buprenorphine and Pulmonary-Edema

buprenorphine has been researched along with Pulmonary-Edema* in 4 studies

Other Studies

4 other study(ies) available for buprenorphine and Pulmonary-Edema

ArticleYear
Exogenous lipoid pneumonia as a contributory factor in a drug-related death.
    Journal of forensic sciences, 2015, Volume: 60, Issue:2

    Postmortem investigation often reveals various conditions, which may or may not have played a part in the death of the individual. The case of a 32-year-old woman is reported, with a long history of drug addiction. She was found dead in her bed. The autopsy revealed diffuse pulmonary edema with congestion of the lungs, brain, liver, and spleen. Microscopic examination of the lungs showed multiple intra-alveolar and interstitial foamy macrophages and extracellular fat droplets surrounded by polynuclear giant cells. Death was attributed to acute polydrug intoxication. As microscopic examination had revealed severe pulmonary lesions, lipoid pneumonia was considered as a contributing factor to death. Lipoid pneumonia is an uncommon entity with the characteristic radiograph features and histologic findings of alveoli filled with vacuolated, lipid-laden histiocytes. It can be either exogenous or endogenous in cause, based on the source of the lipid. Exogenous lipoid pneumonia usually results from aspiration or inhalation of fat-like material, such as mineral oil or petroleum-based lubricants and decongestants, resulting in pulmonary inflammatory reactions.

    Topics: Adult; Buprenorphine; Female; Humans; Lung; Narcotic Antagonists; Pneumonia, Lipid; Pulmonary Edema; Substance-Related Disorders

2015
Toxicological and pathological findings in a series of buprenorphine related deaths. Possible risk factors for fatal outcome.
    Forensic science international, 2012, Jul-10, Volume: 220, Issue:1-3

    Buprenorphine is considered to have little respiratory side effects at therapeutic doses and the partial agonistic properties should produce a "ceiling effect" for respiratory depression at higher doses. Still, there are several reports on buprenorphine related deaths. Most deaths involve drug users and the co-administration of other CNS depressant drugs as well as reduced tolerance have been suggested to be risk factors. The primary aims were to investigate if lack of tolerance and/or co-ingestion of other psychotropic drugs are significant risk factors in buprenorphine fatalities. From July 2005 to September 2009, all autopsy cases where buprenorphine or norbuprenorphine had been detected in femoral blood and where analysis of buprenorphine had been performed in urine were selected. Results from the postmortem examination and toxicology were compiled. Postmortem toxicology was performed using the routine methodology at the laboratory. In total, 97 subjects were included in the study. These were divided into four groups; Intoxication with buprenorphine (N=41), Possible intoxication with buprenorphine (N=24), Control cases where buprenorphine was not the cause of death (N=14), and Unclear (N=18). The metabolite to parent compound ratios in both blood and urine in the Intoxication group were significantly different from those in the Control and Unclear groups. An extensive poly-drug use was seen in all groups with several additional opioids in the Possible group (54%) and in the Unclear group (78%) and hypnotics or sedatives in more than 75% of the Intoxication, Possible, and Unclear cases. Illicit drugs were present in all groups but not to a great extent with amphetamine and tetrahydrocannabinol as the main findings. Interestingly, 4 cases in the Intoxication group presented with no other significant drugs in blood other than buprenorphine. We conclude that a lethal concentration of buprenorphine in blood cannot be defined. Instead the analysis of blood as well as urine can be an important tool to show that the drug was taken shortly before death and to rule out a continuous use of buprenorphine supporting the notion that abstinence is an important risk factor. The presence of alprazolam in more than 40% of the Intoxications and the presence of hypnotics and sedatives in 75% of the Intoxications suggests that these drugs interact with buprenorphine producing toxic effects that buprenorphine alone would not have produced. Still, in 10% of the Intoxication

    Topics: Adult; Buprenorphine; Case-Control Studies; Drug-Related Side Effects and Adverse Reactions; Female; Forensic Pathology; Forensic Toxicology; Humans; Hypnotics and Sedatives; Illicit Drugs; Lung; Male; Middle Aged; Narcotics; Pharmaceutical Preparations; Prescription Drug Misuse; Pulmonary Edema; Respiration; Retrospective Studies; Risk Factors; Substance-Related Disorders; Young Adult

2012
Buprenorphine causes pulmonary edema just like all other mu-opioid narcotics. Upper airway obstruction, negative alveolar pressure.
    Chest, 1995, Volume: 107, Issue:5

    Topics: Analgesics, Opioid; Buprenorphine; Humans; Narcotics; Pulmonary Edema

1995
Noncardiogenic pulmonary edema induced by sublingual buprenorphine.
    Chest, 1994, Volume: 106, Issue:1

    A 21-year-old woman developed noncardiogenic pulmonary edema within 90 min after the use of buprenorphine, 0.2 mg, sublingually for severe dysmenorrhea. No organic cardiovascular illness was detected. The pulmonary edema resolved spontaneously with conservative treatment. The mechanism of pulmonary edema may be an allergic reaction to buprenorphine.

    Topics: Acute Disease; Administration, Sublingual; Adult; Buprenorphine; Dysmenorrhea; Female; Humans; Lung; Pulmonary Edema; Radiography

1994