FRCA Notes

ICU-Acquired Weakness

This topic was an SAQ way back in March 2015 (30% pass rate). Marks were available for definition, classification, risk factors, clinical features, the interpretation of nerve conduction studies and management.

Resources

  • ICU-acquired weakness (ICUAW) can be defined as:

    • Clinically detectable weakness in a critically ill patient, in whom there is no plausible alternative aetiology

  • It develops as a secondary disorder while patients are being treated for other critical illness
  • It is felt to be distinct from a severe disuse muscle atrophy
  1. Critical illness polyneuropathy (CIP)

  2. Critical illness myopathy (CIM)
    • Can be further sub-classified e.g. cachectic myopathy, thick filament myopathy, necrotising myopathy

  3. Critical illness neuro-myopathy (CINM) i.e. a combination of both neurogenic and myogenic disturbances

  • Precise prevalence is difficult to describe owing to varying study populations and diagnostic criteria
  • The prevalence in patients in patients with MODS, septic shock or prolonged (>7 days) mechanical ventilation is in the region of 45%
  • It may be lower in other patient groups, e.g. ∽35% in those with severe ECOPD or status asthmaticus


Pathology Interventional factors Patient factors
Septic shock Vasopressors ↑ age
Multi-organ failure Steroids (any) Female gender
Prolonged mechanical ventilation >7 days / immobility NMBA (any) ↓ albumin
Increased duration of critical illness Aminoglycosides Pre-morbid obesity
Increased severity of illness Need for RRT
Hyperglycaemia Need for TPN


  • The pathophysiology is complex and multimodal in its nature

CIP

  • Leading hypothesis is that CIP is a manifestation of peripheral nervous system organ failure
  • It results from the common pathological processes associated with systemic inflammation, e.g.:
    • Reduced oxygen and nutrient delivery to the axon
    • Macrocirculatory impairment (reduce CO, vasodilation, hypotension)
    • Microcirculatory impairment (endothelial dysfunction, tissue oedema, shunting)

CIM

  • Initial, early decline in muscle strength arises from functional changes:
    • Reduced membrane excitability
    • Decreased synthesis and function of contractile proteins
    • Altered SR function due to reduced calcium uptake/release
    • Mitochondrial dysfunction
    • Increased intracellular glutamine levels

  • Longer-term weakness arises from structural changes
    • There is decreased free intracellular glutamine in skeletal muscle, and decreased protein synthesis
    • Insulin administration causes increased myofibrillar protein synthesis

  • Onset of weakness only after onset of critical illness/ ICU admission
  • Cause of weakness not related to other pathology
  • Typically present beyond the first week of ICU stay

Pattern of weakness

  • Generalised
  • Symmetrical
  • Affects limb muscles proximally > distally
  • Affects respiratory muscles including diaphragm with difficulty weaning from ventilatory support
  • Typically there is sparing of the facial and ocular muscles and cranial nerves

Associated features

  • Reduced muscle tone i.e. flaccid weakness
  • Hyporeflexia: reduced (or normal) deep tendon reflexes
  • Loss of muscle mass
  • Normal conscious level
  • Normal autonomic function
  • MRC power score <48

  • CK - elevated in CIM
  • LP for CSF; may be slightly elevated protein in CIP
  • Nerve conduction studies;
    • Reduced CMAP and SNAP in CIP, but normal conduction velocities/amplitudes
    • Reduced CMAP in CIM, but else normal
  • EMG
    • Assesses motor unit potential (MUP)
    • CIP: long duration, high-amplitude polyphasic MUP
    • CIM: short duration, low-amplitude MUP with early recruitment

  • Muscle biopsy
  • Nerve biopsy
  • MRI brain & spinal cord

  • No intervention has been shown prospectively to improve outcome from ICUAW, so the management of all ICU patients should be to prevent its development
  • Previously early physiotherapy has been recommended, though this may not add benefit and increase risk of adverse events (TEAM ICU, 2022)

  • Avoid risk factors:
    • Avoid hyperglycaemia
    • Avoid early PN
    • Minimise sedation
    • Encourage early mobilisation
    • Good nutrition

  • Neuromuscular electrical stimulation


Short-term Long-term
Sux.-induced hyperkalaemic cardiac arrest ↓ physical functioning
↑ ICU & hospital mortality ↑ Post-ICU mortality
↑ ICU & hospital length of stay ↓ discharge home
↑ hospital costs ↑ discharge to other hospital/rehab centre
↑ mechanical ventilation ↑ rehabilitation LOS
↑ extubation failure
↑ dysphagia


  • Mortality
    • 45% of those who develop ICUAW will die during their admission
    • Of those who survive to discharge, 20% will die within one year

  • Of those who survive to hospital discharge:
    • 60-70% have full recovery
    • 28% have long-term disability