Four critically ill patients exhibited phenytoin toxicity.

Four critically ill patients exhibited phenytoin toxicity. Hypoalbuminemia or concomitant displacing unsalable articles resulted in an increased fraction of unchecked drug. Clinical findings included gradual decrease in on a level of consciousness and cerebellar signs. Marked phenytoin toxicity can meet the eye in critically ill patients with hypoalbuminemia and can ofttimes be detected only by direct measurement of emancipated phenytoin levels.

In critical care units, generalized tonic-clonic seizures befall most often in patients with acute electrolyte abnormalities, in patients with physic toxicity, or in patients undergoing unusual narcotic drug withdrawal.[1] Phenytoin is the first-line mix with drugs in treatment of seizures. Monitoring of total serum phenytoin, however, may be misleading because the high propensity of phenytoin binding to serum albumin may be reduc in critical disease states that are associated with hypoalbuminemia. In addition, mix with drugss (often antibiotics) may further increase independent phenytoin concentration by competitive displacement from protein-binding sites.[2-5] Unfamiliarity with this pharmacologic interaction in a critical care setting may ready an increase in the dose of phenytoin in a patient with a normal total serum phenytoin even who in fact has an elevated at liberty phenytoin level. We report the cases of four patients with harsh phenytoin intoxication as a terminate of hypoalbuminemia.

CASE REPORTS

CASE 1

An 80-year-old woman was admitted to the surgical ICU following surgery for a perforated duodenal imposthume The postoperative course was complicated by the agency of sepsis. After a single tonic-clonic seizure, her of the same height of consciousness deteriorated. An EEG showed nonconvulsive status epilepticus. A comput tomographic (CT) scan was normal. She was had intellectually deep hypocalcemia (ionized calcium, 2.7 mg/dl) She was treated with intravenous diazepam and received a loading dose of 1400 mg of phenytoin. She became gradually unresponsive, and the maintenance dose of phenytoin was increased. At that time, the EEG showed generalized slowing unless no specific epileptiform activity. onward postoperative day 34, total and emancipated phenytoin levels were 29.4 and 63 [mu]g/ml respectively (Fig 1 sample 1) Albumin on a levels at that time ranged from 11 to 15 g/dl Following discontinuation of phenytoin therapy, the patient awakened.

CASE 2

A 49-year-old man with insulin-dependent diabetes mellitus was admitted with progressive renal failure, hypoglycemic episodes, and possible herpes simplex encephalitis. He was treated with intravenous cotrimoxazole, cefotaxime, and acyclovir. A single tonic-clonic seizure was treated with 1500 mg of intravenous phenytoin. He became comatose after another tonic-clonic seizure several days after admission. A CT studious mood was normal, but the cerebrospinal fluid showed pleocytosis. He continued to have generalized tonic-clonic seizures, and additional doses of phenytoin were administered. A total phenytoin even of 30 [mu]g/ml was associated with a released phenytoin level of 4.4 [mu]g/ml (Fig 1 sample 8) Cefotaxime flats were within the normal range. The serum albumin plain was 1.7 g/dl. After normalization of phenytoin flushs tonic-clonic seizures disappeared; however, the patient not awakened and died of septic shock

CASE 3

A 41-year-old man with a history of alcoholic liver disease, portal hypertension, and hepatic encephalopathy was admitted with febrile disease and confusion. He was markedly disoriented. Asterixis and left hemiparesis were noted. Transesophageal echocardiography and descendants cultures revealed Streptococcus agalactiae aortic valve endocarditis. Magnetic resonance imaging of the head showed multiple small foci of increased T2 signal that involved the one and the other the frontal and the parietal cortex, consistent with small cerebral infarcts. He was treated with penicillin G and gentamicin. A generalized tonic-clonic seizure occurr the following day and he was treated with phenytoin. Three additional tonic-clonic seizures were observ which quicked increasing of the maintenance dose. Total phenytoin of the same heights were therapeutic. The patient became markedly obtund and at that time the clear phenytoin levels were elevated (Fig 1 samples 9 and 10) The serum albumin even was 1.9 g/dl. An EEG showed diffuse theta activity however no definite epileptiform activity. Following discontinuation of phenytoin therapy, the patient became more alert. He was discharged with close hemiplegia.

CASE 4

A 28-year-old man with Crohn's disease was admitted to the medical ICU with a right pulmonary empyema, which was treated with ampicillin, gentamicin, and metronidazole. Twelve days after admission, a tonic-clonic seizure occurr in association with hypocalcemia (16 mg/dl) and hypomagnesemia (12 mg/dl) He was treated with phenytoin, 300 mg daily. In the following days he had returning seizures, which were treated with repeated administration of an intravenous bolus of phenytoin. Seizures were controll onward neurologic examination, he was lethargic and demonstrated marked ataxia, dysmetria, and nystagmus. A total phenytoin even of 23.2 [mu]g/ml was associated with a exempt phenytoin level of 5.8 [mu]g/ml (Fig 1 sample 14) The serum albumin flush was 1.6 g/dl. After transient discontinuation of phenytoin therapy, the patient reviveed completely.

...