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Codeine-induced pancreatitis in a previously Cholecystectomized patient: double the trouble
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Abstract
The causality between codeine and acute pancreatitis has not yet been fully deciphered in medical literature. Codeine-induced pancreatitis is a rare entity and the underlying mechanism of action mediated by codeine has not been completely elucidated. One plausible theory is that codeine increases the pressure of the sphincter of Oddi (SOD), which results in spasms and subsequently acute pancreatitis ensues. Codeine-induced pancreatitis has a predilection for patients with a previous surgical history of cholecystectomy. We herein present a case of a 74-year-old male patient presenting for severe epigastric pain radiating to the back after codeine intake for tension headache. His past surgical history was pertinent for a previous cholecystectomy that was done 3 years ago after which he reported no biliary-related symptoms. Upon detailed anamnesis, the patient reported that his pain was directly preceded by the intake of an analgesic medication for his tension headache. The painkiller consisted of 500 mg of acetaminophen, 8 mg of codeine and 30 mg of caffeine. CT scan of the abdomen and pelvis was performed and revealed a prominent pancreatic head with surrounding edema suggestive of acute pancreatitis. Codeine-induced pancreatitis is an uncommon entity. However, it has been documented in medical literature with a preponderance to patients who underwent previous cholecystectomy. Multiple pathophysiological elements come into play, such as decreased bile storage capacity and aberrant nervous wiring at the level of the SOD muscularity. These alterations result in increased SOD pressure and acute pancreatitis ensues. Nonetheless, this article should trigger future studies to further elucidate the causality between codeine and acute pancreatitis.
Oxford University Press (OUP)
Title: Codeine-induced pancreatitis in a previously Cholecystectomized patient: double the trouble
Description:
Abstract
The causality between codeine and acute pancreatitis has not yet been fully deciphered in medical literature.
Codeine-induced pancreatitis is a rare entity and the underlying mechanism of action mediated by codeine has not been completely elucidated.
One plausible theory is that codeine increases the pressure of the sphincter of Oddi (SOD), which results in spasms and subsequently acute pancreatitis ensues.
Codeine-induced pancreatitis has a predilection for patients with a previous surgical history of cholecystectomy.
We herein present a case of a 74-year-old male patient presenting for severe epigastric pain radiating to the back after codeine intake for tension headache.
His past surgical history was pertinent for a previous cholecystectomy that was done 3 years ago after which he reported no biliary-related symptoms.
Upon detailed anamnesis, the patient reported that his pain was directly preceded by the intake of an analgesic medication for his tension headache.
The painkiller consisted of 500 mg of acetaminophen, 8 mg of codeine and 30 mg of caffeine.
CT scan of the abdomen and pelvis was performed and revealed a prominent pancreatic head with surrounding edema suggestive of acute pancreatitis.
Codeine-induced pancreatitis is an uncommon entity.
However, it has been documented in medical literature with a preponderance to patients who underwent previous cholecystectomy.
Multiple pathophysiological elements come into play, such as decreased bile storage capacity and aberrant nervous wiring at the level of the SOD muscularity.
These alterations result in increased SOD pressure and acute pancreatitis ensues.
Nonetheless, this article should trigger future studies to further elucidate the causality between codeine and acute pancreatitis.
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