Introduction:
In intensive care patients, muscular weakness and atrophy have long been linked to a combination of immobility and catabolism. Particular damages to the peripheral nerve, the neuromuscular junction, and the muscle have lately been identified as more likely causes of weakness in these patients. Clinically, the most significant implications are delayed weaning from the ventilator and protracted neurologic rehabilitation. Critical care and mechanical breathing are required in neuromuscular illnesses such as Guillain-Barre syndrome, myasthenia gravis, and various myopathies. In the last decade, it has been recognized that various neuromuscular disorders can develop spontaneously during critical conditions, resulting in delayed weaning from the ventilator, muscle weakness, and a delay in neurologic rehabilitation. Critical illness polyneuropathy is the most common of these neuromuscular diseases; however, neuromuscular transmission disorders and myopathies are becoming more common.
What Is Critical Illness Polyneuropathy?
Though infrequently documented in previous decades, peripheral nerve abnormalities in ICU patients have been researched more systematically since the mid-1980s. French, Canadian, and American investigators identified a diffuse axonal polyneuropathy, later called critical illness polyneuropathy (CIP), as the reason for weaning failure and weakness in the muscles simultaneously. Subsequent studies and case reports backed up the CIP notion. In a prospective trial, it was discovered in 70 % of individuals with sepsis and multiple organ failure.
Critical illness polyneuropathy (CIP) is the sudden onset of severe symmetric weakness in critically ill patients, frequently due to sepsis, airway obstruction, multisystem failure of the organs, or septic inflammatory response syndrome (SIRS). Distal extremities weakness, degeneration, loss of sensory perception, paresthesia, and reduced or absent deep tendon reflexes are all clinical manifestations.
Pathological Process: The pathogenesis of CIP is still unknown and complex, with human research pointing to axonal degeneration.
It is thought to be related to:
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Factors such as drugs, diet, metabolism, and toxicity.
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A lengthy ICU stay.
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The number of invasive operations performed.
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Hyperglycemia.
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Reduced albumin levels.
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The degree of seriousness of multisystem organ failure.
With risk factors such as sepsis, SIRS, multi-organ Failure (MOF), female gender, organ dysfunction duration, ICU stay duration, renal failure, low serum albumin, and hyperglycemia
Clinical Features: CIP clinical characteristics often include:
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Muscle weakness is most noticeable in the lower extremities. This should be suspected if there is diminished limb movement after a painful stimulus to the distal limb. Flaccid weakness can be seen in both directions.
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Cranial nerves are rarely impacted when there is no facial weakness.
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Muscle wasting has been noticed in one-third of patients.
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Reduced muscle Reflexes. Reflexes typically occur at the beginning of the disease, but they gradually fade away.
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Weaning from ventilator difficulties
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Sensory loss is difficult to evaluate in a sedated or intubated patient.
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Impaired consciousness. This is usually indicative of an encephalopathy.
Diagnosis: Although infrequently used, electrodiagnostic testing is still the highest standard for diagnosing critical illness polyneuropathy. Nerve conduction tests and needle electromyography are examples of this. While EMG is the best technique to diagnose CIP, performing a thorough study in ICU settings might be difficult due to electrical interference, anasarca, hypothermia, peripheral edema, or restricted patient participation in the exam.
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There are currently no validated biomarkers available.
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CIP will show signs of denervation and reinnervation with tiny muscle fibers, fiber-type grouping, and fiber group degeneration with extensive axonal degeneration of both motor and sensory nerves, even though it is not routinely performed. Muscle biopsy can reveal thick filament loss, typically linked with CIM, as well as denervation and reinnervation alterations and axonal degeneration related to CIP.
What Is Critical Illness Myopathy?
Critical illness myopathy (CIM), also known as ICU myopathy, acute quadriplegic myopathy, critical care myopathy, acute necrotizing myopathy in intensive care, and thick filament myopathy, is a common cause of ICU-acquired weakness (ICUAW). CIM is the most significant cause of delayed recovery and prolonged mechanical ventilation, resulting in prolonged admission of patients in ICUs, increased mortality and morbidity, and higher healthcare expenses. As a result, understanding the underlying mechanisms of CIM is critical for developing techniques for rapid and precise diagnosis and identifying therapeutic agents and strategies for avoiding or managing CIM.
Diagnosis:
CIM is likely to be underdiagnosed due to a lack of early and practical diagnostic methods and the requirement for a muscle biopsy for a precise diagnosis under current diagnostic criteria. Early detection of evolving CIM may allow clinical studies investigating preventive and therapeutic measures such as glucose management, early mobility, and physical therapy.
According to current standards, CIM should be diagnosed using patient history, physical examination, conventional nerve conduction studies (NCS), electromyography (EMG), and muscle biopsy. As a result, current criteria allow for CIM diagnosis only at an advanced level, putting individuals in the beginning stages in danger of misinterpretation.
What Are Neuromuscular Transmission Disorders?
Disruptions in neuromuscular transmission, like motor neuron disorders and myopathies, produce muscle weakening and respiratory failure without sensory signs. There has been an increase in the number of reports in recent years dealing with prolonged neuromuscular blockade in patients treated with high doses of non-depolarizing neuromuscular-blocking agents (NMBAs) such as Pancuronium, Vecuronium, and Atracurium. In other cases, the drug's metabolism was reduced, resulting in higher plasma levels of the substance and its metabolites.
How Are Neuromuscular Complications Treated?
Management: Following a CIP diagnosis, the inter-professional team of physicians, physical therapists, occupational therapists, speech therapists, dietitians, social workers, and case managers must collaborate to arrange early mobilization and vigorous multidisciplinary rehabilitation.
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Glycemic Control: Research has demonstrated that rigorous insulin therapy for hyperglycemia reduces the risk of critical illness polyneuropathy and myopathy, as well as the length of the intensive care unit stay and the 180-day mortality rate.
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Treatment of Sepsis: Appropriate and timely treatment of sepsis is likely to lessen the occurrence of CIP. Treatment approaches center on semi-recumbent positioning, low tidal volume mechanical ventilation, and no or cautious use of sedative or neuromuscular-blocking agents to limit this risk.
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Muscle Relaxants: Neuromuscular blocking agents (NMBA), strong muscle relaxants, disrupt neuromuscular transmission and produce muscle paralysis. Numerous research has found a link between ICUAW and neuromuscular blockade. It is recommended that when using NMBAs in critically ill patients, continuous vigilance is required, as well as selecting the appropriate NMBA for each setting, following evidence-based protocols to guarantee sufficient sedation and pain relief, using suitable instruments to determine the extent of neuromuscular blockade, and robust rehabilitation regimens throughout periods of decreased mobility.
What Is the Prognosis of CIP and CIM?
CIP and CIM are to be held accountable for extended and, in some cases, severe impairment following a critical illness. There is significant evidence that both conditions (or a combination) can produce persistent weakness months or years after the severe illness has resolved. As a result, 28 % of CIP, CIM, or both patients may never regain independent walking or continuous spontaneous ventilation.
Conclusion:
Neuromuscular difficulties contribute significantly to delayed mechanical ventilation weaning and protracted neurorehabilitation. The most common of these consequences is acute axonal neuropathy, often called CIP. Other causes include long-term use of neuromuscular blocking drugs, which causes chronic inhibition of neuromuscular transmission, and various myopathies.
