💪 Chapter 68: Critical Illness Polyneuropathy & Myopathy (CIP/CIM)

Risk factors (sepsis, SIRS, steroids, neuromuscular blockers, hyperglycaemia) · Flaccid weakness · Failure to wean from ventilator · Preserved cranial nerves · Diagnosis: NCS/EMG · No specific treatment · Prevention: sedation holidays, early mobilisation · Differentiate from GBS

🔍 Core Concepts: CIP/CIM

📌 Definition
Acute polyneuropathy (CIP) and myopathy (CIM) complicating critical illness, especially sepsis, SIRS, and multiorgan failure. Presents with difficulty weaning from ventilator and limb weakness after non-neurological causes excluded.
⚠️ Risk Factors
Sepsis/SIRS (strongest), multiorgan failure, prolonged ICU stay (>4-7 days), hyperglycaemia, steroids, neuromuscular blockers, aminoglycosides, female sex, renal failure, hyperosmolarity.
🩺 Clinical Features
Symmetric flaccid weakness (proximal > distal), difficulty weaning from ventilator (respiratory muscle weakness), preserved cranial nerves, preserved bowel/bladder function. DTRs may be reduced or absent.
🔬 Diagnosis
CIP: axonal degeneration (sensory and motor). CIM: myopathy with sensory sparing. NCS/EMG: reduced CMAP and SNAP amplitudes (CIP), myopathic changes (CIM). Muscle biopsy shows myosin loss.
🆚 Differential Diagnosis
GBS (ascending weakness, albuminocytologic dissociation, history of preceding infection), residual sedation, metabolic disturbances (K, Mg, PO4), propofol infusion syndrome, disuse atrophy.
💊 Management & Prevention
No specific treatment. Prevent/treat sepsis, control glucose, sedation holidays, early mobilisation, minimise steroids and NMBAs. Supportive care, physiotherapy. Slow recovery over months.

🩺 Stepwise Approach: Suspected CIP/CIM

1
Exclude other causes of weakness
Check electrolytes (K, Mg, PO4), glucose, drug levels (sedatives, NMBAs). Consider GBS (LP: albuminocytologic dissociation, history of infection). Propofol infusion syndrome (acidosis, lipaemia).
2
Clinical assessment
Examination: symmetric flaccid weakness, areflexia/hyporeflexia, preserved cranial nerves (unlike GBS), preserved bowel/bladder function. Difficulty weaning from ventilator despite resolving lung pathology.
3
Electrophysiology (NCS/EMG)
CIP: reduced CMAP and SNAP amplitudes (axonal degeneration). CIM: reduced CMAP with normal SNAP, myopathic changes. Muscle biopsy shows myosin loss (CIM).
4
Prevention & management of risk factors
Treat sepsis aggressively, control hyperglycaemia (insulin infusion), minimise steroids and NMBAs (sedation holidays). Early mobilisation (passive/active physiotherapy).
5
Supportive care
Prolonged weaning from mechanical ventilation (slow, pressure support). DVT prophylaxis, nutritional support, pressure ulcer prevention. Speech/swallow therapy if bulbar weakness.
6
Prognosis & rehabilitation
Recovery over weeks to months. Severe axonal loss may have incomplete recovery. Mortality increased in CIP/CIM (associated with underlying sepsis/MOF).