Acute and chronic pancreatitis

Acute pancreatitis defintion
acute inflammatory process of the pancreas
– may also involve peripancreatic tissues and remote organs (kidney, bowel, liver)
-severity is based on the prescence of abscence of necrosis

etiology of acute pancreatitis
BAD SHIT
b- bilary- gall stones blockage
A- alcolhol
d- divisum (malformation/malunion) opening of the major and minor ducts are reversed, drugs(HIV meds, diuretics, ABX
s- surgery
h- hypertriglycreidemia, hypercalcemia, herditary
i- infection, iatrogenic(ERCP)m idiopathic, ischemic
t- tumor, trauma (MVA seatbelt), TRinidad scorpion

B& A account for about 90% of all acute pancreatitis

Acute pancreatits pathophysiology
Not really understood
-Impairement of pancratic microcirculation
-deveopment of pancreatic necrosis
– development of pancreatic infection
-development of systemic compications
**not all patients will progress to most severe

Acute pancreatitis diagnosis
Abdominal pain in epigastic area with radiation to the back, N/V, fever
EXAM- abdominal distension, tendernes,, gaurding, hypoactive bowel sounds
Labs- Pancreatic enzymes elevated
amylase and Lipase 3x normal (lipase is more specific to pancreas)
Imaging- not too helpful except for US with biliary cause, CT only for refractory patients not acute

Ransons’ prognistic criteria
Done at admission and then again at 48 hours
at admission
– >55 yr old
-WBC >16.000
-LDH >350
-Glucose >200
-AST >250
During inital 48 hours
– HCT decrease >10
– BUN increase of >5
-CA <8 -PaO2 <60 - base deficit >4
– Fluid sequestration >6
All of these are worth a point and the more points the more aggressive the treatment and high mortality
*increasei n BUN/CREAT shows lean toward renal failure and fluid sequestration, watch I/O carefully

Mild acute pancreatitis treatment
Fluid replacement- RINGER’s lactate is the best
nothing by mouth
treat pain with analgesia
Almost always resolves in a matter of days

Gallstone pancreatitis treatment
ERCP with sphicnterotomy and stone removal if evidence of cholangitis/bilary obstruction or patient not improving
– this may need to be urgent if a large blockage

Severe pancreatitis treatment
ICU!!!!- aggressive supportive care and extensive monitoring for local or systemic complications (possible respiratory compromise)
– if necorsis or fluid sequestration (need to aspiriate) give Imipenem- for sure if culture is positive but can even give for prophylaxis- done case by case
Nutritional support- espeically if it is greater than 4 hours
– enteral is better but if patient cannot parenteral
*** these patients can get sick very fast

Acute pancreatitis complications
Local- necrosis, peri-pancreatic fluid collections and pseudocysts (false walled cyst will happen over time)
Systemic- WORRY!!!
Secondary to the inflammatory cascade
– GI bleed, shock, coagulopathy, respiratory failure, renal failure, hyperglycemia, hypocalcemia, – very worried about organ failure

Necrotizing pancreatitis
High mortality rate
– suspect if no clinical improvement and/or fever after 5-7 days
– diagnosed by CT
– use Imipenem for fevers
– Pecutaneous aspiration or necrosis
infected- surgical debridement
sterile- usually conservative management
Much higher chance of infection once the pancreas become necrotic
also much higher mortality

Chronic pancreatitis
Chronic inflammatory condition of the pancreas characterized by FIBROSIS, destruction of exocrine tissues and endocrine tissues

can result from multiple acute attacks
These patient can have trouble with diabetes (think of a patient will controlled and then glucose out of control)

Chronic pancreatitis pathophysiology
TOXIN!!!= ETOH a direct pancreatic toxin- lead to pancreatic juice rich in high viscous protein- due to direct damage to pancreas cells
– so precipitation of the protein “plugs” in the small ductules that get blocked and damage the larger ducts
Decreased production of Lithistatin- leads to increase of plug and stone formation

Chronic pancreatitis causes oof
Episodes of recurrent pancreatitis/insults to the pancreas and the pancreatic ductal system leads to fibrosis/necrosis, further ductal changes, strictures, and damage- this means they are at increased risk for pancreatic cancer

Chronic pancreatitis presentation
Pain!!!- mid-epigastric with radiation to the back, worsens with food, chronic and steady
malabsorption- loss of exocrine pancreas
– 80 % of gland destroyed, weight loss, MILD STEATORRHEA with foul smell, vitamin deficiencies
Diabetes- due to loss of endocrine function <10 % of normal function

Chronic pancreatitis imaging
Abdominal x-ray- 30-40% calcifications
US-70% sensitive- dilation of ducts, calcifications, change id pancreatic parenchyma
CT- sensitivity of 75-90%
****ERCP- 95% sensitive
– abnormal main and side branches, stricture, dilation, stones- common to see recurrent cases

Chronic pancreatitis lab testing
Not very helpful
Amylase and lipase can be normal or minimally elevated
Stool for fat, fecal chymotrypsin- both insenstive and time consuming for patient and lab staff

Chronic pancreatitis treatment
Pain- analgesia (narcotics), pancreatic enzymes – inhibit CCK feeback loop on pancreatic stimulation
celiac plexus block
Malabsorption
-pancreatic enzyme replacement – varying amounts of lipase, amylase, and protease
Surgery- due to blockage
– dilated main pancreatic duct
-disease in head of pancreas
-total or near total pancreatectomy

Make sure they stop drinking
harder to treat

Chronic pancreatitis complications
Pseudocyst
Common bile duct obstruction
Pancreatic fistula/leak
Duodenal obstruction
Splenic vein thrombosis
Pancreatic Cancer- low risk but still need to worry about it

Pancreatic cancer
high mortality- not commonly found until very last
Pain is epigastric with radiation to the back- constant
Jaundice
Weight loss
worsening symptoms of diabetes if already diagnosed with diabetes
acute pancreatitis- not common

Risk factors for Pancreatic cancer
Age, male, african american population, Diabetes (think of it when you see a controlled diabetic suddenly out of control), chronic pancreatitis esp. with a longer duration, tobacco (increases risk 2x normal), high fat diet

Pancreatic cancer diagnosis
LABs- CEA adn CA 199, mild amylase & lipase, elevated bilirubin and ALP
Imaging studies- THIS IS THE MAIN WAY TO FIND IT
-CT scan >80% sensitive
-ERCP- 90% sensitive & specificity
Endoscopic ultrasould >90% sensitivity- only really good for tumors <2 cm Uses TNM criteria for staging

Pancreatic cancer surgery
85 % of patient are unresectable
common – pancreatic head surgery- pancreaticduodenectomy (whipple)
Cancer of body and tail- distal
pancreatectomy
surgical resection still has a vrey bad prognosis
only used for patients with no lymph node involement or metastatses (otherwise surgery for pallative care only)

Pancreatic cancer pallative treatment
Pain relief- narcotics, celiac ganglion block
Biliary obstruction- surgical bypass or endoscopic/percuatneous stenting
Dupdenal obstruction- surgical bypass or endoscopic stent
Chemotherpy/radiation

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