Capítulo V. – Pruebas y resultados
5.5 Validación de la hipótesis
5.5.2 Variables de investigación
Diseases of the Gallbladder and Bile Ducts • 65
Therapy
Surgery provides definitive management for most patients with symptomatic gallbladder disease. In patients with cholecystitis, early cholecystectomy (within 24 to 48 hours) is associated with fewer complications and earlier hospital discharge. Compared with open cholecystectomy, laparoscopic cholecystectomy results in shorter hospital stays, less pain, and a more rapid recovery peri- od. When bile duct stones are suspected, intraoperative cholan- giography should be performed at the time of the cholecystec- tomy. If this procedure is not available, postoperative endoscopic retrograde cholangiopancreatography (ERCP) with sphinc- terotomy is an alternative. In patients with severe cholangitis or sepsis, urgent ERCP is essential to remove obstruction and allow biliary drainage.
In most patients with gallstone disease, drug therapy is sup- portive until definitive surgery can be performed. Diclofenac pro- vides pain relief in biliary colic and decreases the risk of develop- ing acute cholecystitis. Nonsteroidal inflammatory drugs are also
helpful in patients with acute cholecystitis with mild to moderate pain; patients with more severe pain may require narcotic analge- sia. Treat patients with acute cholecystitis, especially those with fever, leukocytosis, or complications, with broad-spectrum antibi- otics. Select antimicrobials to cover E. coli, Klebsiella sp., group D
Streptococcus sp., and Enterobacter sp. In critically ill patients,
including those with acute cholangitis, provide coverage for
Bacteroides and Pseudomonas as well. Appropriate antibiotic
regimens include ampicillin, gentamicin and metronidazole; cef- tazidime and metronidazole; or monotherapy with piperacillin/ tazobactam, ampicillin/sulbactam, or ticarcillin/clavulanic acid.
Ursodeoxycholic acid may be used in highly selected patients who are unable or unwilling to undergo surgery. Its use is limited to patients with cholesterol stones, patent biliary tracts, and func- tioning gallbladders.
Follow-Up
Most patients with asymptomatic gallstone disease should be fol- lowed for the development of symptoms. Patients who have had
Table 1. Differential Diagnosis of Acute Cholecystitis Disease Notes
Acute cholecystitis Epigastric and RUQ pain with Murphy’s sign. Bilirubin <4 mg/dL (unless complicated by choledocholithiasis), AST, ALT may be minimally elevated.
Biliary crystals (microlithiasis, sludge) Typical biliary pain and no gallstones on imaging studies. Diagnosis made by aspiration of gallbladder bile from the duodenum or directly from the gallbladder at ERCP and microscopic examination. May cause pain, cholecystitis, or pancreatitis. Treated with cholecystectomy.
Biliary dyskinesia Typical biliary pain, no gallstones on imaging studies and a gallbladder ejection fraction less than 35%-40% at scintigraphy with cholecystokinin infusion. Symptoms usually relieved with cholecystectomy. This is a controversial diagnosis.
Acute cholangitis Charcot's triad (RUQ pain, fever, jaundice) or Reynold's pentad (Charcot's triad plus shock and mental status changes). Bilirubin >4 mg/dL. AST and ALT levels may exceed 1000 U/L.
Acute pancreatitis Mid-epigastric pain radiating to the back, nausea, vomiting, elevated amylase (>2 x normal) and lipase. Vomiting and hyperamylasemia are generally more pronounced than in acute cholecystitis.
Pyelonephritis (right) Costovertebral angle tenderness, evidence of urinary infection. Urinalysis helps to establish the diagnosis. Peptic ulcer disease RUQ or mid-epigastric pain. Perforated ulcer can mimic acute cholecystitis; free air on upright x-ray.
Acute viral hepatitis Prodromal syndrome, jaundice, AST and ALT levels generally >1000 U/L. Bilirubin level generally >4 mg/dL and usually much higher.
Acute alcoholic hepatitis Recent significant alcohol intake. RUQ pain, fever, jaundice, coagulopathy, leukocytosis, AST level usually two to three times greater than ALT level. Bilirubin level generally >4 mg/dL.
Fitz-Hugh-Curtis syndrome RUQ pain, pelvic adnexal tenderness, leukocytosis. Cervical smear shows gonococci. (gonococcal perihepatitis)
AST = aspartate aminotransferase; ALT = alanine aminotransferase; RUQ = right upper quadrant.
Table 2. Imaging Studies for Acute Cholecystitis Test Notes
Right upper quadrant US scan 81%-98% sensitive, 70%-98% specific. Sonographic Murphy's sign (showing maximal tenderness directly over the visualized gallbladder) is >90% predictive of acute cholecystitis.
HIDA scan 85%-97% sensitive, 90% specific.
CT scan Expensive; most useful to diagnose complications such as perforation, cholangitis, and gangrenous cholecystitis. MRI scan or MRCP scan 100% for cystic duct obstruction; 69% for gallbladder wall thickening; 93% for cystic duct obstruction; 83% for
gallbladder wall thickening. Extremely expensive; not universally available.
a cholecystectomy should follow up with their surgeons for eval- uation of post-operative complications such as biliary tract injury or infection. This is particularly important for patients who under- go surgery for cholecystitis because they have a higher rate of post- operative complications.
Book Enhancement
Go to www.acponline.org/essentials/gastroenterology-section .html to view an x-ray showing pneumobilia. In MKSAP for
Students 4, assess yourself with items 21-24 in the Gastro-
enterology and Hepatologysection.
Bibliography
Cohen SM, Kim AI, Faust TW.Acute Cholecystitis. http://pier.acponline .org/physicians/diseases/d642. [Date accessed: 2008 Jan 11] In: PIER [online database]. Philadelphia: American College of Physicians; 2008.
DiSario JA.Gallstones. http://pier.acponline.org/physicians/diseases/ d183. [Date accessed: 2008 Jan 11] In: PIER [online database]. Philadelphia: American College of Physicians; 2008.
Trowbridge RL, Rutkowski NK, Shojania KG. Does this patient have acute cholecystitis? JAMA. 2003;289:80-6. [PMID: 12503981] 66 • Gastroenterology and Hepatology
A
cute pancreatitis occurs when the pancreatic enzyme trypsinogen is prematurely activated to trypsin, which in turn activates pancreatic zymogens. The resulting pan- creatic autodigestion leads to an inflammatory response which causes further pancreatic damage. In severe cases, the inflamma- tion may progress to a systemic inflammatory response, resulting in multiorgan system failure and death. The most common eti- ologies of acute pancreatitis in the United States are biliary obstruction and alcohol. Pancreatitis may be caused by medica- tions such as sulfonamides, estrogens, valproic acid, thiazide diuretics, and furosemide. Other etiologies include familial pan- creatitis, hypertriglyceridemia, hypercalcemia, sphincter of Oddi dysfunction, biliary ductal obstruction, vasculitis, trauma, surgery, endoscopic retrograde cholangiopancreatography (ERCP), cystic fibrosis, and penetrating peptic ulcer. As much as 20% of acute pancreatitis is idiopathic. Mild pancreatitis is usually self-limited, but more severe disease causes significant morbidity and mortali- ty. Repeated episodes of acute pancreatitis may result in chronic pancreatitis and pancreatic endocrine and exocrine insufficiency.Prevention
The best preventive measures for pancreatitis involve avoiding known etiologic agents and medical or surgical management of other precipitating factors. Endoscopic retrograde cholan- giopancreatography is a well-established cause of acute pancre- atitis. Use of safer, non-invasive imaging such as magnetic reso- nance cholangiopancreatography (MRCP) decreases the risk of
procedure-related pancreatitis. However, MRCP cannot replace ERCP for therapeutic drainage of the biliary system.
Diagnosis
The most common symptom of acute pancreatitis is abdominal pain (Table 1). The pain may be epigastric or diffuse. It typically peaks in 30 minutes to a few hours, is moderate to severe, constant, and radiates to the back. The pain usually is not positional, although it may improve when sitting up or leaning forward. Nausea and vomiting are common; the pain of acute pancreatitis is usually not alleviated with vomiting.
Abdominal tenderness is common in pancreatitis, but peri- toneal signs should prompt a search for a perforated viscus. Diminished bowel sounds may point to an associated ileus. Some physical findings may suggest a specific etiology; jaundice suggests biliary obstruction, and eruptive xanthomas suggest hypertriglyc- eridemia. History and physical exam should also evaluate the pos- sibility of complications of acute pancreatitis. Nausea, vomiting, and anorexia frequently result in dehydration, hypotension, and tachycardia. High fever suggests infection. Large pseudocysts may be palpable and painful. Grey-Turner or Cullen’s signs (painless ecchymosis of the flanks and periumbilicus, respectively) suggest retroperitoneal bleeding.
The diagnosis of pancreatitis relies heavily on the serum amy- lase and lipase, which are elevated in 75%-90% of patients. Serum lipase is more specific and stays elevated longer than amy- lase. Leukocytosis and electrolyte abnormalities are common.