Unit 3--GI - Hepatic ^0 Billary Problems--Revised.pdf

NURS20009 Nursing Care 2 Unit 3 Nursing Care of Clients Experiencing Gastrointestinal (Hepatic and Biliary) Problems Unit 3 Topical Outline Definition—Jaundice,, Hepatitis, Hepatic Cirrhosis, Portal Hypertension (Ascites, Oesophageal Varices) (Liver Cancer, Liver Transplant), Cholelithiasis, Acute a...

NURS20009 Nursing Care 2 Unit 3 Nursing Care of Clients Experiencing Gastrointestinal (Hepatic and Biliary) Problems Unit 3 Topical Outline Definition—Jaundice,, Hepatitis, Hepatic Cirrhosis, Portal Hypertension (Ascites, Oesophageal Varices) (Liver Cancer, Liver Transplant), Cholelithiasis, Acute and Chronic Pancreatitis Pathophysiology/ Causes Risk Factors Manifestations Diagnostic Tests Treatment Nursing Interventions (discussion) Complications The Nursing Process (discussion) Case Study and Critical Thinking Functions of the Liver Glucose metabolism Ammonia Conversion Protein metabolism Fat Metabolism Vitamin and Iron Storage Bile Formation Bilirubin Excretion Drug metabolism Physiological (normal) jaundice: occurring in most newborns, this mild jaundice is due to the immaturity of the baby's liver, which leads to a slow processing of bilirubin. It generally appears at 2 to 4 days of age and disappears by 1 to 2 weeks of age. NORMAL BLILIRUBIN VALUES: It is normal to have some bilirubin in the blood. A normal level is: Direct (also called conjugated) bilirubin: 0 to 0.3 mg/dL Total bilirubin: 0.3 to 1.9 mg/dL Jaundice Jaundice Yellow discolouration of tissue Increase in bile pigments (bilirubin) resulting from liver disease A sign of disease Pathophysiology – When a small number of red blood cells die, they are replaced by new ones – Liver removes the old blood cells forming bilirubin – Liver helps break down bilirubin so that it can be excreted as bile through intestines – When too much bilirubin builds up in the body, jaundice may result – Due to overloaded or damaged liver; bilirubin from the liver unable to move through the digestive tract properly Pathophysiology Types of Jaundice Physiologic Jaundice - Common in newborns –livers not fully developed - treated with phototherapy Pathologic Jaundice - Occurs in children and adults – Infants - Starts as physiologic and becomes worse by dehydration or premature birth – Adults - Blood incompatibilities and diseases (hepatitis, cirrhosis, infections and medications) Jaundice Manifestations—Yellow skin and sclera, yellow color inside the mouth, dark or brown colored urine, pale or clay colored stools Diagnostic Tests—Physical exam (swelling of liver), bilirubin blood test, urine and stool sample, hepatitis virus panel, liver function tests, CBC, abdominal ultrasound, abdominal CT scan, liver biopsy, cholesterol level, PTT Jaundice Liver Biopsy Abdominal Ultrasound Jaundice Treatment – Adults—treat underlying cause – Infants—treat with phototherapy, frequent feedings of breast milk or formula Liver Biopsy How to Prepare for the Test Tell your health care provider about: Bleeding problems Drug allergies Medications you are taking Whether you are pregnant You must sign a consent form. Blood tests are sometimes done to test your blood's ability to clot. You will be told not eat or drink anything for the 8 hours before the test. What Happens: Sedation, Image used (US) to guide needle to liver. Biopsy used to diagnose: liver diseases including all the hepatitis family, cancer, infections, cause of elevated enzymes, cause of unexplained enlargement. Hepatitis Hepatitis Hepatitis – swelling and inflammation of the liver Causes – Autoimmune diseases – Genetic abnormalities – Infections from viruses (Hepatitis A, B, C, D and E) – Liver damage from alcohol, poisonous mushrooms, medications (overdose of acetaminophen) Hepatitis Type Transmission Incubation Prevention Hepatitis A Oral fecal route— 2 to 7 weeks food, water, milk, selfish Vaccinations, hand washing Hepatitis B (most prevalent) (More serious as can lead to cirrhosis) Infected blood or plasma, needles, syringes; sexually transmitted through vaginal secretions and semen 6 to 26 weeks Immunizations, safe sex; HB immune globulin for recent contact (infected with body fluids) Hepatitis C (Can lead to cirrhosis, liver cancer) Infected blood or 2 to 20 blood products weeks (transfusions, tattooing); sexual contact No vaccine; no sharing of needles or syringes, safe sex Hepatitis Manifestations—s/s of jaundice, fever, anorexia, nausea and vomiting, liver tenderness, elevated liver enzymes and bilirubin, presence of hepatitis virus in the feces and serum Diagnostic Tests—same as jaundice including serum ammonia levels (if ↑, protein is restricted) Hepatitis The liver normally converts ammonia into urea, which is then eliminated in urine. Ammonia levels in the blood rise when the liver is not able to convert ammonia to urea. This may be caused by cirrhosis or severe hepatitis. Ammonia resulting from protein digestion. High amounts of ammonium ion in the blood affects the brain with a range of symptoms from mild confusion to possible brain damage and death. Typical symptoms of acute hepatitis are: Fever; Appetite loss; Nausea; Abdominal pain; and Jaundice (yellowish colour on the skin and eyeballs). Hepatitis Treatment – Monitor liver function studies – Bed rest with bathroom privileges – High-calorie, high-carbohydrate, high-protein, moderate fat diet – Topical lotions to alleviate dry, itchy skin – Hydrate with IV therapy – Monitor for bleeding tendencies and progression of illness – Blood and body fluid precautions – Monitor patient & family copying – Antiviral in some cases – Supplemental vitamin K accelerates the production of functional clotting factors and helps to decrease the likelihood of serious hemorrhage. Doctors can measure the effectiveness of vitamin K therapy by determining how long it takes your blood to clot. Hepatitis Health Promotion: Prevention of Hepatitis Encourage proper sanitation Instruct patients regarding safe practices for preparing and handling food Promote mandatory reporting of viral hepatitis to local public health department Recommend vaccination all school-age children(in Canada); travelers to developing countries, illegal drug users, men who have sex with men, people with chronic liver disease, & healthcare professionals Hepatic Cirrhosis Hepatic Cirrhosis Chronic disease characterized by replacement of normal liver tissue with diffuse fibrosis that disrupt the function of the liver. Scaring of liver and poor liver function Final phase of liver disease Complication of alcoholism and hepatitis Hepatic Cirrhosis Types Alcoholic cirrhosis: Scar tissue charactistically surrounds the portal areas. Caused by chronic alcoholism; the most common type of cirrhosis. Protnecrotic cirrhosis: There are broad bands of scar tissue. A late result of a previous bout of acute viral hepatitis Biliary cirrhosis: Scarring occurs in the liver around the bile ducts. Usually results from chronic biliary obstruction & infection (cholangitis); its less common type of cirrhosis. Hepatic Cirrhosis Other Factors that lead to cirrhosis: – Nonalcohol fatty liver disease (NAFLD) – Cases of nutrition-related cirrhosis have resulted from extreme dieting, malabsorption, and obesity. – Environmental factors, as well as a genetic predisposition © 2019 Elsevier Canada, a division of Reed Elsevier Canada, Ltd. Hepatic Cirrhosis Early manifestation Compensated – Abdominal pain – Lassitude – Fatigue – Weight loss – Enlargement of liver and spleen Decompensated – Anorexia – Dyspepsia – Nausea/vomiting – Weakness, muscle loss – Change in bowel habits Hepatic Cirrhosis Late manifestations Two causative mechanisms – Liver failure – Portal hypertension Other —liver enlargement, portal obstruction, ascites, infection & peritonitis, gastrointestinal varices, edema, Vit. A,C,&K deficiency, anemia, & mental disorientation. Clinical Manifestations © 2019 Elsevier Canada, a division of Reed Elsevier Canada, Ltd. Hepatic Cirrhosis Diagnostic Tests—Physical exam (swelling of liver), bilirubin blood test, urine and stool sample, hepatitis virus panel, liver function tests, CBC, abdominal ultrasound, abdominal CT scan, liver biopsy, cholesterol level Treatment – Rest with activity as tolerated – Nutritious diet with protein level determined by liver functioning – Monitoring for complications such as ascites, esophageal varices, liver cancer and hepatic coma and providing appropriate nursing care – Drug therapy to reduce ammonia levels, prevent bleeding, reduce edema and provide comfort – End-stage liver disease—Liver transplant Complications Portal hypertension Esophageal and gastric varices Peripheral edema and ascites Hepatic encephalopathy © 2019 Elsevier Canada, a division of Reed Elsevier Canada, Ltd. Portal Hypertension Portal Hypertension An increase in the pressure within the portal vein (vein that carries blood from the digestive organs to the liver—supplies 75% of liver’s blood and 60% of its O₂) Usually develops in people who have liver damage Primary mechanism is increased resistance to blood flow through the liver. Portal Hypertension Pathophysiology: Scar tissue in the liver interrupts normal blood flow causing blood to back up into the portal vein and increasing blood pressure This backup causes the blood to force its way into tiny, thin walled veins at the base of esophagus and in the stomach These fragile blood vessels, known as varices, become stretched, swollen and twisted and may rupture causing hemorrhage and subsequent shock Pathophysiology Portal Hypertension Causes—Cirrhosis, chronic viral hepatitis, thrombosis or clotting in the portal vein Portal Hypertension Manifestations – Esophageal varices (EV) Hematemesis and coffee-ground emesis, melena, tachycardia – Ascites (lack of albumin) Abdominal pain, bloating, increased abdominal girth, weight gain – Encephalopathy (due to ammonia) Lethargy, irritability, confusion and forgetfulness Portal Hypertension Esophageal Varices Encephalopathy Ascites Portal Hypertension Diagnostic Tests – Physical exam(abdominal) and history (alcoholism) – EV—CT scan, ultrasound, endoscopy, blood tests (Hgb, liver function) – Ascites—24-hour urine collection, creatinine and electrolytes, kidney function tests, abdominal percussion(fluid wave) – Encephalopathy—Drug or toxin level, MRI brain, EEG, WBC (↓) Portal Hypertension Treatment for Esophageal Varices – Severe bleeding of varices: IV fluids, blood transfusions, emergency endoscopy – Other procedures: Sclerotherapy, band ligation, balloon tamponade – Medications: Vasodilators, vitamin K (crucial for bld clotting – helps make 4 of the 13 proteins needed for blood clotting) – Surgery: Implanting a stent (relieve pressure) Portal Hypertension Sclerotherapy Balloon Tamponade Stent Placement Band Ligation Portal Hypertension Treatment for Ascites – Lifestyle changes: Avoid alcohol, low sodium diet and diuretics – Reduce abdominal swelling: Paracentesis or abdominal tap Portal Hypertension Treatment for Encephalopathy – Medications (remove toxins from the intestines) Substituting vegetable protein for animal protein Laxatives Lactalose Antibiotics Liver Transplant—Severe variceal bleeding and end-stage liver disease Nutritional Therapy Diet for client without complications – High in calories (3 000 kcal/day) – Increase carbohydrate – Moderate to low fat – Protein restriction rarely justified Protein supplements if protein-calorie malnutrition Low-sodium diet for client with ascites and edema © 2019 Elsevier Canada, a division of Reed Elsevier Canada, Ltd. Nursing Management Monitor In & Out Measure abdominal girth (for ascites) Daily weights Monitor cognitive status Monitor Vitals Monitor daily labs (lytes, ammonia levels, CBC, INR, PTT) Special Diets restrictions (in some cases) – Soft diet/fluids only – Adequate protein – Low sodium Nursing Interventions Assess and document s/s and reactions to tx Administer prescribed medication Provide and encourage prescribed diet Skin care (edema) Monitor vital signs at least 4 hours and report abnormalities Monitor status of ascites Provide planned exercise and rest periods Assist patient with ADLs Monitor skin status and take measures to prevent skin breakdown Reduce risk of injury Increased risk for bleeding Increased risk for confusion Offer emotional support Hepatic Cirrhosis Complication – Liver cancer – Causes: Unknown – Risk factors: Chronic hepatitis B and C, liver cirrhosis, exposure to toxins (fungi— aflatoxin), smoking, Alcohol – Treatment—Radiation, chemotherapy, surgery (resection[lobectomy, local ablation]), liver transplant, support group Liver Cancer Symptoms In the early stages, liver cancer does not cause symptoms. Some common symptoms of advanced liver cancer include: weight loss loss of appetite abdominal pain jaundice fluid in the abdomen How is liver cancer detected? ultrasound blood test to check for increased levels of alpha-fetoprotein (AFP) computer tomography scan (CT) magnetic resonance imaging (MRI) Cholelithiasis Cholelithiasis Cholelithiasis—Presence of gallstones in the gallbladder or biliary tree Cholecystitis: is acute inflammation of the gallbladder. Caused by gallstones. Causes—Precipitated by chemical changes in bile – Bile, stasis, infections of the gallbladder and metabolic changes can precipitate stone formation – Stones may lodge in the biliary tree, causing obstruction and biliary colic Cholelithiasis Cholelithiasis Manifestations—Pain & biliary colic (especially after Indigestion after a meal high in fat), nausea and vomiting, flatulence, belching, right upper-quadrant pain, fever, s/s of jaundice, elevated WBC count, changes in urine(dark color) & stool color(greyish or clay-color), Vit. A,D,E,&K deficiency. Diagnostic Tests—Patient history and physical exam, lab studies (LFT, Lipids), oral cholecystography, IV cholangiography, ultrasound of gallbladder Cholelithiasis Oral Cholecystography Gall bladder Ultrasound IV Cholangiography Cholelithiasis Treatment – – – Hydration with fluids Drug therapy—analgesics, antibiotics Low-fat diet Others – – – Lithotripsy (use of shock waves to disintegrate gallstones) Cholecystectomy (gallbladder) or Cholecystectomy (gallstones) Laparoscopic cholecystectomy (removal through an endoscope inserted through the abdominal wall) Nursing Interventions Nursing Intervention post-op cholecystectomy: Monitor vitals signs Assess breathing pattern Inspect dressing for bleeding T-tube, note color and amount of drainage Inspect skin breakdown around the incision NG tube drainage and suctioning Monitor pain Measure I/O Administer IV fluids if still NPO Nutrition—blended and small meals, avoid fatty foods Nutritional Therapy Diet modifications (cont.) – After laparoscopic cholecystectomy Liquids for day Light meals for several days – After incisional cholecystectomy Liquids to bland diet after return of bowel sounds May need to restrict fats for 4–6 weeks © 2019 Elsevier Canada, a division of Reed Elsevier Canada, Ltd. Patient Teaching Resuming Activity: Light exercise (walking) immediately; Take a shower or bath after 1-2 days Avoid heavy lifting (not >5lbs) after surgery Resume sexual activity when desired Caring for the Wound: Check puncture site daily for signs of infection Wash puncture site with mild soap and water Allow special adhesive strips on the puncture site to fall off Resuming Eating: Resume usual diet If fat intolerance before surgery, gradually add fat as tolerated Patient Teaching Managing pain: Take analgesics as prescribed Sitting upright in bed/chair; walking; or use of heating pad Follow-up Care: Follow-up 7-10 days post surgery Notify surgeon if redness, drainage or pus from incision is noted Report any signs of peritonitis: – Severe abdominal pain, – Chills, – Fever – and vomiting Acute and Chronic Pancreatitis Acute and Chronic Pancreatitis Pancreatitis— ___________________________________ Evolve Video Pancreatitis Acute and Chronic Pancreatitis Manifestations – Acute pancreatitis: Upper left quadrant pain, pain aggravated by eating, nausea and vomiting, fever, hypotension, tachycardia, jaundice, elevated WBC – Chronic pancreatitis: Abdominal pain, weight loss, steatorrhea, DM – Treatment: same as cholelithiasis including NG tube and NPO, control of blood glucose levels Acute and Chronic Pancreatitis Diagnostic Tests—Patient history and physical exam, lab tests (electrolytes, amylase, lipase and liver enzymes), pancreatic scan and ultrasound, endoscopy, x-ray studies Nursing Management Relief pain and discomfort: Analgesics as prescribed, Assess pain & effectiveness of interventions Nonpharmacological interventions – (i.e music, distractions, imagery). Improving breathing pattern: Semi-fowler’s position; change position frequently Pulmonary assessment: pulse oximetry/arterial gases Deep breathing & coughing Nursing Management Improving Nutritional status: Enteral or parenteral nutrition may be prescribed Monitor serum glucose q4-6hrs Reintroduce oral feeding as tolerated A diet high in carbohydrate & low in fat & protein between acute attack Avoid heavy meals & alcoholic beverages. Maintaining Skin Integrity: Assess wound, drainage sites, & skin for signs of – Infection, inflammation, & breakdown. Consult with wound-ostomy nurse Turn patient q2hrs Use specialty beds to prevent skin breakdown Nursing Management Monitoring and Managing Potential Complications: Assess patient's fluids & electrolyte Weight patient daily Measure intake & output Assess and monitor for hypovolemic shock Monitor vital signs Monitor patient for signs of: – neurologic, – cardiovascular, – renal, – and respiratory dysfunction. References Day, R.A., Paul, P., Williams, B., Smeltzer, S.C., Bare, B.. Brunner and Suddarth's Textbook of Canadian Medical-Surgical Nursing (Current Edition). Philadelphia: Lippincott Williams & Wilkins Kwong, J., Reinisch, C., Tyerman, J., Cobbett, S., Hagler, D., Harding, M., & Dott (2023). Lewis's Medical-Surgical Nursing in Canada (5th Edition). Elsevier Health Sciences (US). Lewis, S.L., Bucher, L., Heitkemper, M.M., Harding, M.M., Barry, M.A., Lok, J., Tyerman, J., Goldsworthy, S. (2019). MedicalSurgical Nursing in Canada (4th ed.). CA: Elsevier