A 64-year-old man is evaluated because of weakness and difficulty in weaning from mechanical ventilation. The patient had been admitted to the intensive care unit 2 weeks ago because of septic shock related to alcoholism, pneumonia, and Klebsiella bacteremia. He had developed respiratory failure requiring intubation and mechanical ventilation as well as acute kidney injury. His pulmonary infiltrates had responded to appropriate intravenous antibiotics and his hypotension had responded to intravenous norepinephrine. Now the patient is alert and responsive to verbal commands, is afebrile with blood pressure of 114/74 but has not tolerated several trials of weaning from the ventilator. On physical examination, the patient is cooperative. Cranial nerves are normal. Muscle strength is poor, especially in distal musculature, where he displays only 2/5 strength in the hands and feet. Proximal strength is 3/5. Ankle and knee reflexes are unobtainable. Sensory examination is difficult because of problems communicating with the patient but suggests distal sensory loss in the lower extremities. Laboratory studies show that his creatinine level has spontaneously improved to 2.4 mg/dL. Electrolytes are normal, and the patient has a mild normochromic normocytic anemia with resolving leukocytosis. Serum creatine kinase is 78 units/L (normal <140). What is the most likely cause of his weakness?
Correct Answer: Axonal degeneration of peripheral nerves with denervation potentials in myocytes
Description: This patient suffers from critical care polyneuropathy, which affects 25% to 50% of ICU patients who have suffered multiorgan failure or who have required long-term mechanical ventilation. It typically presents with motor weakness and difficulty in weaning the patient from the ventilator. Cranial nerves are spared. Distal reflex loss, sensory changes in neuropathic distribution, and normal CK help distinguish it from critical care myopathy. Both conditions can coexist in the same patient and distinction between the two conditions may not be important, as treatment of both conditions is supportive. Patients usually improve slowly with time, but prolonged dependence on the ventilator as well as weakness and sensory loss lasting months or years often occur. The cause of critical care polyneuropathy is unknown, but axonal degeneration on nerve conduction studies is characteristic.Loss of myosin characterizes the closely related condition of critical care myopathy, but sensory changes and reflex loss would not be anticipated in a myopathic process. Neuromuscular blockade again would not cause sensory and reflex changes. Thiamine deficiency can be provoked in a malnourished patient (such as one suffering from chronic alcoholism) but would be associated with nystagmus, ataxia, and mental status changes rather than distal weakness and neuropathy. Demyelination (rather than axonal degeneration) is associated with Guillain-Barre syndrome, but this condition would be very unlikely in this ICU patient without antecedent viral or Campylobacter infection.
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