Ch 27: Acute Kidney Injury Flashcards by Tyece Henry

acute kidney injury is rapid loss of kidney function with:

Rise in serum creatinine and/or reduction in urine output
Elevated BUN and K+
Azotemia—accumulation of nitrogenous waste products (BUN, creatinine)

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prerenal causes

factors that reduce systemic circulation causing reduction in renal blood flow which leads to oliguria

Severe dehydration,
heart failure,
decreased CO,
vasodilated states (sepsis, anaphylaxis)

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what is prerenal axotemia

decreased Na+ excretion, increased Na+ and H2O retention and  urine output

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intrarenal failure causes

problems that cause direct damage to kidney tissue

Prolonged ischemia
Nephrotoxins
Hemoglobin released from hemolyzed RBCs
Myoglobin released from necrotic muscle cells
Kidney diseases—acute glomerulonephritis and SLE
CT contrast dye

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the most common cause of intrarenal AKI

acute tubular necrosis (ATN)

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acute tubular necrosis (ATN)

Results from ischemia, nephrotoxins, or sepsis
Severe ischemia causes disruption in basement membrane and patchy destruction of tubular epithelium
Nephrotoxic agents cause necrosis of tubular epithelial cells—clog tubules
Potentially reversible

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causes of postrenal failure

mechanical obstruction of outflow which results reflux into renal pelvis, impairing kidney function

Benign prostatic hyperplasia,
prostate cancer,
calculi,
trauma,
extrarenal tumors
bilateral ureteral obstruction

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what is bilateral ureteral obstruction

hydronephrosis; relieve obstruction in 48 hours increased chance of recovery

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phases of clinical manifestations of AKI

oliguric
diuretic
recovery

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RIFLE classification of AKI

Risk
Injury
Failure
Loss
ESRD

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clinical manifestations - oliguric phase - urinary changes**

Urinary output less than 400 mL/day
Occurs within 1 to 7 days after injury
Lasts 10 to 14 days (longer  poor prognosis)
Urinalysis—casts, RBCs, WBCs, protein
Specific gravity 1.010
Osmolality 300 mOsm/kg

50% patients nonoliguric; greater than 400 mL urine/day

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clinical manifestations - oliguric phase - fluid volume

Hypovolemia may exacerbate AKI
Decreased urine output leads to fluid retention
- Neck veins distended
- Bounding pulse
- Edema
- Hypertension
Fluid overload can lead to heart failure, pulmonary edema, and pericardial and pleural effusions

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clinical manifestations - oliguric phase - metabolic acidosis

Impaired kidney cannot excrete hydrogen ions or acid products of metabolism
Serum bicarbonate (HCO3−) production is decreased
- Reabsorption and regeneration defective
Severe acidosis develops
- Kussmaul respirations—increasing exhaled CO2

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clinical manifestations - oliguric phase - sodium balance

Increased excretion of sodium—damaged tubules
Hyponatremia can lead to cerebral edema

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clinical manifestations - oliguric phase - potassium excess

Impaired ability of kidneys to excrete K+
Increased risk with massive tissue trauma
Usually asymptomatic
ECG changes—peaked T waves, widened QRS, ST depression

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clinical manifestations - oliguric phase - hematologic disorders

Leukocytosis—infection may be fatal
- Urinary and respiratory infections

clinical manifestations - oliguric phase - hematologic disorders

Increased BUN and *serum creatinine levels

clinical manifestations - oliguric phase - neurologic disorders

Fatigue and difficulty concentrating
Seizures, stupor, coma

clinical manifestations and time frame of diuretic phase

(2 to 6 weeks)
Daily urine output is 1 to 3 L; up to 5 L
Osmotic diuresis from high urea and inability of tubules to concentrate urine
Monitor for hypovolemia, hypotension, hyponatremia, hypokalemia, and dehydration

clinical manifestations and time frame of recover phase

(up to 12 months)
Increased GFR, decreased BUN and creatinine
Influenced by severity of injury and complications

diagnostic studies for AKI

Thorough history
Serum creatinine, BUN, electrolytes
Urinalysis
Renal ultrasound
Renal scan
CT scan
Renal biopsy

Contraindications for contrast medium

MRI or MRA with gadolinium contrast medium—may be fatal
Contrast-induced nephropathy (CIN)
Diabetics taking metformin: hold 48 hours before and after use of contrast medium; risk of lactic acidosis
If contrast is needed for high-risk patients—use low-dose and optimal hydration

Interprofessional care goals of AKI

Eliminate cause
Manage signs and symptoms
Prevent complications

Interprofessional Care of AKI

Ensure adequate intravascular volume and cardiac output
- Loop diuretics (e.g., furosemide [Lasix])
- Osmotic diuretics (e.g., mannitol)
Closely monitor fluid intake during oliguric phase
- Fluid restriction calculation: All fluid losses for previous 24 hours + 600 mL (insensible loses)

Hyperkalemia therapies

Temporary—move K+ into cells - Insulin (given with glucose to prevent hypoglycemia) and sodium bicarbonate Decrease dysrhythmias—stabilizes myocardium - Calcium gluconate Remove K+ from body - Sodium polystyrene sulfonate (Kayexalate) or Patiromer (Veltassa) - Dialysis Dietary restriction

Indications for renal replacement therapy (RRT)

Volume overload Elevated serum potassium level Metabolic acidosis BUN level > 120 mg/dL (43 mmol/L) Significant change in mental status Pericarditis, pericardial effusion, or cardiac tamponade Clinical status of patient

types of renal replacement therapy (RRT)

Peritoneal dialysis (PD) - Not frequently used Intermittent hemodialysis (HD) - Emergent therapy Continuous renal replacement therapy (CRRT) - Cannulation of artery and vein - Continuously 24 hours

nutrition therapy for AKI

Maintain adequate caloric intake - Primarily carbohydrates and  fat - Adequate protein to prevent breakdown (30 to 35 kcal/kg and 0.8 to 1.0 g of protein/kg of desired body weight) Restrict sodium, K+, phosphate Calcium supplements or phosphate-binding agents Enteral/parenteral nutrition

nursing assessment of AKI

Measure vital signs Daily weights Strict intake and output Examine urine Assess general appearance Observe dialysis access site Mental status/level of consciousness Oral mucosa Lung sounds Heart rhythm Laboratory values Diagnostic test results

health promotion of AKI

Prevention and early recognition Identify and monitor high-risk populations Control exposure to nephrotoxic drugs and industrial chemicals Prevent prolonged episodes of hypotension and hypovolemia Monitor daily weight, intake and output, and fluid and electrolyte balance Replace significant fluid losses Provide aggressive diuretic therapy for fluid overload Use nephrotoxic drugs sparingly; monitor renal function

acute care of AKI

Accurate intake and output Daily weights Assess for hypervolemia or hypovolemia Assess for potassium and sodium disturbances Meticulous aseptic technique Careful use of nephrotoxic drugs Skin care measures/mouth care

ambulatory care of AKI

Monitor kidney function Regulate protein and potassium intake Follow-up care Teaching Appropriate referrals

Gerontologic Considerations for AKI

Decreased GFR with aging More susceptible to AKI - Dehydration ---Polypharmacy- diuretics, laxatives ---Illness and immobility - Hypotension, diuretic therapy, aminoglycoside therapy, obstructive disorders, surgery, infection, and contrast medium - decrease reduced ability to recover - RRT still an option

calcium gluconate treatment

used with hyperkalemia to protect heart from damage of hyperkalemia