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Nursing Care and Interventions in Managing Chronic Renal Failure
Keith Rischer RN, MA, CEN Top 3 causes of CRF DM 43% HTN 25% Glomerulonephritis 8% African americans 4x more likely to developESRD and 7x more likely to have HTN ESRD #CRF increasing….375,000 Americans receiving tx for ESRD w/275,000 req dialysis 100,000 new cases annually w/75,000 deaths annually Greatest incidence >65 years Since 1973, Medicare pays for dialysis Still have right to refuse dialysis
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Todays Objectives… Review the pathophysiology and causes of chronic renal failure (CRF). Contrast lab findings and physiologic changes associated with acute vs. chronic renal failure. Identify relevant nursing diagnosis statements and prioritize nursing care for clients with CRF including dietary modifications. Compare and contrast the following treatment modalities: peritoneal dialysis, hemodialysis, and continuous renal replacement therapies. Identify nursing care priorities with hemodialysis and peritoneal dialysis. Prioritize teaching needs of clients with CRF.
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Smaller than a fist but together filter 1700 liters blood daily and create 1.5l of urine
Filter physiologically essential electrolytes such as K & na and then selectively reabsorb
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Patho Nephron-each kidney has appx 1 million and consistes of
Glomerulus-basement membrane has pores like a filter and determine the size dependant permeability Size of the pores normally prevents RBC and plasma proteins from passing through into filtrate 125cc filtrate formed every minute this the GLOMERULAR FILTRATION RATE…REABSORPTION OF WATER, UREA, ALONG WITH LYTES, AND AMINO ACIDS ARE DONE PASSIVELY Tubular components of Nephron Proximal convoluted tubule right after glomerulus filtrate…65% of all reabsorption done here Loop of henle…important in controlling the concentration of urine…ADH exerts efect here Reabsorbs more na and cl than water while the proximal tubule reabsorbs na and water in equal amounts Distal convoluted tubule Only 10% of filtered nacl reabsorbed here Thiazide diuretics effect here Collecting tubule 2-5% of nacl reabsorption done here…K+ sparing diuretics such as Aldactone done here
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Patho:Chronic Renal Failure
Progressive, irreversible kidney injury Kidney function does not recover Azotemia Increase nitrogenous wastes such as BUN Creatinine Uremia azotemia with symptoms (chart 75-5 p.1739) Anorexia, N&V, fatigue, SOB Uremic syndrome (urine in the blood) Altered fluid, lyte and acid-base balance clinical and lab manifestations of renal failure More severe weakness, lethargy, confusion…coma..death CRF represents progressive and irreversible destruction of kidney structures Disease states of diabetes, HTN, glomerulonephritis Nephrons damaged and marked decrease in GFR CREATININE Byproduct of skeletal muscle metabolism freely filtered in the glomerulus and is NOT reabsorbed in the tubules Produced at constant rate and any creatinine that is filtered in the glomerulus is lost in the urine rather than being reabsorbed in the blood Serum creatinine can then be an indirect method for assessing the GFR and extent of renal damage
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Patho:Stages of Chronic Renal Failure
Diminished renal reserve GFR ½ normal Compensation w/healthy nephrons Renal insufficiency Nephrons destroyed…remaining adapt BUN, creatinine, uric acid elevate Priorities: fluid volume, diet, control of HTN, End-stage renal disease Severe fluid, acid-base imbalances Dialysis needed or will die End-stage renal disease GFR only 20-25%...kidneys can no longer regulate and then progresses to GFR of only 5% Reduction in renal capillaries and scarring of the glomeruli 6
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Patho:Physiologic Changes
Kidney Decreased GFR Poor H2O excretion Metabolic BUN and creatinine increased Electrolytes Sodium- later stages sodium retention Potassium increased EKG changes Kayexelate Acid-base balance: metabolic acidosis Calcium decreased and phosphorus increased Decreased GFR-in CRF can lose up to 80% nephrons before manifestations and changes present Metabolic BUN and creatinine increased Electrolytes Sodium- later stages sodium retention Reduced nephrons are present to reabsorb sodium…lost in the urine…polyuria Incr sodium as u/o decr Potassium increased Kidneys responsible for excretion…hyperkalemia VT-VF with severe hyperkalemia Acid-base balance: metabolic acidosis As more nephrons lost-acid excretion is reduces with resultant acidosis due to hydrogen ions retained Resp compensation in severe acidosis-kussmauls resp Calcium decreased and phosphorus increased Kidney produces hormone needed to activate vit D which enhances intestinal absorption of calcium In CRF this vitamin deficiency disrupts calcium and phosphate Phosphate increases and calcium decr Hypocalcemia causes more calcium to be demineralized from bones causing bone pain, fractures, osteoporosis
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Patho:Physiologic Changes
Cardiac Hypertension Hyperlipidemia Congestive heart failure Uremic pericarditis Hematologic anemia Gastrointestinal Halitosis Stomatitis PUD Cardiac Hypertension Most CRF have underlying HTN…incr BP causes ongoing damage to fragile glomerular capillaries Fluid overload Malfunction of renin-angiotensin mechanism and Aldosterone secretion-causing sodium retention Hyperlipidemia Changes fat metabolism causing incr triglycerides, total cholesterol and LDL….risk for CAD Congestive heart failure Left ventricular hypertrophy…leading cause of death w/ESRD Uremic pericarditis Pericardial inflammation…pericardial effusion caused by uremic inflammation Sx-SOB-decreasing BP-friction rub and diminished heart tones Hematologic anemia Decreased erythropoetin secretion from kidneys Gastrointestinal Halitosis Normal flora changes from uremia Stomatitis Increased ammonia causes this mouth inflammation
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Patho:Physiologic Changes
Neurologic lethargy Uremic encephalopathy Respiratory pulmonary effusion SOB Urinary proteinuria, oliguria, dilute Skin dry, pallor, pruritus, ecchymosis Neurologic due to uremia lethargy Uremic encephalopathy Respiratory pulmonary effusion SOB Urinary proteinuria, oliguria, dilute Skin …uremia causes more yellowing of pigment dry, pallor, pruritus, ecchymosis
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Drug Therapy chart 75-3 p.1737 Cardioglycides Digoxin/Lanoxin
Calcium channel blockers Diuretics Vitamins and minerals Folic Acid Ferrous Sulfate Biologic response modifiers Erthropoetin (Epogen) Phosphate binders Aluminum hydroxide Stool softeners and laxatives Stool softeners and laxatives…prone to constipation due to decreased fluid intake, iron supplements and phosphate binders 10
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Patho of One Dialysis/ESRD Client
DM II Retinopathy ESRD…hemodialysis 3x/week Anemia CAD PTCA 1994 w/redo 2005 AMI 2005-stent to LAD, Cx CHF 25% EF w/global hypokinesis and severe inferior hypokinesis AFib AAA Neuropathy Obesity Rt Femoral Bypass Rt BKA Medications ASA Phoslo Coumadin Digoxin Epoetin Lantus insulin Novolog per sliding scale Lipitor Neurontin NTG subl prn
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ED Renal Case Study 69yr female
HPI: Hemodialysis earlier in day. Found to have HR in the 40’s afterwards. Did not increase. Has no c/o lightheadedness. Has no other physical c/o VS: T-97.8 P-42 (AFib) R-20 BP-122/76 sats 96% 3l per n/c
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Labs
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Excess Fluid Volume Interventions: Monitor I&O Promote fluid balance
Daily weights 1 kg=1liter fluid Assess for manifestations of volume excess: Crackles in the bases of the lungs Edema Distended neck veins Diuretics Contraindicated w/ESRD
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Decreased Cardiac Output
Interventions: Control hypertension calcium channel blockers ACE inhibitors alpha- and beta-adrenergic blockers vasodilators. Education: monitor blood pressure client’s weight Diet Drug regimen ACE inhibitors-most effective to slow progression of renal failure Calcium channel blockers-improve GFR and renal blood flow
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Potential for Pulmonary Edema
Interventions: Assess for early signs of pulmonary edema Restlessness/anxiety Tachycardia Tachypnea oxygen saturation levels Crackles in bases Hypertension Pulmonary edema secondary to left sided heart failure or fluid overload
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Imbalanced Nutrition Interventions: Dietary evaluation for: Protein
Fluid Potassium Sodium Phosphorus Vitamin supplementation Iron Water soluable vitamins Calcium Vitamin D Less Than body Requirements Risk of malnourishment Hemodialysis increases catabolism Protein Restriction may preserve kidney function Accumulation of waste products/urea from protein intake Protein restriction - why is this changed from going to ESRD to hemodialysis to peritoneal dialysis? Eat protein of high biologic value - meat, eggs Fluid Brush teeth 6-8 times/day, rinse mouth chilled mouth wash or water mixed with lemon juice or vinegar, sour-ball candy, chew gum, before meals - drink water with lemon or eat sherbet or sorbet Fluid restriction - put all the water they can drink in pitcher in AM chew on ice chips Potassium Avoid salt substitutes…bananas What foods are highest in K+ - melons, potatoes (soak in water overnight), prune juice, dried fruit, raw carrots, bananas, avocados, apricots, oranges, swiss chard, spinach, tomatoes, winter squash, peanuts, dried beans, peas Sodium-limit Why??? Phosphorus High protein foods also high in phosphorus What foods are high in phosphorus - chocolate, milk, beef, nuts, legumes Vitamin supplementation Water soluable vitamins removed w/dialysis
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Risk for Infection Interventions: Meticulous skin care
Preventive skin care Inspection of vascular access site for dialysis Monitoring of vital signs for manifestations of infection
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Risk for Injury Interventions: Drug therapy Education prevent fall
pathologic fractures bleeding toxic effects of prescribed drugs Digoxin Narcotics Heparin or Coumadin toxic effects of prescribed drugs Digoxin dig toxicity…N&V, anorexia, confusion, brady or tachycardia Narcotics last longer than healthy kidneys Heparin or Coumadin Poor platelet function and capillary fragility 19
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Fatigue Interventions: Assess for vitamin deficiency anemia
Administer vitamin and mineral supplements anemia Give iron supplements as needed Erythropoietin therapy Buildup of urea S&P 20
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Anxiety Interventions: Health care team involvement
Client and family education Continuity of care Encouragement of client to ask questions and discuss fears about the diagnosis of renal failure S&P 21
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Indications for Dialysis
Uremia Persistent hyperkalemia Uncompensated metabolic acidosis Fluid volume excess unresponsive to diuretics Uremic pericarditis Uremic encephalopathy
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Hemodialysis Client selection Dialysis settings
Irreversible renal failure Expectation for rehab Acceptance of regimen Dialysis settings Acute-hospital Out patient centers 23
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Hemodialysis:Patho Diffusion Dialysate Dialyzer Anticoagulation
Lytes and H2O Dialyzer Anticoagulation Heparin to prevent blood clots in dialyzer or tubing Diffusion Movement of molecules from high to low concentration RBC’s and plasma proteins too large Dialysate Contains balanced mix of electrolytes and water that resemble human plasma During HD waste products move from the blood into dialysate due to differences in concentration (diffusion) K+ and sodium typically move out of plasma into dialysate Dialysate composition changed due to pts lytes and other variables Dialyzer Anticoagulation
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Complications of Hemodialysis
Dialysis disequilibrium syndrome Infectious diseases Hepatitis B and C infections HIV exposure—poses some risk for clients undergoing dialysis S&P 25
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Vascular Access Arteriovenous fistula, or arteriovenous graft for long-term permanent access Hemodialysis catheter, dual or triple lumen, or arteriovenous shunt for temporary access Precautions Bruit & thrill BP restrictions Complications Thrombosis CMS
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Hemodialysis: Nursing Interventions
Predialysis care: Medications to hold…why? Postdialysis care: Monitor for complications such as hypotension, headache, nausea, malaise, vomiting, dizziness, muscle cramps. Monitor vital signs and weight. sepsis Avoid invasive procedures 4 to 6 hours after dialysis. Continually monitor for hemorrhage. Assess for thrill No BP or blood draws on arm
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Peritoneal Dialysis Only for the highly motivated client!!!
Procedure involves siliconized rubber catheter placed into the abdominal cavity for infusion of dialysate. Not as common as PD…have more flexibility Occurs through diffusion and osmosis across the semipermeable membrane of the peritoneum and capillaries Allows solutes and water to move from area of higher concentration in the blood to lower concentration in the dialyzing fluid—diffusion Water removal depends on concentration of dialysate…more glucose becomes more hypertonic and draws more fluid out Continuous cycle PD-exchanges occur at noc while pt sleeps-done q noc
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Peritoneal Dialysis Phases Contraindications history of abd surgeries
Inflow Dwell Drain Contraindications history of abd surgeries recurrent hernias excessive obesity preexisting vertebral disease severe obstructive pulmonary disease
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Complications of Peritoneal Dialysis
Peritonitis (cloudy outflow) Pain Exit site and tunnel infections Poor dialysate flow Dialysate leakage Monitor color of outflow cloudy (peritonitis) brown (bowel) bloody (first week OK) urine (bladder) Peritonitis (cloudy outflow) Major complication due to connection site contamination—meticulous sterile technique when caring for PD catheter and hooking or clamping dialysate bag Pain OK if new to PD should subside in 1-2 weeks Dialysate warm to body temp Exit site and tunnel infections Poor dialysate flow Constipation main cause Dialysate leakage Most common with obese and DM Monitor color of outflow cloudy (peritonitis) brown (bowel) bloody (first week OK) urine (bladder)
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Nursing Care During Peritoneal Dialysis
Pre PD: Vital signs pre and q 15-30” during Weight laboratory tests Continually monitor the client for: respiratory distress pain discomfort Monitor prescribed dwell time and initiate outflow Observe outflow amount & pattern of fluid
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Education Priorities Pathophysiology and manifestations Complications
When to call the doctor Keep record of all labs Take medications and follow plan of care set out by case manager Monitor weight, fatigue levels closely
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