الفهرس 
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Abstract
Weakness in critically ill patients is classified into neuropathy and myopathy. This weakness may develop before the admission to the ICU or affects patients inside the ICU secondary to severe systemic illnesses which is then called ICU acquired weakness (ICU-AW) and includes critical illness polyneuropathy (CIN) and critical illness myopathy (CIM).The main acute neuropathic disorders that need ICU admission and mainly due to expected respiratory failure includes; Certain well-known peripheral neuropathies as Guillain Barre Syndrome(GBS) and acute intermittent porphyria - Neuromuscular junction disorders as myasthenia gravis and botulism.
Two thirds of GBS patients have had a preceding viral or bacterial infection. Most patients present with rapidly progressive areflexic paralysis that typically starts in the legs and spreads proximally, and involves the diaphragm in 25% of cases and the facial muscles in more than 50% of individuals.
General treatment strategy includes close monitoring of respiratory parameters, rapid recognition and management of autonomic dysfunction, nursing care and emotional support. GBS is an immune-mediated disorder, responds to plasma exchange or to intravenous immunoglobulin or both. So, early diagnosis is essential to start treatment early and reduce morbidity.
The most important neuromuscular junction disorder causing acute weakness is myasthenia gravis which is an acquired autoimmune disorder characterized by reduction of postsynaptic nicotinic receptors at NMJ due to either its destruction or inactivation by circulating (Ig G). Most individuals present with ocular muscle weakness (manifested as ptosis and diplopia) and generalized weakness with exaggerated muscle fatigue that worsens with repeated activity and improves with rest. The deficit in myasthenia is purely motor, with no sensory involvement nor autonomic instability. Deep tendon reflexes are usually preserved.
Critical illness polyneuropathy (CIN) is one of the two most common causes of newly ICU-AW. Critical illness polyneuropathy (CIN) affects 75% of patients with severe sepsis and multiorgan failure. It is hypothesized that microvascular endothelial alterations in the endoneurium surrounding the individual nerve fibers are crucial in the development of CIN. Patients with CIN complain of sensorimotor axon-loss polyneuropathy. Distal muscles may be affected to a greater extent than proximal, generalized flaccid weakness with depressed or absent reflexes and distal sensory loss.
Compression neuropathies are common in ICU. Several nerves are particularly at risk, compression of which may increase morbidity as ulnar and peroneal nerves.
Myopathy is a general term for every potential muscle problem (primary structural or functional impairment). Myopathy may be hereditary or acquired. One of the most important causes of myopathy in critically ill patients is critical illness myopathy (CIM) which causes failure of weaning from ventilator
Drug-induced/toxic myopathy is caused by many drugs that have been associated with muscle damage, proximal weakness, an elevated CK level, myopathic findings on EMG, and abnormalities on muscle biopsy. But, it may occur more often with exposure to specific drugs as (cimetidine, D-penicillamine, L-Dopa, cholesterol-lowering agents) Symptoms generally improve after stopping the medication.
Rhabdomyolysis is one of the causes of acute myopathy in which there is striated muscle fiber breakdown that lead to release of myoglobin and potassium. Plasma myoglobin is precipitated in the renal tubules, producing acute renal failure. Potassium release into the blood stream may cause cardiac arrest, so early management is a must by aggressive hydration and forced diuresis.
The distinction between neuropathy and myopathy requires differential diagnosis of the main acute conditions that develop before admission to the ICU and distinguishing between CIM and CIN.
Critical illness polyneuropathy (CIP) & (CIM) are hardly distinguished from their clinical findings and investigation. In the final analysis, both share severe generalized weakness with areflexia and cannot always be reliably differentiated by EMG testing. A biopsy may be helpful in ambiguous situations.