Nursing 4 Lecture 5 Chronic Kidney Disease

  1. Chronic Kidney Disease:
    • -Progressive, irreversible kidney injury
    • -Kidney function does not recover
    • -Can develop over years (insidious), or result from ARF from which the client has not recover

    • End Stage Renal Disease:
    • -When kidney disease becomes too poor to sustain life CKD becomes ESRD

    Azotemia: build up of nitrogenous waste in the blood

    • Uremia: Azotemia which includes
    • -Metallic taste in the mouth
    • -Anorexia
    • -N/V
    • -Muscle cramps
    • -Itching
    • -Fatigue
    • -Lethargy
    • -Hiccups
    • -Edema
    • -Dyspnea
    • -Parasthesia(numbness, tingling, pricking, burning, or creeping on the skin)
  2. Stages of CKD:
    • Normal GFR: 125 mL/min
    • -Controlled by BP and blood flow

      At risk; normal kidney function:
    • ->90 mL/min

    • Mild CKD:
    • -60 to 90 mL/min

    • Moderate CKD:
    • -30 to 59 mL/min

    • Severe CKD:
    • -15 to 29 mL/min

    • ESKD:
    • -<15 mL/min
  3. Kidney Changes:
    -Abnormal urine production, poor water excretion, electrolyte imbalances, and metabolic abnormalities

    • -Healthy nephrons become larger and work harder, so the kidneys can maintain and effective GFR until about 3/4 of kidney function is lost
    • -Homeostasis is maintained until later in the course of kidney failure
    • -As kidney function continues to decline, the BUN increases and urine output decreases
    • -When kidney function decreases to this level, the patient is at risk for fluid overload
  4. Metabolic Changes:
    • -Urea and creatinine excretion are disrupted by kidney failure
    • -Creatinine is derived from proteins present in skeletal muscle
    • -Normal rate of creatinine excretion depends on muscle mass, physical activity, and diet
    • -Without major changes in diet or physical activity the creatinine level remains constant
    • -Creatinine is partially excreted by the tubules and a decrease in kidney function leads to a build up of creatinine

    • -Urea is a produce of protein metabolism and is excreted by the kidneys
    • -The BUN level normally varies directly with protein intake
  5. Electrolyte Changes: Sodium
    • -Early CKD, at risk for hyponatremia
    • -Later stages kidney excretion of sodium is reduced as urine production decreases, sodium retention causes HTN and edema
    • -Even with sodium retention, the serum sodium level may appear normal due to plasma water retention
  6. Electrolyte Changes: Potassium
    • -Potassium excretion is mainly through the kidneys
    • -Normal potassium levels are maintained until the 24 hour urine ouput falls below 500 mL
    • -High potassium levels then develp quickly reaching 7 to 8 mEq/L
    • -Severe EKG changes result from this elevation and fatal dysrhythmias can occur

    • Other Contributings Factors:
    • -Ingestion of potassium in drugs
    • -Failure to restrict potassium in the diet
    • -Tissue breakdown
    • -Blood transfusions
    • -Bleeding or hemorrhage
  7. Acid Base:
    • -Kidneys are unable to excrete excessive hydrogen ions (acids)
    • -Normally, tubular cells move hydrogen ions into the urine for excretion, but ammonium and bicarbonate are needed for this movement to occur
    • -This process leads to a buildup of hydrogen ions and reduced levels of bicarbonate (base deficit)
    • -High potassium levels further reduce renal ammonium production and excretion
  8. Calcium and Phosphate Balance:
    A complex balanced normal relationship exists between phosphate and calcium and is influenced by Vitamin D. The kidney produces a hormone needed to activate vitamin D, which then enhandes intestinal absorption of calcium.

    • -Phosphate retention and a deficiency of active Vitamin D disrupt the calcium phosphate balance
    • -Normally excessive dietary phosphate is excreted by the kidneys in the urine
    • -Parathyroid Hormone controls the amount of phosphate in the blood by causing tubular excretion of phosphate when there is excess
    • -CKD leads to reduced phosphate excretion, which leads to hyperphosphatemia, calcium levels decrease (hypocalcemia), chronic low calcium levels stimulate the realease of PTH, under the influence of additional PTH calcium is released from storage areas in the bones which results in bone densit loss

    -Bone mineral loss, osteomalacia and tooth calcium loss
  9. Cardiac Changes:
    • Hypertension:
    • -Can be the cause or result of CKD
    • -Retention of sodium and water causes circulatory overload which elevates BP

    • Hyperlipidemia:
    • -Occurs from changes in fat metabolism that increase triglyceride, total cholesterol, and LDL levels

    • Heart Failure:
    • -May occur in CKD because it increases the workload on the heart as a result of anemia, hypertension, and fluid overload

    • Pericarditis:
    • -The pericardial sac becomes inflamed by uremic toxins or infection
    • -If not treated this inflammation can lead to pericardial effusion, cardiac tamponade, and death
  10. Hematologic Changes:
    • -Causes of anemia include a decreased erythropoietin level that decreases RBC production
    • -Decreased RBC survival time resulting from uremia, iron and folic acid deficiencies, and increased bleeding as a result of impaired platelet function
  11. Gastrointestinal Changes:
    • -Uremia effects the entire GI system
    • -Normal flora of the mouth changes with uremia
    • -The mouth contains enzyme urease, which breaks down urea into ammonia
    • -Ammonia generated from this reaction causes halitosis (bad breath) and may also cause stomatitis (mouth inflammation)
    • -Anorexia, nausea, vomiting, and hiccups are common in patients with uremia
    • -The specific cause of these problems is unknown but may be related to high BUN and creatinine levels, as well as acidosis
  12. Clinical Manifestations: Neurologic
    • -Lethargy and daytime drowsiness
    • -Inability to concentrate or decreased attention span
    • -Seizures
    • -Coma
    • -Slurred speech
    • -Asterixis
    • -Tremors, twitching, or jerky movements
    • -Myoclonus
    • -Ataxia (alteration in gait)
    • -Paresthesias
  13. Clinical Manifestations: Cardiovascular
    • -Cardiomyopathy
    • -Hypertension
    • -Peripheral edema
    • -Heart failure
    • -Uremic pericarditis
    • -Pericardial effusion
    • -Pericardial friction rub
    • -Cardiac tamponade
  14. Clinical Manifestations: Respiratory
    • -Uremic halitosis
    • -Tachypnea
    • -Deep sighing, yawning
    • -Kussmaul respirations
    • -Uremic pneumonitis
    • -Shortness of breath
    • -Pulmonary edema
    • -Pleural effusion
    • -Depressed cough reflex
    • -Crackles
  15. Clinical Manifestations: Hematologic
    • -Anemia
    • -Abnormal bleeding and bruising
  16. Clinical Manifestations: Gastrointestinal
    • -Anorexia
    • -Nausea
    • -Vomiting
    • -Metallic taste in mouth
    • -Changes in taste acuity and sensation
    • -Uremic colitis (diarrhea)
    • -Constipation
    • -Uremic gastritis (possible GI bleeding)
    • -Uremic fetor (bad breath)
    • -Stomatitis
    • -Diarrhea
  17. Clinical Manifestations: Urinary
    • -Polyuria, nocturia (early)
    • -Oliguria, anuria (later)
    • -Proteinuria
    • -Hematuria
    • -Diluted, strawlike appearance
  18. Clinical Manifestations: Integumentary
    • -Decreased skin turgor
    • -Yellow gray pallor
    • -Dry skin
    • -Pruritis
    • -Ecchymosis
    • -Purpura
    • -Soft tissue calcification
    • -Uremic frost (late, premorbid)
  19. Clinical Manifestations: Musculoskeletal
    • -Muscle weakness and cramping
    • -Bone pain
    • -Pathologic fractures
    • -Renal osteodystrophy
  20. Clinical Manifestations: Reproductive
    • -Decreased fertility
    • -Infrequent or absent menses
    • -Decrased libido
    • -Impotence
  21. Uremic Frost:
    -Uncommon dermatologic manifestation of profound azotemia and occurs when urea and other nitrogenous waste products accumulate in sweat and crystalize after evaporation
  22. Assessment: History
    • -Family history
    • -Diet
    • -Past conditions
    • -Energy levels
    • -Urinary patterns
    • -Normal weight
    • -Medications
  23. Assessment: Psychosocial

    • -Assess for anxiety
    • -Family relations
    • -Social activity
    • -Work patterns
    • -Body image
    • -Sexual activty
  24. Assessment: Laboratory
    • -Creatinine and BUN levels = CHRONICALL HIGH
    • -Creatinine clearance= very low
    • -Electrolyte measurements= high potassium, low sodium
  25. Assessment: Imaging
    Few x-ray findings are abnormal with CKD. Bone x-rays of the hand can show renal osteodystrophy.

    With long term ESKD the kidneys have shrunk and may be 8 to 9 cm or smaller. This small size results from atrophy and fibrosis. If CKD progresses suddenly a kidney ultrasound or CT scan without contrast medium may be used to rule out and obstruction.
  26. Imbalanced Nutrition: Less than body requirements
    • Common changes include:
    • -Control of protein intake
    • -Fluid intake limitation
    • -Restriction of potassium, sodium, and phosphorus intake
    • -Taking vitamin and minerals

    • Protein Restriction:
    • -Early in the course of the disease prevents some of the symptoms of CKD and may preserve kidney function
    • -Protein is restricted on the basis of the degree of kidney impairment (reduced GFR) and the severity of the symptoms
    • -Build up of waste products from protein breakdown is the main cause of uremia
    • -Patients receiving dialysis needs more protein because some protein is lost through dialysis
    • -BUN and albumin levels are used to monitor adequacy of protein intake
    • -Decreased levels indicate poor protein intake
    • -Excessive levels indicate too much protein intake

    • Fluid Management:
    • -Promotion of fluid balance and prevention of complications resulting from abnormal or undesired fluid levels
    • -Maintain accurate intake and output record
    • -Monitor hydration status (moist mucous membranes, adequacy of pulses, and orthostatic blood pressure) as appropriate
    • -Monitor for indications of fluid overload/retention (crackles, elevated CVP or pulmonary capillary wedge pressure, edema, neck vein distension, and ascites) as appropriate
    • -Weigh daily and monitor trends
    • -Monitor laboratory results relevant to fluid retention (increased specific gravity, increased BUN, decreased hematocrit, and increased urine osmolarity levels)
    • -Monitor weight change before and after dialysis
    • -Assess location and extent of edema
    • -Administer prescribed diuretics
    • -Distribute the fluid intake over 24 hours if appropriate
    • -Consuly physician if s/s of fluid volume excess persis or worsen

    • Sodium Restriction:
    • -Needed in patients with little or no urine output
    • -Fluid and sodium restriction cause edema, hypertension, and heart failure
    • -Most pats retain sodium, a few cannot conserve sodium

    • Potassium Restriction:
    • -May be needed when high blood potassium levels can cause dangerous cardiac dysrhythmias
    • -Monitor for EKG for tall, peaked T waves

    • Phosphorus Restriction:
    • -Control of phosphate levels is started early in CKD to avoid osteodystrophy
    • -Monitor serup phosphate levels
    • -Dietary phosphorus restrictions and drugs to assist with phosphate control may be prescribed
    • -Phosphate binders must be taken at meal time
    • -Most patients already restrict there protein intake, and because high protein foods are high in phosphorus, this reduces phosphorus intake

    • Vitamin Supplementation:
    • -Needed daily for most patients with CKD
    • -Low protein diets are also low in vitamins, and water soluble vitamins are removed from the blood during dialysis
    • -Anemia is a problembecause of the limited iron content of low protein diets and decreased kidney production of erythropoietin
    • -Thus supplemental iron is needed
    • -Calcium and Vit D supplements may be needed, depending on the patients serum calcium levels and bone status
  27. Excess Fluid Volume:
    • -Monitor intake and output
    • -Promote fluid balance
    • -Drug therapy includes diuretics

    • Assess for manifestations of volume excess:
    • -Crackles in the bases of the lungs
    • -Edema
    • -Distended neck veins
  28. Decreased Cardiac Output:
    • -Control hypertension with calcium channel blockers, ACE inhibitors, alpha- and beta- adrenergic blockers, and vasodilators
    • -Instruct patient and family to monitor blood pressure, patients weight, diet, and drug therapy
  29. Risk for Infection:
    • -Meticulous skin care
    • -Preventive skin care
    • -Inspectioin of vascular access site for dialysis
    • -Monitoring of vital signs for manifestations of infection

    Risk for infection due to inadequate primary defenses (broken skin), chronic disease or malnutrition
  30. Risk for Injury:
    • -Drug therapy: monitor closely for drug toxicity
    • -Education to prevent fall or injury, pathologic fractures, bleeding, and toxic effects of prescribed drugs

    Risk for injury because of increased susceptibility of bleeding falls and fractures
  31. Fatigue:
    • -Assess for vitamin deficiency, anemia, and buildup of urea
    • -Administer vitamin and mineral supplements
    • -Adminster erythropoietin therapy for bone marrow production
    • -Give iron supplements as needed
  32. Anxitey:
    • -Health care team involvement
    • -Patient and family education
    • -Continuity of care
    • -Encouragement of patient to ask questions and discuss fears about the diagnosis of renal failure
  33. Potential for Pulmonary Edema:
    • -Assess the patient for early signs of pulmonary edema
    • -Monitor serum electrolyte levels, vital signs, oxygen saturation levels, hypertension
  34. 4 Goals or Renal Replacement Therapy:
    • -Remove end products of protein metabolism, such as urea and creatinine from the blood
    • -Maintain safe concentration of serum electrolytes
    • -Correct acidosis and replenish bicarbonate levels of the blood
    • -Remove excess flued from the blood
  35. Diasylate:
    Specially prepared electrolyte solution
Card Set
Nursing 4 Lecture 5 Chronic Kidney Disease
Nursing 4 Lecture 5 Chronic Kidney Disease