Pulse Oximetry Monitoring in Stable Patients

Abstract

ease should not be given the drug or that the quantity administered should be reduced in amount. A wide variety of toxic symptoms may be manifested by patients with renal dysfunction who have been given amantadine. They may become confused, depressed, aggressive, or tense. Ataxia, dizziness, tremulousness, slurred speech, blurred vision, and convulsions have been described. Digestive disturbances, urinary retention, congestive heart failure, and orthostatic hypotension have been noted.’ Striated muscle weakness of the type manifested by the following patient has not, to our knowledge, been described previously. It is another of the adverse reactions that may be encountered in the presence of renal failure. A 59-year-old white woman was referred for emergent treatment because of progressive muscular weakness over a period of 48 h. She was unable to walk, and swallowing and breathing became difficult. The presence of a flulike syndrome had led to the administration of 100 mg of amantadine twice a day for the prior 3 days. She had a history of essential hypertension and right pyelonephritis with a renal calculus. The blood pressure was 190/100 mm Hg, and the respiratory rate was 30 breaths per minute with accessory muscle use. A forced vital capacity of only 500 ml prompted endotracheal intubation with subsequent mechanical ventilation. Pertinent serum values were as follows: potassium, 5.4 mEq/L; phosphate, 9.8 mEq/L; and bicarbonate, 9.0 mEq/L. The blood urea nitrogen level was 111 mg/dl, and the creatinine concentration was 8.0 mg/dL The creatine phosphokinase concentration was 55 U/L. Initial arterial blood gas values after mechanical ventilation was