Transcript Pancreatic diseases

Pancreatic
diseases
WU JIAN
Department of hepatobiliary Surgery
First Affiliated Hospital
Zhejiang University School of Medicine
Pancreas: Anatomy and Physiology
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Retroperitoneal organ
15-20cm in length
Head, neck, body and tail
Uncinate process: curves behind the superior mesenteric
vessels
Neighborhood of the pancreas
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Posterior
L1-2 vertebral
column
Anterior
stomach,
omentum
Right
Duodenum
Left
Splenic hilum
Main duct :
Wirsung ( 1642)
Ampula:
Vater (1720)
Accessory duct : Santorini( 1734)
Pancreas: blood supply
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HEAD：
Superior pancreatoduodenal
A. (from gastroduodenal A.)
Inferior pancreatoduodenal A.
(from SMA)
BODY AND TAIL：
superior pancreatic A.
pancreatic magna A.
transverse pancreatic A.
VEIN：
to splenic vein ,SMV and
portal vein
Lymphatic drainage of pancreas
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Common
pathway
Physiology
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Exocrine：pancreatic juice。
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HCO3- and digestive enzyme
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Endocrine：
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A cell：glycagon
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B cell：insulin
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D cell ：somatostatin
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G cell ：gastrin
 Acute Pancreatitis
Chronic Pancreatitis
 Pancreatic cancer
Periampullary cancer
Endocrinal tumor
Acute Pancreatitis
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Common acute abdomen
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Local inflammatory change in
pancreas
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Systemic change
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Life-threatening inflammatory
disorder of the pancreas
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Abrupt onset and unpredictable course
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Variable severity and duration
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Self-limited but remarkable morbidity
and mortality
Etiology
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Biliary tract disease
Abuse of ethanol
Endoscopic retrograde
cholangiopancreatography
Trauma and operation
Ischemia of pancreas
Drugs
Idiopathic pancreatitis
Hypercalcemia
Hyperlipidemia
Infections and Parasites
Scorpion sting
PATHOGENESIS
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“Self digestion”
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Reflux of bile or duodenal juice
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Trypsinogen was activated
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Trypsin can activate the other zymogens
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Intraparenchymal enzyme activation, tissue
destruction, and ischaemic necrosis.
Pathological and clinical type
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Pathological type
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Acute edematic pancreatitis
Acute hemorrhgic and necrotic pancreatitis (AHNP)
Clinical type
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Mild Acute pancreatitis (MAP)
Severe Acute pancreatitis (SAP)
Fulminant Acute pancreatitis (FAP)
Clinical manifestations
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Abdominal pain
Nausea, vomiting
Distension
Tenderness, rebound tenderness, muscular regard
Fever，jaundice，
Gray-Turner sign: flank ecchymoses
Cullen sign: periumbilical ecchymoses
MODS
laboratory test
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Amylase level in serum and in urine
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Lipase assays
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Blood Rt, liver function, FBS,
PaCO2 ,serum calcium, DIC
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Diagnostic paracentesis
Image findings
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BUS
CT
ERCP
MRCP
Abdomen plain film
Local complication
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Pancreatic necrosis
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Infective pancreatic necrosis
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Sterile pancreatic necrosis
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Pancreatic abscess
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Pancreatic pseudocyst
Acute pancreatic pseudocyst
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Peripancreatic fluid collections occur in
10-20 % of patients
Those persisting beyond the phase of acute
inflammation become pancreatic
pseudocysts
Collection surrounded by fibrous tissue or
granula tissue
Diagnosed by PE or image test
Round or ellipse
Clear cyst wall
Severe Acute Pancreatitis
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Severe Acute pancreatitis (SAP)
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Complicated with MODS
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Necrosis, abscess, pseudocyst
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Or both
Classification system
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General evaluation
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John Ranson score (1974):5 (on admission) +6 (48hr)
Imrie score:8 (WBC,Ca,sugar,PO2,LF)
APACHE II score (1985):12+age＋Chronic health+coma
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Local evaluation
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Atlanta classification system(1992)
Beger’ criteria (1985)
Balthazar CT classification system (1990):I, II, III GRADE
MODS evaluation
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Marshall MODS score system(1995):6 systems/organs involved
Clinical manifestation of SAP
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Abdominal sign: obvious tenderness, rebound tenderness,
muscular regard, distension, lose of bowl sound
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Mass in abdomen, Grey－Turner, Cullen
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MODS
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Irreversible shock
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CT: swelling ， uneven density, invade to outside of
pancreas(Balthazar CT>II)
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APACHE value>8
MODS
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Cardiac function：quick pulse、shock
Pulmonary function ：PaO2<60mmHg，ARDS
Liver function：jaundice， elevated ALT
Renal function：elevated BUN and Creatinine
Digestive function：GI bleeding
Endocrinal function ：glucose>11.1mmol/L
Coagulation system：DIC
Nerve system：unclear consciousness、pancreatic
brain disease
Stage of SAP
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Acute response stage：within 2 weeks
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Systemic infection stage：2 weeks to 2 months
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complicated with shock,ARDS,renal failure
Bacteria or fungus infection
Post-infection stage：after 2  3 months
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Abscess, fistula,
TREATMENT
I.
Non-operative therapy
Acute Response Stage
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ICU ：to prevent MODS
fasting the patient, nasogastric suction
Minimizing pancreatic secretion
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Fluid replacement and Nutritional support
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antacids
5-FU
somatostatin analogues
antiprotease
maintenance of adequate hydration
TPN，glucose ,lipid, amino acid, protein
Analgesia
Antibiotics
Traditional Chinese Medicine
Abdominal lavage
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Operation
Indication of Operation
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Biliary obstruction
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Secondary pancreatic infection
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Shock cannot be reversed,
multiple ogan deteriorate
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Undetermined diagnosis, need to
laparotomy
Principle for treatment of pancreatitis
SAP
MAP
Biliary
Conservative
therapy
Obstuctive
Urgent operation
Or ERCP
Non-obstructive
Conservative
therapy
Elective operation
Non-biliary
Infection
No
infection
Elective operation
Conservative
therapy
Chronic pancreatitis
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Recurrent upper abdominal pain
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With dysfunction of endocrine and
exocrine of pancreas
Clinical manifestition
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Four main symptoms
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Abdominal pain
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Body weight loss
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Diabetes
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Lipid diarrhea
Therapy of chronic pancreatitis
Relieve pain
Drainage of the pancreatic juice
Prevent acute attack
Ameliorate the nutrition
Improve pancreatic function
Non-operation or operation
Pancreatic Cyst
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Pancreatic pseudocyst
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Congenital pancreatic cyst
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Retention pancreatic cyst
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Neoplastic pancreatic cyst
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Pancreatic cystadenoma
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Pancreatic cystadenocarcinoma
Pancreatic pseudocyst
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Indication for operation
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Associated with ongoing pain
More than 6 cm in diameter which persist for 6
weeks
Cyst with haemorrhage and sepsis
Methods
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Percutaneous drainage
Operative drainage
Cystgastrostomy, cystjejunostomy
Resection of pancreatic body and tail
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