Discussion
In summary, this 39-year-old male was diagnosed with hypertriglyceridemia induced acute pancreatitis after an otherwise negative review of personal, social and family history risk factors and biochemical workup. Hypertriglyceridemia is a known risk factor for acute pancreatitis. 3
As two distinct pathological processes were concurrently observed in this patient, the question arises was this due to two separate processes or is a classic case of Occam’s razor with one unifying mechanism as the answer? One must be cautious as confirmation bias may be utilized following the recovery of the patient with a surgical intervention. While exploring the published literatures, only handful of cases of periappendicitis and appendicitis in different patients as the complication of acute pancreatitis have been reported.5,6
One should be aware that there are cases in the literature of similar presentations where amylase and lipase are elevated in the clinical context of acute appendicitis. 7,8 Based on the biochemical profile of a serum lipase elevated more than three times upper limit of normal, in the context of abdominal pain, one can safely conclude that the patient had acute pancreatitis. This diagnosis is supported and validated by the intravenous contrast CT findings when performed on specific time.9
From a radiological perspective, ultrasound has a sensitivity of 86% and a specificity of 81%, compared to computed tomography’s sensitivity of 94% and specificity of 95%, for diagnosing acute appendicitis.10 Ultrasound performed on this patient at the time of admission showed bulky and heterogenous echotexture of pancreas but not the features of acute appendicitis. However, both CT and repeat ultrasound were suggestive of acute appendicitis and this fact was confirmed by the histopathological analysis.
We believe the clinical phenomenon observed in this case could be because of the following:
(1) Hypertriglyceridemia led to acute pancreatitis
(2) Peri-pancreatic fluid and retroperitoneal fluid accumulated, as was observed on the CT scan was exudative fluid of pancreas
(3) Retroperitoneal fluid tracked to the right iliac fossa caused irritation of retroperitoneum leading to periappendicular inflammation
(4) Acute periappendicular inflammation gradually progressed to acute appendicitis.
(5) Per operative observed intraperitoneal fluid may be only reactive fluid of acute appendicitis but not the pancreatic exudate, thus normal amylase and lipase was seen upon analysis
Once again, the patient may have developed appendicitis incidentally and unrelated to the acute pancreatitis. However, given the time course, it makes sense that there is a unifying pathophysiological mechanism.
From a management perspective, we do not believe that there was an antibiotic failure in this case. Frankly, given the aforementioned mechanism, antibiotics may not have even been required in the management of this patient’s appendicitis. Whether or not somatostatin helped this patient is unknown. We added this therapy based on other case reports.6
In summary, this 39-year-old patient with hypertriglyceridemia induced acute pancreatitis concurrently developed acute appendicitis. We think there is a unifying mechanism that we have attempted to hypothesize. Future studies should focus on further elucidation of a pathophysiological mechanism.