ACUTE KIDNEY INJURY AND CHRONIC KIDNEY DISEASE Flashcards
is a rapid loss of renal function due to damage to the kidneys and is accompanied by serum creatinine elevation and/ or reduction in urine output
Acute Kidney Injury
Potentially reversible, but has a high mortality rate
Acute Kidney Injury
Acute Kidney Injury Etiology
-Pre-renal causes
- Intrarenal causes
- Post-renal causes
-External to the kidneys
-Factors that reduce systemic circulation, causing decreased renal blood flow
-Reduced glomerular filtration
- May lead to intrarenal disease if renal ischemia is prolonged
Pre-renal Causes
Conditions that cause direct damage to kidney tissue, resulting in impaired nephron function
Intrarenal Causes
Cause obstruction of intrarenal structures by crystallizing or by causing damage to the epithelial cells of the tubules
Nephrotoxins
Blocks the tubules and causes renal vasoconstriction
Hgb and Myoglobin
Involve mechanical obstruction of urine outflow
Post-renal causes
A 5-tier system and describes the stages of AKI
RIFLE Classification
The RISK, INJURY and FAILURE describe the
SEVERITY
The LOSS and ESKD describe the
OUTCOME
Begins with the initial insults and ends when oliguria develops
Initiation Phase
4 Phases of AKI
-Initiation
-Oliguria
-Diuresis
-Recovery
It is characterized by decreased urine output (less than 400 mL/day or <0.5 mL/kg/hr)
Oliguria Phase
A phase where uremic symptoms begin to appear
Oliguria Phase
Accompanied by an increase in the serum concentration of substances usually excreted by the kidneys
Oliguria Phase
-Marked by a gradual increase in urine output
-The renal function may still be abnormal and uremic symptoms may still be present
Diuresis Phase
This phase may take 3 to 12 months and the laboratory values return to normal
Recovery Phase
In this phase, the patient MUST avoid nephrotoxic agents
Recovery Phase
The most common initial manifestation
Oliguria
Clinical Manifestations of Acute Kidney Injury (AKI)
-Oliguria
-Jugular vein distention
- Bounding pulse
- Edema
- Hypertension
- Kussmaul respirations- rapid, deep respirations
- Hyponatremia, hyperkalemia
-Elevated serum creatinine and BUN
- Neurologic changes
(fatigue)
(Seizure, stupor, coma)
( Asterixis)
Occurs within 24 hours if the _____ is the cause
ISCHEMIA
Delayed up to 1 week if the cause is _________
NEPHROTOXICITY
Clinical manifestations of AKI were flapping tremors when the wrist is extended
Asterixis
Goal of AKI for the Medical Management
Goal: Restore normal chemical balance and prevent complications until repair of renal tissue and restoration of renal function can occur.
-Treat underlying cause
- Maintaining fluid balance
- Renal Replacement therapy
A treatment of hyperkalemia that causes a shift of potassium back into the cell
HR+ D50W
A treatment of hyperkalemia that can correct the acidosis and cause a shift of potassium into cells
NaHCO3 (Sodium Bicarbonate)
A treatment of hyperkalemia that temporarily raises the threshold at which dysrhythmias occur
Calcium Gluconate
Treatment of hyperkalemia that removes potassium from the body
Kayexelate
Most effective therapy to remove potassium
Dialysis
Medical Management for Renal Replacement Therapy
-Volume Overload
-Hyperkalemia
-Metabolic acidosis
-BUN >120 mg/dl
- Significant changes in mental status
- Pericarditis, pericardial effusion, cardiac tamponade
Method of choice when rapid changes are required in a short time
Hemodialysis
Is the most immediate life-threatening imbalances seen in AKI
Hyperkalemia