Pancreatitis Flashcards
No organ failure
No local or systemic complications
Mild Acute Pancreatitis
Transient organ failure (<48 hours) and/or
Local or systemic complications* without persistent organ failure
Moderately Severe Acute Pancreatitis
Persistent organ failure (>48 hours)–single organ or multiorgan
Severe Acute Pancreatitis
acute pancreatitis is best defined clinically by a patient
presenting with 2 of the following 3 criteria
(1) symptoms (e.g., epigastric pain) consistent with pancreatitis
(2) a serum amylase or lipase level greater than 3 times the laboratory’s upper limit of normal,
(3) radiologic imaging consistent with pancreatitis, usually using CT or MRI.
necrotizing pancreatitis have greater than
30% of the gland that is not perfused, with low attenuation
Pancreatic necrosis consists of focal or diffuse nonviable pancreatic parenchyma and is usually accompanied by peripancreatic fat necrosis.
occurs in 30% to 50% of cases of acute
pancreatitis, and most resolve spontaneously
An acute fluid collection
is a fluid collection that persists for 4 to 6 weeks and becomes encapsulated by a wall of fibrous or granulation tissue.
pseudocyst
Pseudocysts
are located adjacent to or off the body of the pancreas.
is more commonly associated with
pseudoaneurysm formation, an erosion of peripancreatic
blood vessels leading to hemoperitoneum
Hemorrhagic pancreatitis
is pancreatic
necrosis that has liquefied after 5 to 6 weeks
WON
Similar to a pseudocyst, a wall develops. However, whereas a pseudocyst always contains fluid, pancreatic necrosis, even if walled off early, contains a significant amount of debris that only becomes liquefied after 5 to 6 weeks.
Draining WON too early (before 4 weeks) should be discouraged because the debris is typically thick, often with the consistency of rubber, early in the course of the disease.
Acute pancreatitis appears to have 2 distinct phases. The first is related to the pathophysiology of the inflammatory cascade.
The second, which develops in fewer than 20% of patients with acute pancreatitis, is related to the anatomic complications that develop, such as pancreatic necrosis. The first phase usually lasts 1 week.
Factors Associated with Severe Pancreatitis
Patient Characteristics Age > 55 years Obesity (BMI > 30 kg/m2 Altered mental status Comorbid disease Systemic inflammatory response syndrome Two or more of the following Pulse > 90/min Respirations > 20/min or PaCO2 < 32 mm Hg Temperature > 38° or < 36°C WBC count > 12,000 or < 4000/mm3 or > 10% band forms Laboratory Findings BUN > 20 mg/dL Rising BUN Hematocrit > 44 Rising hematocrit Elevated serum creatinine level Imaging Findings Pleural effusion(s) Pulmonary infiltrate(s) Multiple or extensive extrapancreatic fluid collections
half the deaths occur
within the first week or 2, usually from multiorgan failure
After the second week of illness, patients
succumb to pancreatic infection associated with multiorgan
failure.
The initial step in the pathogenesis of acute pancreatitis is
conversion of trypsinogen to trypsin, within acinar cells in sufficient quantities to overwhelm normal mechanisms to remove active trypsin
ARDS may be induced by active phospholipase A (lecithinase), which digests lecithin, a major component of lung surfactant
Metabolic complications include
hypocalcemia, hyperlipidemia, hyperglycemia with or without ketoacidosis, and hypoglycemia
Pancreatic infection (infected necrosis and infected pseudocyst) can occur from the
hematogenous route or from translocation
of bacteria from the colon into the lymphatics
The most common obstructive process leading to pancreatitis
is
gallstones, which cause approximately 40%
of cases of acute pancreatitis.
Acute pancreatitis
occurs more frequently when stones are less than
5 mm in diameter
because small stones are more
likely than large stones to pass through the cystic duct and cause ampullary obstruction
Biliary sludge is a viscous suspension in gallbladder bile that may contain small
(<3 mm) stones
Because small stones can hide in biliary sludge, the 2 are commonly referred to together as biliary sludge and microlithiasis
It is usually composed of cholesterol monohydrate crystals or calcium bilirubinate
granules.On US, sludge produces a mobile, low amplitude echo that does not produce an acoustic shadow and that layers in the most dependent part of the gallbladder.
cephalosporin antibiotic ceftriaxone
can form a sludge within the biliary system when its solubility
in bile is exceeded
causes at least 30% of cases of acute pancreatitis
Alcohol
Interestingly, only 10% of chronic alcoholic
patients develop chronic pancreatitis acute pancreatitis can be precipitated in patients with gallstones immediately, alcoholism requires years of toxin exposure.
Alcohol modulates exocrine function
to increase the lithogenicity of pancreatic fluid, leading to the formation of protein plugs and stones
Drug-induced
pancreatitis tends to occur within
4 to 8 weeks of beginning a
drug.
is perhaps the third most common identifiable
cause of pancreatitis after gallstones and alcoholism,
accounting for 2% to 5% of cases
Hypertriglyceridemia
implicated in more than half of gestational pancreatitis cases.
Serum TG concentrations above 1000 mg/dL (11 mmol/L) may precipitate attacks of acute pancreatitis
higher to precipitate acute pancreatitis, perhaps above
2000 mg/dL, and with obvious lactescent (milky) serum due to increased concentrations of chylomicrons. The pathogenesis of hypertriglyceridemic pancreatitis is unclear, but the release of free fatty acids by lipase may damage pancreatic acinar cells or endothelial cells.
Typically, 3 types of patients develop
hypertriglyceridemia-induced pancreatitis.
The first is a poorly controlled diabetic patient with a history of hypertriglyceridemia.
The second is an alcoholic patient with hypertriglyceridemia detected on hospital admission.
The third (15% to 20%) is a nondiabetic, nonalcoholic, nonobese person who has drug- or diet-induced hypertriglyceridemia.
Druginduceddisease is more likely to occur if there is a background of hypertriglyceridemia prior to drug exposure
Most persons who abuse alcohol have moderate but transient elevations of the serum TG level.
are at an increased risk for developing acute pancreatitis.
The risk may be due to the increased prevalence of
gallstones and hypertriglyceridemia in this population.
Diabetics
dyslipidemia, leading to cholesterolsupersaturated
bile resulting in precipitation of cholesterol
crystals.
Also, patients with long-standing diabetes often develop bile stasis in the gallbladder, leading to the precipitation of cholesterol crystals and to gallstones.
is the most common and feared complication
of ERCP, associated with substantial morbidity and
occasional mortality
Acute pancreatitis
Factors That Increase the Risk of Post-ERCP
Pancreatitis
Patient-Related
Young age, female gender, suspected SOD, recurrent
pancreatitis, history of post-ERCP pancreatitis, normal serum bilirubin level
Procedure-Related
Pancreatic duct injection, difficult cannulation, pancreatic sphincterotomy, 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 patient most at risk of developing post-ERCP pancreatitis
was
a woman with suspected choledocholithiasis and normal serum bilirubin, who underwent a sphincterotomy and no stone was found
2-hour serum amylase and lipase were more accurate than a clinical assessment in distinguishing nonpancreatitis abdominal pain from post-ERCP acute pancreatitis.
Serum amylase values
above 276 IU/L (normal 30 to 70) and lipase above 1000 IU/L (normal 45 to 110) 2 hours after completing the procedure had almost a 100% positive predictive value for post-ERCP pancreatitis.
100-mg rectal suppository of diclofenac
reduces the incidence of post ERCP pancreatitis
somatostatin have demonstrated
an efficacy in reducing the incidence of post-ERCP
pancreatitis
majority of studies do not support routine
use of this medication.149-155 Octreotide, the analog of somatostatin, was only effective in reducing post-ERCP hyperamylasemia,
and did not reduce the incidence of post-ERCP
pancreatitis
clearly decreases the risk of
Pancreatic stent placement
post-ERCP pancreatitis in high-risk patients
Placement of
pancreatic duct stents has become a standard practice for patients who are thought to be at high risk for pancreatitis after the procedure
3- to 5-French unflanged
pancreatic stents are used in the following post-ERCP settings:
SOD, difficult cannulation, biliary orifice balloon dilation,
and precut sphincterotomy
whereby the biliary or pancreatic
duct is initially cannulated by a guidewire inserted through the catheter or sphincterotome, has been shown to decrease the risk of pancreatitis
Guidewire cannulation,
is the most common congenital malformation
of the pancreas,
Pancreas divisum
SOD (usually defined as a basal pancreatic sphincter
pressure >_) is the most common abnormality
discovered,
40 mm Hg
Abdominal pain is present at the onset of most attacks of acute
pancreatitis.
Biliary colic may herald or progress to acute pancreatitis.
Pain in pancreatitis usually involves the entire upper
abdomen. However, it may be 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.
Onset of pain is rapid but not as abrupt as that of a perforated viscus
Usually it is at maximal intensity in 10 to 20
minutes
Occasionally, 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.
Pain is absent in 5% to 10% of
attacks, and a painless presentation may be a feature of serious fatal disease
Guarding is more marked in the upper abdomen.
Bowel sounds are reduced and may be absent.
Initially the temperature may be normal, but within 1
to 3 days it may increase to 101°F to 103°F owing to the severe
retroperitoneal inflammatory process and the release of
inflammatory mediators from the pancreas
Uncommon findings in acute pancreatitis include panniculitis
with subcutaneous nodular fat necrosis that may be
accompanied by polyarthritis (PPP syndrome;
thrombophlebitis in the legs, and polyarthritis.
Subcutaneous
fat necroses are 0.5- to 2-cm tender red nodules that
usually appear over the distal extremities but may occur over
the scalp, trunk, or buttocks.
healthy persons, the pancreas accounts for 40% to 45% of serum amylase activity, the salivary glands accounting for the rest.
pancreatic diseases increase serum
pancreatic (P) isoamylase, measurement of P-isoamylase can improve diagnostic accuracy.
The total serum amylase test is most frequently ordered to diagnose acute pancreatitis, because it can be measured quickly and cheaply. It rises within 6 to 12 hours of onset and is cleared fairly rapidly from the blood (half-life, 10 hours).
The serum amylase is usually increased
on the first day of symptoms, and it remains elevated for 3 to 5 days in uncomplicated attacks
limitation of serum amylase is that it is not highly sensitive or specific
Sensitivity is above 85%
Serum amylase also may be falsely normal in hypertriglyceridemia associated
pancreatitis
one half of all patients with an elevated serum
amylase level may not have pancreatic disease.186 In acute
pancreatitis, the serum amylase concentration is usually more
than 2 to 3 times the upper limit of normal; it is usually less
than this with other causes of hyperamylasemia
can cause hyperamylasemia because they produce and secrete salivary (S-type) isoamylase
papillary cystadenocarcinoma of the ovary, benign ovarian cyst, and carcinoma of the
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