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Pancreatitis
Dr. Erwin P. Carabeo July 31, 2015

TOPIC OUTLINE o Lipase: specific to the pancreas

A. Anatomy o Proteases
B. Histology  Secretes bicarbonate
C. Functional Anatomy o Used to neutralize the acidity of the gastric contents
D. Pancreatitis o Mixed with chyme as it passes the duodenum
a. Description o Chyme neutralized because the duodenum is as not as
b. Organ Failure in Severe Acute Pancreatitis resilient as the gastric wall, it cannot withstand the
c. Acute Pancreatitis corrosive effects of gastric juices.
d. Most Common Causes
e. Histologic Presentation (Pathology) PANCREATITIS
f. Pathogenesis  Common condition affecting the pancreas
g. Predisposing Conditions  Pain:
h. Pancreatic Trauma o Severe upper abdominal pain
i. Clinical manifestations o Radiating to the back
j. Laboratory Diagnosis o Aggravated by flat position
k. Miscellaneous Tests o Patients assume the knee-chest position to lessen the pain
l. Tests that Reflect Severity of Pancreatic Injury  ACUTE PANCREATITIS
m. Radiologic Features o Elevated amylase and lipase 3x the normal value
n. CT Scan  SEVERE PANCREATITIS
i. CT Scan Grading system of Baltazar and Ranson o Ductal obstruction
o. Ranson’s Criteria  Contrast enhanced CT scan
p. APACHE II o Distinguishes interstitial pancreatitis from necrotizing
q. Other Markers pancreatitis
r. Other Prognostic Sign  Sequela of acute pancreatitis, development of
s. Goal of Treatment o Diabetes
t. Medical Management of Mild Pancreatitis o Steatorrhea: manifestation of malabsorption
u. Complications o These 2 manifestations indicate the involvement of both the
v. Systemic Complications endocrine and exocrine pancreas
w. Prognosis  Endocrine: injury to the islet cells → insulin insufficiency
*This trans is lecture-based. → diabetes
 Exocrine: injury to the acinus → decreased secretion of
ANATOMY digestive enzymes → steatorrhea
 12-15 cm long
 70 –110g DESCRIPTION
 Lies w/in the curvature of the duodenum  MILD ACUTE PANCREATITIS
 Blood supply: o Minimal or no organ dysfunction
o Celiac artery o Uneventful recovery
o Superior mesenteric artery  SEVERE ACUTE PANCREATITIS
o Organ failure
Celiac artery Superior mesenteric artery o (+) abscess/necrosis/pseudocyst,
↓ o  3 Ranson’s or  8 APACHE II points
Gastroduodenal artery
↓ ↓ ORGAN FAILURE IN SEVERE ACUTE PANCREATITIS
Anterior and Posterior Superior Pancreaticoduodenal arteries  Shock SBP <90 mmHg
 Hypoxemia PaO2 60 mmHg
 Venous drainage flows into the portal system  Azotemia Creatinine >2mg/dl
 Lymphatics terminate in:  GI bleeding >500 ml/24h
o Pancreaticosplenic lymph nodes
o Pancreaticoduodenal lymph nodes ACUTE PANCREATITIS MANIFESTATIONS
o Preaortic lymph nodes  Organ Failure
 Innervation:  Acute Fluid Collection
o Vagal o Occurs 30-50%
o Splanchnic nerves o Resolves spontaneously
o Acute fluid collection
HISTOLOGY  Less than 3cm
 Finely nodular gland  Low attenuation
 No definite fibrous capsule  Pseudocyst Formation
 80% Exocrine: Secretion of digestive enzymes o 4-6 weeks after the acute event
 20% Endocrine: Secretes hormones o encapsulated
 Main cell types:  Pancreatic Necrosis
o Acinar cells o Always correlated with a more severe form of illness
o Ductal cells  Pancreatic Abscess
o Islet cells: Endocrine portion o Late manifestation
 Islet of Langerhans: Cords of polygonal endocrine cells o Presentation 4 weeks after the onset of acute symptoms
 B cells 50-80%: secretes insulin  Other terms in relation with pancreatitis:
 A cells 5-20%: secrets glucagon o Phlegmbon
 PP 10-35 % o Infective pseudocyst
 D cells 5 % o Hemorrhagic pancreatitis
 Exocrine pancreas functional unit: Acinus + draining ducts o Persistent acute pancreatitis
o The lumen of acinus is the origin of secretory duct and
contains centroacinar cells → unique to pancreas
MOST COMMON CAUSES
FUNCTIONAL ANATOMY  Alcohol
 The functional unit of exocrine pancreas is composed of  Gallstones
acinus and draining ductile  Drugs
 Acinus is specialized to synthesize, store and secrete digestive
enzymes
o Amylase: salivary glands and pancreas

Transcribers: CABERO, CALDERON N., DUEÑAS, JAVIER, MONTALBO, MONTES, RAFANAN, UICHANGCO Page 1 of 3
 Pancreatitis 1.19
 Low O2 saturation
2 HISTOLOGIC PRESENTATIONS (PATHOLOGY)  Decreased Ca
 Anatomic derangement: Ultrasound, CT scan, ERCP
Interstitial Pancreatitis  Edema
 Inflammatory infiltrates RADIOLOGIC FEATURES
 No necrosis  Extension of pancreatic exudates into pararenal space and
lesser sac
 No hemorrhage
 Anterior displacement of stomach
Necrotizing Pancreatitis  Macroscopic necrosis  Sentinel loop
 Fat necrosis  Ileus (cecum, duodenum, ileum)
 (+) hemorrhage  Colon cut off sign
 More severe form  Calcified gallstone, pancreatic stones
 Poor prognosis  Ascites
 CXR: atelectasis, pleural effusions, evidence of CHF and ARDS
PATHOGENESIS
 Trypsinogen activation peptide (TAP) concentration correlates CT SCAN
with severity of pancreatic inflammatory response, with  3 main indications:
highest levels with acinar necrosis and pancreatic hemorrhage 1. To rule out mesenteric infarction and perforations
o Protective mechanism: enzyme in inactive form, 2. Staging the severity
sequestered within compartment, protease inhibitors and 3. Define presence of complications
enzyme are separated from lysosomal hydrolases as they
CT Grading System of Balthazar and Ranson
pass the Golgi complex
Grade A Normal appearing pancreas
 Common channel theory
Grade B Focal/diffuse enlargement
o Gallstone impacted in the papilla causes reflux of bile from
CBD into the pancreatic duct Grade C Mild peripancreatic inflammatory changes
o Incompetence of sphincter of Oddi Grade D Fluid collection in a single collection
o Impaction of gallstone in the CBD  raising intraductal Grade E 2 or more fluid collections near the
pancreatic pressure damaging the ductal and acinar cells pancreas or gas within the pancreas or
peripancreatic inflammation
PREDISPOSING CONDITIONS
 Gall stones : 30-70% RANSON’S CRITERIA
 Hereditary pancreatitis: atleast 2 family members have the On admission:
condition  Age >55
 Sphincter of Oddi dysfunction  WBC > 16,000/mm3
 ERCP induced: 5% contributing factor  Glucose > 200mg/dl
 LDH >350 IU/l
PANCREATIC TRAUMA  AST > 250 IU/l
 Penetrating or blunt trauma During initial 48 hours
 In penetrating trauma: laparotomy is essential  Hematocrit decrease of >10mg/dl
 In blunt trauma – is the pancreas injured?  BUN increase of >5mg/dl
 Serum amylase may be increased whether or not the  Ca < 8mg/dl
pancreas is injured  Pao2 < 60 mmHg
 CT scan – show enlargement, contusion, subscapular  Base deficits >4 meq/l
hematoma or E/N within 2 days despite presence of  Fluid sequestration >6L
pancreatic trauma
 ERCP- assess pancreatic ductal injury EARLY PROGNOSTIC SIGNS
Ranson’s:
 5/11 measured at the time of admission reflects the
CLINICAL MANIFESTATIONS
intensity and local inflammation
 Abdominal pain
 6/11 measured within the initial 48 hours reflects the
 Nausea and vomiting
systemic complication and effect of third space loss
 Mild pancreatitis
Ranson’s score was:
 Pancreatic encephalopathy
 1.6 in mild pancreatitis
 Systemic toxicity
 2.4 in severe pancreatitis
 5.6 in lethal pancreatitis
LABORATORY DATA
 Amylase ACUTE PANCREATITIS
o 40-45% from pancreas and 55-60% from salivary gland  Ranson’s score of more than 6 had higher incidence of
o Elevated in 75% of patients with AP from day 1 to day 5-10 complication ,necrosis and infection
of illness  Overall sensitivity 57-85% and specificity of 68-85%
o Not elevated in patients with chronic pancreatitis,
hypertriglyceridemia, and late measurement APACHE II
 Lipase EARLY PROGNOSTIC SIGNS
o Elevated on the first day and remain elevated for longer  APACHE II assess the degree of abnormality of 12
period physiologic variables, age, and chronic health status
o More specific  Score of ≤ 9 within 48h have survived, whereas scores of
o Elevated in patients with renal insufficiency, creatinine ≥13 have likelihood of mortality
clearance less than 20ml/min and in patients with inflamed  Lack sensitivity and appears no better than other scoring
or perforated intestines system
o Non pancreatitis elevation are less than twice the normal
OTHER MARKERS
MISCELLANEOUS TESTS  Amylase does not distinguish mild from severe pancreatitis
 Immunoreactive trypsinogen, elastase, ribonuclease,  CRP is higher in severe and necrotizing pancreatitis; activity
phospholipase A2 peaks 36-48h
 No advantage over amylase and lipase  IL6 peak activity is between 24-36 h
 PAP and PSP as accurate as amylase and may help in  PMN leukocyte elastase higher in severe and necrotizing
establishing diagnosis pancreatitis, with high sensitivity and specificity
 ALT greater than 150 IU/L is specific for gallstone pancreatitis  TAP in urine also assess severity after 48h of symptom
in 96%
OTHER PROGNOSTIC SIGN
TESTS THAT REFLECT SEVERITY OF INJURY  Obese patients have higher incidence of respiratory failure
 Hematocrit less than 50% and severe pancreatitis
 WBC count > 16,000  Obesity is an early prognostic sign
 Increased BUN  Presence of pleural effusion within 72h on CT scan, to 6
 Metabolic acidosis days on CXR correlate with more severe disease

Transcribers: CABERO, CALDERON N., DUEÑAS, JAVIER, MONTALBO, MONTES, RAFANAN, UICHANGCO Page 2 of 3
 Pancreatitis 1.19
 Organ failure and local complications correlate with poor
prognostic disease

ACUTE PANCREATITIS
MILD:
 Minimal or no organ dysfunction, and
 Uneventful recovery
SEVERE:
 organ failure,
 (+) abscess/necrosis/pseudocyst,
 ≥3 Ranson’s or ≥8 APACHE II points
Organ failure:
 Shock
o SBP <90 mmHg
o PaO2 <60 mmHg,
o Creatinine >2mg/dl
o GI bleeding >500 ml/24h
Acute fluid collection
 Less than 3cm,
 Low attenuation,
 Occurs 30-50% and resolves spontaneously

TREATMENT OF ACUTE PANCREATITIS

GOALS OF TREATMENT
 Supportive treatment : fluid resuscitation, pulmonary care,
ICU care
 Limit systemic complication
 Prevent pancreatic necrosis
 Prevent pancreatic infection

LIMITATION OF SYSTEMIC COMPLICATION

 Reduction in pancreatic secretion: Aprotinin
 Inhibition of circulating inflammatory mediator and
peritoneal lavage: ineffective in reducing morbidity and
mortality
 ERCP to remove gallstone in CBD: this eliminated sepsis
but didn’t reduce mortality

MEDICAL MANAGEMENT OF MILD PANCREATITIS

 Adequate fluid resuscitation
 Pain reliever
 NGT insertion
 Refeeding

MEDICAL MANAGEMENT OF SEVERE PANCREATITIS

 Fluid resuscitation may require > 5-6 l/day and at times
more than 10L
 Use of colloids if albumin is less than 2g/l
 If Hct < 25 %- PRBC transfusion
 ARDS is the most serious respiratory complication,
occurring on the 2nd to the 7th day, associated with
dyspnea and progressive hypoxemia
 Cardiovascular care, relief of pain, treatment of infection,
metabolic complication and nutritional support

COMPLICATIONS
 Pancreatic necrosis  systemic toxicity and organ failure
 Infected necrosis  guided percutaneous aspiration 
surgical debridement
 Pancreatic pseudocyst:
 5cm for 6weeks should be decompressed surgically to
prevent bleeding, perforation and infection
 Pseudocyst can be treated surgically, endoscopically and
radiologically
 Pancreatic abscess can be treated with percutaneous
catheter drainage

SYSTEMIC COMPLICATIONS
 Respiratory
 Cardiovascular
 Renal
 CNS
 SQ fat necrosis and bone abnormalities
 GI bleeding
 Splenic hematoma

PROGNOSIS
 Mortality with interstitial AP is close to 0%
 Mortality with Necrotizing AP is 10%
 Alcoholic and gallstone pancreatitis have equally low
mortality
 Higher mortality is associated with idiopathic and
postoperative pancreatitis

Transcribers: CABERO, CALDERON N., DUEÑAS, JAVIER, MONTALBO, MONTES, RAFANAN, UICHANGCO Page 3 of 3