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Suicide
Published in Burkhard Madea, Asphyxiation, Suffocation,and Neck Pressure Deaths, 2020
Frank Musshoff, Burkhard Madea, Elke Doberentz
Considering the autopsy findings, the results of toxicological analysis were consistent with the assumption of a fatal overdose due to tramadol alone. Respiratory depression may be assumed to be the underlying pathophysiological mechanism. Our results support the observations that a high dosage of tramadol may lead to death even in the absence of interacting drugs.
Opioids and Related Agents
Published in Frank A. Barile, Barile’s Clinical Toxicology, 2019
Maintenance of vital functions, including respiratory and cardiovascular integrity, is of paramount importance in the clinical management of acute opioid toxicity. Gastric lavage and induction of emesis are effective if treatment is instituted soon after ingestion. It is possible to reverse the respiratory depression with opioid antagonists. Naloxone (Narcan®) is a pure opioid antagonist available as an injectable only. A 2 mg bolus repeated every 5 minutes, followed by 0.4 mg every 2–3 minutes as needed (up to 24 mg total), dramatically reverses the CNS and respiratory depression (in this capacity, naloxone is also indicated in the diagnosis of suspected acute opioid overdose).* Depending on the extent of narcotic overdose, a continuous infusion of naloxone may be required, especially in the presence of opioids with longer half-lives, such as propoxyphene or methadone. As respiration improves, naloxone, which has a half-life of 60–90 minutes, may be discontinued and resumed as necessary. If there is no response after 10 mg of naloxone, concomitant ingestion with other depressants is likely. It should be noted that naloxone is of little benefit in reversing noncardiogenic pulmonary edema.
Fentanyl and Related Opioids
Published in Ornella Corazza, Andres Roman-Urrestarazu, Handbook of Novel Psychoactive Substances, 2018
Esther Papaseit, Magí Farré, Clara Pérez-Mañá, Adriana Farré, Francina Fonseca, Marta Torrens
At higher doses, the classic elements of opioid toxicity are mental status depression, hypoventilation, miosis, and hypoperistalsis. Eventually, respiratory depression can lead to complete respiratory arrest and potential death. In this scenario, early detection of possible warning signs and drug paraphernalia identification may be key factors (Table 18.2).
Opioid-related adverse drug events in surgical patients: risk factors and association with clinical outcomes
Published in Expert Opinion on Drug Safety, 2022
Chin Hang Yiu, Danijela Gnjidic, Asad Patanwala, Ian Fong, David Begley, Kok Eng Khor, Joanne Rimington, Bernadette Bugeja, Jonathan Penm
To reduce opioid-related harms in hospital systems, the Centers for Disease Control and Prevention (CDC) and the Society of Hospital Medicine (SHM) recommend that clinicians assess patients for ORADE risk factors when prescribing opioids [8,9]. Risk factors that have been identified [5–7,10–13] to increase the risk of general ORADEs for surgical patients have been shown to include patients’ age, gender, and medical conditions such as cardiovascular, respiratory, and renal diseases. As ORADEs include a broad range of adverse events, specific risk factors for gastrointestinal and respiratory adverse events have also been investigated [14–17]. Risk factors for gastrointestinal ORADEs have only been investigated in one previous study [14] that showed age and female gender were risk factors. For respiratory depression, risk factors identified include renal failure, cardiac diseases, sleep apnea, and concurrent use of sedating medications [15–17]. Although the opioid dose has been considered to be a main driver for ORADEs, a recent systematic review of 16 papers found that no previous study has investigated the impact of the opioid dose on the risk of ORADEs in surgical patients [18]. Furthermore, there has been a rise in gabapentinoids use in postoperative pain to reduce opioid consumption [19–21], however none of the previous studies have investigated the impact of gabapentinoids on ORADEs [18]. This gap in the literature will be addressed by this study.
Critical care interventions in children aged 6 months to 12 years admitted to the pediatric intensive care unit after unintentional cannabis exposures
Published in Clinical Toxicology, 2022
James B. Leonard, Thomas Laudone, Elizabeth Quaal Hines, Wendy Klein-Schwartz
Specific CCIs are shown in Table 2. Most common CCIs in the PICU were intubation and sedation in 4.9 and 3.7%, respectively. Most common non-CCI was IV fluids in 44.5% in the PICU and 17.1% in non-PICU patients (Supplemental Table S3). The most common clinically significant effects were respiratory depression in 74 (8.3%) patients admitted to PICU and in 84 (1.4%) not in the PICU (Table 3). This was followed by CNS depression (major) or coma in 73 (8.3%) admitted to PICU and 58 (0.9%) not in the PICU (Table 3). Less common critical effects are shown in Supplemental Table S4. The most frequent non-clinically significant effects were some degree of sedation and tachycardia, followed by vomiting (Supplemental Table S5). Duration of effects for patients admitted to the PICU was less than 24 h for 76.7% of cases, 24 h to 3 d in 19%, 3 d and 1 week in 1.1%, and an unknown duration in 3.2%.
Respiratory failure in confirmed synthetic cannabinoid overdose
Published in Clinical Toxicology, 2022
Alex F. Manini, Alex J. Krotulski, Jonathan Schimmel, Lisa Allen, Yasmin L. Hurd, Lynne D. Richardson, Kavey Vidal, Barry K. Logan
The mechanisms of SC respiratory depression are unclear, and may relate to 1) SC effects on CB1, 2) SC effects on non-CB1 receptors, or 3) Interaction between the endocannabinoid and endogenous opioid systems. SC CB1 agonism has been implicated as the mechanism for respiratory depression in several animal studies, including a rat model in which respiratory changes were blocked by a CB1 antagonist, and this was likely centrally mediated [8]. Another possible mechanism is an unclear interaction between the endocannabinoid and endogenous opioid systems. As evidence for these interactions, opioid antagonists have been found to reduce the reinforcing effects of Δ9-tetrahydrocannabinol in monkeys, and to reduce daily cannabis use in regular users [9,10]. Translating animal findings of cannabinoid respiratory effects to humans must be with the understanding that SC potency varies significantly compared to phytocannabinoids, and that assessing respiratory depression in anesthetized animals may not translate to non-anesthetized humans.