Critical Illness Neuropathy
Asaad Abdelfatah Ali;
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 include; 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. The CSF examination in most patients shows an elevation in protein without increased white cells by the second week of the illness while in CIN the CSF findings are normal. It includes an acute inflammatory demylinating polyneuropathy (AIDP) or acute motor axonal neuropathy (AMAN) forms.Autonomic disturbances are found in 50% of patients and are potentially lethal.
Electrophysiological studies in AIDP shows slow nerve conduction velocities, conduction block.While in AMAN there are low motor amplitudes, normal conduction velocities, and low or absent motor responses and normal sensory responses. Needle electrode electromyogram early may demonstrate only a decreased number of motor unit potentials firing on voluntary effort and later on, active denervation changes as fibrillation potentials may be seen if axon loss has occurred. Electrolytes imbalance as hyponatremia may be present. General treatment strategy includes close monitoring of respiratory parameters, rapid recognition and management of autonomic
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. The CSF examination in most patients shows an elevation in protein without increased white cells by the second week of the illness while in CIN the CSF findings are normal. It includes an acute inflammatory demylinating polyneuropathy (AIDP) or acute motor axonal neuropathy (AMAN) forms.Autonomic disturbances are found in 50% of patients and are potentially lethal.
Electrophysiological studies in AIDP shows slow nerve conduction velocities, conduction block.While in AMAN there are low motor amplitudes, normal conduction velocities, and low or absent motor responses and normal sensory responses. Needle electrode electromyogram early may demonstrate only a decreased number of motor unit potentials firing on voluntary effort and later on, active denervation changes as fibrillation potentials may be seen if axon loss has occurred. Electrolytes imbalance as hyponatremia may be present. General treatment strategy includes close monitoring of respiratory parameters, rapid recognition and management of autonomic
Other data
| Title | Critical Illness Neuropathy | Other Titles | الاعتلال العصبي المكتسب لمرضى الرعاية المركزة | Authors | Asaad Abdelfatah Ali | Issue Date | 2014 |
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