ICU Acquired Weakness
Last updated 27th September 2018 by Tom Heaton
ICU acquired weakness (ICUAW) is a common and important problem for patients recovering from a critical illness episode.
This is quite a decent (if slightly long) video on the topic: https://www.youtube.com/watch?v=eH-eHuz6i-k
This is quite a decent (if slightly long) video on the topic: https://www.youtube.com/watch?v=eH-eHuz6i-k
Definition
ICUAW is defined as: “clinically detectable weakness in critically ill patients in whom there is no other explanation other than critical illness”.
It is recognised as having different components, the main ones being
It is recognised as having different components, the main ones being
- Critical illness polyneuropathy
- Critical illness myopathy
- Critical illness neuromyopathy
Risk Factors
These are under ongoing study.
They appear to be similar for the different types of ICUAW
Probable:
Possible
Some of the studies have shown mixed results when analysing this risk factors.
Indeed, it is important to note that some potentially avoidable risk factors may still be required e.g. neuromuscular blockade in ARDS.
They appear to be similar for the different types of ICUAW
Probable:
- Severe sepsis
- Corticosteroids
- Multiorgan dysfunction (severity and duration of)
- Duration of mechanical ventilation
- Neuromuscular blocking agents
- Hyperglycaemia
- Catabolic state
Possible
- Increasing age
- Vasopressors
- Aminoglycosides
Some of the studies have shown mixed results when analysing this risk factors.
Indeed, it is important to note that some potentially avoidable risk factors may still be required e.g. neuromuscular blockade in ARDS.
Pathophysiology
Much of the injury appears to arise from the same inflammatory processes that lead to the critical illness in the first place, but in this case affecting the nerves and muscles.
Some component also arises from the more general aspect of atrophy from the prolonged immobility that accompanies being so sick.
The pathophysiology of the different forms of ICUAW is different.
Critical Illness Polyneuropathy
This is a distal sensory/motor polyneuropathy that primarily affects motor nerves.
It is characterised by axonal degeneration without demyelination.
Several mechanisms have been described that may lead to the neuronal injury:
Critical Illness Myopathy
This can be considered as both functional and structural.
Some of the functional pathophysiology overlaps with that described for the polyneuropathy, leading to impairment in the muscle’s ability to depolarise:
However, there are subsequent structural changes where muscle mass is lost.
These are related to:
Some component also arises from the more general aspect of atrophy from the prolonged immobility that accompanies being so sick.
The pathophysiology of the different forms of ICUAW is different.
Critical Illness Polyneuropathy
This is a distal sensory/motor polyneuropathy that primarily affects motor nerves.
It is characterised by axonal degeneration without demyelination.
Several mechanisms have been described that may lead to the neuronal injury:
- Microvascular dysfunction with impaired nutrient delivery/utilisation
- Mitochondrial dysfunction
- Sodium channel dysfunction
- Direct glucose cellular toxicity/increased oxidative stress from hyperglycaemia
- Neurotoxin injury
Critical Illness Myopathy
This can be considered as both functional and structural.
Some of the functional pathophysiology overlaps with that described for the polyneuropathy, leading to impairment in the muscle’s ability to depolarise:
- Reduced membrane excitability - sodium channel dysfunction
- Altered sarcoplasmic reticulum function and impact on calcium
- Mitochondrial dysfunction
However, there are subsequent structural changes where muscle mass is lost.
These are related to:
- Catabolic changes from the critical illness state
- Muscle atrophy from disuse
- Muscle denervation (linked to polyneuropathy, neuromuscular blockade)
Epidemiology
This will vary depending only subgroups of critically ill patients (with some being at notably higher risk).
One systematic review described the overall incidence at around 46%.
One systematic review described the overall incidence at around 46%.
Presentation
This has to be taken in parallel with the patient’s presenting illness.
It will usually be following a significant and fairly prolonged critical illness, during which time the extent of treatment may have masked its development e.g. sedation and mechanical ventilation.
It is often in this recovery phase when this problem starts to become apparent.
However, it is important to look back to ensure that the initial presentation may not be part of this weakness e.g. traumatic spinal cord injury, Guillain-Barre.
Examples of presentations include:
The weakness usually affects the limbs in a symmetrical, flaccid pattern, being particularly noticeable in proximal muscle groups.
Facial and ocular muscle are rarely involved.
Weakening of the respiratory muscles can occur.
This may initially manifest as difficulty in weaning a patient from mechanical ventilation, as well as poor clearance of secretions.
Neurological examination is a key part in initial assessment, but is often impeded by the various neurological impairments of ICU (sedation, delirium).
The key feature is clinical assessment of muscle strength.
Muscle strength is assessed in the various muscle groups of the upper and lower limbs (3 muscle groups from each limb) using the Medical Research Council (MRC) scale of 0 to 5.
This gives a score out of 60, with a score of < 48 being diagnostic.
This video gives a nice review of the MRC scale: https://www.youtube.com/watch?v=LjlqP1uMUo0
It will usually be following a significant and fairly prolonged critical illness, during which time the extent of treatment may have masked its development e.g. sedation and mechanical ventilation.
It is often in this recovery phase when this problem starts to become apparent.
However, it is important to look back to ensure that the initial presentation may not be part of this weakness e.g. traumatic spinal cord injury, Guillain-Barre.
Examples of presentations include:
- Generalised weakness
- Failure to wean
The weakness usually affects the limbs in a symmetrical, flaccid pattern, being particularly noticeable in proximal muscle groups.
Facial and ocular muscle are rarely involved.
Weakening of the respiratory muscles can occur.
This may initially manifest as difficulty in weaning a patient from mechanical ventilation, as well as poor clearance of secretions.
Neurological examination is a key part in initial assessment, but is often impeded by the various neurological impairments of ICU (sedation, delirium).
The key feature is clinical assessment of muscle strength.
Muscle strength is assessed in the various muscle groups of the upper and lower limbs (3 muscle groups from each limb) using the Medical Research Council (MRC) scale of 0 to 5.
This gives a score out of 60, with a score of < 48 being diagnostic.
This video gives a nice review of the MRC scale: https://www.youtube.com/watch?v=LjlqP1uMUo0
Investigation
As noted above, the history may mean that the diagnosis of ICUAW might not be applied straight away.
Consideration of other causes should be sought, and often some simple investigations can rule out other possibilities.
Some investigations will be directed at other specific differentials.
More specialist, often electrophysiological testing may be required in some cases where uncertainty is present, but not routinely.
These may include:
Consideration of other causes should be sought, and often some simple investigations can rule out other possibilities.
Some investigations will be directed at other specific differentials.
- Bloods - electrolyte disturbance, creatine kinase
- Medications review - sedatives, muscle relaxants
- Imaging - head and spine imaging
- CSF sampling
More specialist, often electrophysiological testing may be required in some cases where uncertainty is present, but not routinely.
These may include:
- Nerve conduction studies
- Electromyography
- Direct muscle stimulation
- Biopsy (nerve or muscle)
Diagnosis
The criteria for a diagnosis of ICUAW can be said to be met with the following:
- Weakness developing after a critical illness
- Weakness is generalised, symmetrical, flaccid and generally sparing the cranial nerves.
- Other causes of weakness have been excluded
- MRC sum score of <48/60 noted on 2 separate occasions 24h apart.
- Dependence on mechanical ventilation
Management
There remains no treatment for this condition.
Management therefore focuses on avoiding its development as much as possible.
By focusing on some of the key factors that are implemented in its pathophysiology, this can be achieved:
Treating the underlying inflammatory process is clearly important and usually part of the ICU management.
Avoidance of steroids and neuromuscular blockade where possible is important.
Tight glucose control is no longer recommended due to the risks of hypoglycemia, but adherence to the more ‘moderate’ glucose control is still important in reducing the contribution of hyperglycaemia.
Increasing physical activity may take many forms, some of which are recognised as beneficial in other ways:
Management therefore focuses on avoiding its development as much as possible.
By focusing on some of the key factors that are implemented in its pathophysiology, this can be achieved:
- Inflammatory response
- Steroids
- Neuromuscular blockade
- Glucose control
- Physical activity
Treating the underlying inflammatory process is clearly important and usually part of the ICU management.
Avoidance of steroids and neuromuscular blockade where possible is important.
Tight glucose control is no longer recommended due to the risks of hypoglycemia, but adherence to the more ‘moderate’ glucose control is still important in reducing the contribution of hyperglycaemia.
Increasing physical activity may take many forms, some of which are recognised as beneficial in other ways:
- Daily sedation holds
- Ventilation strategies
- Mobilisation/activity regimes
Prognosis
Alongside the psychological impact, the weakness and deconditioning is one of the most challenging parts of the recovery from critical illness.
The improving survival from critical illness means that these problems have been becoming more prevalent.
Neuromuscular dysfunction after critical illness varies significantly between patients.
In most cases some recovery occurs, but this may be incomplete in the majority and can take years.
This can be detected on functional testing as well as physiological testing.
It is important to note that there have been case reports of suxamethonium induced hyperkalemia in patients with ICUAW
The improving survival from critical illness means that these problems have been becoming more prevalent.
Neuromuscular dysfunction after critical illness varies significantly between patients.
In most cases some recovery occurs, but this may be incomplete in the majority and can take years.
This can be detected on functional testing as well as physiological testing.
It is important to note that there have been case reports of suxamethonium induced hyperkalemia in patients with ICUAW
Links & References
- Appleton, R. Kinsella, J. Intensive care unit acquired weakness. CEACCP. 2012. https://academic.oup.com/bjaed/article/12/2/62/251187
- Hudson, D. Critical illness polyneuropathy and polymyopathy. 2016. Youtube. https://www.youtube.com/watch?v=eH-eHuz6i-k
- Bersten, D. Soni, N. Oh’s Intensive Care Manual (7th ed). 2014
- Kress, J. Hall, J. ICU-acquired weakness and recovery from critical illness. NEJM. 2014. 370:1626-1635. https://www.nejm.org/doi/full/10.1056/NEJMra1209390
