Your browser doesn't support javascript.
loading
Sphincter of oddi dysfunction induced by ketamine: A case report.
Sharma, Nava Raj; Basnet, Arjun; Lamichhane, Saral; Tiwari, Kripa; Varghese, Jeffy; Gautam, Sudarshan; Pokhrel, Madalasa.
Afiliação
  • Sharma NR; Manipal College of Medical Sciences Pokhara Nepal.
  • Basnet A; Maimonides Medical Center Brooklyn New York USA.
  • Lamichhane S; Gandaki Medical College Pokhara Nepal.
  • Tiwari K; Maimonides Medical Center Brooklyn New York USA.
  • Varghese J; Maimonides Medical Center Brooklyn New York USA.
  • Gautam S; Maimonides Medical Center Brooklyn New York USA.
  • Pokhrel M; Montefiore New Rochelle Hospital New Rochelle New York USA.
Clin Case Rep ; 12(6): e9016, 2024 Jun.
Article em En | MEDLINE | ID: mdl-38799518
ABSTRACT
Key Clinical Message Chronic ketamine use can lead to sphincter of oddi dysfunction (SOD), causing various hepatobiliary complications. Recognizing substance abuse history is vital for early detection. Timely intervention can prevent irreversible liver and pancreas damage. Abstract Ketamine is commonly abused as a recreational drug worldwide due to its ability to induce euphoria-like effects. Ketamine abuse is associated with many hepatobiliary side effects ranging from cholestasis to biliary sepsis and death. Here we present a case of a young 29-year female with upper abdominal pain due to SOD resulting from chronic use of ketamine. SOD can result in obstruction or dysfunction of the bile and pancreatic ducts. Ketamine induces SOD by activation of the muscarinic receptors in the sphincter of oddi. Detail history of substance abuse is crucial for early identification of ketamine-induced SOD. Early identification and treatment of this rare condition can prevent permanent injury to the liver and pancreas.
Palavras-chave

Texto completo: 1 Base de dados: MEDLINE Idioma: En Revista: Clin Case Rep Ano de publicação: 2024 Tipo de documento: Article

Texto completo: 1 Base de dados: MEDLINE Idioma: En Revista: Clin Case Rep Ano de publicação: 2024 Tipo de documento: Article