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JELINE DIA S.

LABAN BSN 3D

Medical and Nursing Management of Nephrotic Syndrome


Definition Nephrotic syndrome (nephrosis) is not a single disease but a group of symptoms. Symptoms include heavy proteinuria (increase in protein in the urine), hypoalbuminemia (decrease in albumin in the blood), edema, hypercholesterolemia (high serum cholesterol), and normal renal function. II. Risk Factors Collagen vascular disease, such as systemic lupus erythematosus or rheumatoid arthritis Sickle cell disease Diabetes mellitus Malignancy such as leukemia, lymphoma, Wilms tumor or pheochromocytoma Toxins such as bee sting, snake venom Medications including probenecid, captopril, lithium or warfarin Hypertension Heroin use III. Pathophysiology Nephrotic syndrome results from damage to the kidneys glomeruli, the tiny blood vessels that filter waste and excess water from the blood and send them to the bladder as urine. Damage to the glomeruli from diabetes, or even prolonged hypertension causes the membrane to become porous, so that small proteins such as albumin pass through the kidneys into urine. As protein continues to be excreted, serum albumin is decreased, which in turn decreases the serum osmotic pressure. Capillary hydrostatic fluid pressure becomes greater than capillary osmotic pressure, which results in generalized edema. As fluid is lost into the tissues, the plasma volume decreases, stimulating secretion of aldosterone to retain sodium. This additional water also passes out of the capillaries into the tissue leading to even greater edema. IV. Assessment/Clinical Manifestations/Signs and Symptoms Major manifestations is edema (usually periorbital in dependent areas *sacrum, ankles and hands+ and ascites) Malaise, headache, irritability and fatigue Foamy urine Anorexia, abdominal discomfort Laboratory and diagnostic study findings Proteinuria (exceeding 3 to 3.5 g/day) Microscopic hematuria Needle biopsy of the kidney for histologic examination to confirm diagnosis V. Medical Management Objective of management is to preserve renal function. Bed rest for a few days to promote diuresis and reduce edema. Diet with high biologic protein (0.8 g/kg/day) to replenish urinary losses Low sodium, low saturated fat, liberal potassium Pharmacologic therapy Diuretics for severe edema, in combination with angiotensin-converting enzyme (ACE) inhibitors Adrenocorticosteroids to reduce proteinuria Antineoplastic agents (Cytoxan) or immunosuppressive agents VI. Nursing Diagnosis Imbalanced nutrition: less than body requirements Risk for infection Deficient knowledge

JELINE DIA S. LABAN BSN 3D

VII. Nursing Management In the early stages, nursing management is similar to that of acute glomerulonephritis As the disease worsens, management is similar to that of chronic renal failure Monitor intake and output; note signs of low plasma volume and impaired circulation with prerenal acute renal failure Instruct patient receiving steroids or cyclosporine regarding medication and signs and symptoms that must be reported to the physician Instruct patient in selecting a high-protein diet while restricting cholesterol and fat intake

Medical and Nursing Management of Urolithiasis


. Definition Urolithiasis (i.e. renal calculi) is described as calculi in the urinary tract the bladder, the ureters, and the most commonly the kidneys. II. Risk Factors Peaks between ages 30 and 50 years Higher among men than women Immobility Hypercalcemia Urinary tract infection Urine stasis High urine specific gravity Genetic predisposition III. Pathophysiology Calculi are formed by deposition of crystalline substances, including calcium oxalate, calcium phosphate, and uric acid. Most calculi contain calcium or magnesium in combination with phosphorus or oxalate. Calculi may pass through the urinary tract, or they may lodge, causing obstruction leading to infection and possibly hydronephrosis. IV. Assessment/Clinical Manifestations/Signs and Symptoms Vary with the location, size, and cause of calculi and may include: Acute, sharp, intermittent pain (i.e. ureteral colic) Dull, tender ache in the flank (i.e. renal colic) Nausea and vomiting accompanying severe pain. Fever and chills Hematuria Abdominal distention Pyuria Rarely, oliguria or anuria Laboratory and diagnostic study findings Kidneys, ureters, and bladder radiograph reveals visible calculi. Stone analysis detects mineral content of calculi. IV pyelography determines size and location of calculi Renal ultrasonography reveals obstructive changes such as hydronephrosis. V. Medical Management Basic goals are to eradicate the stone, determine the stone type, prevent nephron destruction, control infection and relieve any obstruction that may be present.

JELINE DIA S. LABAN BSN 3D


Stone Removal procedures Cystoscopic examination and passage of small ureteral catheter Chemical analysis of stones to determine composition Extracorporeal shock wave lithotripsy (ESWL) Percutaneous nephrostomy; endourologic methods Electrohydraulic lithotripsy Ureteroscopy: stones fragmented with use of laser, electrohydraulic lithotripsy, or ultrasound and then removed Chemolysis (stone dissolution): alternative for those who are poor risks for other therapies, refuse other methods, or have easily dissolved stones (struvite) Surgical removal is performed in only 1 to 2% of paitents. Pharmacologic and Nutritional therapy Analgesic agents (morphine or meperidine to prevent shock and syncope) and nonsteroidal anti-inflammatory drugs (NSAIDs) Increased fluid intake to assist in stone passage, unless patient is vomiting Increased round-the-clock fluid intake to dilute urine and ensure high urinary output For calcium stones: reduced dietary calcium, protein and sodium intake; liberal fluid intake; medications to acidify urine, such as ammonium chloride, sodium cellulose phosphate (Calcibind), and thiazide diuretics if parathormone production is increased. For phosphate stones: diet low in phosphorus; aluminum hydroxide gel. For uric stones: low-urine and limited protein diet; allopurinol (Zyloprim); alkalinization of urine For cystine stones: low-protein diet; alkalinization of urine For oxalate stones: dilute urine; limit oxalate intake (green leafy vegetables such as spinach, strawberries, rhubarb, wheat bran, chocolate tea, and peanuts) VI. Nursing Diagnosis Pain related to inflammation, obstruction, and abrasion of the urinary tract Deficient knowledge regarding prevention of recurrence of renal stones Ineffective coping related to anxiety, lower activity level and the inability to perform normal activities of daily living Impaired urinary elimination related to renal calculi Risk for infection VII. Nursing Management Provide comfort measures. Encourage bed rest. Teach relaxation techniques. Provide hot baths or moist heat to the flank areas Prepare the client who cannot pas the calculus spontaneously for one of the following nonsurgical procedures: Extracorpeal shock wave lithotripsy which is used to break up calculi so that the client can pass the particles during urination. Ureteroscopy which involves insertion of instruments through a cystoscope to visualize and access the calculus and then remove or fragment it with laser energy or ultrasound. Stone dissolution which involves infusion of chemolytic solutions (i.e. alkylating ore acidifying agents) through a percutaneous nephrostomy tube. This procedure is used for clients who are poor risks for other treatments. Prepare the client for nephrolithotomy (incision into the kidney for removal of the calculus) if nonsurgical methods fail. Monitor for signs and symptoms of dehydration resulting from postobstructive dieresis. Intervene as necessary to restore fluid balance. Inform the client that chemical analysis of the calculus is performed to determine the composition (i.e. calcium oxalate, calcium phosphate). The composition guides further diet therapy. Institute measures to help prevent calculi recurrence. Encourage dietary modifications based on the calculi composition. -Those with calcium calculi should avoid dietary calcium and phosphorus. -Those with uric calculi should avoid food high in purine, such as shellfish, anchovies, asparagus, and organ meats. -Those with oxalate calculi should avoid green leafy vegetables, beans, celery, beets, tea and coffee.

JELINE DIA S. LABAN BSN 3D


Increase fluid intake to 3 to 4 L per day. Instruct the client to drink fluids in the late evening to prevent stasis of urine in kidneys and bladder. Promote increased physical activity. Monitor urine pH. Administer prescribed medications such as: -Aluminum hydroxide which binds with excess phosphorus, causing it to be excreted through the intestinal tract. -Sodium cellulose phosphate which helps prevent calcium stones. -Allopurinol which reduces serum uric acid levels and urinary uric acid excretion. Instruct the client to avoid sudden increases in environmental temperatures, which may cause a fall in urinary volume. Encourage around-the-clock, high-fluid intake if the client is not nauseated or vomiting.

Medical and Nursing Management of Glomerulonephritis


I. Definition Glomerulonephritis is an inflammation of the glomerular capillaries. II. Risk Factors Immune diseases Inflammation of the blood vessels (vasculitis) Infection (poststreptococcal, bacterial endocarditis and viral infections) III. Pathophysiology In patients with glomerulonephritis, the glomeruli becomes inflamed and impair the kidneys ability to filter urine. Eventually, the glomeruli become inflamed and scarred, and slowly lose their ability to remove waste and excess water from the blood to make urine. Glomerulonephritis can be acute, occurring as a sudden attack of inflammation or chronic which develops gradually. IV. Assessment/Clinical Manifestations/Signs and Symptoms Urine is cola-colored as a result of hematuria and proteinuria Headache, malaise, facial edema Flank pain Mild to severe hypertension Tenderness of the costovertebral angle Dyspnea, engorged neck veins Cardiomegaly Pulmonary edema Laboratory and diagnostic study findings Microscopic or gross hematuria Proteinura, increased antistreptolysin-O or antiDNase B titer Elevated BUN and serum creatinine levels and anemia Kidney biopsy is performed for definitive diagnosis V. Medical Management Goal of management are to preserve kidney function and to treat complications promptly. The patient is placed on bed rest during the acute phase until the urine clears and BUN and creatinine levels and blood pressure return to normal.

JELINE DIA S. LABAN BSN 3D


Pharmacologic therapy Penicillin for residual streptococcal infection Diuretics and antihypertensive agents Plasma exchange (plasmapheresis) and treatment with immunosuppressants, corticosteroids, and cytotoxic drugs to reduce inflammatory response in rapidly progressive disease. Dialysis occasionally necessary Nutritional management Dietary protein restricted with renal insufficiency and elevated BUN Sodium restricted with hypertension, edema and congestive heart failure Carbohydrates for energy and to reduce protein catabolism Fluids according to fluid losses and daily body weight and intake and output VI. Nursing Diagnosis Excess fluid volume Risk for infection Deficient knowledge VII. Nursing Management Observe for deteriorating renal function; report changes in fluid and electrolyte status and in cardiac and neurologic status Give emotional support throughout the disease and treatment course by providing opportunities for patient and family to verbalize concerns. Answer questions and discuss options. Educate patient and family about prescribed treatment plan and the risk of noncompliance. Explain about need for follow-up evaluations of blood pressure, urinalysis for protein and casts, blood for BUN, and creatinine to determine if disease has worsened. Instruct in recommended diet and fluid modifications and provide medication teaching. Review fluid and diet restrictions Instruct patient to notify physician if infection or symptoms of renal failure occur: fatigue, nausea and vomiting, diminishing urinary output Give patient and family assistance and support regarding dialysis and long-term complications.

Medical and Nursing Management of Urinary Tract Infections (Upper & Lower UTIs)
Definition Inflammation and infection of urinary tract structures are classified as upper urinary tract infections (UTIs) or lower UTIs. TYPES: Upper UTIs are known as pyelonephritis (e.g. inflammation of the kidney) Lower UTIs include: Cystitis (e.g. inflammation of the bladder wall), the most common type Ureteritis (e.g. inflammation of the ureter) Urethritis (e.g. inflammation of the urethra) II. Risk Factors Women because of their shorter urethra (25% of all women experience UTIs Aging, men peaks after age 50 Pathogenic microorganisms (e.g. Escherichia coli, Proteus, Klebsiella, Enterobacter). Sexual intercourse Indwelling catheterization Urinary stasis Urinary tract instrumentation Residual urine Urinary reflux Bladder overdistention Loss of intact mucosal lining

JELINE DIA S. LABAN BSN 3D


Metabolic disorders III. Pathophysiology An Upper UTI is a bacterial infection of the renal pelvis, tubules, and intesrstitial tissue on one or both kidneys that occurs because of reflux of urine into the ureters. A Lower UTI is an infection that typically ascends from the urethra to the bladder and possibly to the ureter. IV. Assessment/Clinical Manifestations/Signs and Symptoms Upper UTI Flank pain Costovertebral angle tenderness Fever and chills Dysuria Frequency and urgency Malaise Possibly bloody or cloudy urine Lower UTI Frequency and urgency Burning on urination Nocturia Inflamed, edematous meatus in urethritis Laboratory and diagnostic study findings Upper UTI. Urinalysis findings reveal elevated white blood cell count, white cell casts, and bacteria. Lower UTI Urinalysis reveals bacteriuria and red blood cells in urine. Urine culture identifies the causative microorganism. V. Medical Management Drug therapy and patient education are the key treatment measures. UTIs may require 7 to 10 days of medication. Ideal treatment is an antibacterial agent that eradicates bacteria from urinary tract with minimal effects on fecal and vaginal flora. Medications may include sulfisoxazole (Gantrisin); cotrimoxazole (trimethoprim-sulfamethoxaxole) [Bactrim] is the drug of choice. Levofloxacin (Levaquin) may be used for short course therapy. Occasionally, ampicillin or amoxicillin (but E. coli has developed resistance to these agents) If diagnostic evaluation reveals no structural abnormalities, patient may be instructed to begin treatment on own, testing urine with a dipstick whenever symptoms occur, and to contact health provider only with persistence of symptoms at the occurrence of fever, of if the number of treatment episodes exceeds four in a 6-month period. VI. Nursing Diagnosis Pain related to inflammation an infection of the urethra, bladder and other urinary tract structures. Infection related to frequency or burning on urination, fever, elevated white blood cell count, foul-smelling urine, and suprapubic tenderness. Impaired urinary elimination related to excessive urgency and pain with bladder filling. Impaired comfort related to pain with bladder filling. Risk for imbalanced body temperature Pain related to ureteral colic. Fear in response to the diagnosis of pyeloneprhtitis Deficient knowledge related to completion of drug therapy, optimal fluid intake, or need to empty bladder every four hours to reduce bacterial count. Ineffective coping related to anxiety, malaise, and lowered activity level.

JELINE DIA S. LABAN BSN 3D


VII. Nursing Management Provide pain relief. Apply heat to the perineum. Promote measures to prevent infection. Promote measures to maintain fluid and electrolyte balance. Provide client and family teaching. Provide health education on measure to prevent UTIs. Administer prescribed medication.

Medical and Nursing Management of Urinary Retention


I. Definition Urinary retention is urine retained in the bladder in the presence of normal urine production, with an inability to release it even when the micturition reflex is activated. II. Risk Factors Male factors Benign prostatic hypertrophy Urethral stricture Calculi or foreign body in the urethra Urethritis Tumor Phimosis Female factors Urethral obstruction secondary to stricture, calculi, vaginal cysts, tumor or edema Retroverted gravid uterus Male and female factors Reflex spasm of sphincters after surgery or invasive procedures Trauma Neurogenic bladder dysfunction Medications (e.g. anticholinergics, antihistamines) Fecal impaction Psychogenic retention III. Pathophysiology Decreased nerve innervations of the bladder muscle causes the urge to void to be suppressed. Retention may be acute or chronic. Chronic retention can lead to overflow incontinence or residual urine. Other possible complications of chronic urinary retention include urinary tract infection, bladder distention and damage, and hydronephrosis. IV. Assessment/Clinical Manifestations/Signs and Symptoms Inability to void, urinary urgency, urinary hesitancy, and dribbling Lower abdominal pain or discomfort Restlessness and diaphoresis Visible or palpable bladder distention Dullness on bladder percussion Possibly signs and symptoms of lower UTI Laboratory and diagnostic study findings Bladder catheterization commonly reveals residual urine. V. Medical Management Initial management should be urethral catheterization followed by at least one voiding trial. Avoid drugs like tricyclic antidepressants and instructed the patient to drink small volumes of water or tea or to sit in a warm bath or take a warm shower.

JELINE DIA S. LABAN BSN 3D


The patient can be asked to void every three to four hours, regardless of his or her urgency. Ordered diagnostic tests for urinary retention: Urinalysis may give a clue to underlying UTI BUN and serum creatinine may reflect acute renal failure Urinalysis and electrolytes are essential as renal failure often follows chronic retention. If urinary calculus, check urate, calcium and phosphate. Renal ultrasound, IVP, rethrography VI. Nursing Diagnosis Urinary retention Acute pain as related to acute urinary retention VII. Nursing Management Facilitate bladder emptying Provide privacy, run water, have the client assume a normal voiding position and provide pain relief. Promote relaxation of the sphincter by providing sitz baths, warm showers, and hot tea to drink Obtain and record strict urinary output every time the client voids. If the client cannot void, perform intermittent catheterization to prevent overdistention of the bladder. Prepare the client for surgical intervention (e.g. dilation of urethra, cystoplasty), if indicated. Provide health education on measure to prevent UTI.

Bladder Cancer
Etiology and Risk Factors: Carcinogens in the workplace, such as dyes, rubber, leather, ink or paint Recurrent bacterial infection of urinary tract Smoking

Clinical Manifestations: Gross, painless hematuria Urinary frequency Urgency Dysuria Pelvic or back pain with metastasis Treatment: Intravesical into bladder) chemotherapy Radiation therapy Uretoroentero-cutaenous diversions (intestines used) or cutaenous (opening onto abdominal walls)

Medical and Nursing Management of Acute Renal Failure


I. Definition Acute renal failure is defined as sudden, rapid, potentially reversible deterioration of renal function. It can be classified according to underlying cause as: Prerenal azotemia stemming from decreased blood flow to kidneys Intrarenal acute renal failure involving intrinsic damage to renal structures Postrenal obstruction involving obstruction of urine outflow

JELINE DIA S. LABAN BSN 3D


II. Risk Factors Prerenal azotemia is caused by factors that interfere with renal perfusion. Hypovolemia (e.g. hemorrhage, shock, burns) Increased intravascular capacity (e.g. from sepsis, neurogenic bladder) Cardiac disorders (e.g. myocardial infarction, arrhythmias_ Renal artery obstruction Hepatorenal syndrome Intrarenal acute renal failure Acute tubular necrosis which accounts for about 75% of all cases of acute renal failure Acute glomerulonephritis Acute pyelonephritis Postrenal obstruction Ureteral obstruction due to calculi, strictures, trauma, or pregnancy Bladder obstruction (e.g. cancer, prostatic hypertrophy) III. Pathophysiology The exact pathogenesis of acute renal failure is not always known, but it is associated with a severe reduction in the glomerular filtration rate. This may be caused by decreased renal blood flow that leads to increased renalvascular resistance, increased hydrostatic pressure in Bowmans capsule, or a disruption of tubular epithelium. FOUR CLINICAL PHASES OF ACUTER RENAL FAILURE: The onset phase extends from the time of the precipitating event to the beginning of the oliguric-anuric phase. The oliguric-anuric phase is marked by urine output of less than 400 ml/day, volume overload, elevated blood urea nitrogen (BUN) and creatinine levels, electrolyte abnormalities, metabolic acidosis, and uremia. The diuretic phase extends from the time that output becomes more than 400ml/day to the time the BUN stops rising and stabilizes in normal range. During this phase, electrolyte and acid-base problems begin to normalize. The convalescent phase extends from the time the BUN stabilizes until the client returns to normal activity. The client may take up to 2 years to regain 70%to 80% of normal function. Systemic effects of acute renal failure are widespread and may include: Fluid and electrolyte imbalances Acidosis Increased susceptibility to infection Anemia Platelet dysfunction GI disturbances (e.g. anorexia, nausea, vomiting, diarrhea, or constipation, stomatitis) Pericarditis Uremic encephalopathy IV. Assessment/Clinical Manifestations/Signs and Symptoms Altered urine output, may be oliguria, anuria, or rarely polyuria Hypertension or hypotension Tachypnea Signs of fluid overload or extracellular fluid depletion Laboratory and diagnostic study findings Urinalysis Urine osmolality In prerenal values are higher than 900 mOsm/kg In intrarenal parenchymal failure values are less than 250 mOsm/kg In postrenal obstruction values may be normal

JELINE DIA S. LABAN BSN 3D


Blood analysis BUN, serum creatinine, and potassium levels are elevated Blood pH, bicarbonate, hemoglobin, and hematocrit values are decreased V. Medical Management Treatment objectives are to restore normal chemical balance and prevent complications until renal tissues are repaired and renal function is restored. Possible causes of damage are identified and treated. Fluid balance is managed based on daily weight, serial measurements of central venous pressure, serum and urine concentrations, fluid losses, blood pressure, and clinical status. Fluid excesses are treated with mannitol, furosemide to initiate dieresis and prevent or minimize subsequent renal failure. Blood flow is restored to the kidneys with the use of intravenous fluids, albumin or blood product transfusions. Dialysis (hemodialysis, hemofiltration, or peritoneal dialysis) is started to prevent complications of uremia, including hyperkalemia, pericarditis and seizures. Ion exchange resins (orally or by retention enema) Intravenous glucose and insulin or calcium glutamate as an emergency and temporary measure to treat hyperkalemia. Sodium bicarbonate to elevate plasma pH. Parenteral erythropoietin (Epogen) to treat reduced erythropoietin production and prevent anemia Shock and infection are treated if present Arterial blood gases are monitored when severe acidosis is present. If respiratory problems develops, ventilator measures are started. Phosphate-binding agents such as aluminum hydroxide to control elevate serum phosphate concentrations. Dietary protein is limited to about 1g/kg during oliguric phase to minimize protein breakdown and to prevent accumulation of toxic end products. Caloric requirements are met with high-carbohydrate feedings; parenteral nutrition Foods and fluids containing potassium and phosphorus are restricted; potassium intake is limited to 40 to 60 mEq/d. Sodium intake is restricted to 2 g/d. Blood chemistries are evaluated to determine amount of replacement sodium, potassium, and water during oliguric phase. After the diuretic phase, high-protein, high-calorie diet is given with gradual resumption of activities. VI. Nursing Diagnosis Fluid volume excess related to decreased urine output Activity intolerance related to fatigue, toxins and fluid build up Risk for impaired skin integrity related to edema, toxins, or impaired tissue perfusion Risk for infection related to intravenous lines or catheters or uremic toxins Deficient knowledge regarding condition and its treatment VII. Nursing Management Promote measures to ensure normal potassium levels. Monitor potassium level and assess for effects of hyperkalemia. Restrict dietary potassium as necessary. Monitor cardiac telemetry for electrocardiographic changes. Prepare to administer insulin and glucose, which drives potassium back into the cell. Promote measures to maintain acid-base balance. Monitor for acidosis Administer an alkalinizing agent Monitor arterial blood gas values for signs of metabolic acidosis or alkalosis. Be prepared to institute ventilator measures if respiratory problems develop. Promote measures to assess and prevent infection. Assess for infection, especially of the respiratory and urinary tracts. Do not leave the urinary catheter in place. Administer prophylactic antibiotics as prescribed. Monitor for hyperphosphatemia. Administer phosphate-binding agents. Monitor serum phosphorus level.

JELINE DIA S. LABAN BSN 3D


Promote measures to ensure normal calcium levels. Monitor for hypocalcemia Administer calcium supplements Assess for hypercalcemia by checking for Chvosteks and Trousseaus signs. Prevent GI bleeding by administering histamine receptor antagonists and proton pump inhibitors. Promote comfort and encourage bed rest to reduce exertion and metabolic rate. As prescribed, administer shortacting barbiturates to control pain, and assess for central nervous system complications such as drowsiness, confusion, delirium, coma, and convulsions. Provide a high-calorie and low-protein diet, with hyperalimentation if the client cannot eat. If indicated, prepare the client for dialysis to correct hyperkalemia, fluid overload, acidosis, or severe uremia. Administer prescribed medication, which may include alkalinizing agents, antibiotics, phosphate-binding agents, ion exchange resins, calcium supplements, histamine receptor antagonists, and proton-pump inhibitors. Promote measures to maintain fluid balance. Assess fluid balance, and restrict intake to 24-hour urine output plus 500 ml/day. Promote measures to ensure normal sodium and phosphate levels. Instruct the client to restrict sodium intake, drink plenty of fluids, and follow a low-phosphate diet.

Medical and Nursing Management of Chronic Renal Failure


I. Definition Chronic renal failure is the end result of progressive irreversible loss of functioning renal tissue. It usually develops gradually, possibly taking up to several years to develop. In some cases, it may occur rapidly because of an acute disorder (e.g. unresolved acute renal failure) II. Risk Factors Hypertensive nephropathy Diabetic nephropathy Chronic glomerulonephritis Chronic pyelonephritis Lupus nephritis Polycystic kidney disease Chronic hydronephrosis III. Pathophysiology Decreased renal function results in an accumulation of waste products (i.e. uremia) in the bloodstream. Uremia develops and adversely affects every system in the body. THREE BASIC STAGES OF CHRONIC RENAL FAILURE: Decreased renal reserve. During this stage, renal function is 40 to 50% of normal and homeostasis is maintained. Renal insufficiency. During this stage, renal function is 20 to 40% of normal glomerular filtration rate (GFR), clearance, and urine concentration are decreased and homeostasis is altered. End stage renal disease. During this stage, renal function is less than 10% to 15% of normal; all renal functions are severely decreased; and homeostasis is significantly altered.

JELINE DIA S. LABAN BSN 3D


In chronic renal failure, retention of sodium and water leads to edema, heart failure, and hypertension. Conversely, episodes of diarrhea and vomiting may lead to sodium and water depletion, which can exacerbate uremia and produce hypotension and hypovolemia. Metabolic acidosis occurs, interfering with the kidneys ability to excrete hydrogen ions, produce ammonia, and conserve bicarbonate. Decreased GFR results in: Increased serum phosphate Decreased serum calcium Increased parathormone but depleted bone calcium, leading to bone changes (e.g. uremic bone disease, osteomalacia) Erythropoietin production decreases, resulting in anemia. Neurologic complications develop, such as: Altered mental function Personality and behavioral changes Convulsions Coma IV. Assessment/Clinical Manifestations/Signs and Symptoms Clinical manifestations depend on the stage of the disorder: Increased renal reserve Asymptomatic as long as there is no exposure to severe physiologic or psychologic stress. Renal insufficiency. Polyuria Nocturia Signs and symptoms of mild anemia End-stage renal failure Widespread systemic manifestations: 1)Cardiovascular Fluid overload, edema Congestive heart failure Electrolyte imbalance Metabolic acidosis Hypertension Arrhythmias Pericarditis, effusion, and tamponade 2)Gastrointestinal Anorexia, nausea, and emesis Stomatitis, and uremic halitosis Gastritis and bleeding Bowel problems; diarrhea Constipation 3)Hematopoietic Anemia Alteration coagulation Increased susceptibility to infection 4)Integumentary Pallor Yellowness Dryness Pruritus

JELINE DIA S. LABAN BSN 3D


Purpura and ecchymosis Uremic frost (seen only in terminal or severely critically ill clients) 5)Neuromuscular Drowsiness, confusion, coma and irritability Tremors, twitching, and convulsions Peripheral neuropathy (Stage I restless syndrome and paresthesias, Stage II motor involvement, leading to footdrop, Stage III paraplegia) 6)Psychosocial Decreased mentation Decreased concentration Altered perceptions (even to the point of frank psychoses) 7)Respiratory Pulmonary edema Pneumonia or pneumonitis Kussmauls respirations 8)Skeletal Hypocalcemia and hyperphosphatemia Osteodystrophy Metastatic calcifications Laboratory and diagnostic study findings Anemia Elevated blood urea nitrogen (BUN) and serum creatinine levels Elevated serum phosphorus level Decreased serum calcium level Decreased serum protein (particularly albumin( levels Low blood pH V. Medical Management Goal of management are to retain kidney function and maintain homeostasis for as long as possible. All factors that contribute to ESRD and those that are reversible (e.g. obstruction) are identified and treated. Complications can be prevented or delayed by administering prescribed antihypertensives, cardiovascular agents, anticonvulsants, erythropoietin (Epogen), iron supplements, phosphate-binding agents (antacids), and calcium supplements. Dietary intervention is needed, with careful regulation of protein intake, fluid intake to balance fluid losses, and sodium intake and with some restrictions of potassium. Adequate intake of calories and vitamins is ensured. Calories are supplied with carbohydrates and fats to prevent wasting. Protein is restricted; protein must be of high biologic value (dairy products, eggs, meats) Vitamin supplementation Fluid allowance is 500 to 600 mL of fluid or more than the 24-hour urine output Pharmacologic Management Hyperphosphatemia and hypocalcemia are treated with aluminum-based antacids or calcium carbonate; both must be given with food Hypertension is managed by intravascular volume control and antihypertensive medication Heart failure and pulmonary edema are treated with fluid restriction, low-sodium diet, diuretics, inotropoic agents (eg. Digitalis or dobutamine) and dialysis Metabolic acidosis is treated, if necessary, with sodium bicarbonate supplements or dialysis. Hyperkalemia is treated with dialysis; medications are monitored for potassium content; patient is placed on potassium-restricted diet; Kayexalate is administered as needed.

JELINE DIA S. LABAN BSN 3D


Patient is observed for early evidence of neurologic abnormalities (eg. Slight twitching, headache, delirium, or seizure activity) The onset of seizures, type, duration and general effect on patient are recorded; physician is notified immediately and patient is protected from injury with padded side rails. Intravenous diazepam (Valium) or phenytoin (Dilantin) is administered to control seizures. Anemia is treated with recombinant human erythropoietin (Epogen); hematocrit is monitored frequently Heparin is adjusted as necessary to prevent clotting of dialysis lines during treatments. Serum iron and transferring levels are monitored to assess iron states (iron is necessary for adequate response to erythropoietin) Blood pressure and serum potassium levels are monitored Patient is referred to a dialysis and transplantation center early in the course of progressive renal disease. Dialysis is initiated when patient cannot maintain a reasonable lifestyle with conservative treatment. VI. Nursing Diagnosis Excess fluid volume related to decreased urine output, dietary excess, and retention of sodium and water. Imbalanced nutrition: less than body requirements related to anorexia, nausea and vomiting, dietary restriction and altered oral mucous membranes Deficient knowledge regarding condition and treatment regimen VII. Nursing Management Provide conservative therapy, as indicated. Maintain strict fluid control; daily fluid intake should equal 500 ml (insensible loss) plus the amount of the previous 24 hours urine output; daily weight; and strict intake and output Encourage intake of high biologic value protein foods such as eggs, dairy products, and meats (causes positive nitrogen balance needed for growth and healing) Encourage high-calorie, low-protein, low-sodium, and low-potassium snacks between meals. Encourage alternating activity with rest. Encourage independence as much as possible. Assess the client and familys response to chronic illness. Encourage therapeutic conversations to help cope with chronic illness. Provide symptomatic treatment. Be prepared to identify and treat complications, which include hyperkalemia, pericarditis, pericardial effusion, pericardial tamponade, hypertension, anemia, and bone disease. Administer prescribed medication, which may include ion exchange resin, alkalizing agents, antibiotics, erythropoeitin, folic acid supplements, iron supplements, phosphate-binding agents, calcium supplements, histamine receptor antagonists, and proton-pump inhibitors. Prepare the client for peritoneal dialysis, if indicated. Assist with the procedure as instructed, maintaining septic technique and monitoring for signs and symptoms of peritonitis. (rigid, boardlike abdomen, fever, cloudy peritoneal fluid) Prepare the client for and assist with hemodialysis, if indicated. Provide proper shunt care, and assess for possible complications. (bleeding due to heparinization, hypovolemia, hypotension due to excessive water removal, dialysis disequilibrium syndrome (headache, confusion, and seizures) due to rapid removal of urea from plasma.) Prepare the client for kidney transplantation, if indicated. Provide postoperative care for any client who has undergone major surgery with special attention to catheter patency and adequacy, intake and output, fluid replacement, and protection from infection. Monitor for signs and symptoms of complications such as: 1)Graft rejection (fever, elevated white blood cell count, electrolyte abnormalities, abnormal renogram) 2)Infection stemming from immunosuppressive therapy (sepsis pneumonia, wound infection, and urinary tract infection)

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