Page 13 - Acute Pancreatitis (Viêm tụy cấp)

904 PART VII Pancreas

taking thiopurines developed AP. 161 Celiac disease 162 has also pancreas divisum is associated with genetic abnormalities and not
been described in association with pancreatitis, but the relation- solely due to pancreas divisum. This observation along with the
ship remains uncertain. It has been suggested that abnormalities finding that minor papilla endoscopic therapy is associated with
in the normal barrier of the small bowel seen in patients with significant amount of complications like stricture should make
celiac disease may allow excessive absorption of amylase from the one think carefully before subjecting patients with pancreas divi-
intestinal lumen, leading to hyperamylasemia. In the setting of sum and AP to invasive therapy. Every effort should be made to
abdominal pain in a patient with celiac disease, it is not uncom- seek other causes of such attacks of AP. Therefore, it may not be
mon to find elevations in the serum amylase in the absence of the presence of pancreas divisum alone that predisposes to AP,
AP. 163 Pancreatitis has been seen in patients after severe burns. 164 but other factors may be necessary to precipitate an attack. (See
Autoimmune pancreatitis (discussed in the next chapter in the earlier discussion in the section on genetic factors.) 174
more detail). AP or recurrent AP resulting from autoimmune
pancreatitis is rare, seen in type II disease, and is associated with SOD (See Chapter 63)
granulocyte epithelial lesions. 165 Investigators have also described
patients with autoimmune recurrent pancreatitis, especially in SOD is also a controversial cause of AP. Investigators who study
younger women, often without the classic elevation of serum patients with recurrent AP report that SOD (usually defined as a
IgG4. 166 basal pancreatic sphincter pressure >40 mm Hg) is the most com-
As discussed in Chapter 53, PUD (penetrating duodenal or gas- mon abnormality discovered, occurring in approximately 35% to
tric ulcers) can involve the pancreas and cause pancreatitis that 40% of patients. The main argument in favor of this entity as
may be fatal. Though uncommon nowadays, penetrating ulcer a cause of AP is the many observational series that report that
as a cause of pancreatitis should be considered in the appropriate endoscopic pancreatic sphincterotomy or surgical sphinctero-
clinical setting. 167 plasty reduces recurrent attacks of pancreatitis. 174 The arguments
against SOD as a cause of AP include: (1) the lack of any prospec-
tive controlled blinded trials in the treatment of this disorder;
Controversial Causes (2) the short duration of follow-up in the observational reports;
Pancreas Divisum (3) the high risk of pancreatitis (25% to 35%) associated with
ERCP, sphincter of Oddi manometry, and pancreatic sphinc-
Pancreas divisum is the most common congenital malformation terotomy in patients with suspected SOD; (4) the extremely
of the pancreas, occurring in 5% to 10% of the general healthy variable natural history of idiopathic recurrent pancreatitis,
population, the vast majority of whom never develop pancreatitis which may mask the minimal effects of therapy 175 ; and (5) the
(see Chapter 55). Controversy continues to surround the issue relative dearth of data determining the normal range of pancre-
as to whether pancreas divisum with otherwise normal ductular atic sphincter pressure that is the basis for the pathogenesis of
anatomy is a cause of acute recurrent pancreatitis. 168 The pre- SOD. 175 Although one could debate if idiopathic recurrent AP
sumed mechanism of action in those who develop pancreatitis is can be labeled as type 2 SOD, a large number of patients with
that there is relative obstruction to the flow of pancreatic juice abdominal pain after cholecystectomy, but no objective evidence
through the minor papilla. Arguments in favor of attributing of biliary or pancreatic disease is subjected to ERCP, sphincter of
pancreatitis to pancreas divisum include: (1) various series from Oddi manometry, and biliary and or pancreatic sphincterotomy
ERCP referral centers show that patients referred with recur- with a diagnosis of type 3 SOD. For patients with type 3 SOD,
rent AP have a higher frequency of pancreas divisum than would the results of a large rigorously conducted multicenter RCT, the
be expected from the general population; (2) multiple observa- EPISOD trial, has been published. 176 The trial concluded that in
tional series report that performing endoscopic sphincterotomy patients with abdominal pain after cholecystectomy undergoing
or placing a stent across the minor papilla reduces the rate of ERCP with manometry, sphincterotomy versus sham sphincter-
recurrent pancreatitis 169 ; and (3) there is a small randomized otomy did not reduce disability due to pain. These findings do
controlled study suggesting that patients with pancreas divisum not support ERCP and sphincterotomy for these patients.
who undergo duct stenting for 1 year have a lower frequency
of attacks of pancreatitis than those not stented. 170 Arguments CLINICAL FEATURES
against the association include: (1) there are other studies show-
ing that the incidence of pancreatitis in pancreas divisum patients It is difficult to diagnose AP by history and physical examina-
is the same as the general population 171 ; (2) the observational tion, because clinical features are similar to those of many acute
reports are flawed in that follow-up was not long enough (usually abdominal illnesses (Box 58.6).
only 1 to 2 years) and that recurrent AP is a disease of great vari-
ability 151 ; (3) the single randomized study 170 was flawed in that it History
was not blinded, had only 19 patients, and its patients probably
had chronic pancreatitis in that they had multiple pain attacks in Abdominal pain is present at the onset of most attacks of AP.
between attacks of AP. In addition, when considering the lack Biliary pain may herald or progress to AP. Pain in pancreatitis
of evidence, it is worth considering the high risk of endoscopic usually involves the entire upper abdomen. However, it may be
therapy in causing PEP in patients with pancreas divisum, there-
fore making the risk-benefit ratio of treating pancreas divisum
endoscopically questionable. BOX 58 .6 Differential Diagnosis of Acute Pancreatitis

The prevalence of genetic abnormalities in patients with
pancreas divisum and acute recurrent pancreatitis are either the Biliary pain
same 171 or higher 172 than expected in the general population or Acute cholecystitis
population of patients with AP of other etiologies, suggesting a Perforated hollow viscus (e.g., perforated peptic ulcer)
possible genetic contribution. For example, there appears to be Mesenteric ischemia or infarction
a higher incidence of CFTR mutations in patients with pancreas Intestinal obstruction
divisum who develop AP. 173 Because several authors reported Myocardial infarction
associations of SPINK-1 and CFTR mutations in patients with Dissecting aortic aneurysm
AP and pancreas divisum, expert review suggested that idiopathic Ectopic pregnancy
pancreatitis (either acute or acute recurrent) in a patient with