ACUTE BIOLOGIC CRISIS Thyroid Disorder and Hepatic Disorders Dean Gasco GOITER Two major forms: 1.

Endemic goiter Caused principally by nutritional iodine deficiency Need for thyroid hormone (TH) during growth spurts, pregnancy, and lactation Goiter commonly develops in adolescents, pregnant women and nursing mothers who live in iodine- deficient regions 2. Sporadic goiter Major causes: Genetic defects resulting in faulty iodine metabolism 2.

Common form of primary-autoimmune hypothyroidism known as HASHIMOTOS DISEASE

Hypercholesterolemia, hyperlipidemia and proteinemia as a result of T4 changes in the synthesis, mobilization and degradation of serum lipids

Secondary Hypothyroidism - Insufficient stimulation of a normal thyroid gland, resulting in decreased TSH level. Tertiary or Central Hypothyroidism Hypothalamus cannot produce thyroid- releasing hormone (TRH) and subsequently does not stimulate the pituitary to secrete TSH Both TSH and TH levels are again low in the serum Subclinical Hypothyroidism Hypothyroidism that is diagnosed with an elevated TSH level but a normal to low- normal T4 level

3.

Myxedema Coma The most severe complications of hypothyroidism is myxedema coma Drastic decrease in metabolic rate, hypoventilation leading to respiratory acidosis, hypothermia, and hypotension Complicating conditions:

4.

Hyponatremia Hypercalcemia secondary to adrenal insufficiency Hypoglycemia water intoxication May be triggered by stress

Pathophysiology:

Ingestion of large amounts of nutritional goitrogens (goiter-producing agents that inhibit thyroxine [T4 ] production) such as cabbage, soybeans or spinach Ingestion of medicinal goitrogens such as glucocorticoids, dopamine, or lithium

Pathophysiology: The thyroid gland needs iodine to synthesize and secrete thyroid hormones: T4 Triiodothyronine (T3) Thyrocalcitonin (Calcitonin) Production of thyroid hormones depends on the secretion of TSH from the anterior pituitary. Ingestion of adequate protein and iodine. The hypothalamus regulates the pituitary secretion of TSH. Slowing of the basal metabolic rate Leads to achlorhydria (decreased secretion of hydrochloric acid in the stomach), decreased gastrointestinal tract mobility, bradycardia, slowed neurologic functioning and decrease in heat production. Reduction in thyroid hormones causes an increase in serum cholesterol and triglyceride levels and an increase in atherosclerosis, arteriosclerosis and coronary heart disease, anemia. Mild Hypothyroidism Cold Lethargy Dry skin Forgetfulness Depression Weight gain Constipation related to slowed peristaltic action Myxedema dry, waxy type of swelling with abnormal deposits of mucin in the skin Edema is non- pitting and is common in the pretibial and facial areas

Systems involved: 1. Cardiovascular 2. Gastrointestinal 3. Musculoskeletal 4. Integumentary 5. Neurologic 6. Reproductive 7. Others Medical Management: For hypothyroidism to be reversed permanently, - The client must take TH for life. Levothyroxine sodium Myxedema Coma: Desired outcome of the medical management of myxedema coma is to reverse the condition to save the clients life Maintaining a patent airway Giving oxygen Replacing fluids intravenously Client is kept warm Vital signs are closely monitored until the client begins to recover Vasopressors are used to maintain tissue perfusion Levothyroxine sodium is given intravenously with glucose and corticosteroids Medications for Thyroid Disorders: Medications used in the treatment of hyperthyroid conditions are used to reduce thyroid hormone levels Medications used in the treatment of hypothyroid conditions are used to increase thyroid hormone levels Propylthiouracil (PTU) which inhibits thyroid hormone synthesis Radioactive iodine offers a more permanent option because it destroys thyroid tissue. It is not given to pregnant women because it may enter the fetal circulation and destroy fetal thyroid tissue. Thyroid Hormone replacement therapy is also prescribed for clients with goiters because it promotes shrinkage of the gland.

If there is a lack of sufficient dietary iodine or if production of TH is suppressed, the thyroid enlarges in an attempt to compensate for hormonal insufficiency. Goiter is an adaptation to a deficiency of TH. Clinical Manifestations: Diagnosis is confirmed by: a. History b. clinical findings c. laboratory tests Medical Management: When enlargement is a compensatory reaction to iodine deficiency and consequent suppression of T4 secretion, the client can be treated with preparations of iodine and thyroid hormones Lugols solution or saturated solution of potassium iodide (SSKI) drops Iodized salt 50 mg of iodine per day HYPOTHYROIDISM Deficiency of TH resulting in slowed body metabolism, decreased heat production and decreased oxygen consumption by the tissues. Etiology and Risk Factors: 1. Primary Hypothyroidism TH levels are low TSH levels are elevated Pituitary is attempting to stimulate the secretion of thyroid hormones but the thyroid is not responding

Beta- adrenergic blockers may be prescribed to control heart rate and tremors. Acetaminophen may be prescribed for fever.

Graves disease is an autoimmune disorder mediated by immunoglobulin G (IgG) antibody that binds to and activates TSH receptors on the surface of the thyroid cells.

2. 3.

Nursing Management of the Medical Client with Myxedema: Assessment: Periorbital and facial edema Blank facial expression Thick tongue Generalized slowing of all muscle movement Hypothermic Depressed respirations precipitate respiratory acidosis Alterations in heart rate and blood pressure Diagnosis: Risk for Injury: Myxedema Coma Risk for Injury: Myxedema coma related to hypersensitivity to anesthetics, sedatives, and opioids secondary to decreased metabolic rate Interventions: The client should not receive sedatives unless absolutely necessary Self- Care: Evaluate the clients level of knowledge Develop and implement a teaching plan Also provide a written list of the manifestations on Thyroid Supplements, of the manifestations of thyroid deficiency or excess Monitor clients weigh weekly Emphasize the need for iodized salt Advise the client to drink sufficient fluids, increase physical activity and eat a high- fiber diet to prevent constipation Modifications for Older Clients: Autoimmune thyroiditis, Hashimotos disease, previous thyroid surgery or treatment with radioactive agents and noncompliance with prescribed T4 replacements - Remember that a principal hazard in giving T4 to an older client is the development of ischemic heart disease as evidenced by angina. The clients pulse rate should be monitored daily. HYPERTHYROIDISM excessive secretion of TH Etiology and Risk Factors: - Due to over functioning of the entire gland Adenomas of thyroid cancer Graves disease (toxic, diffuse goiter): 1. Hyperthyroidism 2. Thyroid gland enlargement (goiter) 3. Exophthalmos (abnormal protrusion of the eyes) Pathophysiology: Hyperthyroidism is characterized by loss of the normal regulatory controls of TH secretion. Hypermetabolism results with inreased sympathetic nervous system activity Excessive amounts of TH stimulate the cardiac system and increase the number of beta- adrenergic receptors, leading to tachycardia and increased cardiac output, stroke volume, adrenergic responsiveness and peripheral blood flow. Metabolism increases greatly, leading to a negative nitrogen balance, lipid depletion, and a state of nutritional deficiency and weight loss. Results in altered secretion and metabolism of hypothalamic, pituitary and gonadal hormones. Hyperthyroidism results in diminished libido Women also have menstrual irregularities and decreased fertility. Clinical Manifestations: Extremely agitated and irritable Hand tremors at rest Weight loss as a result of the hypermetabolic state Loose bowel movements Heat intolerance Profuse diaphoresis tachycardia Incoordination related to tremors Skin becomes warm, smooth and moist Hair appears thin and soft Mild euphoria to extreme hyperactivity Extreme fatigue and depression - Goiter hyperplasia and hypertrophy of the thyroid cells; cellular overgrowth results in the release of excessive TH into the blood. Enlarged neck Protruding eyes [ Exophthalmos] Agitated expression Restlessness Weight loss Serum cholesterol levels are usually depressed Complications: 1. Exophthalmos Autoimmunity against retro-orbital tissues Fixed stare

It develops as a result of proptosis, lid retraction, muscle swelling, and tissue edema from a prolonged hyperthyroid condition Gritty sensation in the eye Photophobia Lacrimation Inflammatory changes Dyslogia Diuretics may alleviate some periorbital edema Glucocorticoids such as prednisone are given in large doses to reduce inflammation of the periorbital tissues Methylcellulose eye drops help reduce eye irritation Radiation therapy to the retro- orbital tissues may help in severe cases Surgical decompression of the orbits Wear dark eyeglasses Warn the client to avoid getting dust or dirt in the eyes Have the client wear a sleeping mask or lightly tape the eyes shut with non- allergic tape Restrict salt intake to relieve edema

Heart Disease Thyroid Storm (Thyrotoxicosis) Characterized by high fever, severe tachycardia, delirium, dehydration and extreme irritability

Medical Management: Desired outcomes of medical management for clients with Graves disease are to curtail the excessive secretion of TH and to prevent and treat complications. Curtail Excessive Secretion of Thyroid Hormone Iodide - Propylthiouracil corrects hyperthyroidism by impairing TH synthesis; the most serious toxic effect is agranulocytosis Methimazole (Tapazole) Adrenergic blocking agents Iodine therapy is prescribed for 2 reasons: 1. to reduce the vascularity of the thyroid gland before subtotal or total thyroidectomy 2. to treat thyroid storm If iodine is given for a longer period TH floods the circulation and hyperthyroidism becomes more severe than before. Potassium iodide Lugols solution Therapy with radioactive iodine The thyroid gland is unable to distinguish between regular iodine atoms and radioiodine atoms The thyroid gland picks up the radioiodine and concentrates it just as it would As a result, the cells that concentrate radioactive iodine to make T4 are destroyed by the local irradiation, TH secretion diminishes, and the manifestations of hyperthyroidism and goiter disappear.

Major possible complications of radioactive iodine therapy is hypothyroidism

A hypermetabolic state may be obvious from apparent weight loss and exophthalmos may also be obvious.

Follows a respiratory tract infection Genetic predisposition Chronic thyroiditis (Hashimotos disease)

Prevent and Treat Complications Adrenergic blocking agents to control the activity of the sympathetic nervous system Propranolol Catecholamines High- calorie (4000 to 5000 calories) High protein diet to compensate hypermetabolic state and prevent negative nitrogen balance & weight loss High fever is treated with hypothermia blankets Dehydration is reversed with the administration of intravenous fluids Management of thyroid storm involves suppressing hormone release, inhibiting hormone synthesis, blocking conversion of T4 to more active T3, inhibiting the effects of TH on body tissues and treating the precipitating cause, if it is known. Potassium iodide Beta- blockers are given to decrease the effects of sympathetic nervous system Nursing Management of the Medical Client: Assessment: asking questions concerning weight, appetite, activity, heat intolerance and bowel activity assess for the presence of typical manifestations of hyperthyroidism ask about mood alterations Diagnosis: Imbalanced Nutrition: Less Than Body Requirements Imbalanced Nutrition: Less Than Body Requirements related to accelerated metabolic rate resulting in weight loss and decreased energy levels Interventions: Diet high in calories, protein, carbohydrates and minerals Discourage the ingestion of foods that increase peristalsis and thus result in diarrhea, such as highly seasoned, bulky, or fibrous foods Client should be weighed daily Vitamin B complex Surgical Management: Thyroidectomy Complications: a. hemorrhage and infection b. at risk for thyroid storm c. respiratory obstruction d. laryngeal edema e. vocal chord injury

Outcomes of successful preparation for thyroid surgery: The client is euthyroid before entering the operating room. Tests of thyroid function are within normal limits. Manifestations of thyrotoxicosis are greatly diminished or absent. The client appears rested and relaxed. Weight and nutritional status are normal; any weight loss earlier has been regained. Cardiac problems are under control, pulse rate is normal, and perioperative electrocardiograms show no dangerous dysrhythmias. Postoperative Care: Assessment Monitor for Postoperative Complications: a. additional pillows b. oxygen c. suction equipment d. intubation supplies e. tracheostomy set f. Calcium gluconate Monitor and Treat Hypocalcemia a. muscle twitching b. hyperirritability of the nervous system may indicate hypocalcemic tetany c. Hypocalcemia can develop after throidectomy if the parathyroid glands are accidentally removed during surgery d. Monitor the client for Chvosteks and Trousseaus signs Neck Exercises: Show the client how to place the hands at the back of the head when flexing the neck or moving Promote Wound Healing: Teach the client how to care for the incision when it has healed by using lanolin or Vitamin E cream Modifications for Older Clients: - Cardiovascular abnormalities such as heart failure, atrial dysrhythmias and various degrees of heart block may be caused by hyperthyroidism. THYROIDITIS Acute suppurative, subacute thyroiditis ( either granulomatous [painful thyroiditis] or lymphocytic [silent or painless thyroiditis]) Also known as Hashimotos disease Etiology and Risk Factors: Bacterial invasion Streptococcus pyogenes Staphylococcus aureus Pneumococcus pneumoniae Viral in origin

Pathophysiology: Follicular destruction, cell infiltration and colloid depletion occur. Microabscesses form Hashimotos disease is manifested by an enlarged thyroid gland that may produce hypothyroid manifestations if the gland is destroyed by the autoimmune system. A euthyroid state may prevail if the gland is not destroyed.

Clinical Manifestations: Anterior neck pain Fever Diaphoresis Subacute granulomatous thyroiditis is usually painful Radiation to the ear on the ipsilateral side Manifestations of viral infection: Myalgia

Low-grade fever Lassitude Sore throat painless, asymmetrical enlargement of the gland Evaluation of levels of serum T3, FT4, radioiodine uptake, TSH

Medical Management: Parenteral antibiotic therapy Beta- adrenergic blocking agents Antithyroid medications are not indicated Surgical Management: Incision and drainage Diagnosis: Imbalanced Nutrition: Less than Body Requirements (NANDA) related to hypermetabolic state and impaired utilization and storage nutrients. Interventions: 1. Weigh daily 2. Monitor nutritional intake 3. Provide oral hygiene before meals 4. Assess for difficulty swallowing 5. Administer antiemetics as ordered 6. Give fluids by mouth as tolerated 7. Provide small, frequent meals 8. Monitor electrolytes, hemoglobin and hematocrit Diagnosis: Suffocation, Risk for (NANDA) related to potential respiratory obstruction due to hemorrhage, edema of glottis, laryngeal nerve damage or tetany Intervention:

Respiratory obstruction may result from swelling related to the surgical site. Vocal cord paralysis may result from nerve damage.

Nursing Management of the Surgical Client: Preoperative Care

1.

Continuously assess for manifestations of airway obstruction such as increasing restlessness, tachycardia, apprehension, cyanosis, stridulous respiration and retraction of neck tissues. 2. Cough and deep breathe every hour. 3. Suction mouth and trachea if necessary. 4. Use Semi-Fowler position when client is conscious 5. Have tracheostomy set, endotracheal tube 6. Give continuous mist inhalation as ordered. 7. Administer oxygen as ordered. 8. Place the client in the semi- fowler or Fowler position 9. Assess for crackles and increased respirations 10. Administer oxygen and blood products as ordered. Diagnosis: Pain, Acute (NANDA) related to actual postoperative tissue damage Interventions: 1. Assess pain and respiratory status 2. Administer pain medications 3. Support head and neck 4. Use Semi-Fowler position Diagnosis: Impaired Skin Integrity (NANDA) related to surgical incision Interventions: 1. Keep dressings to neck clean and dry 2. Assess wound dressing for tautness 3. Apply emollients (mineral oil, baby oil, lanolin) 4. Use cool, light cotton clothing 5. Keep clothing and bedding dry 6. Keep the environment cool 7. Avoid activities that promote sweating 8. Keep nails short and smooth 9. Administer diphenhydramine HCL (Benadryl) 10. Encourage diversional activities Diagnosis: Risk for Injury (NANDA) Interventions: 1. Check dressing and vital signs every 15 minutes 2. Observe for bleeding at front, sides, and back of neck 3. Examine back of neck and shoulders for bleeding 4. Check dressing for tightness; uncomfortable tautness may indicate bleeding into the tissue 5. Assess client for hypocalcemia 6. Carefully assess for manifestations of thyroid storm THYROID CANCER Pathophysiology: Two most frequent types of Thyroid cancers: 1. Papillary 2. Follicular carcinomas Clinical Manifestations: hard, irregular, painless nodule in an enlarged thyroid gland Cold

Medical Management: Chemotherapy external radiation TSH suppressive therapy used for metastasis Surgical Management: removal of all or part of the thyroid Neck resection HYPERPARATHYROIDISM Etiology and Risk Factors: a. Primary hyperparathyroidism develops when the normal regulatory relationship between serum calcium levels and parathyroid hormone (PTH) secretion is interrupted b. Secondary hyperparathyroidism occurs when the glands are hyperplastic because of malfunction of another organ system is usually the result of renal failure but may also occur as a result of cancers such as multiple myeloma or carcinoma with bone metastasis c. Tertiary hyperparathyroidism occurs when PTH production is irrepressible (autonomous) in clients with normal or low serum calcium levels Pathophysiology: PTH is to increase bone resorption, thereby maintaining the proper balance of calcium and phosphorus ions in the blood. Excessive circulating PTH leads to bone damage, hypercalcemia, and kidney damage. Primary Hyperparathyroidism: excessive PTH stimulates transport of calcium into the blood from the intestine, kidneys and bone Nephrolithiasis is secondary to calcium phosphate kidney stones and deposition of calcium in the soft tissues of the kidney Pyelonephritis may complicate the nephrolithiasis Bone resorption related to hypercalcemia may develop Secondary Hyperparathyroidism: Chronic renal failure and hyperphosphatemia cause secondary hyperparathyroidism As the glomerular filtration rate (GFR) decreases in chronic renal failure, serum phosphorus levels rise, which causes the serum calcium level to fall PTH secretion is stimulated This increase decreases renal tubular absorption of phosphorus, causing serum phosphorus levels to return to normal As the GFR continues to decrease, PTH is secreted in increased amounts to decrease tubular reabsorption of phosphorus and maintain serum phosphorus level at or close to normal limits Clinical Manifestations:

backache Joint pain Bone pain Pathologic fractures Deformity and bending of the bones Osteitis fibrosa Arthritis Osteoporosis Polydipsia Polyuria Polydipsia Appearance of sand, gravel or stones (calculi) in the urine Azotemia Hypertension resulting from renal damage Hypercalcemia produces gastrointestinal manifestations such as: Thirst nausea anorexia constipation ileus abdominal pain decreased neuromuscular bones Osteitis fibrosa with: Osteoclastomas Bone cysts Osteomalacia Stones Renal stones Nephrocalcinosis Polyuria Polydipsia Uremia Abdominal groans Constipation Indigestion, nausea, vomiting Peptic ulcer Pancreatitis Psychic moans Lethargy, fatigue Depression Memory loss Psychoses- paranoia Personality change Confusion, stupor, coma Other Proximal muscle weakness Keratitis, conjunctivitis Hypertension Itching

Medications for Parathyroid Disorders: Furosemide (Lasix)- a loop diuretic may be used to promote calciuria

Plicamycin- is a chemotherapeutic drug that is effective in lowering serum calcium levels Glucocorticoids- may be used to reduce hypercalcemia by decreasing gastrointestinal absorption of calcium Didronel (Etidronate) or Calcitonin- may be used to decrease the release of calcium by bones

grimacing tingling of the fingers laryngospasm dysrhythmias Chvosteks and Trousseaus signs A tracheostomy is required in severe cases

Renal failure sometimes appear as a complication of toxic hepatitis

Known Hepatotoxic Substances Class of Agent Anabolic steroid Antithyroid Antibiotic Oral contraceptive Oral hypoglycemic Tranquilizer Immunosuppressive Calcium channel blocker Oncotherapeutic Anesthetic Antihypertensive Antibiotic Diuretic Antidepressant Anti- inflammatory Antifungal Hydrocarbon Metal Mushroom Analgesic ALCOHOLIC HEPATITIS parenchymal necrosis resulting from heavy alcohol ingestion Assessment: anorexia nausea abdominal pain splenomegaly hepatomegaly jaundice ascites fever encephalopathy elevated serum bilirubin level fatty hepatic tissue Nursing Interventions: High- vitamin, high carbohydrate diet Administering folic acid and thiamine supplements Giving parenteral fluids as ordered Administration of liquid formulas Steroids CIRRHOSIS characterized by widespread fibrosis (scarring) and nodule formation normal flow of blood, bile and hepatic metabolites is altered by fibrosis and changes in the hepatocytes, bile ductules, vascular channels and reticular cells Four major types of Cirrhosis: Example of substances Methyl testosterone Methimazole Erythromycin Rifampin

Nursing Management of the Medical Client: a. Encourage Fluids The client should consume at least 3000 ml of fluids each day b. Prevent Urolithiasis Cranberry juice or prune juice may help make the urine more acidic c. Strain Urine of Stones Surgical Management: Parathyroidectomy Autotransplantation of the parathyroid glands Complications: Edema hemorrhage respiratory distress HYPOPARATHYROIDISM Hyposecretion of the parathyroid glands produces hypoparathyroidism Serum calcium levels are abnormally low Serum phosphate levels are abnormally high Neuromuscular irritability (tetany) may develop Etiology and Risk Factors: a. Iatrogenic (treatment-induced) Causes: accidental removal during thyroidectomy infarction of the parathyroid glands because of an inadequate blood supply to the glands during surgery b. Idiopathic (without a specific cause) Pathophysiology: PTH acts to increase bone resorption, which maintains proper serum calcium levels PTH also regulates phosphate clearance by the renal tubules, thereby maintaining the correct inverse balance between serum calcium and serum phosphate levels Clinical Manifestations: low serum calcium levels hyperventilation ingestion of antacids Acute Hypoparathyroidism accidental damage to parathyroid tissues during thyroidectomy Results in tetany: painful muscle spasms irritability

Chronic Hypoparathyroidism: lethargy thin, patchy hair brittle nails dry, scaly skin personality changes Presence of Chvosteks sign Presence of Trousseaus sign Hyperactive deep tendon reflexes (DTRs) Circumoral paresthesia Numbness and tingling of fingers Medical Management: Elevate Serum Calcium Levels Diet high in calcium but low in phosphorus Tetany and laryngeal spasms may occur suddenly Nursing Management of the Medical Client: 1. Prevent Respiratory Arrest endotracheal tube laryngoscope tracheostomy 2. Monitor and Prevent Tetany intravenous calcium carbonate Self- Care Medications: Vitamin D, except Dihydroxycholecalciferol, are slowly assimilated by the body Modifications: omit cheese and milk products HEPATIC DISORDERS TOXIC HEPATITIS The extent and type of hepatitis: depend on the degree of exposure chemical properties of the hepatotoxin genetic makeup of the individual toxic metabolite formed by the drug metabolizing enzymes within the liver

Clients experiencing a hypersensitivity reaction may demonstrate eosinophilia, fever, arthralgia and sometimes xanthomatosis ( an excessive accumulation of lipids brought about by faulty lipid metabolism ) Adequate rest, promote alleviation Restrict protein intake if evidence of impending hepatic encephalopathy is noted

Alcoholic (Lannecs cirrhosis or portal cirrhosis) b. Postnecrotic c. Biliary d. Cardiac Two major clinical problems in cirrhosis: 1. Decreased liver function 2. Portal hypertension Etiology and Risk Factors: Primary risk factor for cirrhosis: Alcohol ingestion Poor nutritional state Likelihood of damage is greater and the damage is more severe Biliary cirrhosis with intrahepatic cholestasis or obstruction of bile ducts Use of drugs (such as Acetaminophen, Methotrexate or Isoniazid) Hepatic congestion from severe right- sided heart failure Constrictive pericarditis Valvular disease - Alpha1 - antitrypsin deficiency Infiltrative disease (such as amyloidosis, glycogen storage diseases or hemochromatosis) Wilsons disease Nutritional deficits Acetaminophen overdose Pathophysiology: Cirrhotic liver has a nodular consistency, with bands of fibrosis (scar tissue) and small areas of regenerating tissue There is extensive destruction of hepatocytes Periodic exacerbations are marked by bile stasis, precipitating jaundice Portal vein hypertension develops in severe cirrhosis The portal vein receives blood from the intestines and spleen An increase of pressure in the portal vein causes: retrograde increase in pressure resistance and enlargement of the esophageal, umbilical and superior rectus veins, which may result in bleeding varices

a.

Hypoalbuminemia Hyperaldosteronism Gastrointestinal bleeding arises from esophageal varices Hypoprothrombinemia Thrombocytopenia Splenomegaly Anemia Leukopenia Thrombocytopenia may result from splenomegaly Infections may be present as a result of an enlarged, overactive spleen causing leukopenia Bacteria that remain in the portal venous blood bypass the liver and are not removed by Kupffer cells and hence may cause infection Ammonia no longer removed by the liver accumulates to levels toxic to the brain, resulting in encephalopathy Renal failure occurs with rapidly failing hepatic function

Fluids as well as sodium should be restricted in the diet Provide Vitamin Supplements Vitamins A, D, E and K are supplied if fat absorption is adequate Calcium gluconate supplementation

Diagnosis: Activity Intolerance Intervention: Prescribe rest Diagnosis: Risk for Injury Intervention: All known hepatotoxic medications are removed Diagnosis: Ineffective Protection related to alcohol abuse and inadequate nutrition Complications of Cirrhosis: PORTAL HYPERTENSION

Medical Management: Monitor for Complications ascites bleeding esophageal varices hepatic encephalopathy Nutritious diet Restrict sodium and fluids Thiazide diuretic, the diet should be high in potassium B vitamins and fat- soluble vitamins (Vitamins A, D, E and K) are commonly given to clients with alcoholic cirrhosis Alcohol should be avoided Biliary obstruction be removed Avoidance of hepatotoxic substances Drugs to Restrict or Avoid: Acetaminophen Phenobarbital Chlorpromazine Morphine Codeine Alcohol Diagnosis: Ineffective Tissue Perfusion related to bleeding tendencies and varices that may lead to hemorrhage Interventions: Monitor for Hemorrhage Monitor the client for bleeding gums, pupura, melena, hematuria and hematemesis Assess for signs of shock Prevent Hemorrhage Give injections only when absolutely necessary Modify diet Provide ample protein to rebuild tissue but not enough protein to precipitate hepatic encephalopathy Low- fat and low- sodium

persistent increase in blood pressure in the portal venous system occurring as a result in the portal venous system occurring as a result of increased resistance to or obstruction of blood flow through the portal venous system into the liver

Etiology and Risk Factors: Associated with cirrhosis Obstructed by a thrombus Tumor Pathophysiology: Normal blood flow to and from the liver depends on proper functioning of the: portal vein (70% of inflow) hepatic artery (30% of inflow) hepatic veins (outflow) Portal hypertension results either from increased blood flows in the portal vein or from an increased resistance to flow within the portal venous system The most common cause of portal hypertension is cirrhosis The pathophysiologic mechanism in cirrhosis is increased resistance, which is intrahepatic and primarily sinusoidal Portal hypertension may also arise from pre-sinusoidal obstruction, either outside the liver (as in portal vein thrombosis) or within it (as in schistosomiasis) In addition, lesions leading to portal hypertension may be postsinusoidal, either within the liver (as in veno-occlusive disease) or distal to it (as in Budd- Chiari syndrome or right- sided heart failure) Normal portal venous blood pressure is 5 to 10 mm Hg

ascites (the result of osmotic or hydrostatic shifts leading to fluid accumulation in the peritoneum) incomplete clearing of protein metabolic wastes with a resultant increase in ammonia, thus leading to hepatic encephalopathy

Clinical Manifestations: - Hepatomegaly (enlarged liver) - Vascular changes and abnormal results of laboratory tests - Palpation reveals a firm (scarred), lumpy (nodular), usually enlarged liver ( the liver becomes hard and shrunken in late cirrhosis) - Malnutrition - Portal hypertension

Pressure rises 5 mm Hg higher than the inferior vena cava pressure Clinical Manifestations: Tortuous epigastric vessels that branch off the area of the umbilicus and lead toward the sternum and ribs (caput medusae) Enlarged, palpable spleen Internal hemorrhoids Bruits Factors in the Pathogenesis of Cirrhotic Portal Hypertension: Increased resistance to flow Presinusoidal obstruction Portal or splenic vein occlusion (thrombosis, tumors) Schistosomiasis Congenital hepatitis fibrosis Sarcoidosis Sinusoidal Cirrhosis Alcoholic hepatitis Postsinusoidal Veno- occlusive disease Budd- Chiari disease Constrictive pericarditis Increased portal blood flow Splenomegaly not caused by liver disease Arterioportal fistula Complications: Dilation of the superior rectal veins, abdominal wall veins, esophagogastric veins Esophageal veins swell and distend These swollen, dilated veins are called varices Esophageal Bleeding Secondary to Portal Hypertension: - Blood Pressure 90/60 mm Hg Heart rate 100 beats/ min Cool, clammy skin Distal pulses < 2+ on a 0-4+ scale Slowed capillary refill (> 2seconds) Diminished orientation to person, place and time Restlessness Several factors can contribute to rupturing of varices: 1. Increased portal venous blood pressure 2. Increased intrathoracic pressure (coughing and straining at stools) 3. Irritation by food or alcohol 4. Erosion by gastric juices 5. Splenic vein merges with the superior mesenteric vein to form the portal vein 6. Hepatic encephalopathy 7. Blood is a protein; this process increases ammonia in the gut and bloodstream. The excessive ammonia disturbs brain function. Medical Management: a. Sclerotherapy b. Transjugular intrahepatic portosystemic shunt

c. d. e. f. g. h.

i.
j. k. l. 1.

Administration of vasopressin Balloon tamponade Beta- adrenergic blocking agents Endoscopic electrocautery Direct ligation of bleeding varices Transhepatic embolization of the left gastric vein urgent Portacaval shunt surgery Cold saline lavage Volume expanders Blood products Control Hemorrhage Sclerotherapy passes an endoscope into the esophagus and injects a sclerosing agent (e.g. morrhuate sodium) that flows into the varices the sclerosing agent initially causes inflammation of the vein wall and then fibrosis Transjugular Intrahepatic Portosystemic Shunt Expandable metal stent is advanced with the aid of fluoroscopy to the hepatic veins during an angiogram and then through the liver to create a direct portacaval channel Stents frequently undergo stenosis or occlude over a period of months, prompting the need for another TIPS or another approach Vasopressin IV vasopressin is administered to stop variceal bleeding Achieves temporary lowering of portal pressure These agents reduce portal venous blood flow by constricting afferent arterioles Direct infusion of vasopressin into the superior mesenteric artery is most effective Side effects: a. Hypothermia b. myocardial and gastrointestinal tract ischemia c. acute renal failure Vasopressin may be given in conjunction with nitroglycerin To minimize vasoconstrictive side effects Beta- adrenergic Blocking Agents Propranolol [Inderal] Metoprolol [Lopressor] Nadolol [Cogard] For management of acute variceal bleeding Balloon Tamponade Applying pressure to ruptured varices via balloon tamponade may stop hemorrhage Inserts a Sengstaken- Blakemore or Minnesota tube into the stomach and inflates the esophageal and gastric balloons The pressure of the esophageal balloon against the varices may stop the bleeding You should have scissors at the bedside to be able to remove the tube in an emergency Complications include aspiration pneumonitis as well as esophageal rupture

Nursing Management of the Medical Client Assessment: Assessing tube function after placement of a Sengstaken-Blakemore or Minnesota tube Diagnosis: Ineffective Tissue Perfusion related to portal hypertension and rupture and hemorrhage of esophageal varices Interventions: a. Prevent Hemorrhage o Avoid straining maneuvers that increase intraabdominal or intrathoracic pressure o Avoid rough foods, which may traumatize the esophagus and spicy foods which may irritate the esophageal mucosa o Develop an emergency plan in case severe esophageal varices should rupture o List of all emergency telephone numbers o Monitor blood pressure, pulse rate, respiration and urine output o Assist with interventions to restore circulating blood volume Diagnosis: Impaired Gas Exchange related to decreased oxygen supply secondary to aspiration pneumonitis or obstruction occurring after balloon tamponade with the SengstakenBlakemore tub b. Prevent Esophageal Necrosis o Must release the pressure on the esophagus periodically to prevent tissue damage c. Prevent Aspiration Pneumonia o Inflated balloon in the esophagus prevents saliva and secretions from reaching the stomach d. Prevent Nares Erosion o Clean and lubricate the external nares o Provide padding if necessary Prevent Airway Obstruction o Gastric balloon deflates or breaks and traction on the tube pulls the esophageal balloon up into the oropharynx o Keep scissors at the bedside o Cut the tube and pull it out to restore airway patency Diagnosis: Acute Confusion related to portosystemic encephalopathy and hepatic coma occurring in conjunction with gastrointestinal bleeding and accumulation of ammonia f. Monitor Level of Consciousness o Assess the client regularly for the development of asterixis (liver flap or flapping tremor) o Monitor for evidence of gastrointestinal bleeding, including melena or hematemesis, because bleeding can precipitate hepatic coma g. Protect from Injury o Keeping the side rails up and the bed in the lowest position e.

2.

3.

4.

5.

Endoscopic Band Ligation o Esophageal varices are ligated and strangulated with small elastic )-rings placed in the appropriate place during endoscopy i. Portosystemic Shunt o Portosystemic shunt reduces portal hypertension by sending portal venous blood directly into the inferior vena cava, bypassing the liver Contraindications: Poor general health so that the client is not able to withstand the trauma, blood and fluid loss and anesthesia of surgery Complications: Major complications after a shunt procedure: Bacteremia DIC Heart failure Shunt clotting Hepatic encephalopathy Preoperative Care: Appraisal of the clients general physical condition and readiness for surgery along with assessment of the clients neurologic, respiratory and renal systems to establish a baseline - Blood-clotting mechanisms are analyzed Postoperative Care: Inspect the operative site carefully for any manifestations of shunt clotting, such as pain, distention or nausea Monitor for the following: Presence of hemorrhage Fluid and electrolyte imbalance Respiratory rate and rhythm Hypoalbuminemia Hypoglycemia Manifestations of infection Pain levels Mental status (alertness) Assess for Excess Fluid Volume Detect development of ascites Monitor weight and intake and output Monitor and Treat Postprocedure Complications Administer Vitamin K Turning, coughing and deep breathing Administering IV fluids plus blood or volume expanders Monitoring blood and urine values Eliminating medications that sedate, depress the CNS Maintaining nutrition Maintaining sterile technique Assisting the client and the clients family to cope with postoperative discomfort

h.

HEPATIC ENCEPHALOPATHY cause of this disorder is the livers inability to metabolize ammonia to form urea so that it can be excreted Ammonia is a CNS depressant There is reduced mental alertness, confusion and restlessness, loss of consciousness, seizures and irreversible coma Pathophysiology: Characterized by elevations of ammonia levels in the blood and cerebrospinal fluid (CSF) Ammonia is produced in the gastrointestinal tract when protein is broken down by bacteria, by the liver and in lesser amounts, by gastric juices and peripheral tissue metabolism False neurotransmitters, elevated levels of mercaptans (organic chemicals that contain the sulfhydryl radical, formed when the oxygen of an alcohol molecule is replaced by sulfur), phenol, and short- chain fatty acids Liver converts ammonia into glutamine, which is stored in the liver and is later converted to urea and excreted through the kidneys Failure of the liver to perform this function may be due to liver cell damage and necrosis Ammonia also is a CNS toxin, affecting glial and nerve cells It leads to altered CNS metabolism and function Hepatocellular failure Portosystemic shunt surgery Clinical Manifestations: mental confusion to deep coma impairs memory, attention, concentration and rate of response Handwriting and speech slow significant changes as intellectual deterioration occurs Hyperventilation with respiratory alkalosis develops because of high ammonia levels stimulate the respiratory center - Presence of methylmercaptan causes a characteristic odor on the breath called fetor hepaticus Monitor serum ammonia levels, electrolyte levels, blood gases and hepatic function test results Prognosis: Client may die of circulatory or respiratory complications, infection or delirium and convulsions Medical Management: 1. Identify and Treat Precipitating Causes a. Gastrointestinal bleeding b. Increased dietary protein c. Constipation d. Infection e. CNS- depressant drugs f. Dehydration

Only fruit juices and IV fluids Vegetable and dairy protein Diet high in vegetables and dairy products 2. Reduce Nitrogenous Waste (Ammonia) in Blood and Bacteria in Colon o Neomycin exerts a powerful effect on the intestinal bacteria that are responsible for ammonia production o Neomycin is nephrotoxic, its use must be avoided in clients with renal insufficiency o Lactulose, which helps decrease blood ammonia levels by reducing absorption of ammonia, is given to clients to produce two to four stools a day 3. Maintain Fluid Volume Balance o Monitoring the quantity and rate of administration 4. Assessment: o Clients normally neat handwriting become sloppy and difficult to read o Is speech slow and slurred? o Observe the client for personality changes and elicit liver flap or flapping tremor (asterixis) Diagnosis: Ineffective Family Therapeutic Regimen Management related to reduction in protein in the diet and long- term pharmacologic intervention with neomycin 5. Promote Low-Protein Diet 6. Monitor for Gastrointestinal Hemorrhage 7. Encourage Bowel Cleansing 8. Administer oral Lactulose 9. Prevent Hypoxemia 10. Prevent infection with accumulation of protein from tissue catabolism 11. Prevent Ammonia Toxicity and Hypokalemia o Be alert to possible harmful accumulations of ammonia as a result of diuretic therapy o Hypokalemia from the use of diuretics contributes to hepatic encephalopathy by increasing ammonia production in the kidney 12. Avoid Sedation o Agents with CNS depressant effects may precipitate coma, and their use should thus be avoided 13. Prevent Complications of Immobility o Prevent pneumonia and skin breakdown 14. Medications o Lactulose, diuretics and vitamin supplements 15. Diet Modifications o Limitations on dietary protein, sodium and water 16. Home Modifications 17. Follow-Up Assessments FATTY LIVER (HEPATIC STENOSIS) lipid infiltration may lead to hepatic stenosis or fatty liver

causes liver enlargement and increased firmness and may result in decreased function Major causes of lipid infiltration: Chronic alcoholism protein malnutrition Diabetes Mellitus Obesity Cushings syndrome Jejunoileal bypass Prolonged IV hyperalimentation Chronic illnesses that involve impaired nutrition or malabsorption Hepatotoxins (carbon tetrachloride) DDT [dichlorodiphenyltrichloroethanel] Reyes syndrome Clients with massive infiltration experience anorexia, abdominal pain, and sometimes jaundice Elevated serum alkaline phosphatase and bilirubin levels Fat embolization may occur and can cause death Nursing Interventions: Directing attention to correction of the cause (abstinence from alcohol, control of diabetes mellitus, weight loss or correction of the intestinal absorptive defect) Preparing the client for diagnostic procedures Giving supportive physical care including adequate nutritional intake Designing teaching guidelines that promote proper diet and prevent recurrence