Critical Illness Polyneuropathy

The occurrence of muscle weakness in patients with sepsis and multiple organ failure managed in the intensive care unit has been recognized with increasing frequency in the last 15 years. This weakness is due to an axonal polyneuropathy, otherwise called critical illness polyneuropathy. It must be differentiated from myopathy or disturbance of the neuromuscular junction that can also occur in the intensive care setting. y Neither the cause nor the exact mechanism of critical illness polyneuropathy has been elucidated. Nutritional, toxic, metabolic, and vascular factors have all been proposed as likely causes, but none has been proved so far. y

The difficulty in examining critically ill patients may explain why this complication has only recently been recognized. The presence of encephalopathy or generalized edema can make the clinical diagnosis difficult to obtain. Predominantly proximal weakness can lead to quadriparesis. The facial muscles can be mildly weak, but the muscles of the eyes, tongue, and jaw are relatively spared. y Deep tendon reflexes are partially preserved. Nevertheless, the signs of limb weakness and loss of previously elicited tendon reflexes are not present in all patients, even those who are subsequently shown by electrophysiological studies to have a moderately severe polyneuropathy. y

Electrophysiological studies demonstrate acute axonal damage to the peripheral nerves. Signs of primary demyelination, such as marked slowing of nerve conduction velocities, prolongation of distal latencies, dispersion of compound muscle action potentials, conduction block, and increased F-wave latencies, are absent even in severe cases of polyneuropathy. y Parenchymatous axonal damage and marked neurogenic atrophy are constant features of nerve biopsy.

Before the recognition of critical illness polyneuropathy, these cases were usually misdiagnosed as acute demyelinating Guillain-Barre syndrome. The essentials for diagnosis of Guillain-Barre syndrome (e.g., absent reflexes, albuminocytological dissociation in the CSF, and evidence of demyelination in the electrophysiological studies), however, are not present in most critically ill patients with neuromuscular weaning failure. Furthermore, prolonged neuromuscular blockade following long-term treatment with muscle relaxant drugs; aminoglycoside antibiotics; neuromuscular blocking agents in combination with high-dose corticosteroids for treatment of life-threatening status asthmaticus; and infectious, metabolic, or toxic myopathies or neuropathies should be included in the differential diagnosis of weakness and prolonged dependence on the ventilator. y , y

Sepsis and multiple organ failure still has a high mortality rate, even in fully equipped intensive care units. Clinical recovery from the neuropathy is rapid and nearly complete in those patients who survive, although it may appear to be incomplete on electrodiagnostic studies. Thus, neuropathy acquired during critical illness, although causing a delay in weaning from ventilatory support and hospital discharge, does not worsen long-term prognosis. y

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Peripheral Neuropathy Natural Treatment Options

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