Assessment and Management of Hepatic and Biliary Disorders PDF

Assessment and management of patients with Hepatic and Biliary Disorders Chapter 49 &50 1 2 Jordan University of Science and Technology Faculty of Nursing 3 4 5 ...

Assessment and management of patients with Hepatic and Biliary Disorders Chapter 49 &50 1 2 Jordan University of Science and Technology Faculty of Nursing 3 4 5  Functions of the Liver: Glucose Metabolism and regulation of blood glucose concentration. Ammonia conversion to urea that can be excreted in the urea. Protein Metabolism: Synthesis almost all plasma proteins+ clotting factors. Fat Metabolism: Breakdown of fatty acids for the production of energy and Ketone bodies Vitamin and Iron Storage: A, B12 and D And several of the B-Complex. Drug Metabolism Bile formation: Composed mainly from water, lecithin, and electrolytes and contain some fatty acids, chol., bilirubin and bile salts. Bilirubin Excretion 6  Gerontologic consideration Decreases in size and weight Reduced drug metabolism Increase risk of GB stone Higher risk of biliary tract diseases 7 Assessment 8  Health History: Present or previous exposure or ingestion of hepatotoxic agents, drugs Family history or history of cirrhosis, hepatitis, cancer History of blood transfusions, injection, dental treatment, hemodialysis Hepatic vein thrombosis Dietary intake Duration and onset of present symptoms 9  Physical Examination Skin Inspection  Pallor, Jaundice: Skin, Mucosa, and Sclera  Muscle atrophy, Edema, Skin excoriation from scratching (pruritis)  Petechia, Echomosis, Spider angiomas, and palmar erythema. Abdominal Assessment:  Dilated abdominal wall veins, Ascites, Abdominal dullness.  Palpation for liver tenderness, Size (Firm, sharp ridge with a smooth surface). Cirrhosis of the liver: smooth, hard, shrunken, fibrotic Acute Hepatitis: Soft edges and easily moves  Percussion of upper and lower borders. 10  Cognitive / neuro assessment Recall, memory, abstract thinking 11  Diagnostic Evaluation: Liver Function Tests Liver Biopsy Other Diagnostic Tests - Ultrasonography: guide the biopsy - Computed Tomography (CT): identify normal structure - Magnatic Resonance Imaging: identify normal structure - Laproscopy - A radio-Isotop Liver scan (Liver size and hepatic flow) 12  Common Liver Function Tests (table 39-1 p1121) 70% damage to notice change Serum Bilirubin Test (Direct, Total) http://www.youtube.com/watch?v=bFdTgty0T0I Serum Albumin Test Prothrombin Time (PT) Test Serum Alkaline Phosphatase Test: Elevation indicate an obstruction of bile flow, liver injury, or certain liver cancer Serum Ammonia 13  Serum Aminotransferases (transaminases): Released from damaged liver cells Alanin Transaminase (ALT) Test,: Released from damaged Liver cells. It is good indicator for the progress or worsening of the Liver Aspartate Transaminase (AST): Released from damaged liver, heart, muscle, or brain cell Gamma Glutamyl transpiptidase (GGT) and LDH: Increase in biliary cholistasis 14 15  Liver Biopsy chart 39-2 p 1122 Needle Aspiration of liver tissue to examine liver cells ( An Invasive Procedure) Out-patient procedure. - Location 6th intercostal space, Mid Axillary Line Preparation: - Check PT, PTT, And platelet count, and check for compatible donor blood. - Check for consent form. - Vital signs - Patient education is essential for preparation - anesthesia: local 16  During Procedure Nursing Care: - Position: Supine with RT arm above head. - Expose the Rt side of the patient’s upper ` abdomen (Rt hypochondriac region) - Instruct the patient to inhale and exhale several time then exhale and hold. - physician may create incision before introducing the needle 17  Post-Procedure Nursing Care: Turn the patient onto the Rt side, place the pillow under the costal margin for several hours ( Recumbent and immobile) for 1h, then on the back for 3h. - Assess vital signs q 10-15 min for 1 hr - observe puncture site for hemorrhage after test - if the patient discharge ask him to avoid heavy lifting and strenuous activity for 1 week - Major complications are liver injury, bleeding, and peritonitis, and Pneumothorax. Page 39-2 Video:http://www.youtube.com/watch?v=ug3n7bvq2Wg&featur e=related 18  Hepatic Dysfunction Clinical Manifestations of Liver Dysfunction: Jaundice: Increase concentration of Bilirubin Portal Hypertension Ascites Nutritional deficiencies: Result from the inability of the liver cells to metabolize certain vitamins. Hepatic Encephalopathy or coma: Due to accumulation of ammonia in the serum due to impaired protein metabolism. 19  Hepatic Disorders: 1. Jaundice: Bilirubin is (more than 2.5 mg/dl). Yellow- or green-tinged body tissues, sclera, and skin due to increased serum bilirubin levels 20 21  Types and causes: 1. Pre-hepatic (Hemolytic) Jaundice: Result of excess breakdown of RBC’s and liver is presented with more bilirubin than it’s capable of excretion - Hemolytic transfusion reaction - Hemolytic Disorders ( hereditary or acquired) - Hemolytic disease of the newborn - Autoimmune hemolytic anemia - increase urine and stool urobilinogen (formed in intestines, by bacterial reabsorbed) 2. Intra-hepatic (Hepatocellular): Decreased bilirubin uptake by damaged liver cells - Hepatitis - Cirrhosis - Cancer of the liver – Change in LFT 22  Cont…….. 3. Post-hepatic ( Obstructive) Jaundice: due to occlusion of the bile ducts - Gallstone ( cholelithiasis). - Inflammatory process - Tumor - pressure from enlarged organ 4. Hereditary Hyperbilirubinemia: due to several inherited disorders. - Gilbert’s syndrome - Dubin-Johnson syndrome Causes 1. Impaired Hepatic intake 2. Conjugation of bilirubin 3. Excretion of bilirubin into biliary system 23  Continue: Hepatocellular and obstructive jaundice types are most associated with liver disease. Signs and Symptoms Associated with Hepatocellular and Obstructive Jaundice Hepatocellular – Patient may appear mildly or severely ill. – Lack of appetite, nausea, weight loss – Malaise, fatigue, weakness – Headache, chills, and fever if infectious in origin Obstructive – Dark orange-brown urine and light clay-colored stools – Dyspepsia and intolerance of fats, impaired digestion – Pruritus 24  Clinical Manifestations Yellow Sclera Yellowish-orange Skin Clay-colored feces Tea-colored urine Pruritis Fatigue Anorexia Laboratory diagnostic tests: Increased serum bilirubin, alkaline phosphatase, cholesterol, serum bile salts, prolonged PT. 25  II. Portal Hypertension: Obstructed blood flow through damaged liver results in increased BP through the portal Venous system Consequences: 1. The formation of esophageal, gastric, and hemorrhoidal varices: Rupture cause massive bleeding 2. Ascites: Accumulation of fluid in the abdominal cavity\ 3. May cause splenomegaly The 2 main manifestations are: Ascites and varices 26  1. Ascites: Ascites: Fluid in Peritoneal Cavity Due To: Portal hypertension resulting in increased capillary pressure and obstruction of venous blood flow Vasodilatation of splanchnic circulation (blood flow to the major abdominal organs) Changes in the ability to metabolize aldosterone, increasing fluid retention Decreased synthesis of albumin, decreasing serum osmotic pressure Movement of albumin and fluid into the peritoneal cavity 27 Pathogenesis of Ascites p 1129 28  Manifestation 1. Increased abdominal girth 2. Bulging flanks 3. Striae 4. Distended veins 5. Rapid weight gain 6. SOB 7. Fluid and electrolyte imbalance 29  Assessment of Ascites Record abdominal girth and weight daily. Paient may have striae, distended veins, and umbilical hernia. Assess for fluid in abdominal cavity by percussion for shifting dullness or by fluid wave. Monitor for potential fluid and electrolyte imbalances. 30 Assessing for Abdominal Fluid Wave 31  Management Of Ascites Dietary modification: 1- negative Na balance to reduce fluid retention 2- no more than 2 g /day of sodium: if fluid accumulation is not relieved use 500 mg regimen and diuretics administered. 3- read food labels 4- taste of un-salted food can be adjusted using lemon juice, herbs, …etc 5- avoid salt substitutes: they contain K+ 6- teach patient: home care Dietary modification is only 10 % effective 32  Diuretics Successful in 90% Meds: 1- aldosteron blocking agent: Spironolactone, prevent K+ loss 2- Lasix: long use may cause Na depletion 3- Ammonium Chloride and Diamox: contraindicated, can cause coma. Daily weight loss should not > 2kg No fluid restriction unless Na level is very low Complication of diuretics: Electrolyte disturbance, dehydration/hypovolemia, Encephalopathy: K+ Ammonia 33  Bed rest: Upright position stimulates Renin-Angiotensin- Aldosteron system which decreases the response to diuretics http://www.youtube.com/watch?v=PDE2qdS2 ZvY 34  Paracentesis table p 1126 Primarily diagnostic But can be used in refractive ascites. 5-6 L can be removed Colloid fluid (salt-poor Albumin) to reduce risk of circulatory dysfunction after paracentesis 35  TIPS transjagular intrahepatic portosytemic shunt Treatment of choice for refractive ascites - reduce portal hypertension - decrease Na retention - improve response to diuretics - prevent recurrence of fluid accumulation 36 TIPS 37  Nursing Interventions: Monitor I/O, Nutritional status Monitor and prevent edema: Daily Wt and measurements of abd girth Promotion of breathing Monitor serum ammonia level Monitor electrolyte level Monitor cognitive status Monitor and promote skin integrity Promote comfort Teaching: Rx plan, avoid alcohol Continued care: home visit, adherence to Rx 38  2. Esophageal Varices: Are dilated tortuous veins found on the submucosa of lower esophagus Caused by portal hypertension which is due to portal venous circulation obstruction Bleeding Esophageal varices can lead to hemorrhagic shock, decreased cerebral, hepatic, and renal perfusion Encephalopathy risk is increased due to increased nitrogen load in GI tract from bleeding and increased serum ammonia levels Hemorrhage may result from: Lifting heavy objects, straining at stool, coughing, Vomiting, poorly chewed food, irritating fluids, reflux of stomach contents, and medication 30-50% mortality rate in 1st bleeding episode. Patho: blood seeks new routes (collatral circulation) due to the obstruction in vessels in submucusal layer. 39  Cont…… Clinical Manifestation 1. Hematemesis 2. Melena 3. General deterioration in mental or physical status 4. Cold clammy skin 5. Hypotension 6. Tachycardia 40  Cont….. Assessment and diagnostic Findings: to identify the bleeding site: 1. Endoscopy: NPO till gag reflex return 2. Barium swallow 3. Ultrasonography 4. CT 5. Angiography - Portal hypertension measures: indirect insertion of fluid-filled balloon catheter into the antecubital or femoral vein to the hepatic vein. Reading over 20 ml saline is abnormal. - Laboratory tests such as liver function test, blood flow and clearance studies to assess cardiac output and hepatic bld flow Managing Esophageal Varices: - monitor V/S, monitor signs of hypovolemia, O2 administration, Pharmacological therapy to decrease portal pressure ( Vasopressin and Beta Blockers), Balloon Tamponade: Sengstaken-Blakemore tube 41  Medical Management of Bleeding Esophageal Varices monitor circulating volume: central line V/S O2 IVF: caution for overhydration Balloon tamponade: Control Bleeding By applying pressure on the cardiac portion of the stomach and against the bleeding varices by a double-balloon tamponade (Sengstaken-Blakemore tube) - Has four opening: Gastric Aspiration, Esophageal aspiration, inflating of the gastric balloon, and inflating of the esophageal balloon - The pressure in the balloon should be 25-40 mmHg and to be checked q 2-4 hrs - Overinfalting and leaving balloon for long time may cause injury from ulceration and necrosis of the mouth nose or stomach mucosa - Displacement of tube may result in obstruction of airway and asphyxia from aspiration - Overinfalting may result in sudden rupture and aspiration of gastric content into the lung. - Frequent assessment for bleeding and inflation of balloons are needed in order to minimize the complications. 42 Balloon tamponade 43 Endoscopic therapy (injection sclerotherapy) Useful in GI bleeding, less effective in 1st and subsequent variceal bleeding Complications: esophageal stricture, perforation, aspiration pneumonia. Give antiacids post procedure to control sclerosing and reduce acid reflux. Esophageal Banding Therapy (Band Ligation) Treatment of choice Can be combined with pharmacologic treatment. Less risky than sclerosing Complications: lacerations, dysphagia, stricture (rare) TIPS 44  Surgical management of varices 1- surgical bypass: to reduce portal pressure 2- devascularization and transection Very risky: cause encephalopathy 2nd line management if everything else failed Summary available p1134 45  3. Hepatic Encephalopathy and Coma Results from accumulation of Ammonia and other toxic metabolites in the blood (eg. False neurotransmitters). Amonia: excited certain receptors on astrocyte cells, increases neurosteroid production, increases GABA neurotransmitor, depression of CNS Hepatic Coma represents most advanced stages of hepatic encephalopathy. (See stages in table 39-3, p1134) Ammonia is a result of enzyme and bacterial digestion of dietary and blood protein in the GI tract. GI bleeding in Esophageal Varices increases ammonia. Survival rate: 40% in 1 yr, after 1st episode. So, pt should be referred for liver transplant 46  Clinical manifestation Early symptoms: Mental changes Motor disturbances Alteration in mood Changes in personality Altered sleep pattern ( day and night reversal) Then: Asterixis( Flapping tremor of hands) - impaired writing and in ability to draw line or figures ( This way used to assess the improvement of the patient) - Constructional apraxia ( in ability to draw simple figures) EEG slowing of brain Waves Potential seizures Fetor Hepaticas: Sweet slightly fecal odor to the breath of intestinal origin 47 Asterixis 48 Effects of Constructional Apraxia 49  Medical Management: Eliminate the cause Lactulose: promotes excretion of ammonia through stool to reduce serum ammonia levels - Causes intestinal bloating and cramps - Monitor for hypokalemia and dehydration - For comatose pt give through NG tube or enema IV administration of glucose to minimize protein breakdown Administration of vitamins to correct deficiency Correct electrolyte imbalance 50  Cont.. Moderate restriction of protein intake( at least.5g/kg usually 1gkg-1.5g/kg) chart 39-5,p 1136 Small frequent meals and complex CHO Substitute vegetable protein for animal protein Reduction of ammonia from GI tract by gastric suction, enemas, oral antibiotics Discontinue sedatives, analgesics, and tranquilizers. Monitor for and promptly treat complications and infections. 51  Nursing management: Prevent injury, assess pt (neuro), assess respiration, intubation if needed, communicate with the family, teach self care. 52  Hepatitis—See Chart 39-6 Viral hepatitis: a systemic viral infection that causes necrosis and inflammation of liver cells with characteristic symptoms and cellular and biochemical changes. –A –B –C –D –E – Hepatitis G and GB virus-C Nonviral hepatitis—toxic and drug induced 53  Hepatitis A (HAV) Fecal–oral transmission Spread primarily by poor hygiene; hand-to-mouth contact, close contact, or through food and fluids Incubation: 15–50 days Illness may last 4–8 weeks Mortality is 0.5% for younger than age 40 and 1–2% for those over age 40 Manifestations: mild flu-like symptoms, low-grade fever, anorexia, later jaundice and dark urine, indigestion and epigastric distress, enlargement of liver and spleen Anti-HAV antibody in serum after symptoms appear 54  Management Prevention – Good hand washing, safe water, and proper sewage disposal – Vaccine: about 100% effective (2-3 doses) – See Chart 39-7 – Immunoglobulin for contacts to provide passive immunity Bed rest during acute stage Nutritional support (see Chart 39-8) 55  Hepatitis B (HBV) Transmitted through blood found in blood, saliva, semen, and vaginal secretions, sexually transmitted, transmitted to infant at the time of birth A major worldwide cause of cirrhosis and liver cancer Risk factors (see Chart 39-9) incubation period; 1–6 months. >90% recovers after that Manifestations: insidious and variable, similar to hepatitis A The virus has antigenic particles that elicit specific antibody markers during different stages of the disease 56  Management Prevention – Vaccine: for persons at high risk, routine vaccination of infants – Passive immunization for those exposed – Standard precautions/infection control measures – Screening of blood and blood products Bed rest Nutritional support Medications for chronic hepatitis type B include alpha interferon and antiviral agents: lamividine (Epivir), adefovir (Hepsera) 57  Hepatitis C Transmitted by blood and sexual contract, including needle sticks and sharing of needles The most common blood-borne infection A cause of 1/3 of cases of liver cancer and the most common reason for liver transplant Risk factors (see Chart 39-10) Incubation period is variable Symptoms are usually mild Chronic carrier state frequently occurs 58  Management Prevention Screening of blood Prevention of needle sticks for health care workers Measures to reduce spread of infection as with hepatitis B Alcohol encourages the progression of the disease, so alcohol and medications that effect the liver should be avoided Antiviral agents: combine 2 antivairal agents, interferon and ribavirin (Rebetol) 59  Hepatitis D and E Hepatitis D – Only persons with hepatitis B are at risk for hepatitis D. (needs HBsAG to replicate) – Transmission is through blood and sexual contact. Common in drug users. – Symptoms and treatment are similar to hepatitis B but more likely to develop fulminant liver failure and chronic active hepatitis and cirrhosis. – Rx: under investigation, interferon therapy. Hepatitis E – Transmitted by fecal–oral route, – Incubation period 15–65 days, – Resembles hepatitis A and is self-limited with an abrupt onset. No chronic form. 60  Other Liver Disorders Nonviral hepatitis – Toxic hepatitis – Drug-induced hepatitis Fulminant hepatic failure Rx: symptomatic, maintain fluid & E balance 61  Hepatic Cirrhosis Is a chronic disease characterized by replacement of normal liver tissue with diffuse fibrosis that disrupt the structure and function of the liver. Irreversible process http://www.youtube.com/watch?v=ex5wUWrZu bo&feature=related 62  Type of Hepatic cirrhosis: 1. Alcoholic cirrhosis: The scar tissue surrounds the portal areas and is the most common type. 2. Postnecrotic cirrhosis: There are broad bands of scar tissue as a late result of acute viral hepatitis 3. Biliary cirrhosis: Scarring occurs in the liver around the bile ducts. Usually is the result of chronic biliary obstruction and infection (Cholangitis). Less common type. The portion of the liver involved in cirrhosis consist of portal and periportal spaces where the bile canaliculi communicated to form the liver bile ducts These portions become inflamed and the bile duct become occluded with thickened bile an pus. 63  Pathophysiology ( Causes of Hepatic cirrhosis):. 1. Nutritional deficiency with reduced protein intake 2. Excessive alcohol intake ( Most common cause) 3. Exposure to certain chemecals ( carbon tetrachloride, chlorinated naphthalene, arsenic, or phosphorus) or exposure to infection Twice as many men as women are affected Most patients are between 40 and 60 years of age. 64  Clinical Manifestation: 1. Liver enlargement: Early symptoms, liver loaded with fatty tissue (firm and has sharp edge, producing abd pain, later the liver decreases in the size due to contraction of scar tissue and the edges become nodular. 2. Portal obstruction and ascites 3. Infection and peritonitis 4. Gastrointestinal varices 5. Edema 6. Vitamin deficiency and anemia 7. Mental deterioration 65  Cont…. Clinical manifestation: Compensated Decompensated Intermittent mild fever Ascites Vascular spider Jaundice Palmer erythema weakness Unexplained epistaxis Muscle wasting ankle edema weight loss Vague morning indigestion Continuous mild fever Flatulent dyspepsia purpora Abdominal pain spontaneous bruising Firm, enlarged liver Epistaxis splenomegaly Hypotension spares body hair white nails Gonadal atrophy Diagnostic Tests: LFT, CT, MRI, Ultrasound scanning and then confirmed by liver biopsy 66  Medical Management: Based on presenting symptoms Monitor for complications Maximize liver function - Antiacids to decrease gastric distress and minimize the possibility of gastric bleeding - Adequate rest, Vitamins and nutritional support to promote healing of damaged liver cells -Potassium sparing diuretics: for ascites - Avoidance of alcohol - adequate calories and protein ( unless if there is encephalopathy) - Fluid and elect. Restriction - Colchicine: anti inflammatory 67 Nursing Process: The Care of the Patient with Cirrhosis of the Liver: Assessment p1152 Focus on onset of symptoms and history of precipitating factors. Alcohol use/abuse Dietary intake and nutritional status Exposure to toxic agents and drugs Assess mental status. Abilities to carry out ADL/IADLs, maintain a job, and maintain social relationships Monitor for signs and symptoms related to the disease, including indicators for bleeding, encephalopathy, fluid volume changes, and lab data. 68  Diagnosis Activity intolerance Imbalanced nutrition Impaired skin integrity Risk for injury and bleeding 69  Collaborative Problems/Potential Complications Bleeding and hemorrhage Hepatic encephalopathy Fluid volume excess 70  Planning Goals may include increased participation in activities, improvement of nutritional status, improvement of skin integrity, decreased potential for injury, improvement of mental status, and absence of complications. 71  Activity Intolerance Rest and supportive measures Positioning for respiratory efficiency Oxygen Planned mild exercise and rest periods Address nutritional status to improve strength. Measures to prevent hazards of immobility 72  Imbalanced Nutrition I&O Encourage patient to eat. Small, frequent meals may be better tolerated. Consider patient preferences. Supplemental vitamins and minerals, especially B complex; provide water-soluble forms of fat-soluble vitamins if patient has steatorrhea High-calorie diet, sodium restriction for ascites Protein is modified to patient needs. Protein is restricted if patient is at risk for encephalopathy. 73  Other Interventions Impaired skin integrity – Frequent position changes – Gentle skin care – Measures to reduce scratching by the patient Risk for injury – Measures to prevent falls – Measures to prevent trauma related to risk for bleeding – Careful evaluation of any injury related to potential for bleeding 74  Nursing Management of Cirrhosis: 1. Adequate Nutrition 2000-3000 cal/day High protein to help liver regenerate unless encephalopathy is there High CHO - Restrict F/E intake if Ascites or edema presents Rest frequently Control temperature Antiemetic, antiacids, antidiarrheal as ordered Vitamins supplements (Fat soluble) 2. Removal all hepatotoxic drugs 3. Avoid alcohol, and give antibiotic if ordered 75  Cancer of the liver: May be malignant or Benign (uncommon) Primary liver cancer are associated with - Chronic liver disease - Hepatitis B, and C infection - Cirrhosis Type of primary Liver cancer:(few) 1. Hepatocellular carcinoma (HCC): Most common type. nonresectable 2. Cholangiocellular carcinoma: Resectable if early detected 3. Hepatocellular and cholangiocellular carcinoma: Most of liver cancers are metastasized from other organs( Secondary) 76  Clinical Manifestation: Pain, continuous dull ache in the right upper Quadrant, epigastrium or back Wt loss Loss of strength Anorexia Anemia may occur Enlarged liver and irregular in palpation Jaundice and Ascites Assessment and Diagnostic tests X-ray. LFT, increase alpha fetoprotien (AFP)/tumor marker, histology/biopsy. 77  Medical Management: 1. Nonsurgical Management: Radiation therapy Chemotherapy Percutaneous Biliary drainage: are used to reestablish biliary drainage, relieve pressure and pain and decrease pruritus and jaundice. (Catheter inserted through the abd wall pass the obstruction then to DU after days the catheter is opened to external drainage to assess the bile amount, color and content). Laser hyperthermia: Using heat and direct it to tumor Immunotherapy: under investigation 78  Cont….. 2. Surgical Management: Lobectomy: Surgical resection of part of the liver up to 90%(Most common surgical procedure Local ablation: if not candidate for transplant. E.g. radiofrequency ablation. Complication: pain, bleeding Liver transplantation: Replacement the liver with healthy donor organ. Recurrence of primary tumor is 70-80% after transplantation. 79 Liver, Biliary System, and Pancreas 80  Biliary Conditions: Definition of terms: Biliary (chart 40-1) Cholecystitis: Inflamation of the gallbladder Cholelithiasis: the presence of calculi in the gallbladder Cholecystectomy: removal of the gallbaldder Cholecystostomy: opening and drainage of the gallbladder Choledochotomy:opening into the common duct Choledocholethiasis: stone in the common duct 81  Cont….. Choledochlithotomy: incision of common bile duct for removal of stones Choledochoduodenostomy: anastomosis of common duct to DU Choledochojejunostomy: anastomosis of CD to jejunom Lithotripsy: disintegration of gallstones by shock waves Laparoscopic chlecystectomy: removal of gallbladder by endoscopic procedure Laser Cholecystectomy: Removal of gallbladder using laser. 82  Cholecystitis: Acute infection of the gallbladder causes pain, tenderness, and rigidity of the upper Rt abd and associated with nausea and vomiting and positive Murphy’s sign. Pain may radiate to midsternal or to RT shoulder 83  Types: 1. Calculous: gallbladder stone obstruct bile outflow causing back up of the bile in the gallbladder leading to autolysis and edema. Vascular supply is compromised and leads to gangrene and perforation 2. Acalculous: Acute gallbladder inflammation in the absence of obstruction by gallstones (major surgical procedure, trauma, or burns, cystic duct obstruction, primary bacterial infection, multiple blood transfusion 84  Cholithiasis Calculi, or gallstone usually formed in the gallbladder from the solid constituent of the bile and vary in size, shape and composition 1. Pigment stone: precipitating of unconjugated pigment in the bile to form stones represent one third of cases. Causes cirrhosis, hemolysis and infection of the biliary tree 2. Cholesterol stones: more common, Cholesterol is insoluble in water, solubility depend on bile acid and lecithin (phospholipid) in bile. Decreased bile acid and increase cholesterol synthesis in liver cause bile supersaturation with cholesterol which precipitate and form stone 85  Cont… Four time more women than men develop cholelesterol stones and gallbladder disease (due to estrogen and contraceptive use which increase cholesterol saturation) Risk factors : Obesity, multi parous, Frequent changes in Wt, Rapid Wt loss, oral contraceptive, estrogens, cystic fibrosis, DM, and increases with age due to more cholesterol synthesis and decreased bile acid synthesis 86  Clinical Manifestations: Silent, producing no pain and only mild GI symptoms( detected accidentally). Pain and biliary colic, jaundice, change in urine (dark) and stool color (light), vit deficiency (fat-soluble) Two type of Symptoms ( which may be acute or chronic) 1. From disease of the gallbladder itself: epigastric distress following fatty meal( fullness, abdominal distention) vague pain in the RUQ 2. From Obstruction of the bile passage by gallstone fever palpable mass Colicky pain ( Rt abdominal pain radiated to the back or Rt shoulder) Nausea and vomiting Murphy’s sign (inspiratory pain): Positive Jaundice (commonly occurs with obstruction of common bile duct) Changes in Urine color (dark color) and stool color ( clay-colored) Vitamin deficiency ( fat-soluble vitamins) 87  Diagnostic Tests: Abdominal X-ray U/S Radionuclide imaging: IV radioactive agent Cholecystography: oral iodine contrast agent used 10-12 hrs before X-ray, NPO Endoscopic retrograde cholengiopancretography (ERCP): Direct observation through fiberoptic scope inserted through esophagus into DU ( Discuss nursing implication). Percutaneous transhepatic Cholengiography: inject the dye directly into the biliary tree. 88  Cont……… Medical management: Treatment of acute symptoms Nutritional and supportive treatment: Low- fat, liquid diet, rest, IV fluids, nasogastric suction, analgesia and antibiotics Pharmacological therapy to dissolve small, radiolucent gallstones composed primarily of cholesterol (ursodeoxycholic acid and chenodeoxycholic acid) 89  Nonsurgical removal of gallstones Dissolving gall stone: infusion of solvent into the gallbladder Extracorporeal shockwave lithotripsy (through water bath): Pt should have < 4 stones,< 3 cm in diameter, and no liver or pancreas disease. Contraindicated inflammatory disease of the biliary system Intracorporeal lithotripsy: by ultrasound, pulsed laser By Instrumentation: such as ERCP 90  Surgical Management: Laparoscopic Cholecystectomy Cholecystectomy Mini-Cholecystectomy Choledochostomy Surgical Cholecystostomy: opening the gallbladder to remove the stone or the pus by drainage when severely inflamed before removal. Percutaneous Cholycystostomy. 91  Nursing Process: Undergoing Surgery for Gallbladder Disease: Assessment Patient history Knowledge and teaching needs Respiratory status and risk factors for postop respiratory complications Nutritional status Monitor for potential bleeding. GI symptoms: after laparoscopic surgery, assess for loss of appetite, vomiting, pain, distention, fever-- potential infection or disruption of GI tract. 92  Diagnosis: Acute pain Impaired gas exchange Impaired skin integrity Imbalanced nutrition Deficient knowledge 93  Collaborative Problems/Potential Complications Bleeding Gastrointestinal symptoms Complications as related to surgery in general: atelectasis, thrombophlebitis Planning Goals may include relief of pain, adequate ventilation, intact skin, improved biliary drainage, optimal nutritional intake, absence of complications, and understanding of self-care routines. 94  Postoperative Care Interventions Low Fowler’s position May have NG tube NPO until bowel sounds return, then a soft, low-fat, high-carbohydrate diet postoperatively Care of biliary drainage system Administer analgesics as ordered and medicate to promote/permit ambulation and activities, including deep breathing. Turn, and encourage coughing and deep breathing, splinting to reduce pain. Ambulation 95  Patient Teaching (See Chart 40-3) Medications Diet: at discharge, maintain a nutritious diet and avoid excess fat. Fat restriction is usually lifted in 4-6 weeks. Instruct in wound care, dressing changes, care of T-tube. Activity Instruct patient and family to report signs of gastrointestinal complications, changes in color of stool or urine, fever, unrelieved or increased pain, nausea, vomiting, and redness/edema/signs of infection at incision site. 96  Pancreatitis A severe disorder that can lead to death. Acute pancreatitis does not usually lead to chronic pancreatitis. Acute pancreatitis: pancreatic duct becomes obstructed and enzymes back up into the pancreatic duct, causing autodigestion and inflammation of the pancreas Chronic pancreatitis: a progressive inflammatory disorder with destruction of the pancreas. Cells are replaced by fibrous tissue, and pressure within the pancreas increases. Mechanical obstruction of the pancreatic and common bile ducts and destruction of the secreting cells of the pancreas occur. 97  Causes: Biliary tract disease: Stones Long term use of alcohol Bacterial or viral infection Blunt abd trauma, peptic ulcer, ischemic vascular disease Hyperlipidemia, hypercalcemia Use of corticosteriods, thiazide diuretics, and oralcontraceptivr ERCP or surgeries near to pancreas. 98  Assessment and diagnostic findings History of Abd pain Serum amylase and Lipase Increase WBC’s X-Ray studies Ultrasound Abd CT-Scan ERCP rarely used because patient is acutely ill. 99  Manifestations Acute: Severe abdominal pain Patient appears acutely ill. Abdominal guarding Nausea and vomiting Fever, jaundice, confusion, and agitation may occur. Ecchymosis in the flank or umbilical area may occur. Patient may develop respiratory distress, hypoxia, renal failure, hypovolemia, and shock. Chronic: Recurrent attacks of severe upper abdominal and back pain accompanied by vomiting Weight loss Steatorrhea 100  Nursing Process: Assessment Focus on abdominal pain and discomfort. Fluid and electrolyte status Medications Alcohol use GI assessment and nutritional status Respiratory status Emotional and psychological status of patient and family; anxiety and coping 101  Diagnosis: Acute pain Ineffective breathing pattern Imbalanced nutrition Impaired skin integrity Collaborative Problems/Potential Complications: Fluid and electrolyte disturbances Necrosis of the pancreas Shock Multiple organ dysfunction syndrome DIC Planning: Major goals include relief of pain and discomfort, improved respiratory function, improved nutritional status, maintenance of skin integrity, and absence of complications. 102  Relieving Pain and Discomfort Use of analgesics Nasogastric suction to relieve nausea and distention Frequent oral care Bed rest Measures to promote comfort and relieve anxiety 103