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Fluids & Electrolytes
As Mr. R, 66, is going about his daily activities, he experiences severe upper-abdominal pain. He describes the pain as a pressure that begins in the epigastrium and spreads in a bandlike distribution to the left and right upper quadrants, radiating to the upper back. It increases in intensity to 8 on a 0-to-10 scale over 1 to 2 hours. The pain is exacerbated by movement and associated with nausea, vomiting, chills, and rigors.
Mr. R is jaundiced and his urine is dark amber. His liver function tests (LFTs), including serum bilirubin levels, are markedly elevated.
Given Mr. R's history and signs and symptoms, his healthcare provider suspects a biliary obstruction: a blockage of the flow of bile from the liver to the small intestine.
A RELATIVELY COMMON disorder, biliary obstruction affects approximately 5 per 1,000 people.1 Jaundice (icterus) is a key sign of biliary obstruction. The word icterus derives from an ancient Greek word that also signified a yellow bird (see Recognizing the yellow bird of jaundice). This article describes the various possible causes of biliary obstruction, diagnostic studies and treatment options, and nursing considerations for patients with this disorder.
In biliary obstruction, the interruption of bile flow can occur at any level within the biliary system. (See How bile travels to the duodenum.) Bile, the liver's exocrine secretion, is produced continuously by liver cells (hepatocytes). It contains water, cholesterol, bile salts, which aid in the digestion of fats, and waste products such as bilirubin, which causes bile's familiar yellow-green color.
Bilirubin is formed by the breakdown of hemoglobin from red blood cells as they pass through the spleen. The process of bilirubin metabolism can be affected by an alteration in the steps involving uptake, storage, conjugation, and secretion.
Unconjugated bilirubin (UCB) is minimally soluble in water and is transported in blood attached to albumin, which limits renal excretion and diffusion into tissues. UCB is cleared from the bloodstream mainly by hepatocytes, which convert it to a water-soluble conjugated bilirubin (CB). This in turn is secreted into bile. The secreted CB travels in bile down the biliary tree to the intestine, where bacteria in both the small and large intestine hydrolyze the conjugates, yielding UCB again. Colonic anaerobes then reduce UCB to urobilinogens that are eliminated mainly in the feces.2
Bilirubin is normally absent in urine. But when excess CB is present in the blood, it can be secreted by the kidneys into urine, giving the urine a dark amber ("coca cola") color.
The normal serum total bilirubin concentration is less than 1 mg/dL. An accumulation of bilirubin in the bloodstream (hyperbilirubinemia) and subsequent deposition in the skin and sclerae causes jaundice (icterus). Scleral icterus is generally a more sensitive sign of hyperbilirubinemia than generalized jaundice. Jaundice is a term often used interchangeably with hyperbilirubinemia, which may not be clinically detected until bilirubin levels are at least 3 mg/dL.3
Mr. R undergoes further evaluation to determine the origin of his signs and symptoms.
Cholestasis, defined as obstruction of biliary flow, can be caused by mechanical factors, such as biliary strictures, or by metabolic factors such as hepatotoxicity due to certain medications, pregnancy, and sepsis (due to the effects of released cytokines). These processes can damage or impair hepatocyte function, resulting in hyperbilirubinemia (see Identifying causes of cholestasis).
Cholestasis can also have either intrahepatic or extrahepatic etiologies. Intrahepatic cholestasis generally occurs at the level of the hepatocyte or biliary canalicular membrane. The most common causes of intrahepatic cholestasis are hepatitis and cirrhosis.3
Hepatitis is an inflammation of the liver characterized by diffuse or patchy necrosis. Causes of hepatitis include viruses, drugs, and alcohol. Cirrhosis is characterized by generalized disorganization of hepatic architecture with nodule formation and scarring of the parenchyma. Cirrhosis results from chronic liver inflammation.2
Primary biliary cirrhosis (PBC), another possible cause of intra hepatic cholestasis, is a chronic, autoimmune, granulomatous destruction of the intrahepatic ducts.1 In contrast to patients with other types of liver disease, 95% of those with PBC are women. Most patients with PBC are asymptomatic in the early stages of disease; fatigue and pruritus are the most common presenting signs and symptoms at later stages.4
Extrahepatic cholestasis can be subdivided into those that are intraductal or extraductal. Intraductal causes include choledocholithiasis (gallstone in the common bile duct [CBD]), biliary strictures, primary sclerosing cholangitis (PSC), sphincter of Oddi dysfunction, and neoplasms such as cholangiocellular carcinoma. Extraductal obstruction caused by external compression of the biliary ducts may be secondary to neoplasms, such as pancreatic carcinoma, pancreatitis, or cystic duct stones with subsequent gallbladder distension.1
Stone disease is the most common cause of biliary obstruction. More than one million Americans are diagnosed with cholelithiasis (gallstones) every year.5 Many factors increase the risk of developing gallstones, including:
* advancing age
* gender; gallstones are more common in women5
* family history and genetics
* certain medications, such as estrogens
* diet, especially a diet low in fiber and high in saturated fats
* sedentary lifestyle.
Gallstones can become lodged in the CBD and cause complete obstruction, with increased intraductal pressure throughout the biliary tree. In Mirizzi syndrome, an impacted cystic duct stone causes inflammation and compression of the common hepatic duct and thus biliary obstruction.1 The vast majority of stones, however, are smaller than 1 cm and don't obstruct the ducts. (See Hard facts about gallstones.)
Other causes of intraductal cholestasis include:
* benign biliary strictures caused by surgical anastomosis, operative injury, or chronic pancreatitis.
* sphincter of Oddi dysfunction or dyskinesia.
* PSC, a chronic disorder of unknown etiology characterized by inflammation, fibrosis, and stricturing of ducts in the biliary tree.
* benign and malignant neoplasms.
Malignant or benign neoplasms can also cause external compression of the bile duct, resulting in obstruction. Causes of extraductal neoplastic obstruction include tumors arising locally from the gastrointestinal (GI) tract (such as pancreatic cancer) and metastatic cancers from outside the GI tract (such as breast cancer). Benign extraductal causes of biliary obstruction include acute and chronic pancreatitis.
A former kitchen cabinet salesperson, Mr. R has been unemployed for the past year and pays for his own insurance. He's proud to be with his wife of 42 years. He reports drinking alcohol infrequently (one to three beers a month) and denies any history of tobacco or illicit drug use. He has no family history of biliary tract disorders, liver disease, pancreatitis, pancreatic cancer, or inflammatory bowel disease, and he denies any significant medical or surgical history.
Mr. R's vital signs are: BP, 128/82; heart rate, 71; respiratory rate, 12; temperature, 97.4[degrees] F; weight, 176 lb (80 kg). His abdomen is soft, nontender, and nondistended with no masses and no hepatosplenomegaly. He's jaundiced with scleral icterus. No rash is noted.
The diagnostic approach to identifying biliary diseases begins with a careful history, physical assessment, and screening lab studies. When taking the patient's history and performing a physical exam, focus on gathering this information.1,6
* the presence or absence of pain, including the onset, duration, location, and characteristics of the pain
* unexplained weight loss
* systemic symptoms, such as anorexia and malaise, which may indicate viral hepatitis
* gallstone disease
* diarrhea of recent onset
* use of medications, including over-the-counter products and herbal and nutritional supplements
* alcohol use
* inherited disorders, including liver diseases and hemolytic disorders
* HIV status
* recent travel
* recent exposure to toxic substances
* acholic (pale) stools due to the lack of bilirubin in the intestinal tract
* GI bleeding
* dark amber urine
* ascites, which suggests cirrhosis
* fever (particularly when associated with chills or right upper quadrant pain, which suggests acute cholangitis)
* xanthomata (fatty deposits in the skin), a sign of PBC
* excoriations (from pruritus), which suggest prolonged cholestasis.
Mr. R's blood test results include an albumin of 3.2 (normal, 3.5 to 4.8 g/dL), total bilirubin 6.4 (normal, 0.3 to 1 mg/dL), conjugated (direct) bilirubin 3.5 (normal, 0 to 0.2 mg/dL), aspartate transaminase (AST) 128 (normal, 14 to 20 U/L), alanine aminotransferase (ALT) 403 (normal, 10 to 40 U/L), alkaline phosphatase (ALP) 269 (normal, 25 to 100 U/L), prothrombin time 14.2 (normal, 11 to 13 seconds), white blood cell count 11,000 cells/mm3 (normal, 4,500 to 10,500 cells/mm3), hematocrit 46% (normal, 42% to 52%), and platelets 222,000 cells/mm3 (normal, 140,000 to 400,000 cells/mm3).
Various LFTs reflect the liver's condition, the most common being serum transaminases ALT, AST, bilirubin, ALP, albumin, and prothrombin time. (See Matching assessment findings to a diagnosis.)
Regardless of the cause of cholestasis, serum bilirubin values are usually elevated and can't be relied upon to determine the obstruction's etiology. Blood levels of ALP rise due to increased synthesis of the enzyme induced by the biliary tract obstruction.7
The degree of serum transaminase elevation can occasionally help in differentiating between hepatocellular and cholestatic processes. While AST and ALT values less than eight times normal may be seen in either hepatocellular or cholestatic liver disease, values greater than 25 times normal primarily develop in hepatocellular diseases.8
Other blood tests, such as hepatitis serologies, may be indicated to differentiate viral from other causes of hepatitis.1
Mr. R undergoes multiple imaging studies. Transabdominal ultrasonography shows a normal gallbladder with no bile duct dilation. Magnetic resonance cholangiopancreatography reveals focal intrahepatic duct dilation in segments of both the right and left lobes of the liver.
Transabdominal ultrasonography (US) is the procedure of choice for the initial evaluation of cholestasis. It's the least expensive, safest, and most sensitive imaging study for visualizing the gallbladder. US can show cholelithiasis, but it's not as useful for CBD stones because bowel gas may obscure visualization.6
Endoscopic ultrasound (EUS) allows complete visualization of the biliary system, can detect small CBD stones, and is also highly accurate for detecting pancreatic tumors. EUS has been reported to have up to a 98% diagnostic accuracy in patients with obstructive biliary disease.1
A computed tomography (CT) scan is usually considered more accurate than US for helping determine the specific cause and level of obstruction. It also provides better visualization of liver structures. The use of contrast media helps define vascular structures and the pancreas.
Magnetic resonance cholangiopancreatography (MRCP) provides visualization and measurements of the bile and pancreatic ducts. MRCP provides a diagnostic cholangiogram in 90% to 100% of patients and reveals the level of obstruction in 80% to 100% of cases.1
Endoscopic retrograde cholangiopancreatography (ERCP) combines endoscopic and radiologic modalities to visualize both the biliary and pancreatic duct systems. It's considered the gold standard for imaging the biliary tree. It's also used therapeutically; some obstructions discovered during ECRP can be treated by performing a sphincterotomy, removing stones, and placing stents.
Mr. R and his wife listen intently as their healthcare provider discusses diagnostic and treatment strategies for his presumed biliary obstruction. After reviewing the risks and benefits with the healthcare provider, Mr. R agrees to pursue ERCP, which is performed in an outpatient setting. The procedure reveals segmental dilation, beading, and stricturing of the intrahepatic ducts consistent with PSC. The extrahepatic ducts are nondilated and nonstrictured but contain multiple fillingdefects consistent with stones. Endoscopic sphincterotomy (ES) and stone extraction is performed.
ES involves cutting the deep muscle layers of the sphincter of Oddi to facilitate stone extraction.9 Biliary obstruction secondary to bile duct strictures of pancreatic, biliary, or metastatic origin are treated by placing a plastic or metal stent within the bile duct to ensure patency and proper drainage of bile.
The need for surgical intervention depends on the cause of biliary obstruction. For example, cholecystectomy may be the treatment of choice in cases of symptomatic stone disease.
Liver transplantation is another treatment option in certain patients, such as those with PSC.
Patient teaching is essential to prepare the patient for ERCP. Following facility policy, instruct the patient to eat nothing after midnight on the day before the procedure. Assess the patient for allergies, a history of adverse reactions to iodinated contrast media, and for implanted medical devices that might be affected by the use of cautery. For women, a focused medical history includes pregnancy status. Perform medication reconciliation and assess for anticoagulant use.
Immediately before the procedure, obtain baseline vital signs and confirm that the patient has given informed consent and signed the consent form.
After the procedure, be prepared to prevent or recognize complications. The most common complications of ERCP with ES are pancreatitis (about a 5% risk), cholangitis, bleeding, and perforation.10 Monitor the patient for the following signs and symptoms:
* severe abdominal pain
* a firm, distended abdomen
* fever or chills
* difficulty swallowing (dysphagia)
* a crunching feeling under the skin (subcutaneous emphysema)
* melena or hematochezia.
Like other invasive procedures, endoscopic procedures also have the potential for sedation-related complications. However, with the judicious use of moderate sedation/analgesia and careful monitoring, the risk can be reduced significantly. These complications can range in severity from transient oxygen desaturation to life-threatening events such as respiratory arrest, cardiac dysrhythmias, and myocardial infarction. The patient should have continuous cardiac monitoring, with vital signs monitored every 5 minutes throughout the procedure.
Closely monitor the patient's level of consciousness and pulmonary status, including continuous SpO2 monitoring and/or capnography.
Mr. R's ERCP is successful. After recovering from the procedure and moderate sedation/analgesia, he's discharged home.
Before discharge, educate the patient about signs and symptoms to report immediately, such as severe abdominal pain, nausea, vomiting, chills or fever (which may indicate cholangitis), difficulty swallowing or neck stiffness, and signs of bleeding, such as vomiting blood or dark tarry stools. The patient should also be instructed to avoid alcohol and drugs that may interfere with normal coagulation, such as aspirin and ibuprofen, as instructed by the healthcare provider.11 Ensure that a responsible adult drives the patient home after discharge.
In addition, discharge planning includes educating the patient about the disease process, including risk factors, signs and symptoms of biliary obstruction, and prescribed management. For example, discuss recommended dietary changes and review medications to identify any that may increase the risk of cholestasis. Encourage the patient to lose weight if indicated, and explain how a sedentary lifestyle can increase risks.
Unlike the ancients, we don't have a "yellow bird" to cure our ailments. But with advancements in current diagnostic modalities and treatments, complications of biliary obstruction can be prevented.
Jaundice was recognized by ancient Greeks and Romans as a sign of disease. The word jaundice stems from the Latin word galbinus, which described a light greenish yellow color. Icterus is a Latinized form of the Greek word ikteros, which to the ancient Greeks signified both jaundice and a "yellow bird." The ancient treatment for jaundice included the use of yellow birds as a cure, as is described in Pliny the Elder's Naturalis Historia XXX:XXVII (written in AD 77): "There is a bird called jaundice from its color. If one with jaundice looks at it, they are cured of that complaint, and the bird dies."2
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Pfadt E, Carlson DS. Spotlight on sphincter of Oddi dysfunction. Nursing. 2011;41(8):42-45.
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