Laparoscopic cholecystectomy is a minimally invasive surgical procedure for removal of a diseased gallbladder. This technique essentially has replaced the open technique for routine cholecystectomies since the early 1990s. At this time, laparoscopic cholecystectomy is indicated for the treatment of cholecystitis (acute/chronic), symptomatic cholelithiasis, biliary dyskinesia, acalculous cholecystitis, gallstone pancreatitis, and gallbladder masses/polyps. These indications are the same for an open cholecystectomy. Cases of gallbladder cancers are usually best treated with open cholecystectomy. Approximately 20 million people in the United States have gallstones. Of these people, there are approximately 300,000 cholecystectomies performed annually. Ten percent to 15% of the population has asymptomatic gallstones. Of these, 20% are symptomatic (biliary colic). Of the 20% who are symptomatic approximately 1% to 4% will manifest complications (acute cholecystitis, gallstone pancreatitis, choledocholithiasis, gallstone ileus). The incidence of gallstones increases with an increase in age, with females more likely to form gallstones than males. Age 50 to 65 approximately 20% of women and 5% of men have gallstones. Overall, 75% of gallstones are composed of cholesterol, and the other 25% are pigmented. Despite the composition of gallstones the clinical signs and symptoms are the same.
The gallbladder lives on the inferior aspect of the liver bed, more specifically under liver segments 4b and 5. The gallbladder can be up to 10 cm in length and physiologically can hold up to 50 cc of fluid (bile). A line from the gallbladder to the inferior vena cava separates the liver into right and left lobes. There are four anatomical sections to the gallbladder: fundus, body, infundibulum, and neck. There is great variation in the biliary ductal anatomy. The cystic duct most commonly arises from the common bile duct and inserts at the neck of the gallbladder. The branch point of the cystic duct from the common bile duct marks the beginning of the common hepatic duct superiorly. The blood supply to the gallbladder is from the cystic artery which originates approximately 90% of the time from the right hepatic artery. Again, there is great variation in the course and origin of the cystic artery. The hepatocystic triangle (triangle of Calot) is a surgical anatomical landmark created by the cystic duct laterally, the common hepatic duct medially, and the liver edge superiorly. This triangle is of surgical importance because this is the location for the most common path of the cystic artery to the gallbladder. There sentinel lymph node of the gallbladder resides within the hepatocystic triangle, also known as Lund's node (and erroneously referred to as the node of Calot).
Please note that although gallbladder cancer was once a contraindication to a laparoscopic cholecystectomy, the current literature supports laparoscopic intervention.
The patient should be medically optimized preoperatively.
Preoperative antibiotics should be given within 30 minutes of incision per protocol.
An aseptic surgical field is created from just above the bilateral costal margins to the pubic tubercle and laterally to the right and left flanks. The sterile surgical field should allow for the possibility of an open procedure if needed.
After induction of anesthesia and intubation, the laparoscopic cholecystectomy may begin.
First, insufflation of the abdomen is achieved to 15 mmHg using carbon dioxide. Next, four small incisions are made in the abdomen for trocar placement (supraumbilical x1, subxiphoid x1, and right subcostal x2). Utilizing a camera (laparoscope) and long instruments the gallbladder is retracted over the liver. This allows for exposure of the proposed region of the hepatocystic triangle. Careful dissection is carried out to achieve the critical view of safety. This view is defined as (1) clearance of fibrous and fatty tissue from the hepatocystic triangle, (2) the presence of only two tubular structures entering into the base of the gallbladder, and (3) the separation of the lower third of the gallbladder from the liver to visualize the cystic plate. Once this view is adequately achieved, the operating surgeon can proceed with confidence that he/she has isolated the cystic duct and cystic artery. Both structures are carefully clipped and transected. Electrocautery or harmonic scalpel is then used to separate the gallbladder from the liver bed completely. Hemostasis should be achieved after the abdomen is allowed to deflate to 8 mmHg for 2 minutes. This technique is employed to avoid missing potential venous bleeding that can be tamponaded by elevated intra-abdominal pressure (15 mmHg). The gallbladder is removed from the abdomen in a specimen pouch. All trocars should be removed under direct visualization. Closure of port sites is surgeon specific; this author recommends fascial closure of trocar sites greater than 5 mm to avoid incisional hernias in the postoperative period.
Common complications include but are not limited to bleeding, infection, and damage to surrounding structure. Bleeding is a common complication as the liver is a very vascular organ. Experienced surgeons must be knowledgeable in regards to anatomical anomalies of arteries to prevent potential significant blood loss. The most serious complication is an iatrogenic injury of the common bile/hepatic duct. Injury to either of these structures may require a further surgical procedure to divert the flow of bile into the intestines. This procedure usually requires a specially trained hepatobiliary surgeon.
Lastly, although not a complication, conversion to an open procedure has become a rare event as the experience of surgeons has increased over the years. Conversion to an open procedure creates a larger abdominal incision, causes significant pain control issues postoperatively, and leads to a cosmetically displeasing scar. Please note that conversion to an open procedure should not be viewed as a complication but seen as a well-educated decision made by an experienced surgeon to safely care for the patient.
The etiology of gallbladder disease is associated with a poorly functioning gallbladder and superconcentrated bile. Normally, the gallbladder empties its contents in response to physiologic changes associated with digestion (cholecystokinin, vagal input from antral distension, migrating myoelectric complex). High concentrations of cholesterol within the gallbladder is a known cause for precipitation of cholesterol gallstones. Pigmented stones precipitate typically from hemolytic diseases (black stones) or from infection (brown stones) where bacterial enzymes break down bilirubin into an insoluble content. Stasis within the gallbladder or bile ducts increases the likelihood of stone formation. Gallbladder disease is exemplified by obstruction of the cystic duct. Patients may experience acute obstruction of the cystic duct by stones, or occasionally, in most critically ill patients, there is acute acalculous cholecystitis, where there is no mechanical obstruction but a functional obstruction. This obstruction, mechanical or not, in conjunction with attempted bile excretion for digestion will cause acute inflammation of the gallbladder.
A classic finding for gallbladder disease is right upper quadrant or epigastric abdominal pain. The pain typically has an onset 30 minutes to two hours after consumption of fatty foods. The pain can last from one to two hours, up to more than 24 hours. Pain lasting more than 24 hours is associated with a secondary infection known as acute cholecystitis. Pain radiates from the right upper quadrant to the right flank, and occasionally to the right shoulder due to sympathetic innervation. Associated symptoms include but are not limited to nausea, vomit (bilious), fever, chills, and diarrhea. Less specific symptoms may be experienced like indigestion, GERD-like symptoms, PUD symptoms, and dyspepsia. Earlier in the disease process pain will be intermittent and associated with oral intake of fatty foods. As the process progresses, pain may become more frequent and occur regardless of oral intake.
Complete a thorough history and physical examination, including abdominal examination, and specifically check for a “Murphy’s Sign.”
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