Page 4 - Acute Pancreatitis (Viêm tụy cấp)

CHAPTER 58 Acute Pancreatitis 895

collections. Approximately 30% to 50% of cases of AP, mainly BOX 58 .2 Factors Associated With Severe Acute

the interstitial type, have peripancreatic fluid collections, which 58
typically resolve. After a period of approximately 4 weeks, if the Pancreatitis
acute peripancreatic fluid collections persist and develop a wall,
then they are called a “pseudocyst.” Because most of these col- PATIENT CHARACTERISTICS
lections resolve, true pseudocysts are uncommon, although most Age >55 yr 11,13,210,327
of the persistent fluid collections are loosely described as “pseu- Obesity (BMI >30 kg/m )
2 313
docyst.” Pseudocysts are located adjacent to or off the body of Altered mental status 223,224
the pancreas. At times, these enzyme-rich fluid-filled sacs can Comorbid disease 11
be found distantly in the pelvis or chest. When a pseudocyst is Systemic inflammatory response syndrome (SIRS) 11,20,217,223,224
located within the body of the pancreas, the cyst may contain Two or more of the following (SIRS criteria)
necrotic pancreatic debris on MRI and EUS, even when the Pulse >90/min
pseudocyst is fluid appearing with low attenuation on CT. Such Respirations >20/min or PaCO 2 <32 mm Hg
“pseudocysts” are more correctly called necrotic collections. Temperature >38°C or <36°C
Necrotic collections, which may also be peripancreatic, develop WBC count >12,000 or <4000/mm or >10% band forms
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a wall after 4 weeks and are then referred to as WON. The term LABORATORY FINDINGS
pancreatic abscess, defined in the original Atlanta classification, was 225
omitted because this is usually the end result of infected necrosis BUN >20 mg/dL or rising BUN level
314
and is also rare. Similarly the term infected pseudocyst is also dis- Elevated serum creatinine level 231
couraged as spontaneous infection without intervention is rare. Hematocrit >44% or rising hematocrit
Of all these terms, the most important distinction is that IMAGING FINDINGS
between pancreatic necrosis and pseudocyst. WON is pancreatic Pleural effusion(s) 195
necrosis that has liquefied after 5 to 6 weeks. Similar to a pseudo- Pulmonary infiltrate(s) 11
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cyst, a wall develops. However, whereas a pseudocyst always con- Multiple or extensive extrapancreatic fluid collections 203
tains fluid, pancreatic necrosis, even if walled off early, contains a
significant amount of debris that only becomes liquefied after 5 to BUN, Blood urea nitrogen level.
6 weeks. Draining WON too early (before 4 weeks) is discouraged
because the debris is typically thick, often with the consistency of
rubber, early in the course of the disease. After 4 weeks, WON can
be treated similarly to a pseudocyst and drained surgically, endo- cytokine-mediated SIRS; if organ failure is persistent, then AP
scopically, or percutaneously (see Chapter 61). is considered severe.
The first phase of AP usually lasts 1 week. During this phase,
COURSE OF THE DISEASE the disease severity is directly related to extrapancreatic organ
failure from the patient’s SIRS elicited by acinar cell injury. Mul-
AP appears to have 2 distinct phases. The first phase usually lasts tiple cytokines are involved, including platelet activating factor
a week and is characterized by systemic symptoms that may result (PAF), TNF-α, nuclear factor κB (NF-κB), and numerous inter-
in organ failure. The pancreatic inflammation may lead to the leukins (ILs; see Chapter 2). During this first week, the initial
systemic inflammatory response syndrome (SIRS). Infectious state of inflammation evolves dynamically, with variable degrees
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complications are uncommon in this phase. Fever, tachycardia, of pancreatic and peripancreatic ischemia or edema toward either
hypotension, respiratory distress, and leukocytosis are typically resolution, irreversible necrosis and liquefaction, or the develop-
related to SIRS (Box 58.2). Failure of the respiratory, circulatory ment of fluid collections in and around the pancreas. The extent
and renal systems are usually associated with persistent SIRS. GI of the pancreatic and peripancreatic changes is usually propor-
bleeding, liver failure, and coagulation disturbances have been tional to the severity of extrapancreatic organ failure. However,
included in some older studies, but the revised Atlanta classifica- organ failure may develop independent of pancreatic necrosis.
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tion removed them because they are rare and data regarding Conversely, patients with pancreatic necrosis may have no evi-
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these complications is sparse. Most organ failure observed in the dence of organ failure. The development of organ failure appears
first week is also present on day 1, and at that time, one should to correlate with the persistence of the systemic inflammatory
consider (and treat) the patient as having severe AP. If the organ response cascade (discussed later).
failure persists beyond 48 hours, severe AP is confirmed. If organ Approximately 75% to 80%, of patients with AP have a reso-
failure resolves within 48 hours and local complications evolve, lution of the disease process (interstitial pancreatitis) and do not
the case would be classified as moderately severe AP. If no local enter a second phase. However, in ∼20% of patients, a more pro-
complications are seen, the revised Atlanta classification still clas- tracted course develops, typically related to the necrotizing pro-
sifies the patient as moderately severe pancreatitis; however, the cess (necrotizing pancreatitis) lasting weeks to months. Mortality
original description of moderately severe AP described patients in this second phase is related to a combination of factors, includ-
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with local complications but without organ failure. Future clas- ing organ failure secondary to sterile necrosis, infected necrosis,
sifications may address patients with simple fluid collections, local complications from the severe necrotic process, or compli-
transient organ failure alone and exacerbation of preexisting cations from surgical/minimally invasive intervention. 18-20
medical comorbidities differently than as moderately severe AP. There are 2 time peaks for mortality in AP. Most studies in the
The second phase usually starts after 7 days and is mainly USA and Europe reveal that about half the deaths occur within
characterized by the local complications and ensuing infec- the first week or 2, usually from multiorgan failure. 18-20 Death
tion of such local complications. The organ failure seen in the can be very rapid. For example, in Scotland about one quarter of
first phase may continue and contribute to late morbidity and all deaths occurred within 24 hours of admission, and one third
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mortality, usually with infected necrosis. Hence, by definition, within 48 hours. After the second week of illness, patients suc-
mild AP is not associated with the second phase, except rare cumb to pancreatic infection associated with multiorgan failure.
patients who continue to have pain without any organ failure Some studies in Europe report a very high late mortality rate
or local complications. Organ failure occurs in ∼5% of intersti- from infection. It is unclear if this is related to endogenous
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tial pancreatitis (often synonymous with mild severity) due to infection of the pancreatic necrosis or to surgical interventions