Acute Kidney Injury (slides 20-49)

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

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

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)


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


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


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!!!


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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