Acute Pancreatitis

Xia, Zhongsheng

Department of Gastroenterology,

Sun Yat-sen Memorial Hospital,

Sun Yat-sen University.

Teaching Objective

To know the etiology and pathogenesis of acute pancreatitis

To master the clinical features and key points of diagnosis for different types of acute pancreatitis

To master the therapy principles of acute pancreatitis

Definition

Acute pancreatitis is a inflammation of the

pancreas induced by the activation of the

pancreatic enzymes derived from various

causes.

Etiology

Biliary duct diseases: gallstone, acute and chroni

c cholecystitis, ascariasis accompanied with infl

ammatory stricture at the level of the papilla.

Common channel hypothesis Alcohol and/ or square meal hyperlipidemia Postoperation: post-ERCP, abdominal operation.

Etiology

Metabolic diseases: hyperparathyroidism, hypercal

cemia, etc.

Drugs: glucocorticords, diuretics, azathioprine, estr

ogen, etc.

Autoimmune diseases: SLE, RA, vasculitis, etc.

Viral infections: mumps, coxsackie virus , HIV, etc

Idiopathic pancreatitis.

Pathogenesis

trypsinogen→ trypsin

trypsin →pancreatic enzymes, complement

system and kinin system

Pathophysiological changes: leukocyte che

motaxis, release of active agents, oxygenic s

tress, microcirculation disorder and bacteria

transposal.

Trypsin activates other proenzymes and results in proteolysis, edema and vascular damage

Lipase produces extrapancreatic fat necrosis Phospholipase degrades the lecithin into the lysolecithin w

hich induces pancreatic necrosis and hemorrhage Kallikrein and elastase cause vascular destruction Bradykinin peptidase and vasoactive substance induce vas

odilatation, increase vascular permeability and edema Cytokine, oxygen free radicals, platelet activating factor, p

rostaglandins, blood circulation disturbance, systemic inflammation response syndrome (SIRS)

Pathology

Mild form (interstitial or edematous

pancreatitis)

focal or diffused edema

slight leukocyte infiltration

Severe form (necrotic or hemorrhagic pancreatitis) marked acinar destruction with hemorrhage extensive leukocyte infiltration necrosis of parapancreatic fat grossly an inflammatory tumor-like mass with dif

fused hemorrhagic change secondary infection induces the formation of absc

ess or pseudocysts

Symptoms abdominal pain: located in epigastrium and radiates to the b

ack. The lateral kneel-chest position with the neck flexed may relieve the abdominal pain.

Nausea, vomiting, abdominal distention: 90% patients Fever: low-grade fever in mild pancreatitis; high fever sugg

ests coexisting infection. Hypotension or shock: often in severe pancreatitis

Clinical manifestations

Signs

MAP: signs are mild. Abdominal tenderness and diminished bowel sounds are present.

SAP: peritoneal irritation sign bowel sounds are diminished or absent ascites or shifting dullness Grey-Turner sign Cullen sign jaundice Pancreatic pseudocyst

Complications

Local complications Pseudocyst: occur 2 weeks after the onset. Acute fluid collection: occur in the early stage. Pancreatic abscess: after 4 weeks on the basis of pse

udocyst Pancreatic necrosis infection: usually after 2 weeks

Systemic complications

ARDS acute renal failure heart failure and cardiac arrhythmia gastrointestinal bleeding Septicemia disorders of hemostasis: thrombosis, DIC. disorders of CNS: pancreatic encephalopathy Hyperglycemia disorders of water, electrolytes and acid-base bala

nce

Laboratory Studies

blood count: leukocytes count is more than 10,000/mm3

Hematocrit (Hct): is high (over 50%) because of loss of plasma into the retroperitoneal space

Amylase

normal values of the serum amylase: 40 to 180 Somogyi units or 8 to 64 Winslow uni

ts over 500 Somogyi units are strongly suggested a

cute pancreatitis. there is no significant correlation between the se

verity of the pancreatitis and the levels of the serum amylase

normal values of urinary amylase: < 256 Winslow units over 256 Winslow units are suggested acute panc

reatitis

False positive amylase elevation in serum or urine may occur in many conditions other than pancreatitis, such as the other acute abdominal diseases, proximal renal tubular malfunction, including thermal burns, diabetic acidosis and postoperative states or macroamylasemia.

kinetic changes of serum and urine enzymes in acute pancreatitis

0

1

2

3

4

5

6

oh 6h 12h 1d 2d 3d 4d 5d 6d 7d 8d

norm

al h

igh

limi

t

serum amylase

urine amylase

serum lipase

Biochemical test Hypocalcemia Hyperglycemia Hyperbilirubinemia Hypoxemia

Imaging examination

X-ray: Abdominal X-ray sentinel loop colon cut-off Chest X-ray: may reveal the complications of

lung such as pleural effusion, pulmonary edema and interstitial inflammation.

Ultrasonography It is a useful method to find an enlarged pancr

eas, a pseudocyst, ascites, biliary stone, dilated common bile duct and other pancreatic mass

CT & MRI

正常胰腺 CT 平扫

肝右叶

胰头

肠管

肾

腹主动脉

下腔静脉

胰腺体、尾部胆

囊

肝右叶 脾

肠管

下腔静脉

膈脚 腹主动脉

Normal pancreas

Contrast CT showing pancreatic necrosis

Diagnosis-criteria

symptoms: acute, severe constant epigastric pain.

Nausea and vomiting.

Physical examination: epigastric tenderness with

or without rebound tenderness.

Laboratory studies: elevated serum amylase (≥3 ti

mes of high limit of normal value)

Imaging examinations: morphological changes of

pancreas or not

Excluding the other acute abdominal diseases.

Clinical manifestations Scoring systems: Ranson CT grading Serum biomarkers: CRP, IL-6

Diagnosis-evaluation of patients’ condition

Diagnosis-classification

MAP (mild acute pancreatitis): Acute pancreatitis No dysfunction of organ or local complications Ranson’s score <3 or CT grading: A, B, C or CTSI <2

Diagnosis-classification

SAP (severe acute pancreatitis): Acute pancreatitis Local complications or organ failure or Ranson’s score >3 or CT grading: D, E or CTSI >3.

Differential diagnosis

Perforated peptic ulcer Acute calculous cholecystitis Acute ileus Mesenteric vascular embolism Rupture of the spleen Acute appendicitis Angina pectoris Acute myocardial infarction

Therapy-MAP

Monitoring: should be monitored for at least 3 days.

Supportive treatment: volume repletion with crystalloids an

d colloids to keep balance.

Relieve severe pain: Dolantin is preferred over morphine.

inhibit excrine of the pancreas:

No oral alimentation and continuous nasogastric suction

H2RA or PPI

Somatostatin and its long-acting analogue (Sandostatin)

Antibiotics is required especially in infection of biliary duct.

Therapy-SAP

Monitoring Nutritional support: parenteral nutrition→enteral nutrition maintain balance of water, electrolytes and acid-base. essential diet Prevention of infection: oral antibiotics intravenous infusion of antibiotics enteral feeding

inhibit excrine of pancreas and pancreatic enzymes:

No oral alimentation and continuous nasogastric suction

H2RA or PPI

Somatostatin and its long-acting analogue (Sandostatin)

Prevention and treatment of enteral failure oral antibiotics enteral microecological preparations glutamine enteral feeding Treatment of multiple organs failure

Endoscopic therapy: ERCP+EST+ENBD Surgical operation: indications necrotic pancreatitis with infection pancreatic abscess early severe acute pancreatitis (ESAP) abdominal compartment syndrome (ACS) pancreatic pseudocyst: >6cm diagnosis remain unclear and GI perforation is suggested

Emerging drugs: CCK receptor antagonist: loxiglumide Prostaglandins: PGE1

Platelet activating factor (PAF) antagonist TNF monoclonal antibody: Infliximab

prognosis

MAP: good

SAP: poor. 10~30% mortality

Risk factors: age, hypotension, hypoalbuminem

ia, hypoxemia, hypocalcemia, miscellaneous co

mplications.

Questions

What are the clinical manifestations of acute pancreatitis?

What is the diagnostic key points of acute pancreatitis?

What is the therapy of acute pancreatitis?

necrotic pancreatitis

Grey-Turner sign

Cullen sign

jaundice

Pseudocyst of pancreas

Sentinel loop. A segment of air-filled small intestine

Colon cut-off sign. Supine abdominal radiograph obtained in a patient with acute pancreatitis shows an abrupt termination of air in the left side of the transverse colon (arrows).

Pseudocyst of pancreasEdematous pancreas

On admission: Age >55 Leukocyte count >16,000/mm3

Blood glucose >11mmol/L LDH >350 IU/L AST >250

After 48 hours: Hct increase >10% BUN rise >5 mmol/L Serum calcium <2 mmol/L PaO2 <60mmHg Base deficit >4mmol/L Estimated fluid sequestration >6 L

Ranson’s scoring system

CT grading

Grade A: normal pancreas Grade B: enlargement of pancreas Grade C: Grade B + peripancreatitis Grade D: Grade C + one area of fluid collection Grade E: multiple region of fluid collection