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Biomedical subjects

E Sindrup

Publications and source records attributed to E Sindrup.

10 recordsLinked to original sources
PubMed1982

Overdosage of antidepressants: clinical and pharmacokinetic aspects.

Twenty-nine cases of self-poisoning with antidepressants (amitriptyline, imipramine, clomipramine, maprotiline, doxepine, nortriptyline, opipramol) were examined by frequent observation of CNS effects, heart rate, blood pressure and standard ECG, 24h-ECG-monitoring, measurement of systolic time intervals, EEG recordings and frequent measurement of serum levels of antidepressants and primary metabolites. None of the patients died. Maximum total serum antidepressant level (parent compound + desmethyl metabolite) ranged from 20 to 2200 micrograms/l, with concentrations above 500 micrograms/l in 11 cases. The serum amitriptyline concentration remained high for 3-4 days in some of the severely intoxicated patients and the decay curves were compatible with partly saturated elimination. A degree of unconsciousness and the occurrence of excitation and hallucinations were generally seen in cases with total serum antidepressant levels above 500 micrograms/l. Grand mal seizures occurred more frequently at high antidepressant levels, but could not be predicted from the EEG recordings. Increased heart rate and prolonged QRS- and QTc-intervals were significantly correlated with the total serum antidepressant level. 24 h-ECG-monitoring revealed no serious arrhythmias or instances of heart block. Hypotension was only seen initially in few patients. Systolic time interval measurements showed changes suggesting impaired myocardial performance (elevated PEP/LVET ratio) at intermediate (60-500 micrograms/l) but not high (greater than 500 micrograms/l) total serum antidepressant levels. Measurement of serum concentration in antidepressant intoxication is important for identification of patients with high serum levels and the corresponding risk of developing toxic reactions, and to exclude patients with a low concentration who do not require intensive observation.

Adult↗
PubMed1979

'alpha pattern coma' following cerebral anoxia.

In 30 patients, who were all comatose as a result of cerebral anoxia after cardiac arrest, at least one EEG with activity in the alpha frequency range was recorded. Regionally the activity of the above mentioned characteristic was often diffusely distributed or most pronounced occipitally, whereas a tendency to affect other regions was rarely observed. In 50% of the patients, where more than one EEG was recorded, the 'alpha' rhythm was still present in the following record. Only one of the patients survived, and even so, with considerable mental defects. In 4 patients the level of consciousness improved, but 3 of them never reached a definite level of cortical function and died as a result of cerebral anoxia.

Adult↗
PubMed1978

Electroencephalographic prediction of anoxic brain damage after resuscitation from cardiac arrest in patients with acute myocardial infarction.

The short-term prognostic value of routine electroencephalography (EEG), carried out on the days after cardiac arrest, was evaluated in a consecutive study of 185 patients with acute myocardial infarction together with an episode of clinical cardiac arrest. The individual EEGs were classified on a 5-grade scale. Of the 89 patients who survived, 18 had signs of anoxic brain damage; 96 patients died, 76 as a result of cerebral anoxia. Only 2 patients survived out of the total of 72 for whom the first EEG was classified as grades III--V. The EEGs of both these patients were recorded within a few hours after the cardiac arrest. None of the patients with an EEG of grade I died of cerebral anoxia, while all degrees of brain damage were otherwise observed in connection with EEGs of both grades I and II. It is concluded that an EEG of grades III--V indicates a fatal outcome, provided it has been recorded more than 24 hours after the cardiac arrest. A grade III--V EEG that is recorded within 24 hours after a cardiac arrest should be repeated some days later. It is not possible, on the basis of a single EEG, to predict the extent of the anoxic brain damage.

Acute Disease↗