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
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
Critical illness polyneuropathy
Critical illness myopathy
Critical illness neuromyopathy
They are strongly interconnected, but are different in their pathophysiology.
These are under ongoing study. They appear to be similar for the different types of ICUAW
Multiorgan dysfunction (severity and duration of)
Duration of mechanical ventilation
Neuromuscular blocking agents
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.
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:
Microvascular dysfunction with impaired nutrient delivery/utilisation
Sodium channel dysfunction
Direct glucose cellular toxicity/increased oxidative stress from hyperglycaemia
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:
Altered sarcoplasmic reticulum function and impact on calcium
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)
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%.
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:
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.
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.
Bloods - electrolyte disturbance, creatine kinase
Medications review - sedatives, muscle relaxants
Imaging - head and spine imaging
More specialist, often electrophysiological testing may be required in some cases where uncertainty is present, but not routinely. These may include:
Nerve conduction studies
Direct muscle stimulation
Biopsy (nerve or muscle)
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
And one of:
MRC sum score of <48/60 noted on 2 separate occasions 24h apart.
Dependence on mechanical ventilation
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:
Daily sedation holds
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