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Management of Patient with Renal Disorders | | | | | | | |Submitted by: | |Inac, Sarah Gaile T. |BSN III | | | |Submitted to: | |Prof. Frederick Calara PTRP, RN,RM,MAN | FLUID AND ELECTROLYTE IMBALANCES IN RENAL DISORDERS ?if fluid intake is inadequate, the pt is said to be volume depleted and may show s/sx of fluid volume deficit. ?the fluid intake and output (I&O) record, a key monitoring tool, is used to document important fluid parameters, including: -fluid taken (orally and parenterally) volume of urine -other fluid losses (diarrhea, vomiting, diaphoresis) ?pt weight is also important and documenting trends in weight is key assessment strategy essential for determining the daily fluid allowance and indicating signs of fluid overload or deficit. Nursing Alert: the most accurate indicator of fluid loss or gain in an acutely ill pt is WEIGHT. An accurate daily weight must be obtained and recorded.

A 1-kg wt gain is equal to 1000ml of retained fluid. GERONTOLOGIC CONSIDERATIONS ?with aging, kidney is less able to respond to acute fluid and electrolyte changes. elderly pt may develop atypical and non-specific s/sx of disturbed renal function and fluid and electrolyte imbalances. ?fluid balance deficit in elderly: -constipation -falls -medications toxicity -urinary tract and respiratory tract infection -delirium -seizures -electrolyte imbalances -hyperthermia -delayed wound healing RENAL DISORDERS CHRONIC KIDNEY DISEASE ?umbrella term that describes kidney damage or a v in the GFR for 3 or more months. ?can result in end stage renal dse and necessitate renal replacement therapy (dialysis or kidney transplant). RISK FACTORS: ?Cardiovascular Dse Diabetes, primary source of CKD. ?Hpn, 2nd leading cause ?Obesity PATHOPHYSIOLOGY ?early stages of CKD, there can be significant damage to the kidneys w/o s/sx. ?damage to the kidney is thought to be caused by prolonged acute inflammation that is not organ specific and thus has subtle systemic manifestations. STAGES OF CKD ?based on the GFR.

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Normal GFR: 125 ml/min/1. 73m? STAGE 1 ?GFR ? 90ml/min/1. 73m? ?kidney damage with normal or ^GFR STAGE 2 ?GFR = 60-89ml/min/1. 73m? ?mild v in GFR STAGE 3 ?GFR = 30-59ml/min/1. 73m? ?moderate v in GFR STAGE 4 ?GFR = 15-29ml/min/1. 73m? ?severe v in GFR STAGE 5 GFR < 15ml/min/1. 73m? ?kidney failure (End stage renal dse) ?pt with CKD are at risk for cardiovascular dse – leading cause of morbidity and mortality. CLINICAL MANIFESTATIONS ?Elevated Serum Creatinine –indicate underlying kidney dse. ?Anemia – due to v erythropoietin production by the kidney and metabolic acidosis; abnormalities in calcium and phosphorus. ?Fluid Retention – evidenced by edema and CHF, develops. ?Abnormalities in electrolytes ?

Heart failure worsens ?Hpn becomes more difficult to control. ASSESSMENT AND DIAGNOSTIC FINDINGS ?GFR- amount of plasma filtered through the glomeruli per unit of time. Creatinine Clearance- measure of the amount of creatinine the kidneys are able to clear in a 24hr period. ?calculation of GFR, important assessment perimeter in CKD. MEDICAL MANAGEMENT ?Regular clinical and laboratory assessment is important to keep the BP below 130/80mmHg. ?It also includes early referral for initiation of renal replacement therapies as indicated by the pt’s renal status. ?Prevention of complications is accomplished by controlling cardiovascular risk factors: ?treating hyperglycemia ?treating anemia ?smoking cessation ?weight loss ?exercise program as needed ?reduction in Na and alcohol intake

GERONTOLOGIC CONSIDERATIONS ?Changes in kidney function with normal aging ^ the susceptibility of elderly pt to kidney dysfunction and renal failure. ?Predisposing older adults to renal dse associated with these disorders: ?atherosclerosis ?Hpn ?heart failure ?diabetes ?cancer Therefore, acute problems must be prevented if possible and treated quickly to avoid kidney damage. ?Elderly pt undergo extensive diagnostic or when new medications (eg, diuretic agents) are added, precautions must be taken to prevent dehydration, w/c can compromise marginal renal function and lead to renal failure. Elderly pt frequently take OTC drugs ^ the risk for medication – associated changes in renal function, precautions are indicated with all medications. NEPHROSCLEROSIS ?Hardening of the renal arteries. ?most often due to prolonged hpn and diabetes. ?major cause of CKD and ESRD secondary to many disorders.

PATHOPHYSIOLOGY 2 forms of Nephrosclerosis: ?Malignant (accelerated) – often associated with significant hpn (diastolic BP higher than 130mmHg) -occurs in young adults and twice as often in men compared to women. -v blood flow to the kidney resulting in patchy necrosis or the renal parenchyma. overtime, fibrosis occurs and glomeruli are destroyed. -without dialysis, more than half of pt die due to uremia (excess of urea and other nitrogenous wastes in the blood) ? Benign – can be found in older adults, associated with atherosclerosis and hpn. ASSESSMENT AND DIAGNOSTIC FINDINGS ?Symptoms are rare early in the dse, eventhough the urine usually contains protein and occasional casts. ?Renal insufficiency and associated s/sx occur late in the dse. MEDICAL MANAGEMENT ?Aggressive antihypertensive therapy ?Angiotensin-Converting Enzyme (ACE) inhibitor, alone or in combination with other antihypertensive medications.

PRIMARY GLOMERULAR DISEASE ?destroy the glomerulus of the kidneys are the third most common cause of Stage 5 CKD. ?glomerular capillaries are primarily involved. ?antigen-antibody complexes form in the blood and become trapped in the glomerular capillaries (the filtering portion of the kidney), including an inflammatory response. ?IgG (major immunoglobulin [antibody]) found in the blood, can be detected in the glomerulus capillary walls. ?Major clinical manifestations of glomerular injury: ?proteinuria ?hematuria ?vGFR ?vexcretion of Na ?edema ?hpn TERMS TYPICALLY USED WHEN DESCRIBING GLOMERULAR DISEASE Primary – dse mainly in glomeruli. ?Secondary – glomerular dse that are the consequence of systemic dse. ?Idiopathic – cause is unknown. ?Acute – occurs over days or weeks. ?Chronic – occurs over months or years. ?Rapidly progressing – constant loss of renal function with minimal change of recovery. ?Diffuse – involves all glomeruli. ?Focal – involves some glomeruli. ?Segmental – involves portions of individual glomeruli. ?Membranous – evidence of thickened glomerular capillary walls. ?Proliferative – number of glomerular cells involved is increasing. ACUTE NEPHRITIC SYNDROME ?Clinical manifestation of glomerular inflammation.

Glomerulonephritis – an inflammation of the glomerular capillaries that can occur in acute and chronic forms. PATHOPHYSIOLOGY ?Primary glomerular dse includes: ?post infectious glomerulonephritis ?rapidly progressive glomerulonephritis ?membrane proliferative glomerulonephritis ?membranous glomerulonephritis ?Post infectious causes Group A beta hemolytic streptococcus infection of the throat that precedes the onset of glomerulonephritis by 2-3weeks. ?It may also follow impetigo (infection of the skin) and acute viral infection (infection of upper respiratory tract, mumps, varicella zoster virus, Epstein-Barr virus, hep B, and HIV infection) ?

In some pt, antigens outside the body (eg. Medications, foreign serum) intiate the process, resulting in antigen-antibody complexes being deposited in the glomeruli. ?In other pt, kidney tissue itself serves as the inciting antigen. SEQUENCE OF EVENTS IN ACUTE NEPHRITIC SYNDROME Antigen (Group A Beta Hemolytic Streptococcus) v Antigen-antibody product v Desposition of antigen-antibody complex in glomerulus v ^ production of epithelial cells lining the glomerulus v Leukocyte infiltration of the glomerulus v Thickening of glomerular filtration membrane v Scarring and loss of glomerular filtration membrane v glomerular filtration rate (GFR) CLINICAL MANIFESTATIONS ?Primary presenting features of an acute inflammation: ?Hematuria – may be identifiable through microscopic or macroscopic. -urine may be appeared cola-colored because of RBC and protein plugs or casts. -RBC casts indicate glomerular injury. ?Proteinuria – due to ^ permeability of the glomerular membrane may also occur with associated pitting edema, hypoalbuminemia, hyperlipidemia and fatty casts in the urine. -BUN and Serum Creatinine levels may ^ as urine output decreases. -anemia may be present. ?

Azotemia – abnormal concentration of nitrogenous wastes in the blood. Complain of headache ?Malaise ?Flank Pain ?Elderly pt may experienced circulatory overload with dyspnea, engorged neck veins, cardiomegaly and pulmonary edema. ?Atypical symptoms include confusion, somnolence, seizure which often confused with the symptoms of a primary neurologic disorder. ASSESSMENT AND DIAGNOSTIC FINDINGS ?Kidneys becomes large, edematous and congested. ?All renal tissues including the glomeruli, tubules and blood vessels are affected to varying degrees. ?Pt with IgA nephropathy have an elevated serum IgA and low to normal complement levels. Electron microscopy and immunofluorescent analysis help identify the nature of the lesion. ?Kidney Biopsy may be needed for definitive diagnosis. ?Some pt develops severe uremia within weeks and require dialysis for survival. ?After a period of apparent recovery, insidiously develop chronic glomerulonephritis. COMPLICATIONS ?Hypertensive encephalopathy – medical emergency and therapy is directed toward reducing the Bp without impairing renal function. ?Heart Failure ?Pulmonary Edema ?ESRD MEDICAL MANAGEMENT ?Corticosteroids ?Managing Hypertension ?Controlling proteinuria If residual streptococcal infection is suspected, penicillin is the agent of choice. ?Dietary protein is restricted when renal insufficiency and nitrogen retention (elevated BUN) develop. ?Sodium is restricted when pt has hpn, edema, and heart failure. NURSING MANAGEMENT ?Carbohydrates are given liberally to provide energy and reduce the catabolism of protein. ?I&O ?Fluids are given based on the pt’s fluid losses and body wt. ?Other nsg interventions focus on pt education about the dse process, explanation of laboratory and other diagnostic tests and preparation for safe and effective self-care at home.

CHRONIC GLOMERULONEPHRITIS ?Due to repeated episodes of acute nephritic syndrome, hypertensive nephrosclerosis, hyperlipidemia, chronic tubulointerstitial injury, or hemodynamically mediated glomerular sclerosis. ?Secondary glomerular diseases that can have systemic effects include lupus erymatosus, Goodpasture’s syndrome (caused by antibodies to the glomerular basement membrane), diabetic glomerulosclerosis and amyloidosis. PATHOPHYSIOLOGY ?Kidneys are reduced to as little as one-fifth their normal size (consisting largely of fibrous tissue). ?The cortex layer shrinks to 1-2mm in thickness or less. Bands of scar tissue distort the remaining cortex, making the surface of the kidney rough and irregular. ?Numerous glomeruli and their tubules become scarred, and the branches of the renal artery are thickened. ?The resulting severe glomerular damage can progress to stage 5 CKD and require renal replacement therapies. CLINICAL MANIFESTATIONS ?Some pt with severe disease have no symptoms at all for many years. ?It may discovered when hypertension or elevated BUN and Serum Creatinine levels are detected. ?Loss of weight and strength ?Increasing irritability ?Nocturia (increased need to urinate at night) Headaches, dizziness, and digestive disturbances. ?The pt appears poorly nourished, with a yellow-gray pigmentation of the skin and periorbital and peripheral (dependent) edema. ?Bp may be normal or severely elevated. ?Retinal findings include hemorrhage, exudates, narrowed tortuous arterioles and papilledema. ?

Anemia causes pale mucous membranes. ?Cardiomegaly, a gallop rhythm, distended neck veins, and other s/sx of heart failure may be present. ?Crackles can be heard in the bases of the lungs. ?Perpheral neuropathy with diminished deep tendon reflexes and neurosensory changes occur late in the dse. Pt becomes confused and demonstrates a limited attention span. ?Evidence of pericarditis with a pericardial friction rub and pulsus paradoxus (difference of Bp during inspiration and expiration or greater than 10mmHg). ASSESSMENT AND DIAGNOSTIC FINDINGS ?

Urinalysis reveals a fixed specific gravity of about 1. 010, variable proteinuria, and urinary casts (proteins secreted by damaged kidney tubules). ?As renal failure progresses and the GFR falls below 50ml/min, the ff changes occur: ?Hyperkalemia due to decreased potassium excretion, acidosis, catabolism, and excessive potassium intake from food and medications. Metabolic acidosis from decreased acid secretion by the kidney and inability to regenerate bicarbonate. ?Anemia secondary to decreased erythropoiesis (production of RBCs) . ?Hypoalbuminemia with edema secondary to protein loss through the damaged glomerular membrane. ?Increased serum phosphorus level due to decreased renal excretion of phosphorus. ?Decreased serum calcium level (calcium binds to phosphorus to compensate for elevated serum phosphorus levels). ?Mental status changes. ?Impaired nerve conduction due to electrolyte abnormalities and uremia. ?Chest x-rays show cardiac enlargement and pulmonary edema. ECG may be normal or may indicate left ventricular hypertrophy associated with hpn and signs of electrolyte disturbances such as tall, tented (or peaked) T waves associated with hyperkalemia. ?CT and MRI scans show a decrease in the size of the renal cortex. MEDICAL MANAGEMENT ?If pt has hpn, efforts are made to reduce the Bp with Na and w

ater restriction and antihypertensive agents. ?Wt is monitored daily and diuretic medications are prescribed to treat fluid overload. ?Proteins of ^ biologic value (dairy products, eggs, meats) are provided to promote good nutritional status. UTI must be treated promptly to prevent further renal damage. ?Dialysis is initiated early in the course of the dse to keep the pt in optimal physical condition, prevent fluid and electrolyte imbalances and minimize the risk of complications of renal failure. NURSING MANAGEMENT ?Changes in fluid and electrolyte status and in cardiac and neurologic status are reported promptly to the physician. ?Emotional support by providing opportunities for the pt and the family to verbalize their concerns, have their questions answered, and explore their options. ?Instructions to the pt include explanation and scheduling for follow-up evaluations: BP ?Urinalysis for protein and casts ?Laboratory studies of BUN and serum creatinine levels. ?If longterm dialysis is needed, nurse teaches the pt and family about the procedure, how to care for the acess site, dietary restrictions and other necessary lifestyle modifications. ?Explanations about recommended diet and fluid modifications and medications (purpose, desired effects and adverse effects, dosage and administration schedule). ?

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