Pancreatic, Hepatic and Biliary Disease: An Overview
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Transcript Pancreatic, Hepatic and Biliary Disease: An Overview
Pancreatic and
Biliary Disease: An
Overview
Tory Davis PA-C
Table of Contents
Pancreatic disease
– Acute pancreatitis
– Chronic pancreatitis
Gallbladder disease
– Cholelithiasis
– Cholecystitis
Acute Pancreatitis
Inflammation of pancreas (+/-adjacent
tissue)
– caused by release of activated pancreatic
enzymes within gland (autodigestion)
Several possible etiologies
Range from mild (abd pain, vomitinginflammation confined to gland, 5%
mortality) to severe (really bad, maybe
dead: pancreatic necrosis, systemic
inflammatory process, shock, multi-organ
failure- up to 50% mortality)
What’s happening
Pancreatic enzymes (trypsin,
phospholipase A2, elastase) get
activated within the gland
Cause tissue damage directly AND
Activate complement and inflammatory
cascades, producing cytokines
inflammation, edema, tissue necrosis
Then what?
Cytokines and enzymes in peritoneum
cause chemical burns, fluid thirdspacing
In systemic circ systemic
inflammatory response capillary
permeability and vascular tone
– acute respiratory distress, renal failure
Who’s responsible for
this mess?
EtOH- 100 g/d x 3-5 yrs
(lots)pancreatic enzyme proteins to
precipitate in small
ductulesobstructionpremature
activation of enzymes
Biliary/structural- gallstone in
Sphincter of Oddi ductal pressures
Etiology
80% caused by alcohol or biliary tract
disease/structural disorders
– Stones
– ERCP (dx imaging study)
– Trauma
– Ischemia
– Vasculitis
– Pancreas divisum – predisposes for
pancreatitis
Etiology
20% caused by “other”
– Drugs: ACE-I, sulfa, NSAIDs
– Infectious: CMV, mumps, Coxsackie B
– Inherited: CF, other gene mutations
– Metabolic: hypertrigs, hypercalcemia,
hyperparathyroid
– Other: pregnancy, embolism
Causes of Acute
Pancreatitis: GET SMASH'D
Gallstones (most common reason for acute
pancreatitis with amylase >1000 units/L)
Ethanol (alcohol)
Trauma (usually blunt abdominal injury)
Steroids
Mumps
Autoimmune
Scorpion bites (akin to zebra bites in Maine)
Hyperlipidemia (particularly
hypertriglyceridemia)
Drugs (ACE-I, sulfa)
Acute Pancreatitis S&S
Steady, boring deep epigastric pain
– Radiates to the back in 50%
Sudden onset with gallstone pancreatitis,
gradual sx increase over days with EtOH
Nausea and vomiting common
Alleviated by sitting upright, lean forward
Aggravated by vigorous movement, deep
inspiration, coughing
Weakness, anxiety, diaphoresis
Physical Exam
Acutely ill appearing
Febrile
Mild jaundice possible
Tachycardic, diaphoretic, pale
Tachypneic with shallow respirations
diaphragmatic excursion
– Why? Don’t want to breath
Postural hypotension
Blunted sensorium
Exam
Marked upper and mild lower abd
tenderness with guarding
Mild-moderate upper abd rigidity
Rectum nontender, neg FOBT
Hypoactive BS, maybe absent (ileus)
Evidence of extravasation of hemorrhagic
exudate
– Grey Turner’s sign: flank ecchymosis
– Cullen’s sign: umbilical ecchymosis
Work-up
Lipase more specific, elevated up to 14
days
Amylase elevate early, recedes 3-5 days
Non-specific to pancreas
CMP– elevated glucose, Ca
– elevated alk phos and bilirubin indicating
obstruction
LDH- elevated from tissue necrosis
Work-up
CBC with diff– WBC up to 12-20
– Hct 50-55% (indicating 3rd spacing)
EKG- r/o MI
U/S to image biliary tree
– Start here - it’s faster and cheaper
– Stones easily observable and fixable
CT to image pancreas itself
– Necrosis, vascular involvement, mass
Ddx
Perforated ulcer
(gastric, duodenal)
Mesenteric
infarction
Strangulating
intestinal
obstruction
Dissecting
aneurysm
Biliary colic
Appendicitis
Inferior wall MI
Splenic hematoma
Abd muscle
hematoma
Ranson’s Criteria for
Pancreatitis Mortality
Determine and document at admission
–
–
–
–
–
Age >55
Glucose>200
Serum LDH>350
AST>250
WBC>16,000
If 3 or more present at admission, severe
course predicted with 60-80% sensitivity
Ranson’s Criteria: Part 2
Development of these in 1st 48h
heralds worsening prognosis
– HCT > 10%
– BUN > 5mg/dL
– Ca <8mg/dL
– PaO2 <60 mmHg
– Fluid sequestration >6L
– Base deficit over 4 meq/L
Ranson’s Criteria
Mortality proportional to # of criteria
Download to your PDA for IM rotations…
Number of Criteria
0-2
3-4
5-6
7-8
Mortality
1%
16%
40%
100%
Treatment
Adequate fluids- up to 6-8 L/day IV fluid
with lytes- dilute enzymes, reduce
inflammatory markers
NPO until acute inflammation subsides
– To avoid stimulation or release of enzymes
– Until pain/tenderness resolved, nl labs, appetite
present, feels better- may take days to weeks
– NG tube for pts with ileus, abd distention,
vomiting
Acute pancreatitis Tx
Pain relief- parenteral opioids
– such as demerol
Anti-emetics
H2 blockers and/or PPI
– why? Stop stomach acid production
(doesn’t stimulate pancreas)
IVF
Surgical consult for severe pancreatitis
Treatment
ICU admission if oliguric, hypotensive,
Ranson’s 3, or pancreatic necrosis
by CT >30%
Humidified O2 if hypoxic
Treat heart failure, renal failure,
hyperglycemia, hypomagnesemia etc
Abx (imipemem x 1 wk)
Tx
If gallstone pancreatitis:
80% will pass stone spontaneously within
24h
If not…ERCP w/ sphincterotomy and stone
removal
If they DO pass the stone spontaneously,
may elect lap cholecystectomy later
Oh and..
After 5-7d, necrotic tissue can become
infected
If pt initially stabilizes, then
deteriorates OR if pt appears toxic, w/
high temp, high WBCs, suspect
infection with enteric bacteria
100% mortality unless aggressive tx
with surgical debridement or drainage
Other complications
Intravascular volume depletion, shock
Prerenal azotemia
– May require peritoneal or hemodialysis
ARDS- acute respiratory distress
syndrome
Pancreatic abscess- needs drainage
GI bleed
Chronic
Pancreatitis
Persistent inflammation of pancreas
permanent structural damage
decrease in endocrine and exocrine
functions
Chronic Pancreatitis
In US, 70-80% from alcohol, 15-25%
idiopathic
Mechanism: ductal obstruction from
protein plugs
– Chronic obstructionchronic and
persistent inflammation fibrosis and
alternating ductal stricture and dilation
– Neuronal sheath hypertrophy and
peri-neural inflamchronic pain
– DM in 20-30% in 10-15 yrs due to loss of
endocrine function
S&S
Episodic abd pain in 85-90%
– Severe pain, lasts hours to days
– Episodes subside in 6-10 years, after acinar
cells destroyed
Steatorrhea when lipase and protease are
<10% of normal
– Greasy stools, oil droplet leakage
– Sort of like eating a bag of Olestra WOW! Chips
Weight loss
Dx Chronic Pancreatitis
Difficult to dx
Amylase/lipase are normal early
Typical alcohol hx helps
X-ray show calcification in 30%- but not
until late in disease process
Without typical hx, must r/o malignancy with
abd CT
– If nl, ERCP, endoscopic US, secretin pancreatic
function testing
Tx
Similar to acute pancreatitis
Acutely: NPO, fluids, opioids
Long term: EtOH cessation, low-fat
diet to pancreatic enzyme secretion
Often these don’t help; may need
opioids, with real concern for
addiction
Surgery (pancreatic resection) for pts
abstinent from EtOH who can manage
DM
Drugs
Tx steatorrhea with pancreatic
supplements
– 30,000 units of lipase given before,
during, after meals
acid-stimulated release of secretin
– H2 blocker (ranitidine150 mg BID
– PPI (omeprazole 20-60 mg qday)
– Sodium bicarb 650 mg ac and pc
Gallbladder
Anatomy 101
Anatomy of Biliary Tree
– R & L hepatic ducts from liver form
Common Hepatic Duct
– Joins Cystic Duct from GB to form
Common Bile Duct
– Pancreatic Duct joins at Ampulla of Vater,
has Sphincter of Oddi
– Enters duodenum at Major Duodenal
Papilla
Biliary Disease
Cholestasis – impairment of bile formation
or transport from metabolic, autoimmune,
infectious, genetic, or toxic abnormalities
Most biliary disease is caused by gallstones
– Found in 20% ♀ and 8% ♂ > 40 y.o.
Biliary sludge: thick mucoid stuff contains
phospholipids, cholesterol and Ca++ crystals
– Precursor to gallstones
Gallstone Formation
Gallstones mostly cholesterol, bilirubin, and
Ca++ salts, plus proteins and other materials
80% of stones are cholesterol stones, 20%
are pigment stones
– Cholesterol stones form when bile
supersaturated with cholesterol
– Multilaminar vesicles of phospholipid and
cholesterol form nucleus of stone
– Insoluble cholesterol crystals laminate onto
surface and grow within mucin gel
– Polar bile proteins then fuse crystals into stones
Pigment Stones
Ca++ salts of bilirubin
– Often in polymers with mucin glycoproteins,
some cholesterol
About 15% of stones can be seen on X-ray,
and 2/3 of these are pigment stones (more
calcified)
Why these form is not well understood, but
some links to infection and other processes
Etiol/Epidemiology
Cholesterol stone formation factors are proportions
of cholesterol, phospholipid, and bile acids in gall
bladder
Stones form when cholesterol output increased or
bile acid secretion decreased or combination of
both
Process enhanced by estrogen and cholesterol
– Female, OCP, multiparous, over forty
– Obesity; rapid weight loss and fasting
– Serum cholesterol not a predictor
Cholelithiasis
Presence of one or more calculi in
gallbladder
In US, 20% of people >65 have stones
Most disorders of biliary tract are
caused by stones
80% asymptomatic
Sx and disease when stones cause
obstruction
Cholelithiasis
Consequences:
– Cholecystitis
– Bile tract obstruction/biliary colic
– Infection (cholangitis)
– Gallstone pancreatitis
Biliary colic
Caused by transient cystic duct
obstruction
RUQ pain, poorly localized
Sudden onset, peaks in 15-30 min,
steady for 1-6h, dissipates over 30-60
min, leaving dull ache
– If lasts >6h, suspect pancreatitis or
cholecystitis, not colic
Biliary Colic
Intensify 30-60 minutes after eating
(why?), resolves in hours
Eructation, N/V, dyspepsia, flatulence,
reflux
Mild transient elev serum bili >5
Broad, scary DDx, incl PUD,
pancreatitis, cardiac syndromes, SBO,
AAA, pleurisy, hepatitis,
gastroenteritis, PTX
Biliary colic
Pain- severe
N/V, no F/C
Labs normal
Feels FINE between episodes
Tests:
– Abd US 95% specific for stones
– CT, MRI
– Endoscopic US if other tests equivocal
Cholelithiasis
Prognosis
Asymptomatic stones get symptomatic at
average rate of 2% per year
– Diabetics prone to complications, so recommend
cholecystectomy even in absence of sx
Symptomatic: Colic resolves spontaneously
but recurs in 20-40% of pts per year
Complications: cholecystitis,
choledocholithiasis, cholangitis, gallstone
pancreatitis
Cholelithiasis
Treatment
Elective cholecystectomy
– Open
– Laparoscopic
Converts to open in 5% due to difficulty in identifying
anatomy or complications
Non surgical
– High risk (age, comorbidities)
– Stones can be dissolved with oral bile salts
made from bear bile. $$$, lots of SEs, lifetime tx
Cholecystitis
Inflammation of gallbladder
Usually cystic duct obstruction by stone
Stone lodges obstructionbile
stasisrelease of inflammatory enzymes
Damaged mucosa secretes more fluid into
gallbladderdistension inflammatory
mediatorsworse mucosal damage
ischemiamore inflammation
Cholecystitis
Most commonly a complication of
cholelithiasis
But 5-10% are acalculous
Common for pts to have hx biliary colic
RUQ pain and tenderness
Develops over hours
+/- nausea, vomiting, fever, chills
Can lead to bacterial infection, necrosis,
perforation
S&S
Like biliary colic, but worse and
doesn’t resolve
Vomiting
R subcostal tenderness
+ Murphy’s sign
R sided guarding
Low grade fever
IF…
… abd pain, fever, rigors, + rebound
tenderness- think empyema or
perforation
…accompanied by jaundice, think
common duct obstruction
…untreated, 10% will have local
perforation, 1% free perfperitonitis
Dx and Tx
Dx: US- (incl ultrasonographic Murphy’s
sign)
If unequivocal, cholescintography (HIDA
scan)
Check CBC, LFTs, amylase/lipase
– Expect leukocytosis with L shift, nl LFTs
Tx: NPO, IV fluids, opioids, parenteral abx,
admit, cholecystectomy in next 24-48h
Cholecystitis
Complications
Emphysematous cholecystitis: result of
gangrene, gas-producing bacteria
(usually Clostridium)
Porcelain GB: repeated inflammation
causes deposition Ca++ salts in GB
wall
Fistula
Ileus
Choledocholithiasis
Common duct stones
Most passed from GB, some form in
CBD
Sx of gallstones plus possible
pancreatitis
Charcot’s Triad: RUQ pain, jaundice,
fever (usually with chills)
ERCP - possible stent, sphincterotomy
Cholangitis
Painful inflammation of biliary tree
If infection occurs, then can be suppurative
Ascending Cholangitis: rises to infect liver
May form obstructing empyema, abscess,
gangrene, perforation fulminant liver
failure, peritonitis, sepsis (death, too)
Suppurative cholangitis is life threatening SCU admission, abx, supportive care,
surgical consult
Primary Biliary
Cirrhosis
Inflammation & necrosis of cholangiocytes
in small and mid-size bile ducts
Immunologic process
Cholestatic process results in liver dz
Signs/Sx of biliary obstruction
– Pruritis, RUQ pain, indigestion, xanthomas and
xanthelasmas, eventual cirrhosis and liver failure
Mostly ♀ > 40 with co-morbid auto-immune
disorders
Biliary Dyskinesia
Can have all sx of cholecystitis, but no
stones, no sludge
Usually dysfunction at Sphincter of Oddi