NR 325 Week 3 Acute Kidney Injury CAE PNCI Medical Surgical

NR 325 Week 3 Acute Kidney Injury CAE PNCI Medical Surgical

Name

Chamberlain University

NR-325 Adult Health II

Prof. Name

Date

Acute Kidney Injury (AKI): Pathophysiological Changes, Diagnostic Differentiation, and Management

Pathophysiology of Acute Kidney Injury

Acute kidney injury (AKI) represents a sudden decline in kidney function, often due to an obstruction that disrupts normal urine flow. When urine outflow is blocked, it causes reflux into the renal pelvis, ultimately compromising kidney function. Bilateral ureteral obstruction specifically leads to hydronephrosis, which causes kidney dilation and increases hydrostatic pressure and tubular blockage, progressively reducing kidney efficiency. If this obstruction is cleared within 48 hours, recovery of kidney function is possible; however, prolonged blockage can cause tubular atrophy and irreversible kidney fibrosis. Additionally, severe ischemia disrupts the basement membrane and destroys portions of the tubular epithelium.

Classification of AKI: Prerenal, Intrarenal, and Postrenal

AKI is categorized based on the causative factor: prerenal, intrarenal, and postrenal. Prerenal AKI is often due to hypovolemia (dehydration, hemorrhage), decreased cardiac output (heart failure, myocardial infarction), or reduced vascular resistance (shock, neurologic injury). Intrarenal causes involve nephrotoxins like aminoglycosides or contrast media, infections such as acute pyelonephritis, and conditions like lupus. Postrenal causes include obstructions from benign prostatic hyperplasia, calculi, or neuromuscular disorders. Common signs and symptoms of AKI include oliguria, shortness of breath, peripheral edema, chest pain, fatigue, and, in severe cases, seizures or coma.

Electrolyte and Fluid Imbalances in AKI

AKI often disrupts electrolyte balance, causing abnormalities like hyperkalemia, hyponatremia, and hypocalcemia. Hyperkalemia, often due to renal insufficiency or metabolic acidosis, presents with muscle weakness, bradycardia, and dysrhythmias. Hyponatremia may result from dehydration or fluid overload, causing confusion, dry mucous membranes, and headache. Hypocalcemia is linked to elevated phosphorus levels secondary to decreased glomerular filtration rate, with symptoms including tetany and tingling around the mouth or extremities.

NR 325 Week 3 Acute Kidney Injury CAE PNCI Medical Surgical

Table 1: Overview of AKI Characteristics, Causes, Symptoms, and Management

Management and Treatment of AKI

Managing AKI involves treating the underlying cause and closely monitoring fluid balance, electrolyte levels, and kidney function. Fluid administration can promote perfusion, with oral diuretics or IV fluids as needed. Electrolyte disturbances are managed with specific treatments like IV insulin to address hyperkalemia or sodium bicarbonate for acidosis. Dialysis may be necessary for severe cases, particularly if conservative measures do not stabilize the patient. Sodium polystyrene sulfonate enemas may be used to treat hyperkalemia by replacing potassium with sodium in the intestines.

NR 325 Week 3 Acute Kidney Injury CAE PNCI Medical Surgical

Nursing actions in dialysis include using aseptic techniques, avoiding compression of the access site, and monitoring for complications like hypotension or disequilibrium syndrome. Patient education covers the importance of hand hygiene, infection prevention, and adherence to prescribed medications. For those with MRSA, isolation and careful wound care are crucial to minimize the risk of spreading infection within healthcare settings.

References

• Kidney Disease: Improving Global Outcomes (KDIGO) Acute Kidney Injury Work Group. (2012). KDIGO clinical practice guideline for acute kidney injury. Kidney International Supplements, 2(1), 1-138.
• 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

• Thomas, R., & Balogun, R. A. (2018). Dialysis modalities: An evidence-based review. Clinics in Chest Medicine, 39(3), 557–566. https://doi.org/10.1016/j.ccm.2018.04.009