Acute Kidney Injury (slides 20-49)

cdunbar4's version from 2016-11-02 22:19

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 respirations, irritability, arythmias
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

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