acute kidney injury in critical care

NRS 400

What is AKI?

A sudden-onset and usually reversible decrease in kidney function.

What are the 3 types of AKI?

Prerenal, intrarenal, and postrenal.

What is prerenal AKI?

Reduced blood flow to the kidneys causing decreased GFR without structural kidney damage.

What is intrarenal AKI?

Damage to the functional part of the kidney.

What is postrenal AKI?

A urinary-system problem below the kidney that prevents urine from draining.

What is CKD?

A progressive, irreversible loss of kidney function that alters waste/fluid excretion, electrolytes, hormone synthesis, and metabolism.

What eGFR value is listed in the CKD review?

≥90.

What is hemodialysis (HD)?

A treatment in which a hemodialyzer filters waste from blood while washing the blood with dialysate.

What can guide dialysis decisions?

Urea reduction ratio plus hyperkalemia, acidosis, hyperphosphatemia, and the amount of fluid removal.

What should be monitored during HD?

BP/hemodynamic stability and fluids/electrolytes.

What HD access is listed?

AV fistula/graft or hemodialysis central venous catheter.

Is AKI usually isolated in critically ill patients?

No. It usually develops as a complication of another illness or injury.

Which organ often first shows poor perfusion?

The kidneys.

What can AKI signal in critical illness?

Worsening stages of shock from prolonged hypotension.

What shock types are associated with AKI?

Septic, cardiogenic, and hemorrhagic shock.

What other injuries/conditions are listed with AKI?

Burns and trauma.

What medication-related cause of AKI is listed?

Nephrotoxic medications.

What contrast-related cause of AKI is listed?

Contrast dye.

What muscle-related cause of AKI is listed?

Rhabdomyolysis.

What is the key shock-AKI relationship?

Shock → poor perfusion → kidney injury → worsening shock.

What urine-output change is listed with AKI?

Oliguria to anuria.

What fluid-retention findings are listed with AKI?

JVD, peripheral edema, and anasarca.

What electrolyte abnormality causes peaked T-waves in the lecture?

Hyperkalemia.

What other electrolyte abnormalities are listed with AKI?

Hypocalcemia, hyperphosphatemia, and hyponatremia.

What acid-base abnormality is listed with AKI?

Metabolic acidosis.

What happens to pH in AKI metabolic acidosis?

pH decreases.

What happens to HCO3− in AKI metabolic acidosis?

HCO3− decreases.

What happens to BUN in AKI?

BUN increases.

What happens to creatinine in AKI?

Creatinine increases.

What happens to GFR in AKI?

GFR decreases.

What is the AKI shock cascade?

Shock → poor renal perfusion → acute tubular injury → fluid retention → acidosis → hyperkalemia → pulmonary edema/dysrhythmias → worsening shock → death.

What can fluid retention in AKI lead to?

Pulmonary edema and worsening shock.

What are the 5 priority goals of AKI management?

Restore perfusion; prevent further injury; manage fluid balance; correct electrolyte imbalances; support other organs.

Why may some AKI patients need fluids?

Fluid resuscitation may be needed to promote organ perfusion during shock.

What can excessive fluid balance cause?

Fluid overload, worsening tissue edema, and impaired oxygenation.

What may be required for volume overload?

Diuretic therapy or dialysis therapy.

Why is hyperkalemia dangerous in AKI?

Impaired potassium excretion can cause life-threatening hyperkalemia.

What ECG finding is associated with hyperkalemia?

Peaked T-waves.

What cardiac complication is associated with hyperkalemia?

Dysrhythmia risk.

What is the D in the hyperkalemia mnemonic?

Dextrose.

What is the I in the hyperkalemia mnemonic?

Insulin.

What is the C in the hyperkalemia mnemonic?

Calcium gluconate or calcium chloride.

What is the K in the hyperkalemia mnemonic?

Kayexalate.

What other potassium-removal methods are listed?

Diuretics and renal replacement therapy.

What complications can occur if the kidneys do not recover quickly?

Refractory hyperkalemia, severe acidosis, fluid overload, and inability to clear toxins.

Why can intermittent HD be dangerous in ICU patients?

It removes larger fluid amounts in a shorter time and can cause hemodynamic instability.

How can HD-related hypotension affect an ICU patient?

It can worsen organ perfusion.

What is CRRT?

Continuous Renal Replacement Therapy.

Why is CRRT important in critical care?

It provides blood purification for critically ill patients with AKI and is useful in shock.

What happens when decreased perfusion causes the kidneys to stop functioning?

Toxins and fluid accumulate, causing systemic alterations.

What systemic problems from kidney failure are listed?

Acid/base imbalances, fluid overload, and encephalopathy.

How is CRRT tolerated compared with intermittent HD?

CRRT is gradual and continuous, so it is more easily tolerated.

What are complications of CRRT?

Catheter-related complications, hemorrhage, infection, pneumothorax, and air embolism.

What molecules are removed by HD in the comparison table?

Low molecular weight molecules.

What molecules are removed by CRRT?

Small and middle molecules.

What are listed uses of HD?

CKD inpatient/outpatient, AKI in hemodynamically stable patients, and hyperkalemia.

What patients are listed for CRRT?

Critically ill patients with AKI who are hemodynamically unstable.

What access is listed for HD?

Temporary HD line or AV fistula/graft.

What access is listed for CRRT?

Temporary HD line.

How long does HD run for AKI/inpatients?

3–4 hours.

How often does HD run for CKD?

3–4 times/week.

How long does CRRT run?

24 hours/day.

What can happen during or immediately after intermittent HD?

Hemodynamic instability and hypotension.

What type of shifts can occur with intermittent HD?

Large volume and electrolyte shifts in a short period.

What neurologic complication is listed with intermittent HD?

Cerebral edema.

Are anticoagulants needed during the HD run according to the table?

No.

Why is CRRT used for hemodynamically unstable patients?

They may not tolerate large/quick volume shifts.

How does CRRT remove fluid and toxins?

Continuously at smaller/slower rates.

Why does CRRT need anticoagulation?

To keep the filter from clotting.

What are typical CRRT patients?

Septic shock, ARDS with fluid overload, cardiogenic shock, severe burns/trauma, and liver failure.

What are the nursing considerations for CRRT?

Hourly I/Os, hemodynamic monitoring, electrolyte monitoring, access assessment, anticoagulation, and filter-clotting monitoring.

How often should I/Os be monitored during CRRT?

Hourly.

What should be monitored hemodynamically during CRRT?

Hemodynamic status.

What lab category should be monitored during CRRT?

Electrolytes.

What access-related nursing assessment is required with CRRT?

Access assessment.

What anticoagulation issue should be watched during CRRT?

Filter clotting.

A patient in septic shock develops oliguria, rising BUN/creatinine, hyperkalemia, and metabolic acidosis. What does the lecture point toward?

AKI.

A patient in shock develops AKI. What cycle does the lecture emphasize?

Poor renal perfusion causes kidney injury, which can worsen shock.

An AKI patient has JVD, edema, and anasarca. What problem is suggested?

Fluid retention/fluid overload.

An AKI patient has peaked T-waves. What should the nurse recognize?

Hyperkalemia.

An AKI patient has dangerous hyperkalemia. Which medication is included to protect against dysrhythmia?

Calcium gluconate or calcium chloride.

Which two medications are paired in the D-I portion of hyperkalemia treatment?

Dextrose and insulin.

What additional methods can remove potassium?

Diuretics and renal replacement therapy.

An AKI patient has refractory hyperkalemia, severe acidosis, fluid overload, and inability to clear toxins. What may be needed?

Renal replacement therapy.

A shock patient needs fluid resuscitation. Why?

To promote organ perfusion.

A patient becomes fluid overloaded after treatment. What can this worsen?

Tissue edema and oxygenation.

A hemodynamically unstable ICU patient cannot tolerate rapid fluid removal. Which therapy is emphasized?

CRRT.

Why would CRRT be preferred over intermittent HD in an unstable patient?

It provides smaller/slower continuous fluid and toxin removal and is more easily tolerated.

A patient develops hypotension during intermittent HD. Why is this concerning?

Hypotension can worsen organ perfusion.

A patient on CRRT develops bleeding. What complication is listed?

Hemorrhage.

A patient on CRRT develops a catheter problem. What complication category is listed?

Catheter-related complication.

A patient on CRRT develops infection. Is infection a listed complication?

Yes.

A patient on CRRT develops a pneumothorax. Is this a listed complication?

Yes.

A patient on CRRT develops an air embolism. Is this a listed complication?

Yes.

What does the page 9 AKI cascade show?

Shock → poor renal perfusion → acute tubular injury → fluid retention → acidosis → hyperkalemia → pulmonary edema/dysrhythmias → worsening shock → death.

What does the page 10 management slide identify as priority goals?

Restore perfusion, prevent further injury, manage fluid balance, correct electrolyte imbalances, and support other organs.

What does the page 16 HD vs CRRT table emphasize?

HD involves larger/quick shifts and can cause hypotension; CRRT is continuous, slower, and intended for hemodynamically unstable patients.

What is the major duration difference between HD and CRRT?

HD is 3–4 hours for AKI/inpatients, while CRRT runs 24 hours/day.

What is the major anticoagulation difference in the table?

Anticoagulants are not needed during the HD run; CRRT needs anticoagulation to prevent filter clotting.

What is the major access difference in the table?

HD may use a temporary HD line or AV fistula/graft; CRRT uses a temporary HD line.