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Nursing2011 l Octoberwww.Nursing2011.com ANCC CONTACT HOURSAs 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 radiating to the upper back. It increases in intensity to 8 on Mr. R is jaundiced and his urine is dark amber. His liver function tests (LFTs), including serum bilirubin levels, are 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.(icterus) is a key sign of biliary obstruction. The word icterusderives 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.What can go wrong?In biliary obstruction, the interruption of bile flow can occur at any level within the biliary system. (See ) Bile, the liver’s exocrine secretion, By Habiba A. Habib, BSN, RN, and Michael Saunders, MD The yellow bird Recognizing biliary obstruction. P. MARAZZIHOTOESEARCHERS www.Nursing2011.com October l Nursing2011 of jaundice: Nursing2011 l Octoberwww.Nursing2011.comis produced continuously by liver water, cholesterol, bile salts, which waste products such as bilirubin, which causes bile’s familiar yellow-green color.Bilirubin is formed by the break-down of hemoglobin from red blood cells as they pass through the spleen. The process of bilirubin metabolism can be affected by an alteration in conjugation, and secretion.albumin, which limits renal excre-tion and diffusion into tissues. UCB is cleared from the bloodstream vert it to a water-soluble conju-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.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.bloodstream (hyperbilirubinemia) and subsequent deposition in the a more sensitive sign of hyperbiliru-Jaundice is a inter-detected until bilirubin levels are at Mr. R undergoes further evaluation to determine the origin of his signs and tion of biliary flow, can be caused by mechanical factors, such as biliary Recognizing “the yellow bird” of jaundiceJaundice was recognized by ancient Greeks and Romans as a sign of disease. The word jaundice stems from the Latin , which described a light greenish yellow colorwhich 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 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.” How bile travels to the duodenum(CBD). The remaining 50% is stored in the gallbladder. In response to a meal, this bile is released from the gallbladder via thcystic duct, which joins the common hepatic duct from the liver. The CBD courses through the head of the pancreas for approximately 2 cm before passing through the hepatopancreatic ampulla (ampulla of Vater) into the duodenum. DiaphragmLiverGallbladderCystic ductCommon bile ductHepatopancreaticampullaDuodenumHead of the pancreasPancreatic ductTail of thepancreasCommon hepatic ductSpleen www.Nursing2011.com October l Nursing2011strictures, or by metabolic factors medications, pregnancy, and sepsis (due to the effects of released cyto-kines). These processes can damage resulting in hyperbilirubinemia (see generally occurs at the level of the hepatocyte or biliary canalicular membrane. The most common causes of intrahepatic cholestasis are hepatitis and cirrhosis.the liver characterized by diffuse or patchy necrosis. Causes of hepatitis Cirrhosis is characterized by gener-alized disorganization of hepatic architecture with nodule formation and scarring of the parenchyma. Cirrhosis results from chronic liver Primary biliary cirrhosis (PBC), hepatic cholestasis, is a chronic, auto-destruction disease, 95% of those with PBC are women. Most patients with PBC are disease; fatigue and pruritus are the most common presenting signs and can be subdivided into those that are intra-ductal 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 neo-plasms, such as pancreatic carcinoma, pancreatitis, or cystic duct stones with Stone disease is the most common cause of biliary obstruction. More than one million Americans are diag-nosed with cholelithiasis (gallstones) every year. Many factors increase gender; gallstones are more com- family history and geneticsestrogens 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 inflammation and compression of the common hepatic duct and thus biliary obstruction. The vast majority of stones, however, are smaller than 1 cm and don’t obstruct the ducts. Hard facts about gallstones benign biliary strictures caused by surgical anastomosis, operative injury, or chronic pancreatitis. PSC, a chronic disorder of unknown tion, fibrosis, and stricturing of ducts in the biliary tree.also cause external compression of the bile duct, resulting in obstruc-locally from the gastrointestinal tract (such as pancreatic cancer) and metastatic cancers from outside the GI tract (such as breast cancer). ary obstruction include acute and chronic pancreatitis.Patient history and lab resultsA former kitchen cabinet salesperson, Mr. R has been unemployed for the past He’s proud to be with his wife of 42 years. He reports drinking alcohol infre-quently (one to three beers a month) and denies any history of tobacco or illicit Identifying causes of cholestasis primary sclerosing cholangitis infiltrative diseases, such as amyloidosis Scleral icterus is generally Nursing2011 l Octoberwww.Nursing2011.com Hard facts about gallstonesMore than 1 million Americans are diagnosed with gallstones (cholelithiasis) each year.lesterol gallstones in their composition and etiology. To form pigment gallstones, an excess of bilirubin in bile combines withother constituents, mainly calcium. These gallstones are black to dark brown and much harder than cholesterol gallstones.Most patients with gallstones are asymptoma

tic. When gallstones do cause problems, biliary pain (colic) is the most common Choledocholithiasis (stone in bile duct) occurs in 15% to 20% of patients with cholelithiasis. In addition, approximately 5% of Liver and gallbladderLiver(right lobe) Liver (left lobe)Gallbladder Gallstones inGallbladderGallstonesCystic duct www.Nursing2011.com October l Nursing2011drug use. He has no family history of bil-iary tract disorders, liver disease, pancre-atitis, pancreatic cancer, or inflammatory cant medical or surgical history.Mr. R’s vital signs are: BP, 128/82; heart rate, 71; respiratory rate, 12; temperature, 97.4° F; weight, 176 lb (80 kg). His abdomen is soft, nontender, no hepatosplenomegaly. He’s jaundiced with scleral icterus. No rash is noted.The diagnostic approach to identi-fying biliary diseases begins with a careful history, physical assessment, and screening lab studies. When tak-ing the patient’s history and perform-ing a physical exam, focus on gathering the presence or absence of pain, systemic symptoms, such as anorexia and malaise, which may indicate viral diarrhea of recent onset use of medications, including over-the-counter products and herbal and surgeries inherited disorders, including liver diseases and hemolytic disorders recent travel recent exposure to toxic substances ascites, which suggests cirrhosis excoriations (from pruritus), which suggest prolonged cholestasis.Review lab studies to check 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), aspar-tate transaminase (AST) 128 (normal, 14 to 20 U/L), alanine aminotransfer-ase (ALT) 403 (normal, 10 to 40 U/L), alkaline phosphatase (ALP) 269 (nor-mal, 25 to 100 U/L), prothrombin time 14.2 (normal, 11 to 13 seconds), (normal, 4,500 to 10,500 cells/mm), hematocrit 46% (normal, 42% to (normal, 140,000 to 400,000 cells/Various LFTs reflect the liver’s con-dition, the most common being serum transaminases ALT, AST, bilirubin, ALP, albumin, and prothrombin time. Regardless of the cause of cho-lestasis, 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 The degree of serum t

ransaminase differentiating between hepatocellu-lar and cholestatic processes. While AST and ALT values less than eight disease, values greater than 25 times tis serologies, may be indicated to differentiate viral from other causes Mr. R undergoes multiple imaging ies. Transabdominal ultrasonogra-phy shows a normal gallbladder with no bile duct dilation. Magnetic reso-nance cholangiopancreatography reveals focal intrahepatic duct dilation lobes of the liver. Matching assessment findings to a diagnosis Lab test/clinical findingIntrahepatic/hepato-�75% of patientsSerum bilirubin levelsIncreasedUsually 3x normal&#x-100;Usually 3x normal(ALT, AST)&#x-100;1,000 IUMildly elevated, 00 IU, The ancient treatment Nursing2011 l Octoberwww.Nursing2011.comTransabdominal ultrasonography is the procedure of choice for It’s the least expensive, safest, and visualizing the gallbladder. US can show cholelithiasis, but it’s not as gas may obscure visualization.biliary system, can detect small CBD detecting pancreatic tumors. EUS has been reported to have up to a 98% obstructive biliary disease.scan is usually considered more accurate than US for helping deter-obstruction. It also provides better visualization of liver structures. The vascular structures and the pancreas.Magnetic resonance cholangio-pancreatography (MRCP) provides visualization and measurements of the bile and pancreatic ducts. MRCP provides a diagnostic cholangiogram reveals the level of obstruction in Endoscopic retrograde cholangio-pancreatography (ERCP) combines endoscopic and radiologic modalities to visualize both the biliary and pan-creatic duct systems. It’s considered the gold standard for imaging the bil-iary tree. It’s also used therapeutically; some obstructions discovered during ECRP can be treated by performing a sphincterotomy, removing stones, Treatment optionsMr. 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 set-ting. 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 Endoscopic sphincterotomy (ES) and

stone extraction is performed. Biliary obstruction secondary to bile duct strictures of pancreatic, biliary, or metastatic origin are treated by plac-the bile duct to ensure patency and proper drainage of bile.The need for surgical interven-tectomy may be the treatment of treatment option in certain patients, Patient teaching is essential to pre-pare the patient for ERCP. Following facility policy, instruct the patient to eat nothing after midnight on the 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 medi-cal history includes pregnancy status. Perform medication reconciliation Immediately before the procedure, obtain baseline vital signs and confirm that the patient has given informed 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 Monitor the patient for severe abdominal pain difficulty swallowing (dysphagia)Like other invasive procedures, endoscopic procedures also have the potential for sedation-related complications. However, with the 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 myocar-dial infarction. The patient should have continuous cardiac monitor-with vital signs monitored every 5 minutes throughout the procedure.Closely monitor the patient’s level of consciousness and pulmonary sta-itoring and/or capnography.Mr. R’s ERCP is successful. After recov-ering from the procedure and moder-ate sedation/analgesia, he’s discharged 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), Educate the patient about www.Nursing2011.com October l Nursing2011difficulty swallowing or neck stiff-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 pro-vider.Ensure that a responsible adult d

rives the patient home after discharge.In addition, discharge planning the disease process, including risk ary obstruction, and prescribed recommended dietary changes and review medications to identify any that may increase the risk of cho-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. REFERENCES1. Bonheur JL, Ells, PF. Biliary obstruction. eMedi-cine Gastroenterology. 2009:1-20. http://emedicine.medscape.com/article/187001-overview.2. Ostrow J, Saunders M, Silverstein B. The Gut Course Syllabus, Human Biology 551. 41st ed. Univer-sity of Washington Division of Gastroenterology. 2010:112-171.3. Roy-Chowdhury N, Roy-Chowdhury J. Classifi-cation and causes of jaundice or asymptomatic hyperbilirubinemia. UpToDate. 2011:1-11. http://www.uptodate.com/patients/content/topic.do?topicKey=~OqyqJgCSG93Ec.4. Kaplan MM. Clinical manifestations, diagnosis, and natural history of primary biliary cirrhosis. UpToDate. 2010:1-12. http://www.uptodate.com/patients/content/topic.do?topicKey=~zgfICtNw8rsAg.5. Zakko SF. Patient information: Gallstones. UpToDate. 2010:1-6. http://www.uptodate.com/contents/patient-information-gallstones?source=search_result&selectedTitle=2~150.6. Roy-Chowdhury N, Roy-Chowdhury J. Diag-nostic approach to the patient with jaundice or asymptomatic hyperbilirubinemia. UpToDate2010:1-7. http://www.uptodate.com/patients/content/topic.do?topicKey=~Z_vlV7O4fQHgw.7. Kaplan MM. Enzymatic measures of cholestasis (eg, alkaline phosphatase, 5´-nucleotidase, gamma-glutamyl transpeptidase). UpToDate. 2011:1-12. http://www.uptodate.com/contents/enzymatic-measures-of-cholestasis-eg-alkaline-phosphatase-5-nucleotidase-gamma-glutamyl-transpeptidase.8. Kaplan MM. Approach to the patient with abnor-mal liver function tests. UpToDate. 2011:1-20.http://www.uptodate.com/patients/content/topic.do?topicKey=~d9TdAFObj4HGCV.9. Raijman I. Endoscopic management of bile duct stones: standard techniques and mechanical litho-tripsy. UpToDate. 2010:1-10. http://www.uptodate.com/patients/content/topic.do?topicKey=~mp5ZXedWCD6DPA.10. Carr-Locke D. Endoscopic retrograde cholangio-pancreatography (ERCP). AccessMedicine. 2010:1-6. http://www.accessmedicine.com.offcampus.lib.washi

ngton.edu/content.aspx?aID=6203895/.11. Bruesehoff MP. ERCP: much ado about block-ages. Nursing. 2010;40(9):46-50.12. Zakko S. Uncomplicated gallstone disease. UpToDate. 2010:1-16. http://www.uptodate.com/contents/uncomplicated-gallstone-disease?source=search_result&selectedTitle=2~150.RESOURCEPfadt E, Carlson DS. Spotlight on sphincter of Oddi dysfunction. Nursing. 2011;41(8):42-45.Habiba A. Habib is a staff nurse at the University of Washington Medical Center, Digestive Disease Center, Seattle, Wash. Michael Saunders is a Clinical Professor and Director of the Digestive Disease Center at the University of Washington Medical Center, Seattle, Wash.The authors have disclosed that they have no financial relationships relating to this article.DOI-10.1097/01.NURSE.0000405102.68864.c2INSTRUCTIONSThe yellow bird of jaundice: Recognizing biliary obstruction DISCOUNTS and CUSTOMER SERVICE Send two or more tests in any nursing journal published by Lippincott Williams & Wilkins  We also offer CE accounts for hospitals and other healthcare facilities on nursingcenter.1-800-787-8985 for details. journal, will award 2.3 contact hours Your certificate is valid in all states. The ANCC’s accreditation status of Lippincott Williams & Wilkins Department of Continuing Education refers only to its continuing nursing educational activities and does not imply TEST INSTRUCTIONS To take the test online, go to our secure website at http://www.nursingcenter.com/ce/nursing On the print form, record your answers in the test answer section of the CE enrollment form on page 36. Each question has only one correct answer. You may  Complete the registration information and course evaluation. Mail the completed form and registration fee of $21.95 to: Lippincott Williams & Wilkins, CE , 2710 Yorktowne Blvd., Brick, NJ 08723. We will mail your certificate in 4 to 6 weeks. For faster service, include a fax number and we will fax your certificate  You will receive your CE certificate of earned contact hours and an answer key to review your results. There is no minimum passing grade. Registration deadline is October 31, 2013. For more than 27 additional continuing education articles related to gastrointestinal topics, go to NursingCenter.com/CE Earn CE credit online: Go to http://www.nursingcenter.com/CE/nursing and receive a certificate within minute