Propofol-induced acute pancreatitis

Csomor, J.; Murínová, Irena; Broulíková, Karolina; Kučerka, Ondřej; Sedloň, Pavel; Jarosek, J; Urbánek, Petr; Zavoral, Miroslav

doi:10.1111/jcpt.12524

Cited by 15 publications

(13 citation statements)

References 9 publications

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“…Artificial ventilation, hemodialysis, intensive care and total parenteral nutrition were needed in the remaining patients. One patient underwent 14 operations for infected pancreatic necrosis and died [34]. AP was improved with a median duration of 7 days (range, 3–35 days).…”

Section: Resultsmentioning

confidence: 99%

Acute pancreatitis associated with intravenous administration of propofol: evaluation of causality in a systematic review of the literature

Haffar¹,

Kaur

Garg

et al. 2018

Gastroenterology Report

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Acute pancreatitis (AP) associated with intravenous administration of propofol has been described with unknown causal relation. We therefore assessed this causality in a systematic review. Multiple databases were searched on 16 August 2017; studies were appraised and selected by two reviewers based on a priori criteria. Propofol causality was evaluated with the Naranjo scale and Badalov classification.We identified 18 studies from 11 countries with a total of 21 patients, and the majority had adequate methodological quality. The median age was 35 years (range, 4–77) and 10 (48%) were males. Overall, propofol was administrated in 8 patients as sedative along with induction/maintenance of anesthesia in 13 patients; median dose was 200 mg, with intermediate latency (1–30 days) in 14 (67%). Serum triglycerides were >1000 mg/dL in four patients. Severe AP was observed in four patients (19%). AP recurrence occurred in one out of two patients who underwent rechallenge. Mortality related to AP was 3/21(14%). Propofol was the probable cause of AP according to the Naranjo scale in 19 patients (89%).Propofol-induced AP has a probable causal relation and evidence supports Badalov class Ib. Hypertriglyceridemia is not the only mechanism by which propofol illicit AP. Propofol-induced AP was severe in 19% of patients with a mortality rate related to AP of 14%. Future research is needed to delineate whether this risk is higher if combined with other procedures that portend inherent risk of pancreatitis such as endoscopic retrograde cholangiopancreatography.

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Section: Resultsmentioning

confidence: 99%

Acute pancreatitis associated with intravenous administration of propofol: evaluation of causality in a systematic review of the literature

Haffar¹,

Kaur

Garg

et al. 2018

Gastroenterology Report

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“…The case report publication rate was highest from 1990 to 1999 (n = 241, 24.1 cases/year), and has slowed in recent years (2010-early 2019: 19.1 cases/year). In most case reports, the causes of AP that were excluded to arrive at a diagnosis of DIP were poorly reported, with only two recent case reports having data reported for all ten non-drug causes for which we extracted data [14,15]. Similarly, 81% of cases did not conduct a formal causality assessment.…”

Section: Plos Onementioning

confidence: 99%

“…When we required all ten causes of AP to be excluded instead of only four for a diagnosis of DIP, only two recently published cases met the more rigorous diagnostic criteria for DIP [14,15]. These two cases implicated amoxicillin/clavulanic acid and propofol, respectively.…”

Section: Sensitivity Analysesmentioning

confidence: 99%

Drug induced pancreatitis: A systematic review of case reports to determine potential drug associations

et al. 2020

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“…Autopsy and histological findings observed in lethal cases resulting from propofol overdose usually report cerebral and pulmonary edema, polyvisceral congestion, lungs with some petechial hemorrhages on pleural surface, hemorrhagic pancreatitis, and hepatic steatosis [ 158 , 160 , 178 ]. Although claimed as very rare idiosyncratic reaction (<1/10,000) and with a an estimated incidence of 0.1%–2% of all pancreatitis cases, hypertriglyceridaemia has been suggested as a causal relationship between propofol and pancreatitis since it is formulated as a fat emulsion [ 179 ].…”

Section: Adverse Effects Fatal Intoxications and Autopsy Findinmentioning

confidence: 99%

“…Although claimed as very rare idiosyncratic reaction (<1/10,000) and with a an estimated incidence of 0.1%–2% of all pancreatitis cases, hypertriglyceridaemia has been suggested as a causal relationship between propofol and pancreatitis since it is formulated as a fat emulsion [ 179 ]. Therefore, patients who develop hypertriglyceridaemia are at risk of developing pancreatitis, and serum triglyceride concentrations should be routinely monitored in these patients and alternative sedation strategies should be considered when hypertriglyceridemia is detected [ 178 , 179 ]. Nevertheless, some case reports describe the development of propofol-induced acute pancreatitis in the absence of hypertriglyceridaemia [ 180 ].…”

Section: Adverse Effects Fatal Intoxications and Autopsy Findinmentioning

confidence: 99%

Metabolic Profiles of Propofol and Fospropofol: Clinical and Forensic Interpretative Aspects

Dinis-Oliveira

2018

BioMed Research International

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Propofol is an intravenous short-acting anesthetic widely used to induce and maintain general anesthesia and to provide procedural sedation. The potential for propofol dependency and abuse has been recognized, and several cases of accidental overdose and suicide have emerged, mostly among the health professionals. Different studies have demonstrated an unpredictable interindividual variability of propofol pharmacokinetics and pharmacodynamics with forensic and clinical adverse relevant outcomes (e.g., pronounced respiratory and cardiac depression), namely, due to polymorphisms in the UDP-glucuronosyltransferase and cytochrome P450 isoforms and drugs administered concurrently. In this work the pharmacokinetics of propofol and fospropofol with particular focus on metabolic pathways is fully reviewed. It is concluded that knowing the metabolism of propofol may lead to the development of new clues to help further toxicological and clinical interpretations and to reduce serious adverse reactions such as respiratory failure, metabolic acidosis, rhabdomyolysis, cardiac bradyarrhythmias, hypotension and myocardial failure, anaphylaxis, hypertriglyceridemia, renal failure, hepatomegaly, hepatic steatosis, acute pancreatitis, abuse, and death. Particularly, further studies aiming to characterize polymorphic enzymes involved in the metabolic pathway, the development of additional routine forensic toxicological analysis, and the relatively new field of ‘‘omics” technology, namely, metabolomics, can offer more in explaining the unpredictable interindividual variability.

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Propofol-induced acute pancreatitis

Abstract: We present a rare case of propofol-induced acute necrotising pancreatitis, which is to the best of our knowledge the first fatal case reported in an adult patient.

Cited by 15 publications

References 9 publications

Acute pancreatitis associated with intravenous administration of propofol: evaluation of causality in a systematic review of the literature

Acute pancreatitis associated with intravenous administration of propofol: evaluation of causality in a systematic review of the literature

Drug induced pancreatitis: A systematic review of case reports to determine potential drug associations

Metabolic Profiles of Propofol and Fospropofol: Clinical and Forensic Interpretative Aspects

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