Syringe infusion pump versus gravity-feed minibottle: evaluation of systems.

Abstract

betes mellitus, and a focal seizuredisorder secondary to a previous infarct of the left frontoparietal region. Her daughters added that she had been unusually lethargic and had not been following a consistent diet. Her chief complaint at the time of admission consisted of seeing worms in her stools as well as having worms "crawl out her nose and mouth." She also noted the presence of "strange sounds coming from the back of the house" which were later unsubstantiated. Her medications consisted of captopril ISO mg/d, clonidine 0.6 mg/d, aspirin 325 mg/d, dipyridamole 225 rng/d, glyburide 25 mg/d, and phenytoin 400 mg/d. Due to the patient's mental condition, compliance was difficult to assess. Steady-state phenytoin concentrations were not monitored on an outpatient basis, and there was no evidenceor prior history of alcohol or substance abuse. Upon admission, physical examination revealed a well-developed, mildly obese Mexican-American woman in no acute distress. She was cooperative but complained of seeingworms in her clothes. Blood pressure was 164170mm Hg; pulse 72 beats/min and regular; respiration 16 breaths/min; and temperature 37°C. Laboratory values were phenytoin 36.2I'g/ml (normal 10-20); vitamin B" 498 pg/ml (normal 220-749); and folic acid 5.6 ng/ml (normal 1.7-15.5). A serial multiple analysis was unremarkable with the exception of a mildly elevated aspartate aminotransferase and alkaline phosphatase. A complete blood cell count was within normal limits and urinalysis was negative. There was no evidenceof nystagmus or ataxia and she denied diplopia. Thyroid function was normal, as well as morning and evening serum cortisol levels. The patient was hospitalized and preadmission medications, other than phenytoin, were resumed. Stool was tested for ova and parasites and was negative. An electroencephalogram recorded no abnormalities and a computed tomography scan of the head recorded the prior infarction. Over the subsequent days her mental status gradually improved. Serum phenytoin concentrations were further evaluated on hospital days 3and 4 with the results reported as 24and 221'g/ ml, respectively. A psychiatric consultation was performed on day 2. The patient did not experience any psychomotor abnormalities. Mood was appropriate and thinking was logical and coherent. There was no evidenceof a psychotic process. She denied auditory and visual hallucinations except for residual delusions regarding worms in her stool. She described psychosocial stressors, including her 81· year-old husband's alcohol abuse and questions of a daughter's drug use. The patient was diagnosed with delerium secondary to phenytoin toxicity with no further treatment indicated. Shewas discharged on day 4 in good condition with follow-up of her mental status to be conducted by the consulting psychiatrist. Phenytoin was withheld on discharge. Reynolds' and Herberg' identified several predisposing factors to chronic phenytoin toxicity, such as multiple drug use, age, variations in drug metabolism and distribution, poor diet, diabetes, and hypoalbuminemia. Kato added mild organic brain syndrome and mental retardation as predisposing factors to chronic phenytoin intoxication. ' Herberg described four cases of "psychosis with organic brain syndrome" which were later diagnosed as phenytoin intoxication.' In 1979, Franks and Richter noted three patients with organic brain syndrome or borderline mental retardation who developed psychosis associated with anticonvulsant toxicity that lacked the typical neurological signs of toxicity.' Other authors have described similar experiences.": Hyperglycemia, concurrent drug interference, and folic acid deficiency have been associated with psychosis as a result of chronic phenytoin toxicity. Phenytoin toxic psychosis with associated hyperglycemia has been documented previously in the literature."II Wesseling and Mols-Thurkow confirmed that in patients taking phenytoin, concurrent administration of tolbutamide may increase non-protein-bound phenytoin, thereby enhancing the likelihood of toxicity. t2 Because the patient presented in this case was receiving phenytoin with glyburide, a highly protein-bound sulfonylurea, the interaction cannot be ruled out. A free phenytoin concentration was not obtained during the patient's hospitalization to confirm the possibility of this interaction. Because phenytoin reduces the absorption of folic acid, a controversial relationship exists between folate deficiency and phenytoin psychosis. IJ. 14 It has been suggested that oral administration of folic acid improves the mental status of some patients with phenytoin psychosis.' Phenytoin-induced psychosis as a result of chronic intoxication is often difficult to diagnose. Nystagmus, ataxia, slurred speech, and other physical signs of toxicity may be absent. Although a phenytoin concentration may be helpful, it is not conclusive. Several authors described patients with subtherapeutic concentrations later diagnosed with phenytoin-induced psychosis. Clinicians should be familiar with the predisposing factors associated with this phenomenon, which may include organic brain syndrome or mental retardation, drug-drug interference, altered drug metabolism, poor diet, and diabetes. It is essential that a thorough workup be performed to exclude the more common causes of psychosis before arriving at a final diagnosis. The patient presented in this report showed no traditional signs of acute intoxication. An immediately determined phenytoin concentration in addition to a psychiatric evaluation aided in the final diagnosis.