ABSTRACT
Poisoning may also lead to both coma and multiple organ failure, also in youngsters without a known major medical history. As not all toxic agents are routinely screened when a poisoning is suspected, it is useful to consider less frequently encountered poisons in certain cases. We describe the occurrence of asystole and multiple organ failure which occurred in a young man after a suspected tramadol overdose. The tramadol concentration on admission in the ICU was indeed 8 microg/ml (mg/l), far above the therapeutic range. Subsequently, the patient developed severe acute liver failure, finally leading to death. Post-mortem toxicology did not reveal any other poison responsible for this unfavourable course as only very high serum and tissue tramadol and desmethyltramadol concentrations were found. Only a few fatal poisonings attributable to tramadol alone, as observed in our case, have been reported. An overview of these cases is presented.
Subject(s)
Analgesics, Opioid/poisoning , Tramadol/poisoning , Adult , Analgesics, Opioid/blood , Analgesics, Opioid/pharmacokinetics , Drug Overdose , Forensic Toxicology , Heart Arrest/chemically induced , Humans , Male , Multiple Organ Failure/chemically induced , Tissue Distribution , Tramadol/blood , Tramadol/pharmacokineticsSubject(s)
Phosphodiesterase Inhibitors/analysis , Piperazines/analysis , Postmortem Changes , Sulfones/analysis , Citric Acid/chemistry , Forensic Medicine/methods , Gas Chromatography-Mass Spectrometry , Humans , Molecular Weight , Phosphodiesterase Inhibitors/chemistry , Phosphodiesterase Inhibitors/pharmacokinetics , Piperazines/chemistry , Piperazines/pharmacokinetics , Purines/analysis , Purines/chemistry , Purines/pharmacokinetics , Sildenafil Citrate , Specimen Handling , Sulfones/chemistry , Sulfones/pharmacokinetics , Tissue DistributionABSTRACT
OBJECTIVE: To report a case of D-lactic acid acidosis owing to massive oral ingestion of propylene glycol. CASE REPORT: A 72-year old man with known congestive failure was admitted to the ICU with encephalopathy. Twelve hours prior to admission he had erroneously ingested a large amount of propylene glycol (PG). The laboratory revealed high anion gap (anion gap = 27 meq/l) acidosis (arterial pH = 7.16) and an increased osmolal gap. Toxicological analysis revealed a low serum propylene glycol level. Biochemical analysis indicated that very high amounts of D-lactic acid (up to 110 mmol/l), but not of the usual type of L-lactic acid, were responsible for the metabolic acidosis. Hemodialysis was initiated and associated with a decline of both the acidosis and D-lactic acid levels. The patient regained conciousness. CONCLUSION: Ingestion of massive doses of propylene glycol, previously not reported as a cause of D-lactic acidosis, should be added to the differential diagnosis of this rare condition.
