NR 325 Week 3 Acute Kidney Injury CAE PNCI Medical Surgical

Student Name

Chamberlain University

NR-325 Adult Health II

Prof. Name

Date

Acute Kidney Injury – CAE PNCI Medical-Surgical Preparation

Pathophysiology of Acute Kidney Injury

Acute Kidney Injury (AKI) is characterized by a sudden decline in renal function, leading to reduced glomerular filtration rate (GFR), retention of nitrogenous waste products, fluid imbalance, and electrolyte disturbances. The pathophysiological changes depend on the underlying cause but often involve impaired renal perfusion, tubular injury, or urinary tract obstruction.

In cases of urinary tract obstruction, urine flow is impeded, causing backward pressure (urinary reflux) into the renal pelvis. This increases hydrostatic pressure within the nephron and reduces GFR. Bilateral ureteral obstruction leads to hydronephrosis (dilation of the kidney), tubular blockage, and progressive loss of renal function.

If obstruction is relieved within 48 hours, renal recovery is usually complete. However, prolonged obstruction results in tubular atrophy and irreversible interstitial fibrosis.

In ischemic AKI, severe reduction in renal blood flow causes damage to the tubular basement membrane and patchy necrosis of the tubular epithelium, further impairing filtration and concentrating ability.

Etiology, Clinical Features, and Diagnostic Patterns

Causes of AKI

AKI is classified into prerenal, intrarenal, and postrenal categories.

Type of AKI	Common Causes	Signs and Symptoms	Diagnostic Findings
Prerenal	Hypovolemia (dehydration, hemorrhage, diarrhea, vomiting, excessive diuresis, burns, hypoalbuminemia), decreased cardiac output (heart failure, MI, dysrhythmias, cardiogenic shock), decreased systemic vascular resistance (anaphylaxis, septic shock, neurological injury), decreased renal blood flow (bilateral renal vein thrombosis, renal artery thrombosis, hepatorenal syndrome).	Oliguria, hypotension, tachycardia, dry mucous membranes, poor skin turgor, confusion.	Urine sodium <20 mEq/L, high urine osmolality (>500 mOsm/kg), bland urinary sediment.
Intrarenal	Nephrotoxic agents (aminoglycosides, vancomycin, amphotericin B, contrast dye, hemolytic transfusion reactions, crush injury, ethylene glycol, lead, arsenic), interstitial nephritis (NSAIDs, ACE inhibitors, sulfonamides, rifampin, viral/fungal/bacterial infections), other (acute glomerulonephritis, malignant hypertension, lupus nephritis, thrombotic disorders).	Edema, fatigue, flank pain, hematuria, oliguria.	Urine sodium >40 mEq/L, muddy brown granular casts, low urine osmolality (<350 mOsm/kg).
Postrenal	Benign prostatic hyperplasia, bladder/prostate cancer, kidney stones, urethral strictures, neuromuscular bladder dysfunction, spinal cord injury, pelvic trauma.	Lower abdominal discomfort, hesitancy, fluctuating urine output, anuria in complete obstruction.	Imaging showing hydronephrosis or bladder distention; elevated post-void residual volume.

Fluid and Electrolyte Imbalances in AKI

Renal impairment affects electrolyte regulation, leading to potentially life-threatening abnormalities.

Disturbance	Causes	Clinical Manifestations
Hyperkalemia	Reduced potassium excretion due to renal insufficiency; metabolic acidosis causing potassium shift from intracellular to extracellular space.	Muscle weakness, paresthesias, bradycardia, irritability, leg cramps, dysrhythmias, abdominal cramps, diarrhea.
Hyponatremia	Dilution from fluid retention; sodium loss in hypo/hypervolemic states.	Abdominal cramping, headache, confusion, dry mucous membranes.
Hypocalcemia	Hyperphosphatemia from reduced GFR; impaired vitamin D activation.	Tetany, perioral/finger/toe tingling, positive Trousseau’s & Chvostek’s signs, irritability, bronchospasm.

Management of Acute Kidney Injury

Medical and Nursing Goals

1. Treat the underlying cause promptly.
2. Restore and maintain adequate renal perfusion.
3. Prevent fluid overload and correct electrolyte imbalances.
4. Support kidney recovery and prevent complications.

Key Interventions

• Strict I&O and daily weights.
• Continuous cardiac monitoring for dysrhythmias.
• IV fluid challenges for prerenal AKI (avoid in volume-overloaded patients).
• Loop diuretics for volume overload.
• IV insulin with dextrose for hyperkalemia.
• Sodium bicarbonate for metabolic acidosis.
• Calcium gluconate for cardiac membrane stabilization in hyperkalemia.

Sodium Polystyrene Sulfonate

Sodium polystyrene sulfonate exchanges sodium ions for potassium in the colon, facilitating potassium excretion in stool. It is contraindicated in patients without bowel sounds due to the risk of bowel necrosis.

Dialysis-Related Complications and Prevention

Peritoneal Dialysis

Complications:

• Peritonitis from poor aseptic technique.
• Exit-site infection.
• Dialysis-induced hypotension in elderly patients.

NR 325 Week 3 Acute Kidney Injury CAE PNCI Medical Surgical

Prevention:

• Use aseptic technique during exchanges.
• Avoid pressure or needle sticks on access arm.
• Monitor for thrill/bruit.
• Check for redness, swelling, drainage.

Hemodialysis

Complications:

• Disequilibrium syndrome from rapid solute removal.
• Hypotension from fluid shifts.
• Access site infection or clotting.

Prevention:

• Start with slow dialysis rates.
• Monitor neurological status.
• Manage hypotension with fluids; stop dialysis if persistent.

Teaching Plan for AKI Patients

• Understand and follow prescribed treatment regimens.
• Actively participate in care decisions.
• Use effective coping strategies to manage illness stress.
• Maintain activity within tolerance limits.
• Attend dietary consultations.
• Increase fluid intake as directed.

MRSA Overview and Prevention

MRSA (Methicillin-Resistant Staphylococcus aureus) is a resistant strain of staph bacteria that can cause difficult-to-treat infections, particularly in hospitalized or long-term care patients. It can spread to the community through direct contact.

Prevention Measures:

• Perform hand hygiene before and after patient contact.
• Use gloves and gowns for wound care.
• Isolate infected patients.
• Administer antibiotics on schedule.
• Educate patients about hygiene, avoiding sharing personal items, and proper disposal of dressings.

Peritoneal vs. Hemodialysis

Feature	Hemodialysis	Peritoneal Dialysis
Mechanism	Blood pumped through dialyzer outside body.	Dialysate instilled into peritoneal cavity.
Membrane Used	Artificial semipermeable membrane.	Peritoneal membrane.
Invasiveness	Requires vascular access.	Requires peritoneal catheter.
Session Duration	3–4 hours, 3 times/week.	Several exchanges daily or overnight cycles.

Case Progression and Interventions

State 1 – Initial Postoperative Decline

• Findings: Low urine output (250 mL/12 hr), abdominal distention, hypotension, tachycardia, hypoxia.
• Labs: Na 150, K 5.2, Cl 116, CO₂ 18, BUN 50, Creatinine 2.6.
• Likely cause: AKI due to vancomycin nephrotoxicity and hypovolemia (intrarenal).

Interventions:

• O₂ therapy.
• ECG monitoring.
• IV normal saline bolus.
• Notify provider of unstable vitals and low urine output.
• Discontinue nephrotoxic drugs.

State 2 – Deterioration

• Findings: Fluid overload (crackles, bounding pulses), K 6.7, BUN 40, Creatinine 3.2.
• Management:
  • Stop IV fluids.
  • Calcium gluconate to protect heart from hyperkalemia effects.
  • IV insulin with dextrose to shift potassium intracellularly.
  • Sodium polystyrene sulfonate for potassium excretion (if bowel sounds present).
  • Cardiac monitoring.

State 3 – Pre-Dialysis

• Findings: Persistent oliguria (10 mL), patient inquiring about dialysis.
• Teaching: Purpose of hemodialysis, procedure steps, potential benefits, and risks.
• Prep: Obtain informed consent, check labs, monitor ECG, assess weight.

State 4 – Post-Dialysis Improvement

• Findings: 1 L fluid removed, improved vitals, clear lung sounds, stable O₂ saturation.
• Ongoing Care:
  • Monitor for dialysis complications (hypotension, infection, disequilibrium syndrome).
  • Educate patient on fistula care and infection prevention.

References

American Nephrology Nurses Association. (2021). Nephrology nursing standards of practice and guidelines for care. ANNA.

Bellomo, R., Kellum, J. A., & Ronco, C. (2019). Acute kidney injury. The Lancet, 394(10212), 1949–1964. https://doi.org/10.1016/S0140-6736(19)32563-2

Khwaja, A. (2012). KDIGO clinical practice guidelines for acute kidney injury. Nephron Clinical Practice, 120(4), c179–c184. https://doi.org/10.1159/000339789

National Institute for Health and Care Excellence. (2019). Acute kidney injury: Prevention, detection and management. NICE Guideline

NR 325 Week 3 Acute Kidney Injury CAE PNCI Medical Surgical

[NG148]. https://www.nice.org.uk/guidance/ng148

Palevsky, P. M. (2020). Acute kidney injury: Epidemiology, outcomes, diagnosis, and management. UpToDate.