IM MINI REVALIDA

CASE:
Prepared by: ​CC Pornillos, Ma. Eloisa Joanne & CC Priela, Benedict

DEFINITION

Types:
1. Interstitial Pancreatitis
○ Pancreas blood supply is maintained
○ Self-limiting
2. Necrotizing Pancreatitis
○ Pancreas blood supply is interrupted
○ Extent of necrosis may correlate with the severity of the attack and its systemic complications

Acute Pancreatitis : Pancreatic inflammation with little or no fibrosis vs Chronic: Already structural damage to the
pancreas

EPIDEMIOLOGY

Acute pancreatitis is the ​most common inpatient principal gastrointestinal diagnosis​.

Occurs most frequently in the second and third decades of life, highest in the 10-to-19-year-old age group
Hospitalization rate
● Increases with age
● Higher among blacks
● More prevalent in males than females

ETIOLOGY/RISK FACTORS

A. Common Causes
Remember the mnemonic ​“GATED”
1. G​allstones
○ Leading cause (30-60%)
○ At Least one gallstone < 5mm = 4x risk of acute pancreatitis
○ Smaller gallstone is worse
2. A​lcohol
○ Second most common cause (15-30%)
○ Not solely responsible
3. Hyper​T​riglyceridemia
○ Serum TGL > 1000-2000 mg/dL
○ Prone to RECURRENT episodes of pancreatitis
○ Factor that causes an abrupt increase in TGs (drugs and alcohol) may precipitate acute pancreatitis
○ Apolipoprotein C2 deficiency
○ Increased incidence of pancreatitis
○ ApoC2 activates lipoprotein lipase -> clearing of chylomicrons from bloodstream
○ DM with ketoacidosis and OCPs may lead to high TG levels
4. E​RCP
○ Especially after biliary manometry
○ Risk reduced by prophylactic duct stent and NSAIDs
5. D​rugs
6. Others
○ Hypersensitivity
○ Generation of a toxic metabolite
○ Trauma
○ Postoperative

PATHOPHYSIOLOGY

Autodigestion
● Currently accepted pathogenic theory
● Pancreatitis results when proteolytic enzymes (trypsinogen, chymotrypsinogen, proelastase, and lipolytic
enzymes) are activated in the pancreas acinar cell rather than in the intestinal lumen.
● Factors leading to premature activation of trypsin
○ Endotoxins
○ Exotoxins
○ Viral infections
○ Ischemia
○ Oxidative stress
○ Lysosomal calcium
○ Direct trauma
○ Spontaneous activation
A. Initial Phase
● Intrapancreatic digestive enzyme activation and acinar cell injury.
● Trypsin activation​ appears to be mediated by lysosomal hydrolases such as cathepsin B that become
colocalized with digestive enzymes in intracellular organelles.
● Acinar cell injury​ is the consequence of trypsin activation.
B. Second Phase
● Activation, chemoattraction, and sequestration of leukocytes and macrophages​ in the pancreas, resulting
in an enhanced intrapancreatic inflammatory reaction.
● Neutrophils can activate ​trypsinogen​. Intrapancreatic acinar cell activation of trypsinogen could be a two-step
process.
● Neutrophil depletion induced by antineutrophil serum has been shown to reduce the severity
C. Third Phase
● Activated proteolytic enzymes and cytokines are released by the inflamed pancreas on distant organs.
● Trypsin digests pancreatic and peripancreatic tissues and activates elastase and phospholipase A2.
● The active enzymes and cytokines digest cellular membranes leading to:
○ Proteolysis
○ Edema
○ Interstitial hemorrhage
○ Vascular damage
○ Coagulation necrosis
○ Fat necrosis
○ Parenchymal cell necrosis
● Cellular injury and death result in the liberation of bradykinin peptides, vasoactive substances, and histamine
leading to:
○ Vasodilation
○ Increased vascular permeability
○ Edema
● The systemic inflammatory response syndrome (SIRS) and acute respiratory distress syndrome (ARDS), as
well as multiorgan failure, may occur as a result of this cascade of local and distant effects.

CLINICAL MANIFESTATIONS

A. Approach to Abdominal Pain

● Abdominal pain is the major symptom of acute pancreatitis.
● Pain is steady and boring in character.
● Located in the epigastrium and periumbilical region, and may radiate to the back, chest, flanks, and lower
abdomen.
● Nausea, vomiting, and abdominal distention due to gastric and intestinal hypomotility and chemical peritonitis
are also frequent complaints
B. Physical Examination
● Distressed and anxious patient
● Low-grade fever
● Tachycardia
● Hypotension
● Shock
○ Hypovolemia secondary to exudation of blood and plasma proteins into the retroperitoneal space
○ Increased formation and release of kinin peptides (vasodilation and increased vascular permeability)
○ Systemic effects of proteolytic and lipolytic enzymes
● Jaundice - infrequent
○ Due to edema of the head of the pancreas with compression of the intrapancreatic portion of the
common bile duct or passage of a biliary stone or sludge
○ Erythematous skin nodules due to subcutaneous fat necrosis
● Pulmonary findings
○ Basilar rales
○ Atelectasis
○ Pleural effusion (most frequently left sided)
● Abdominal tenderness and muscle rigidity
● Bowel sounds are usually diminished or absent
● Palpable pancreas (4-6 weeks)
○ Acute fluid collection
○ Walled off necrosis
○ Pseudocyst
● Cullen's Sign
○ A faint blue discoloration around the umbilicus (result of hemoperitoneum)
● Turner's Sign
○ A blue-red-purple or green-brown discoloration of the flanks (tissue catabolism of hemoglobin)
C. Laboratory Data
● Serum amylase or lipase 3-fold or more above normal virtually clinch the diagnosis of gut perforation, ischemia,
and infarction are excluded
○ Serum lipase is preferred.
■ Total serum amylase returns to normal after 3-7 days
 ■ Isoamylase and lipase remain elevated for 7-14 days
■ Patients with acidemia (DKA) can also have increased serum amylase
○ No correlation between serum lipase/amylase levels with severity of pancreatitis
● Leukocytosis is frequent.l
● Patients with more severe disease may show:
○ Hemoconcentration with hematocrit values >44%
■ Harbinger for more serious disease
■ Sequestration of fluid into the third space
○ Prerenal azotemia with a blood urea nitrogen (BUN) level >22 mg/dL
■ Result from loss of plasma into the retroperitoneal space and peritoneal cavity
■ Risk factor for mortality
● Hyperglycemia
● Hypocalcemia (~25%)
○ Saponification of calcium by fatty acids in areas of fat necrosis
● Hyperbilirubinemia (~10%)
○ Serum bilirubin >68 mmoL or >4.0 mg/dL
○ Jaundice is transient
○ Serum bilirubin returns to normal in 4-7 days
● Aspartate aminotransferase & alkaline phosphatase
○ Transient elevation
○ May point to gallbladder-related disease or inflammation in the pancreatic head
● Hypertriglyceridemia (~5-10%)
○ Serum amylase levels in these individuals are often spuriously normal
● Hypoxemia (~5-10%)
○ May herald the onset of ARDS
● Electrocardiogram
○ Resembles MI (ST-segment and T-wave abnormalities)
● Ultrasound
○ Initial diagnostic imaging modality and is most useful to evaluate for gallstone disease and the
pancreatic head
● CT:
○ Interstitial pancreatitis
○ Necrotizing pancreatitis
○ Acute pancreatic fluid collection
○ Pancreatic pseudocyst
○ Acute necrotic collection (ANC)
○ Walled-off pancreatic necrosis (WON)

DIFFERENTIAL DIAGNOSIS

● Perforated viscus, especially peptic ulcer

● Acute cholecystitis and biliary colic
○ Elevated serum amylase in BOTH
○ Pain of biliary tract origin (Cholecystitis) is more right-sided or epigastric and can be more severe; ileus
is usually absent
● Acute intestinal obstruction
○ History of crescendo-decrescendo pain, findings on abdominal examination, and CT of the abdomen
showing changes in characteristic of mechanical obstruction
● Mesenteric vascular occlusion
○ Usually suspected in elderly debilitated patients with brisk leukocytosis, abdominal distention, and
bloody diarrhea, confirmed by CT or magnetic resonance angiography
● Renal colic
● Inferior myocardial infarction
● Dissecting aortic aneurysm
● Connective tissue disorders with vasculitis
○ Pancreatitis can occur as a complication
● Pneumonia
● Diabetic ketoacidosis
○ Accompanied by abdominal pain and elevated total serum amylase levels
○ Serum lipase level is not elevated in diabeticketoacidosis

DIAGNOSTIC PLAN

(​Bases of each test, expected findings with normal/reference values)

Establish diagnosis if ⅔ is present
1. Typical​ abdominal pain​ in the epigastrium that may radiate to the back
2. Serum Amylase or Lipase 3- fold or more above normal
a. Lipase preferred - remain elevated for 7-14 days
b. Amylase - return to normal after 3-7 days
3. Confirmatory finding of AP on imaging - Gadolinium-DTPA (Gd-DTPA)-enhanced MRI
 a. Best of with 3-5 days into hospitalization when patient are not responding to supportive care
b. Interstitial Pancreatitis
i. 90-95% admission; persistent organ failure >48 h
ii. Diffuse gland enhancement, Contrast enhancement, Mild inflammatory changes or
peripancreatic stranding
iii. Resolve with a week of hospitalization
c. Necrotizing Pancreatitis
i. 5-10%
ii. Lack of pancreatic parenchymal enhancement by IV contrast
iii. Presence of peripancreatic necrosis
- Other morphological features of AP
d. Acute Pancreatic fluid collection
i. Peripancreatic fluid associated with interstitial edematous pancreatitis with no
associated necrosis
ii. Term is only applied if ​within 4 weeks​ after onset of pancreatitis
iii. CT: homogenous collection with fluid density
e. Pancreatic pseudocyst
i. Encapsulated ​collection of fluid ​with well defined inflammatory wall
ii. Occurs​ >4 weeks ​after onset
iii. CT: well circumscribed homogenous fluid density
f. Acute necrotic (ANC)
i. Collection of​ both fluid and necrosis
ii. CT: heterogenous and non liquid density; no capsule
g. Walled-off necrosis (WON)
i. Mature, encapsulated ​collection of pancreatic and or peripancreatic necrosis
ii. CT: heterogeneous with liquid and non liquid density; well -defined wall completely
encapsulated

Other imaging:
1. Ultrasound
a. may visualize abnormal findings associated with the etiology and morbidity, such as ascites,
gallstones, and cholangiectasis.
b. It is particularly important to check for the presence of cholecholithiasis and cholangiectasis
when judging whether endoscopic sphincterotomy for gallstone pancreatitis is required.
Laboratory
1. Inc Hematocrit (hemoconcentration) ​- d ​ ue to sequestration of edematous fluid in the retroperitoneum
2. Inc BUN and Creatinine - due to severe fluid loss leading to prerenal azotemia
3. Hyperglycemia
4. Hypoalbuminemia
5. Hypocalcemia

MANAGEMENT

● 85-90% are self limiting and subside spontaneously

● After diagnosis in ER/ Initial management:
1. Aggressive fluid resuscitation
a. LRS(preferred) or NSS initially at 15-20 ml/kg, followed by 3mg/kg/h to maintain urine
output of >0.5ml/kg/hr
b. Reason: to maintain renal perfusion and hemodynamic stability
2. NPO to rest pancreas
3. IV narcotics(morphine) for abdominal pain
4. 2L supplemental oxygen
5. Monitor Hct and BUN every 8-12 hours
a. If decrease = sufficient fluids
b. If increase BUN = inadequate hydration
i. Treat with repeat fluid challenge- 2L crystalloid bolus followed by increasing
fluid rate by 1.5mg/kg/L
6. Prophylactic antibiotic - not recommended
a. Use only if with extrapancreatic infections (ex. Pneumonia, UTI)
● Local complications ​- still with signs despite tx and fluid → transfer to ICU
○ Ones mentioned above (WON, ACN…)
● Nutritional therapy
○ Low fat solid diet
○ Enteral nutrition 2-3 days after admission
○ Reason: maintain gut barrier integrity, limits bacterial translocation less expensive
 PROGNOSIS

● 85-90% are self limiting and subside spontaneously

● Assessment of severity / Prognostication factor
1. BISAP - >3 or more increase risk for in- hospital mortality
a. BUN >25 mg/dL
b. Impaired mental status (GCS<15)
c. SIRS
d. Age >60 yrs
e. Pleural effusion on radiography
2. Ranson’s Criteria
a. <3 positive criteria: Mild, uncomplicated
b. >6 positive, Severe dx with mortality risk 50%
3. APACHE II
4. More severe AP
a. Elevated Hct >44%
b. Admission BUN > 22 mg/dl

Links to References:
- Harrisons
- MED 2 trans 2018
- Include links to videos for History/PE
- Include links to CPGs pertinent to the case