Exploratory Laparotomy Case Study


If the affected part is cancerous, this surgery removesthe cancer and some of the surrounding tissue and lymphglands to help reduce the chance of a recurrence. Thesurgeon preserves the colon's tubelike shape, allowingwaste to pass through it easily, and retain normal bowelfunction.Some common colon problems include:


which are tissue growth in the colon linings. If caught early, they frequently are not cancerous, but asthey grow larger it becomes more likely they will becomecancerous. Thus, removing the polyp early may decreasethe risk of colon cancer.

Diverticulosis and Diverticulitis

are two other relatedcolon conditions. Diverticulosis occurs when smallpouches form on the lining of the colon. Diverticulitisoccurs when one of these pouches becomes infected andinflamed. In some cases, the pouch also may break.

Inflammatory bowel disease (IBD)

is a condition thatcauses swelling, inflammation, and sores in the digestivesystem. Patients with untreated IBD may be at higherrisk of colon cancer.

Overview & Description

An abdominal exploration, or laparotomy, is a surgicalprocedure that allows a surgeon to look inside theabdominal cavity.

Who is a candidate for the procedure?

An exploratory laparotomy is often done when a personcomplains of abdominal pain. It can also be performedafter an injury to the abdomen. The operation allows thesurgeon to examine internal organs. Disease or damage


The gold standard for making a diagnosis of BA is exploratory laparotomy with intraoperative cholangiogram, because sometimes even the histology on liver biopsy can be ambiguous. BA is the most common surgically correctable liver disorder in infancy (Sokol et al, 2003). Outcome after Kasai portoenterostomy is dependent on the timing of the procedure, with best results achieved earlier in the course of the disease. However, establishing a diagnosis early remains a challenge, because there are no convenient means of screening newborns. The American Academy of Pediatrics currently recommends that infants who are jaundiced at 3 weeks of age should have a measurement of total and conjugated bilirubin (Sokol et al, 2007). A conjugated bilirubin that is more than 20% of an elevated serum bilirubin is diagnostic of cholestasis and potentially serious liver disease. Asking about the color of stools and examining the color of a fresh specimen of stool is helpful in distinguishing between cholestasis (acholic, pale) and unconjugated hyperbilirubinemia (pigmented, green/yellow). In some countries, especially in Asia, a stool card is used to allow identification of acholic stools by parents to facilitate early diagnosis of BA (Hsiao et al, 2008).

Ultrasonography plays an important role in distinguishing BA from other causes of neonatal cholestasis. Using the gallbladder shape and wall structure sonography could identify BA with a sensitivity of 90% and specificity of 92.4% in 346 infants with conjugated hyperbilirubinemia (Farrant et al, 2000). Some find the triangular cord sign, which represents a cone-shaped fibrotic mass cranial to the bifurcation of the portal vein, very useful in the diagnosis of BA (Choi et al, 1996), but others are unable to detect it sonographically (Shneider et al, 2006a). Absence of the common bile duct can sometimes be defined on imaging, as can situs inversus and some of the other malformations associated with the fetal type and the BASM subgroup in BA. On T2-weighted MRI, moderately high signal intensity along the portal tract that extends from the porta hepatis correlated with periductal edema and inflammatory cell infiltration (Schneider et al, 2006). Although BA can be diagnosed on the basis of lack of visualization of either common bile duct or the common hepatic duct, findings on MRI should always be interpreted in conjunction with the clinical information.

Hepatobiliary scintigraphy is a noninvasive way for ruling out extrahepatic biliary atresia. Technetium-99m iminodiacetic acid derivatives are excreted from the blood by hepatocytes and excreted into the bowel through the biliary system. Infants characteristically need to be primed with phenobarbitone for 3 to 5 days before the test, because it increases bilirubin conjugation and has a choleretic effect. If there is excretion of labeled tracer in the intestine, then BA is ruled out. Conversely, if there is no excretion of tracer, then the diagnosis is not necessarily BA, but is also seen in severe neonatal hepatitis and interlobular bile duct paucity (Gilmour et al, 1997). The scintigraphy test is of value in infants in the intensive care unit who are of low birthweight or on oxygen where excretion of tracer in the gut rules out BA and allows the liver biopsy to be postponed/avoided. In the older infant above 6 to 7 weeks, the test may not be as useful, because it causes delay by a week, given the need for phenobarbitone priming and the fact that a definitive diagnosis is not possible without a liver biopsy with or without an intraoperative cholangiogram. Some have used scintigraphy in combination with serum γ-glutamyl transpeptidase levels (Arora et al, 2001; Stipsanelli et al, 2007), and others have primed with ursodeoxycholic acid in an effort to improve sensitivity of the test (Poddar et al, 2004). Duodenal fluid may be obtained to assess the bilirubin content, and if fluid is bile stained, then BA is ruled out. Endoscopic retrograde cholangiopancreatography permits visualization of the biliary tree in young infants, but is technically challenging in the newborn (Guelrud et al, 1991).

Liver biopsy is an essential tool in the evaluation of an infant with conjugated hyperbilirubinemia and should be performed preferably before 8 weeks of age. The histologic features of BA (Figure 74-1) include cholestasis, periportal ductular proliferation, and the presence of bile plugs in cholangioles and interlobular bile ducts (Ishak and Sharp, 2002). These findings are highly suggestive of biliary obstruction, but bile ductular proliferation can also be seen in α1-antitrypsin deficiency. Giant-cell transformation is seen in 15% of cases. Fibrosis is progressive with eventual development of biliary cirrhosis (Lefkowitch et al, 1998).

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