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emmedonline
Dr. Ajith Kumar J MD
Dept. of Emergency Medicne
Travancore Medicity, Kollam
India
editor
CRITICAL ILLNESS NEUROPATHY
It is seen in the setting of prolonged critical illness, sepsis, multisystem organ failure.
It is suspected when there is failure to wean from mechanical ventilation despite improvement of underlying sepsis & critical illness
Patients will have
Diffuse weakness
Decreased reflexes
Distal sensory loss
EEG: Diffuse symmetric distal axonal sensorimotor neuropathy
Pathology : Axonal degeneration.
Mechanism : Precise mechanism is still unclear. Probably due to cytokines associated with sepsis & SIRS.
Aggressive control of glycemia with insulin decreases the risk of critical illness polyneuropathy.
Spontaneous recovery is usually seen, but may take weeks to months.
Disorders of neurotransmission
A defect in neuromuscular transmission may be source of weakness in critically ill patient.
Drugs like aminoglycoside, beta blockers , non depolarsing muscle relaxants are associated.
Risk factors for prolonged action are females, metabolic acidosis & renal failure.
Prolonged neuromuscular blockade doesnot appear to damage the PNS.
Once the offending drugs are removed, full strength is restored over days.
MYOPATHY
Critically ill patient develop muscle wasting; often in face of seemingly adequate nutritional support.
Catabolic myopathy : Due to elevated cortisol & catecholamine release, other circulating factors induced by SIRS.
Septic myopathy : Characterised by weakness progressing to a profound level over just a few days.It is assosciated with elevation in serum creatinine kinase & urine myoglobin. Both EMG & muscle biopsy may be normal initially but eventually show abnormal spontaneous activity & panfacialuar necrosis with an accompanying inflammatory reaction.
Acute quadriplegic myopathy
It describes a clinical syndrome of severe weakness in a setting of glucocorticoid & non depolarising NMBA use.
It is recognized when patient fails to wean from mechanical ventilation despite resolution of primary pulmonary process.
There will be vacular changes in type I & II muscle fibers with evidence of regulation.
Prognosis is usually good.
Since it is due to actual muscle damage recovery takes weeks to months.
Tracheostomy & prolonged ventilation is required.
Some patients will have residual long term weakness with atrophy & fatigue limiting ambulation.
Updated on 19/4/13
Reference : Harrison
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emmedonline
Dr. Ajith Kumar J MD
Dept. of Emergency Medicne
Travancore Medicity, Kollam
India
editor