Clinical features in 28 consecutive cases of laboratory confirmed massive poisoning with carbamazepine alone.

A retrospective study of consecutive cases of massive carbamazepine poisoning treated in an intensive care unit during the period 1981-1991 was performed, mainly to determine whether serum carbamazepine levels were predictive of toxicity. Out of a total of 51 admissions with a diagnosis of carbamazepine self-poisoning, 28 (25 patients) were included. The reasons for exclusion were coingestion of other drugs (11 cases), incorrect diagnosis or inadequate information (6 cases), a peak observed serum concentration of carbamazepine below 76 mumol/L [18 mg/L] (4 cases), and lack of any documented serum carbamazepine assay (2 cases). The peak serum concentrations ranged from 78 to 285 mumol/L [18.4 to 67.4 mg/L]. It was found that serum levels equal to or above 170 mumol/L [40 mg/L] were significantly associated with an increased risk of serious complications such as coma, seizures, respiratory failure and cardiac conduction defects. In 60% of the 10 patients with a serum level > or = 170 mumol/L at least two of these symptoms occurred, in 50% at least three, and in 40% all four. There were two fatalities. Among the 16 patients (18 admissions) with a serum carbamazepine concentration below 170 mumol/L, only one was comatose and none had any of the other severe symptoms. It is concluded that serum carbamazepine levels accurately predict the severity of toxicity in massive carbamazepine poisoning in adults.

Considerations for the treatment of ethylene glycol poisoning based on analysis of two cases.

The clinical picture as well as the principles of treatment in ethylene glycol poisoning differ with the time after ingestion. These time-related differences are illustrated by two case reports. During the first hours of ethylene glycol poisoning, the patient suffers from drunkenness, vomiting and somnolence due to the intoxicant effect of ethylene glycol on the central nervous system. In the following hours a poisoning with glycolate and oxalate develops, with increasing acidosis, renal and brain damage. A patient admitted within a few hours of an overdose, with no or only slight metabolic acidosis, may be successfully treated with ethanol. If the serum concentration of ethylene glycol is very high, hemodialysis may be deferred until the necessary staff and equipment are available. If the patient is admitted with severe metabolic acidosis, hemodialysis must be started immediately. The need for ethanol administration during hemodialysis merits reevaluation.

Hexapropymate self-poisoning causes severe and long-lasting clinical symptoms.

Cases of hexapropymate poisoning requiring intensive care in an urban region of Sweden (420,000 inhabitants) were collected over 2.5 years (1985 to 1987). Only patients with serum hexapropymate concentrations above 5.5 mg/L (30 mumol/L) and with a negative history for intake of tricyclic antidepressants, phenothiazines, barbiturates, antihistaminic drugs and opiates were included. Clinical data about 8 intoxication events in 6 patients were evaluated retrospectively. Initial symptoms included coma, hypotension, hypothermia, and hypoventilation. Maximum coma depth (Glasgow coma score) was 3 to 5 in 5 out of 8 events. On 7 occasions assisted ventilation was required (for 12 hours or more in 5 events). There was no relationship between serum concentrations of hexapropymate and severity of clinical symptoms. All patients survived. Detailed analysis of the drug elimination in one patient showed a terminal elimination half-life of 21 hours, which is longer than previously reported (5 hours). The indications for use of this hypnotic drug may vary between doctors since an 8-fold variation was seen in drug prescription between Swedish counties in 1987. Poisoning with hexapropymate is a serious condition which may require symptomatic treatment in the intensive care unit. The clinical picture is similar to that seen in patients with burbiturate intoxication. There is no role for active forced elimination of the drug. It is questionable whether the clinical value of the drug is outweighted by its toxicity.

Cerebral blood flow and metabolic rate of oxygen, glucose, lactate, pyruvate, ketone bodies and amino acids.

The cerebral blood flow (CBF) and cerebral metabolic rate (CMR) of oxygen, glucose, lactate, pyruvate, ketone bodies and 24 amino acids were examined in 12 patients with presenile dementia and in seven with normal-pressure hydrocephalus. Both groups of patients showed significantly lower values of CBF and cerebral uptake of oxygen and glucose than 10 healthy subjects examined concurrently. The values decreased roughly in proportion to the degree of clinical deterioration. Furthermore, the patients exhibited a significant release of lactate and pyruvate. A positive correlation was found between CMR and arterial concentration of ketone bodies. The group with presenile dementia showed no uptake of amino acids, but a significant release of phenylalanine; in addition, CMR of alanine and threonine was significantly lower than in the healthy subjects. These findings suggest a cerebral catabolic state. Four patients with normal-pressure hydrocephalus were also studied after shunt operations. All showed an increase of CMR glucose and a decrease of CMR ketone bodies, acetoacetate as well as D-beta-hydroxybutyrate, which could not be attributed to a consistent decrease of arterial levels of ketone bodies.

Cerebral blood flow and metabolic rate of oxygen, glucose, lactate, pyruvate, ketone bodies and amino acids.

The cerebral blood flow (CBF) and cerebral metabolic rate (CMR) of oxygen, glucose, lactate, pyruvate, ketone bodies, and 24 amino acids were examined in 10 healthy subjects, five 21-24 and five 55-65 years old. The subjects were free from drugs. The results of psychometric and neurological examinations were negative. CBF was determined with the nitrous oxide method on the subjects who were awake and normocapnic and had fasted overnight. No differences were found between the young and the old groups except in arterial levels of four amino acids, viz. aspartic acid, methionine, lysine, and tryptophan. In the whole group of 10 subjects, a significant cerebral net uptake (expressed as median values in mumol X kg-1 X min-1) was found not only for oxygen (1719) and glucose (248), but also for acetoacetate (4.3), D-beta-hydroxybutyrate (6.2), arginine (2.0), leucine (5.2), and isoleucine (1.2). There was a significant net release of lactate (-28). CBF was positively correlated to the CMR of oxygen and D-beta-hydroxybutyrate. Arterial concentrations and CMR were positively correlated for ketone bodies, glutamic acid, proline and taurine. It is of particular interest that the whole group of healthy subjects showed a significant cerebral uptake of branched-chain and dibasic amino acids.

Cytomegalovirus infection associated with severe encephalitis.

A previously healthy 37-year-old woman had a 5-week febrile disease starting 10 days after delivery, which was complicated by disseminated intravascular coagulation and treated with fresh blood transfusions. She developed severe encephalitis with coma. She also had signs of perimyocarditis and enlargement of liver and lymph nodes. The encephalitis was completely reversible. There was a 16-fold rise in complement-fixing antibodies against cytomegalovirus.