PHYSICS OF SOUND Powerpoint Presentation

PHYSICS OF SOUND

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Slide 1 :

Cirrhosis of the Liver andLiver Failure Developed by Cheryl McConnell RN MSN

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Pathophysiology Slow, insidious, progressive, chronic Fibrous bands replace normal liver structure Cell degeneration occurs Liver attempts to regenerate cells but cells are abnormal and disorganized Causes abnormal blood and lymph flow Results in more fibrous tissue formation

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Normal Liver

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Incidence of Cirrhosis Tenth leading cause of death in US At least 25,000 deaths annually Higher death rates for men than women ? mortality in African Americans and Hispanics

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Types of Cirrhosis Laennec’s (alcoholic) Postnecrotic Biliary Cardiac

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Laennec’s Cirrhosis Most common type of cirrhosis Also called alcoholic or portal Alcohol causes inflammation to liver cells Leads to fatty deposits and hepatomegaly Scarring formed and liver cells destroyed Malnutrition and more alcohol accelerate the damage

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Postnecrotic Cirrhosis Caused by viral hepatitis or hepatotoxins Scar tissue destroys liver lobes Liver initially enlarges but then shrinks in size 10 – 30% of all cirrhoses

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Biliary Cirrhosis Caused by chronic biliary obstruction or stasis of bile, biliary inflammation, or hepatic fibrosis Excessive bile leads to liver cell destruction and formation of nodules in the lobes 5 – 10% of all cirrhoses

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Cardiac Cirrhosis Seen with right sided heart failure Liver is engorged with venous blood Becomes enlarged, edematous, and dark Venous congestion results in anoxia Cell necrosis results

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Diagnostic Data ? AST, ALT, LDH, Alk phos ? bilirubin, ammonia, ? coagulation studies Serum protein levels depend on disease ? with acute liver disease ? with chronic liver disease

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More Diagnostics Abdominal x-ray Upper GI series Angiography Abdominal CT EGD Liver biopsy Nuclear scan

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Signs and Symptoms Neurological Asterixis Paraesthesias LOC Sensory disturbances Behavorial changes Cognitive changes Skin Spider angiomas Palmar erythma Jaundice Pruitis ? hair production caput medusa ? pigmentation Bruising White Nails

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Caput Medusae

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Spider Angiomas

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Palmar Erythema

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More Signs and Symptoms GI Abdominal pain Anorexia Ascites Diarrhea Clay colored stools Fetor hepaticus Gastritis GI bleeding N/V Varices Malnutrition

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“White Nails”

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More Signs and Symptoms Cardiovascular Dysrhythmias Portal hypertension Collateral circulation Fatigue Peripheral edema Endocrine Gynecomastia Amenorrhea ? aldosterone, ADH, estrogens, glucocorticoids

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More Signs and Symptoms Respiratory Dyspnea Hypoxia Blood Anemia DIC Thrombocytopenia ? WBCs Hypokalemia Hypocalcemia Hypo/Hypernatremia Hypomagnesia

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More Signs and Symptoms Immune ? Susceptibility to infections Leukopenia Renal ? Urinary output

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Complications Portal hypertension Ascites Varices Coagulation defects Jaundice PSE (portal systemic encephalopathy) Hepatorenal syndrome

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Portal Hypertension Increased pressure within the portal vein Results in obstruction of blood flow through the portal vein Blood tries to find new ways around obstructed area = collateral circulation Causes venous distention in entire GI tract

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Ascites Accumulation of plasma in the peritoneal cavity Caused by increased pressure forcing fluid out of intravascular space into cavity Plasma contains albumin so circulating proteins decreased ? serum osmotic pressure Intravascular fluid depletion stimulates kidney to conserve sodium and water = ? hydrostatic pressure and creates more ascites

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Ascites

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Varices Occur anywhere in the GI tract especially Esophageal Hemorrhoids Bleeding esphageal varices Caused by thin walled veins that are irritated, distended and eventually rupture Chemical irritants Mechanical trauma Esophagus pressure Prone to hemorrhage – medical emergency

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Esophageal Varices

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Coagulation Defects Susceptible to bleeding Bruises easily Does not clot Esophageal varices bleeding

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Jaundice Due to hepatocellular destruction or hepatic obstruction Hepatocellular – cannot metabolize bilirubin so it builds up Obstruction – clogs bile ducts so excretion is not possible

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Jaundice

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PSE Also known as hepatic coma Seen in end stage hepatic failure Can be insidious or rapid onset depending on the severity of liver disease Caused by impaired ammonia metabolism

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PSE Continued Usually protein breaks down into ammonia in GI tract, then ammonia into urea --- excreted by the kidneys Liver cannot convert ammonia into urea Results in ? serum ammonia levels Toxic to the central nervous system

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PSE Continued Other factors that add to PSE: High protein diet Infection Hypovolemia Constipation GI bleeding Medications

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Stages of PSE #1 - Prodomal – very subtle changes Personality/behavior changes Impaired thinking/concentration Emotional highs and lows Fatigue, drowsiness Slurred or slow speech Sleep pattern disturbance

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Stages of PSE #2 – Impending Continued mental deterioration Confusion Disoriented Asterixis

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Stages of PSE #3 – Stuporuous Marked mental confusion Drowsy but arousable Abnormal EEG Muscle twitching Hyperreflexia Continued asterixis

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Stages of PSE #4 – Comatose (85% mortality rate) Unresponsive Responds to painful stimuli only No asterixis Positive Babinski’s sign Muscle rigidity Fetor hepaticus Seizures

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Hepatorenal Syndrome A primary cause of death with hepatic failure/cirrhosis Kidneys cannot excrete ammonia and bilirubin Results in acute tubular necrosis Signs/symptoms Sudden ? urinary output ? BUN, Cr, urine osmolarity ? Urine Na

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Treatment Diet ? Sodium (< 2 grams) ?Carbohydrate, moderate fats ? Protein Unless PSE present then ? protein Fluid restriction (total of = 1500cc/day) Vitamin supplements

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Treatment Continued Medications Diuretics Electrolyte replacement Antacids Must be low sodium – Riopan Lactulose Facilitates evaculation of ammonia Neomycin Eliminates intestinal flora = ? protein breakdown Levadopa For PSE – repairs damaged neurotransmitters

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More Treatments Ascites control Paracentesis Shunts Le Veen Shunt - drains ascites fluid into superior vena cava Denver Shunt – subcutaneous pump that is manually compressed Post op care: same as with any abdominal surgery, watch for fluid volume overload and bleeding disorders, measure abdominal girth every shift

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Le Veen Shunt

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More Treatments Hemorrhage from varices Esophagogastric balloon tamponade Sengstaken-Blakemore tube – balloon inflates in esophagus and puts pressure on varices Blood transfusions Medications Beta blockers to decrease HR and BP Pitressin (vasopressin) IV or into superior mesenteric artery (via endoscopy) Sclerotherapy Sclerosing agents injected into varices during EGD Transjugular intrahepatic portal systemic shunt (TIPS) Shunt between portal and hepatic vein to ? pressure = ? bleeding Other portal system shunts – poor prognosis

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Sclerosing Procedure

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Blakemore Tube

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Another Blakemore Tube

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More Treatments PSE Low protein diet May need TPN Control GI bleeding Medications Neuro checks Look for signs and symptoms of the stages of PSE

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Home Care Diet ? calories, vitamins, protein (unless PSE) ? sodium Medications Diurectics Antacids, H2-receptor antagonists No OTC medications No alcohol consumption ? activity – rest periods Home care equipment

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Evaluation Outcomes Patient will ? in ascites Electrolytes WNL B/P WNL No bleeding or complications from bleeding PSE managed immediatley Optimal quality of life

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