Critical illness neuromyopathy
Critical illness neuromyopathy (CINM) includes critical
illness neuropathy and critical illness myopathy, which
often co‑exist, but usually myopathy predominates. It is
common in the mechanically ventilated (25–60% patients
ventilated for >7 days) patients. Multiple pathogenic
factors are involved in its causation including axonopathy,
mitochondrial dysfunction, microvascular ischemia,
sodium channelopathy, catabolism, and immobility.
CINM is associated with sepsis, systemic inflammation,
poor glycemic control, steroids, neuromuscular blocking
agents, immobility, and malnutrition.[20] CINM presents as
flaccid quadriparesis with hypo or areflexia and confirmed
by nerve conduction and electromyography studies.[11,21]
Optimal therapy for this condition is unknown. Treatment
is usually supportive therapy with intensive glycemic control,
minimizing the use of corticosteroids and neuromuscular
blockade, early mobilization, neuromuscular stimulation,
electrolyte replacement, and optimizing nutrition. Nearly,
70% of survivors recover completely over 4–5 months.[22]
Low body mass index and wasting in COPD patients
predisposes to CINM and prevention and treatment need
early extubation with the use of NIV. Physiotherapy with
early mobilization of critically ill patients is a relatively new
management strategy advocated to address and to reduce
the disability associated with ICU‑acquired weakness.[23] This
therapeutic approach has been reported in clinical studies
and is recommended by the European Respiratory Society