Critical illness polyneuropathy and myopathy (ICU-acquired weakness) !

Severe weakness that develops in very sick patients in intensive care because nerves and muscles are damaged, making it hard to wean from the ventilator.

Updated 2026-11-01

Structures involved

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Why it happens

What it is

ICU-acquired weakness is generalised, symmetric, flaccid weakness that appears during critical illness with no other explanation. It includes critical illness polyneuropathy (axonal damage to sensory and motor nerves), critical illness myopathy (primary muscle damage) and, often, both together (polyneuromyopathy).

Who gets it

Common in intensive care: it is reported in roughly a quarter to a half of patients ventilated for a week or more and in up to two thirds of patients with sepsis and multiple organ failure. It is seen in ICUs across Colombia and Latin America, where long ventilation and sepsis are frequent; it is often recognised only when weaning fails.

Causes

Sepsis and systemic inflammatory response
Multiple organ failure
Prolonged mechanical ventilation and immobility
Corticosteroids, especially combined with non-depolarising neuromuscular blockers (mainly myopathy)
Hyperglycaemia

Risk factors

Severity of illness and multiple organ dysfunction
Sepsis
Long duration of ventilation and bed rest
High-dose corticosteroids
Prolonged neuromuscular blockade
Poor glucose control
Older age and pre-existing frailty

Pathophysiology

Inflammation impairs the microcirculation of nerves and muscles, increases vascular permeability and leads to energy failure in axons, producing axonal degeneration. In muscle, sodium channels become inexcitable (an acquired channelopathy), thick (myosin) filaments are lost, and catabolism and disuse cause atrophy. Corticosteroids and denervation from blockers make muscle more susceptible. Respiratory muscles are involved, which delays weaning.

Classification

Critical illness polyneuropathy (CIP): axonal sensorimotor neuropathy
Critical illness myopathy (CIM): including thick-filament myosin loss and necrotising forms
Combined critical illness polyneuromyopathy

Symptoms and signs

Symmetric flaccid weakness of the limbs, worse proximally in myopathy and distally in neuropathy
Reduced or absent tendon reflexes (often preserved in pure myopathy)
Muscle wasting
Failure to wean from the ventilator
Distal sensory loss in polyneuropathy
Facial muscles relatively spared; patient may grimace to pain but not move limbs

Diagnosis

Clinical: Suspected in an alert, cooperative ICU patient with generalised weakness. Manual muscle testing with the Medical Research Council (MRC) sum score; a score below 48 out of 60, measured more than once, defines ICU-acquired weakness. Handgrip dynamometry is a quick alternative.
Tests: Nerve conduction studies and EMG: reduced motor and sensory amplitudes in polyneuropathy; reduced motor amplitudes with normal sensory responses and inexcitable muscle on direct stimulation in myopathy. CK is normal or mildly raised. Muscle biopsy (loss of myosin filaments) is reserved for unclear cases. Electrolytes, magnesium and phosphate are checked.
Imaging: Not routinely needed; brain or spine MRI when central causes are suspected. Muscle ultrasound can track loss of muscle thickness.

Differential diagnosis

Guillain-Barré syndrome
Myasthenia gravis and prolonged neuromuscular blockade
Botulism and Lambert-Eaton syndrome
Spinal cord injury or compression
Brainstem stroke
Electrolyte disorders (low potassium, phosphate or magnesium) and rhabdomyolysis

Goal of treatment

There is no specific drug; the aim is to treat the critical illness, limit risk factors, and rehabilitate early to restore breathing and walking.

Treatment

Acute: Rapid control of sepsis and organ support; avoid prolonged neuromuscular blockade and unnecessary high-dose corticosteroids.
Medical: Avoid hyperglycaemia without causing hypoglycaemia; daily sedation minimisation or interruption; adequate nutrition and correction of electrolytes.
Rehabilitation: Early mobilisation and physiotherapy in the ICU (passive then active exercise, cycle ergometry, sitting and standing), inspiratory muscle training and staged weaning.
Follow-up: Nursing priorities: daily strength and weaning assessments, repositioning and pressure-injury prevention, thromboprophylaxis, aspiration prevention and delirium screening.

Complications

Prolonged mechanical ventilation and tracheostomy
Longer ICU and hospital stay and higher mortality
Pressure injuries and venous thromboembolism
Long-term weakness, fatigue and disability (post-intensive care syndrome)
Contractures and foot drop

Prognosis

Pure myopathy often recovers within weeks to months; polyneuropathy recovers more slowly and may leave lasting weakness or sensory loss. Many survivors have reduced physical function for a year or longer.

Prevention

Early treatment of sepsis
Minimal sedation with daily interruption
Limited use of neuromuscular blockers and high-dose corticosteroids
Avoidance of hyperglycaemia
Early mobilisation in the ICU

Test yourself

Think of the answer, then tap the question to see it.

A septic patient ventilated for two weeks is awake but cannot lift his arms or be weaned, with absent reflexes. What is the likely diagnosis?

ICU-acquired weakness from critical illness polyneuropathy and/or myopathy.

What MRC sum score defines ICU-acquired weakness?

Below 48 out of 60.

Which drug combination is classically linked to critical illness myopathy?

Corticosteroids together with non-depolarising neuromuscular blockers.

How do nerve studies distinguish neuropathy from myopathy?

Neuropathy reduces both motor and sensory amplitudes; myopathy spares sensory responses and muscle is inexcitable on direct stimulation.

Which intervention has the best evidence for prevention?

Early mobilisation, together with minimal sedation and avoidance of hyperglycaemia.

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Educational information, not medical advice. For any symptom, see a health professional.

Sources: Intensive Care Unit Acquired Weakness (ICU-AW): a brief and practical review (Reviews in Health Care (Godoy DA, Vaz de Mello L, Masotti L, Di Napoli M), 2015).

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