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.