What is the recommended treatment for critical‑illness polyneuromyopathy (CIPNM) in an adult ICU patient who is mechanically ventilated and receiving sedatives, including corticosteroids and neuromuscular blocking agents?

Treatment of Critical Illness Polyneuromyopathy (CIPNM)

There is no specific pharmacologic treatment for CIPNM; management focuses on prevention through strict glycemic control, early mobilization, minimizing corticosteroid and neuromuscular blocking agent exposure, and structured physiotherapy once the condition develops. 1, 2, 3

Primary Treatment Strategy: Prevention is Key

Since no curative pharmacologic therapy exists for CIPNM, the cornerstone of management is preventing its development through modifiable risk factor control 2, 4:

Glycemic Control

• Maintain blood glucose below 180 mg/dL in all mechanically ventilated ICU patients receiving neuromuscular blocking agents 1
• Strict glycemic control (80-110 mg/dL) was shown to be an independent protective factor against CIPNM development in surgical ICU patients, though this must be balanced against hypoglycemia risk (11.3% vs 1.8% with conventional therapy) 1
• Targeting 100-150 mg/dL may be advantageous in specific populations if achievable without significant hypoglycemia risk 1

Minimize Neuromuscular Blocking Agent Exposure

• Discontinue NMBAs as soon as clinically possible—administration beyond 1-2 days substantially increases CIPNM risk 5, 6
• Prolonged continuous infusion of NMBAs (particularly in medical ICU patients) is an independent risk factor for CIPNM 1
• When NMBAs are necessary, use cisatracurium as first-line due to organ-independent elimination and lower risk profile 6
• Implement daily drug holidays to reduce cumulative exposure 6
• Mandatory train-of-four (TOF) monitoring to optimize dosing and prevent excessive blockade 6

Corticosteroid Management

• Limit total corticosteroid doses to less than 1 gram methylprednisolone equivalent 5
• The combination of corticosteroids plus NMBAs dramatically increases CIPNM incidence to as high as 30% 5
• Use the lowest effective dose for the shortest duration necessary 2, 4

Active Treatment Once CIPNM Develops

Structured Physiotherapy Protocol

• Initiate a structured regimen of physiotherapy immediately upon diagnosis, even in patients still receiving NMBAs or sedation 1
• Early mobilization and physical rehabilitation are critical interventions that directly impact recovery 2, 4, 7
• For patients who can actively participate: bedside cycle ergometry and progressive resistance exercises 1
• For sedated or paralyzed patients: passive range-of-motion exercises for all extremities 1
• Rehabilitation should start as early as possible once diagnosis is established—delay from diagnosis to rehabilitation start correlates with worse functional recovery 7

Multicomponent Nonpharmacologic Interventions

• Implement an ABCDEF bundle approach (Awakening trials, Breathing coordination, Delirium monitoring, Early mobility, Family engagement) 1
• Cognitive stimulation: reorientation, use of clocks, music therapy 1
• Sleep optimization: minimize light and noise, reduce sedation 1
• Sensory support: enable use of hearing aids and eyeglasses 1
• These bundled interventions reduce delirium (OR 0.59,95% CI 0.39-0.88) and shorten ICU length of stay 1

Sedation Management

• Prefer dexmedetomidine over benzodiazepines for sedation in mechanically ventilated patients 8
• Target light sedation (RASS -1 to 0) using validated sedation scales 8
• Dexmedetomidine has opioid-sparing effects and may reduce delirium duration 8
• For patients with agitation preventing weaning: dexmedetomidine is specifically recommended 8

Diagnostic Confirmation and Monitoring

Clinical Assessment

• Use Medical Research Council (MRC) sum score—values <48 out of 60 define ICU-acquired weakness 5
• Handgrip strength: <10 kg at discharge and <15 kg at one month indicates significant weakness 5
• Monitor for characteristic features: flaccid paralysis, preserved sensory function, reduced/absent reflexes, marked muscle wasting 5

Electrophysiologic Studies

• Electromyography and nerve conduction studies are the gold standard for diagnosis 2
• Look for severely reduced compound motor action potential amplitudes with normal conduction velocities (distinguishing from demyelinating disorders like Guillain-Barré) 5
• Evidence of acute denervation on EMG confirms diagnosis 5

Critical Pitfalls to Avoid

Do not confuse CIPNM with Guillain-Barré syndrome—CIPNM is an axonal polyneuropathy with normal conduction velocities, whereas Guillain-Barré shows slowed conduction from demyelination 5. The clinical context (sepsis, prolonged ventilation, NMBA/corticosteroid exposure) and electrophysiology distinguish these conditions 5.

Do not delay rehabilitation—waiting for complete resolution of critical illness before starting physiotherapy worsens outcomes 7. Even patients on continuous NMBA infusions should receive passive range-of-motion exercises 1.

Do not use benzodiazepines for routine sedation—they increase delirium and may worsen neuromuscular outcomes compared to dexmedetomidine 8.

Prognosis and Long-Term Management

Recovery is prolonged and often incomplete 5, 2:

• 64% of ICU survivors have functional impairments at 3 months, 56% at 12 months 5
• Axonal injury requires extended convalescence periods 5
• Increased rehospitalization rates and ongoing morbidity are common 5
• Comprehensive rehabilitation combining established functional scales with ICF assessment is recommended for tracking recovery 7