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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