry site is identified..

Tetanospasmin is taken up and transmitted by motor neurones to the central
nervous system where it preferentially binds to GABA inhibitory
interneurones.

Tetanospasmin cleaves synaptobrevin preventing neurotransmitter release thereby blocking these pathways and allowing uninhibited afferent stimuli.

C. tetani is difficult to culture and only identified in about one-third of cases.

Question 4

What is the natural course of the disease?

Answer 4

The incubation period is between 3 and 21 days (average 7 days). There is a
prodrome of non-specific stiffness, fever, malaise, headache and dysphagia.
This is followed by the classical symptoms of:

1. Trismus ‘Lockjaw’ due to masseter spasm
2. Risus sardonicus Rigidity and spasm in the facial muscles
3. Opisthotonus
   Arched body secondary to paravertebral muscle spasm
4. Painful spasms may eventually compromise respiration
5. Sympathetic overactivity
   Tachycardia, arrhythmias, paroxysmal
   hypertension, sweating, pyrexia and
   gastrointestinal stasis.

The spasms can be precipitated by noise, handling or even light. Several
grading systems of severity of the disease are in use but the most widely used
is that proposed by Ablett (Grades I–IV represent mild to very severe).

Question 5

How would you treat this man?

Answer 5

In the first instance an ABC approach is adopted and further management
guided by clinical findings.

The wound should be cleaned and debrided.

Give metronidazole for 7–10 days to eradicate the causative organism.
Penicillin use results in significantly worse mortality rates.

To neutralise the free toxin, human tetanus immunoglobulin is given i.m.
General nursing care is very important. These patients should be nursed in a
quiet, isolated, darkened room.

Diazepam or chlorpromazine should be given initially to try and control the
spasms.
Dantrolene and intrathecal baclofen have been used in the treatment of
tetanic spasms.

Magnesium may also be used to control spasms.
Intensive care may be indicated with paralysis and ventilation.
Ventilation is likely to be prolonged if required and early tracheostomy
should be considered.
Autonomic dysfunction often occurs after the onset of respiratory
symptoms. Treatment with -blockers is controversial since their use has
been associated with sudden cardiac arrest and unresponsive hypotension.
Esmolol, because it is short acting, may be the most suitable drug in this
class.
Other general ICU measures include nutritional support and
thromboprophylaxis.
Mortality, even with supportive intensive care, is around 11%
Patients die from aspiration, hypoxia, respiratory failure and cardiac arrest.