Treatment of Acute Kidney Injury After Cardiac Arrest
The treatment of acute kidney injury (AKI) after cardiac arrest centers on close monitoring of kidney function, optimizing hemodynamics through goal-directed fluid therapy and vasopressor support, avoiding nephrotoxic medications, and initiating renal replacement therapy when indicated, particularly in cases with fluid overload. 1, 2
Monitoring and Early Detection
- Monitor kidney function closely including urine output and serum creatinine throughout post-cardiac arrest care, as patients are at high risk for developing AKI. 1
- AKI occurs in approximately 37-52% of cardiac arrest survivors, with onset typically within 1-2 days after return of spontaneous circulation (ROSC). 3
- In pediatric patients, 37% develop AKI after cardiac arrest, with 11.5% developing severe AKI and 6.4% requiring renal replacement therapy within 48 hours of ROSC. 1, 2
- Urinary biomarkers (tissue inhibitor of metalloproteinases-2 and insulin-like growth factor-binding protein 7) can identify at-risk patients as early as 1 hour after cardiopulmonary bypass in cardiac surgery patients. 2
Hemodynamic Optimization
Goal-directed fluid therapy is critical and should use standardized algorithms targeting specific hemodynamic parameters. 2, 4
Fluid Management
- Use isotonic crystalloids rather than colloids for volume expansion in patients at risk of AKI. 2
- Avoid starch-containing fluids in at-risk patients. 2
- Implement goal-directed fluid therapy with quantified targets for blood pressure, cardiac index, systemic venous oxygen saturation, and urine output. 2
- Volumetric (extravascular lung water index, global end-diastolic volume index) and arterial waveform-derived variables (pulse pressure variation, stroke volume variation) can guide fluid therapy and reduce AKI incidence. 4
- In one study, hemodynamic-guided fluid therapy (averaging 5449±1438 mL in first 24 hours) significantly reduced severe AKI compared to conventional monitoring (4375±1285 mL), with RIFLE 'I'/'F' occurring in only 4.3% versus 28.6%. 4
Blood Pressure Goals
- Target a mean arterial pressure of at least 65 mm Hg, though optimal blood pressure goals remain uncertain. 1
- Use vasopressors (such as norepinephrine) in conjunction with fluids in patients with vasomotor shock to maintain adequate perfusion pressure. 1, 2
- Titrate inotropic agents (such as dobutamine) and inodilators (such as milrinone) as needed to optimize cardiac output and systemic perfusion. 1
- Monitor central venous oxygen saturation with a target of 70% as a reasonable goal. 1
Medication Management
Nephrotoxic medications must be avoided or used with extreme caution. 1, 2
- Discontinue ACE inhibitors and angiotensin II receptor blockers for 48 hours post-cardiac arrest. 2
- Use aminoglycosides only when no suitable, less nephrotoxic alternatives are available, and when necessary, administer as a single daily dose with close monitoring of drug levels. 2
- Adjust medication dosages for patients with impaired kidney function. 1
- Closely monitor serum concentrations of nephrotoxic medications. 1
- Avoid radiocontrast agents when possible in at-risk patients. 2
Medications NOT Recommended
- Do not use low-dose dopamine to prevent or treat AKI. 2
- Do not use fenoldopam to prevent or treat AKI. 2
- Do not use atrial natriuretic peptide to prevent or treat AKI. 2
- Do not use recombinant human IGF-1 for AKI prevention or treatment. 2
- Diuretics should not be used to prevent AKI but may be used to manage volume overload once AKI is established. 2
Metabolic Management
- Target moderate glycemic control (144-180 mg/dL or 8-10 mmol/L) in adult patients with ROSC after cardiac arrest. 1
- Do not attempt tight glucose control (80-110 mg/dL) due to increased risk of hypoglycemia and potential for worse outcomes. 1
- Maintain plasma glucose between 110-149 mg/dL (6.1-8.3 mmol/L) in pediatric patients to avoid hyperglycemia. 2
Renal Replacement Therapy
Consider early initiation of RRT, particularly in cases with fluid overload. 2, 5
- Approximately 33% of AKI patients after cardiac arrest require RRT, with only 2% remaining dialysis-dependent at 30 days. 3
- The decision to initiate RRT should be based on clinical status including degree of fluid overload, electrolyte abnormalities, and acid-base status. 5
- Use of vasopressors is strongly associated with both development of AKI and continued need for post-discharge dialysis. 6
- Post-discharge dialysis is associated with significantly increased mortality risk (HR 2.57). 6
Nutritional Support for Established AKI
- Provide 20-30 kcal/kg/day total energy intake for patients with any stage of AKI. 2
- Do not restrict protein intake to prevent or delay RRT initiation. 2
- Administer protein at 0.8-1.0 g/kg/day in noncatabolic AKI patients without dialysis, and 1.0-1.5 g/kg/day in patients on RRT. 2
- Provide nutrition preferentially via the enteral route. 2
Risk Factors and Prognosis
Understanding risk factors helps identify patients requiring more aggressive monitoring and intervention:
- Major risk factors include: abnormal baseline creatinine, in-hospital arrest location, higher number of epinephrine doses during arrest (both total doses and rate of dosing), post-cardiac arrest acidosis (pH <7.21), initial non-shockable rhythm, longer duration of arrest, presence of shock, and higher blood lactate after resuscitation. 1, 7, 3
- AKI is associated with significantly increased mortality (OR 2.63, HR 1.35) and poor neurological outcomes (OR 2.22-2.27). 6, 8, 3
- Hospital mortality is 69.4% in AKI patients versus 52.0% in non-AKI patients. 6
Follow-up Care
- Ensure early follow-up after discharge for patients with AKI, as they are at higher risk for developing chronic kidney disease. 5
- Pediatric patients should receive follow-up within 3 months post-discharge, especially those with severe AKI. 5
- At 30 days post-cardiac arrest, many survivors achieve normal kidney function (eGFR >75 mL/min/1.73 m²), particularly younger male patients. 8
Common Pitfalls to Avoid
- Avoid under-resuscitation: Inadequate fluid therapy guided only by conventional monitoring increases AKI risk compared to hemodynamic-guided approaches. 4
- Avoid nephrotoxic medication exposure: This is a modifiable risk factor that requires vigilant attention in the post-arrest period. 1, 2
- Avoid delayed RRT initiation: Early consideration of RRT, particularly with fluid overload, may improve outcomes. 2, 5
- Avoid ignoring epinephrine dosing: Both total number and rate of epinephrine administration during arrest impact AKI risk and severity, suggesting potential epinephrine toxicity. 7