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Advanced Topics Exam 2 Acute Kidney Injury
Terms in this set (44)
Previously known as acute kidney failure or acute renal failure.
Usually develops over hours or days with progressive elevations in BUN, creatinine, & K+ w/or w/o oliguria.
Rapid loss of kidney function with progressive azotemia.
Can be reversible, but has high mortality rate.
3-4 phases (initiating/onset (1-7 days, treat here), oliguric <400/24h, diuretic-increased UOP, recovery)
1. Maintain fluid & acid base balance
2. Regulate blood pressure
3. Detoxify the blood by eliminating wastes (urea-breakdown of ammonia, uric acid, creatinine, Ca+, K+, Phos, Mg++, Nitrogen)
4. Aiding RBC formation
Build up of nitrogenous waste in the body.
Usually bilateral unless solitary kidney.
Better indicator for AKI
Influenced by age, race, gender, & muscle mass
Influenced by catabolic, fever, steroid, GI bleeding, protein intake
May reach 180-200 mg/dL before symptoms begin in AKI.
Most accurate indicator.
Factors external to kidney that reduce renal flow such as hypovolemia, decreased CO, that can lead to decreased glomerular perfusion & filtration.
Oliguric phase has high SG & low Na+
Conditions that cause direct damage to the renal tissue, resulting in impaired neprhon function. Acute tubular necrosis accounts for most cases.
Can occur from nephrotoxic substances such as certain antibiotics, sickle cell, rhabdomyolosis, aminoglycosides ("mycin"s), NSAIDs, chemo, CT dye, arteriograms (emboli), antifreeze.
Oliguric phase has low SG & high Na+
Mechanical obstruction of urinary outflow such as BPH, prostate cancer, calculi, trauma, and tumors.
If relieved w/in 48 hours, complete recovery of GFR can be recovered.
UOP < 400 ml/day
UOP <100 ml/day or essentially no UOP
Low BP, sepsis, blockage (tumor, clot), decreased fluid/blood volume
For low BP
Give fluid & vasopressor
Acute Tubular Necrosis
Causes cellular death
Damage can come fro ischemia, drugs, etc.
Damaged cells slough off and clog up nephrons which leads to increased pressure.
Decreased renal flow, decreased glomerular capillary pressure, decreased glomerular filtration rate.
All leads to decreased UOP & increased BUN
Decreased GFR, build up of waste products, decreased or absent UOP
Get peak & trough to prevent kidney damage.
End stage kidney disease
Agitation or lethargy
Decrease bowel sounds
Tall T waves
Kidneys cannot synthesie ammonium which is needed for H+ excretion.
Kidney can't excrete acid products
Hematologic disorders such as decreased RBCs
Na+ (up, down, or normal)
Can't reabsorb bicarb
Hematologic effects of AKI
Anemia d/t decreased erythropoietin, loss of RBCs, altered WBCs, and platelet abnormalities.
Immunodeficiencies leading to infection which is most common cause of death with AKI.
Meticulous aseptic technique & electrolyte monitoring.
Sodium effects of AKI
Urinary excretion may increase d/t damaged tubules that cannot conserve.
May be normal or low.
Potassium effects of AKI
Increased because kidneys can't excrete it.
More is released from cells if there is tissue trauma.
If acidotic, it increases due to H+ into cells.
Cardiac muscle very intolerant of acute increase.
Nephrons not functioning properly.
Urine output begins to increase.
Anywhere from 1-5 L per day.
Risk for hypotension from hypovolemia.
Monitor for hyponatremia, hypokalemia, hypovolemia.
May last 1-3 weeks.
May still be making urine, but it may not have all the waste products it should.
GFR begins to increase.
BUN & creatinine begin to decrease.
Improvements in the first 1-2 weeks, but may last for 1 year.
If it does not take place, client progresses to CKD.
Looks at kidney to see if there is something pressing on it & to measure kidney size.
Used to assess blood flow
Used to look for tumors & obstructions.
Avoid contrast to prevent further damage.
Looking for cells, casts, & crystals.
Prerenal: no cells, but possible hyaline casts. Na+<10. High specific gravity.
Intrarenal: Low SG.
Postrenal: may see stones, sediment, & clots.
ATN: coarse, muddly brown casts. Na+ >40 due to impaired reabsorption.
1-2 mcg/kg/min to increase perfusion to kidney.
Treatment for hyperkalemia
D50W & insulin to drive back into cells.
Sodium bicarb to shift back into cells.
Calcium gluconate raises the excitatioin threshold (protective)
Kayexlate (exchanges Na for K): give orally or rectally
Restrictions & no salt substitutes.
Restrictions for AKI
Na (to prevent edema, HTN, & HF), possibly K & phos.,
Continuous renal replacement therapy (CRRT)
Dialysis modality used to treat critically ill, hospitalized pts in intensive care unit who develop AKI.
More gradual solute removal than hemodialysis.
Better tolerated in acutely ill.
Can use arterial & venous access or venous to venous
Maintained by CCU nurse
Hourly hemodynamic status, I/O, volume.
1:1 pt to nurse ratio.
Indications for dialysis
Fluid overload w/pulmonary edema.
systolic BP + 2x diastolic BP/3
Leading cause of death in AKI
Most common cause of ARF
Volume depletion leading to prerenal azotemia.
Access to big vessels (AV fistulas, grafts, ports, shunts)
Auscultate graft for bruit & fell for thrill.
Cleans blood through diffusion & ultrafiltration
Takes 3-4 hours
Monitor for hypotension
No BP on the same side
Usually hold med before, especially BP lowering meds.
Ecchymosis over flank
Peri-umbilical bruising indicative of retroperitoneal hemorrhage due to renal trauma
Can come from cadaver such as one with anoxic brain damage due to MVA, GSW
Postop immunosuppressive therapy to prevent rejection of the transplanted organ & maintain immunity to prevent infection.
Nashville has 3 centers: Vanderbilt, Centennial, & St. Thomas
CI: disseminated malignancies, refractory or untreated cardiac disease, chronic resp. failure, extensive vascular disease, chronic infections, unresolved psychosocial problems such as noncompliance, alcoholism, drug addiction.
Will go in below existing failed kidney.
Pt. may diurese so check BP to make sure new kidney is getting blood flow & O2.
Immunosuppressive agents for renal transplants
Calcineurin inhibitors: prevent cell mediated attacks
Prophylactic antibiotics & antifungals (acyclovir)
Occurs minutes to hours after transplantation.
Antibody medicated humoral rejection.
No treatment except removal of organ.
Uncommon d/t crossmatching
Most commonly occurs days to months after transplantation.
T-cytotoxic lymphocytes will attack the transplant graft..
Usually treatable with additional immunosuppressive therapy.
Occurs over months to years & is irreversible.
Can be difficult to manage.
Changing immunosuppression therapy may sometimes help.
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