- Etiology
- Pathogenesis
- Pathology
- Pathophysiology
- Epidemiology
- Management & Treatment
- Prevention
- Complications
- Prognosis
- Research Frontier
- Clinical Case Studies
- Study Questions
1. Gallstones for gallstone disease
2. Ischemia for acalcuous cholecystitis
Obstruction of the cystic duct by a gallstone leads to gallbladder distention, inflammation, and edema of the gallbladder wall.
In <1% of acute cholecystitis, the cause is a tumor obstructing the cystic duct.
Acute cholecystitis is caused by persistent obstruction of the cystic duct with stones resulting in gallbladder inflammation and pain.
It may be complicated with necrosis, infection, and gangrene.
The test of choice is a RUQ ultrasound. Cholescinitigraphy (HIDA scan) is useful when the pretest probability is high and ultrasound is nondiagnostic. Nonvisualization of the gallbladder suggests cystic duct obstruction and is highly specific for acute cholecystitis.
In acute cholecystitis, the gallbladder wall becomes grossly thickened and reddish with subserosal hemorrhages. Pericholecystic fluid often is present. The mucosa may show hyperemia and patchy necrosis. In severe cases, about 5% to 10%, the inflammatory process progresses and leads to ischemia and necrosis of the gallbladder wall. More frequently, the gallstone is dislodged and the inflammation resolves.
Initially, acute cholecystitis is an inflammatory process, probably mediated by the mucosal toxin lysolecithin, a product of lecithin, as well as bile salts and platelet-activating factor. An increase in prostaglandin synthesis amplifies the inflammatory response.
Complication of gallstone disease. In 90% of patients it is caused by a transient or permanent obstruction of the cystic duct by a stone. It represents an inflammatory response to mechanical, chemical, or bacterial causes. The increased intraluminal pressure and distention of the gallbladder result in ischemia of the mucosa and the wall of the gallbladder. Inflammatory agents, such as lysolecithin, and local tissue factors may be released.
Bacterial inflammation playing a role in 50–85% of patients with acute cholecystitis, in general, is a secondary event occurring late in the course. The organisms most frequently isolated by culture of gallbladder bile in these patients include Escherichia coli, Klebsiella, Streptococcus, and Clostridium species.
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1. Admit
2. No oral intake
3. Nasogastric suction
3. Treat hypovolemia from vomiting.
4. Correct of electrolyte disorders
4. Control of pain: nonsteroidal anti-inflammatory drugs (NSAIDs) or opioids (meperidine)
5. Empiric Antibiotics
| Dose | |
| Single-agent regimen | |
| Ertapenem | 1 g IV once daily |
| Piperacillin-tazobactam | 3.375 g IV every 6 hours |
| Combination regimen with metronidazole* | |
| ONE of the following: | |
| Cefazolin | 1 to 2 g IV every 8 hours |
| OR | |
| Cefuroxime | 1.5 g IV every 8 hours |
| OR | |
| Ceftriaxone | 2 g IV once daily |
| OR | |
| Cefotaxime | 2 g IV every 8 hours |
| OR | |
| Ciprofloxacin | 400 mg IV every 12 hours or 500 mg PO every 12 hours |
| OR | |
| Levofloxacin | 750 mg IV or PO once daily |
| PLUS: | |
| Metronidazole* | 500 mg IV or PO every 8 hours |
*For empiric therapy cover streptococci, Enterobacteriaceae, and anaerobes.
The antibiotic doses listed are for adult patients with normal renal function.
Administered prophylactically to protect against sepsis and wound infection [7].
Continue until the gallbladder is removed or the cholecystitis clinically resolves.
The chosen agent(s) covers the most common pathogens of the Enterobacteriaceae family, including gram-negative rods and anaerobes [6].
The most frequent isolates from the gallbladder or common bile duct were Escherichia coli (41 percent), Enterococcus (12 percent), Klebsiella (11 percent), and Enterobacter (9 percent).
5. Laparoscopic cholecystectomy
Optimal timing of surgery depends on patient stabilization and should be performed as soon as feasible.
The localized edema associated with acute cholecystitis aides with dissection of tissue planes and facilitates cholecystectomy.
Compared to delayed cholecystectomy (after 7 days of symptoms), this approach is associated with a decreased conversion rate to open operation (2% vs 30%) and decreased recovery time (12 vs 28 days).
Many patients present, however, outside the initial 72-hour window. Most current recommendations extend the period for safely performing laparoscopic cholecystectomy during acute cholecystitis to within one week of symptom onset. If outside of this 7-day window, many surgeons advocate a course of intravenous and (later) oral antibiotics with a plan to perform cholecystectomy in a delayed fashion at least 6 weeks later. This delay will allow the scarring in the right upper quadrant to subside, allowing for safer and easier dissection during laparoscopy.
If the patient has continued pain or recurrence of cholecystitis during this waiting period, laparoscopic cholecystectomy should be attempted immediately. The patient should be counseled on the high probability of conversion to an open operation.
Delayed surgery is reserved for pts with high risk of emergent surgery.
8. Percutaneous tube cholecystotomy
For patients who are not operative candidates, percutaneous tube cholecystotomy remains a viable option to drain the infected bile as a bridge to elective cholecystectomy when the patient has stabilized.
[Untreated cholecystitis can lead to gallbladder ischemia, necrosis, or perforation, resulting in biliary leak or fistula formation to the surrounding structures.
The potential for choledocholithiasis and common bile duct injury must be considered in patients presenting with jaundice after cholecystectomy.]
Empyema, hydrops, gangrene, perforation, fistulization, gallstone ileus, porcelain gallbladder.
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Question 1 of 1
A 42-year-old African-American man has been diagnosed with hypertension for the past 10 years and treated with medication. One morning, he is found unresponsive by his wife. He is taken to the emergency department and pronounced dead by the physician. An autopsy revealed cardiac hypertrophy and a narrowing of the aorta just distal to the ligamentum arteriosum, with dilation of the intercostal artery's ostia. How could the death have possibly been prevented?