Acute Kidney Injury PDF

Acute Kidney Injury By Dr. Angela Banks, RN, PhD How do the kidneys function? Responsible for maintaining fluid and electrolyte homeostasis Ridding the body of water soluble wastes Regulating the amount an...

Acute Kidney Injury By Dr. Angela Banks, RN, PhD How do the kidneys function? Responsible for maintaining fluid and electrolyte homeostasis Ridding the body of water soluble wastes Regulating the amount and composition of the urine Performing 2 important endocrine functions Electrolytes Potassium 3.5-5.0 mEq/L Sodium level 135-145 mEq/L Calcium 8.5-10.5 mg/dL Phosphorus 3.0-4.5 mg/dL  Hormonal Regulation Erythropoietin Stimulates erythrocyte development in bone marrow Regulator of RBC production Vitamin D Osteodystrophy Vitamin D is impaired Poor calcium reabsorption Decreased calcium Stimulus for parathyroid release Leads to parathyroid hormone release  Addressing Clinical Problems Reduction in red blood cells leads to anemia Erythropoietin (Epogen) replacement Reduced blood flow Activation of the Renin-Angiotensin Aldosterone System Hypertension Damages the capillaries in the glomerulus Leads to End Stage Kidney Disease  Types of Renal Azotemia Types of Azotemia Cause Pathophysiology Key Lab Findings Prerenal Reduced blood flow to the kidneys Decreased kidney perfusion without Elevated BUN-to-creatinine ratio (>20:1). Azotemia structural damage. The kidneys retain The kidneys are still reabsorbing more the ability to concentrate urine and urea nitrogen compared to creatinine. reabsorb BUN. If untreated, it can Low urine sodium concentration (40 urine. Common causes include acute mEq/L) due to direct damage to the tubular necrosis (ATN), and kidney’s tubules which impairs their glomerulonephritis (Inflammation of the ability to reabsorb sodium. glomeruli) Postrenal Obstruction of outflow (e.g., kidney Obstruction causes urine to back up BUN-to-creatinine ratio (starts elevated, Azotemia stones, enlarged prostate, tumors) into the kidneys, increasing pressure then normalizes) and damaging renal tissue if prolonged. High urine sodium can occur due to Initially, the kidneys may still impaired tubular reabsorption as a result concentrate urine, but over time, tubular of the obstruction. function is lost.  Types of Renal Injury and Treatment Approach Type of Renal Treatment Approach Injury Prerenal Azotemia 1. Identify and Address Underlying Cause: Assess for dehydration, heart failure, or hypovolemia. Administer IV fluids (e.g., isotonic saline) for volume resuscitation. If due to heart failure, optimize cardiac output with diuretics and other heart failure medications. 2. Monitor and Support Kidney Function: Regularly monitor serum creatinine, electrolytes, and urine output. Avoid nephrotoxic agents (e.g., NSAIDs, certain antibiotics) during recovery. Intrinsic Renal 1. Identify and Treat Underlying Cause: In cases of Acute Tubular Necrosis (ATN): Remove nephrotoxic agents (e.g., Azotemia contrast dyes, certain medications). Manage electrolyte imbalances (e.g., hyperkalemia). 2. Supportive Care: Maintain adequate hydration. May require dialysis if severe electrolyte imbalances or fluid overload occur. 3. Monitor Renal Function: Regularly check kidney function (serum creatinine, electrolytes) and adjust treatment based on progress. Postrenal Azotemia 1. Relieve Obstruction: Identify the cause of obstruction (e.g., kidney stones, tumors, enlarged prostate). Use catheterization or surgical intervention (e.g., nephrostomy, ureteral stent placement) to relieve the obstruction. 2. Support Kidney Function: Monitor kidney function (serum creatinine, urine output) during recovery. Manage any resulting electrolyte imbalances. 3. Post-Obstruction Assessment: Assess for potential renal recovery post-relief of obstruction and adjust treatment accordingly. Prerenal Injury (Azotemia) 1. Hemorrhage 2. Dehydration 3. Burns 4. Heart failure 5. Myocardial infarction Prerenal Acute Kidney Injury NSAIDS - Motrin cause vasoconstriction of afferent arterioles Ace inhibitors reduce glomerular perfusion pressure → ↓GFR Lisinopril (Zestril) Captopril (Capoten) Angiotensin II Receptor Blockers (ARBs) reduce glomerular perfusion pressure → ↓GFR Losartan (Cozaar) Valsartan (Diovan) Candesartan (Atacand) Intrarenal (Intrinsic) Acute Kidney Injury (AKI)  Acute Tubular Necrosis Initiation Phase Pathophysiology During this phase, the kidney tubules start to suffer damage due to insufficient oxygenation or exposure to toxic substances. Symptoms: Decreased urinary output with mild ↑ BUN and Creatinine levels Reversibility: If recognized early less damage is done Acute Tubular Necrosis (Maintenance Phase) acidosis  Acute Tubular Necrosis Recovery Phase (Diuretic Phase) Urinary output > 400 cc/hr Osmotic Diuresis Gradual Normalization of the BUN and Creatinine levels Fluid and Electrolyte depletion Postrenal Acute Kidney Injury  Clinical Manifestations Elevated blood pressure S3 heart sound indicates ↓ left ventricular function of heart failure Pulmonary crackles - volume excess Jugular venous distention - due to volume excess Anemia due to suppression of erythropoietin secretion  Diagnostic Tests Urinalysis Proteinuria RBCs & WBCs Tubular epithelial cells Elevated Serum Creatinine Normal.6-1.2 mg/dL Elevated Blood Urea Nitrogen Normal 6-20 mg/dL Serum Electrolytes Potassium Elevated Sodium Decreased Arterial Blood gases Metabolic Acidosis Complete Blood Count Renal Ultrasonography Used to identify obstructive cause of renal failure and to differentiate AKI from End Stage Renal Disease (ESRD) Medications Loop Diuretics Bumetanide (Bumex) Ethacrynic acid (Edecrin) Furosemide (Lasix) Torsemide (Dermadex) Osmotic Diuretics will pull extracellular water into the vascular system Mannitol- (Osmitrol) Urea (Ureaphil)  Electrolyte Modifiers Calcium Chloride Calcium Gluconate (Kalcinate) Sodium Bicarbonate (Sellymin) Sodium Polystyrene Sulfonate (Kayexalate) Three Types of Dialysis Hemodialysis Peritoneal dialyses Continuous Renal Replacement Therapy Dialysis is a life saving intervention Removes excess toxins Lowers elevated drug levels Hemodialysis Access Hemodialysis Arteriovenous (AV) fistula Arteriovenous (AV) graft Central Venous Catheter (CVC) catheter Peritoneal Dialysis Peritoneal Catheter Peritoneal Dialysis Peritoneal Dialysis Machine  Implementation of Care Monitor hourly Intake and output Daily weights Assessing Vital signs every 4 hours Assess breath sounds Monitoring serum electrolytes Hyperkalemia Hyponatremia Hyperphosphatemia Fluid Restriction is pivotal