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ICU acquired weakness

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ICU acquired weakness

Updated February 2015 by Charles Gomersall

Difficult to distinguish between critical illness polyneuropathy and critical illness myopathy and it may be preferable to group the two together as ICU acquired weakness

Epidemiology

  • occurs in 25-63% of patients who have been mechanically ventilated for 1 week
    • 70-100% of those who are also septic
  • rare in children
  • more common in females
  • associated with:
    • sepsis, SIRS
    • multiorgan dysfunction
    • neuromuscular blocking agents
    • corticosteroids (in some but not all studies)
    • hyperglycaemia (independent factor in one trial)
    • cytotoxics
    • status asthmaticus with neuromuscular blockade

Pathophysiology

Critical illness myopathy

  • primary myopathy
  • microvascular ischaemia
  • catabolism
  • immobility

Critical illness polyneuropathy

  • predominantly motor neuropathy
  • secondary myopathy due to denervation
    • proposed mechanisms:
    • microvascular injury with nerve ischaemia
    • dysfunction of sodium channels
    • nerve mitochondrial injury

Clinical features

  • often presents with difficulty in weaning
  • flaccid
  • symmetrical weakness predominantly affecting limbs and respiratory muscles
    • tends to cause distal muscle weakness (as do inflammatory, diabetic, porphyria neuropathy), particularly affecting lower limbs
    • cranial nerves unaffected (cf Guillain Barre) - in common with other axonal neuropathies. Discrepancy between facial grimacing and decreased limb movement on painful stimulus often striking
    • reflexes usually disappear during the course of the illness but absent reflexes are not a prerequisite for diagnosis
  • no/little sensory disturbance
  • subclinical in 50%
  • NB features may be modified by presence of co-existing septic encephalopathy

Investigations

  • EMG & nerve conduction
     
    Critical illness polyneuropathy Critical illness myopathy
    Normal to minimally reduced nerve conduction velocity
    Reduced amplitude of muscle compound action potentials
    Decreased amplitude of sensory nerve action potentials
    Normal to minimally reduced nerve conduction velocity
    Reduced amplitude of muscle compound action potentials
    Reduced muscle excitability on direct stimulation
    Increased duration of muscle compound action potentials
    Normal sensory nerve action potentials
  • muscle biopsy
  • CPK: normal or near normal in most patients
  • CSF: at most, mildly raised protein

Differential diagnosis

  • Guillain-Barre syndrome
  • other causes of predominant motor neuropathy (eg lead poisoning, botulism)
  • diabetic neuropathy
  • porphyria
  • acute quadriplegic myopathy
    • more common in patients with severe asthma treated with high dose corticosteroids but may occur in the absence of steroid use
    • sensation and reflexes relatively spared
    • may be distinguished from critical illness polyneuropathy and myopathy by EMG
    • CPK elevated
  • acute cervical myelopathy
  • myasthenia gravis

Prevention

  • subgroup analysis suggests that intensive insulin therapy/tight glucose control may reduce the incidence but not generally recommended simply to prevent ICU acquired weakness
  • early mobilization

Treatment

  • no specific treatment
  • treat underlying condition

Prognosis

  • associated with increased mortality, prolonged mechanical ventilation and prolonged rehabilitation
  • in patients who required prolonged mechanical ventilation neuromuscular recovery is typically prolonged and incomplete

Further reading

Kress JP, Hall JB. ICU-acquired weakness and recovery from critical illness. N Engl J Med, 2014; 370:1626-35


© Charles Gomersall December 1999, May 2007, February 2015


©Charles Gomersall, February, 2015 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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