Acute Kidney Injury Flashcards
Acute Kidney Injury
Rapid loss of kidney function Elevates serum creatinine Decreases urine output/oliguria Potentially reversible Severity levels: -Mild -Azotemia
Azotemia
An accumulation of nitrogenous waste products like urea nitrogen, creatinine in the blood
AKI can develop…
over hours or days with progressive elevations of BUN, creatinine, and potassium with or without a reduction in urine output
Prerenal
Causes are factors external to the kidneys that reduce renal blood flow
-severe dehydration
-heart failure
-decreased CO
Decreases glomerular filtration rate
Causes oliguria
Autoregulatory mechanisms attempt to preserve blood flow
Intrarenal
Causes include conditions that cause direct damage to kidney tissue
Potentially reversible as long as basement membrane is not destroyed
Intrarenal results from:
Prolonged ischemia
Nephrotoxins
Hemoglobin released from hemolyzed RBCs
Myoglobin released from necrotic muscle cells
Acute tubular necrosis (ATN)
Intrarenal
Results from ischemia, nephrotoxins, or sepsis
Severe ischemia causes disruption in basement membrane
Nephrotoxic agents cause necrosis of tubular epithelial cells
Potentially reversible
Postrenal causes
Benign prostatic hyperplasia Prostate cancer Calculi Trauma Extrarenal tumors
Postrenal causes include
mechanical obstruction in the outflow of urine
What is hydronephrosis?
Kidney dilation as a result from bilateral ureteral obstruction
Increases hydrostatic pressure
Tubular blockage results in progressive decline in kidney function
RIFLE Classification
Used to describe the stages of AKI Standardizes the diagnosis of AKI Risk Injury Failure Loss End-stage kidney disease
R
Risk
First stage of AKI where GFR is decreased by 25%
I
Injury
Second stage where GFR is decreased by 50% and then increases in severity to the final or third stage
F
Failure
GFR is decreased by 75%
Two outcome variables are L and E
L
Loss
Outcome from failure and decreased GFR
Complete failure of kidneys
E
End stage kidney disease
Outcome from failure and decreased GFR
Complete failure of kidneys
Oliguric Phase
Urinary changes -Output less than 400mL/day -Occurs within 1-7 days after injury -Lasts 10-14 days -Urinalysis may show casts, RBCs, WBCs Fixed urine specific gravity and osmolality -Fixed plasma osmolality -Proteinuria if glomerular dysfunction
Oliguric phase: Fluid Volume
Hypovolemia may exacerbate AKI
W/ decreased urine output, fluid retention occurs
-neck veins distended
-bounding pulse
-edema
-hypertension
Fluid overload can lead to HF, pulmonary edema, and pericardial/pleural effusions
Oliguric phase clinical manifestations
Fluid volume Metabolic acidosis Sodium balance Potassium excess Hematologic disorders Waste product accumulation Neurologic disorders
Oliguric phase: Metabolic Acidosis
Serum bicarbonate level decreases
Severe acidosis develops
-Kussmaul respirations
Bicarbonate is used to buffer hydrogen ions because kidneys cannot synthesize ammonia which is needed for hydrogen ion excretion
Oliguric phase: Sodium Balance
Increased excretion of sodium
Hyponatremia can lead to cerebral edema
Damaged tubules cannot conserve sodium. Uncontrolled hyponatremia or water excess can lead to cerebral edema
Oliguric phase: Potassium Excess
ECG changes
Levels may increase because kidney’s normal ability to excrete potassium is impaired. Massive tissue trama and damaged cells release additional K and ECF.
How does hyperkalemia cause changes in the ECG?
Peaked T waves
Widening of the QRS complex
ST segment depression
Oliguric phase: Hematologic Disorders
Leukocytosis
Oliguric phase: Waste product accumulation
Elevated BUN and serum creatinine levels
Urea
end product of protein metabolism
Creatinine
end product of endogenous muscle metabolism
Diuretic phase clinical manifestations
Daily urine output is 1-3 L
May reach 5 L or more
Monitor for hyponatremia, hypokalemia, and dehydration
Recovery phase clinical manifestations
May take up to 12 months for kidney function to stabilize
Begins when GFR increases, allowing BUN and creatinine to plateau then decrease
Improvements occur in first 1-2 weeks
Diagnostic studies
Thorough history Serum creatinine Urinalysis Kidney ultrasonography Renal scan CT scan Renal biopsy
Collaborative care
Ensure adequate intravascular volume and cardiac output -IV/oral fluids based on urine output -Loop diuretics -Osmotic diuretics Therapies for hyperkalemia
Nutritional therapy
Maintain adequate caloric intake
Restrict sodium K
Increase dietary fat
Enteral nutrition
Health promotion
Identify and monitor populations at high risk
Control exposure to nephrotoxic drugs and industrial chemicals
Prevent prolonged episodes of hypotension and hypovolemia
Gerontologic considerations for being more susceptible to AKI
Polypharmacy (5+ prescribed drugs a day) Hypotension Diuretic therapy Aminoglycoside therapy Obstructive disorders Surgery Infection
