Pocket Medicine: The Massachusetts General Hospital Handbook of Internal Medicine (43 page)

↑ lipase
: more specific than amylase

 false
: renal failure, other abd process, diabetic ketoacidosis, HIV, macrolipasemia

ALT >3 × ULN suggests gallstone pancreatitis (
Am J Gastro
1994;89:1863);  AΦ, bili not helpful

Other labs (see “Prognosis”): ↑ WBC, ↑ or ↓ Hct, ↑ BUN, ↓ Ca, ↑ glc, ↑ CRP

• Imaging studies

KUB/CXR: can see “sentinel loop” air in small bowel in LUQ, atelectasis, effusion

Abd CT
: not required for dx, but test of choice to make dx. Helps exclude other dx, stage severity, & r/o complications. CT w/ IV contrast on day 3 of presentation in severe cases to evaluate for pancreatic necrosis (avoid on presentation b/c theoretical concern of ↑ necrosis w/ IV contrast; defer if concomitant AKI).

Abd U/S
: typically not useful to visualize pancreas (obscured by bowel gas), but helpful to investigate biliary etiology (ie, gallstones and BD dilatation); can see pseudocyst

MRI/MRCP: can detect necrosis; also used to assess for stones & ductal disruption

Endoscopic U/S (EUS): limited role acutely; useful for occult biliary disease (microlithiasis)

Treatment
(
Lancet
2008;371:143;
AJG
2012;107:1146)
• Supportive therapy: in mild cases, bowel rest is usually sufficient

Fluid resuscitation
LR may be superior to NS (↓ SIRS, CRP at 24 h; contraindicated if ↑ Ca); at least 250 mL/h, may need up to
10 L
/
d
if severe; titrate to UOP ≥0.5 mL/kg/h

Nutrition
: if mild, initiate oral nutrition when pain, nausea allow.

If severe and NPO >7 d expected, early (w/in 48 h) enteral nutrition indicated and preferred over TPN; ↓ infectious complications & disease severity, & trend toward ↓ mortality (
BMJ
2004;328:1407). Ideally NJ tube, but NG okay.

Analgesia
: IV meperidine, morphine, hydromorphone (theoretical risk of sphincter of Oddi spasm by opiates, but has not been shown to adversely affect outcome)

• Prophylactic systemic
abx
(eg, imipenem) to ↓ mortality & prevent conversion of sterile to infected necrosis controversial (
Am J Surg
2009;197:806;
Gastro
2007;132:2022); ? reserve for severe pancreatitis w/ >30% necrosis by CT, & no >14 d • Debridement: infected necrosis usually requires percut, endoscopic or surgical debridement. Improved outcomes by delaying surgery ≥2 wk if possible to allow organization of necrosis. CCY if gallstones (w/in 48 h if mild, o/w w/in 14 d;
Surg
2009;145:260;
Ann Surg
2010;251:615) • ERCP + sphincterotomy: in acute setting, reserved for severe cholangitis/sepsis and T bili >5 (ie, presumptive obstructive BD stone). Otherwise, early ERCP does not reduce risk of local or systemic pancreatitis complications (
Ann Surg
2007;245:10).

Complications

• Systemic: shock, ARDS, renal failure, GI hemorrhage, DIC

• Metabolic: hypocalcemia, hyperglycemia, hypertriglyceridemia •
Acute fluid collection
(30–50%): seen early, no capsule, no Rx required •
Pseudocyst
(10–20%): fluid collection, persists for 4–6 wk, encapsulated suggested by persistent pain & elevation of amylase or lipase, or mass on exam most resolve spont.; if >6 cm or persists >6 wk + pain → endo/perc/surg drainage •
Sterile pancreatic necrosis
(20%): area of nonviable pancreatic tissue ? prophylactic abx (see above); supportive measures, surgery if Pt unstable •
Infection
(5% of all cases, 30% of severe): usually 2° enteric GNR

infected pancreatic necrosis
: new SIRS after 7 d typical; perc drainage followed by min invasive surg debridement or endoscopic necrosectomy superior to open necrosectomy; FNA no longer routinely recommended (
Pancreas
2012;41:1176)

pancreatic abscess
: circumscribed collection of pus (usually w/o pancreatic tissue) treat with abx + drainage (CT-guided if possible), usually seen ≥4 wk into course

•
Ascites or pleural effusion
: occurs due to disrupted pancreatic duct; consider early ERCP w/ stent across duct; can also occur from draining pseudocyst
Prognosis
(
Gastro
2007;132:2022)
• Severe pancreatitis (20%) = organ failure
or
local complications (necrosis, pseudocyst) • Scoring systems: HAPS, BISAP, APACHE II, Ranson’s criteria, CT Severity Index

HAPS
: no abd tenderness or rebound on exam plus nl Hct and Cr on admission predicts non-severe course w/ 98% accuracy (
Clin Gas Hep
2009;6:702)

BISAP
: 5-point scoring system on admission (BUN >25, GCS <15, SIRS, age >60, and pleural effusion) identifies Pts at risk for ↑’d mortality (
Am J Gastro
2009;104:966)

APACHE II
(
www.mdcalc.com/apache-ii-score-for-icu-mortality
): severe if score ≥8

Chronic pancreatitis
(
Lancet
2011;377:1184)
• 70–80% due to EtOH, also consider autoimmune pancreatitis. Smoking major risk factor.

• Often, but not always, recurrent acute attacks → inflammatory infiltrate → fibrosis → exocrine then endocrine insufficiency (eg, diabetes) • Sxs include epigastric pain, N/V; over time will be painless and p/w steatorrhea and wt loss • Amylase/lipase ↑ early, but may be nl later.
fecal fat, ↓’d stool elastase & chymotrypsin, Ca
^2
+
in pancreas on KUB/CT.

• ERCP/MRCP/EUS high Se for dx: stricture, dilated ducts, honeycombing of parenchyma • Treatment is low-fat diet and enzyme replacement. Avoid EtOH & tobacco. Analgesia w/ NSAID ± mild opioid (eg, tramadol). Surgery in selected cases.

ABNORMAL LIVER TESTS

Tests of hepatocellular injury or cholestasis

•
Aminotransferases
(AST, ALT): intracellular enzymes released 2° necrosis/inflammation

ALT more specific for liver than is AST (heart, skeletal muscle, kidney, brain, RBC/WBC)

ALT > AST → viral hepatitis or fatty liver/nonalcoholic steatohepatitis (precirrhotic)

AST: ALT >2:1 → alcoholic hepatitis, cirrhosis; nonhepatic source

ALT/AST >15× ULN → etiologies of acute liver failure (↑↑↑ LDH → ischemia/toxic)

•
Alkaline phosphatase
(AΦ): enzyme bound in hepatic canicular membrane

besides liver, also found in bone, intestines, kidney and placenta

confirm liver origin with: ↑ 5′-NT, ↑ GGT or AΦ heat fractionation

↑ levels seen with biliary obstruction or intrahepatic cholestasis (eg, hepatic infiltration)

Tests of hepatic function

•
Albumin
: marker for liver protein synthesis, ↓ slowly in liver failure (t
_1
/2
~20 d) •
Prothrombin time
(PT): depends on synthesis of coag factors by liver (except FVIII); b/c t
_1
/2
of some factors (eg, V, VII) is short, ↑ PT can occur w/in hrs of liver dysfxn •
Bilirubin
: product of heme metab (unconjugated, “indirect”) carried by alb to liver where taken up for conjugation (“direct”) to make soluble, then excreted into bile; most sensitive test to detect parenchymal disease; in those w/ normal LFTs, high nl Tbili (? marker of ↑ heme oxygenase) a/w ↓ resp disease & death (
JAMA
2011;305:691)
Patterns of liver injury

•
Hepatocellular
: ↑↑ aminotransferases, ± ↑ bilirubin or AΦ

↑↑↑ ALT & AST (>1000): severe viral hepatitis, drugs, ischemia, Wilson’s, AIH

•
Cholestasis
: ↑↑ AΦ and bilirubin, ± ↑ aminotransferases •
Isolated hyperbilirubinemia
: ↑↑ bilirubin (direct or indirect), nl AΦ and aminotransferases •
Infiltrative
: ↑ AΦ, ± ↑ bilirubin or aminotransferases •
Jaundice
is a clinical sign seen when bilirubin >2.5 mg/dL (esp. in sclera or under

tongue); if hyperbilirubinemia conjugated → ↑ urine bilirubin

Figure 3-3 
Approach to abnormal liver tests with hepatocellular pattern