Acute Kidney Injury (AKI)

kidneys receive __% of cardiac output
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kidneys receive __% of cardiac output
20-25%
normal GFR
80-125 ml/min
What two hormones play a role in water reabsorption?
aldosterone and ADH
About how much of the filtrate is reasborbed
99%
AKI
sudden decline in kidney function causing disturbances in fluid,electrolyte and acid base balances because of a loss in small solute clearance and decreased GFR
Cardinal features of AKI
azotemia
olguria
Azotemia
increased in BUN and serum Cr.
accumulation of nitrogenous wastes
Olguira
UOP less than 0.5ml/kg/hr
KDIGO
Clinical practice guidelines for AKI
KDIGO pt 2
Stage 1
Stage 2
Stage 3
FYI•The Acute Kidney Injury Network (AKIN) identifies three stages that correspond to the RIFLE system (risk, injury, failure) but assesses changes over 48 hours.The RIFLE criteria is used to assessthe progression of AKIAKI causescan be:Prerenal Intrarenal PostrenalPrerenal AKI-results from diminished blood flow/inteference with renal perfusion -most cause are related to impairment of autoregulation and GFR -typically can reverse by treating the cause or will progress to intrarenalMost common cause of prerenal AKISEPSISIntrarenal AKI-directly effecting the functioning kidneys -glomerualr,vascular or hematological issuesMost common cause of intrarenal AKIAcute tubular necrosis (ATN)ATN occurs as a result ofprolonged ischemia ,exposure to nephrotoxic meds or bothPostrenal AKI-results from obstruction of flow of urine -leads to a decrease GFR -reverses when obstruction is removedThe term used to described accumulation of nitrogeous wasteazotemiaA treatment for postrenal AKI isureteral stent placementInitiation Phase-from the time precpitating event to signs of decreaed renal perfusion -last from several hours to 2 days -potentially reversible if caught earlyWhat actions and treatments can reverse AKI in the intitiation phase?aggressive treatment of shockMaintainence Phase-Urine volume is at its lowest point -pt may be olguric/anuric -requires renal replacement therapyRecovery Phase-renal tissue recovers and repairs itself -can last 4-6 months -residual impairment of GFRPredisposing factorsHTN,DM,immunological disease,heridatary disorders,hypotensive episodes,exposure ot nephrotoxic agentsClinical presentation of AKI-presentation varies based on etiology -VS and temp may be altered -BP changes depend on etiologyPrerenal ,intrarenal and post renal presentationbased on kidney function,UOP and labsPhysical findings of AKISigns of uremia (malaise, fatigue, disorientation, and drowsiness) Color and texture of skin Bruising, petechiae, and edema Current and admission body weight and intake and output Dehydration/fluid overloadLab test for AKI-Serum cr.-more specific to renal injury -serum BUN--not a reliable indicator has many influences -BUN Cr ratio- normal 10:1 to 20:1Normal serum Cr0.6-1.2 Normal BUN 7-20urine creatinine clearanceprovides an estimate of GFR -normal 84-138Lab findings-can help determine what stage of AKI the are in Specific gravity Urine osmolality Urine sodium Microscopic examination BUN/Creatinine ratio FENa (the factional excretion of sodium)Urine test for AKIurine electtolyes,specifc gravity and osmalityWhich intervention is most important in assessing fluid balance in the patient with AKI?daily weightNursing Diagnosis-Assesment status of fluid volume status is the most important -Excess volume can be an issue:daily weight and I &OsNursing Diagnosis pt 2-fluid volume imbalance -electrolyte imbalance -risk for infection (antibiotics:monitor peak and trough levels) -imbalanced nutrition,anxiety,knowledge deficitWhat agents are nephrotoxic?aminoglycosides ,NSAIDS,and contrast agents (not a drug)Fluid and Electolyte Imbalanceshyperkalemia hyponatremia hypocalcemia hyperphosphatemia hypermagnemiaMedical management-early recognition -fluid/volume replacement -caution in pts with cardiac disorders -Treatment: typically fluid and inotropesPost renal managementalleviate the obstruction using a catheter or stentATN management-medications -specialized diets -management of fluid and electrolyte imbalance -dialysis or CRRTDiureticsmay cause more harm than good controversialDrug therapy-dopamine-controversial -ACETYLCYSTEINE- prevent kidney damage from contrast dye -epotein alfa-treat anemiaDietary Management-Higher-than-normal basal requirement -Provide adequate energy, protein, and micronutrients -25 to 35 kcal/kg of ideal body weight per day _Restricted Protein Sodium Potassium Fluid intake (output + 600-1000 mL)Hyperkalemiacommon in AKI due to decreased GFRTreating hyperkalemia•Calcium gluconate, given IV over 5 minutes;prevent and tx cardiac toxicity caused by hyperkalemia during cardiac resuscitation •Albuterol -shifts potassium into the intracellular space •Sodium bicarbonate, severe acidosis with pH < 7.2 or serum HCO3 < 15mEq/L; shifts K temporarily from the extracellular fluid to the intracellular fluid •Insulin shifts K temporarily into the extracellular fluid;dextrose prevents hypoglycemia •Lasix increases renal excretion of potassium •Kayexalate increase fecal excretion of potassium by exchanging sodium ions for potassium ions -Dextrose treats hypoglycemiaHypoatremiarelated to fluid overload treat with fluid restriction,specifically of free water intakeMetabolic acidosistreatment based on severity may need IV bicarb monitor calcium levelsrenal replacement therapy-life saving treatment -primary treatment for AKI pts -includes: hemodialysis, peritoneal dialysis, CRRTDialysistwo principles diffusion and ultrafiltrationDialysis indications-Fluid overload -Electrolyte imbalances hyperkalemia -Acid base disturbances metabolic acidosis -Uremia -fluid managementpercutaneous catheters-temporary -internal jugular preferred siteVascular access- Arteriovenous (AV) fistula or graft for long-term permanent accessHemodialysisUsually done at the bedside in the ICU Pre- and postdialysis labs and weight Monitor for complications -volume depletion -Dysrhythmias -Hypoxemia -Disequilibrium syndrome -Vascular access infections -Hypotension most common as a result of hypovelmiaCRRT-used in pts too unstable for hemodialysis Advantages -More gradual solute removal -Flexible fluid administration -Minimal heparin -Can be done by staff nurses at the bedside Disadvantages -Bed rest -One-to-one nursing careCRRT types1. Slow continuous ultrafiltration (SCUF) fluid removal 2. Continuous venovenous hemofiltration (CVVH) fluid and some uremic waste product removal 3. Continuous venonvenous hemodialysis (CVVHD) fluid and maximal uremic waste removal 4. Continuous venovenous hemodiafiltration (CVVHDF) maximal and uremic waste removal; the closest to native kidney functionPeritoneal Dialysis-Removal of solutes and fluids using the peritoneal membrane as a filter -Rarely used in the critical care setting because it is less efficient -High risk of peritonitis -usually only used if pt already has itPrerenal presentationmost distinct factor is something that has to do a diminish in perfusionIntrarenal causesthe most important factor is something causes direct trauma to the renal tissuePostrenal causesthe most important factor is that there is an obstruction of blood flow