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Clinical Course: We present a potentially fatal case of acute methaqualone (M) poisoning with very low serum concentrations of M but extremely high levels of its metabolite, 2-methyl-3-(2-hydroxymethyl-phenyl)-4 (3H)-chinazoline (Met-1). A 23-year-old man was admitted to the intensive care unit 2 days after ingestion of 4-5 g M in an suicidal attempt. On admission he was somnolent and poorly responsive to painful stimuli. Physical examination revealed a heart rate of 95 bpm, a blood pressure of 125/65 mmHg, and a normal body temperature. His chest was clear to auscultation, respirations were shallow, and the skin was cyanotic. The electrocardiogram was unremarkable. The chest radiograph showed a normal heart size without pulmonary infiltrates or venous congestion. The pupils were dilated but reactive to light. The neurologic examination was further remarkable for increased limb reflexes, myoclonia, and positive pyramidal signs. During the next 2 days the patient became comatose and developed respiratory insufficiency due to non-cardiogenic pulmonary oedema, which was confirmed by chest radiograph and haemodynamic investigations by means of right heart catheterisation. He required mechanical ventilation for 6 days. Finally, he recovered completely and was discharged in good condition., Diagnostics: A lumbar puncture revealed neither blood nor pleocytosis in the cerebrospinal fluid. Cranial computed tomography was carried out on an emergency basis, but no abnormality was disclosed. An electroencephalogram did not exhibit any significant pathological findings. Testing for infectious diseases or porphyria gave negative results. Toxicological screening based on enzyme immunoassays (ELISA) was negative for alcohol, tricyclic antidepressants, benzodiazepines, barbiturates, and morphine, but gave a positive result for M. From the moment of admission daily blood samples were taken and analysed by combined gas chromatography and mass spectrometry. These showed very low levels of M but extremely high levels of Met-1., Therapy: After gastric lavage, continuous enteric lavage with activated charcoal and mannitol was initiated to minimise intestinal absorption. Since M was hardly detectable in the serum, haemoperfusion was not regarded as indicated for drug elimination and treatment was restricted to general supportive measures. To rule out a central anticholinergic syndrome, an anticholinesterase drug (physostigmine) was administered but remained without therapeutic effect., Conclusions: The presented case is the first report of a life-threatening intoxication after M ingestion primarily caused by Met-1. It supports the significance of this metabolite for the toxic effects of the drug. A toxicological screening test based on ELISA proved helpful due to its cross-reactivity with metabolites. In cases similar to ours, resin haemoperfusion may be indicated to remove the metabolites despite low detectable concentrations of the parent substance in the serum.

Due to the multitude of invasive procedures of today's intensive care medicine, infections from central venous catheters have gained increasing attention. The incidence of bacteremias arising from such devices ranges from less than 0.1 to 0.6 cases per 100 catheter-days. Factors influencing the incidence of catheter-associated infections are related to patient characteristics as well as the purpose and material of the catheter. Silicone catheters seem to carry a lower risk of infection than common polytetrafluorethylene catheters. The most frequently isolated bacteria in catheter-associated infections are coagulase-negative and coagulase-positive staphylococci, enterococci, and pseudomonas species. Septicemias due to Candida albicans frequently complicate the course of immune-compromised patients receiving total parenteral nutrition (TPE). Catheter-associated bacteremias (CAB) can arise from the contaminated hub, from which pathogens migrate intraluminally to the blood stream. When the catheter entry site is infected, bacteria may reach the blood via the extraluminal route and cause septicemia. Endemic outbreaks of CAB often originate from contaminated infusion fluids. As the clinical presentation of "catheter infections" is often uncharacteristic and insidious, a definite diagnosis depends on bacteriological examination of the catheter. Quantitative and semiquantitative culture techniques of the catheter tip help to distinguish colonization from contamination by numbers of colony-forming units per milliliter culture medium. Preliminary results can be obtained by simple Gram or acridine-orange staining of the catheter tip. The most important prophylactic measures to prevent CAB are strictly aseptic conditions when catheters are placed and meticulous care thereafter, preferably by specially trained nurses or "TPE teams".(ABSTRACT TRUNCATED AT 250 WORDS)