Liver and Pancreas

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Transcript Liver and Pancreas

Liver, Pancreas, Gallbladder, and
Biliary Board Review
Elizabeth Paine, MD
July 18, 2015
** I have no financial interests regarding the
content of my presentation **
Liver enzyme elevations
Hepatocellular diseases
(predominant ALT/AST
elevations)
Cholestatic diseases
(predominant Alkaline
phosphatase/GGT elevations)
NAFLD
Chronic viral hepatitis
Autoimmune hepatitis
Wilson’s disease
Hereditary hemochromatosis
Alcoholic liver disease
Drug toxicity
Alpha 1 antitrypsin deficiency
Gallstones with biliary obstruction
Primary biliary cirrhosis
Cancer
Drug toxicity
Primary sclerosing cholangitis
Sarcoidosis
Autoimmune cholangiopathy
Adapted from Aragon and Younossi. CCJM 2010 March;77(3):195-204.
Elevated ALT/AST workup
Aragon and Younossi. CCJM 2010;77:195-204
Elevated Alkaline Phosphatase
A.
Give albumin now and wait to start
antibiotics until cultures return
Aragon and Younossi. CCJM 2010;77:195-204
Question
A 56 year old man with diabetes, hypertension and
obesity (BMI 31) is found to have an ALT 67 and AST
40 with a normal albumin, total bilirubin, and
alkaline phosphatase. He states that he has never
been a drinker and has no family history of liver
diseases. What is the most likely etiology of his
abnormal liver enzymes from the choices below?
A.
B.
C.
D.
Autoimmune hepatitis
Non-alcoholic fatty liver disease
Wilson disease
Hereditary hemochromatosis
Question
A 56 year old man with diabetes, hypertension and
obesity (BMI 31) is found to have an ALT 67 and AST
40 with a normal albumin, total bilirubin, and
alkaline phosphatase. He states that he has never
been a drinker and has no family history of liver
diseases. What is the most likely etiology of his
abnormal liver enzymes from the choices below?
A.
B.
C.
D.
Autoimmune hepatitis
Non-alcoholic fatty liver disease
Wilson disease
Hereditary hemochromatosis
Nonalcoholic fatty liver disease (NAFLD)
• Broad term (steatosis 
cirrhosis)
• Associated with metabolic
syndrome and obesity
• Diagnosis inferred by
absence of other etiologies
of liver disease
• Treatment
Chalasani et al. Hepatology 2012;55(6): 2005-2023
http://liverbasics.com/hepaticsteatosis.html
Autoimmune Hepatitis
• Range of
presentations
• Fatigue, jaundice,
malaise
• Types 1 and 2
• Autoantibodies seen:
ANA, ASMA, IgG,
LKM1
• Treatments
Manns MP, Lohse AW, Vergani D. Autoimmune hepatitis
– Update 2015. J. Hepatol. 2015 Apr;62(1S):S100-S111
Wilson’s disease
• Rare, autosomal recessive
disorder
• Usually a young patient with
neuropsychiatric symptoms
• Very low alkaline phosphatase
• Low ceruloplasmin
• Kayser-Fleischer rings
• Can present in acute liver
failure
http://www.wilsonsdisease.org/
wilson-disease/kayserfleischerrings.php
Iron overload syndromes
• Hereditary hemochromatosis
• Iron loading anemias (chronic hemolytic
anemias, sideroblastic anemia, thal major)
• Chronic liver disease (alcoholic, viral hepatitis,
NAFLD)
• Parenteral iron overload (RBC transfusions,
long standing HD)
Hereditary Hemochromatosis
• Most common genetic
disease in Caucasians
• Iron saturation >45%
• HFE genes C282Y and
H63D
• Clinical features
• Treatment:
phlebotomy with goal
ferritin <50
https://cornellbiochem.wikispaces.com/Hereditary
+Hemochromatosis
Viral Hepatitis
• Transmission
- Fecal-oral: Hep A an E
- Sexual: Hep B and D, also C
• Clinical features
• Typical course
Question
Mr. Smith presents to your clinic and reports a 2 weeks
history of fatigue and feeling “sick to my stomach.” He
also reported that he saw another provider 1 week ago
who mentioned something was abnormal with his liver.
You order a CBC, CMP, and Hepatitis panel and find that
he has positive IgM anti-HAV, positive Hepatitis B surface
antibody, and elevated ALT/AST. What is the most likely
etiology of his clinical picture?
A.
B.
C.
D.
Hepatitis B
Hepatitis C
Hepatitis A
Hepatitis D
Question
Mr. Smith presents to your clinic and reports a 2 weeks
history of fatigue and feeling “sick to my stomach.” He
also reported that he saw another provider 1 week ago
who mentioned something was abnormal with his liver.
You order a CBC, CMP, and Hepatitis panel and find that
he has positive IgM anti-HAV, negative IgG anti-HAV,
positive Hepatitis B surface antibody, and elevated
ALT/AST. What is the most likely etiology of his current
clinical picture?
A.
B.
C.
D.
Hepatitis B
Hepatitis C
Hepatitis A
Hepatitis D
Hepatitis B
• Incubation period
• Multiple modes of
transmission
• Can present with serum
sickness
• Extraintestinal
manifestations:
remember association
with PAN
Hepatitis B
http://www.bio-rad.com/en-us/product/hepatitis-b/monolisa-anti-hbc-igm-eia
Hepatitis B serologies
HBsAg
anti-HBs
anti-HBc
IgM
anti-HBc
IgG
HBeAg
+
-
+
-
+
+
-
-
+
+/-
-
+
-
-
-
-
+
-
+
-
-
-
+
-
-
-
-
-
+
-
DX
Acute
infection
Chronic
infection
Vaccinated
Exposed
immune
Acute
window
Exposed,
Ab lost
Hepatitis B treatment options
•
•
•
•
•
•
Entecavir
Tenofovir
Adefovir
Lamivudine (if not resistant)
PEG IFN
Telbivudine
Hepatitis B treatment
Hep B eAg
HBV DNA
ALT
Treatment strategy
Positive
>20K
<2 x ULN
Primarily observe until ALT elevated,
can consider bx and tx if significant
fibrosis
Positive
>20K
>2 x ULN
Observe for 3-6 months and treat if no
seroconversion
Negative
>20K
> 2x ULN
Treat, endpoint not defined
Negative
>2K
1-2 x ULN
Treat if liver bx shows significant
necroinflammation or fibrosis
Negative
<2K
< ULN
Observe
Pos or Neg
Detectable
Cirrhosis
If DNA > 2K, treat. If < 2K, consider tx if
ALT elevated
Pos or Neg
Undetectable
Cirrhosis
Compensated: observe
Decompensated: refer for transplant
Adapted from Lok and McMahon. Chronic Hepatitis B: Update 2009. Hepatology September 2009.
Caveats with Hepatitis B
• If Hepatitis B eAg positive patient is treated,
treat for 6 months after seroconversion to Hep
B eAb positive
• Pregnancy and Hep B
• HCC screening
Hepatitis C
•
•
•
•
•
Risk factors
Genotypes – gt1 is most common in US
Screening: HCV Ab
Confirmation: PCR testing
CDC guidelines: Adults born 1945-1965
should be tested once (without prior
ascertainment of HCV risk factors)
• Disease progression
Hepatitis C treatment
• Rapidly changing
• Doubt this will be testable now since it is
changing by the month with new drugs
Hep C Extraintestinal manifestations
• Cryoglobulinemia
• Porphyria cutanea tarda
• Membranoproliferative
glomerulonephritis
• Inflammatory arthritis
• Sjogren’s syndrome
http://www.porphyriaprofessionals.uct.ac.za/ppb/professional/gallery/skind
isease
Hepatitis D
•
•
•
•
•
Requires co-existent Hepatitis B
Usually found in IVDA
Coinfection vs. superinfection
Diagnosis
Treatment
Alcoholic hepatitis
• Jaundice, fever,
ascites, AST/ALT >2
• Path
• Treatment
• Reassess in 7 days
with Lille score
http://missinglink.ucsf.edu/lm/IDS_106_Liver_
histo_path/Assets/Liver_path.htm
Primary biliary cirrhosis
https://www.pathology.med.umich.edu/g
reensonlab/pbc2.jpg
• Usually middle
aged female
• Itching and fatigue
• Increased alkaline
phosphatase
• Elevated AMA
• Treat with ursodiol
• Manage cirrhosis
Primary Sclerosing Cholangitis
• Autoimmune
• Fibrosis of large bile
ducts
• RUQ pain, fatigue, weight
loss
• 70% associated with UC
• Increased risk of
cholangiocarcinoma
• Diagnosed with MRCP or
ERCP
http://openi.nlm.nih.gov/detailedresult.php?i
mg=2880347_ijgm-3-143f3&req=4
PSC Pathology
http://library.med.utah.edu/WebPath/LIVEHTML/LIVER054.html
Question
A 63 year old patient presents because of abnormal
liver function tests including AST 123, ALT 143,
alkaline phosphatase 143. He drinks 1 glass of wine
daily. He takes amiodarone, losartan, and
metformin. A liver biopsy is done and shows
Mallory hyaline bodies consistent with fatty
deposition. What is the most likely cause?
A.
B.
C.
D.
Alcohol
Metformin
Amiodarone
Losartan
Question
A 63 year old patient presents because of abnormal
liver function tests including AST 123, ALT 143,
alkaline phosphatase 143. He drinks 1 glass of wine
daily. He takes amiodarone, losartan, and
metformin. A liver biopsy is done and shows
Mallory hyaline bodies consistent with fatty
deposition. What is the most likely cause?
A.
B.
C.
D.
Alcohol
Metformin
Amiodarone
Losartan
DILI evaluation
Chalasani et al. Am J. Gastroenterol 2014/109:950-966
DILI evaluation
Chalasani et al. Am J. Gastroenterol 2014/109:950-966
Drugs Commonly Associated with DILI
Drug
Pattern
Features
Amiodarone
Macrovesicular fat
“Bright” on non-contrast
CT
Acetaminophen
Acute hepatitis
ALT >5000, renal injury
Amoxicillin/clavulanate
TMP/SMX
Cholestasis
May occur after treatment
finished
Valproate
Microvesicular fat
Encephalopathy
Nitrofurantoin
Minocycline
Mimics autoimmune
hepatitis
Can occur after months on
the drug; may require
steroids
Methotrexate
Fibrosis
Probably rare
Phenytoin
Mixed
Hypersensitivity features
Adapted from Mayo Clinic Gastroenterology and Hepatology Board Review 2013
Question
A 22 year old woman who is 23 weeks pregnant
presents to clinic complaining of itching. This
itching is primarily on her palms and soles and is
worse at night. She denies any tylenol usage or
usage of other OTC medications except a prenatal
vitamin. Her abdominal ultrasound is normal.
Which of the following is the most likely diagnosis?
A. Intrahepatic cholestasis of pregnancy
B. HELLP (Hemolysis, Elevated Liver Enzymes, Low
Platelets) syndrome
C. Acute fatty liver of pregnancy
D. Acute Hepatitis A
Question
A 22 year old woman who is 23 weeks pregnant
presents to clinic complaining of itching. This
itching is primarily on her palms and soles and is
worse at night. She denies any tylenol usage or
usage of other OTC medications except a prenatal
vitamin. Her abdominal ultrasound is normal.
Which of the following is the most likely diagnosis?
A. Intrahepatic cholestasis of pregnancy
B. HELLP (Hemolysis, Elevated Liver Enzymes, Low
Platelets) syndrome
C. Acute fatty liver of pregnancy
D. Acute Hepatitis A
Intrahepatic cholestasis of pregnancy
• Usually 3rd trimester,
sometimes 2nd
• Pruritus - particularly palms
and soles
• Less than ¼ develop jaundice
• Treatment
Williamson and Geenes. Obstet Gynecol. 2014 July;124(1):120-33.
HELLP diagnosis
• Combination of clinical features
• Abdominal imaging
• Common lab features:
H: LDH >600, abnormal smear
EL: AST >70, AST/ALT elevation up to
10:10-20 fold
LP: platelets <150,000
Acute Fatty Liver of Pregnancy
•
•
•
•
•
Often presents as fulminant hepatic failure
Usually late 3rd trimester
Occurs in 1 in 6700 3rd trimester pregnancies
Associated factors
Treatment
Liver Diseases in Pregnancy
ICP
HELLP
AFLP
% Pregnancies
0.1% (USA)
0.2%–0.6%
0.005%–0.01%
Onset/trimester
25–32 weeks
3 or postpartum
3 or postpartum
Family history
Often
No
Occasionally
Preeclampsia
No
Yes
50%
Typical clinical features
Pruritus, mild
jaundice, increased
bile acids, dec vit K
Hemolysis
Thrombocytopenia
Liver failure with
coagulopathy, HE
hypoglycemia, DIC
Aminotransferases
Mild to 10–20-fold ↑
Mild to 10–20-fold ↑
300–500 but varies
Bilirubin
<5 mg/dL
<5 mg/dL unless
massive necrosis
often <5 mg/dL, higher
if severe
Hepatic imaging
Normal
Hepatic infarcts,
hematomas, rupture
Fatty infiltration
Histology
Nl–mild cholestasis,
no necrosis
Patchy/extensive
necrosis, hemorrhage
Microvesicular fat in
zone 3
Recurrence in
subsequent pregnancies
45%–70%
4%–19%
(LCHAD) defect—yes
Gilbert’s disease
•
•
•
•
Unconjugated hyperbilirubinemia
Autosomal dominant
Jaundice worsens with stress and fasting
Usually not treated
Cirrhosis
Taylor CR. Cirrhosis Imaging. http://emedicine.medscape.com/article/366426-overview
Cirrhosis complications
•
•
•
•
•
Ascites
Spontaneous bacterial peritonitis
Hepatic encephalopathy
Hepatorenal syndrome
Hepatocellular carcinoma
Question
A 53 y/o man with DM2 and HTN presents to your clinic
with a 2 month history of his pants becoming progressively
tighter. He drinks a case of beer on the weekends but denies
drug use. On exam, his BP is 99/55 with pulse of 75/minute and
T 98.2°F. His abdomen is tense with no tenderness or rebound.
Labs: WBC 5, Hb 9.2, platelets 160,000, creatinine 2,
albumin 3.4, AST 67, INR 1.4. Abdominal CT shows a large
amount of ascites and some coarsening of the liver parenchyma.
He underwent a 7L paracentesis with fluid studies as follows:
fluid albumin 2, fluid total protein 1.5, fluid PMN’s 287.
Which of the following is the best next step?
A. Start Vancomycin 1g IV daily
B. Give albumin now and wait to start antibiotics until cultures
return
C. Begin ciprofloxacin 250mg po weekly for SBP
D. Start Cefotaxime and albumin
Question
A 53 y/o man with DM2 and HTN presents to your clinic
with a 2 month history of his pants becoming progressively
tighter. He drinks a case of beer on the weekends but denies
drug use. On exam, his BP is 99/55 with pulse of 75/minute and
T 98.2°F. His abdomen is tense with no tenderness or rebound.
Labs: WBC 5, Hb 9.2, platelets 160,000, creatinine 2,
albumin 3.4, AST 67, INR 1.4. Abdominal CT shows a large
amount of ascites and some coarsening of the liver parenchyma.
He underwent a 7L paracentesis with fluid studies as follows:
fluid albumin 2, fluid total protein 1.5, fluid PMN’s 287.
Which of the following is the best next step?
A. Start Vancomycin 1g IV daily
B. Give albumin now and wait to start antibiotics until cultures
return
C. Begin ciprofloxacin 250mg po weekly for SBP
D. Start Cefotaxime and albumin
Ascites on CT
Poggi et al. International Journal of Case Reports and Images. 2013;4(1):32-36.
Serum-ascites albumin gradient (SAAG)
SAAG (g/dL)
≥ 1.1
< 1.1
Cirrhosis
Nephrotic syndrome
Total protein (g/dL)
< 2.5
Acute liver failure
≥ 2.5
CHF
Peritoneal
carcinomatosis
Constrictive
pericarditis
TB peritonitis
Budd-Chiari
syndrome
Pancreatic ascites
Veno-occlusive
disease
Chylous ascites
Ascites therapy: dietary and diuretics
• Sodium restriction < 2 grams/day
• Spironolactone/furosemide in a
ratio of 100/40
• Goal is weight loss of 0.5-1kg/day
• Diuretics are titrated to achieve
weight loss without complications
Runyon and AASLD Practice Guideline Committee. Management of Adult Patients with Ascites Due to Cirrhosis. 2013.
Refractory ascites
• Definition
• Reversible
factors
• Treatment
options
• TIPS
https://www.uic.edu/com/virtualpatient/part3/data/surgeryhtml/1310detail.htm
Runyon and AASLD Practice Guideline Committee. Management of Adult Patients with Ascites Due to Cirrhosis. 2013.
Spontaneous bacterial peritonitis (SBP)
•
•
•
•
Definition
Frequency
Clinical manifestations
Diagnosis: absolute
PMN > 250
• Bacterial culture
Example ascitic fluid
labs in patient with
SBP:
WBC 5300/mm3
87% neutrophils
Albumin <1
Runyon and AASLD Practice Guideline Committee. Management of Adult Patients with Ascites Due to Cirrhosis. 2013.
SBP treatment
• Need to control ascites
• Cefotaxime 2g IV q8
hours
• Uncomplicated SBP
outpatient can be
treated with oral
ofloxacin
• Albumin infusion
Runyon and AASLD Practice Guideline Committee. Management of Adult Patients with Ascites Due to Cirrhosis. 2013.
Primary and secondary prophylaxis
• Primary prophylaxis:
- IV cefotaxime or BID norfloxacin
- Indicated for the following patients:
 cirrhotic with GI bleed (for 7 days)
 pts w ascitic fluid protein <1.5 and Cr≥1.2, BUN≥25,
Na ≤130, CTP ≥9, bili≥3 (long term abx can be considered)
• Secondary prophylaxis:
- Norfloxacin 400mg daily or bactrim/cipro daily.
Daily dosing recommended over weekly dosing.
- For patients who previously had SBP
Runyon and AASLD Practice Guideline Committee. Management of Adult Patients with Ascites Due to Cirrhosis. 2013.
Question
A 42 year old woman with cirrhosis presents to
the ER with active hematemesis and an emesis
basin full of bright red blood. What is the most
likely etiology of her upper GI bleeding?
A.
B.
C.
D.
Dieulafoy lesion
Portal hypertensive gastropathy
Angioectasia/AVM
Esophageal varices
Question
A 42 year old woman with cirrhosis presents to
the ER with active hematemesis and an emesis
basin full of bright red blood. What is the most
likely etiology of her upper GI bleeding?
A.
B.
C.
D.
Dieulafoy lesion
Portal hypertensive gastropathy
Angioectasia/AVM
Esophageal varices
Esophageal varices
• ~1/4 to 1/3 of cirrhotics hemorrhage at least
once from varices
• Have portal HTN with pressures > 12mmHg
• Esophageal variceal hemorrhage
• Management of bleeding esophageal varices
Garcia-Tsao et al. Hepatology 2007:46(3):922-934.
Esophageal varices
http://www.clevelandclinicmeded.com/medicalpubs/diseasemanagement/hepatology/variceal-hemorrhage/
Question
A 65 year old man with cirrhosis is brought in to the
clinic by his wife after he had several days of staying
up all night and sleeping all day, along with
intermittent periods of “not making sense.” He has
asterixis on exam. What should be done for this
patient?
A.
B.
C.
D.
Start lactulose and titrate for 3 loose stools daily
Restrict the protein in his diet
Initiate metronidazole
Start furosemide
Question
A 65 year old man with cirrhosis is brought in to the
clinic by his wife after he had several days of staying
up all night and sleeping all day, along with
intermittent periods of “not making sense.” He has
asterixis on exam. What should be done for this
patient?
A.
B.
C.
D.
Start lactulose and titrate for 3 loose stools daily
Restrict the protein in his diet
Initiate metronidazole
Start furosemide
Hepatic encephalopathy
• Describes the spectrum of
potentially reversible
neuropsychiatric abnormalities
in patients with liver
dysfunction
• Presumed mechanism
• Early feature is sleep
disturbance
• Later features are asterixis,
hyperactive DTRs, transient
decerebrate positioning
Vistrup et al. Hepatology 2014 Aug;60(2):715-35.
Hepatic encephalopathy management
• Identification and avoidance of precipitants
• Lactulose 30mL BID-TID, titrated for 2-4 BM daily
Rifaximin 550mg po BID
• Protein restriction is no longer recommended for
most patients
• Treatment of post-TIPs hepatic encephalopathy
Vistrup et al. Hepatology 2014 Aug;60(2):715-35.
Question
A 55 year old man with history of cirrhosis and
ascites undergoes his q6 month surveillance
imaging. On ultrasound, he was found to have a
new 2.6cm liver lesion. AFP was 532. Subsequent
3phase liver CT showed the same lesion with
arterial enhancement and portal venous washout.
What is the most likely diagnosis?
A.
B.
C.
D.
Hemangioma
Hepatocellular carcinoma
Metastasis
Hepatic cyst
Question
A 55 year old man with history of cirrhosis and
ascites undergoes his q6 month surveillance
imaging. On ultrasound, he was found to have a
new 2.6cm liver lesion. AFP was 532. Subsequent
3phase liver CT showed the same lesion with
arterial enhancement and portal venous washout.
What is the most likely diagnosis?
A.
B.
C.
D.
Hemangioma
Hepatocellular carcinoma
Metastasis
Hepatic cyst
Hepatocellular carcinoma
• Cirrhotic patients
have increased risk
for HCC
• Hep B patients can
develop HCC without
cirrhosis
• Common
signs/symptoms
• Diagnosis
Bruix and Sherman. Management of Hepatocellular
Carcinoma. AASLD guideline 2011.
Barcelona criteria
Sherman M et al. Current Oncology 2011. 18(5):228-240.
Question
A 65 year old man with alcoholic cirrhosis is admitted to
House Medicine with spontaneous bacterial peritonitis.
He has not been taking NSAIDs or diuretics. His initial
serum creatinine is 1.1 but 4 days later, his creatinine has
risen to 3.6 and he is anuric. His creatinine does not
improve after receiving 2 days of albumin infusions.
Which of the following statements is true?
A. He likely has type I hepatorenal syndrome
B. He likely has type II hepatorenal syndrome and will
improve without treatment
C. He should be given vasodilators to improve renal
perfusion
D. He should be given furosemide and aldactone in a
40/100 ratio
Question
A 65 year old man with alcoholic cirrhosis is admitted to
House Medicine with spontaneous bacterial peritonitis.
He has not been taking NSAIDs or diuretics. His initial
serum creatinine is 1.1 but 4 days later, his creatinine has
risen to 3.6 and he is anuric. His creatinine does not
improve after receiving 2 days of albumin infusions.
Which of the following statements is true?
A. He likely has type I hepatorenal syndrome
B. He likely has type II hepatorenal syndrome and will
improve without treatment
C. He should be given vasodilators to improve renal
perfusion
D. He should be given furosemide and aldactone in a
40/100 ratio
Hepatorenal syndrome diagnosis
Diagnostic criteria (Salerno et. al 2007)
• Cirrhosis with ascites
• Serum Cr >1.5
• No improvement after 2 days of diuretic withdrawal
and plasma volume expansion with albumin
(100g/day)
• Absence of shock
• No current or recent nephrotoxic drugs or
vasodilation
• Absence of parenchymal kidney disease with
proteinuria <500, no US evidence of obstructive
uropathy or microhematuria
Salerno et al. Gut 2007;56:1310-1318.
Hepatorenal syndrome
• Types:
- Type 1 HRS
- Type 2 HRS
• Treatment
- Prevention
- Therapy
Runyon and AASLD Practice Guideline Committee. Management of Adult Patients with Ascites Due to Cirrhosis. 2013.
Schistosomiasis – Hepatic involvement
• In adults with chronic infection
– “pipestem fibrosis”
• Portal HTN & splenomegaly
• GI varices
• Often no abnormalities in LFTs
• Gold standard for dx is
microscopy of stool or urine
sample for schistosome eggs
• Treatment: praziquantel 40-60
mg/kg
http://www.microbiologybook.or
g/parasitology/sch3.jpg
Acute pancreatitis
• Acute onset
persistent epigastric
abdominal pain
• Usually with
nausea/vomiting
• Elevated amylase,
lipase
• Imaging
Munoz and Katerndahl. Am Fam Physician 2000
July 1;62(1):164-174
Etiologies of acute pancreatitis
•
•
•
•
•
•
•
Alcohol abuse
Gallstones
Hypertriglyceridemia
Post-ERCP
Pancreatic malignancy
Medications
Hypercalcemia
Medications:
Furosemide
Thiazides
Estrogens
Azathioprine
5-ASA
Tetracyclines
Sulfonamides
Anti-HIV drugs
Valproic acid
Some diabetes drugs
Poor prognostic indicators in acute
pancreatitis
•
•
•
•
•
•
•
•
•
SBP <90 with HR >130
PO2 < 60mmHg
Urine output <50mL/hr
Altered mental status
Pancreatic necrosis
Altered mental status
Low calcium (<8mg/dL) and albumin <3.2 g/dL
Hemoconcentration (Hct > 44%)
APACHE 2 score > 8
Complications of acute pancreatitis
•
•
•
•
•
Necrosis
Pseudocyst
Abscess
Shock
Left sided pleural
effusion
• Splenic vein
thrombus
http://www.top5plus5.com/Pseudocyst%20of%20the%20Pan
creas_files/Pseudocysts%20Images.html
Management of acute pancreatitis
•
•
•
•
•
•
Supportive care
NPO initially but early enteral feeding as able
IVF
Systemic antibiotics if infected or severe
Pain control
ERCP for cholangitis or sepsis
Chronic pancreatitis
• Usually result of
chronic ETOH
• Early sx: recurrent
abdominal pain
• Late sx: steatorrhea
and DM
• Imaging
http://www.nytimes.com/imagepages/2007/08/
01/health/adam/1157PancreatitischronicCTscan.
html
Complications of chronic pancreatitis
• Pancreatic cancer (~ 4% of pts with chronic
pancreatitis >20 years)
• Brittle DM, prone to hypoglycemia
• Splenic vein thrombosis
• B12 malabsorption
Management of chronic pancreatitis
• Pancreatic enzymes (start with 500 lipase
units/kg/meal) with antacids
• Decrease fat in diet
• Add medium-chain TG
• Avoid ETOH
• Stop smoking
Autoimmune pancreatitis
• Often have painless
obstructive jaundice
• Can have elevated
IgG4
• Imaging findings
• Tx: steroids
Chruch et al. Am. J. Gastroenterol 2007(102):24172425.
Pancreatic cancer
• Jaundice, weight
loss, abdominal pain
• If in pancreatic
head: painless
jaundice
• If in body/tail: pain,
weight loss
• Diagnosis
• Treatment
http://www.aboutcancer.com/pancreas1_images.htm
Question
A 65 y/o veteran is found to have the following
ultrasound but is asymptomatic with normal
labs. What should be done next?
A.
B.
C.
D.
Observation
Referral to Surgery
Abdominal CT
MRI
Question
A 65 y/o veteran is found to have the following
ultrasound but is asymptomatic with normal
labs. What should be done next?
A.
B.
C.
D.
Observation
Referral to Surgery
Abdominal CT
MRI
Cholelithiasis
• Very common
• Association with obesity, OCP, ileal
disease/resection
• Symptoms: post-prandial RUQ pain
• US to diagnose
• If asymptomatic, do nothing
• If symptomatic  refer to surgery
Choledocholithiasis
• Stones in CBD
• Elevated AlkPhos and
bilirubin
• Can also see CBD
dilation on US
• Tx: ERCP with
sphincterotomy in
most cases
http://www.healthhype.com/gallbladder-testsultrasound-ct-hida-scan-ercp.html
Acute Cholecystitis
•
•
•
•
•
•
RUQ pain, fever, leukocytosis
Calculous vs. acalculous
Frequently have positive “Murphy’s sign”
Ultrasound
HIDA scan
Tx: cholecystectomy (if good surgical
candidate), percutaneous cholecystotomy
with abx if very sick
Porcelain gallbladder
Acute cholangitis
•
•
•
•
Charcot’s triad
Complication of choledocholithiasis or cancer
Need antibiotics
Also need ERCP with endoscopic
sphincterotomy or surgery if ERCP isn’t
available
Liver/Biliary history pearls
• Pruritus/cholestasis
PBC/PSC
• Undercooked food, oysters, daycare
Hepatitis A
• ICU, hypotension, right sided CHF
Hepatic congestion
• Neuropsych findings
Wilson’s disease
Liver/Biliary history pearls
• Metabolic syndrome, mildly elevated ALT/AST
Fatty liver
• Hyperpigmentation
Hemochromatosis or PBC
• Kayser-Fleischer rings/sunflower cataracts
Wilson’s disease
Liver/Biliary history pearls
• Splenomegaly
Portal hypertension or infiltrative process
• Pulsatile liver
Tricuspid insufficiency
• Hepatic bruits
Hepatocellular carcinoma
Questions?