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Cholecystitis & biliary colic chap. 85 tintinalli’s emergency medicine robert moosally, do. 4 major biliary tract emergencies: Biliary colic (symptomatic cholelithiasis) Cholecystitis Gallstone pancreatitis Ascending cholangitis 4 “F’s” (the classical presenting pt) Female Forty Fat
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Cholecystitis & biliary colicchap. 85tintinalli’s emergency medicinerobert moosally, do
4 major biliary tract emergencies: • Biliary colic (symptomatic cholelithiasis) • Cholecystitis • Gallstone pancreatitis • Ascending cholangitis • 4 “F’s” (the classical presenting pt) • Female • Forty • Fat • Flatulence
specific presentations • Kids: infrequent; gallstones may be idiopathic or due to hemolytic disorders, cystic fibrosis, obesity, ileal resection or long-term TPN • Pregnancy: increase of GB sludge/gallstones, predisposes cholelithiasis but rarely cholecystitis • Elderly: more likely to present with biliary sepsis/GB gangrene; increased perioperative mortality (19%)
risk factors • Table 85-1 (tintinalli’s) • Familial tendencies • Asian descent (pigmented stones) • Chronic biliary tract infection • Parasitic infection • Chronic liver dz (esp. alcoholics) • Chronic intravascular hemolysis (SCA)
pathophysiology • Bile is made and secreted by hepatocytes; stored in GB • Wall of GB innervated with sympathetic & parasympathetic nerves from celiac plexus
Bile • Water (80%) • Bile acids (10%) • Lecithin & other phospholipids (4-5%) • Cholesterol (1%) • Conjugated bilirubin • Electrolytes • Mucous • Various proteins • Cholecystokinin (CCK) is stimulus for release of bile into small intestine
types of gallstones • Cholesterol (70%) • Radiolucent (calcium content lower here) • Pigment (20%) • Black (pts w/ adv. liver dz & hemolytic d/o) • Brown (pts of Asian descent, bacterial/parasitic infection) • Radiopaque (more calcium here) • Mixed (10%)
clinical features of biliary colic • RUQ pain (w/w/out gallstones) • Upper abd/epigastric pain • Radiation of pain to left upper back • Pain persisting 2-6 hrs. • Not colicky • Episodes infrequent • Up to 1/3 of pts will have sxs NOT related to food/meal time
Clinical features of acute cholecystitis • Pain persisting > 6 hours • Nausea & vomiting, anorexia • Fever +/- chills • Hx of similar attacks/documented gallstones • Pain becomes more localized to RUQ • Murphy’s sign (est. at 97% sensitive for a.c.) • Signs of systemic toxicity, dehydration • Localized peritoneal toxicity, distention • Hypoactive bowel sounds
Clinical features of acalculous cholecystitis • 5-10% of pts with acute cholecystitis • More rapid, malignant course • Elderly • Hx of DM • Multiple trauma, burns, prolonged labor, major surgery, GB torsion, systemic vasculitic states, bacterial/parasitic infxn. • Frequently occurs as a result of another process going on and these pts are SICK!!!!!!
differential diagnosis • Gastritis • GERD • Pancreatitis • Hepatitis • PUD • Atypical MI • Renal colic • Pyelonephritis • Appendicitis • PID/Fitzhugh-Curtis Syndrome/Ectopic • Pneumonia/pleural effusion
diagnosis • High clinical suspicion • US (modality of choice); CT not as sensitive • Labs will most likely be normal • CBC, CMP normal range • Lipase to r/o pancreatitis • Urine to r/o pyelo, uti, ectopic, kidney stones • Plain films (esp. CXR to r/o pneumonia) • EKG to r/o AMI; ACS • HIDA (sens. of 97% and spec. of 90%)
complications • Mallory-Weiss tears • Fluid & electrolyte abnormalities • Gallstone pancreatitis • Ascending cholangitis (mortality can reach 100% if no tx or improper tx) • Cholecystitis leading to GB empyema • Emphysematous (gangrenous) cholecystitis
Treatment & disposition • Table 85-3 (tintinalli’s) • If pt presents in shock, then IV fluids +/- vasopressors, broad spectrum axbx & surgery to decompress biliary tree • GB empyema develop gm neg. sepsis • Broad spectrum axbx, fluids, stat surgery • Gangrene of GB (segmental ischemia of GB wall) – risk of perforation -> surgery • Emphysematous cholecystitis (gangrene of entire GB); pts are in septic shock
Contrast CT scan showing emphysematous cholecystitis with gallbladder wall disruption (arrow), gas formation (arrowhead), and a biloma Contrast CT scan showing gallstones (arrow) with gallbladder rupture and fluid localized at the gallbladder fossa (arrowhead)
A false-positive case, with poor enhancement of the mucosa of the ventral portion of the gallbladder and suspected gallbladder disruption. Gallstones with acute cholecystitis and gallbladder wall gangrene (arrow) were found during surgery. No disruption of the gallbladder wall was noted. A false-positive case: gallbladder rupture with liver penetration suspected before surgery. Actually, only chronic cholecystitis and a separated liver abscess (arrow) were found during surgery.
Abdominal radiograph of acalculous emphysematous cholecystitis demonstrating curvilinear air pattern conforming to the shape of the gallbladder wall CT images of emphysematous cholecystitis - same patient
Ultrasound findings of acalculous cholecystitis include marked gallbladder wall thickening and pericholecystic fluid. Transverse ultrasound demonstrates marked gallbladder wall thickening and pericholecystic fluid collection in a patient with AIDS who was managed conservatively
How would you like to stick the US probe on a pt and see HIM waving back at you!!! Ascaris lumbricoides of the GB
treatment & disposition cont. • Antispasmodic agents (glycopyrrolate) • Opiate analgesics (meperidine) • Antiemetics (promethazine) • NSAIDS (ketorolac) • NGT (if protracted vomiting) • IVF’s (once hydrated, can try PO fluids) • If stable and pain controlled, can arrange for outpt. surgical follow-up