Intensive Care Acquired Weakness

Intensive Care Acquired Weakness

A cardiovascularly fit 65 year old man was admitted with septic shock secondary to community acquired pneumonia, which progressed to multi-organ failure. During his recovery it was noted that he had generalised weakness with no focal neurology. He underwent respiratory weaning, and rehabilitation therapy over the next 4 weeks but had persistent weakness at his ICU discharge.

How can ICU-acquired weakness be diagnosed and managed?

Tahir Ali

ICU-acquired weakness (ICUAW) is defined as ‘clinically detected weakness
in critically ill patients in whom there is no plausible aetiology other than
critical illness’.(1) It can be further sub-classified into ‘critical illness
polyneuropathy’ (CIPN), critical illness myopathy (CIM), or critical illness
neuromyopathy (CINM).

Various risk factors have been described for ICUAW including patients with
severe sepsis, multiorgan failure, prolonged mechanical ventilation (greater
than 7 days), muscle inactivity, hyperglycaemia, use of corticosteroids and
neuromuscular blockers,(2) post liver transplantation(3), and patients with status
asthmaticus(4) and severe COPD(5)

The pathophysiology is incompletely understood. The hypothesis is that there
is peripheral nervous system damage due to various systemic inflammatory
processes. These include decreased oxygen and nutrient delivery to nerve
axons(6), and impaired mitochondrial oxygen utilization. This leads to
subsequent impaired ATP generation due to nitric oxide and oxygen free

The main clinical feature is variable, symmetrical, proximal and distal muscle
weakness with cranial nerve sparing following critical illness.
Investigations are predominantly in order to rule out other differential
diagnoses (Guillain–Barre´ syndrome, Myasthenia Gravis, spinal cord disease
etc). These include blood tests (electrolytes, CK, ESR, autoantibodies),
lumbar puncture and MRI scans. Various neurophysiological investigations
can aid in the diagnosis and differentiation between the types of ICUAW.
However since they require specialist neurophysiology input, they are not
readily utilised in critical care.

No specific treatments have been described for ICUAW and therefore
management relies upon prevention and reducing the risk factors described.
Various therapies have been trialled (nutritional supplements, antioxidants,
growth hormones, immunoglobulins) with no obvious benefits. Tight glycaemic
control has been shown to reduce the incidence of ICUAW(8) however the
NICE-SUGAR trial(9) demonstrated increased absolute risk (2.6%) of death.
This has resulted in movement to a glucose range of 6-10mmol/l and
therefore tight control cannot be used until continuous glucose monitoring is
readily available in critical care.

In 2009, NICE published specific research recommendations intended to
optimise recovery and rehabilitation of critically ill patients, rather than survival
alone. Various methods were used aiming to reduce the physical and
psychological implications of critical illness.

Rehabilitation requires close co-ordination by the appropriate healthcare
professional with other members of the multidisciplinary team. This includes
the physiotherapists, microbiologists and nursing and medical staff. .
The key principles of rehabilitation include starting an individualised and
structured programme as soon as clinically possible, ideally on day 1, with
regular follow up reviews. Avoiding and reducing ‘physical’ and ‘non-physical’
morbidity, and provision of adequate nutritional support are essential aspects
of recovery and rehabilitation. A risk assessment should be performed as
early as possible and both the patient and family should be involved in the

Various studies have been reviewed during the development of the NICE
guidelines. However, with regards to screening and assessment tools for
physical morbidity (mobilisation, muscle strength and swallowing), Collen et al
(1991) conferred low quality evidence in terms of sample size (23) and study

Various studies have looked at early progressive physical and occupational
therapy, including cycle ergometry, inspiratory muscle training and
ambulation. Quality of evidence was varied, most being level 2-4 with one
RCT, and studied outcomes including ‘muscle strength’, ‘functional mobility’
and ‘quality of life’.(10,11) Furthermore the literature supported improvement in
functional mobility using objective measures such as Barthel Index and
Functional Independence Measure (FIM).(10.11,12)

The rehabilitation plan should be modified prior to discharge (home or
community care) and regular follow up should be provided by skilled
healthcare professionals. Prolonged weakness is a major cause of morbidity
for many months following critical illness. Studies that assessed muscle
strength demonstrated improvement by the time of discharge and in the postacute
setting but no improvement in ICU. Some patients may require referrals
for psychiatric or psychological support to address anxiety, post-traumatic
stress disorder and other ‘non-physical’ causes of morbidity.

Learning points

ICUAW is an important cause of morbidity during ICU admission and post
discharge. Latronico N et al looked at 263 critical care patients with ICUAW
and demonstrated 68.4% complete recovery and 28% with persistent severe
disability(13). This highlights the severity of this condition, the likelihood of
complete recovery, and the importance of not taking an entirely pessimistic
view towards patients with evidence of ICUAW such as the ‘slow ventilator

Efforts must be made to reduce the risk factors as much as clinically possible.
Early progressive physiotherapy and occupational therapy improves muscle
strength and functional mobility, and therefore should be appropriately
incorporated into the weaning plan of critically ill patients.


1. Herridge MS, Cheung AM, Tansey CM et al. One-year outcomes in
survivors of the acute respiratory distress syndrome. NEJM 2003; 348:
2. De Jonghe B, Lacherade JC, Sharshar T, Outin H. Intensive care unitacquired
weakness: risk factors and prevention. Crit Care Med. 2009.
Oct;37(10 Suppl):S309-15.
3. Campellone JV, Lacomis D, Kramer J, Van Cott AC, Giuliani MJ. Acute
myopathy after liver transplantation. Neurology 1998; 50: 46–53
4. Douglass JA, Tuxen DV, Horne M et al. Myopathy in severe asthma.
Am Rev Respir Dis 1992; 146: 517–9
5. Amaya-Villar R, Garnacho-Montero J, Garcı´a-Garmendı´a JL et al.
Steroid-induced myopathy in patients intubated due to exacerbation of
chronic obstructive pulmonary disease. Intensive Care Med 2005; 31:

6. Bolton CF: Neuromuscular manifestations of critical illness. Muscle
Nerve 2005, 32:140-163.
7. Brealey D, Brand M, Hargreaves I, Heales S, Land J, Smolenski R,
Davies NA, Cooper CE, Singer M: Association between mitochondrial
dysfunction and severity and outcome of septic shock.
Lancet 2002, 360:219-223.
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review: Critical illness polyneuropathy and myopathy. Crit
Care. 2008; 12(6): 238.
9. Intensive versus Conventional Glucose Control in Critically Ill Patients.
The NICE-SUGAR Study Investigators. NEJM 2009; 360:1283-1297.
10. Schweickert WD, Pohlman MC, Pohlman AS. Early physical and
occupational therapy in mechanically ventilated, critically ill patients: a
randomized controlled. Lancet. 2009;373:1874-1882.
11. Burtin C, Clerckx B, Robbeets C, et al. Early exercise in critically
patients enhances short-term functional recovery. Crit Care Med.
12. Chiang LL, Wang LY, Wu CP, Wu HD, Wu YT. Effects of physical
training on functional status in patients with prolonged mechanical
ventilation. Phys Ther. 2006;86:1271-1281.
13. Latronico N, Shehu I, Seghelini E. Neuromuscular sequelae of critical
illness. Curr Opin Crit Care 2005; 11: 381–90.


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