ACUTE PANCREATITIS Flashcards
Inflammation of the pancreas due to activation of enzymes within the pancreas
Acute pancreatitis
Pathologic spectrum of acute pancreatitis
Interstitial pancreatitis
Necrotizing pancreatitis
Difference between interstitial pancreatitis and necrotizing pancreatitis
Interstitial - mild and self limited disorder
Necrotizing pancreatitis - more severe form
Currently accepted pathogenic theory of acute pancreatitis
Autodigestion Proteolytic ernzymes ( trypsinogen,chymotrypsinogen, proelastase) are activated in the pancreas rather than in the intestinal lumen
Common etiologies of pancreatitis
GATED
Gallstones - most common cause
Alcohol- second most common cause
Hypertriglyceridemia (usually with serum triglycerides >1000 mg/dL)
Endoscopic retrograde cholangiopancreatography
Drugs
Trauma
Postoperative
Sphincter of Oddi dysfunction
For recurrent attacks of acute pancreatitis the 2 most common cause are
Alcohol and cholelithiasis
Symptoms of acute pancreatitis
Abdominal pain
Nausea
Vomiting
Abdominal distention
Character of abdominal pain in acute pancreatitis
Quality: steady and boring in character
Location: epigastrium and periumbilical region
Radiation: back, chest, flanks,lower abdomen
Effects of position changes: more intense when supine, relieved upon sitting with the trunk flexed and knees drawn up
General PE of acute pancreatitis
Distressed and anxious patient
Low grade fever
Tachycardia
Hypotension
What causes shock in patients with acute pancreatitis
Hypovolemia secondary to exudation of blood and plasma proteins into the retroperitoneum
Systemic effects of proteolytic and lipolytic enzymes released into the circulation
What causes disorientation, hallucination, agitation and coma in acute pancreatitis patients
Alcohol withdrawal Hypotension/ shock Electrolyte imbalance ( hyponatremia) Hypoxemia Fever Toxic effects of pancreatic enzymes to CNS
Abdominal PE of patient with acute pancreatitis
Compared with the intense abdominal pain, there may be unimpressive abdominal tenderness.
Guarding - more marked in the upper abdomen
Decreased or absent bowel sounds
What causes jaundice (although infrequent) in patients with acute pancreatitis
Due to edema of the pancreatic head with compression of the intrapancreatic portion of the CBD Possible choledocholithiasis (gallstone pancreatitis) Co-existenr liver disease
Pulmonary findings in acute pancreatitis
Bnasilar rales, atelectasis, pleural effusion (most frequently left sided) ARDS
Blue discoloration around the umbilicus (results from hemoperitoneum)
Cullen’s sign
Blue-red-purple or green-brown discoloration of the flanks reflecting tissue catabolism of hemoglobin
Turner’s sign
0.5- 2 cm tender red nodules that commonly appear over the distal extremities but may also occur over the scalp, trunk and buttocks
Panniculitis with subcutaneous fat necrosis
Panniculitis with subcutaneous fat necrosis may also be accompanied by
Polyarthritis (PPP syndrome) and
Thrombophlebitis in the legs
Morphologic features of acute pancreatitis (revised atlanta definitions)
Intestitial pancreatitis Necrotizing pancreatitis Acute pancreatic fluid collection Pancreatic pseudocyst Acute necrotic collection Walled- off necrosis (WON)
Acute inflammation of the pancreatic parenchyma and peripancreatic tissues
No recognizable tissue necrosis
Interstitial pancreatitis
Inflammation associated with parenchymal and or peripancreatic necrosis
Necrotizing pancreatitis
Peripancreatic fluid associated with intestitial edematous pancreatitis
No associated necrosis
Applies only to areas of fluid seen within the first 4 weeks after onset of interstitial edematous pancreatitis and without features of pseudocyst
Acute pancreatic fluid collection
Encapsulated collection of fluid with a well-defined inflammatory wall usually outside the pancreas with minimal or no necrosis
Pancreatic Pseudocyst
Pancreatic pseudocyst usually occurs
> 4 weeks after onset of interstitial edematous pancreatitis
Collection containing variable amounts of both fluid and necrosis associated with necrotizing pancreatitis
Acute necrotic collection (ANC)
Mature encapsulated collection of pancreatic and or peripancreatic necrosis that haas developed a well-defined inflammatory wall
Usually occurs after >4 weeks after onset of necrotizing pancreatitis
Walled- off necrosis (WON)
Phases of acute pancreatitis
Early < 2weeks
Late > 2weeks
In early acute pancreatitis what is expected
Most exhibit SIRS and are predisposed to organ failure
What organs should be assessed to define organ failure in early pancreatitis
3 organs : respiratory, cardiovascular, renal
Most important clinical finding with regard to severity of acute pancreatitis episode
Persistent organ failure > 48 hours
Late acute pancreatitis is characterized by a protracted course of illness and may require ___ to evaluate for local complications
Imaging
Supportive measures for late acute pancreatitis
Dialysis
Ventilator support
TPN
What is mild acute pancreatitis
Without local complications or organ failure
Self-limited disease and subsides within 3-7 days after tx is instituted
What characterizes moderately severe acute pancreatitis
Transient organ failure (resolves < 48 hours) or
Local or systemic complications in the absence of persistent organ failure
What characterizes severe acute pancreatitis
Persistent organ failure > 48 hours
When can oral intake be resumed in mild acute pancreatitis patients
If patient is hungry
Normal bowel function
No nausea or vomiting
What diagnostic modality is employed for severe acute pancreatitis
CT scan or MRI- to assess for necrosis and or complications
2 types of pancreatitis are recognized on imaging
Interstitial
Necrotizing
CT imaging in acute pancreatitis is best evaluated when
3-5 days into hospitalization when patients are not responding to supportive care to look for local complications such as necrosis
When will perfusion defects after IV contrast may not appear until
48-72 hours after onset of acute pancreatitis
Diagnostics employed in acute pancreatitis.
Amylase inc more than 3 fold
Lipase - inc more than 3 fold
CBC - leukocytosis (15000 -20000 - uL)
-hemoconcentration with hematocrit 44% and a failure to decrease levels in 24 hours from admission -predictors of necrotizing pancreatitis
Renal function - azotemia with BUN >22 mg /dL (associated with inc mortality) due to loss of plasma into retroperitoneal space and peritoneal cavity
serum chemistry -
hyperglycemia
hypocalcemia
hyperbilirubinemia
serum ALP and AST elevated - acute biliary obstruction
ALT conc 150 IU/L (3 fold elevation)- gallstone pancreatitis
Markedly elevated serum LDH levels - poor prognosis
Hypertriglyceridemia >1000 mg/dL
ABG - hypoxemia (aterial PO2 <60 mmHg)- herald onset of ARDS
Abdominal CT scan - indicating the severity of acute pancreatitis and risk of morbidity and mortality; evaluates for complications of acute pancreatitis
sonography- evaluate gallbladder if gallstone disease is suspected
amylase returns to normal after
3-7 days
differentials for elevated amylase
macroamylasemia papillarycystadenocarcinoma of the ovary benign ovarian cyst carcinoma of the lung intestinal infarction perforated viscus
more specific test for acute pancreatitis
a. amylase
b. lipase
b. lipase
lipase is elevated when
for 7 - 14 days
diagnostic that is predictive of necrotizing pancreatitis
hemoconcentration with HCT value of >44%
and failure to decrease in 24 hours from admission
what causes azotemia in acute pancreatitis
due to loss of plasma into the retroperitoneal space and peritoneal cavity
what causes hyperglycemia in acute pancreatitis
due to decreased insulin release
increased glucagon release
increased output of adrenal glucocorticoids and cathecholamines
what causes hypocalcemia in acute pancreatitis ?
due to decreased albumin (calcium is normally bound to albumin ) which is lost into the peritoneum as albumin-rich intravascular fluid that extravasates intro he peritoneum or retroperitoneum
Hyperbilirubinemia, serum ALP and AST levels are transiently elevated in Acute pancreatitis particularly in
acute biliary obstruction from choledocholithiasis
which diagnostic tests for acute pancreatitis are associated with gallstone pancreatitis
hyperbilirubinemia, elevated serum ALP and AST levels, ALT conc 3 fold elevation
what is indicated by elevated serum LDH levels in acute pancreatitis
poor prognosis
hypertriglyceridemia >1000 mg/dL secondary to acute pancreatitis is also increased with concomitant
alcohol use
uncontrolled diabetes
this elevated diagnostic serum chemistry may precipitate attacks of acute pancreatitis
hypertriglyceridemia
helpful in indicating the severity of acute pancreatitis and the risk of morbidity and mortality
abdominal CT scan
aids in evaluating for complications of acute pancreatitis
abdominal CT scan
useful in acute pancreatitis to evaluate the gallbladder if gallstone disease is suspected
sonography
risk factors for severity of acute pancreatitis
age >60 years old
Obesity, BMI >30
Comorbid disease ( Charlson comorbidity index)
markers of severity on admission or within 24 hours of acute pancreatitis
SIRS
APACHE II
hemoconcentration >44% Hct
Admission BUN >22 mg/dL
BISAP >/= 3 - inc risk of in-hospital mortality BUN >25 mg/dL Impaired mental status GCS <15 SIRS >/=2 of 4 present Age >60 years old pleural effusion
Organ failure - modified marshall score
Cardiovascular SBP <90 mmHg, HR 130 bpm
pulmonary PaO2 <60 mmHg
Renal: serum creatinine >2 mg/dL
Markers of severity of acute pancreatitis during hospitalization
persistent organ failure > 48 hours
pancreatic necrosis `
is acute pancreatitis self limited?
Usually self-limited
when does acute pancreatitis resolve after treatment
3-7 days after tx
conventional measures for acute pancreatitis
analgesics for pain
no oral alimentation
oxygen via nasal canula
the most important intervention for acute pancreatitis
safe and aggressive IV fluid resuscitation
how to do fluid resuscitation for acute pancreatitis
initial IVF - LR or PNSS 15-20 cc/kg bolus followed by 3 mg/kg /hr infusion to maintain urine output >0.5 cc/kg/hr
how to monitor adequacy of fluid resuscitation for acute pancreatitis
measure Hct and BUN every 8-12 hours and serum electrolytes daily to ensure adequacy of fluid resuscitation
does antibiotics have a role in interstitial or necrotizing pancreatitis
None
role of CT scan in acute pancreatitis
to evaluate for necrosis and other local complications if the patient still exhibits evidence of severe disease and or organ failure > 72 hours despite adequate resuscitation
when is ERCP indicated for management of acute pancreatitis
for SEVERE ACUTE BILIARY PANCREATITIS with
ORGAN FAILURE and or cholangitis within 24-72 hours
when is resumption of diet allowed in acute pancreatitis
early refeeding -> improve outcome and allow early discharge
mild acute pancreatitis - oral feedings can be started immediately (low fat solid diet or clear liquids) - if there is NO NAUSEA & VOMITING, ABDOMINAL PAIN RESOLVED
severe acute pancreatitis - enteral nutrition- prevent infectious complications
when is parenteral nutrition advised for acute pancreatitis
unless the enteral route is NOT tolerated, NOT available, or NOT meeting caloric requirements
what is indicated if the conventional measures for management for acute pancreatitis if no improvement in 7-28 days
FNA (fine needle aspiration) of pancreas for culture
role of surgery in acute pancreatitis
GALLSTONE PANCREATITIS - cholecystectomy should be done prior to discharge to prevent recurrence
ASYMPTOMATIC PSEUDOCYSTS and PANCREATIC and or EXTRAPANCREATIC NECROSIS - do not warrant intervention
local complications of acute pancreatitis
necrosis (sterile or infected)
Pancreatic fluid collections (Pseudocyst and abscess)
Pancreatic ascites
Obstructive jaundice
Bowel compression or fistulization (usually to the left colon)
which part of bowel is most probably affected (bowel compression or fistulization) by acute pancreatitis
usually to the left colon
systemic complications of acute pancreatitis
pulmonary - ARDS, effusion, pneumonitis
cardiovascular - hypotension, sudden death
hematologic - DIC
gastrointestinal - ulcer formation, gastritis, mallory-weiss, rupture of splenic artery/ vein leading to gastric varices, hemosuccus pancreaticus (bleeding into pancreatic duct from pseudoaneurysm)
renal- oligura, azotemia, acute tubular necrosis
Metabolic - hyperglycemia, hypocalcemia
others: pancreatic encephalopathy (agitation, hallucination, confusion, disorientation, coma)
Putscher’s retinopathy (flame-shaped hemorrhages with cotton wool spots)
