विवरण
Managing acute kidney failure, also known as acute kidney injury (AKI), is a critical medical intervention that requires prompt diagnosis and treatment. Rapidly identify the signs and symptoms of AKI, including decreased urine output, fluid retention, and elevated creatinine and blood urea nitrogen (BUN) levels. Determine and address the underlying cause of AKI, which can include dehydration, infections, medication toxicity, or underlying medical conditions. Carefully manage fluid balance, as both dehydration and fluid overload can worsen AKI. Tailor fluid administration to the patient's needs. Diuretics may be used cautiously to manage fluid overload, but their use should be monitored closely. Review and adjust medications, especially nephrotoxic drugs, which can exacerbate kidney injury. Monitor and correct electrolyte imbalances, such as hyperkalemia or hyponatremia, which can occur in AKI. Consider renal replacement therapy (hemodialysis or peritoneal dialysis) in severe cases to remove waste products and excess fluids from the bloodstream.
सारांश
- Acute kidney injury (AKI) is a common complication in critical care settings, representing a syndrome with multiple facets and significant implications for patient morbidity and mortality. Early diagnosis is crucial for effective management.
- AKI diagnosis relies on serum creatinine levels and urine output. A creatinine increase of ≥0.3 mg/dL within 48 hours or ≥1.5 times baseline in 3-7 days, alongside urine output <0.5 ml/kg/hour for 6 hours, indicates AKI. These parameters are influenced by various factors beyond kidney function.
- The KDIGO (Kidney Disease: Improving Global Outcomes) guidelines stage AKI into three levels based on creatinine and urine output criteria. Creatinine levels 1.5-1.9 times baseline define Stage 1, 2-2.9 times baseline define Stage 2, and ≥3 times baseline (or ≥4 mg/dL) define Stage 3. Urine output is categorized as Stage 1/2: <0.5 ml/kg/hour for 6-12 hours and Stage 3: 24 hours or anuria for >12 hours.
- Serum creatinine, a metabolite of creatine phosphate, is influenced by production rate (affected by muscle mass and liver function), volume of distribution (impacted by fluid resuscitation), and tubular secretion. This can lead to delayed diagnosis or misdiagnosis of AKI.
- Oliguria, or decreased urine output, can result from physiological causes like dehydration or pathological causes such as renal hypoperfusion. Careful consideration of both factors is necessary to avoid overdiagnosis of AKI.
- Cystatin C, produced by all nucleated cells and filtered by the glomerulus, is proposed as a marker of kidney function that is less influenced by GFR than creatinine. However, conflicting studies question its reliability.
- The Furosemide Stress Test involves administering 1 mg/kg of furosemide (or 1.5 mg/kg if the patient recently received the medication) to assess renal tubular function. A urine output of >200 mL in the subsequent two hours suggests adequate function.
- Future AKI diagnostics may incorporate novel urinary biomarkers (e.g., NGAL, KIM-1, IL-18) in conjunction with creatinine and urine output to improve sensitivity and prognostic capabilities.
- Diagnostic workup includes blood counts, urine dipstick tests, urine microscopy, renal ultrasound, and serum calcium levels. Additional tests may be necessary to determine the underlying etiology of AKI, with nephrology consultation being often required.
- Risk factors for AKI include non-modifiable factors (age, gender, ethnicity, pre-existing conditions) and modifiable factors (sepsis, hypovolemia, nephrotoxins, major surgery, trauma, contrast media, COVID-19). Sepsis is the leading cause of AKI requiring renal replacement therapy (RRT).
- The pathophysiology of AKI involves damage to the endothelial cells of the peritubular capillaries and the proximal tubular cells, leading to fluid overload, electrolyte disturbances, uremia, and acid-base imbalance.
- AKI is classified by time frame: AKI within 7 days, Acute Kidney Disease (AKD) from 7-90 days, and Chronic Kidney Disease (CKD) beyond 90 days if serum creatinine does not return to baseline. Long-term effects of AKD include increased mortality and morbidity.
- AKI management involves careful fluid management, preferring crystalloids over colloids. Balanced crystalloid solutions and normal saline are both acceptable choices. Diuretics are only used to treat fluid overload, not for AKI prevention or treatment. Hemodynamic management with vasopressors aims to increase renal perfusion.
- A care bundle approach involves identifying high-risk patients, discontinuing nephrotoxic agents, ensuring euvolemia, monitoring hemodynamics and renal function, avoiding hyperglycemia, using safer contrast agents, and considering RRT.
- The timing of RRT is guided by trials showing that delaying treatment may reduce dialysis days but worsening clinical parameters require timely intervention. Early recognition and treatment of AKI are crucial to minimize further damage.
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