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Disease/Disorder

Definition

Critical illness myopathy (CIM) also referred to as intensive care unit (ICU) myopathy, is a form of generalized weakness involving the muscles of the extremities, trunk, and respiration that frequently occurs in conjunction with severe illness and is associated with significant morbidity and mortality.1 This is the most common form of ICU-acquired myopathy presenting with flaccid quadriparesis usually affecting limb muscles proximally equally or more pronounced than distal muscles. Sensation is usually intact as opposed to other pathologies commonly seen in ICU patients such as Critical illness polyneuropathy (CIP) and Critical illness polyneuromyopathy (CIPNM).2 CIM has also been termed acute quadriplegic myopathy (AQM), acute illness myopathy, and myopathy associated with thick filament (myosin) loss.3

Etiology

While the exact etiology is unknown, most reported cases are multifactorial. The pathophysiology of CIM is complex and thought to involve microcirculatory changes, metabolic alterations, electrical muscle alterations with abnormal excitation-contraction coupling, and energetic failure with mitochondrial dysfunction.4

Epidemiology including risk factors and primary prevention

It is estimated that 25-83% of critically ill patients suffer from either CIM, CIP, or CIPNM.Major risk factors include sepsis, multi-organ failure, acute respiratory distress syndrome (ARDS), prolonged intubation, lengthy ICU stay, prolonged immobilization, malnutrition, female gender, older age, impaired glucose homeostasis, and the use of catecholamines and aminoglycosides. It is unknown whether modifying risk factors can prevent CIM.5,6 Although CIM may develop in the absence of exposure to IV glucocorticoids in critically ill patients, neuromuscular blocking agents are still associated with neuromuscular dysfunction.7 In the setting of the recent pandemic, patients with COVID-19 related lengthy ICU stays had a high risk for ICU acquired weakness. Greater than 25 percent of patients who were mechanically ventilated in the ICU for at least seven days were noted to develop CIM.6

Patho-anatomy/physiology

Although this is an acute illness, the exact time of onset is difficult to pinpoint. CIM is characterized by severe muscle atrophy, with a preferential loss of myosin, the main component of the thick filaments. The initial phase may have some involvement of ion channel dysfunction followed by malfunctioning mitochondria and membrane dysfunction triggering Ca 2+ imbalance. Atrophy of the muscle fibers and selective loss of numerous myosin thick filaments from the A bands can be seen. Histologic findings have revealed disaggregated myosin monomers are retained but have no enzyme activity. Myosin monomers likely disaggregate due to ionic imbalance in the sarcoplasm.6 The most prominent clinical feature is generalized flaccid weakness affecting appendicular, truncal, and cranial musculature. There is usually no myalgia or muscle tenderness. An important manifestation is neck flexor weakness, which correlates with diaphragmatic muscular weakness and difficulty in weaning from mechanical ventilation. A pupil-sparing ophthalmoparesis may be present however must be distinguished from another neuromuscular junction transmission disorder. The loss of deep tendon reflexes is a variable finding, although in most cases they are depressed.8 One study demonstrated that impaired GLUT4 translocation to the sarcolemmal membrane is a mechanism of impaired glucose supply to muscle cells in patients with CIM. Impaired GLUT4 translocation was not eliminated despite treatment with insulin. Skeletal muscles fibers were then deprived of glucose which is particularly detrimental to glycolytic metabolism dependent type 2 muscle fibers. Electrical muscle stimulation restored GLUT4 translocation to the sarcolemmal membrane and rescued fiber atrophy in patients with CIM.9,10

Disease progression including natural history, disease phases or stages, disease trajectory (clinical features and presentation over time)

A typical clinical scenario usually involves a patient who has been in the ICU for at least 7 days secondary to an underlying disease process, such as sepsis or ARDS, with subsequent multi-organ failure who requires ventilatory support.4 The severe generalized muscle weakness usually becomes evident when the systemic illness subsides, often as attempts are made to wean the patient from the ventilator. Most patients with acute myopathy recover over a period of 6 to 12 weeks after the corticosteroid agent has been greatly reduced in dose or withdrawn, but a few have remained weak for as long as a year. Serum CK is elevated, at least early in the process. Electromyography (EMG) discloses the characteristic features of a myopathy; often there are fibrillations, theorized to be a result of separation of the motor endplate region from intact segments of muscle fibers. Muscle biopsy shows varying degrees of necrosis and vacuolation affecting mainly type 2 fibers. The identifying histologic feature is a striking loss of myosin. It is important to be mindful of the degree of muscle necrosis and elevation of CK levels which can cause myoglobinuria leading to renal failure.

By definition, patients are or were critically ill, and weakness should have started after onset of critical illness. For a diagnosis of critical illness myopathy, the patient meets criteria for ICU-acquired weakness (ICUAW), sensory nerve action potential amplitudes are >80% of the lower limit of normal in two or more nerves, needle electromyogram in two or more muscle groups demonstrates short-duration, low-amplitude motor unit potentials with early or normal full recruitment with or without fibrillation potentials, and direct muscle stimulation demonstrates reduced excitability (muscle-to-nerve ratio, and muscle histology is consistent with a myopathy.11

Specific secondary or associated conditions and complications

When approaching patients with acute neuromuscular weakness, especially those who have difficulty weaning off a ventilator, it is important to consider a broad set of differential diagnoses. Common causes that must be worked up include, but are not limited to, disease processes that affect the motor neuron, neuromuscular junction, and muscle itself. CIP, amyotrophic lateral sclerosis, Guillain-Barre syndrome, sarcoidosis, myasthenia gravis, botulism toxicity, metabolic neuropathies, toxic neuropathies, toxic myopathies, and neuropathies secondary to nutritional deficiencies can all result in prolonged intubation and flaccid muscle tone.12 Of note, CIM can be difficult to distinguish from CIP, especially since often times they co-exist resulting in the condition known as CIPNM (critical illness polyneuromyopathy). Many experts believe that CIP is much more uncommon than CIM.7,13 The main differentiating factor between CIM and CIP is that sensory nerves are spared in CIM whereas CIP has both sensory and motor involvement which can be determined on physical exam as well as electrodiagnostic study.14,15

CIM-related complications are usually secondary to immobility rather than the disease process itself such as deep vein thrombosis and the development of pressure injuries. Therefore, for CIM patients, special attention should be given to prophylactic anticoagulation and frequent skin checks.15 In light of the recent COVID pandemic, a post-mortem study showed a spectrum of myopathic changes, suggesting CIM as a common diagnosis in post-mortem patients. Evidence shows that patients with SARS-CoV-2 infection may develop various neurological complications as a direct or indirect viral action.16 The COVID-19-associated CIM may show not only conventional CIM features described in non-COVID-19 patients, but also COVID-19-associated myopathic changes, such as autophagic vacuoles, SARS-CoV immunostaining+ granules, variable inflammation, and additional mitochondrial abnormalities.16

Essentials of Assessment

History

Most patients with neuromuscular weakness in the ICU are usually identified because of difficulty weaning from mechanical ventilation.17 Consequently, it may not always be possible to obtain an accurate history and timeline of the weakness from patients as they are frequently intubated and sedated. However, it is still very important to understand the patients’ underlying conditions and the course of illness during their ICU stay to rule out other possibilities of muscle weakness. If a patient is conscious important questions to consider are prior history of weakness, onset of current episode of weakness, pattern of the weakness, difficulty swallowing, newly started medications, and the presence or lack of sensory complaints.12

Physical examination

Patients with CIM typically present with diffuse symmetric muscle weakness, proximal greater than distal, with characteristic involvement of neck flexors and respiratory muscles. Facial muscles, especially extraocular muscles, are rarely involved with CIM, and the presence of facial weakness should raise suspicion for other neurologic disorders where bulbar function is compromised. If possible, muscle strength should be evaluated using the Medical Research Council (MRC) System to assess 12 muscle groups. CIM patients typically exhibit at least a 4/5 grade on all testable muscles, or an average MRC sum score of less than 48.12,18 Muscle tone is usually flaccid. There is no sensory involvement unless patients have an underlying neurologic condition that affects sensory function. Deep tendon reflexes are typically normal but can be reduced.19,20 Of note, a thorough physical exam may not always be possible in the acute hospitalization phase while patients are still intubated and is often deferred until a patient undergoes a sedation holiday or is extubated and able to actively participate.18

Functional assessment

Beginning evaluation in the ICU is particularly important for those with suspected ICU-acquired weakness. ICUAW is the most common form of physical impairment occurring in 25 percent or more of ICU survivors. Early assessment identifies those with weakness who might begin therapy early in their course. In a large cohort of ventilated patients, at three months 32 percent of patients were disabled in their ADLs and 26 percent were disabled in instrumental ADLs. Disability was prominent in those with and without pre-existing functional disability and persisted in most patients at 12 months.5

Most patients are intubated in the ICU and have altered mental status. Functional level is largely dependent on conditions of their underlying disease(s) and cognitive status. In the early stages, self-care and bed mobility usually require maximal assistance because of proximal muscle weakness and underlying conditions. Despite having some residual weakness from disuse atrophy, most patients with CIM eventually recover and are able to achieve total independence or return to pre-hospitalization functional status.10,19

Laboratory studies

Serum Creatinine phosphokinase (CPK) level may be normal or mildly elevated.12 Although there are some reports of high CK levels (up to 10 times higher than upper normal level) in CIM, such high levels of CK should prompt investigation for other conditions, such as rhabdomyolysis or toxic myopathies. Comprehensive laboratory evaluation is often performed to rule out other diseases, but there are no validated biomarkers unique to CIM currently available. CSF is usually normal.12,20

Imaging

Careful neuraxial imaging is often necessary to rule out other possibilities of weakness, such as stroke or spinal cord infarct, especially when patients are non-communicative. Magnetic resonance imaging of muscle tissue using a myositis protocol can show enhancement in short-tau inversion-recovery images when there is diffuse muscle edema. However, this finding is nonspecific and can be associated with rhabdomyolysis or inflammatory myositis. Currently there is no specific imaging modality or finding known to be uniquely associated with CIM.21,22

Muscle ultrasound may help evaluate muscle thickness and echogenicity in neuromuscular conditions. In a prospective study of 95 patients with critical illness, probable CIM/CIP was diagnosed in 17. Among 67 patients in whom ultrasound of the muscles was performed, increased echogenicity in any muscle was found to be 82 percent sensitive and 57 percent specific for CIM/CIP. An abnormal ultrasound was associated with a lower chance of discharge to home, suggesting that ultrasound may also have potential as a prognostic tool.7 

Supplemental assessment tools

Electrodiagnostic studies are a crucial part of diagnosis yet may be difficult to perform in patients with diminished level of consciousness in the ICU setting, and typically requires greater than 3 weeks of symptoms to arrive at a diagnosis.23

Nerve Conduction Study14,18,24-26  

  • Sensory nerve action potentials should be > 80% of the lower limit for at least two nerves unless there is a history of peripheral neuropathy or coexisting diagnosis of CIP.
  • CMAP amplitudes are often markedly reduced (<80% of the lower limit) in at least 2 nerves without conduction block. Distal latencies and conduction velocities remain normal.

Electromyography14,18,24-26

  • Requires collaborative and conscious patient able to perform voluntary muscle contraction.
  • Motor unit action potentials demonstrate short duration, low-amplitude, and early or normal recruitment with or without fibrillation potentials.

Direct Muscle Stimulation:14,18,24-26

  • Does not require cooperative or conscious patient.
  • Compares CMAPs elicited by direct stimulation of the nerve (neCMAP) and the muscle (mfCMAP) and is helpful distinguishing myopathy from a polyneuropathy such as CIM vs CIP.
  • In a polyneuropathy mfCMAP remains normal and only the neCMAP is reduced.
  • In a myopathy both the neCMAP and mfCMAP are reduced signifying reduced excitability of the muscle membrane inexcitable muscle.
  • Although this technique is rarely adopted, because distinguishing CIM from CIP will not likely change the management of patients in the ICU, and because of technical difficulties in performing this method, particularly in the ICU.

Muscle biopsy can also be helpful in leading to the diagnosis of the primary myopathy CIM. CIM can be further categorized pathologically as either thick filament myopathy, acute myopathy with scattered necrosis, acute myopathy with diffuse necrosis, disuse cachectic myopathy, or rhabdomyolysis.4 Because of myosin loss, some fibers characteristically demonstrate the lack of adenosine triphosphatase staining at both higher and lower hydrogen ion concentrations. One study showed increased expression of calcium-activated protease, calpain, suggesting abnormal intracellular calcium homeostasis as an important part of pathogenesis.27 Biopsies have also show low glutamine levels, low protein/DNA levels, and high concentrations of extracellular water, indicating that a deficiency of glutamine may be pathogenically linked to CIM.23,28

Professional issues

Because most patients cannot express themselves and may be dealing with life and death issues, it is important to identify the person who has power of attorney and closely communicate with legitimate members of family and social circles.

Rehabilitation Management and Treatments

Available or current treatment guidelines

Specific rehabilitation strategies needed to improve functional outcomes in CIM have not yet been established. There is no specific pharmacologic treatment for CIM. Instead, prevention, and early recognition of this disorder appear to be the most important factors in management to improve subsequent outcomes. From a medical perspective, prevention of CIM may be possible by minimizing risk factors and through aggressive medical management of critically ill patients.29 Some studies also support strict glycemic control with glucose levels between 80 and 110 mg/dl via insulin therapy to decrease of risk of developing CIM.24 In addition to medical management numerous studies argue that early rehabilitation and mobilization of patients in the ICU results in improved short term outcomes and reduction of sequelae associated with deconditioning and immobility.8,30 There is convincing evidence that early mobilization should be started soon after patients are admitted to the ICU, and that these measures are likely to improve short-term outcomes. Neuromuscular electrostimulation and nutritional supplementation may also be considered.31

Coordination of care

The interdisciplinary team should include physicians, nurses, respiratory therapists, physical, occupational, and possibly speech therapists. Follow-up with a physiatrist and/or primary care provider should be arranged for functional reassessment at 2 to 3 months after the patient’s discharge from critical care.32

The COVID-19 pandemic amplified patient communication impairment in intensive care unit leading to miscommunication, misinterpretation and poorer outcomes. Health care professionals and therapists had to become creative to bridge the gap between interaction which is a staple for their therapy and family teaching.33

Patient & family education

The patient’s family and/or caregiver should also be involved in the rehabilitation goals. Some critical care units use patient diaries as a way to deliver information to the patient and their families and/or caregivers. It is also important to communicate with both the patient and their family regarding the gradual nature of recovery from this disease process.

Emerging/unique interventions

  • Some studies showed that electrical muscle stimulation implemented in patients with CIM, especially those that are intubated and sedated, can improve muscle strength and lead to earlier mobilization.4
  • Early delivery of physical therapy while in the ICU has also shown short-term benefits.8
  • The use of early mobility and walking programs has also shown to be beneficial in short and long term outcomes.4
  • Nutritional supplementation with proteins, antioxidants, and amino acids such as glutamine and arginine may help facilitate more rapid recover of muscle catabolism that occurs during CIM.34
  • Due to the effects of the COVID pandemic, many system-based gaps in medicine were found, such as the lack of bilingual communication modalities and delayed utilization of therapy resources due to contact precautions. Often times, patients had impaired cognitive and motor function associated with a variety of post-COVID-19 sequelae increasing their therapy needs and a delayed transition to a speaking valve due to the secretion burden.33

Translation into practice: practice “pearls”/performance improvement in practice (PIPs)/changes in clinical practice behaviors and skills

Traditionally, bedrest has been considered the ICU activity standard, with physical therapy postponed until after ICU discharge. However, prevention appears to be one of the most successful treatment for CIM. Changing ICU attitudes and beliefs toward early mobilization of ICU patients is of the utmost importance. This involves creating a culture sensitive to patient-focused outcomes and improved interdisciplinary teamwork. Mobility has been shown to be facilitated by an ICU culture where activity is a key component of care.35

Cutting Edge Concepts and Practice

  • Early and regular mobilization of ICU patients.
  • Early delivery of ICU-Based Physical Therapy.
  • Neuromuscular electric stimulation.
  • Quantitative neuromuscular ultrasound in evaluation of neuromuscular pathology early in critical illness.36
  • Use of nutritional therapies (e.g., glutamine and glutathione supplementation), and hormonal therapy may be beneficial.36

Gaps in the Evidence-Based Knowledge

  • Development of strategies to most effectively identify patients at risk of critical illness-associated physical morbidity, psychologic morbidity, and cognitive dysfunction.
  • Studies to elucidate the mechanisms by which immobility and other aspects of critical illness lead to neuromuscular dysfunction and injury.
  • Studies examining the possible preventative effects of electrical muscle stimulation.
  • Comparative studies evaluating the resources needed to safely mobilize and exercise an ICU patient.
  • Randomized controlled trials evaluating early rehabilitation strategies and optimal timing during critical illness including a comparison of ICU based versus acute inpatient rehabilitation physical therapy.
  • Prospective studies examining the long-term consequences and co-morbidities associated with CIM.
  • Retrospective studies examining the effects of rehabilitation in patients who have recovered from SARS2-COVID and CIM.
  • Studies examing the financial plausibility of early mobilization in an ICU setting.

References

  1. Brown D, Williams K, Cuccurullo S. Myopathies. In: Maitin IB, Cruz E. eds. CURRENT Diagnosis & Treatment: Physical Medicine & Rehabilitation. McGraw Hill; 2014. Accessed September 05, 2023. https://accessmedicine-mhmedical-com.ezaccess.libraries.psu.edu/content.aspx?bookid=1180&sectionid=70378701
  2. Schweickert W, Kress JP. ICU-Acquired Weakness. In: Hall JB, Schmidt GA, Kress JP. eds. Principles of Critical Care, 4e. McGraw Hill; 2014. Accessed September 05, 2023. https://accessmedicine-mhmedical-com.ezaccess.libraries.psu.edu/content.aspx?bookid=1340&sectionid=80035955
  3. Doughty, Christopher T., and Amato Anthony  A. “109 Disorders of Skeletal Muscle.” Bradley and Daroff’s Neurology in Clinical Practice, 2-Volume Set, ELSEVIER – HEALTH SCIENCE, S.l., 2021.
  4. Zhou C, Wu L, Ni F, Ji W, Wu J, Zhang H. Critical illness polyneuropathy and myopathy: a systematic review. Neural Regen Res. 2014;9(1):101-110. doi:10.4103/1673-5374.125337
  5. Price DR, Mikkelsen ME, Umscheid CA, Armstrong EJ. Neuromuscular Blocking Agents and Neuromuscular Dysfunction Acquired in Critical Illness: A Systematic Review and Meta-Analysis. Crit Care Med. 2016 Nov;44(11):2070-2078. doi: 10.1097/CCM.0000000000001839. PMID: 27513545.
  6. Dubowitz, Victor, et al. “Toxic and Drug-Induced Myopathies.” Muscle Biopsy: A Modern Approach, Ballière Tindall, London, 1985.
  7. Lacomis D, Petrella JT, Guiliani MJ. Cause of neuromuscular weakness in the intensive care unit: A study of ninety-two patients. Muscle Nerve. 1998;21:610-617.
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  9. Weber-Carstens S, Schneider J, Wollersheim T, Assmann A, Bierbrauer J, Marg A, Al Hasani H, Chadt A, Wenzel K, Koch S, Fielitz J, Kleber C, Faust K, Mai K, Spies CD, Luft FC, Boschmann M, Spranger J, Spuler S. Critical illness myopathy and GLUT4. Am J Respir Crit Care Med.2013;187(4)387-396.
  10. Koch S, Wollersheim T, Bierbrauer J, Haas K, Mörgeli R, Deja M, Spies CD, Spuler S, Krebs M, Weber-Carstens S. Long-term recovery In critical illness myopathy is complete, contrary to polyneuropathy. Muscle Nerve. 2014 Sep;50(3):431-6. doi: 10.1002/mus.24175. Epub 2014 Jul 14. PMID: 24415656
  11. Herridge M (2013). Chapter 68. long-term outcomes after mechanical ventilation. Tobin M.J.(Ed.), Principles and Practice of Mechanical Ventilation, 3e. McGraw Hill. https://accessmedicine-mhmedical-com.ezaccess.libraries.psu.edu/content.aspx?bookid=520&sectionid=41692317
  12. Taylor, Christopher. Intensive Care Unit Acquired Weakness. Anaesthesia & Intensive Care Medicine, vol. 19, no. 3, Feb. 2018, pp. 79–82., doi:10.1016/j.mpaic.2017.12.009.
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  14. Latronico, Nicola; Bolton, Charles F.The Lancet Neurology;London Vol. 10, Iss. 10, (Oct 2011): 931-41.
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  17. Dhand UK. Clinical approach to the weak patient in the intensive care unit. Resp Care. 2006;51(9):1024-1040.
  18. ZʼGraggen WJ, Tankisi H. Critical Illness Myopathy. J Clin Neurophysiol. 2020 May;37(3):200-204. doi: 10.1097/WNP.0000000000000652. PMID: 32358245.
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  21. Bunnell A, Ney J, Gellhorn A, Hough CL. Quantitative neuromuscular ultrasound in intensive-care acquired weakness: a systematic review. Muscle Nerve. 2015; 52:701-708.
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  25. Lefaucheur JP, Nordine T, Rodriguez P, Brochard L. Origin of ICU acquired paresis determined by direct muscle stimulation. J Neurol Neurosurg Psychiatry. 2006;77:500-506.
  26. Marrero HG and Stålberg EV. Optimizing testing methods and collection of reference data for differentiating critical illness polyneuropathy from critical illness myopathies. Muscle Nerve.2016;53:555-563.
  27. Showalter CJ, Engel AG. Acute quadriplegic myopathy: analysis of myosin isoforms and evidencefor calpain-mediated proteolysis. Muscle Nerve. 1997;20:316-322.
  28. Hermans G, De Jonghe B, Buryninckx F, Van den Berghe G. Interventions for preventing critical illness polyneuropathy and critical illness myopathy. Cochrane Database of Systemic Reviews. 2014;1:1-24.
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  30. Jang MH, Shin MJ, Shin YB. Pulmonary and Physical Rehabilitation in Critically Ill Patients. Acute Crit Care. 2019;34(1):1-13. doi:10.4266/acc.2019.00444
  31. Pauley, Ellen, et al. “Physical rehabilitation and critical illness.” Anaesthesia &amp; Intensive Care Medicine, vol. 22, no. 11, 2021, pp. 690–692, https://doi.org/10.1016/j.mpaic.2021.07.021.
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  34. Burnham EL, Moss M, Ziegler TR. Myopathies in critical illness: characterization and nutritional aspects. J Nutr. 2005;135:1818S-1823S.
  35. Bailey PP, Miller RR 3rd, Clemmer TP. Culture of early mobility in mechanically ventilated patients. Crit Care Med. 2009;37(10 Suppl):S429-435.
  36. Bunnell A, Ney J, Gellhorn A, Hough CL. Quantitative neuromuscular ultrasound in intensive-care acquired weakness: a systematic review. Muscle Nerve. 2015; 52:701-708.

Original Version of the Topic

Erik Hoyer, MD, MA. Critical Illness Myopathy. 11/27/2012

Previous Revision(s) of the Topic

Erika Moody, MD, John Harrell, MD. Critical Illness Myopathy. 8/18/2016

Mollie Elizabeth Andreae, MD, Justin Sup Hong, MD. Critical Illness Myopathy. 12/10/2020

Author Disclosure

Almeet Kaur, DO
Nothing to Disclose

Justin S. Hong, MD
Nothing to Disclose