Colicky pain typically waxes and wanes, with periods of intense pain (such as from a ureter intermittently contracting in the presence of a stone) followed by relief. The pain from gallstones is constant, may last from minutes to hours, and then dissipates. A better term is symptomatic cholelithiasis.

Female gender, pregnancy, oral contraceptive use (excess estrogen leads to higher cholesterol in bile and decreased gallbladder motility) as opposed to obesity (decreases bile salts), high-fat diet (increases bile cholesterol), hereditary (higher incidence in Hispanics, Pima Indians), Crohn’s disease and terminal ileal resection (loss of bile salts), and rapid weight loss after gastric surgery (impaired gallbladder emptying).

Symptomatic cholelithiasis is usually managed as an outpatient, with eventual elective laparoscopic cholecystectomy. Acute cholecystitis requires hospital admission, intravenous (IV) antibiotics, and urgent cholecystectomy.

An urgent case can be booked during the next available operating room (OR) time slot, while an emergent case requires a patient to be rushed to the OR immediately.

It suggests a biliary origin of the pain. Fatty food ingestion triggers the release of cholecystokinin, which leads to contraction of the gallbladder. Gallstones may obstruct the cystic duct so that the gallbladder is unable to empty bile as it attempts to contract after fatty food ingestion. The ensuing distention of the gallbladder stretches the visceral peritoneum that surrounds it, leading to RUQ and/or epigastric pain that is vague and mild to moderate in severity (symptomatic cholelithiasis).

The gallbladder and the scapula share the same cutaneous dermatome from the same spinal cord levels. The scapula receives cutaneous innervation from the supraclavicular nerves. Since the same spinothalamic pathways (pain and temperature) are activated, gallbladder distention/inflammation triggers scapular pain via the phrenic nerve.

This physical examination finding is called Murphy’s sign and is thought to be specific to acute cholecystitis. It represents focal peritonitis of the anterior abdominal wall parietal peritoneum due to inflammation of the adjacent gallbladder. When the patient inspires, the diaphragm moves caudad, as does the gallbladder. Palpating deep in the RUQ causes the gallbladder to then come into contact with the parietal peritoneum, further irritating the inflamed parietal peritoneum and causing cessation of inspiration secondary to pain.

Somatic pain is well localized and typically secondary to peritoneal irritation. Patients can often point to where it hurts. In contrast, visceral pain is more difficult to localize and results from mechanical stretching of the abdominal (visceral) organs.

The presence of systemic signs of infection, such as fever and tachycardia, suggests a more severe biliary disease such as acute cholecystitis or acute cholangitis. Symptomatic cholelithiasis (biliary colic) does not present with systemic symptoms.

Recurrent bouts of symptomatic cholelithiasis often lead to chronic inflammation of the gallbladder with fibrotic changes seen on histologic examination. As such, biliary colic, symptomatic cholelithiasis, and chronic cholecystitis are interchangeable terms.

Acute cholecystitis is caused by sustained obstruction (impaction) of the cystic duct, most often by a gallstone. This obstruction leads to inflammation and edema of the gallbladder wall and then eventually bacterial overgrowth and invasion of the gallbladder wall. This can progress to ischemia and necrosis (gangrenous cholecystitis) and rarely gallbladder perforation.

The most common organisms found in biliary cultures from patients with acute cholecystitis are Escherichia coli, Bacteroides fragilis, Klebsiella, Enterobacter, Enterococcus, and Pseudomonas species.

The three main components of bile are bile salts, cholesterol, and lecithin (a phospholipid). Bile also contains water, electrolytes, proteins, and bile pigments.

The two main types of gallstones are cholesterol (70–80 % of gallstones in the USA) and pigment.

Cholesterol gallstones form when the concentration of cholesterol in the bile exceeds its solubility, which causes precipitation of cholesterol crystals. The solubility of cholesterol is dependent on the concentration of cholesterol, bile salts, and lecithin in the bile. Lower concentrations of bile salts or lecithin favor precipitation of cholesterol, as does high levels of cholesterol.

These stones comprise the remaining 20–30 % of gallstones seen in the USA. Pigmented stones are classified as black or brown and contain less than 30 % cholesterol. The dark coloration is a result of the presence of calcium bilirubinate within the stones. Black stones are often associated with hemolytic disease such as hereditary spherocytosis or sickle cell disease. As a result of the breakdown of red blood cells, the amount of unconjugated bilirubin increases, leading to the formation of black stones. Black stones are most often found within the gallbladder. Brown stones, in comparison, most often form within the bile ducts. They are larger and softer than black stones and usually are associated with bacterial infection and parasites. They are more common in Asian countries.