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.
ecchymosis in 1 of both flanks
Gray Turner sign
about the peri- umbilical area
Cullen sign
Band keratopathy (an infiltration on the lateral margin of the cornea)
occurs with hypercalcemia.
It rises within 6 to 12 hours of onset and is cleared fairly rapidly from the blood (half-life, 10 hours)
remains elevated for 3 to 5 days in uncomplicated attacks.
In AP, the serum amylase concentration is usually more than 2 to 3 times the upper limit of normal
Amylase
Standard Blood Tests
WBC count frequently is elevated, often markedly so in severe pancreatitis
Serum AST, ALT, alkaline phosphatase, and bilirubin also may increase, particularly in gallstone pancreatitis.
Abdominal Plain Film
Findings on a plain radiograph range from no abnormalities in mild disease to localized ileus of a segment of small intestine (“sentinel loop”) or the colon cutoff sign in more severe disease.
spread of exudate to specific areas of the colon may produce spasm of that part of the colon and either no air distal to the spasm (the colon cutoff sign) or dilated colon proximal to the spasm.
Abdominal US
intraductal or parenchymal calcification(s) and dilation of the PD.
CT
CT is the most important imaging test for the diagnosis of AP and its intra-abdominal complications.
3 main indications for a CT in AP are to (1) exclude other serious intra-abdominal con- ditions (e.g., mesenteric infarction or a perforated peptic ulcer), (2) stage the severity of AP, and (3) determine whether complica- tions of pancreatitis are present (e.g., involvement of the GI tract or nearby blood vessels and organs, including liver, spleen, and kidney).
Alcoholic pancreatitis
requently in men approximately 40 years old.
The first clinical episode usually occurs after 5 to 10 years of heavy alcohol consumption.
serum ALT concentration greater than 150 IU/L (≈3-fold elevation) is 96%; the PPV is 95%, but the sensitivity is only 48%
biliary pancreatitis
more frequent in women, and the first clinical episode is often after the age of 40 years.
predictors of persistent organ failure (severe AP) and infected pancreatic necrosis
blood urea nitrogen (BUN) level for prediction of persistent organ failure after 48 hours of admission and procalcitonin for prediction of infected pancreatic necrosis in patients with confirmed pancreatic necrosis
following
predictors at admission to be useful while considered together
with clinical judgement:
advanced age (>60 years), BMI, Charl-
son’s comorbidity index, pleural effusions or infiltrates on the
admission chest radiograph, elevated hematocrit, elevated BUN
level, elevated serum creatinine level, and CRP >15 mg/dL at 48 hours.
most validated system for many years and none of the later scoring systems
APACHE II
Ranson and colleagues identified 11 signs that had prognostic significance during the first 48 hours.
BISAP (Bedside Index for Severity in AP), assigns each parameter 1 point: BUN greater than 25 mg/dL, Impaired mental status, SIRS, Age older than 60 years, and Pleural effusion, for a possible total of 5 points. A BISAP score of 4 or 5 is associated with a 7- to 12-fold increased risk of developing organ failure.
CT Grading System of Balthazar and the CT Severity Index (CTSI)
A: Normal pancreas consistent with mild pancreatitis
B: Focal or diffuse enlargement of the gland, including contour irregularities and inhomogeneous attenuation but without peripancreatic inflammation
C: Grade B plus peripancreatic inflammation
D: Grade C plus associated single fluid collection
E: Grade C plus 2 or more peripancreatic fluid collections or gas in the pancreas or retroperitoneum
Initial Management During the First Week
The patient is usually kept NPO until any nausea and vomiting have subsided.
Intravenous Fluid and Electrolyte Resuscitation
extravasation of protein-rich intravascular fluid into the peritoneal cavity and retroperitoneum, resulting in hemoconcentration and decreased renal perfusion with the associated elevation in the BUN level and, later, the serum creatinine level.
admission hematocrit of more than 44% and a failure of the admission hematocrit to decrease at 24 hours
predictors of necrotizing pancreatitis
Associated with increased mortality.
elevation and/or rising BUN
One could suggest a fluid rate of 5 to 10 mL per kilogram body weight per hour or 250 to 500 mL per hour of probably lactated Ringer solution, preferably during the first 24 hours after admission
Lactated Ringer solution is supposed to reduce intracellular acidosis in the pancreas and thus the tryptic activity.
Metabolic Complications
Hyperglycemia may present during the first several days of severe pancreatitis but usually disappears as the inflammatory process subsides.
Hypocalcemia is mainly due to a low serum albumin.
Serum albumin is lost as albumin-rich intravascular fluid extrava- sates into peritoneum and retroperitoneum, as well as the nega- tive phase reactant effect on reducing albumin synthesis during the acute illness phase
Antibiotics
Imipenem, fluoroquinolones (ciprofloxacin, ofloxacin, pefloxacin), and metronidazole emerged as the drugs that achieved the highest inhibitory concentrations in pancreatic tissue
ERCP
mild biliary AP, same-admission laparo- scopic cholecystectomy is the standard therapy
ERCP within 72 hours for cholangitis and possibly for persistent biliary obstruction defined by elevated liver tests and/or the pres- ence of a stone in the common bile duct on imaging.
cute biliary pancreatitis, urgent ERCP within 24 to 48 hours is indicated if the patient has cholangitis, total serum bilirubin >5 mg/dL, clinical deterioration (worsening pain and white cell count and worsening vital signs), or a stone documented in the common bile duct on imaging.
Nutrition
In mild AP, possible to feed patients immediately, even with a full solid diet without standard practice of NPO initially, and others reporting that feeding can be with low fat solid diet versus clear liquids or soft diet versus clear liquids, immediately without waiting for the pain to subside or the enzymes to normalize
AP enteral nutrition is preferred to TPN if the patient is not able to tolerate oral feed- ing for prolonged period
TPN
severe or established necrotizing pancreatitis starting enteral nutrition early on, preferably in the first 24 hours
feeding?
For those patients who can do not tolerate anything by mouth due to vom- iting and/or worsening pain after 3 to 5 days, a low-fat diet given by nasogastric tube and, if not tolerated, a postpyloric feeding should be given.
Cholecystectomy
include urgent (24 to 72 hours) ERCP, elective ERCP before cholecystectomy for gallstones, and cholecystectomy as the definitive treatment.
recurrence of further attacks of AP is 18% in 6 weeks if cholecystectomy is not performed at the time of index attack of biliary pancreatitis
Pancreatic Fluid Collections
After the initial phase of 2 weeks, pancreatic fluid collections appear to become more demarcated and develop a wall, usually by 4 weeks.
an entity when a significant amount of pancreatic body necrosis disconnects the PD in the proximal and distal segments.
Disconnected PD syndrome
Disconnected PD syndrome
diagnosis is made usually by necrosis of the middle part of the pancreas initially, a persistent fluid collection in the area of necrosis, complete cutoff of the PD on ERCP in the same region, and a viable enhancing distal segment of the pancreas.
self-expanding metal stent can be used for short duration of 3 weeks, subsequent treatment would be pigtail catheters either from a single entrance from the stomach into the fluid collection or multiple gait ways for better egress of pancreatic secretions.
most frequently used minimally invasive technique for drainage or debridement of pancreatic fluid collections on a worldwide basis
Percutaneous drainage
Long-Term Sequelae of Acute Pancreatitis
Exocrine and endocrine insufficiency after an attack of AP is common.
sustained intra-abdominal pressure greater than 20 mm Hg (typically determined by a pressure-recording catheter in the urinary
bladder) that is associated with the development of organ dysfunction or failure
Abdominal Compartment Syndrome
discrete flame-shaped hemorrhages with cotton wool spots) can cause sudden blindness.181 It is thought to be due to microembolization in the choroidal and retinal arteries.
Purtsher retinopathy
In idiopathic AP,
recent guidelines and reviews recommend obtaining EUS
obtaining EUS after
a period of 8 to 12 weeks to look for causes like microlithiasis
in the common bile duct, small tumors near the PD causing
obstruction, chronic pancreatitis presenting as an AP attack, and
some anatomical abnormalities missed on CT scan
Pancreatic secretory trypsin inhibitor
called SPINK1) binds and inactivates about 20% of the trypsin activity.
SPINK1 protects the pancreatic acinar cell by inhibiting prematurely activated trypsin.
Mutations in the CFTR gene have also been implicated in pancreatitis
predictors at admission to be useful
advanced age (>60 years), BMI, Charlson’s comorbidity index, pleural effusions or infiltrates on the
admission chest radiograph, elevated hematocrit, elevated BUN
level, elevated serum creatinine level, and CRP >15 mg/dL at 48 hours.
prognostic significance during the first 48 hours.
Ranson and colleagues identified 11 signs
