Ch 27: Acute Kidney Injury

Question 1

acute kidney injury is rapid loss of kidney function with:

Answer 1

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

Question 2

prerenal causes

Answer 2

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)

Question 3

what is prerenal axotemia

Answer 3

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

Question 4

intrarenal failure causes

Answer 4

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

Question 5

the most common cause of intrarenal AKI

Answer 5

acute tubular necrosis (ATN)

Question 6

acute tubular necrosis (ATN)

Answer 6

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

Question 7

causes of postrenal failure

Answer 7

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

Question 8

what is bilateral ureteral obstruction

Answer 8

hydronephrosis; relieve obstruction in 48 hours increased chance of recovery

Question 9

phases of clinical manifestations of AKI

Answer 9

oliguric
diuretic
recovery

Question 10

RIFLE classification of AKI

Answer 10

Risk
Injury
Failure
Loss
ESRD

Question 11

clinical manifestations - oliguric phase - urinary changes**

Answer 11

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

Question 12

clinical manifestations - oliguric phase - fluid volume

Answer 12

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

Question 13

clinical manifestations - oliguric phase - metabolic acidosis

Answer 13

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

Question 14

clinical manifestations - oliguric phase - sodium balance

Answer 14

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

Question 15

clinical manifestations - oliguric phase - potassium excess

Answer 15

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

Question 16

clinical manifestations - oliguric phase - hematologic disorders

Answer 16

Leukocytosis—infection may be fatal
- Urinary and respiratory infections

Question 17

clinical manifestations - oliguric phase - hematologic disorders

Answer 17

Increased BUN and *serum creatinine levels

Question 18

clinical manifestations - oliguric phase - neurologic disorders

Answer 18

Fatigue and difficulty concentrating
Seizures, stupor, coma

Question 19

clinical manifestations and time frame of diuretic phase

Answer 19

(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

Question 20

clinical manifestations and time frame of recover phase

Answer 20

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

Question 21

diagnostic studies for AKI

Answer 21

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

Question 22

Contraindications for contrast medium

Answer 22

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

Question 23

Interprofessional care goals of AKI

Answer 23

Eliminate cause
Manage signs and symptoms
Prevent complications

Question 24

Interprofessional Care of AKI

Answer 24

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)

Question 25

Hyperkalemia therapies

Answer 25

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

Question 26

Indications for renal replacement therapy (RRT)

Answer 26

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

Question 27

types of renal replacement therapy (RRT)

Answer 27

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

Question 28

nutrition therapy for AKI

Answer 28

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

Question 29

nursing assessment of AKI

Answer 29

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

Question 30

health promotion of AKI

Answer 30

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

Question 31

acute care of AKI

Answer 31

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

Question 32

ambulatory care of AKI

Answer 32

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

Question 33

Gerontologic Considerations for AKI

Answer 33

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

Question 34

calcium gluconate treatment

Answer 34

used with hyperkalemia to protect heart from damage of hyperkalemia