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Acute Kidney Injury (slides 20-49)

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olanjones's version from 2017-04-05 18:54

General Etiologies

Question Answer
Characterized by a rapid loss of kidney function causing a rise in ______ ______ and/or a reduction in _____ ________.serum creatinine; urine output
AKI is not good, it is reversible, if chronic....high mortality; dialysis, eventually transplantation
Usually develops over hours or days with progressive ↑in serum _____, _______, ______.BUN; creatinine; K (azotemia)
May have normal UO (better prognosis) or may have oliguria < ___ cc/day400 = ↑ mortality rate
What is the major cause of death? What can you do as a nurse, knowing this this a major risk?Infection: motivate patient, vaccinations, jump on infections **room with non-infectious roommates (this is usually nurses' job!)
How does HTN lead to AKI?prolonged HTN (↓ perfusion)
How does hypovolemia lead to AKI?↓ cardiac output and ↓ perfusion
Acute Tubular Necrosis (most common intrarenal) is the result of (3)ischemia, nephrotoxins or sepsis ; can be differentiated in urine if "casts" are present (WBCs, RBCs, kidney cells, proteins, fats)
What are some risk factors for AKI?IDDM or NIDDM is 40%; HTN; hypovolemia; prolonged exposure to drugs excreted by kidney (acetaminophen)
Nephrotoxic drugsACE inhibitors; aminoglycosides; cephalosporins; sulfonamides; tetracycline; vancomycin; immunosuppressants
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Pre, Intra, Post-renal

Question Answer
Most common 55-60% of AKI'spre-renal
How do pre-renal risk factors cause renal failure ?↓ circulation → leads to a ↓ glomerular perfusion → ↓GFR
How is the oliguria in prerenal different from the oliguria intrarenal?pre is d/t lack of blood volume (no tissue damage) whereas intra is due to damaged kidney parenchyma
Which is MOST treatable of the three?Post-renal
Post-renalOBSTRUCTION: blockage and backflow
Pre-renal EXTERNAL: ↓ in blood flow
Intra-renalDAMAGE: renal tissue damage → ischemia
35-40% of all casesintra-renal
Examples of events that can alter pre-renal flowshock; hemorrhage/burns; sepsis; anaphylaxsis
Examples of intrarenal disordersAcute tubular necrosis (90% if all intrarenal); Nephrotoxins ;Acute glomerulonephritis; acute pyelonephritis
Post renal is < _________% of all cases; examples?<5%; stones, strictures, tumors
Complicated ATN: Ischemia pathoIschemia→basement membrane disruptions→tubular destruction→(hypovolemia & ↓ renal blood flow)→peripheral constriction →↓ blood flow→↓GFR→tubular dysfunction→oliguria
Damaged tubules leads to ______ cells and ____ which caused a reduce in _________.necrotic; debris; filtration (plugged up)
What are the 4 phases of progression AKI ?Initiating phase; oliguric; diuretic; recovery
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Phases of AKI progression

Question Answer
Initiating phaseinsult until s/s are noticed: can be hours to days
Oliguric phase is <___cc/day (most common 1st sign) occurs in _________%400; 50%
If the cause is ischemia, oliguria can occur within __hours and can last up to ______ or ______.24; weeks or months (The longer it lasts, the worst the prognosis)
Pre-renal oliguric phase process: ↓ BV→ auto-regulatory attempts to preserve blood to vital organs→vasoconstriction & Na/water retention
Pre-renal oliguric phase UA findings (What is low/high?)Low sodium & High Specific Gravity
Intra-renal oliguric phase process:Protein, blood, etc. pass through damaged glomeruli via "holes" in the filter
Intra-renal oliguric phase UA findingshigh Na, Plasma SG=1.010; WBC's, RBC's & necrotic sloughing of kidney cells (casts)
Fluid Volume changes: oliguric phase UO↓'s = fluid retention (edema, HTN, fluid overload, jugular vein distention, edema, HF, pericardial/pleural effusions)
Metabolic changes: oliguric phasekidneys can no longer synthesize NH3 or excrete acid products d/t HCO3- depleted → metabolic acidosis (Kussmaul respirations)
Sodium Balance changes: oliguric phaseDamaged tubules can't conserve sodium=> ↑ in urinary Na loss => low serum sodium (do not ↑ intake of Na, can lead to HTN, volume expansion; could lead to hyponatremia)
Hematologic Disorders: oliguric phasemultifactoral; leukocytosis is usually present; thrombocytopenia; systemic lupus erythematosus
Waste Product Accumulation: oliguric phase↑ levels of serum creatinine & BUN (can't excrete it out)
Neurologic Disorders: oliguric phasenitrogen accumulates in brain or other nervous tissue (flappy tremor when wrist extends; fatigue; stupor; can't concentrate)
Diuretic Phase processkidneys can now excrete, but can't concentrate (output increases)
In which phase will sodium, potassium and fluid be lost, why?Diuretic: osmotic diuresis d/t high concentration of filtrate & inability of tubules to concentrate the urine
Complications & things to watch for in diuretic phase?Hypotension; hypovolemia; monitor for hyponatremia, hypokalemia & dehydration
What happens to the creatinine clearance & serum creatinine/ BUN in diuretic phase?creatinine clearance low; serum BUN/creatinine high
S/S hyponatremialethargy, h/a, confusion, increased BP (Fluid Retention)
S/S hypokalemiamuscle weakness, constipation, shallow respiration, irritability, arrhythmias
Recovery PhaseGFR ↑'s-BUN/creatinine plateau then decreases (12m to full recovery, depends on overall health, age, if not = ESRF)
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Miscellaneous

Question Answer
Normally, what does bicarbonate do?goes out & collects acidic hydrogen ions in plasma
Normally, Nitrogenis a by product of protein metabolism & the kidney collects it via NH4 (ammonium) ion
Kidney collects ____ ions (via bicarbonate ion) & nitrogen (via ammonium ion) to produce ________, which is then excreted.H; NH3 (ammonia)
If kidneys can't produce & excrete ammonia, there is a systemic build up of both Nitrogen & H which results inmetabolic acidosis & azotemia
Diagnosing AKI via good history of potential pre-renal problems likedehydration, blood loss, heart disease (anything REDUCING blood flow to kidneys)
Diagnosing AKI via good hx of potential intra-renal problems likenephrotoxic drugs, prolonged HTN or hypovolemia
24 hour urine collection: nurse responsiblitymost need preservatives, nurse must be sure the container has the preservatives it needs.
Precautions in 24 hour urine collectionNo TP in specimen; poo before peeing (void & flush 1st pee of the day); adequate fluid intake; avoid vigorous exercise
Collaborative Care primary goalCardiac Output-MUST PERFUSE THE KIDNEYS
If there is adequate perfusion aka good CO, what else should be watched for?Fluid overload (loop diuretics are ok, watch fluids & sodium)
Most common cause of death with AKIINFECTION so maintain asepsis
CC PotassiumDangerous: kayexalate or dialysis will help if hyperkalemic
If renal failure is a result of a traumatic event (crushing or burn), there is a much higher risk for increased ____ and __________________.BUN and Potassium
Indications for dialysis (3)↑ fluid volume overload (respiratory compromise); ↑ K with EKG changes; Metabolic acidosis → <15 bicarbonate;
Nutrition is a huge challenge. What does adequate nutrition help prevent?Catabolism (increased K and N; destructive metabolism)
Nutrition: % of calories you want from fat30-40%; you always want carbs
Dietary Management also includesfluid restriction; K restriction; high carbs; low protein; calcium supplement; Vit D supplements; phosphate binders with meals (TUMS)
Gerontologic ConsiderationsNot so good d/t fewer functioning cells to start with = less able to handle fluid overload = more chance of underlying condition = less room for error
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CRRT

Question Answer
What it doesRemoves uremic toxins & fluids, slowly and continuously adjusts acid-base status & electrolytes in a hemodynamically unstable patient
ContraindicationsLife-threatening manifestations of uremia (hyperkalemia, pericarditis) that require rapid resolution (CRRT can be used in conjunction with HD)
Vascular accessDouble-lumen catheter placed in the jugular or femoral vein (a blood pump is used to propel the blood through the circuit)
What is ultrafiltrateplasma water & non-protein solutes removed from the blood via the hollow-fiber hemofilter (the remaining fluid continues through the filter and returns to the pt)
What should ultrafiltrate look likeClear yellow; if it becomes bloody/blood tinged, rupture in filter membrane should be suspected, & suspended treatment immediately to prevent blood loss & infection
Ultrafiltration rate0 to 500 mL/hr
What is used to prevent blood clotting during CRRTHeparin (as a bolus at the initiation of CRRT or through the heparin infusion port before the hemofilter)
Is a dialysate usedNo, solute is removed via convection, osmosis, and diffusion
How does it differ from HD-Continuous rather than intermittent; Large volumes (200-800 mL) of fluid can be removed over days (24 hrs-more than 2 weeks) versus hours (3-4 hrs)
-It causes less hemodynamic instability (e.g., hypotension)
-Requires monitoring by a trained ICU nurse (rather than HD nurse)
-Does not require complicated HD equipment (blood pump is needed for venovenous therapies)
How long can a pt be on CRRT30-40 days - hemofilter should be changed every 24-48 hrs because of loss of filtration efficiency or potential for clotting
NI-Obtain weights, Monitor & document lab values DAILY for adequate F&E balance
-HOURLY I&O, VS, & hemodynamic status
Should there be a change in MAP or CO when pt is on CRRTVery little; CVP & pulm artery pressure are expected
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Dialysis

Question Answer
AEIOUAcid-base problems, Electrolyte problems, Intoxications, Overload of fluids, Uremic symptoms
Principles of dialysis*Diffusion (movement of solutes from area of ↑concentration to area of ↓concentration)
*Osmosis (movement of fluid from ↓concentration to ↑concentration)
*Ultrafiltration (water & fluid removal by increasing the osmolality of the dialysate)
CUP OF TEA principleThe longer the stronger - relates to dialysis; the longer dialysis is performed the more solutes will be shifted
Disequilibrium syndrome Initial nausea/HA &/or jerk/twitch (from mild cerebral edema -> rapid solute loss from extracellular fluid), Can be minimized by dialyzing in smaller bites
Peritoneal dialysisPerformed through abd wall (into cavity), Two types:
*Automated (machine cycles while pt sleeps, leave fluid in during the day)
*Continuous ambulatory (done manually, can be disconnected, variable sched)
How long does it take PD catheter to seal?about 1 to 2 weeks
PD benefits-More independence (can be done at home), fewer dietary restrictions
-Avoids venous access problems (e.g. older pts w/ CVD)
-Diabetics (better BP control, gradual fluid shift, insulin put in dialysate, no heparin)
PD complications-Hyperglycemia or hyperlipidemia, Protein loss
-Peritonitis (s/s: fever, pain, drainage cloudy, hypoactive BS, N&V)
-Infection (from: poor hand washing, contaminated dialysate, poor catheter care)
-Inflammation (rxn to dialysate, wrong concentration of dialysate)
HemodialysisBlood removed and run through a dialyzer membrane then returned to the body (done when BUN=80, Creatinine=8, maybe K+=6.0 w/ EKG changes?
HD accessBest - Fistulas (anastomosis of artery & vein), less likely to clot, must have good BV
Graft (synthetic), more easily infected & more likely to clot, Site must be protected (no BP/IV/venipuncture)
Rare – Shunts (external), not used much anymore
HD benefits-Rapid fluid removal, rapid removal of urea & creatinine, effective K+ removal
-Less protein loss, lowering of triglycerides
-Home dialysis possible
HD complications-Vascular access problems, Heparin used
-Dietary/fluid restrictions
-Requires extensive equipment/specially trained people, Is time consuming (3xs/wk-4hrs @ a time)
ND for dialysisRisk for infection (high), Risk for impaired circulation, Fluid volume excess, Pain r/t phosphate overload in bones, Activity intolerance secondary to anemia
Continuous Renal Replacement Tx?I know what the fuck that is now!!!
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Transplants

Question Answer
Why is perfect compatibility not an issue?Can remove incompatible blood from donor kidney
Immunosuppressive drugs are used (but are usually responsible for most long-tern problems)
Signs of rejectionFever, Weight gain, Decreased UO, Increased BP (hour by hour monitoring UO, then cc by cc)
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