CITU MS2 Liver, Gallbladder, Pancreas Disorders PDF

HEPATO PANCREATO BILIARY DISORDERS Learning Objectives General Objective: After 16 hours of varied teaching – learning activities, the BSN 3 students will be able to acquire essential knowledge, demonstrate vital skills and develop deeper appreciation in the care of patients with Hepatobiliary...

HEPATO PANCREATO BILIARY DISORDERS Learning Objectives General Objective: After 16 hours of varied teaching – learning activities, the BSN 3 students will be able to acquire essential knowledge, demonstrate vital skills and develop deeper appreciation in the care of patients with Hepatobiliary and Gastrointestinal Disorders. 1. Review the ANATOMY AND PHYSIOLOGY of the liver, gallbladder and pancreas (hepatobiliary system) 2. Describe and define cholecystitis in terms of its manifestations, and types. 3. Define and describe cholelithiasis. 4. Enumerate the risk factors for cholelithiasis. 5. Illustrate the pathophysiology of cholelithiasis. 6. Analyze the clinical manifestations of the disease process. 7. Compare the different assessment and diagnostic procedures and findings of cholelithiasis. 8. Explain the Medical and Surgical Management of cholelithiasis. 9. Develop a plan of care for patients with cholelithiasis. 10. Appreciate the important role of the nurse in the care of patients with cholecystitis and cholelithiasis.  Review of ANATOMY & PHYSIOLOGY The LIVER Largest gland of the body, can be considered a chemical factory that manufactures, stores, alters, and excretes a large number of substances involved in metabolism. Anatomy of the Liver Anatomy of the Liver o a large, highly vascular organ located behind the ribs in the upper right portion of the abdominal cavity. o It weighs between 1200 and 1500g and is divided into four lobes (right, left, caudate, and quadrate). Anatomy of the Liver o 80% of the blood supply comes from the portal vein, which drains the GI tract and is rich in nutrients but lacks oxygen. o The remainder of the blood supply enters by way of the hepatic artery and is rich in oxygen. Anatomy of the Liver o Terminal branches of these two blood vessels join to form common capillary beds, which constitute the sinusoids of the liver. o The sinusoids empty into venules that occupy the center of each liver lobule and are called the central veins. The central veins join to form the hepatic vein, which constitutes the venous drainage from the liver and empties into the inferior vena cava. Anatomy of the Liver o In addition to hepatocytes, phagocytic cells belonging to the reticuloendothelial system are present in the liver. o In the liver, these cells are called Kupffer cells. As the most common phagocyte in the human body, their main function is to engulf particulate matter (eg, bacteria) that enters the liver through the portal blood. Anatomy of the Liver o The smallest bile ducts, called canaliculi, are located between the lobules of the liver. The canaliculi receive secretions from the hepatocytes and carry them to larger bile ducts, which eventually form the hepatic duct. o The hepatic duct from the liver and the cystic duct from the gallbladder join to form the common bile duct, which empties into the small intestine. The sphincter of Oddi, located at the junction where the common bile duct enters the duodenum, controls the flow of bile into the intestine. Physiology of the Liver glucose is taken up from the portal venous blood by the liver and converted into glycogen, which is stored in the hepatocytes. Subsequently, the glycogen is converted back to glucose (glycogenolysis) and released as needed into the bloodstream to maintain normal levels of blood glucose. Additional glucose can be synthesized by the liver through a process called gluconeogenesis. For this process, the liver uses amino acids from protein breakdown or lactate produced by exercising muscles. This process occurs in response to hypoglycemia Physiology of the Liver Use of amino acids from protein for gluconeogenesis results in the formation of ammonia as a byproduct. The liver converts this metabolically generated ammonia into urea. Ammonia produced by bacteria in the intestines is also removed from portal blood for urea synthesis. In this way, the liver converts ammonia, a potential toxin, into urea, a compound that is excreted in the urine Physiology of the Liver The liver also plays an important role in protein metabolism. It synthesizes almost all of the plasma proteins (except gamma-globulin), including albumin, alpha-globulins and beta-globulins, blood clotting factors, specific transport proteins, and most of the plasma lipoproteins. Vitamin K is required by the liver for synthesis of prothrombin and some of the other clotting factors. Amino acids are used by the liver for protein synthesis Physiology of the Liver Fatty acids can be broken down INTO ketone bodies (acetoacetic acid, beta-hydroxybutyric acid, and acetone) which can be used by muscles as sources of energy when glucose metabolism is limited or unavailable. Fatty acids and their metabolic products are also used for the synthesis of cholesterol, lecithin, lipoproteins, and other complex lipids Physiology of the Liver Vitamins A, B, and D and several of the B- complex vitamins are stored in large amounts in the liver. Certain substances, such as iron and copper, are also stored in the liver. Physiology of the Liver Bile is continuously formed by the hepatocytes and collected in the canaliculi and bile ducts. It is composed mainly of water and electrolytes such as sodium, potassium, calcium, chloride, and bicarbonate, and it also contains significant amounts of lecithin, fatty acids, cholesterol, bilirubin, and bile salts. Physiology of the Liver Bilirubin is a pigment derived from the breakdown of hemoglobin by cells of the reticuloendothelial system, including the Kupffer cells of the liver. Hepatocytes remove bilirubin from the blood and chemically modify it through conjugation to glucuronic acid, which makes the bilirubin more soluble in aqueous solutions. The conjugated bilirubin is secreted by the hepatocytes into the adjacent bile canaliculi and is eventually carried in the bile into the duodenum. In the small intestine, bilirubin is converted into urobilinogen, which is partially excreted in the feces and partially absorbed through the intestinal mucosa into the portal blood. Much of this reabsorbed urobilinogen is removed by the hepatocytes and secreted into the bile once again (enterohepatic circulation). Some of the urobilinogen enters the systemic circulation and is excreted by the kidneys in the urine. Elimination of bilirubin in the bile represents the major route of its excretion. Physiology of the Liver The liver metabolizes many medications, such as barbiturates, opioids, sedatives, anesthetics, and amphetamines. Metabolism generally results in drug inactivation, although activation may also occur. One of the important pathways for medication metabolism involves conjugation (binding) of the medication with a variety of compounds, such as glucuronic acid or acetic acid, to form more soluble substances. These substances may be excreted in the feces or urine, similar to bilirubin excretion. Bioavailability is the fraction of the administered medication that actually reaches the systemic circulation. The bioavailability of an oral medication (absorbed from the GI tract) can be decreased if the medication is metabolized to a great extent by the liver before it reaches the systemic circulation; this is known as first-pass effect. Some medications have such a large first-pass effect that their use is essentially limited to the parenteral route, or oral doses must be substantially larger than parenteral doses to achieve the same effect. The GALLBLADDER Pear-shaped, hollow, saclike organ located at the inferior surface of the liver. Anatomy of the Gallbladder pear-shaped, hollow, saclike organ, 7.5 to 10 cm (3 to 4 in) long, lies in a shallow depression on the inferior surface of the liver, to which it is attached by loose connective tissue. The capacity of the gallbladder is 30 to 50 mL of bile. Its wall is composed largely of smooth muscle. Physiology of the Gallbladder Storage depot for bile. Between meals, when the sphincter of Oddi is closed, bile produced by the hepatocytes enters the gallbladder. During storage, a large portion of the water in bile is absorbed through the walls of the gallbladder, so that bile in the gallbladder is five to 10 times more concentrated than that originally secreted by the liver. When food enters the duodenum, the gallbladder contracts and the sphincter of Oddi (located at the junction of the common bile duct with the duodenum) Relaxes. Relaxation of this sphincter allows the bile to enter the intestine. This response is mediated by secretion of the hormone cholecystokinin- pancreozymin (CCK-PZ) from the intestinal wall. The PANCREAS The pancreas is a vital organ located in the abdomen, playing a crucial role in both the digestive and endocrine systems. Anatomy of the Pancreas  Anatomy of the Pancreas o Location: The pancreas is situated in the upper abdomen, behind the stomach and in front of the spine. It lies across the back of the abdomen, extending horizontally from the right side to the left side. o Shape and Size: It is elongated, somewhat flat, and resembles a tadpole, with a length of about 15-20 cm (6-8 inches). The pancreas is divided into four main parts: the head, neck, body, and tail.  Anatomy of the Pancreas Duct System o Main Pancreatic Duct (Duct of Wirsung): This duct runs the length of the pancreas, collecting digestive enzymes produced by the exocrine cells. It merges with the common bile duct near the head of the pancreas before emptying into the duodenum at the ampulla of Vater. o Accessory Pancreatic Duct (Duct of Santorini): A secondary duct that may be present and drains into the duodenum above the main pancreatic duct. Anatomy of the Pancreas Exocrine Tissue: o Composed of acinar cells, this tissue produces digestive enzymes (amylase, lipase, proteases) that are secreted into the pancreatic duct system. o The acinus is the functional unit, where enzyme production occurs. Endocrine Tissue (Islets of Langerhans): o Scattered throughout the pancreas, these clusters of cells produce important hormones, such as insulin, glucagon, somatostatin, and pancreatic polypeptide, which are released directly into the bloodstream. o The islets contain several types of cells: o Alpha cells: Produce glucagon. o Beta cells: Produce insulin. o Delta cells: Produce somatostatin. o PP cells: Produce pancreatic polypeptide. Physiology of the Pancreas The Exocrine Pancreas The secretions of the exocrine portion of the pancreas are collected in the pancreatic duct, which joins the common bile duct and enters the duodenum at the ampulla of Vater. The secretions of the exocrine pancreas are digestive enzymes high in protein content and an electrolyte-rich fluid. The secretions, which are very alkaline because of their high concentration of sodium bicarbonate, are capable of neutralizing the highly acid gastric juice that enters the duodenum. Pancreatic enzyme secretion is normally 1500 to 2500 mL/day. The enzyme secretions include amylase, which aids in the digestion of carbohydrates; trypsin, which aids in the digestion of proteins; and lipase, which aids in the digestion of fats. Other enzymes that promote the breakdown of more complex foodstuffs are also secreted. Hormones originating in the GI tract stimulate the secretion of these exocrine pancreatic juices. The hormone secretin is the major stimulus for increased bicarbonate secretion from the pancreas, and the major stimulus for digestive enzyme secretion is the hormone CCK-PZ. The vagus nerve also influences exocrine pancreatic secretion. Physiology of the Pancreas The Endocrine Pancreas Insulin A major action of insulin is to lower blood glucose by permitting entry of glucose into the cells of the liver, muscle, and other tissues, where it is either stored as glycogen or used for energy. Insulin also promotes the storage of fat in adipose tissue and the synthesis of proteins in various body tissues. In the absence of insulin, glucose cannot enter the cells and is excreted in the urine. Glucagon The effect of glucagon (opposite to that of insulin) is chiefly to raise the blood glucose by converting glycogen to glucose in the liver. Glucagon is secreted by the pancreas in response to a decrease in the level of blood glucose. Somatostatin Somatostatin exerts a hypoglycemic effect by interfering with release of growth hormone from the pituitary and glucagon from the pancreas. Physiology of the Pancreas Endocrine Control of Carbohydrate Metabolism Glucose required for energy is derived by metabolism of ingested carbohydrates and also from proteins by the process of gluconeogenesis. Glucose can be stored temporarily in the form of glycogen in the liver, muscles, and other tissues. The endocrine system controls the level of blood glucose by regulating the rate at which glucose is synthesized, stored, and moved to and from the bloodstream. Through the action of hormones, blood glucose is normally maintained at less than 100 mg/dL (5.5 mmol/L). Insulin is the primary hormone that lowers the blood glucose level. Hormones that raise the blood glucose level are glucagon, epinephrine, adrenocorticosteroids, growth hormone, and thyroid hormone.  BILIARY DISORDERS CHOLECYSTITIS acute inflammation of the gallbladder. causes pain, tenderness, and rigidity of the upper right abdomen that may radiate to the midsternal area or right shoulder and is associated with nausea, vomiting, and the usual signs of an acute inflammation. An empyema of the gallbladder develops if the gallbladder becomes filled with purulent fluid (pus). Calculous Cholecystitis cause of more than 90% of cases of acute cholecystitis. In calculous cholecystitis, a gallbladder stone obstructs bile outflow. Bile remaining in the gallbladder initiates a chemical reaction; autolysis and edema occur; and the blood vessels in the gallbladder are compressed, compromising its vascular supply. Gangrene of the gallbladder with perforation may result. Bacteria play a minor role in acute cholecystitis; however, secondary infection of bile occurs in approximately 50% of cases. The organisms involved are generally enteric (normally live in the GI tract) and include Escherichia coli, Klebsiella species, and Streptococcus. Bacterial contamination is not believed to stimulate the actual onset of acute cholecystitis. Acalculous Cholecystitis acute gallbladder inflammation in the absence of obstruction by gallstones. Usually occur after major surgical procedures, severe trauma, or burns. Other factors associated with this type of cholecystitis include torsion, cystic duct obstruction, primary bacterial infections of the gallbladder, and multiple blood transfusions. It is speculated that acalculous cholecystitis is caused by alterations in fluids and electrolytes and alterations in regional blood flow in the visceral circulation. Bile stasis (lack of gallbladder contraction) and increased viscosity of the bile are also thought to play a role. CHOLELITHIASIS Calculi, or gallstones, usually form in the gallbladder from the solid constituents of bile; they vary greatly in size, shape, and composition. They are uncommon in children and young adults but become more prevalent with increasing age, affecting 30% to 40% of people by the age of 80 years. RISK FACTORS OTHER RISK FACTORS Frequent changes in weight Ileal resection or disease Rapid weight loss (leads to Cystic fibrosis rapid development of Diabetes mellitus gallstones and high risk of symptomatic disease) Treatment with high-dose estrogen OR EVEN low- dose estrogen Clofibrate  2 Major Types Pigment Stones Cholesterol Stones ▪ Formed when unconjugated ▪ account for most of the remaining pigments in the bile precipitate to 75% of cases of gallbladder disease. form stones. ▪ Decreased bile acid synthesis and ▪ about 10% to 25% of cases. increased cholesterol synthesis in the ▪ increased risk in patients with liver result in bile supersaturated with cirrhosis, hemolysis, and infections of cholesterol, which precipitates out of the biliary tract. the bile to form stones.  Cause: UNCONJUGATED BILIRUBIN PIGMENT STONES Bilirubin Breakdown product of Hgb Normally CONJUGATED (bilirubin + glucuronic acid) Conjugated bilirubin is water soluble and excreted in the bile BUT some remains unattached to C6H10O7 RISKS HEMOLYSIS (sickle cell disease / hereditary UNCONJUGATED Bilirubin spherocytosis) – increased Hgb destruction Bacterial Infections in the Bile Ducts – can Increased concentration binds to Ca ions to form deconjugate bilirubin leading to increase in calcium bilirubinate (is poorly soluble and tends to unconjugated bilirubin precipitate out). CIRRHOSIS – impairs normal bilirubin conjugation Leads to the formation of pigment stones. PIGMENT STONES classified into: black pigment stones (primarily seen in conditions like hemolysis or cirrhosis) and brown pigment stones (more common in bile duct infections and associated with bacterial activity). ▪ Both types are formed from the precipitation of unconjugated bilirubin. ▪ Pigment stones cannot be dissolved and must be removed surgically.  Cause: CHOLESTEROL CHOLESTEROL STONES Normal constituent of the Bile BUT is INSOLUBLE in water Its solubility depends on BILE ACIDS and lecithin (phospholipids) in bile: Cholic Acid: One of the main primary bile acids synthesized in the liver from cholesterol. It helps emulsify fats and aids in the absorption of fat-soluble vitamins, contributing to keeping cholesterol dissolved in bile. Chenodeoxycholic Acid (CDCA): Another primary bile acid that is critical in reducing bile supersaturation. CDCA has been used therapeutically to dissolve cholesterol gallstones by reducing cholesterol secretion into bile and increasing bile acid RISKS concentrations. Secondary bile acids, like deoxycholic acid and lithocholic acid, are formed from primary bile acids through bacterial action in the intestines. The F’s and Others cholesterol-saturated bile predisposes to the formation of gallstones and acts as an irritant that produces inflammatory changes in the gallbladder.  Risk Factor: Frequent changes in weight and Rapid weight loss Increased Cholesterol Secretion: During rapid weight loss, particularly from very low-calorie diets or bariatric surgery, the liver secretes more cholesterol into the bile. This excess cholesterol can supersaturate the bile, leading to the formation of cholesterol crystals, which can eventually aggregate into gallstones. Reduced Gallbladder Motility: During periods of rapid weight loss, especially in the context of very low-calorie diets, the gallbladder empties less frequently. This bile stasis (lack of regular emptying) allows bile to remain in the gallbladder longer, increasing the chance of cholesterol precipitating out of the bile to form stones. Fluctuations in Hormones: Weight cycling can lead to fluctuations in hormones such as insulin, estrogen, and leptin, all of which can influence bile composition and gallbladder function. For example, increased estrogen levels (which can occur during periods of weight gain or with certain medications) can raise cholesterol levels in bile, promoting gallstone formation. Chronic Low-Grade Inflammation: Frequent weight changes can cause stress on the body, leading to chronic low-grade inflammation. Inflammation has been linked to various metabolic disturbances, including alterations in cholesterol metabolism and gallbladder function, which may contribute to an increased risk of gallstones.  Risk Factor: Treatment with High Dose or even Low Dose Estrogen Increased Cholesterol Secretion: Estrogen increases the synthesis of cholesterol in the liver and its secretion into bile. High levels of estrogen can lead to an increased concentration of cholesterol in the bile, making it more likely to become supersaturated. Supersaturated cholesterol can crystallize, forming cholesterol gallstones. Reduced Bile Acid Synthesis: Estrogen can inhibit the conversion of cholesterol into bile acids. Bile acids are crucial for dissolving cholesterol in bile. When estrogen reduces bile acid synthesis, the bile becomes less effective at keeping cholesterol in solution, further promoting cholesterol crystallization and gallstone formation. Gallbladder Hypomotility: High estrogen levels can affect gallbladder motility. Estrogen has a relaxing effect on smooth muscle, which includes the gallbladder. This relaxation can reduce the frequency and strength of gallbladder contractions, leading to bile stasis (prolonged retention of bile in the gallbladder). Bile stasis allows more time for cholesterol to precipitate and form gallstones. Increased Risk of Obesity and Metabolic Changes: High-dose estrogen therapy can lead to weight gain or central obesity, which is associated with increased cholesterol levels and insulin resistance. These metabolic changes can further exacerbate the risk of gallstone formation. Hormonal Imbalance: High levels of estrogen can disrupt the balance of other hormones involved in lipid metabolism, such as insulin and progesterone. Hormonal imbalances can affect liver function and bile composition, increasing the risk of gallstones. Altered Lipid Metabolism and Lipids and Bile Composition: Estrogen affects lipid metabolism, leading to increased levels of serum lipids and changes in bile lipid composition. High estrogen levels can result in a higher concentration of cholesterol relative to bile acids in the bile, contributing to the formation of cholesterol gallstones.  Risk Factor: Prolonged use of Clofibrate a fibrate drug used primarily to reduce cholesterol and triglyceride levels, can increase the risk of cholelithiasis (gallstone formation) due to its effect on bile composition. ✓ Increased Cholesterol Secretion in Bile: Clofibrate lowers blood cholesterol by promoting the excretion of cholesterol into bile. This increases the cholesterol content in bile, leading to supersaturation. ✓ Cholesterol Crystallization: When bile becomes supersaturated with cholesterol, it can precipitate out and form cholesterol crystals, which can gradually coalesce into gallstones. ✓ Reduced Bile Acid Synthesis: Clofibrate may also reduce the synthesis of bile acids, which are necessary to keep cholesterol dissolved in bile. A reduction in bile acids further predisposes bile to cholesterol crystallization. Risk Factor: Ileal Resection or GI Disease ✓ Ileal Resection or Bypass: The ileum is the primary site for the reabsorption of bile acids from the intestine back into the liver (enterohepatic circulation). When the ileum is resected or bypassed (as in bariatric surgery), bile acids are not efficiently reabsorbed. This leads to bile acid depletion in the liver and bile, resulting in bile that is less capable of keeping cholesterol in solution. Consequently, bile becomes supersaturated with cholesterol, which can lead to cholesterol crystal formation and eventually gallstones. ✓ GI Diseases (e.g., Crohn's Disease): Chronic inflammatory conditions affecting the small intestine, particularly the ileum (as seen in Crohn's disease), can also impair bile acid reabsorption. This has the same effect as ileal resection, leading to reduced bile acid levels and increased cholesterol saturation in bile. Risk Factor: Ileal Resection or GI Disease ✓T-Tube Fistula: A T-tube is used to drain bile after certain biliary surgeries. Chronic bile drainage through a T-tube can lead to significant loss of bile acids, reducing the bile acid pool in the body. With lower bile acid levels, the bile becomes more concentrated with cholesterol, which promotes gallstone formation. ✓Malabsorption Conditions: In conditions where there is fat malabsorption (such as in celiac disease or chronic pancreatitis), unabsorbed fatty acids can bind with calcium in the intestines, forming insoluble soaps that trap bile acids. This further reduces the bile acid pool, increasing the risk of cholesterol supersaturation in bile and gallstone formation.  Risk Factor: Cystic Fibrosis ✓ Dehydrated Secretions: Cystic fibrosis is characterized by defective chloride and sodium ion transport across epithelial cells, leading to thick and dehydrated secretions in various organs, including the liver and bile ducts. This results in thickened, viscous bile, which can promote bile stasis (poor flow of bile) and increase the risk of bile components precipitating into gallstones. ✓ Pancreatic and Hepatic Dysfunction: In CF, the pancreas and liver are often affected. Pancreatic insufficiency leads to impaired digestion and malabsorption of fats, which can alter bile composition. Additionally, CF-related liver disease can reduce bile acid secretion. Bile acids are necessary to keep cholesterol dissolved in bile, so reduced bile acid levels can lead to supersaturation of cholesterol in bile, promoting gallstone formation. ✓ Delayed Gallbladder Emptying: Cystic fibrosis can also affect the motility of the gallbladder, leading to delayed or incomplete emptying. This can cause bile to remain in the gallbladder for extended periods, increasing the chance of cholesterol precipitation and stone formation.  Risk Factor: Diabetes Mellitus ✓ People with diabetes, especially TYPE 2 DIABETES, have an increased risk of cholelithiasis (gallstone formation) due to a combination of factors related to metabolic disturbances and gallbladder function. ✓ Gallbladder Hypomotility (Reduced Gallbladder Contraction): In diabetes, especially if poorly controlled, autonomic neuropathy can occur. This can affect the nerves that control the contraction of the gallbladder, leading to gallbladder hypomotility (sluggish or incomplete emptying of the gallbladder). When the gallbladder does not empty fully, bile remains in the gallbladder for longer periods, allowing more time for cholesterol to precipitate and form gallstones. ✓ Increased Cholesterol Saturation in Bile: People with type 2 diabetes often have insulin resistance, which is associated with dyslipidemia (abnormal lipid levels). Dyslipidemia can result in increased levels of cholesterol in the blood, which in turn can increase cholesterol secretion into bile. Bile that is supersaturated with cholesterol is more likely to lead to the formation of cholesterol gallstones. ✓ Obesity: Obesity is common in people with type 2 diabetes and is an independent risk factor for gallstones. In obesity, there is increased cholesterol synthesis and secretion into bile, leading to supersaturation of bile with cholesterol, which promotes gallstone formation. This risk is exacerbated by insulin resistance, a hallmark of type 2 diabetes. ✓ Hypertriglyceridemia: People with diabetes, particularly those with metabolic syndrome, often have elevated triglyceride levels. Hypertriglyceridemia can be associated with changes in bile composition, making it more prone to forming gallstones. ✓ Hyperinsulinemia: High insulin levels, which are common in the early stages of type 2 diabetes and in insulin-resistant states, may stimulate cholesterol synthesis in the liver. This increases the cholesterol content in bile, predisposing individuals to cholesterol gallstones. CLINICAL MANIFESTATIONS Maybe Asymptomatic (SILENT CHOLELITHIASIS). Symptomatic patient may develop TWO TYPES of symptoms: A. Due to disease of the gallbladder itself B. Due to obstruction of the bile passages by a gallstone. The symptoms may be ACUTE or CHRONIC. Epigastric distress, such as fullness, abdominal distention, and vague pain in the right upper quadrant of the abdomen, may occur WHICH usually follow a meal rich in fried or fatty foods.  Usually follows after gallstone obstruction in the cystic PAIN AND BILIARY duct leading to gallbladder distention, inflammation, and eventually infection (acute cholecystitis). COLIC Excruciating upper right abdominal pain that radiates to the back or right shoulder Occurs during deep inspiration and prevents full inspiratory excursion. Caused by contraction of the gallbladder, which cannot release bile because of obstruction by the stone. Associated with N&V, and it is noticeable several hours after a heavy meal. Observable patient restlessness. Require the use of analgesics to control pain. The use of morphine has traditionally been avoided because of concern that it could cause spasm of the sphincter of Oddi, and meperidine (Demerol) has been used instead. This is controversial, because morphine is the preferred analgesic agent for management of acute pain, and some metabolites of meperidine are toxic to the central nervous system (CNS).  ▪ Occurs in patients with JAUNDICE AND gallbladder disease, usually with PRURITUS obstruction of the common bile duct. ▪ Bile is no longer carried to the duodenum, is absorbed by the blood and gives the skin and mucous membranes a yellow color. ▪ This is frequently accompanied by marked pruritus (itching) of the skin. Changes in URINE and STOOL COLOR ▪ The excretion of the bile pigments by the kidneys gives the urine a very dark color. ▪ The feces, no longer colored with bile pigments, are grayish, like putty, or clay-colored. VITAMIN DEFICIENCIES ▪ Obstruction of bile flow interferes with absorption of the fat-soluble vitamins A, D, E, and K. Patients may exhibit deficiencies of these vitamins if biliary obstruction has been prolonged. ▪ For example, a patient may have bleeding caused by vitamin K deficiency (vitamin K is necessary for normal blood clotting). ASSESSMENT AND DIAGNOSTICS Abdominal X-Ray Ultrasonography ▪ If gallbladder disease is suspected, ▪ Ultrasonography has replaced an abdominal x-ray may be obtained cholecystography as the diagnostic to exclude other causes of procedure of choice because it is rapid symptoms. and accurate and can be used in patients with liver dysfunction and jaundice. ▪ However, only 15% to 20% of gallstones are calcified sufficiently to ▪ It does not expose patients to ionizing radiation. be visible on such x-ray studies. ▪ The procedure is most accurate if the patient fasts overnight so that the gallbladder is distended. ▪ Ultrasonography can detect calculi in the gallbladder or a dilated common bile duct with 95% accuracy. ASSESSMENT AND DIAGNOSTICS Radionuclide Imaging / ▪ Used successfully in the diagnosis of Cholescintigraph / acute cholecystitis, blockage of a bile Hepatobiliary duct, and biliary dyskinesia. Iminodiacetic Acid (HIDA) ▪ In this procedure, a radioactive agent is administered intravenously. Scan ▪ It is taken up by the hepatocytes and excreted rapidly through the biliary tract. ▪ The biliary tract is then scanned, and images of the gallbladder and biliary tract are obtained. ▪ This test is more expensive than ultrasonography, takes longer to perform, exposes the patient to radiation, and cannot detect gallstones. It is often used when ultrasonography is not conclusive. ASSESSMENT AND DIAGNOSTICS Radionuclide Imaging / Patient Preparation Cholescintigraph / 1. Fasting Hepatobiliary ❖The patient is usually instructed to fast Iminodiacetic Acid (HIDA) for at least 4-6 hours before the procedure. Scan ❖Fasting is necessary to ensure the gallbladder is properly distended and to avoid any interference from recently ingested food. 2. Medication Review ❖The healthcare provider will review any medications the patient is taking, as some drugs (e.g., opiates) can affect gallbladder function and alter the results of the test. ❖These medications may need to be temporarily discontinued. ASSESSMENT AND DIAGNOSTICS Radionuclide Imaging / Radiotracer Injection Cholescintigraph / Hepatobiliary Administration of Radiotracer Iminodiacetic Acid (HIDA) ❖A small amount of a radioactive tracer (typically technetium-99m-labeled Scan iminodiacetic acid analogs) is injected into a vein in the patient's arm. ❖The tracer is taken up by the liver and excreted into the bile. Waiting Period ❖After the injection, there is a brief waiting period (usually about 5-10 minutes) to allow the tracer to be processed by the liver and excreted into the bile ducts and gallbladder. ASSESSMENT AND DIAGNOSTICS Radionuclide Imaging / Imaging Acquisition Cholescintigraph / Gamma Camera Scanning Hepatobiliary Iminodiacetic ❖The patient lies on an imaging table, and a Acid (HIDA) Scan gamma camera is positioned over the abdomen. ❖The camera detects the gamma rays emitted by the radioactive tracer and creates images of the liver, gallbladder, bile ducts, and small intestine. Sequential Imaging ❖Images are typically taken at intervals to track the flow of bile through the biliary system. ❖The scanning can last between 30 minutes to a few hours, depending on the specific clinical question being addressed. For example, delayed images may be necessary if bile flow is slow or obstructed. ASSESSMENT AND DIAGNOSTICS Radionuclide Imaging / Post-Procedure Monitoring Cholescintigraph / Observation Hepatobiliary ❖Once the imaging is complete, the patient is usually monitored briefly for Iminodiacetic Acid (HIDA) any adverse reactions to the radiotracer, Scan although complications are rare. ❖The radioactive tracer will naturally decay and be excreted from the body over time. Resume Normal Activities ❖The patient can typically resume normal activities immediately after the procedure, ❖Advise to drink plenty of fluids to help eliminate the radioactive material from patient’s body.  ASSESSMENT AND DIAGNOSTICS ▪ Although cholecystography has been replaced by ultrasonography as the test of choice, it is still used if Cholecystography ultrasound equipment is not available or if the ultrasound results are inconclusive. ▪ Oral cholangiography may be performed to detect gallstones and to assess the ability of the gallbladder to fill, concentrate its contents, contract, and empty. ▪ If the patient is not allergic to iodine or seafood, an iodide containing contrast agent that is excreted by the liver and concentrated in the gallbladder is administered 10 to 12 hours before the x-ray study. ▪ The normal gallbladder fills with this radiopaque substance. If gallstones are present, they appear as shadows on the x-ray film. ▪ Oral cholecystography is likely to continue to be used as part of the evaluation of the few patients who have been treated with gallstone dissolution therapy or lithotripsy. ASSESSMENT AND DIAGNOSTICS Patient Preparation Cholecystography / Fasting ❖The patient is instructed to fast for 8-12 hours Oral Cholecystography before the procedure to ensure that the / OCG gallbladder is fully distended and that there is no interference from food or recent bile secretion. Oral Contrast Agent ❖Oral contrast tablets (usually iodine-based agents like iopanoic acid) the night before the procedure. ❖These tablets are absorbed in the intestines, processed by the liver, and excreted into the bile, which accumulates in the gallbladder. Medication Review Some drugs (e.g., anticholinergics) may interfere with the function of the gallbladder.  ASSESSMENT AND DIAGNOSTICS Radiographic Imaging Cholecystography / X-Ray Imaging Oral Cholecystography ❖After a period of 10-15 hours (usually the next morning), the patient undergoes a series of X-ray / OCG images of the abdomen. ❖The radiologist or technician will take images with the patient in different positions to fully visualize the gallbladder. Visualization of the Gallbladder ❖If the gallbladder is functioning properly, it will concentrate the contrast agent, and the gallbladder will appear clearly on the X-ray images. ❖If the gallbladder fails to fill with the contrast agent, this may indicate gallbladder disease, such as obstruction of the cystic duct or severe cholecystitis.  ASSESSMENT AND DIAGNOSTICS Post-Procedure Cholecystography / Resume Normal Activities Oral Cholecystography ❖After the procedure, the patient / OCG can usually resume normal activities. ❖There is no radioactive material or long-lasting effects from the contrast agent. Follow-Up ❖The referring physician discusses the results with the patient and determines if further tests or treatments are needed, based on the findings.  ASSESSMENT AND DIAGNOSTICS ▪ permits direct visualization of structures that previously could be seen only during laparotomy. Endoscopic Retrograde ▪ The examination of the hepatobiliary system is Cholangiopancreatography carried out via a side-viewing flexible fiberoptic (ERCP) endoscope inserted through the esophagus to the descending duodenum. ▪ Multiple position changes are required to pass the endoscope during the procedure, beginning in the left semi-prone position. ▪ Fluoroscopy and multiple x-rays are used during ERCP to evaluate the presence and location of ductal stones. ▪ Careful insertion of a catheter through the endoscope into the common bile duct is the most important step in sphincterotomy (division of the muscles of the biliary sphincter) for gallstone extraction via this technique.  ASSESSMENT AND DIAGNOSTICS Nursing Implications Endoscopic Retrograde ▪ The procedure requires a cooperative patient to permit Cholangiopancreatography insertion of the endoscope without damage to the GI tract structures, including the biliary tree. (ERCP) ▪ Before the procedure: ▪ the patient is given an explanation of the procedure and his or her role in it. The patient takes nothing by mouth for several hours before the procedure. ▪ Moderate sedation is used, and the sedated patient must be monitored closely. It may be necessary to administer medications, such as glucagon or anticholinergics, to make cannulation easier by decreasing duodenal peristalsis. ▪ The nurse observes closely for signs of respiratory and central nervous system depression, hypotension, oversedation, and vomiting (if glucagon is administered).  ASSESSMENT AND DIAGNOSTICS Nursing Implications Endoscopic Retrograde ▪ During ERCP: Cholangiopancreatography ▪ the nurse monitors intravenous (IV) fluids, (ERCP) administers medications, and positions the patient. ▪ After the procedure: ▪ the nurse monitors the patient’s condition, observing vital signs and monitoring for signs of perforation or infection. ▪ The nurse also monitors the patient for side effects of any medications received during the procedure and for return of the gag and cough reflexes after the use of local anesthetics.  ASSESSMENT AND DIAGNOSTICS ▪ Percutaneous transhepatic cholangiography involves the injection of dye directly into the biliary tract. Because of Percutaneous Transhepatic the relatively large concentration of dye that is introduced into the biliary system, including the hepatic ducts within Cholangiography the liver, the entire length of the common bile duct, the cystic duct, and the gallbladder is outlined clearly. ▪ This procedure can be carried out even in the presence of liver dysfunction and jaundice. It is useful for: (1) distinguishing jaundice caused by liver disease (hepatocellular jaundice) from that caused by biliary obstruction, (2) investigating the GI symptoms of a patient whose gallbladder has been removed, (3) locating stones within the bile ducts, and (4) diagnosing cancer involving the biliary system.  ASSESSMENT AND DIAGNOSTICS ▪ This sterile procedure is performed under moderate sedation on a patient who has been fasting; the patient Percutaneous Transhepatic receives local anesthesia and moderate sedation. Cholangiography ▪ Coagulation parameters and platelet count should be normal to minimize the risk of bleeding. ▪ Broad-spectrum antibiotics are administered during the procedure because of the high prevalence of bacterial colonization from obstructed biliary systems. ▪ After infiltration with a local anesthetic agent has occurred, a flexible needle is inserted into the liver from the right side in the midclavicular line immediately beneath the right costal margin. ▪ Successful entry of a duct is noted when bile is aspirated or on injection of a contrast agent.  ASSESSMENT AND DIAGNOSTICS ▪ Ultrasound can be used to guide puncture of the duct. Percutaneous Transhepatic ▪ Bile is aspirated and samples are sent for bacteriology and cytology. Cholangiography ▪ A water-soluble contrast agent is injected to fill the biliary system. ▪ The fluoroscopy table is tilted and the patient is repositioned to allow x-rays to be taken in multiple projections. ▪ Delayed x-ray views can identify abnormalities of more distant ducts and determine the length of a stricture or multiple strictures. ▪ Before the needle is removed, as much dye and bile as possible are aspirated to forestall subsequent leakage into the needle tract and eventually into the peritoneal cavity, thus minimizing the risk of bile peritonitis.  ASSESSMENT AND DIAGNOSTICS Percutaneous Transhepatic Nursing Alert Cholangiography o MONITOR the patient for symptoms of bleeding, peritonitis, and septicemia. o ASSESS the patient for pain and indications of these complications and reports them promptly to the physician. o ADMINITER antibiotic agents are often prescribed to minimize the risk of sepsis and septic shock. MEDICAL MANAGEMENT GOALS: 1.TO reduce the incidence of acute episodes of gallbladder pain and cholecystitis by supportive and dietary management. 2. TO remove the cause of cholecystitis by pharmacologic therapy, endoscopic procedures, or surgical intervention. SUMMARY OF MEDICAL MANAGEMENT 1. Nutritional and Supportive 6. Surgical Management Therapy Laparoscopic Cholecystectomy 2. Pharmacologic Therapy Cholecystectomy 3. Nonsurgical Removal of Gallstones Mini-Cholecystectomy ▪ Dissolving Gallstones ▪ Stone Removal by Instrumentation Choledochostomy 4. Intracorporeal Lithotripsy Surgical Cholecystostomy 5. Extracorporeal Shock Wave Percutaneous Cholecystostomy Lithotripsy MEDICAL MANAGEMENT ▪ Diet required immediately after an episode is usually limited to low-fat liquids. Nutritional and ▪ These can include powdered supplements Supportive Therapy high in protein and carbohydrate stirred into skim milk. ▪ Cooked fruits, rice or tapioca, lean meats, mashed potatoes, non–gas-forming vegetables, bread, coffee, or tea may be added as tolerated. ▪ The patient should avoid eggs, cream, pork, fried foods, cheese, rich dressings, gas-forming vegetables, and alcohol. ▪ It is important to remind the patient that fatty foods may induce an episode of cholecystitis. MEDICAL MANAGEMENT ▪ Ursodeoxycholic acid (UDCA [URSO, Actigall]) and chenodeoxycholic acid (chenodiol or CDCA [Chenix]) have been used to dissolve small, Pharmacologic radiolucent gallstones composed primarily of cholesterol. Therapy ▪ UDCA has fewer side effects than chenodiol and can be administered in smaller doses to achieve the same effect. It acts by inhibiting the synthesis and secretion of cholesterol, thereby desaturating bile. ▪ Treatment with UDCA can reduce the size of existing stones, dissolve small stones, and prevent new stones from forming. ▪ 6 to 12 months of therapy are required in many patients to dissolve stones, and monitoring of the patient for recurrence of symptoms or the occurrence of side effects (eg, GI symptoms, pruritus, headache) is required during this time. ▪ Indicated for patients who refuse surgery or for whom surgery is considered too risky. ▪ Patients with significant, frequent symptoms; cystic duct occlusion; or pigment stones are not candidates for therapy with UDCA. ▪ Laparoscopic or open cholecystectomy is more appropriate for symptomatic patients with acceptable operative risk. MEDICAL MANAGEMENT DISSOLVING GALLSTONES NON-SURGICAL REMOVAL OF ▪ Dissolve gallstones by infusion of a solvent (mono- GALLSTONES octanoin or methyl tertiary butyl ether [MTBE]) into the gallbladder. ▪ Solvent can be infused through the following routes: through a tube or catheter inserted percutaneously directly into the gallbladder; through a tube or drain inserted through a T-tube tract to dissolve stones not removed at the time of surgery; endoscopically with ERCP; or via a transnasal biliary catheter. MEDICAL MANAGEMENT STONE REMOVAL BY INSTRUMENTATION NON-SURGICAL REMOVAL OF ▪ A catheter and instrument with a basket attached are threaded through the T-tube tract or fistula formed at the GALLSTONES time of T-tube insertion; the basket is used to retrieve and remove the stones lodged in the common bile duct. ▪ The patient is observed closely for bleeding, perforation, and the development of pancreatitis or sepsis. ▪ Useful in diagnosis and treatment of patients who have symptoms after biliary tract surgery, patients with intact gallbladders, and patients for whom surgery is particularly hazardous. MEDICAL MANAGEMENT STONE REMOVAL BY INSTRUMENTATION NON-SURGICAL REMOVAL OF GALLSTONES MEDICAL MANAGEMENT INTRACORPOREAL LITHOTRIPSY NON-SURGICAL REMOVAL OF ▪ Stones in the gallbladder or common bile duct may be fragmented by means of laser pulse technology. GALLSTONES ▪ The laser pulse produces rapid expansion and disintegration of plasma on the stone surface, resulting in a mechanical shock wave. ▪ Repeated procedures may be necessary because of stone size, local anatomy, bleeding, or technical difficulty. ▪ This approach allows time for improvement in the patient’s clinical condition until gallstones are cleared endoscopically, percutaneously, or surgically. MEDICAL MANAGEMENT EXTRACORPOREAL SHOCK WAVE NON-SURGICAL REMOVAL OF LITHOTRIPSY GALLSTONES ▪ Lithotripsy, a noninvasive procedure, uses repeated shock waves directed at the gallstones in the gallbladder or common bile duct to fragment the stones. ▪ The waves are transmitted to the body through a fluid-filled bag or by immersing the patient in a water bath. ▪ Procedure requires no incision and no hospitalization MEDICAL MANAGEMENT SURGICAL ▪ Surgical treatment of gallbladder MANAGEMENT disease and gallstones is carried out to relieve persistent symptoms, to remove the cause of biliary colic, and to treat acute cholecystitis. ▪ Surgery may be delayed until the patient’s symptoms have subsided, or it may be performed as an emergency procedure, if necessitated by the patient’s condition. MEDICAL MANAGEMENT Preoperative Measures SURGICAL MANAGEMENT ▪ Tests: Chest x-ray, electrocardiogram (ECG), and liver function tests ▪ Vitamin K may be administered if the prothrombin level is low. ▪ May be necessary to provide IV glucose with protein supplements to aid wound healing and help prevent liver damage. ▪ Instruct to do turning and deep breathing (prevents postoperative pneumonia and atelectasis) MEDICAL MANAGEMENT Laparoscopic Cholecystectomy ▪ New standard for therapy of symptomatic gallstones SURGICAL ▪ If the common bile duct is obstructed by a MANAGEMENT gallstone, an ERCP with sphincterotomy may be performed to explore the duct before laparoscopy. ▪ Performed through a small incision or puncture made through the abdominal wall at the umbilicus. ▪ The patient does not experience the paralytic ileus that occurs with open abdominal surgery and has less postoperative abdominal pain. ▪ Conversion to a traditional abdominal surgical procedure may be necessary if problems are encountered during the laparoscopic procedure. MEDICAL MANAGEMENT SURGICAL Laparoscopic MANAGEMENT Cholecystectomy ▪ The most serious complication after laparoscopic cholecystectomy is a bile duct injury ▪ Common postoperative symptom: drowsiness MEDICAL MANAGEMENT Cholecystectomy SURGICAL ▪ gallbladder is removed through an abdominal MANAGEMENT incision (usually right subcostal) after the cystic duct and artery are ligated. ▪ Procedure is performed for acute and chronic cholecystitis ▪ A drain is placed close to the gallbladder bed and brought out through a puncture wound if there is a bile leak ▪ Usually only a small amount of serosanguineous fluid drains in the initial 24 hours after surgery; afterward, the drain is removed ▪ Complications: Bile duct injury MEDICAL MANAGEMENT Mini-Cholecystectomy SURGICAL MANAGEMENT ▪ Mini-cholecystectomy is a surgical procedure in which the gallbladder is removed through a small incision. ▪ If needed, the surgical incision is extended to remove larger gallbladder stones. ▪ The procedure is controversial because it limits exposure to all the involved biliary structures. MEDICAL MANAGEMENT Choledochostomy SURGICAL MANAGEMENT ▪ Choledochostomy is reserved for the patient with acute cholecystitis who may be too ill to undergo a surgical procedure. ▪ It involves making an incision in the common duct, usually for removal of stones ▪ Laparoscopic cholecystectomy is planned for a future date after acute inflammation has resolved. MEDICAL MANAGEMENT Surgical Cholecystostomy SURGICAL ▪ Cholecystostomy is performed when the patient’s MANAGEMENT condition precludes more extensive surgery or when an acute inflammatory reaction is severe. ▪ High mortality rate (20% to 30%) because of the underlying disease process ▪ Percutaneous Cholecystostomy has been used in the treatment and diagnosis of acute cholecystitis in patients who are poor risks for any surgical procedure or for general anesthesia. ▪ Includes: patients with sepsis or severe cardiac, renal, pulmonary, or liver failure ▪ Immediate relief of pain and resolution of signs and symptoms of sepsis and cholecystitis have been reported with this procedure. MEDICAL MANAGEMENT ▪ Surgical intervention for disease of the Gerontologic biliary tract is the most common operative Considerations procedure performed in the elderly. ▪ Elderly patient may not exhibit the typical symptoms of fever, pain, chills, and jaundice. ▪ Common symptoms: accompanied or preceded by those of septic shock, which include oliguria, hypotension, changes in mental status, tachycardia, and tachypnea ▪ Elective cholecystectomy is usually well- tolerated NURSING PROCESS ▪ Focus on respiratory status ▪ Health History: smoking, previous respiratory problems, shallow respirations, a persistent or ASSESSMENT ineffective cough, and the presence of adventitious breath sounds ▪ Health Teaching: Instruct patient about the need to avoid smoking and use of aspirin or other agents that alter coagulation ▪ Nutritional Status: dietary history and a general examination performed at the time of preadmission testing; review laboratory results  Common postoperative Nursing Diagnoses: NURSING PROCESS ▪ Acute pain and discomfort related to surgical incision DIAGNOSIS ▪ Impaired gas exchange related to the high abdominal surgical incision (if traditional surgical cholecystectomy was performed) ▪ Impaired skin integrity related to altered biliary drainage after surgical intervention ▪ Imbalanced nutrition, less than body requirements, related to inadequate bile secretion ▪ Deficient knowledge about self-care activities related to incision care, dietary modifications (if needed), medications, and reportable signs or symptoms (eg, fever, bleeding, vomiting) NURSING PROCESS DIAGNOSIS Collaborative Problems/Potential Complications ▪ Bleeding ▪ GI Symptoms (biliary leak or injury to the bowel) PLANNING AND ▪ Main Goals: relief of pain, adequate ventilation, intact skin and improved biliary drainage, optimal nutritional intake, absence GOALS of complications, and understanding of self-care routines NURSING PROCESS General Post-Operative ▪ Position patient to low Fowler’s position Nursing ▪ Administer water and other fluids within hours after Interventions laparoscopic procedures ▪ Diet: Soft diet is started after bowel sounds return (usually the next day) Relieving Pain ▪ Administer analgesic agents ▪ Help the patient turn, cough, breathe deeply, and ambulate ▪ Use of pillow or binder  Improving Respiratory Status NURSING PROCESS ▪ Note: Patients are prone to pulmonary complications ▪ Deep breaths and cough every hour to prevent Post-Operative atelectasis Nursing ▪ Use of incentive spirometry Interventions ▪ Early ambulation ▪ Complications are more likely in elderly, obese, with health hx Maintaining Skin Integrity and Promoting Biliary Drainage ▪ Drainage tube must be connected immediately to a drainage receptacle. Monitor for proper drainage. Elevate above abdomen. ▪ Monitor for signs of infection NURSING PROCESS Maintaining Skin Integrity and Promoting Biliary Drainage Post-Operative Nursing ▪ Drainage tube must be connected Interventions immediately to a drainage receptacle. Monitor for proper drainage (amount, color, character). Elevate above abdomen. ▪ Monitor for signs of infection ▪ Clamp drainage for 1 hour before and after each meal ▪ Observe stool color ▪ Laboratory: Urine and stool for bile pigments ▪ Maintain I&O  Improving Nutritional Status NURSING PROCESS ▪ Immediate Post-Operative Diet: low in fat and high in carbohydrates and proteins Post-Operative Nursing ▪ Hospital Discharge Diet: avoid excessive fats (restricted for 4 to 6 weeks) Interventions Monitoring and Managing Potential Complications ▪ Monitor for bleeding ▪ Monitor V/s ▪ Inspect incision site for bleeding ▪ Assess abdomen tenderness or rigidity ▪ Monitor for infection ▪ Anorexia, vomiting, pain, abdominal distension, temperature elevation  Promoting Home and Community-based NURSING PROCESS Care ▪ Health Teaching Post-Operative Nursing ▪ Prescribed medication Interventions ▪ Symptoms to be reported: jaundice, dark urine, pale-colored stools, pruritic, signs of inflammation and infection (fever or pain) ▪ Drainage Tube Management: ▪ Report promptly any changes in the amount or characteristics of drainage ▪ Signs of Infection ▪ Emphasize importance of follow up appointments NURSING PROCESS ▪ Reports decrease in pain EVALUATION ▪ Demonstrates proper respiratory function ▪ Exhibits normal skin integrity around biliary drainage, or pus around drainage tube ▪ Obtains relief from dietary intolerance ▪ Absence of complications DISORDERS OF THE PANCREAS PANCREATITIS DEFINITION ▪ Inflammation of the pancreas ▪ autodigestion of the pancreas ▪ Categorized into: Acute & Chronic ▪ Cause: specific cause unknown, believed to be caused by temporary obstruction of pancreas accompanied by hypersecretion of the exocrine enzymes ▪ Mechanism: enzymes enter bile duct > enzymes become activated > bile and enzymes back up into the pancreatic duct > pancreatitis  ACUTE PANCREATITIS DEFINITION ▪ medical emergency associated with a high risk of life-threatening complications and mortality. ▪ Characteristics: ▪ edema, ▪ inflammation confined to the pancreas, ▪ minimal organ dysfunction ▪ Return to normal function usually occurs within 6 months  ACUTE PANCREATITIS DEFINITION ▪ Has risk for hypovolemic shock, F&E disturbance, sepsis ▪ Characteristics of SEVERE ACUTE PANCREATITIS: widespread and complete enzymatic digestion of the gland ▪ Local Complications: pancreatic cysts or abscesses and acute fluid collections in or near the pancreas ▪ Systemic Complications: organ failure, such as pulmonary insufficiency with hypoxia, shock, renal failure, and GI bleeding. ACUTE PANCREATITIS GERONTOLOGIC CONSIDERATIONS ▪ Mortality rate increases with age ▪ Younger patients develop local complications ▪ Systemic complications increase with age ACUTE PANCREATITIS PATHOPHYSIOLOGY gallstones enter common bile duct and lodge at ampulla of Vater >> obstructed flow of pancreatic juice >> reflux of bile from common bile duct to pancreatic duct >> pancreatic enzymes activates >> vasodilation >> increased vascular permeability, necrosis, erosion, hemorrhage ▪ Mortality rate (2% to 10%) due to shock, anoxia, hypotension, F&E imbalance ACUTE PANCREATITIS PATHOPHYSIOLOGY  ACUTE PANCREATITIS CLINICAL MANIFESTATIONS ▪ Major symptom: SEVERE ABDOMINAL PAIN & BACK PAIN ▪ Other symptoms: ▪ Abdominal distention ▪ Poorly defined, palpable abdominal mass ▪ Decreased peristalsis ▪ Vomiting without relieved pain or nausea ▪ Abdominal guarding ▪ Nausea and vomiting (common) ▪ Fever, jaundice, mental confusion, agitation (not as common) ▪ Hypotension due to hypovolemia (leads to tachycardia, cyanosis, cold & clammy skin) ▪ Acute renal failure ▪ Respiratory disease and hypoxia (common) ACUTE PANCREATITIS ASSESSMENT AND DIAGNOSTIC ▪ Assessment is based on a history of abdominal pain, presence of risk factors, physical examination findings, and diagnostics ▪ Serum amylase and lipase levels ↑ ▪ Urinary amylase levels ↑ and remain elevated longer than serum amylase levels. ▪ WBC ↑ ▪ Hypocalcemia ▪ Transient hyperglycemia and glucosuria ▪ Hematocrit and Hemoglobin = monitor for bleeding ▪ Peritoneal fluid = ↑ pancreatic enzymes ▪ Diagnostics: X-Ray, Ultrasound, CT Scan ACUTE PANCREATITIS MEDICAL MANAGEMENT GENERAL MANAGEMENT ▪ Management is directed toward relieving symptoms and preventing or treating complications ▪ Oral intake is withheld to inhibit stimulation of the pancreas ▪ Histamine-2 (H2) antagonists: cimetidine (Tagamet) and ranitidine (Zantac) = decrease pancreatic activity by inhibiting secretion of gastric acid PAIN MANAGEMENT ▪ Administration of analgesia = reduces pain and restlessness ▪ Administration of parenteral opioids (morphine, fentanyl, hydromorphone) ▪ Opioids stimulate the sphincter of Oddi which worsens pancreatitis ▪ Administration of antiemetics = prevents vomiting ACUTE PANCREATITIS ACUTE PANCREATITIS MEDICAL MANAGEMENT INTENSIVE CARE ▪ Maintain fluid volume and prevent renal failure ▪ ABG monitoring ▪ Hemodynamic monitoring ▪ Antibiotic administration ▪ Glycemic control RESPIRATORY CARE ▪ ABG Monitoring ▪ Humidified oxygen intubation ▪ Mechanical ventilation ACUTE PANCREATITIS MEDICAL MANAGEMENT BILIARY DRAINAGE ▪ Placement of biliary drains (external drainage) and stents (indwelling tubes) SURGICAL INTERVENTION ▪ Used in diagnosing (diagnostic laparotomy) POSTACUTE MANAGEMENT ▪ Antacids may be used after acute pancreatitis begins to resolve ▪ Oral feedings that are low in fat and protein are initiated gradually ▪ Caffeine and alcohol are eliminated from the diet. ACUTE PANCREATITIS NURSING MANAGEMENT RELIEVING PAIN AND DISCOMFORT The current recommendation for pain management in this population is parenteral opioids, including morphine, hydromorphone, or fentanyl Parenteral fluids and electrolytes are prescribed to restore and maintain fluid balance. The acutely ill patient is maintained on bed rest to decrease the metabolic rate and reduce the secretion of pancreatic and gastric enzymes IMPROVING BREATHING PATTERN Oral food or fluid intake is not permitted. Assess the patient’s nutritional status and to note factors that alter the patient’s nutritional requirements Enteral or parenteral nutrition may be prescribed. ACUTE PANCREATITIS NURSING MANAGEMENT MAINTAINING SKIN INTEGRITY assesses the wound, drainage sites, and skin for signs of infection, inflammation, and breakdown. wound care as prescribed and takes precautions to protect intact skin from contact with drainage. MONITORING AND MANAGING POTENTIAL COMPLICATIONS Fluid and electrolyte disturbances are common complications because of nausea, vomiting, movement of fluid from the vascular compartment to the peritoneal cavity, diaphoresis, fever, and the use of gastric suction. Pancreatic necrosis is a major cause of morbidity and mortality in patients with acute pancreatitis because of resulting hemorrhage, septic shock, and multiple organ failure. ACUTE PANCREATITIS NURSING MANAGEMENT MONITORING AND MANAGING POTENTIAL COMPLICATIONS Monitor V/S Administer prescribed fluids, medications, and blood products; assisting with supportive management Shock and multiple organ failure may occur with acute pancreatitis. The nurse closely monitors the patient for early signs of neurologic, cardiovascular, renal, and respiratory dysfunction. PROMOTING HOME AND COMMUNITY-BASED CARE Instructs the patient about the factors implicated in the onset of acute pancreatitis and about the need to avoid high- fat foods, heavy meals, and alcohol A referral for home care is often indicated. CHRONIC PANCREATITIS DEFINITION ▪ Chronic pancreatitis is an inflammatory disorder characterized by progressive destruction of the pancreas. ▪ Alcohol consumption in Western societies and malnutrition worldwide are the major causes of chronic pancreatitis. ▪ Median age of patients diagnosed with chronic pancreatitis is 37 to 40 years. ▪ Long-term alcohol consumption causes hypersecretion of protein in pancreatic secretions, resulting in protein plugs and calculi within the pancreatic ducts. ▪ Smoking is another factor in the development of chronic pancreatitis  CHRONIC PANCREATITIS CLINICAL MANIFESTATIONS ▪ Major symptom: recurring attacks of severe upper abdominal and back pain + vomiting that cannot be relieved by opioids ▪ Other symptoms: ▪ Dull, nagging pain ▪ Some are painless ▪ Weight loss ▪ Anorexia or fear CHRONIC PANCREATITIS ASSESSMENT AND DIAGNOSTIC ▪ Imaging: MRI, CT Scans, Ultrasound for diagnostic evaluation ▪ Glucose tolerance test evaluates pancreatic islet cell function ▪ Abnormal glucose tolerance test indicate presence of diabetes associate with pancreatitis ▪ Steatorrhea is best confirmed by laboratory analysis of fecal content CHRONIC PANCREATITIS MEDICAL MANAGEMENT NONSURGICAL MANAGEMENT ▪ Endoscopy to remove pancreatic duct stones, correct strictures, and drain cysts may be effective in selected patients to manage pain and relieve obstruction ▪ Management of abdominal pain and discomfort is similar to that of acute pancreatitis CHRONIC PANCREATITIS MEDICAL MANAGEMENT SURGICAL MANAGEMENT Chronic pancreatitis is not often managed by surgery. Surgery may be indicated to relieve persistent abdominal pain and discomfort, restore drainage of pancreatic secretions, and reduce the frequency of acute attacks of pancreatitis and hospitalization CHRONIC PANCREATITIS MEDICAL MANAGEMENT SURGICAL MANAGEMENT Pancreaticojejunostomy (also referred to as Roux-en-Y), with a side-to-side anastomosis or joining of the pancreatic duct to the jejunum, allows drainage of the pancreatic secretions into the jejunum. Whipple resection (pancreaticoduodenectomy) can be carried out to relieve the pain of chronic pancreatitis. Patients who undergo surgery for chronic pancreatitis may experience weight gain and improved nutritional status; this may result from reduction in pain associated with eating rather than from correction of malabsorption. Even after undergoing these surgical procedures, the patient is likely to continue to have pain and impaired digestion secondary to pancreatitis, unless alcohol is avoided completely. DISORDERS OF THE LIVER LIVER CIRRHOSIS Scarring of the liver A chronic disease characterized by replacement of normal liver tissue with diffuse fibrosis that disrupts the structure and function of the liver. Portal and Periportal spaces become the sites of inflammation, and the bile ducts become occluded with inspissated (thickened) bile and pus. The liver attempts to form new bile channels; hence, there is an overgrowth of tissue made up largely of disconnected, newly formed bile ducts and surrounded by scar tissue. LIVER CIRRHOSIS TYPES Alcoholic Cirrhosis Is the most common type of cirrhosis and frequently caused by chronic alcoholism Characterized by scar tissue that surrounds the portal areas Post-necrotic Cirrhosis As a result of a previous bout of acute viral hepatitis broad bands of scar tissue Biliary Cirrhosis much less common than the other two types, results from chronic biliary obstruction and infection (cholangitis) scarring occurs in the liver around the bile ducts.  LIVER CIRRHOSIS CLINICAL MANIFESTATIONS Signs and symptoms of cirrhosis increase in severity as the disease progresses. Severity categorized as compensated or decompensated cirrhosis. LIVER CIRRHOSIS CLINICAL MANIFESTATIONS Compensated With its less severe, often vague symptoms, may be discovered secondarily at a routine physical examination. Signs and Symptoms Compensated Vague morning indigestion Intermittent mild fever Flatulent dyspepsia Vascular spiders Abdominal pain Palmar erythema (reddened palms) Firm, enlarged liver Unexplained epistaxis Splenomegaly Ankle edema LIVER CIRRHOSIS CLINICAL MANIFESTATIONS Decompensated Cirrhosis Results from failure of the liver to synthesize proteins, clotting factors, and other substances and manifestations of portal hypertension Signs and Symptoms Ascites Purpura (due to decreased platelet count) Jaundice Spontaneous bruising Weakness Epistaxis Muscle wasting Hypotension Weight loss Sparse body hair Continuous mild fever White nails Clubbing of fingers Gonadal atrophy LIVER CIRRHOSIS CLINICAL MANIFESTATIONS Liver Enlargement Early in the course of cirrhosis, the liver tends to be large, and the cells are loaded with fat. Portal Obstruction and Ascites Portal obstruction and ascites, late manifestations of cirrhosis, are caused partly by chronic failure of liver function and partly by obstruction of the portal circulation. Infection and Peritonitis Bacterial peritonitis may develop in patients with cirrhosis and ascites in the absence of an intra-abdominal source of infection or an abscess; spontaneous bacterial peritonitis (SBP). Edema Reduced plasma albumin concentration predisposes the patient to the formation of edema. LIVER CIRRHOSIS CLINICAL MANIFESTATIONS Gastrointestinal Varices The obstruction to blood flow through the liver caused by fibrotic changes also results in the formation of collateral blood vessels in the GI system and shunting of blood from the portal vessels into blood vessels with lower pressures. Vitamin Deficiency and Anemia Because of inadequate formation, use, and storage of certain vitamins (notably vitamins A, C, and K), signs of deficiency are common, particularly hemorrhagic phenomena associated with vitamin K deficiency. Mental Deterioration Additional clinical manifestations include deterioration of mental and cognitive function with impending hepatic encephalopathy and hepatic coma, as previously described. LIVER CIRRHOSIS ASSESSMENT AND DIAGNOSTIC FINDINGS Severe parenchymal liver dysfunction Decrease: Serum Albumin Level, Serum Cholinesterase Level Increase: Serum Globulin Level, Serum Alkaline Phosphatase, AST, ALT, and GGT, Bilirubin tests, Prolonged: Prothrombin Time Ultrasound scanning is used to measure the difference in density of parenchymal cells and scar tissue. CT, MRI, and radioisotope liver scans give information about liver size and hepatic blood flow and obstruction. Diagnosis is confirmed by liver biopsy. Arterial blood gas analysis may reveal a ventilation perfusion imbalance and hypoxia. LIVER CIRRHOSIS MEDICAL MANAGEMENT Antacids or Histamine-2 (H2) antagonists are prescribed to decrease gastric distress and minimize the possibility of GI bleeding. Vitamins and nutritional supplements promote healing of damaged liver cells and improve the patient’s general nutritional status. Potassium-sparing diuretics such as spironolactone or triamterene (Dyrenium) may be indicated to decrease ascites, if present; these diuretics are preferred because they minimize the fluid and electrolyte changes commonly seen with other agents. An adequate diet and avoidance of alcohol are essential. Although the fibrosis of the cirrhotic liver cannot be reversed, its progression may be halted or slowed by such measures. LIVER CIRRHOSIS MEDICAL MANAGEMENT Preliminary studies indicate that colchicine, an anti-inflammatory agent used to treat the symptoms of gout, may increase survival time in patients with mild to moderate cirrhosis. Angiotensin system inhibitors, statins, diuretics, immunosuppressants, and glitazones. have shown to possess antifibrotic activity for the treatment of cirrhosis. These medications have reasonable safety profiles, but their long- term safety and efficacy in patients with cirrhosis has yet to be demonstrated (Schuppan & Afdhal, 2008) Milk thistle (Silybum marianum) for many patients who have end-stage liver to treat jaundice and other symptoms disease (ESLD) Ursodeoxycholic acid (Actigall, URSO) for primary biliary to improve liver function. LIVER CIRRHOSIS GENERAL NURSING MANAGEMENT Promoting Rest Monitor weight and fluid intake and output Establish rest and other supportive measures to permit the liver to reestablish its functional ability. Adjusts the patient’s position in bed for maximal respiratory efficiency, which is especially important if ascites is marked, because it interferes with adequate thoracic excursion. Oxygen therapy may be required in liver failure to oxygenate the damaged cells and prevent further cell destruction After nutritional status improves and strength increases, the nurse encourages the patient to increase activity gradually. LIVER CIRRHOSIS GENERAL NURSING MANAGEMENT Improving Nutritional Status Encourages the patient to eat nutritious, high-protein diet, if tolerated, supplemented by vitamins of the B complex, as well as A, C, and K. Patients with fatty stools (steatorrhea) should receive water-soluble forms of fat-soluble vitamins A, D, and E (Aquasol A, D, and E). Protein is restricted if encephalopathy develops. Incorporating vegetable protein to meet protein needs may decrease the risk for encephalopathy. Sodium restriction is also indicated to prevent ascites. Patients with prolonged or severe anorexia and those who are vomiting or eating poorly for any reason may receive nutrients by the enteral or parenteral route. LIVER CIRRHOSIS GENERAL NURSING MANAGEMENT Providing Skin Care Frequently change patient’s position to prevent pressure ulcers. Avoid use of Irritating soaps and adhesive tape to prevent trauma to the skin. Apply lotion sooth irritated skin Establish measures to minimize scratching by the patient. Reducing Risk of Injury Protect the patient from falls and other injuries. Raise and pad side rails with blankets or other materials Orient the patient to time and place and explains all procedures to prevent agitation Instruct the patient to ask for assistance to get out of bed. Carefully evaluate any injury because of the possibility of internal bleeding. LIVER CIRRHOSIS MONITORING AND MANAGING POTENTIAL COMPLICATIONS Bleeding and Hemorrhage Patients with advanced chronic liver disease develop cardiovascular abnormalities. These occur due to an increased cardiac output and decreased peripheral vascular resistance, possibly resulting from the release of vasodilators. Hepatic Encephalopathy Monitor the patient’s mental status closely and reports changes so that treatment of encephalopathy can be initiated promptly. Administer oxygen if oxygen desaturation occurs. Monitors for fever or abdominal pain, which may signal the onset of bacterial peritonitis or other infection. Perform intensive nursing interventions aimed at providing for patient safety and prevention and early identification of life-threatening complications such as respiratory failure and cerebral edema. LIVER CIRRHOSIS MONITORING AND MANAGING POTENTIAL COMPLICATIONS Fluid Volume Excess Administer diuretics, implementing fluid restrictions, and enhancing patient positioning can optimize pulmonary function Monitor intake and output, daily weight changes, changes in abdominal girth, and edema formation is part of nursing assessment in the hospital or in the home setting. Monitor for nocturia and, later, for oliguria, because these states indicate increasing severity of liver dysfunction (Rodes, et al., 2007). LIVER CIRRHOSIS PROMOTING HOME AND COMMUNITY- BASED CARE Teaching Patients Self-Care Discharge plan should include exclusion of alcohol from the diet and also avoid the consumption of raw shellfish. Sodium restriction will continue for a considerable time, if not permanently. Instruct the patient and family about symptoms of impending encephalopathy, possible bleeding tendencies, and susceptibility to infection The nurse has a significant role in offering support and encouragement to the patient and in providing positive feedback when the patient experiences success. LIVER CIRRHOSIS PROMOTING HOME AND COMMUNITY-BASED CARE Continuing Care Referral for home care may assist the patient in dealing with the transition from hospital to home. The use of alcohol may have been an important part of normal home and social life in the past. The home care nurse assesses the patient’s progress at home and the manner in which the patient and family are coping with the elimination of alcohol and the dietary restrictions. The nurse also reinforces previous teaching and answers questions that may not have occurred to the patient or family until the patient is back home and trying to establish new patterns of eating, drinking, and lifestyle. CANCER OF THE LIVER Hepatic tumors may be malignant or benign. Benign liver tumors were uncommon until oral contraceptives were in widespread use. Benign liver tumors occur most frequently in women in their reproductive years who are taking oral contraceptives. CANCER OF THE LIVER Primary Liver Tumors Few cancers originate in the liver. Primary liver tumors usually are associated with chronic liver disease, hepatitis B and C infections, and cirrhosis. Hepatocellular carcinoma (HCC) is the most common type of primary liver cancer, with more than half a million cases diagnosed each year on a worldwide basis. HCC is the third leading cause of cancer related mortality worldwide. Risk Factors: cigarette smoking, alcohol use, aflatoxin, unrefrigerated foods Causes: Cirrhosis, chronic infection with hepatitis B and C, and exposure to certain chemical toxins (eg, vinyl chloride, arsenic) Other types of primary liver cancer include cholangiocellular carcinoma and combined hepatocellular and cholangiocellular carcinoma. CANCER OF THE LIVER Liver Metastases Metastases from other primary sites, particularly the digestive system, breast, and lung, are found in the liver 2.5 times more frequently than tumors due to primary liver cancers (Rodes, et al., 2007). Malignant tumors are likely to reach the liver eventually, by way of the portal system or lymphatic channels, or by direct extension from an abdominal tumor. Moreover, the liver apparently is an ideal place for these malignant cells to thrive. Often the first evidence of cancer in an abdominal organ is the appearance of liver metastases; unless exploratory surgery or an autopsy is performed, the primary tumor may never be identified. CANCER OF THE LIVER Liver Metastases – Clinical Manifestations The early manifestations of malignancy of the liver include: Pain—a continuous dull ache in the right upper quadrant epigastrium, or back. Weight loss, loss of strength, anorexia, and anemia may also occur. The liver may be enlarged and irregular on palpation. Jaundice is present only if the larger bile ducts are occluded by the pressure of malignant nodules in the hilum of the liver. Ascites develops if such nodules obstruct the portal veins or if tumor tissue is seeded in the peritoneal cavity. CANCER OF THE LIVER Liver Metastases – Assessment and Diagnostic Findings The diagnosis of liver cancer is based on clinical signs and symptoms, the history and physical examination, and the results of laboratory and x-ray studies. Increased serum levels of bilirubin, alkaline phosphatase, AST, GGT, and lactic dehydrogenase may occur. Leukocytosis (increased white blood cells) Erythrocytosis (increased red blood cells) Hypercalcemia, hypoglycemia, and hypocholesterolemia may also be seen on laboratory assessment. The serum level of alpha-fetoprotein (AFP), which serves as a tumor marker, is elevated in 30% to 40% of patients with primary liver cancer. The level of carcinoembryonic antigen (CEA), a marker of advanced cancer of the digestive tract, may be elevated. CANCER OF THE LIVER Liver Metastases – Assessment and Diagnostic Findings X-rays Liver scans CT scans Ultrasound studies MRI arteriography, and laparoscopy may be part of the diagnostic workup and may be performed to determine the extent of the cancer. Positive emission tomograms (PET) scans are used to evaluate a wide range of metastatic tumors of the liver CANCER OF THE LIVER Liver Metastases – Medical Management Radiation Therapy Chemotherapy Percutaneous Biliary Drainage Other Nonsurgical Treatments Laser hyperthermia has been used to treat hepatic metastases. Heat has been directed to tumors through several methods to cause necrosis of the tumor cells while sparing normal tissue. Radiofrequency thermal ablation Immunotherapy Transcatheter arterial embolization Ultrasound-guided injection of alcohol for multiple small lesions CANCER OF THE LIVER Liver Metastases – Surgical Management Lobectomy Removal of a lobe of the liver is the most common surgical procedure for excising a liver tumor. Local Ablation In patients who are not candidates for resection or transplantation, ablation of HCC may be accomplished by chemicals such as ethanol or by physical means such as radiofrequency ablation or microwave coagulation. Liver Transplantation Removing the liver and replacing it with a healthy donor organ is another way to treat liver cancer. CANCER OF THE LIVER Liver Metastases – General Nursing Management Before surgery, provide support, explanation, and encouragement to help the patient prepare psychologically for the surgery. After surgery, be attentive to potential problems related to cardiopulmonary involvement. A constant infusion of 10% glucose may be required in the first 48 hours to prevent a precipitous fall in the blood glucose level that results from decreased gluconeogenesis. Blood and IV fluid infusions may be needed. The patient requires constant, close monitoring and care for the first 2 or 3 days, similar to postsurgical abdominal and thoracic nursing care. If the patient is to receive chemotherapy or radiation therapy in an effort to relieve symptoms, he or she may be discharged home while still receiving one or both of these therapies. LIVER ABSCESSES Types Amebic Liver Abscesses most commonly caused by Entamoeba histolytica occurs in the developing countries of the tropics and subtropics because of poor sanitation and hygiene. Pyogenic Liver Abscesses much less common but are more common in developed countries than the amebic type. LIVER ABSCESSES Clinical Manifestations Sepsis like signs and symptoms: Fever with chills and diaphoresis Malaise Anorexia Nausea Vomiting, and Weight loss Dull abdominal pain and tenderness in the right upper quadrant of the abdomen. Hepatomegaly, jaundice, anemia, and pleural effusion may develop. Sepsis and shock may be severe and life-threatening with 100% mortality rate in the past due vague clinical symptoms, inadequate diagnostic tools, and inadequate surgical drainage of the abscess. With the aid of ultrasound, CT, MRI, and liver scans, early diagnosis and surgical drainage of abscesses have greatly reduced the mortality rate. LIVER ABSCESSES Assessment and Diagnostic Findings Blood cultures: unidentified organism Aspiration of the liver abscess, guided by ultrasound, CT, or MRI, may be performed to assist in diagnosis and to obtain cultures of the organism. Percutaneous drainage of pyogenic abscesses is carried out to evacuate the abscess material and promote healing. A catheter may be left in place for continuous drainage; the patient must be instructed about its management. LIVER ABSCESSES Medical Management Treatment includes IV antibiotic therapy Specific antibiotic used in treatment depends on the organism identified. Continuous supportive care is indicated because of the serious condition of the patient. Open surgical drainage may be required if antibiotic therapy and percutaneous drainage are ineffective. LIVER ABSCESSES General Nursing Management Monitor drainage and skin care for patients who underwent evacuation and drainage of an abscess. Implement strategies in containing the drainage and to protect the patient from other sources of infection. Monitor vital signs are monitored to detect changes in the patient’s physical status. Deterioration in vital signs or the onset of new symptoms such as increasing pain, which may indicate rupture or extension of the abscess, is reported promptly. Administer IV antibiotic therapy as prescribed. Monitor the white blood cell count and other laboratory test results closely for changes consistent with worsening infection. Prepare the patient for discharge by providing instruction about symptom management, signs and symptoms that should be reported to the physician, management of drainage, and the importance of taking antibiotics as prescribed.