1. 1. Presenter : Dr. Kumar Neuromuscular weakness related to critical illness
2. 2. Introduction Neuromuscular weakness is a common occurrence in patients who are critically ill, developing in 25 percent of patients who are in the ICU and ventilated for at least seven days. Weakness is partly a consequence of improved survival in patients with multiorgan failure and sepsis, but is also a consequence of treatments administered in the ICU, including i.v glucocorticoids and paralytic agents. Neuromuscular weakness in the ICU is most often due to
3. 3. CRITICAL ILLNESS MYOPATHY The most common form of intensive care unit (ICU)-acquired myopathy is critical illness myopathy (CIM). This disorder is also known by other names, including acute quadriplegic myopathy and thick filament myopathy.
4. 4. Epidemiology and risk factors patients with status asthmaticus or COPD and 7 percent who receive a liver transplant develop CIM. Patients with other critical illnesses, such as ARDS, may also be affected. Each of these disorders is typically associated with intravenous (IV) glucocorticoid therapy. Triggering factors may include a higher illness severity index, hyperglycemia, hyperthyroidism ,
5. 5. Clinical features Critical illness myopathy usually begins several days after IV glucocorticoid treatment is initiated. The time of onset of the myopathy may not be known in patients who are comatose or encephalopathic. The most common presenting features of CIM are 1. Flaccid quadriparesis that may affect proximal more than distal muscles 2. Failure to wean from mechanical ventilation
6. 6. Laboratory and electrodiagnostic findings in CIM The increase in serum CK peaked around four days after initial treatment with glucocorticoids, and lasted for as long as 16 days. major nerve conduction findings of CIM are normal to low motor amplitudes with occasional broadening of the compound muscle action potential . Phrenic motor amplitudes may also be low. Needle electromyography shows early or normal full recruitment
7. 7. Direct muscle stimulation- muscles exhibit electrical inexcitability This inexcitability is due to a defect in muscle membrane depolarization, which may be related to increased inactivation of sodium channels at the resting potential
8. 8. pathogenesis of CIM The major histopathologic finding in CIM is relatively selective loss of myosin, which can be identified as a lack of reactivity to myosin ATPase in non-necrotic fibers. atrophy of myofibers, type 2 more than type 1
9. 9. Diagnosis of CIM
10. 10. By definition, patients are or were critically ill, and weakness should have started after onset of critical illness. 1. For a definite diagnosis of critical illness myopathy , patients should have all four major features and one or more supportive features. 2. For probable critical illness myopathy , patients should have any three major features and one or more supportive feature. 3. For possible critical illness myopathy , patients should have either major features 1 and 3, or 2 and 3, and one or more supportive feature.
11. 11. Treatment and prognosis of CIM Treatment of CIM is directed toward 1. discontinuation or reduction of glucocorticoids as soon as possible, 2. aggressive management of medical conditions 3. avoidance of additional complications such as venous thrombosis and 4. rehabilitation
12. 12. two studies have reported that intensive insulin therapy (target blood glucose 80 to 110 mg/dL [4.4 to 6.1 mmol/L]) may lower the incidence of CIM and CIP among critically ill patients who remain in the intensive care unit for seven or more days. Critical illness myopathy is usually reversible over weeks to months , but leads to prolonged ICU stays and increased length of hospital stay overall
13. 13. CRITICAL ILLNESS POLYNEUROPATHY 1. second neuromuscular condition that is commonly acquired in the intensive care unit (ICU) 2. Critical illness polyneuropathy appears to be a common complication of severe sepsis 3. mechanism of axonal injury in CIP is unknown 4. speculation focuses on injury to the microcirculation of distal nerves, causing ischemia and axonal degeneration. 5. During the early stages of sepsis, electrical inexcitability due to sodium channel inactivation may be present in
14. 14. Clinical features of CIP Affected patients manifest a sensorimotor polyneuropathy characterized clinically by 1. Limb muscle weakness and atrophy 2. Reduced or absent deep tendon reflexes 3. Loss of peripheral sensation to light touch and pin prick 4. Relative preservation of cranial nerve function
15. 15. Laboratory and electrodiagnostic findings Nerve conduction studies in patients with CIP typically reveal low motor and sensory amplitudes. Needle EMG may show fibrillation potentials in subacute to chronic patients. The serum CK levels are normal and muscle biopsy shows findings consistent with neurogenic atrophy
16. 16. Treatment and prognosis of CIP CIP with mild or moderate nerve injury, recovery of muscle strength generally occurs over weeks to months Patients with severe CIP may remain quadriplegic. treatment of CIP is supportive and includes aggressive management of sepsis and underlying medical conditions, avoidance of additional complications such as venous thrombosis, and
17. 17. COMBINED CRITICAL ILLNESS MYOPATHY AND POLYNEUROPATHY Combined CIM and CIP, sometimes called critical illness polyneuromyopathy, is increasingly recognized as a cause of neuromuscular weakness in the ICU. Sepsis and the systemic inflammatory response syndrome may be a common pathologic mechanism underlying the development of both CIM and CIP. Nerve conduction studies may be predictive of neuromuscular dysfunction as early as 72 hours after onset of critical illness.
18. 18. PROLONGED NEUROMUSCULAR JUNCTION BLOCKADE A rare disorder occurring in the ICU is prolonged neuromuscular junction blockade. This disorder is related to prolonged use (days) of paralytic agents, often in the setting of renal or hepatic insufficiency, leading to prolonged circulation of drug metabolites . These curare-like paralytic agents bind reversibly to ach receptors on the motor end-plates of nmjs, thereby inhibiting neuromuscular transmission
19. 19. The commonly used aminosteroid blocking agents, such as pancuronium and vecuronium , are normally cleared from the circulation within several hours, primarily by the liver. in patients with decreased renal function (creatinine clearance