Critical Illness Weakness

Combination of myopathy and neuropathy that occurs in the ICU patient, that is:

Formal diagnosis of CIN/CIM requires electrophysiology studies, which are rarely performed in practice and are predominantly a research tool. Criteria include:

CIN
- ↓ AP amplitude
  ⩾2 nerves have amplitude <80% LLN for both:
  - Compound muscle
  - Sensory nerve
- Normal nerve conduction velocity
- No change on repetitive stimulation
CIM
- Preserved sensory nerve function
- ↓ Muscle excitability in ⩾2 muscle groups

Characterised by:
- Proximal myopathy
- Symmetrical flaccid weakness
- Hyporeflexia
Subdivided into Critical Illness:
- Myopathy
  Almost universal in the critically ill, and contributes to the majority of ICU acquired weakness.
- Neuropathy
  Rarer than CIM.
- Neuromyopathy
  Combination of neuropathy and myopathy.

Epidemiology and Risk Factors

Weakness is common in ICU patients:

65% of patients after 5-7 days of ventilation

Risk factors relate predominantly to ↓ muscle mass:

Patient factors have substantial overlap, are mutually reinforcing, and could broadly be summarised as frailty.

Patient factors
- Age
- Low-baseline muscle mass
- Chronic disease
Disease factors
- Severity of illness
- ICU length of stay
- Hyperglycaemia

Notably, muscle relaxants are not associated with ↑ CIM/CIN

Pathophysiology

Myopathy:

Loss of muscle mass
- Rapid ↓ in muscle mass within 3 days of ICU admission:
  - 10% ↓ in thickness and cross-sectional area within first 3 days
  - Further 10% ↓ over following 4 days
    Usually 2-3%/day.
- ↑↑ Speed of wasting with ↑ number of organ failures
↓ Anabolism
- Altered protein metabolism
- Generalised inflammation
Myonecrosis
↓ Skeletal muscle ATP synthesis

Neuropathy:

Acquired channelopathy of voltage-gated sodium channels
Widely present but poor correlation with dysfunction.
Axonal degeneration
- Associated with ↑ BSL

Aetiology

Clinical Manifestations

Diagnostic Approach and DDx

Differential diagnoses of weakness include:

Brainstem
- CVA
- Locked-in syndrome
Spinal cord
- Transverse myelitis
- Mass effect
  - Tumour
  - Haemorrhage
Peripheral nerve
- GBS
- CIN
- Toxins
  - Arsenic
  - Thallium
NMJ
- Neuromuscular blockade
- MG
- Lambert-Eaton syndrome
- Toxins
  - Organophosphate
  - Botulism
Muscle
- Steroid myopathy
- Alcoholic myopathy
- Polymyositis
- Dermatomyositis
- Toxic myopathy
- CIM

Investigations

Bedside:

Laboratory:

Imaging:

Other:

Electrophysiology
- Rarely performed in practice
- Required for diagnosis of peripheral nerve injury

Management

Specific therapy:

Pharmacological
Procedural
Physical

Supportive care:

E
- Physiotherapy
  - ↓ Catabolic effects of immobilisation and bed rest
  - ↑ Anabolism
G
- Feeding
  ↑ Anabolism.
- Insulin
  ↑ Anabolism.

Disposition:

Preventative:

Minimise sedation and ventilation time
- Early wakening
- Spontaneous breathing
- Early mobilisation

Marginal and Ineffective Therapies

Electrical stimulation
No ↑ muscle mass, possibly due to:
- Impaired anabolic response
- Electrical damage to muscle
Extra nutrition
No ↑ muscle mass or outcome improvement.
Tight glucose control
Does ↓ muscle mass loss, but results in ↑↑ hypoglycaemia and ↑ mortality.

Anaesthetic Considerations

Complications

Death
D
- Persistent weakness
E
- ↑ Osteoporosis and fracture risk

Prognosis

Significant morbidity and mortality:

Mortality
↑ Short-term and 5-year mortality.
Morbidity
Severe functional limitations occur among survivors:
- At 6-12 months
  - 70% have substantial limitations
  - 30% are carer-dependent

Key Studies

References

Nakanishi N, Oto J, Tsutsumi R, Iuchi M, Onodera M, Nishimura M. Upper and lower limb muscle atrophy in critically ill patients: an observational ultrasonography study. Intensive Care Med. 2018 Feb;44(2):263-264.
Bersten, A. D., & Handy, J. M. (2018). Oh’s Intensive Care Manual. Elsevier Gezondheidszorg.