ICU-acquired weakness: what is preventing its rehabilitation in critically ill patients?

Table 1 Clinical, electrophysiological, and histological features of intensive care unit-acquired weakness (ICUAW)

Investigation	CIP	CIM	CINM
Physical examination	Distal muscle weakness	Proximal muscle weakness	Proximal and distal muscle weakness
	Distal sensory deficit	Normal sensory testing	Distal sensory deficit
	Normal or depressed deep tendon reflexes	Normal or depressed deep tendon reflexes	Depressed deep tendon reflexes
Electrophysiology studies	Decreased CMAP and decreased SNAP	Decreased CMAP and normal SNAP	Decreased CMAP and SNAP
	Normal MUAP	Decreased MUAP	Decreased MUAP
	Normal or near-normal conduction velocity	EMG shows short duration, low amplitude activity	EMG shows short duration, low-amplitude activity
Histology	Axonal degeneration of distal motor and sensory nerves	Thick filament (myosin) loss, type II fiber (fast twitch) atrophy, necrosis	Axonal degeneration and evidence of loss in myosin, type II fiber atrophy, and necrosis

CIM = critical illness myopathy; CINM = critical illness neuromyopathy; CIP = critical illness polyneuropathy; CMAP = compound muscle action potential; EMG = electromyography; MUAP = muscle unit action potential; SNAP= sensory nerve action potential.

ISSN: 1741-7015