Intensive care unit-acquired weakness

The following statements regarding intensive care unit (ICU)-acquired weakness are

true EXCEPT which one?

a) The incidence of critical illness polyneuropathy among septic shock patients on the

ICU is 80%

b) Muscles of facial expression are spared by critical illness polymyopathy

c) Presence of normal deep tendon reflexes does not eliminate the diagnosis of critical

illness polyneuropathy

d) Persistent hyperglycaemia is an independent risk factor for ICU-acquired weakness

e) Electrophysiological studies typically show a reduced nerve conduction velocity

Answer: e

Explanation

Acquired weakness is common among intensive care unit patients especially in those

who have suffered systemic inflammatory conditions with multiorgan dysfunction.

The exact aetiology remains to be elucidated but the demonstration of cytokineinitiated

skeletal muscle breakdown does imply a chemical messenger-mediated

process. The distinction between critical illness polyneuropathy and critical illness

polymyopathy depends on detailed electroneurography, needle electromyography

and a muscle biopsy. The exact clinical relevance of these invasive studies is debated

given that therapeutic interventions are limited and are not specific to either variant.

Focus should be on recognition of the at-risk population, preventative measures and,

once symptomatic, exclusion of other (even pre-morbid) neurological conditions

before arriving at the diagnosis. Risk factors are sepsis and other causes of systemic

inflammation, multiorgan dysfunction, predicted prolonged immobility or ventilator

dependence, hyperglycaemia and use of corticosteroids or non-depolarising muscle

relaxants. Preventative measures involve avoiding those risks if possible and using

minimal sedation techniques with frequent sedation holds to reduce complete immobility.

Passive muscle exercises, ventilator-weaning regimens and optimising electrolytes

and nutrition are also beneficial. In those patients who are able to co-operate with

physical examination, serial neurological examination demonstrating symmetrical

weakness with facial muscle sparing may obviate the need for invasive studies providing

a slow improvement is demonstrable. In other circumstances, electrophysiological

studies with or without muscle biopsy are required for diagnosis. In both critical illness

polyneuropathy and myopathy, nerve conduction velocity is normal. However, in the

neuropathy, compound muscle action potential and sensory nerve action potential are

reduced. Differential diagnoses to be considered are diabetic neuropathy, porphyria,

Guillian–Barré syndrome, myasthenic syndromes, subacute combined degeneration of

the cord or muscular dystrophy. Also recall that low plasma phosphate, sodium, and

potassium concentrations can be responsible for significant muscular weakness.