NSC 386: Comprehensive Study Guide on Acute Kidney Injury (AKI)

Acute Kidney Injury (AKI): Overview and Epidemiology

• Definition of Acute Kidney Injury (AKI)
      - AKI is defined as a rapid decline in kidney function.
      - It is primarily characterized by:
          - Decreased urine output ($UOP$).
          - Increased serum creatinine ($SrCr$).
      - It is often a reversible process, though it can result in significant morbidity.
• Laboratory Significance
      - Serum Creatinine ($SrCr$): This is considered the most reliable indicator of kidney function. AKI is identified when current levels rise above the patient's known baseline. Normal levels indicate adequate perfusion; elevations suggest a problem (e.g., $\text{shock}$, $\text{hypovolemia}$, or $\text{decreased perfusion/blood pressure}$).
      - BUN (Blood Urea Nitrogen): Not considered the most reliable indicator on its own as it can be influenced by other factors like protein intake or hydration status.
• Risk Factors for AKI
      - Increasing age.
      - Diabetes Mellitus ($DM$).
      - Hypertension ($HTN$).
      - Heart Failure ($HF$).
      - Chronic Kidney Disease ($CKD$).
      - Sepsis.
      - Medications: Specific nephrotoxic triggers include certain antibiotics, metformin, and contrast media.
      - Surgery: AKI can occur up to $30$ days post-operatively.
• Epidemiology and Mortality
      - Approximately $2\text{--}5\%$ of all hospitalized patients will develop AKI.
      - Up to $50\%$ of critically care patients (ICU) will develop AKI.
      - There is a significantly increased mortality rate for patients who develop AKI.

Etiology and Classification of AKI

• Prerenal Causes (External to the Kidney)
      - These factors reduce systemic circulation, causing a decrease in renal blood flow and perfusion.
      - Examples: Heart Failure ($HF$), hypovolemia, cardiogenic shock, septic shock, Myocardial Infarction ($MI$), burns, dehydration, and excessive diuresis.
      - Key characteristic: There is "nothing wrong with the kidney itself"; the issue is lack of perfusion (e.g., hypotension/low BP).
• Intrarenal Causes (Direct Damage)
      - These involve problems that cause direct damage to the kidney tissue, resulting in impaired nephron function.
      - Examples: Nephrotoxic medications (antibiotics), contrast media, and hemolytic blood transfusion reactions.
      - Metaphor: This is described as a "shotgun blast" directly to the kidney tissue.
• Postrenal Causes (Mechanical Obstruction)
      - These involve a mechanical obstruction in the outflow of urine. Urine refluxes into the renal pelvis, impairing kidney function.
      - Examples: Kidney stones, Benign Prostatic Hyperplasia ($BPH$), and bladder cancer ($CA$).
      - Result: Dilation of the renal pelvis occurs due to backflow.

AKI Criteria and Staging (RIFLE / Network Scale)

• Stage I: Risk
      - Urine Output ($UOP$): Low for $6$ hours.
      - Serum Creatinine ($SrCr$): Increased $1.5\text{--}2 \times$ baseline.
• Stage II: Injury
      - Urine Output ($UOP$): Low for $12$ hours.
      - Serum Creatinine ($SrCr$): Increased $2\text{--}3 \times$ baseline.
• Stage III: Failure
      - Urine Output ($UOP$): Anuria (no urine).
      - Serum Creatinine ($SrCr$): Increased > 3 \times baseline.
• Loss of Function
      - Complete loss of function requiring dialysis for > 4 weeks.
• End-Stage Renal Disease (ESRD)
      - Complete loss of function requiring dialysis for > 3 months.

Clinical Phases of AKI

• Oliguric Phase
      - Timeline: Occurs within $1\text{--}7$ days of the injury; lasts $10\text{--}14$ days.
      - Urine Output: Decreased to < 400\,mL/24\,hours. Dark color may indicate concentrated urine or infection.
      - Laboratory Changes: Increased $SrCr$ and $BUN$.
      - Fluid Volume Overload (FVO): Leads to edema and potential hypertension.
      - Electrolyte Imbalances:
          - Increased Potassium ($K$): The kidney is the primary route for $K$ excretion.
          - Increased Phosphorus.
          - Decreased Sodium ($Na$): Often dilutional due to fluid retention.
          - Decreased Calcium ($Ca$): The kidney is responsible for activating Vitamin D; without it, calcium cannot be processed.
      - Metabolic Acidosis: Caused by the kidney's inability to excrete acid or regenerate bicarbonate.
      - Hematologic Changes: Anemia due to decreased production of Erythropoietin by the kidneys.
      - Neurological Changes: Mental status changes due to the buildup of nitrogenous waste products (azotemia).
• Diuretic Phase
      - Timeline: Lasts $1\text{--}3$ weeks.
      - Clinical Presentation: Gradual increase in daily urine output, usually $1\text{--}3\,L/day$, but can reach up to $5\,L/day$.
      - Mechanism: The nephrons are not yet fully functional (cannot concentrate urine), but the body is beginning to filter out waste. $BUN$ and $SrCr$ begin to stabilize.
      - Complications: Hypovolemia, hypotension, hyponatremia, and hypokalemia due to massive fluid and electrolyte loss.
• Recovery Phase
      - Timeline: Can take several months to $1\text{--}2$ years.
      - Clinical Presentation: GFR (Glomerular Filtration Rate) increases and $SrCr$ normalizes to baseline.
      - Outcome: Some patients achieve normal function, while others may remain in an early stage of Chronic Kidney Disease ($CKD$).

Treatment and Nursing Care for AKI

• Primary Goals
      - Eliminate the cause of the injury.
      - Manage signs and symptoms.
      - Prevent complications during kidney recovery.
• Initial Assessment and Perfusion
      - Determine if there is adequate intravascular volume and cardiac output for kidney perfusion.
      - Fluid Challenge: If the patient does not show signs of Fluid Volume Overload (no JVD, no crackles, no pedal edema), a bolus of $0.5\text{--}1\,L$ of normal saline ($NS$) may be given to "jump start" the kidneys.
• Fluid Management
      - If FVO is present: Fluid restriction is necessary (e.g., < 1,000\,mL/day).
      - Diuretics: Furosemide ($Lasix$) may be administered at $0.5\,mg/kg/hr$. If there is no response, the nurse must look for other interventions.
• Nursing Interventions
      - Strict intake and output (I&O).
      - Daily weights (monitoring for retention).
      - Vital signs (monitoring BP and HR).
      - Monitor lab trends (the goal is for $SrCr$ to plateau and then decrease).
• Medication: Furosemide (Lasix)
      - Therapeutic effects: Increased urine output and decreased blood pressure.
      - Side effects: Hypotension, hypokalemia ($\downarrow K$), and ototoxicity/transient hearing loss.
• Nutrition
      - Monitor dietary protein: Hard to digest for compromised kidneys.
      - Protein requirement: $0.8\text{--}1\,g/kg$ of body weight.
      - Calculation Example: If a client weighs $140\,lbs$ ($63.6\,kg$) and is ordered $0.8\,g/kg$, they should receive approximately $51\,grams$ of protein in $24$ hours.

Management of Hyperkalemia

• Mild to Moderate Treatment
      - Sodium Polystyrene Sulfonate (Kayexalate): Administered PO or as a retention enema. It causes diarrhea to excrete potassium. Nurses should never hold this medication because the diarrhea is the desired effect.
      - Dietary Restriction: Potassium intake should be < 40\,mEq/day. (Example: Remove high-potassium foods like bananas and yogurt from trays).
• Severe or Symptomatic treatment ($K > 6\,mEq/L$)
      - Cardiac Monitoring: Required immediately due to dysrhythmia risk.
      - Regular Insulin: $10\text{--}20$ units administered IV over $1$ hour. It shifts potassium into the cells.
      - Dextrose (D50): Administered with insulin to prevent hypoglycemia.
      - Nursing Note: If Blood Glucose ($BG$) drops too low (e.g., level of $30$) and the patient is lethargic, administer one amp of $D_{50}$ IV immediately.
      - IV Calcium Gluconate: Given concurrently to improve cardiac contractility and stabilize the myocardium.
      - Sodium Bicarbonate: Treats metabolic acidosis and helps shift potassium into cells.

Dialysis and Renal Replacement Therapy

• Indications for Dialysis
      - Potassium ($K$) levels > 6.5\,mEq/L.
      - Pulmonary edema (indicated by crackles or pink frothy sputum).
      - Uremia (urea buildup in the blood causing confusion).
• Continuous Renal Replacement Therapy (CRRT)
      - Used to treat AKI specifically in the ICU setting.
      - Uses a temporary access device (e.g., subclavian).
      - Decreases fluids and toxins slowly over $24$ hours to days rather than a rapid few-hour session.
      - Benefit: Decreases the risk of hemodynamic instability (less stress on BP).
      - Nursing Care for CRRT: Hourly I&O, daily weights, vital signs, and monitoring labs ($SrCr$/$BUN$).

Questions & Discussion

• Case Study 1: Gentamicin and Dark Urine
      - Scenario: A client with COPD is receiving Gentamicin IV (an antibiotic known to be nephrotoxic). At $12:00\,pm$, the nurse empties $125\,mL$ of dark urine from a catheter last emptied at $6:00\,am$. Labs: BUN $24$, SrCr $1.9$, K $5.0$. Lungs are CTA (clear to auscultation), no pedal edema.
      - Conclusion: Underperfused or damaged kidneys are holding onto fluid/waste; SrCr is high. The diagnosis is AKI.
• Case Study 2: Response to Treatment
      - Scenario: Patient receives $1,000\,mL$ NS bolus and $40\,mg$ Furosemide. Next day: Bilateral crackles at lung bases, $UOP$ is $120\,mL$ over $5$ hours. BP $160/92$, HR $88$, RR $26$, $O_2$ Sat $88\%$. Labs: SrCr $2.5$, BUN $95$, eGFR <45, K $5.5$.
      - Findings: The treatment was not effective. The patient is in fluid overload and hyperkalemic. Priority is based on ABCs (Airway, Breathing, Circulation) due to respiratory distress from fluid in lungs.
• Learning Check: Insulin for Hyperkalemia
      - Question: After insulin, the client's BG is $30$, they are lethargic and confused. What is the intervention?
      - Answer: Give one amp of $D_{50}$ IV now.
• Learning Check: Potassium Restricted Diet
      - Question: Which food should be removed from the lunch tray?
      - Answer: Banana and yogurt parfait (High Potassium).