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Differential Diagnosis
Epigastric abdominal pain radiating to the back, in a
patient with a history of heavy alcohol consumption and a
family history of hypertriglyceridemia, suggests acute
pancreatitis. However, in a patient who is tachycardic,
hypotensive, and vomiting, the differential diagnosis would
also include perforated gastroduodenal ulcer disease and
esophageal rupture (Boerhaave’s syndrome). Cholecystitis
and cholangitis are other important considerations, as
these patients may present with fever, tachycardia,
hypotension, and abdominal pain.
Presentation Continued
The patient has been hospitalized in the past for acute
pancreatitis. He has no history of gallstone disease.
Laboratory tests were notable for lipase of 18,200 U/L,
amylase of 7,800 U/L, and mildly elevated
transaminases (AST of 124 IU/L and ALT of 79 IU/L).
Alkaline phosphatase, total bilirubin, and creatinine
were within normal limits. Serum glucose was elevated
at 230 mg/dL and lactate dehydrogenase (LDH) was
411 IU/L. He had a hematocrit of 48% and an elevated
white blood cell (WBC) count of 16,400 cells/cm3.
Triglycerides were 1,100 mg/dL. His respiratory rate
was 16 and an arterial blood gas was notable for a pH
of 7.31 and a PaO2 of 72 mm Hg. A Ranson score of 3
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was calculated upon admission (Table 1).
A contrast-enhanced computerized tomographic
(CT) scan of the abdomen and pelvis reveals stranding,
inflammation, and edema within the peripancreatic
area and extending inferiorly along the paracolic gutters
to the pelvis (Figure 1). The low attenuation area in the
tail of the pancreas is consistent with necrosis and
represents approximately 30% of the pancreatic
parenchyma (Figure 2). Bowel wall thickening was also
seen at the hepatic flexure of the transverse colon.
There was no free air or evidence of biliary disease,
and no occlusion or thrombosis of the peripancreatic
vasculature.
TABLE 1. Ranson Criteria
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FIGURE 1 • CT scan of the abdomen with IV and oral contrast reveals
stranding, inflammation, and edema within the peripancreatic area.
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FIGURE 2 • CT scan of the abdomen with IV and oral contrast reveals low
attenuation of the tail of the pancreas. This is consistent with necrosis and
represents approximately 30% of the pancreatic parenchyma.
Workup
This patient presents with severe acute necrotizing
pancreatitis. The most common etiology of acute
pancreatitis is obstructive biliary tract disease, responsible
for up to 40% of cases. Excessive alcohol use is the
second most common cause of pancreatitis, responsible
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for approximately 35% of cases. Other causes include
hypertriglyceridemia, endoscopic retrograde
pancreatography (ERCP), anatomic abnormalities (e.g.,
pancreatic divisum), and abdominal trauma.
Nearly 20% to 30% of patients with acute pancreatitis
have pancreatic necrosis; therefore, it is vital to determine
the severity of pancreatitis. The Ranson score, based on
the presence of 11 clinical signs (five measured at the time
of admission and six measured 48 hours after admission),
indicates the risk of systemic complications and the
likelihood of pancreatic necrosis (Table 1). The presence
of three or more Ranson criteria (or if the patient is in
shock, renal insufficiency, or pulmonary insufficiency)
indicates severe pancreatitis and a greater likelihood of
necrosis. Severe pancreatitis is associated with multiple
organ dysfunction syndrome (MODS) and mortality rates
that typically exceed 15%. In contrast, patients with mild
disease generally recover completely with conservative
management.
Contrast-enhanced abdominal CT is the gold standard
for noninvasive diagnosis of pancreatic necrosis. CT is
>90% accurate in diagnosing necrosis if more than 30% of
the gland is affected. There are several CT-based
classification schemes that predict disease severity and
mortality. However, several recent studies revealed that the
associated radiation exposure was significant and that,
after CT imaging, changes in clinical management were
infrequent. Subsequently, it is recommended that the use of
CT be restricted to patients with severe pancreatitis.
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Diagnosis and Treatment
Initial treatment of the patient with severe pancreatitis
includes monitoring, fluid resuscitation, and pain control
with patient-administered or epidural analgesia (PCA). A
Foley catheter to measure urine output should be
considered. Oxygenation should be monitored closely and
early intubation should be considered in the patient whose
respiratory function is deteriorating. Caloric support should
be initiated early in the hospital course, and enteral feeding
via a nasojejunal tube is preferred if the patient’s ileus is
not too severe.
In patients who are appropriately resuscitated,
infectious complications are considered to be the main
cause of mortality in severe pancreatitis. Multiple trials have
examined the value of prophylactic antibiotics and this
remains controversial; selection for resistant organisms
and
Candida
species may be associated with even worse
outcomes.
For patients with MODS and signs of sepsis, CTguided (FNA) of the necrotic areas should be performed to
determine the presence of bacterial contamination.
Although these developments may be the result of infection,
MODS and the systemic inflammatory response syndrome
can result from pancreatic necrosis alone. Infected
pancreatic necrosis is an indication for intervention with
either surgical or radiologic drainage. In extremely ill
patients, a percutaneous drain placed at the time of the
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FNA can help stabilize the patient prior to surgery, and may
be used to temporize or even definitively treat infected
necrosis. If possible, waiting at least 4 weeks prior to
necrosectomy will allow demarcation of necrosis, thereby
minimizing resection of viable pancreas and the
accompanying morbidity. Sterile necrotizing pancreatitis,
on the other hand, has not been shown to benefit from
drainage or debridement and may be managed
nonoperatively. In patients who develop abdominal
compartment syndrome, surgical decompression may
improve respiratory, cardiovascular, and renal parameters,
but it is unclear if this is associated with an improvement in
mortality.
Presentation Continued
The patient was admitted to the intensive care unit. His
pain was controlled with a PCA, and his electrolytes
were closely monitored. A postpyloric feeding tube was
placed under endoscopic guidance. Although he initially
stabilized, on the eighth hospital day, the patient
became tachycardic and hypotensive. His WBC count
continued to rise, and his creatinine became elevated.
An intra-abdominal pressure was measured at 15 mm
Hg. He became increasingly dyspneic and required
intubation. CT-guided FNA revealed gram-negative
rods, and a percutaneous drain was placed. Despite
this, the patient continued to deteriorate and the
decision was made to proceed with surgical
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debridement.
Surgical Approach
The approach to pancreatic debridement is determined by
the interval to operation. Over time, the pancreatic necrosis
becomes increasingly organized, permitting a more
focused and even minimally invasive approach. In patients
undergoing operation prior to a month after onset, open
pancreatic necrosectomy is often required.
Open pancreatic necrosectomy
(Table 2). Preoperative
imaging should be used to guide placement of the incision.
A vertical midline or Chevron incision may be employed.
The greater omentum is usually separated from the middle
of the transverse colon for a distance sufficient to expose
the pancreas. When the collection extends into the
mesocolon and the small bowel mesentery, a direct
approach from below the transverse colon may be more
appropriate. Once the pancreas is exposed, the capsule is
opened and all purulent material and necrotic tissue is
removed from the pancreatic bed, being careful to preserve
viable pancreatic tissue. Sharp dissection is usually
avoided; it is typically sufficient to remove tissue that
comes easily with a ring forceps or irrigation. The
transverse colon should be inspected for viability; if the
colon is compromised, an extended right hemicolectomy
should be performed. Care should be taken to minimize
intra-operative hemorrhage. Depending on the organization
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of the necrosis, the anticipated need for further
debridement, and the degree of hemorrhage, it may be
appropriate to pack the pancreatic bed and plan
reoperation. In cases where the laparotomy incision will be
closed, Jackson-Pratt (JP) drains should be placed to
maximize postoperative drainage of debris. Closed
continuous lavage of the retroperitoneum may be
appropriate in patients where ongoing necrosis is
anticipated.
TABLE 2. Key Technical Steps and Potential Pitfalls in Open Pancreatic
Necrosectomy
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Laparoscopic pancreatic necrosectomy.
For critically ill,
hemodynamically unstable patients or if the necrosis is not
yet organized, laparoscopic intervention is contraindicated.
However, some case series suggest that laparoscopic
necrosectomy is appropriate in patients who have
undergone prior percutaneous drainage and/or have
limited areas of necrosis that will benefit from a singlestage procedure. Full laparoscopic procedures with carbon
dioxide pneumoperitoneum and modified laparoscopic
procedures aided by a hand port have been described.
Postoperative drainage is recommended with both
techniques. Other minimally invasive techniques, such as
endoscopic transgastric or transduodenal necrosectomy or
retroperitoneal percutaneous necrosectomy, may be
alternatives to surgical intervention, but a full description of
these techniques and their indication is beyond the scope
of this text.
Special Intraoperative Considerations
Pancreatic necrosectomy may be combined with
cholecystectomy if exposure is simple and mobilization is
thought to be safe. However, in the patient with severe
pancreatitis, even if secondary to gallstones,
cholecystectomy should be deferred to a later date if the
gallbladder is not easily accessible.
A subcostal incision can be performed if focal areas of
necrosis are in the tail or in the head of the gland. Formal
mobilization of the gastrocolic gutters is typically not
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