AKI Flashcards
What is AKI?
Rapid loss of renal function
What do you see during AKI?
Increase in serum creatinine 0.3mg/dl or more in 48 hours,
decreased urine volume less than 0.5ml/kg/hr for 6 hours
Best indicator of kidney function
Glomerular filtration rate which is mirrored in the creatinine clearance. Normal GFR is 125/ml. It decreases as one ages.
Difference between AKI and CKD
AKI happens over a short period of time, within 48 hours whereas CKD happens over 3 months time.
AKI affects most body systems but CKD affects all body systems.
Metabolic complications of AKI
metabolic acidosis(The kidney cannot get rid of the hydrogen ions)
Hyperlipidemia(due to Insulin resistance), when they are in oliguric phase they experience hyperkalemia.
During Diuretic phase, they experience hypokalemia. They experience hyponatremia,
CKD
s/s:hyperkalemia, hypernatremia
AKI and CKD experience hypocalcemia due to the phosphate increases. The kidney cannot eliminate phosphate. They both can have gout. They both have carbohydrate resistance
Neurologic complication
Uremia syndrome(BUN is very elevated, patient is symptomatic from the high BUN), irritability, weakness, confusion, asterixis,seizure,slurred speech,fatigue,headache,sleep disturbances,hypertensive retinopathy.
Cardiovascular complication
HTN,heart failure(prevention-take anti-hypertensive medications and treat DM),
Arterial heart disease,Pericarditis(uremia is irritating to serrous membranes), pericardial effusion, tamponade, pulmonary embolism, anasarca, and peripheral edema, pulmonary edema.
Anybody with high creatinine is at risk for MI.
GI complications
VAN, decreased peristalsis,ulcer formation and bleeding, uremic fetor, gastritis, malnutrition. They can’t tolerate enteral nutrition.
They have special renal nutrition.
Renal and Immune complication
With CKD and ESKD(stage 5 CKD): pneumonia and sepsis, uremia can burst RBC-anemia, CKD- kidney can no longer produce erythropoietin hence low RBC, the CKD will have chronic anemia.
Uremia makes the thrombocytes not function well, hence they are at high risk for bleeding.
Uremia makes WBC not to be effective hence they can develop sepsis
Causes of AKI
Prerenal causes(due to low perfusion like shock) Intrarenal causes(injury intrinsic in the kidney like drug, contrast medium, NSAIDS,) Postrenal causes(due to obstruction like BPH, renal calculi, neurogenic bladder)
To prevent AKI
question patient on nephrotoxic medications such as gentamycin, avoid dehydration(if they are not oliguric), look at the urine characteristics, monitor I&O,evaluate fluid status, monitor peak and trough level, daily weights, renal function studies, report urinary output less than 0.5ml/kg/hr that persists for more than 2 hours, make sure people with renal insuffiency are pretreated with fluid before contrast dye, 1L NS with sodium bicarb or acetylsteine, then give furosemide or mannitol to flush out the kidney.
Phases of AKI
Onset
Oliguric- s/s-low urinary output, sediments in the urine, protein in the urine(if cause is intrarenal),
Diuresis
Recovery
Oliguric Phase
Monitor for symptoms of fluid overload like crackles, S3, dependent edema, anasarca, low O2, increased CVP, increased wedge, confusion, tachpnea. They will have signs and symptoms of cardiogenic pulmonary edema,
Typical fluid restriction for kidney disease is 500-600 + urinary output for 24 hours before.
For example a patient has 1500ml output. Tomorrow he can get 2000-2100ml of fluid.
Diet during Oliguric phase (diet similar to CKD)
Low phosphate low potassium and low protein