ICU-Acquired Weakness

Posted by Sara Fazio • April 25th, 2014

Stays in intensive care units are commonly accompanied by muscle weakness. The latest article in the Critical Care series reviews the basis for this condition and provides guidance on how to prevent, diagnose, and treat it.

Weakness acquired in the intensive care unit (ICU) is caused by many different pathophysiological mechanisms that are not mutually exclusive. This is not surprising, given the diverse diseases that precipitate critical illness, the drugs used during its management, and the consequences of protracted immobility.

Clinical Pearls

What is critical illness polyneuropathy?

Critical illness polyneuropathy is characterized by a primary axonal degeneration, without demyelination, that typically affects motor nerves more than sensory nerves. It affects the limbs (particularly the lower extremities) in a symmetric pattern. Weakness is most notable in proximal neuromuscular areas (e.g., the shoulders and hip girdle). In addition, involvement of the respiratory muscles can occur and can impede weaning from mechanical ventilation. Facial and ocular muscles are rarely involved. Creatine kinase levels are not elevated in patients with critical illness polyneuropathy. The condition is distinct from the Guillain-Barre syndrome because demyelination is not seen.

What is critical illness myopathy?

As distinct from a secondary myopathy resulting from muscle denervation, critical illness myopathy is a primary myopathy. It is often difficult to distinguish this myopathy from critical illness polyneuropathy by means of a simple bedside examination. Both conditions are manifested by limb and respiratory-muscle weakness and retained sensory function; however, because altered mental status is common in patients in the ICU, sensory examination may be difficult to perform. In patients with critical illness myopathy, electrophysiological studies show reduced amplitude and increased duration of CMAPs. Histopathological analysis shows selective loss of thick filaments in muscle, which reflects myosin loss as well as muscle necrosis. Creatine kinase levels may be mildly elevated, except that in occasional cases of necrotizing myopathy, such levels are markedly elevated. Critical illness myopathy occurs more frequently than critical illness neuropathy, and it is associated with a higher rate of recovery.

Morning Report Questions

Q: What is the appropriate diagnostic approach to ICU-acquired weakness?

A: The diagnosis of ICU-acquired weakness is made with the use of the Medical Research Council (MRC) scale for grading the strength of various muscle groups in the upper and lower extremities. The scale ranges from 0 to 5, with higher scores indicating greater muscle strength; a combined score of less than 48 is diagnostic of ICU-acquired weakness. Patients with ICU-acquired weakness according to the MRC examination should undergo serial evaluations, and if persistent deficits are noted, electrophysiological studies, muscle biopsy, or both are warranted. Patients with persistent coma after discontinuation of sedation should undergo studies of the central nervous system such as cranial computed tomography or magnetic resonance imaging. If such studies are normal, electrophysiological studies, a muscle biopsy, or both should be performed.

Table 1. Electrophysiological Features of ICU-Acquired Weakness.

Q: What are the risk factors for ICU-acquired weakness?

A: The reported incidence of ICU-acquired weakness ranges from 25 to 100%. It is clear that sepsis, persistent systemic inflammation, and multiorgan system failure are important risk factors. Hyperglycemia in the ICU was reported to be an independent risk factor in one trial. Glucocorticoid therapy has been reported to be a risk factor in some trials. In a study reported by De Jonghe and colleagues, ICU-acquired weakness was more than four times as likely to develop in women as in men. There is evidence that aggressive glucose control may reduce the risk of critical illness polyneuropathy (and myopathy) and result in a decreased need for prolonged mechanical ventilation. However, because of the increased risk of adverse events associated with aggressive glucose control, it is not recommended solely for the prevention of critical illness polyneuropathy.

Table 3. Clinical Risk Factors and Pathophysiological Features of Critical Illness Polyneuropathy and Critical Illness Myopathy.

7 Responses to “ICU-Acquired Weakness”

  1. Dr.Prakash Katakia says:

    Is there any preventive or curative therapy available as on date?

  2. Amol Patil says:

    I think this feature is slightly misleading. Critical care Neuropathy and Myopathy do NOT occur in isolation. Hence this phenomenon is called Critical care NeuroMoypathy (CINM). Accordingly the EMG, NCV findings are mixed as is the CK elevation.
    One of the risk factors not mentioned is systemic paralytics. High dose steroids and paralytics are a potent combination.

  3. Gladys Farfán Townsend says:

    Thanks!

  4. khawaja ikram ul haq says:

    the weakness that u state is similar to that of people aging or starting to age…obviously people in hospitals should be given some sort of movement so that their muscles and nerves donot stop working…

  5. Imran says:

    Good job

  6. Ali Ahmad says:

    B. It is a demyelinating condition

  7. Rebecca Sebo says:

    What is the prognosis of CIM for a 44 y.o. male, mv x 13 days due to ARDS secondary to pneumonia, sepsis, acute renal failure (which returned) and improper nutrition x 14 days. He hasn’t walked in 5 months but was very strong and physically active prior ti incident. Has lost almost 100lbs since this started.

    I’m just concerned that his physical therapy isn’t progressing as it should. Any advice or comments would be very helpful.

Leave a Reply

Please note: Comment moderation is enabled and may delay your comment. There is no need to resubmit your comment.

Submitting a comment indicates you have read and agreed to the Terms and Conditions.