Critical Illness Myopathy - Causes, Symptoms, Treatment, and Recovery

Introduction

Critical illness polyneuropathy and myopathy are common causes of neuromuscular weakness in patients admitted to the intensive care unit. Approximately 25 to 83 percent of people with critical illness suffer from critical illness polyneuropathy or myopathy. The diagnosis of critical illness myopathy is challenging. Myopathy affects skeletal muscles and muscle fibers, causing muscle weakness. The treatment should include the withdrawal of medications and improved patient functional outcomes.

What Is Critical Illness Myopathy?

Critical illness myopathy develops in patients admitted to the intensive care units for more than two weeks. This condition is characterized by muscle weakness and failure of weaning from mechanical ventilation. It involves the muscles of respiration and limbs due to prolonged immobility and drugs used in critical care, such as steroids, sedatives, or muscle relaxants.

What Causes Critical Illness Myopathy?

The exact etiology of critical illness myopathy is not known. Common causes and risk factors of critical illness myopathy include the following.

• Prolonged intubation.

• Prolonged immobilization.

• Use of steroids, neuromuscular blockade agents

• Sedatives.

• Muscle relaxants.

• Sepsis.

• Multi-organ failure.

• Acute respiratory distress syndrome (ARDS).

• Malnutrition.

• Older age.

• Impaired glucose homeostasis.

• Status asthmaticus.

• Chronic obstructive pulmonary disease (COPD).

These factors can disrupt the structure and function of muscle, leading to muscle atrophy and degeneration of muscle fibers.

What Is the Pathophysiology of Critical Illness Myopathy?

The pathophysiology of critical illness myopathy has yet to be entirely understood. It involves the alterations in the following mechanisms of muscles.

Microvascular Alterations:

• Vasodilation.

• Cytokine production.

• Increased permeability.

• Endo neural edema.

• Hypoxemia.

• Extravasation.

Metabolic Alterations:

• Hyperglycemia.

• Activation of proteolytic pathways.

• Hypoalbuminemia.

• Amino acid deficiency.

• Hormone imbalance.

Electrical Alterations:

• Ion channel dysfunction.

• Cell depolarization.

• Cell in-excitability.

• Altered calcium homeostasis.

• Contraction coupling.

Bioenergetic Failure:

• Antioxidant depletion.

• Reactive oxygen species increase.

• Apoptosis.

• Mitochondrial dysfunction.

What Are the Symptoms of Critical Illness Myopathy?

The most common symptoms of critical illness myopathy include the following.

• Muscle weakness is more on the proximal side.

• Sensory preservation.

• Atrophy of the muscles.

What Is the Pathological Classification of Critical Illness Myopathy?

The pathological classification of critical illness myopathy includes the following.

• Thick filament myopathy occurs due to the loss of thick filaments.

• Acute myopathy with scattered necrosis.

• Cachectic myopathy caused by normal or type 2 fiber atrophy.

• Acute myopathy with diffuse necrosis occurs due to marked necrosis.

• Rhabdomyolysis caused by normal or mild necrosis.

How to Diagnose Critical Illness Myopathy?

The diagnosis of critical illness myopathy includes the following.

History:

Understanding the patient’s underlying medical conditions and history of their illness is essential. If a patient is conscious, a history of weakness, past medical history, the pattern of weakness, difficulty swallowing, presence of sensory complaints, and history of medications are taken and recorded.

Physical Examination:

Patients with critical illness myopathy exhibit the following characteristic features on physical examination.

• Symmetric diffuse muscle weakness.

• Proximal muscle weakness is more significant than distal.

• Involvement of respiratory muscles and neck flexors.

• Evaluation of muscle strengths using the Medical Research Council (MRC) system to access muscle groups.

• Flaccid muscle tone.

Physical examination for patients under sedation is complex.

Functional Assessment:

Patients intubated in the intensive care unit have altered mental statuses, limited physical activities, and cognitive impairment. The healthcare team will assess the physical and mental disabilities for better treatment and rehabilitation.

Laboratory Studies:

There are no biomarkers for the diagnosis of critical illness myopathy. Comprehensive laboratory evaluation detects critical illness myopathy and other diseases. Serum creatinine phosphokinase (CPK) is measured to diagnose critical illness. The CPK levels become ten times higher than the average level.

Imaging:

There is no specific imaging to rule out critical illness myopathy. Some standard imaging diagnostic tests include the following.

• Neuraxial Imaging to rule out stroke and spinal cord infarct in non-communicative patients.

• Magnetic resonance imaging (MRI) of muscles detects diffuse muscle edema.

• Ultrasound uses muscle thickness to identify myopathy.

Supplemental Assessment Tools:

Electrodiagnostic studies are challenging to perform in unconscious patients in the ICU setting. The following are some diagnostic tools to assess critical illness myopathy.

• Nerve conduction study detects sensory nerve action potentials and CMAP amplitudes.

• Electromyography is performed on conscious patients to examine voluntary muscle contraction.

• Direct muscle stimulation is performed on unconscious patients to detect critical illness myopathy.

Muscle biopsy detects primary critical illness myopathy.

What Are the Rehabilitation Management and Treatments for Critical Illness Myopathy?

There are no specific pharmacological treatments and rehabilitation strategies for critical illness myopathy. Prevention and early recognition of this condition are essential for the management of this condition. The following are some management and rehabilitative techniques.

Coordination of Care:

An interdisciplinary team containing physicians, nurses, physiotherapists, occupational therapists, and speech therapists. Follow-up care for functional reassessment 2 to 3 months after the patient’s discharge from critical care.

Patient and Family Education:

The involvement of family and caregivers is essential for successful rehabilitation. Communication about the patient’s condition and recovery process with family and caregivers helps manage critical illness myopathy.

Emerging Interventions:

• Electrical muscle stimulation for sedated or intubated patients with critical illness myopathy improves muscle strength and earlier mobilization.

• Earlier initiation of physical therapy in the intensive care unit gives short-term benefits.

• Early mobility and walking improve the physical condition of the patients.

• Early mobilization and kinesiotherapy reduce hospitalization and mechanical ventilation duration and help faster recovery and physical functions.

• Nutritional supplementation, including proteins, amino acids (glutamine and arginine), and antioxidants, provide rapid muscle catabolism recovery.

Hyperglycemia is a risk factor for critical illness myopathy, strict glycemic control with insulin can prevent critical illness myopathy.

How to Improve the Prevention of Critical Illness Myopathy?

The strategies to improve the prevention of critical illness myopathy include the following.

• Development of strategies to identify the patients at risk of developing comorbidities in the ICU.

• Evaluation of factors associated with neuromuscular dysfunction and injury.

• Evaluation of resources needed for the safety mobilization of patients in the ICU.

• Examination of long-term consequences and comorbidities associated with critical illness myopathy.

Conclusion

Patients admitted to the intensive care unit may suffer from critical illness polyneuropathy, myopathy, or a combination of both. It is vital to diagnose and distinguish the condition to provide appropriate treatment. More research is needed to find diagnoses and treatment plans for critical illness myopathy.