acute, chronic pancreatitis and pancreatic cancer
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Acute, Chronic Pancreatitis and pancreatic cancer. Pathophysiology of acute pancreatitis. Triggering mechanism not exactly understood - PowerPoint PPT PresentationTRANSCRIPT
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Acute, Chronic Pancreatitis and pancreatic cancer
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Pathophysiology of acute pancreatitis Triggering mechanism not exactly
understood When pancreas becomes damaged or
ducts become blocked, trypsin inhibitor accumulates and activates pancreatic secretions that escape into the surrounding tissue, resulting in inflammation, thereby causing acute pancreatitis
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Pathophysiology Release of kallikrein and chymotrypsin results in
increased capillary membrane permeability, leading to leakage of fluid into the interstitium and development of edema and relative hypovolemia
Elastase is the most harmful in terms of direct cell damage, it causes dissolution of the elastic fibers of blood vessels leading to hemorrhage
Phospholipase A in the presence of bile, destroys phospholipids of cell membranes causing severe pancreatic and adipose tissue necrosis
Lipase flows into damaged tissue and is absorbed into systemic circulation, resulting in fat necrosis of the pancreas and surrounding tissues
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Edematous (Interstitial) Pancreatitis
Usually mild Resolves in about
7 days Results in fluid
accumulation and swelling
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Severe or Necrotizing Pancreatitis Associated with a
high degree of complications and mortality
Caused by the release of cytokines and other proinflammatory mediators that produce a hyperinflammatory reaction, resulting in cell death and tissue damage
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Acute Pancreatitis: Damage and Destruction
If pancreatitis damages the islets of Langerhans, diabetes mellitus may result
Severe sudden pancreatitis may cause diabetic acidosis, shock and coma
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Causes of Acute Pancreatitis
Alcohol abuse} Gallstones } both 80%
Mechanical/structural injury Sphincter of Oddi
dysfunction Blunt trauma Post-ERCP 5% Pancreatic malignancy PUD ( penetrating)
Medications Azathiprine Sulfonamides Furosemide
Metabolic Hypertriglyceridemia Hypercalcemia
Infectious Viral (mumps, rubella,
CMV)
Idiopathic 10%
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Clinical Presentation Epigastric pain rapidly increasing in severity Diffuse abdominal pain with radiation to
back Pain rarely only in left upper quadrant Restlessness Prefer to sit and lean Nausea/Vomiting Fever Tachycardia
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Abdominal Examination Decreased or absent bowel sounds Abdominal tenderness Guarding Palpable mass in epigastric area Jaundice if there’s obstruction of the bile
duct Cullen’s sign Grey Turner’s sign
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Clinical Manifestations
Abdominal distention Abdominal guarding Abdominal tympany Hypoactive bowel
sounds Severe disease:
peritoneal signs, ascites, jaundice, palpable abdominal mass, Grey Turner’s sign, Cullen’s sign, and signs of hypovolemic shock
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Investigation Serum amylase raises within hours and
remains for 4-5 d ( 3-5 x normal) Urine amylase increased for 1-2 weeks Elevated WBC Decreased serum calcium Elevated serum bilirubin, AST, ALT, LDH,
and alkaline phosphatase Abdominal XRAYS and CT’s showing
pleural effusions and bowel dilation and ileus
Serum triglycerides >150mg/dl
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Amylase
levels greater than three times the upper limit is needed for dx ( isoamylase is more specific)
Serum amylase levels may be normal if due to alcohol abuse or hypertriglyceridemia
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Other causes of Amylase Elevation
Abdominal Source Biliary obstruction Bowel obstruction Perforated ulcer Appendicitis Mesenteric
ischemia Peritonitis
Salivary Parotitis
Unknown Source Renal failure Head trauma Burns Postoperative DKA
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Diagnostic Evaluation Serum lipase is more sensitive and
specific An elevation of greater than three
times the normal value usually confirms acute pancreatitis
A lipase-to-amylase ratio of greater than 2 is usually evident with pancreatitis related to alcohol abuse
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Imaging Plain abdominal x-rays for visualizing
gallstones or a gas-filled transverse colon ending at the area of pancreatic inflammation colon cut-off sign
Abdominal ultrasound Cholelithiasis, biliary sludge, bile duct
dilation, and pseudocysts CT of abdomen MRCP EUS
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Ranson’s criteria of severityAt admission:
Age > 55 WBC > 16,000 Glucose > 200 LDH > 2x normal ALT > 6x normalDuring initial 48 hr: PaO2 < 60 mmHg B.Urea ↑ >5 mg/dl S. Ca < 8 mg/dl ↓ in PCV > 10% Base deficit > 4mEq/l Estimated fluid sequestration > 600 mlMortality: 1% if <3 scores, 10-20% if 3-5, > 50% if ≥ 6
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Complications – Local Necrosis
Sterile Infected - abscess
Pseudocyst Ascites Intraperitoneal hemorrhage Thrombosis Bowel infarction Obstructive jaundice
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Complications – Systemic Pulmonary
Pleural effusions Atelectasis Mediastinal abscess ARDS
Cardiovascular Hypotension Sudden death Pericardial effusion
Hematologic DIC
Gastrointestinal PUD Erosive gastritis Blood vessel
erosion Portal vein
thrombosis Renal
ARF Renal artery/vein
thrombosis
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Management
Fluid Management Nutritional support
Rest gut TPN
Pain management Supporting other organ systems
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Treatment
IV replacement of fluids, proteins, electrolytes and blood
Withholding food and fluids to rest the pancreas
NG tube suctioning Drugs Peritoneal lavage Surgical drainage Laparotomy to remove
obstruction
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Fluid Resuscitation
Patients with acute pancreatitis may have fluid shifts of 4 to 12 L into retroperitoneal space and peritoneal cavity due to inflammation
In severe acute pancreatitis, blood vessels in and around the pancreas may also become disrupted, resulting in hemorrhage.
Replace fluids with colloids, crystalloids, or blood products
Monitor for S&S of hemorrhage ( chart)
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Rest the Pancreas NPO status Resting the gut is recommended until the patient
no longer reports abdominal pain and serum amylase has returned to normal
Provide nutrition enterally using a jejunal tube to prevent pancreatic enzyme secretion.
If parenteral therapy is used, the solution is usually a mixture of hypertonic glucose and amino acids.
The use of lipid emulsion is contraindicated during acute phase because it increases pancreatic exocrine secretion.
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Pharmaceutical Treatment
Pethidine for pain Morphine causes spasm of Sphincter
of Oddi Pneumatic compressions
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Management - Antibiotics Infected necrosis has significant
mortality (40%) prophylactic antibiotics in severe
pancreatitis with necrosis Imipenem, cefuroxime, ceftazidime +
amikacin + metro, Ofloxacin + metro, cipro + metro your choice
If used, it should be given no longer than 7 to 14 days
Gut decontamination is not recommended
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Goals for Treatment Supportive care
Pain control Antiemetics IVF NPO
Lessening inflammation and necrosis ERCP with stone extraction or stent
placement Treating complications Preventing recurrence
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ERCP IN ACUTE PANCREATITIS
Emergency ERCP with biliary sphincterotomy and stone extraction when stones are identified in the common bile duct improves outcome in severe acute pancreatitis. Greatest benefit occurs in those patients who have ascending cholangitis
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Prognosis
~90% mild, self-limited Usually resolves in 3-7 days
~10% severe requiring ICU admission Mortality may approach 50% in
severe cases
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Chronic pancreatitis Pathophys - irreversible parenchymal
destruction leading to pancreatic dysfunction
most frequent in men with peak incidence between the age 35 and 45 years.
Weight loss is multifactorial: maldigestion, fear of eating, anorexia, nausea, and vomiting
Constipation, flatulence Steatorrhea- does not occur until 90% of pancreatic
function is lost. Diabetes- when more than 80% of the gland is destroyed.
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Clinical picture
Abdominal pain occurs in 50% to 80% , pain is dull or boring in quality and worsens after eating. The pain is located in the epigastric area and often radiates to the back.
Two patterns of pain Short, relapsing episodes lasting days to
weeks, separated by pain-free intervals.
Prolonged, severe, unrelenting pain.
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Chronic pancreatitis
#1- etiology is chronic alcohol abuse (90%)
Gallstones Hyperparathyroidism Congenital malformation(pancreas divisum) Idiopathic
MRCP of pancreas divisum
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Evaluation
or normal amylase and lipase Plain AXR / CT may show calcified
pancreas Pain management critical
Alcohol cessation may improve pain Narcotic dependency is common
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ERCP
ERCP is a highly sensitive radiographic test for CP.
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CT features
The cardinal CT features of CP are pancreatic atrophy, calcifications, and main pancreatic duct dilation .
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Direct PFTs require placement of double-lumen, gastroduodenal tubes for pancreatic fluid collection after intravenous CCK or secretin stimulation. Direct tests are sensitive for early CP.
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TREATMENT(1)
Pain relief — Avoiding alcohol Modifying meals Non-narcotic analgesics : NSAIDs such as ibuprofen Pancreatic enzyme
supplements Narcotic analgesics
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TREATMENT(2)
Treatment of fat malabsorption and steatorrhea —
Reducing fat intake Lipase supplements Medium chain triglycerides
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INTERVENTION IN CHRONIC PANCREATITIS
Endoscopic therapy Dilatation or stenting of pancreatic
duct strictures Removal of calculi (mechanical or
shock-wave lithotripsy)
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Intervention…
Surgical methods Partial pancreatic resection,
preserving the duodenum Pancreatico-jejunostomy
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Complications Exocrine insufficiency typically
manifests as wt loss and steatorrhea If steatorrhea present, a trypsinogen level
< 10 is diagnostic for chronic pancreatitis Manage with low-fat diet and pancreatic
enzyme supplements (Pancrease, Creon) Endocrine insufficiency - from islet cell
destruction which leads to diabetes
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Pancreatic Cancer
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Incidence
One of the leading causes of cancer mortality
Incidence increases with age Rarely before 50 y/o – usually 60 to
70 y/o Slightly more in men Less than 20% live longer than one
year
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Etiology of Pancreatic Cancer
Exact cause unknown Smokers at high risk High fat, high protein, high
caffeine, high alcohol diets May be genetic
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Pathophysiology Usually arises from epithelial cells of
the pancreatic ducts Tumor discovered in late stages so
has spread throughout pancreas Can be a result of metastatic
disease from lung, breast, thyroid, kidney, or skin
Rapid growing with spread to surrounding tissue
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More Patho
Most common site is the head of the pancreas
Necrotic pancreatic tumors increase thromboplastic factors
Thrombophlebitis seen as a result
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Diagnostics
No specific blood tests to diagnose Elevated amylase, lipase, alkaline
phosphatase, bilirubin, CEA, C19-9 CT, Ultrasonography Needle biopsy Paracentesis ERCP – most definitive diagnostic
test
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Signs and Symptoms
Vague, dull, abdominal pain Weight loss, weakness Anorexia, nausea, vomiting Glucose intolerance Flatulence GI bleeding Ascites Leg DVT Jaundice (if head of pancreas involved)
Clay colored stools Dark urine
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Clinical Management
Goal is to prevent spread of tumor Chemotherapy or radiation Pain control Total resection Head of pancreas removal Whipple procedure
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Whipple Procedure Radical pancreaticoduodenectomy Used for cancer of the pancreas head only Removal of:
Pancreas head Duodenum Stomach Portion of jejunum Gallbladder Spleen Duct anastomoses: pancreatic& common bile to
jejunum
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Clinical Management Continued
Nutritional support: TPN, tube feeding
Needs critical care nursing postoperatively
Fluid and electrolyte replacement Glucose monitoring