L18 Management of Acute Kidney Injury Flashcards
Staging of Acute Kidney Disease?
Look at Serum Creatinine!!
Classification of Acute Kidney Disease?
Management depends on cause:
Postrenal
Obstructive uropathy
Reversible if obstruction promptly relieved
Prerenal
Azotemia (blood accumulation of nitrogen-bearing waste products ( urea))
Reversible renal dysfunction caused by decreased renal perfusion
Intrarenal
Intrinsic
AKIRenal vascular, glomerular, tubulointerstitial pathology
Causes/Risk Factors/Exam Indicators/Imaging of Post-Renal Acute Kidney Injury?
Obstruction of collecting system or extrarenal drainage
Risk factors of obstruction:
SINGLE KIDNEY
Prostatic causes
Neurologic, and spinal disorders
Metastatic cancers
Nephrolithiasis
Medications (crystals)
Exam Indicators: Anuria (NO urine), Increased serum creatinine
Imaging: Ultrasound
Treatment of Urinary Tract Obstrution (Post Renal Acute Kidney Injury)
Discontinuation of anticholinergic drugs, crystal-inducing drugs, such as indinavir
Foley Indwelling Catheter
Interventional radiology, surgery
Therapy of Shock/Acute Pre-Renal Kidney Injury?
Initial therapy of hypotension ± shock should be with IV Fluid boluses (Cystaloids), in the absence of congestive heart failure/pulmonary edema!!
In hypotensive patients who are unresponsive to fluid therapy, catecholamine vasoactive drugs support circulation
Therapy of the cause of shock (bleeding, infection/sepsis ) is critically important
Functional AKI vs. Structural AKI
Acute kidney injury is divided into Prerenal Azotemia (Functional AKI) and Acute Tubular Necrosis (Structural AKI) on the basis of serum creatinine (sCr) and urinary biomarkers.
Prerenal azotemia: tubular function is intact and is responding to renal hypoperfusion.
Structural AKI Pathogenesis (acute tubular necrosis): Increased Vasoconstriction (excess Cl- through ascening loop at macula densa) => Increased endothelial leucocytes-endothelial adhesion => vascular obstruction
Azotemia= blood accumulation of nitrogen-bearing waste products (urea)
Supportive Care of Acute Kidney Disease?
Maintain adequate perfusion (Fluid restrict once adequately resuscitated)
Dietary restrictions (K, phosphorous)
Dose medications for GFR <10ml/min
Diuretics
Monitor for uraemic complication
Hyperkalemia Therapy?
STOP K Intake
Hold drugs that increase K: RAAS inhibitors, NSAIDs
Do Not Use Low-Dose Dopamine in AKI
Stabilize: Continuous cardiac monitoring, IV Calcium
Shift K:
IV Insulin (10U IV) and Glucose (50ml 50% dextrose)
Nebulised β2-agonist (salbutamol)
Sodium bicarbonate if acidosis
Increase K excretion:
Cation exchange resins
Increase urine output: Fluids (if hypovolemic) or Diuretics
Acute Dialysis
Indications for Renal Replacement Therapy?
May be required for patients with severe AKI
Uremia (Encephalopathy, Pericarditis, Bleeding diathesis)
Volume Overload
Hyperkalemia
Metabolic Acidosis
Severe hyperphosphatemia
Good to wait for, if started prematurely can actually lead to worse outcomes
