Liver Cirrhosis

Scenario A Manuel with his wife was admitted to hospital because of shortness of breathing and severe epigastria pain and repeated episodes of vomiting of blood (hematemesis). His blood pressure was 90/40 and his pulse rate was 120/min. His appearance was somewhat un-kept. Upon questioning his drinking habits, he reported he often went on "binges", sometimes drinking a quart of alcohol within a few days. The patient revealed that he had exhibited upper gastrointestinal bleeding on previous occasions, but never so profusely.

The patient's skin and conjunctivae were slightly yellow (jaundiced). His eyes appeared to be slightly sunken. His abdomen was enlarged and rounded, giving the appearance of being fluid filled (ascites). There was protrusion and considerable downward displacement of his umbilicus. Palpation of the patient's abdomen revealed his liver measured 14 cm in the mid-clavicular line, indicating an enlargement of the liver (hepatomegaly) and his spleen was palpable 3 cm below the left costal margin (splenomegaly).

Liver Cirrhosis

Camacho, Jaymie Ann Rose Esmatao, Analyn Talens, Famela Bandiola, Revalyn Relox, Ariane Deleon, Glayzel

I. II.

Introduction Patient Profile Nursing Health history II.A Present Health History II.B Past Health History II.C Family Health History

III. IV. V. VI. VII. VIII. IX. X. XI.

Gordons Review of system Physical assessment Anatomy and physiology Pathophysiology Nursing Care Plan Drugs Health Teaching Discharge plan

Liver Cirrhosis

Cirrhosis of liver is a chronic disease that causes cell destruction and fibrosis (scarring) of hepatic tissue. Fibrosis alters normal liver structure and vasculature, impairing blood and lymph flow and resulting in hepatic insufficiency and hypertension in the portal vein. Cirrhosis is a potentially life-threatening condition that occurs when scarring damages the liver. This scarring replaces healthy tissue and prevents the liver from working normally. Cirrhosis usually develops after years of liver inflammation. When chronic diseases cause the liver to become permanently injured and scarred, condition is called cirrhosis, cirrhosis harms the structure of the liver and blocks the flow of blood. The loss of normal liver tissue slows the processing of nutrients, hormones, drugs, and toxins by the liver. Also the production of proteins and other substances made by the liver is suppressed. People with cirrhosis often have few symptoms at first. The person may experience fatigue, weakness, and exhaustion. Loss of appetite is usual, often with nausea and weight loss. As liver function declines, water may accumulate in the legs and the abdomen (ascites). A decrease in proteins needed for blood clotting makes it easy for the person to bruise. Bleeding or infection. In the later stages of cirrhosis, jaundice (yellowish skin) may occur, caused by the buildup of bile pigment that is passed by the liver into the intestines. The liver of a person with cirrhosis also has trouble removing toxins, which may build up in the blood. Drugs taken usually are filtered out by the liver, and this cleansing process also is slowed by down cirrhosis. People with cirrhosis often are very sensitive to medications and their side effects. The doctor often can diagnose cirrhosis from the patients symptoms and from laboratory tests. During physical exam, the doctor could notice a change in ho w your liver feels or how large it is/ if the doctor suspects cirrhosis. You will be given blood tests. The purpose of tests is to find out if some cases, other tests that take pictures of the liver are performed Etiology: Laennecs Cirrhosis

Laennecs Cirrhosis also known Alcoholic Cirrhosis is caused by excessive alcohol ingestion, especially when excess alcohol combined with lack of dietary protein.

Postnecrotic Cirrhosis Postnecrotic Cirrhosis may result from massive exposure to hepatoxins, viral hepatitis, or infection.

Biliary Cirrhosis Biliary Cirrhosis is caused by chronic inflammation and obstruction of the gallbladder and bile ducts

Cardiac Cirrhosis Cardiac Cirrhosis is caused by chronic severe congestion of the liver from heart failure. The liver congestion causes death of liver cells from lack of nutrient and oxygen.

Complication of Cirrhosis

HEPATORENAL SYNDROME

Is a secondary kidney failure that occurs in about one-third of liver failure patients Symptoms of hepatorenal syndrome include oliguria without detectable kidney damage, reduced glomerular filtration rate (GFR) with essentially no urine output or less than 200 Ml per day, and nearly total sodium retention. Hepatorenal syndrome is considered an ominous sign.

CLOTTING DEFECTS. Blood clotting defects may develop because of impaired prothrombin and fibrinogen production in the liver. Further, the absence of bile salts essential for some blood clotting factors. Patients with chronic liver failure have tendency to bruise easily and may progress to disseminated intravascular coagulation (DIC) or hemorrhage.

ASCITES Ascites is an accumulation of serous fluid in the abdominal cavity. The fluid accumulates primary because of low production of albumin by the failing liver. An amount of protein in the capillaries causes plasma to seep into the abdominal cavity. The accumulated fluid causes a markedly enlarged abdomen. The fluid may cause severe respiratory distress as a result of elevation of the diaphragm.

PORTAL HYPERTENSION

Portal hypertension is a persistent blood pressure elevation in the portal circulation of the abdomen. Liver damage causes a blockage of blood flow in the portal vein. Increased resistance from delayed drainage causes enlargement of the visible abdominal veins around the umbilicus(called caput medusa), rectal hemorrhoids, enlarged spleen, and esophageal VARICES(dilated veins)(Fig.35.1) the most serious result of portal hypertension is bleeding esophageal varices. The walls of the esophageal veins are thin and tear easily. Varices usually develop from the fundus of the stomach upward and may extend into the upper esophagus. The blood-filled, thin-walled varices nay tear easily from sudden excessive pressure, such as the intra-abdominal pressure that results from coughing, lifting, or straining, causing severe bleeding.

HEPATIC ENCEPHALOPATHY Hepatic encephalopathy is cause by the accumulation of noxious substances in the circulation. The failing liver is unable to make the toxic substances water soluble for excretion in the urine. Ammonia, a by-product of protein metabolism, is most commonly the substance causing symptoms. Signs and symptoms of hepatic encephalopathy include progressive confusion: ASTERIXIS, or flapping tremors in the hands caused by toxins at peripheral nerves; and FETOR HEPATICUS, or foul

II. Nursing Health History Patient profile Name: Manuel Tambago Age: 54 yrs. Old Birthday: march 3 1959 Sex: male Civil status: married Nationality: Filipino Religion: catholic Occupation: mechanic Date of admission: February 28, 2013 /8:00 Pm

Review of system Integumentary system -Edema, Jaundice, palmar erythema, severe Itching Respiratory system -Shortness of breathing -abnormal respiratory rate Cardiovascular system -abnormal pulse and heart rate Gastrointestinal -Irregular bowel movements - -Enlargement of liver -unable to absorb nutrients -no protection against toxics Excretory system -Tea colored urine Musculoskeletal

- Weakness

Laboratory Result Blood -Alanine amino transferase cells -albumin result -Ammonia -Bilirubin -AST -PT Urine -Urobilinogen Ultrasound -Liver <4mg/24hr increases in urine because of filtration of excessive bilinogen in blood 15-19ug/dl 0.3-3.0mg/dl 8-20U/L 8.8-11.6 increased because live cannot metabolize protein end product Increased because liver is unable to use it to produce bile high concentration in liver cell Liver can no longer make prothrombin; patient bleed easily 3.5- 5.5 g/dl decreased because of impaired protein synthesis: edema and ascites may Normal value 5-35 IU/ml abnormal findings

High concentration in liver cells: released with death of liver

Chief complaint: abdominal pain, hematemesis, shortness of breathing Informant: Wife Present Health History Hematemesis Nausea Continuous vomiting for 3 days up to now Shortness of breathing Lack of consciousness Anorexia High temperature past few day Hematemesis (upon admission)

Past health history 3 years ago he developed hypertension which controlled by medication

Family history Both parents are alive and well His grandfather in father side died in hypertension His grandmother in father side died in heart failure

Health teaching Teach the patient how liver cirrhosis is affecting their bodies. Patient need to know how to give importance to their body. Discharge plan Diet -Diet that low in sodium and high protein -Low in Potassium chloride if posible -Avoid self-medication or unprescribed medicine -Avoid fatty foods and high cholesterol foods -Avoid alcoholic beverage Medication -Diuretics medication for edema & ascites (Spironolactone & Propranolol) -Vasopressin, Lactulose, Neomycin, Ferrous sulfate, docusate. Exercise and Activity -Encourage to do physical activities

-Do daily exercise

Nursing Prioritization:

Ineffective Breathing pattern Imbalanced diet: less than body requirement Chronic pain Deficient fluid volume Excess fluid volume Risk for bleeding Risk for infection Risk for acute confusion Self-esteem/disturbed body image Knowledge deficit

Assessment

Diagnosis

Desire outcome

Planning

Intervention

Evaluation

-Abnormal pulse rate -dyspnea for 1week -fatigue

Ineffective breathing pattern related to ascites as evidence by shortness of breathing

-Maintain effective respiratory pattern; be free of dyspnea and cyanosis, with ABGs and vital capacity within acceptable range.

-After two hours if intervention the client will feel comfortable and will lessen the shortness of breathing -the patient will no longer suffer from dyspnea

Monitor respiratory rate, depth, and effort. Rationale - Rapid shallow respirations/dyspnea may be present because of hypoxia and/or fluid accumulation in abdomen.

Auscultate breath sounds, noting crackles, wheezes, rhonchi. -Indicates developing complications (e.g., presence of adventitious sounds reflects accumulation of fluid/secretions; absent/diminished sounds suggest atelectasis), increasing risk of infection.

Investigate changes in level of consciousness. -Changes in mentation may reflect hypoxemia and respiratory failure, which often accompany hepatic coma.

Keep head of bed elevated. Position on sides. -Facilitates breathing by reducing pressure on the diaphragm, and minimizes risk of aspiration of secretions.

Encourage frequent repositioning and deep-breathing exercises/coughing as appropriate. -Aids in lung expansion and mobilizing

secretions.

Imbalanced nutrition: less than body requirements related to Anorexia as evidence by weight loss

-Demonstrate progressive weight gain toward goal with clientappropriate normalization of laboratory values. -Experience no further signs of malnutrition.

Measure dietary intake by calorie count. -Provides information about intake, needs/deficiencies.

Weigh as indicated. Compare changes in fluid status, recent weight history, and skinfold measurements. -It may be difficult to use weight as a direct indicator of nutritional status in view of edema/ascites. Skinfold measurements are useful in assessing changes in muscle mass and subcutaneous fat reserves.

Assist/encourage patient to eat; explain reasons for the types of diet. Feed patient if tiring easily, or have SO assist patient. Consider preferences in food choices.

-Improved nutrition/diet is vital to recovery. Patient may eat better if family is involved and preferred foods are included as much as possible. Encourage patient to eat all meals/supplementary feedings. - Patient may pick at food or eat only a few bites because of loss of interest in food or because of nausea, generalized weakness, and malaise. Recommend/provide small, frequent meals. - Poor tolerance to larger meals may be due to increased intraabdominal pressure/ascites. Provide salt substitutes,

if allowed; avoid those containing ammonium. - Salt substitutes enhance the flavor of food and aid in increasing appetite; ammonia potentiates risk of encephalopathy. Restrict intake of caffeine, gas-producing or spicy and excessively hot or cold foods. -Aids in reducing gastric irritation/diarrhea and abdominal discomfort that may impair oral intake/digestion. Suggest soft foods, avoiding roughage if indicated. -Hemorrhage from esophageal varices may occur in advanced cirrhosis. Encourage frequent mouth care, especially before meals. - Patient is prone to

sore and/or bleeding gums and bad taste in mouth, which contributes to anorexia. Promote undisturbed rest periods, especially before meals. --Conserving energy reduces metabolic demands on the liver and promotes cellular regeneration. Recommend cessation of smoking. -Reduces excessive gastric stimulation and risk of irritation/bleeding. Monitor laboratory studies, e.g., serum glucose, prealbumin/albumin, total protein, ammonia.

-Glucose may be decreased because of impaired glycogenesis, depleted glycogen stores, or inadequate intake. Protein may be low because of impaired metabolism, decreased hepatic synthesis, or loss into peritoneal cavity (ascites). Elevation of ammonia level may require restriction of protein intake to prevent serious complications.

Edema ascites

Excess fluid volume related to excess sodium/flui d intake as evidence by edema and ascites

-Demonstrate stabilized fluid volume, with balanced I&O, stable weight, vital signs within patients normal range, and absence of edema.

Measure I&O, noting positive balance (intake in excess of output). Weigh daily, and note gain more than 0.5 kg/day. Reflects circulating volume status, developing/resolution of fluid shifts, and response to therapy. Positive balance/weight gain often reflects continuing fluid retention. Note: Decreased circulating volume (fluid shifts) may directly affect renal function/urine output, resulting in hepatorenal syndrome. Monitor BP (and CVP if available). Note JVD/abdominal vein distension. BP elevations are usually associated with fluid volume excess but may not occur because of fluid shifts out of the vascular space. Distension of external jugular and abdominal veins is associated with vascular congestion. Assess respiratory status, noting increased respiratory rate, dyspnea. Indicative of pulmonary congestion/edema. Auscultate lungs, noting diminished/absent breath sounds and developing adventitious sounds (e.g., crackles). Increasing pulmonary congestion may result in consolidation, impaired gas exchange, and complications, e.g., pulmonary edema. Monitor for cardiac dysrhythmias. Auscultate heart sounds, noting development of S3/S4 gallop rhythm. May be caused by HF, decreased coronary arterial perfusion, and electrolyte imbalance. Assess degree of peripheral/dependent edema. Fluids shift into tissues as a result of sodium and water retention,

decreased albumin, and increased antidiuretic hormone (ADH). Measure abdominal girth. Reflects accumulation of fluid (ascites) resulting from loss of plasma proteins/fluid into peritoneal space. Note:Excessive fluid accumulation can reduce circulating volume, creating a deficit (signs of dehydration). Encourage bedrest when ascites is present. May promote recumbency-induced Decreases sensation of thirst. Decreased diuresis. Provide frequent mouth care; occasional ice chips (if NPO). Monitor serum albumin and electrolytes (particularly potassium and sodium). serum albumin affects plasma colloid osmotic pressure, resulting in edema formation. Reduced renal blood flow accompanied by elevated ADH and aldosterone levels and the use of diuretics (to reduce total body water) may cause various electrolyte shifts/imbalances. Monitor serial chest x-rays. Vascular congestion, pulmonary edema, and pleural effusions frequently occur. Restrict sodium and fluids as indicated. Sodium may be restricted to minimize fluid retention in extravascular spaces. Fluid restriction may be necessary to correct/prevent dilutional hyponatremia. Administer salt-free albumin/plasma expanders as indicated. Albumin may be used to increase the colloid osmotic pressure in the vascular compartment (pulling fluid into vascular space),

thereby increasing effective circulating volume and decreasing formation of ascites. Administer medications as indicated:Diuretics, e.g., spironolactone (Aldactone), furosemide (Lasix); Potassium; Positive inotropic drugs and arterial vasodilators. Used with caution to control edema and ascites, block effect of aldosterone, and increase water excretion while sparing potassium when conservative therapy with bedrest and sodium restriction does not alleviate problem. Serum and cellular potassium are usually depleted because of liver disease and urinary losses. Given to increase cardiac output/improve renal blood flow and function, thereby reducing excess fluid.

region

Type of assessment

Normal findings

Actual findings

Physical Assessment

Skin, hair and nails

Palpate and inspect

-no clubbing of nail -no seborrhea -no edema -brown pigmentation

-clubbing of nails -yellowish skin -bruises -ascites -spider naevi -hair fall Yellowish in sclera

eyes

Inspect and palpate

-Pinkish conjunctivae -moist -no ulcer

Ear

Inspect and palpate

-Hear sound equally in both ears -no lesion -no discharge of

Hear the sound equally both side -no lesion -no discharge of fluid

fluid -no pain Nose Inspect and palpate -in the middle of the -no discharge Mouth Inspect and palpate -pinkish -no edema Neck Inspect and palpate -straight -no masses and lumps Lungs Inspect, percuss and auscultate -

-no pain

-in the middle no discharge -bleeding gums -no edema -pinkish -straight -no masses and lumps

Heart

Inspect, Palpate and percuss

-pulsation of the apical impulse maybe visible

-apical impulse is visible

Abdomen

Inspect, palpate and percuss

-skin color is uniform -no lesion -liver cant easily palpate

-large abdomen -spider naevi -palpable liver

Musculoskeletal