Pocket Medicine: The Massachusetts General Hospital Handbook of Internal Medicine (52 page)

Clinical manifestations

• May be asx; biliary pain in
2%/y; once sx, rate of complications
2%/y •
Biliary pain (“colic”)
=
episodic RUQ or epigastric abd pain
that begins abruptly, is continuous, resolves slowly and lasts for 30 min–3 h; ± radiation to scapula; nausea •
May be precipitated by fatty foods

• Physical exam: afebrile, ± RUQ tenderness or epigastric pain

Diagnostic studies

• RUQ U/S: Se & Sp >95% for stones >5 mm; can show complications (cholecystitis); should be performed only after fasting ≥8 h to ensure distended, bile-filled gallbladder
Treatment

• Cholecystectomy (CCY), usually laparoscopic, if symptomatic

• CCY in asx Pts w/: GB calcification (~7% risk of ca) (
Surgery
2001;129:699), GB polyps >10 mm, Native American, stones >3 cm or bariatric surgery or cardiac transplant candidates • Ursodeoxycholic acid (rare) for cholesterol stones w/ uncomplicated biliary pain or if poor surgical candidate; also reduces risk of gallstone formation with rapid wt loss • Biliary pain: NSAIDs (eg, diclofenac 50 mg IM) drug of choice, efficacy
opiates & ↓ complications (
Aliment Pharmacol Ther
2012;35:1370)
Complications

• Cholecystitis: 20% of sx biliary pain → cholecystitis w/in 2 y

• Choledocholithiasis → cholangitis or gallstone pancreatitis

• Mirizzi’s syndrome: common hepatic duct compression by cystic duct stone → jaundice, biliary obstruction • Cholecystenteric fistula: stone erodes through gallbladder into bowel

• Gallstone ileus: SBO (usually at term ileum) due to stone in intestine that passed thru fistula • Gallbladder carcinoma (~1% in U.S.)

CHOLECYSTITIS (
NEJM
2008;358:2804)

Pathogenesis

• Acute cholecystitis: stone impaction in cystic duct → inflammation behind obstruction → GB swelling ± secondary infection (50%) of biliary fluid

• Acalculous cholecystitis: gallbladder stasis and ischemia → inflammatory response; occurs mainly in critically ill, hosp. Pts (postop major surgery, TPN, sepsis, trauma, burns, opiates, immunosuppression, infxn [eg, CMV,
Crypto, Campylobacter
, typhoid fever])

Clinical manifestations

• History: RUQ/epigastric pain ± radiation to R shoulder/back, nausea, vomiting, fever

•
Physical exam: RUQ tenderness
, Murphy’s sign = ↑ RUQ pain and inspiratory arrest with deep breath during palpation of R subcostal region, ± palpable gallbladder

• Laboratory evaluation: ↑ WBC, ± mild ↑ bilirubin, AΦ, ALT/AST and amylase; AST/ALT >500 U/L, bili >4 mg/dL or amylase >1000 U/L → choledocholithiasis

Diagnostic studies

•
RUQ U/S
: high Se & Sp for stones, but need
specific signs of cholecystitis
: GB wall thickening >4 mm, pericholecystic fluid and a sonographic Murphy’s sign

•
HIDA scan
: most Se test (80–90%) for acute cholecystitis. IV inj of HIDA (selectively secreted into biliary tree). In acute cholecystitis, HIDA enters BD but not GB. 10–20% false
(cystic duct obstructed from chronic cholecystitis, lengthy fasting, liver disease).

Treatment

• NPO, IV fluids, nasogastric tube if intractable vomiting, analgesia

•
Antibiotics
(
E. coli
,
Klebsiella
and
Enterobacter
sp. are usual pathogens) ([2nd-or 3rd-generation cephalosporin or FQ] + MNZ) or piperacillin-tazobactam

• Early CCY (usually w/in 72 h). Delaying surgery 2–3 mo ↓ operative time w/o Δ rate of complications or conversion to open procedure (
Am J Surg
2008;194:40).

• If unstable for surgery, EUS-guided transmural or ERCP-guided transcystic duct drainage is equivalent to cholecystostomy (
Gastro
2012;142:805)

• Intraoperative cholangiogram or ERCP to r/o choledocholithiasis in Pts w/ jaundice, cholangitis or stone in BD on U/S

Complications

• Gangrenous cholecystitis: necrosis w/ risk of empyema and perforation

• Emphysematous cholecystitis: infection by gas-forming organisms (air in GB wall)

• Post CCY: bile duct leak, BD injury or retained stones, cystic duct remnant, sphincter of Oddi dysfxn

CHOLEDOCHOLITHIASIS

Definition

• Gallstone lodged in bile duct (BD)

Epidemiology

• Occurs in 15% of Pts w/ gallbladder stones; can form de novo in BD

Clinical manifestations

• Asymptomatic (50%)

• RUQ/epigastric pain due to obstruction of bile flow → ↑ BD pressure, jaundice, pruritus, nausea
Diagnostic studies

• Labs: ↑ bilirubin, AΦ; transient spike in ALT or amylase suggests passage of stone • RUQ U/S: BD stones seen ~50% of cases; usually inferred from dilated BD (>6 mm) • ERCP preferred dx modality when likelihood high; cholangiogram (percutaneous, operative) when ERCP unavailable or unsuccessful; EUS/MRCP to exclude BD stones when suspicion low
Treatment

• ERCP & papillotomy w/ stone extraction (± lithotripsy)

• CCY typically w/in 6 wk unless contraindication (>15% Pts will develop indication for CCY if left unRx’d)
Complications

• Cholangitis, cholecystitis, pancreatitis, stricture

CHOLANGITIS

Definition & etiologies

• BD obstruction → infection proximal to the obstruction

•
Etiologies: BD stone
(~85%)

Malignant (biliary, pancreatic) or benign stricture

Infection w/ fluke (
Clonorchis sinensis
,
Opisthorchis viverrini
)

Clinical manifestations

• Charcot’s triad: RUQ pain, jaundice, fever/chills; present in ~70% of Pts • Reynolds’ pentad: Charcot’s triad + shock and Δ MS; present in ~15% of Pts
Diagnostic studies

• RUQ U/S

• Labs: ↑ WBC, bilirubin, AΦ, amylase;
BCx • ERCP; percutaneous transhepatic cholangiogram (if ERCP unsuccessful)
Treatment

•
Antibiotics
(broad spectrum) to cover common bile pathogens (see above) ampicillin + gentamicin (or levofloxacin) ± MNZ (if severe); carbapenems; pip/tazo • ~80% respond to conservative Rx and abx → biliary drainage on elective basis •
~20% require urgent biliary decompression
via ERCP (papillotomy, stone extraction and/or stent insertion). If sphincterotomy cannot be performed (larger stones), decompression by biliary stent or nasobiliary catheter can be done; otherwise percutaneous transhepatic biliary drainage or surgery.

ACID-BASE DISTURBANCES

GENERAL

Definitions

•
Acidemia
→ pH <7.36,
alkalemia
→ pH >7.44

•
Acidosis
→ process that increases [H+];
alkalosis
→ process that decreases [H+]

• Primary disorders: metabolic acidosis or alkalosis, respiratory acidosis or alkalosis

• Compensation

respiratory: hyper-or hypoventilation alters P
_a
CO
₂
to counteract 1° metabolic process renal: excretion/retention of H+/HCO
₃
to counteract 1° respiratory process respiratory compensation occurs in minutes; renal compensation takes hours to days
compensation never fully corrects pH;
if pH normal, consider mixed disorder

Workup

• Determine
primary disorder
: ✓ pH, P
_a
CO
₂
, HCO
₃

• Determine if
degree of compensation
is appropriate