Critical Illness Neuromuscular Weakness (CINMW) is a spectrum of acquired neuromuscular disorders seen in ICU patients, most commonly Critical Illness Polyneuropathy (CIP) and
Critical Illness Myopathy (CIM).
It causes symmetric weakness of limb and respiratory muscles, leading to prolonged ventilation, delayed weaning, and higher morbidity/mortality.
π About
- Diffuse, symmetric limb and respiratory muscle weakness.
- Occurs in critically ill patients with sepsis, multi-organ failure, or prolonged ventilation.
- Delays rehabilitation and worsens quality of life post-ICU.
β οΈ Risk Factors
- Prolonged mechanical ventilation (immobility, sedation, NM blockers).
- Sepsis & SIRS (systemic inflammation damaging nerves/muscles).
- Corticosteroids (prolonged/high-dose β atrophy, myopathy).
- Neuromuscular blockers (especially non-depolarising, prolonged).
- Immobility (disuse atrophy).
- Multi-organ failure (e.g., ARDS, renal/hepatic failure).
- Hyperglycaemia (poor control worsens nerve injury).
- High severity of illness (higher APACHE II score = higher risk).
𧬠Types
- Critical Illness Polyneuropathy (CIP):
- Axonal sensorimotor neuropathy, often with sepsis/SIRS.
- Features: symmetric weakness, distal sensory loss, absent reflexes, respiratory involvement.
- Critical Illness Myopathy (CIM):
- Primary myopathy (fibre atrophy, necrosis, myosin loss); linked to steroids/NMBAs.
- Features: proximal > distal weakness, reflexes reduced/preserved, respiratory weakness.
- Overlap Syndrome: combination of CIP + CIM.
π Causes of Weakness in ICU (Differentials)
- π Medication-induced: corticosteroids, NMBAs, aminoglycosides, zidovudine, amiodarone.
- 𧬠Pre-existing neuromuscular disease: myasthenia gravis, Lambert-Eaton, polymyositis, mitochondrial myopathies.
- π§ Spinal cord pathology: ischaemia, compression (abscess/haematoma), trauma, transverse myelitis.
- π¦ Critical illness weakness: CIP, CIM, overlap syndrome.
- πͺ Muscle mass loss: cachexia, disuse atrophy, rhabdomyolysis.
- β‘ Electrolyte disorders: hypokalaemia, hypophosphataemia, hypermagnesaemia, hypercalcaemia, hyponatraemia.
- π Systemic illnesses: porphyria, HIV, vasculitis, paraneoplastic syndromes, toxins (organophosphates, heavy metals).
π©Ί Clinical Presentation
- Prolonged ventilator dependence (respiratory muscle weakness).
- Generalised flaccid weakness (quadriparesis/plegia).
- Reduced/absent reflexes (especially in CIP).
- Facial weakness may occur, but extraocular movements are usually preserved.
- Sensory loss in CIP (not in CIM).
- Alertness intact (distinguishes from central causes such as stroke or coma).
βοΈ Key Differentials
- Guillain-BarrΓ© Syndrome: Ascending weakness, areflexia, raised CSF protein.
- Rhabdomyolysis: CK >10,000, myoglobinuria, risk of AKI.
- Myasthenia Gravis: Fluctuating weakness, ocular/bulbar signs, preserved reflexes.
- Spinal Cord Injury: Weakness + sensory level, later spasticity.
- Electrolyte Disorders: Hypokalaemia, hypophosphataemia (reversible if corrected).
π§ͺ Investigations
- Bloods: FBC, U&E, LFTs, glucose, CK (mild β in CIM, very high in rhabdomyolysis), TFTs, B12/folate.
- Nerve Conduction Studies (NCS):
- CIP β β CMAP/SNAP amplitudes (axonal loss).
- CIM β normal sensory studies, reduced CMAPs.
- EMG: CIP = denervation; CIM = low-amplitude, short-duration MUAPs.
- CSF: If GBS suspected β albuminocytologic dissociation.
- Muscle biopsy: CIM = myosin loss, fibre necrosis; CIP = axonal degeneration.
- MRI spine: If spinal cord disease suspected.
π Management
- Optimise ICU care: minimise sedation, avoid prolonged NMBAs, judicious steroid use, strict glycaemic control.
- Early mobilisation: passive β active physiotherapy, OT input.
- Ventilator weaning: protocols, inspiratory muscle training.
- Nutrition: adequate protein/calories; prefer enteral feeds.
- Prevention: DVT prophylaxis, pressure sore prevention, contracture prevention.
- Rehabilitation: multidisciplinary (neuro, rehab, dietetics, psychology).
π Prognosis
- Most improve over weeksβmonths with rehabilitation.
- Some develop persistent weakness & disability, particularly if prolonged ICU stay.
- Early mobilisation and prevention strategies improve outcomes.
π References
- Bolton CF. Neuromuscular manifestations of critical illness. Muscle Nerve. 2005.
- Latronico N, Bolton CF. Critical illness polyneuropathy and myopathy. Lancet Neurol. 2011.
- Hermans G, et al. ICU-acquired weakness. Crit Care Med. 2008.
- Stevens RD, et al. Neuromuscular dysfunction in critical illness. Intensive Care Med. 2007.
- Schweickert WD, et al. Early PT/OT in ventilated ICU patients. Lancet. 2009.