Acute Pancreatitis Flashcards
2012 Atlanta Classification Revision of Acute Pancreatitis
MILD ACUTE PANCREATITIS
No organ failure
No local or systemic complications
MODERATELY SEVERE ACUTE PANCREATITIS
Transient organ failure (<48 hr) and/or
Local or systemic complications* without persistent organ failure
SEVERE ACUTE PANCREATITIS
Persistent organ failure (>48 hr)___single organ or multiorgan
Acute Pancreatitis
best defined physiologically as an acute inflammatory process of the pancreas with variable involvement of other regional tissues or remote organ systems,
defined by a patient meeting 2 of the following 3 criteria:
(1) symptoms (e.g., acute onset epigastric and/or left upper quad- rant pain, often radiating to the back) consistent with pancreatitis,
(2) a serum amylase or lipase level greater than 3 times the upper limit of the laboratory’s reference range, and
(3) radiologic imaging consistent with pancreatitis, usually using CT or MRI.
After a period of approximately 4 weeks, if the acute peripancreatic fluid collections persist and develop a wall
located adjacent to or off the body of the pancreas.
Pseudocyst
Necrotic collections, which may also be peripancreatic, develop a wall after 4 weeks
WON is pancreatic necrosis that has liquefied after 5 to 6 weeks
WON
Factors Associated With Severe Acute Pancreatitis
PATIENT CHARACTERISTICS
Age >55 yr
Obesity (BMI >30 kg/m2)
Altered mental status
Comorbid disease
Systemic inflammatory response syndrome (SIRS)
Two or more of the following (SIRS criteria) Pulse >90/min
Respirations >20/min or PaCO2 <32 mm Hg Temperature >38°C or <36°C
WBC count >12,000 or <4000/mm3 or >10% band forms
LABORATORY FINDINGS
BUN >20 mg/dL or rising BUN level
Elevated serum creatinine level
Hematocrit >44% or rising hematocrit
IMAGING FINDINGS
Pleural effusion(s)
Pulmonary infiltrate(s)
Multiple or extensive extrapancreatic fluid collections
AP appears to have 2 distinct phases.
The first phase usually lasts a week and is characterized by systemic symptoms that may result in organ failure.
Most organ failure observed in the first week is also present on day 1, and at that time, one should consider (and treat) the patient as having severe AP
AP appears to have 2 distinct phases.
The second phase starts after 7 days and is mainly characterized by the local complications and ensuing infection of such local complications.
First phase
the disease severity is directly related to extrapancreatic organ failure from the patient’s SIRS elicited by acinar cell injury.
initial state of inflammation evolves dynamically, with variable degrees of pancreatic and peripancreatic ischemia or edema toward either resolution, irreversible necrosis and liquefaction, or the development of fluid collections in and around the pancreas
The initial step in the pathogenesis of AP
conversion of trypsinogen to trypsin within acinar cells in sufficient quantities to overwhelm normal mechanisms to remove active trypsin
Gallstone Pancreatitis
factors that may initiate gallstone pancreatitis include
reflux of bile into the PD or obstruction of the PD at the ampulla from stone(s) or from edema result- ing from the passage of a stone.
Reflux of bile into the PD could occur when the distal bile and PDs form a common chan- nel and a gallstone becomes impacted in the duodenal papilla.
The pathophysiology of AP
starts with acinar injury that, if unchecked, leads to local inflammatory complications, a systemic inflammatory response, and even sepsis.
microcirculatory injury, leukocyte chemoattrac- tion, release of pro- and anti-inflammatory cytokines, oxidative stress, leakage of pancreatic fluid into the region of the pancreas, and bacterial translocation to the pancreas and systemic circula- tion.
Conditions That Predispose to Acute Pancreatitis
Obstruction Gallstones Tumors Parasites Duodenal diverticula Annular pancreas Choledochocele
Alcohol/other toxins/drugs Ethyl alcohol Methyl alcohol Scorpion venom Organophosphorus insecticides Drugs
Metabolic abnormalities Hypertriglyceridemia Diabetes mellitus Hypercalcemia Infection
Vascular disorders
Vasculitis
Emboli to pancreatic blood vessels Hypotension/ischemia
Trauma Postoperative state Post-ERCP Hereditary/familial/genetic Controversial Pancreas divisum SOD Miscellaneous Idiopathic
the most common obstructive process leading to pancreatitis
Gallstones
Gallstone Pancreatitis
more common in women
AP occurs more frequently when stones are less than 5 mm in diameter
The triad of serum GGT ≥40 U/L, ALT ≥150 U/L, and lipase ≥15× ULN within 48 hours of presentation
Biliary Sludge and Microlithiasis
Biliary sludge is a viscous suspension in gallbladder bile that may contain small (<3 mm) stones (i.e., microlithiasis)
It is usually composed of cholesterol monohydrate crystals or calcium bilirubinate granules
Treatment choices include cholecystectomy, ursodeoxycholic acid therapy, endoscopic sphincterotomy, or watchful waiting.
Sludge may result from functional bile stasis, such as that associated with prolonged fasting or TPN, or from mechanical stasis, such as occurs in distal bile duct obstruction.
Tumors
Pancreatic tumors, presumably by obstructing the PD, infrequently cause acute and recurrent AP
The most common tumor that presents in this manner is intraductal papillary mucinous neoplasm
second most common cause of AP after gallstones and causes at least 30% of the cases.
most common etiology of chronic pancreatitis in developed countries
Prolonged alcohol consumption (more than 4 to 5 drinks per day for at least 5 years)
Ethyl Alcohol
Independent risk factor
Cigarette smoking has been shown to be an
independent risk factor for AP
Drug-induced pancreatitis tends to occur within 4 to 8 weeks of beginning a drug.
The most common is a hypersensitivity reaction. This tends to occur 4 to 8 weeks after starting the drug and is not dose related.
drug-induced pancreatitis tends to be mild and self-limited.
Drugs
third most common identifiable cause of pancreatitis
from 2% to 5%1 to 20% of cases.
Serum TG concentrations above 1000 mg/dL (11 mmol/L) may precipitate attacks
Hypertriglyceridemia
Factors That Increase the Risk of Post-ERCP Pancreatitis
PATIENT-RELATED
Young age, female gender, suspected SOD, history of recurrent pancreatitis, history of post-ERCP pancreatitis, normal serum bilirubin level
PROCEDURE-RELATED
Pancreatic duct injection, difficult cannulation, pancreatic sphinc- terotomy, precut access, balloon dilation
OPERATOR OR TECHNIQUE-RELATED
Trainee (fellow) participation, nonuse of a guidewire for cannulation, failure to use a pancreatic duct stent in a high-risk procedure
The 3 major modalities shown to reduce the risk are post- ERCP pancreatitis
prophylactic pancreatic stents, pre- procedural intravenous fluids, and rectal administration of NSAID
prophylactic PD stents are either a 3 French or 5 French and can be less than 5 cm or greater than 5 cm in length and placed temporarily to cover the 2- to 3-day period of ampullary edema.
most common congenital malformation of the pancreas, occurring in 5% to 10% of the general healthy population, the vast majority of whom never develop pancreatitis
Pancreas Divisum
CLINICAL FEATURES
Abdominal pain; epigastric, in the right upper quadrant, or, infrequently, confined to the left side.
Pain in the lower abdomen may arise from the rapid spread of pancreatic exudation to the left colon.
maximal intensity in 10 to 20 minutes.
pain gradually increases and takes several hours to reach maximum intensity.
Pain is steady and moderate to very severe. There is little pain relief with changing position. Frequently, pain is unbearable, steady, and boring.
Band-like radiation of the pain to the back occurs in half of patients.
