AKI Flashcards
Prerenal AKI:
- Renal hypoperfusion occurs; ↓ blood flow to kidney
- Related to low cardiac output, hypotension, bleeding, vasodilation, thrombosis
- Oliguraia is a classic finding- less than 400 ml
- Could be bc of contrast media or hypovolemia – prerenal causes
- (prolonged hypotension (sepsis, vasodilation)
- prolonged low cardiac output (HF, cardiogenic shock)
- prolonged volume depletion (hydration, hemorrhage)
- renovascular thrombosis (thromboemboli))
Intrarenal AKI
- Ischemic or toxic insult directed at the nephron
- Ischemia is related to substances that damage the renal tubular endothelium (antimicrobials, contrast dye)
- When internal filtering structures are affected, this is known as acute tubular necrosis (ATN)
- Nephrotic syndrome
- (kidney ischemia (advanced stage of prerenal acute kidney injury)
- endogenous toxins (rhadbdomylsis. Tumor lysis syndrome)
- exogenous toxins (radiocontrast dye, nephrotoxic drugs)
- infection (acute glomerulophritis, intersitial nephritis))
Postrenal AKI
- Caused by any obstruction that hinders flow of urine from beyond the kidney
- Not common
- Sudden development of anuria should prompt nurse to check patency of Foley catheter
- Stones
- (obstruction (urethra, prostate, or bladder)
- rare as a cause in critical care)
ARF blood gas interoperation
Metabolic acidosis occurs as a result of the accumulation of unexcreted waste products.
BUN ARF values
BUN will be elevated and the value is changed by protein intake, blood in the GI tract, cell catabolism, and is diluted by fluid administration.
Creatinine ARF values
Creatinine is completely excreted with normal kidney function, therefore creatinine is elevated when the kidneys are not working
Creatinine Clearance ARF values
Creatinine clearance is decreased with kidney failure. Even small changes will represent a significant decrease in GFR.
Potassium and Magnesium values with ARF
Potassium values will rise.
Magnesium values will rise.
Fractional excretion of sodium value with ARF
Fractional excretion of sodium value below 1% suggests a prerenal compromise. This is because resorption of almost all the filtered sodium is a response to decreased perfusion to the kidneys. If the value is above 2% then the damage is intrarenal and the kidney cannot concentrate the sodium.
treatment of hyperkalemia
• Hyperkalemia may lead to lethal cardiac dysrhythmias
• Treatment may include
o Diuretics (if producing urine)
o Intravenous insulin and glucose – quickest! As insulin carries glucose into cells, also carries potassium
o Kayexalate
Onset phase
occurs from initial insult until cell injury develops
• GFR decreases
• If treatment initiated, damage is reversible
Oliguric/anuric phase
lasts 5-16 days depending on degree of oliguria
• The more oliguric, the more severe the injury
• See further decrease in GFR, greater increase in BUN and Creatinine, worsening electrolyte/acid-base imbalances (metabolic acidosis)
• Pt will not make urine for 2-3 wks
• Worried about hyperkalemia, hypermagnesim, and can see high phosophorus
• Oliguria period is when there is an increase in the serum concentration of substances usually excreted by the kidneys (urea, creatinine, uric acid, organic acids, potassium, and magnesium). In this phase uremic symptoms first develop and life threatening conditions such as hyperkalemia develops
Diuretic phase:
last 7-14 days
• GFR improves
• Polyuria with u/o of 2-4 L/day-tubles are recovering, no longer obstructed but edema and scarring remain
• Kidneys can clear volume but not solutes
• Watch for HYPOVOLEMIAA in this phase
• Worried about hypokalemia, hypomagnesium
• The diuresis period is when there is a gradual increase in the urine output. This signals that glomerular filtration has started to recover. Lab values will stabilize then decrease. Renal function may still be abnormal even though there might be a normal volume of urinary output. Dehydration may occur which would cause the uremic symptoms to increase.
Recovery phase:
last weeks-years
• Kidney function slowly returns to normal or near normal
• Approx. 62% eventually recover normal function 33% have residual damage and 5% require long term dialysis
• The recovery period is when renal function is improving and may take 3-12 months. Lab values return to normal. There may be a 1-3% reduction in GFR but is not significant.
acute tubular necrosis
• When internal filtering structures are affected, this is known as acute tubular necrosis (ATN)
Description
• Nephrotoxic or ischemic injury
• Damages kidney tubular epithelium
• In severe cases extends to basement membrane
Epidemiology and etiology
• Damage prevents normal concentration of urine, filtration of wastes, and regulation of acid-base, electrolyte and water balance
• Accounts for 76% of AKI in critically ill patients
Pathophysiology
• Tubular obstruction
• Tubular edema
• Tubular cell injury
When the internal filtering structures of the kidney are pathologically affected it was known as acute tubular necrosis. Now the term AKI is used more often
At-risk Disease States and Acute Kidney Injury
At-risk Disease States and Acute Kidney Injury • Underlying chronic kidney disease • Risk of AKI • Older age and AKI • Heart failure and AKI • Respiratory failure and AKI • Sepsis and AKI • Trauma and AKI • Contrast-induced nephrotoxic injury and AKI
Who is at risk?
• “Typically, a patient is not admitted to the ICU with acute kidney injury alone; there is always coexisting hemodynamic cardiac, pulmonary, or neurologic compromise.”
contrast-induced nephrotoxic injury
intrarenal
CIN is when there is an increase in serum creatinine levels above 0.5 or more, or 25% increase from the pts baseline within 3 days of exposure to contrast medium without another explanation of development of AKI.
Pts at highest risk are: pre-existing CKD, baseline serum creatinine levels above 1.5 mg/dL, dehydration, diabetes, heart failure, or older than 75
Medical Management of AKI
Prevention
Compensations for deterioration of kidney function
Regeneration of remaining kidney capacity
Fluid balance
•Fluid resuscitation
o Crystalloids
o Colloids
•Fluid restriction
•Fluid removal
•It’s a challenge to get volume and blood circulating in kidneys
Pharmacologic Management of AKI
• Eliminate any nephrotoxic medications • Diuretics • Loop diuretics • Thaizide diuretics • Osmotic diuretics • Heart failure o Natriuretic peptides o Aldosterone agonists Controversies • Dopamine o Low dose at 2 to 3 mg/kg per min o Increases urine output in short term o Critically ill patients may develop dopamine-renal-receptor tolerance • Acetylcysteine o Vasodilates the tubule and scavenges oxygen free radicals o Fenoldopam
How is the AKI patient managed medically?
Key treatment focuses on prevention strategies, fluid balance, anemia, medications, and electrolyte imbalances.
Crystalloids and colloids are different types of IV fluids used for volume management. The purpose of volume replacement is to replace fluid and electrolyte loses and prevent ongoing loss. Maintenance IV fluid therapy is initiated when oral fluid intake is inadvisable.
Fluid restriction is used to prevent circulatory overload and the development of interstitial edema when the kidneys cannot remove the excess fluid. Pts are usually restricted to 1 L of fluid per 24 hrs if the urine output is less than 500 ml.
Fluid removal may be needed. During early stages of AKI diuretics may be used. When later stages develop hemodialysis may be needed.
Discuss dietary management for the patient in acute renal failure.
Diet is designed to account for the diminished excretory capacity of the kidney. Energy intake is between 20-30 kilocalories/kg per day with 1.2-1.5 grams/kg of protein. Fluids are limited. Potassium, sodium, and phosphorus are limited.
