Renal unit- AKI, Rhabdo, dialysis Flashcards
functions of kidney
A WET BED
A-acid-base balance
W-Water removal
E-erythropoiesis production
T- toxin, medication, metabolic waste removal
B- Blood pressure regulation
E-electrolyte balance + osmolality
D- vitamin D activation
What is AKI?
sudden decrease in kidney function (changes take place within few hours to few days)
characterized by decrease urine output, elevated BUN and Creatinine
Types of AKI: Prerenal (define + causes)
Lack of blood flow/pressure to the kidneys that decreases kidney function
Can turn into intrinsic kidney injury if not treated promptly
caused by absolute volume loss (loss from the body; hemorrhage, dehydration), relative volume loss (vasodilation, decreased cardiac output; hypovolemic = shock), occlusion (thromboembolism), medications that alter perfusion or are nephrotoxic (ACEIs, ARBs, cyclosporins, contrast agents, amphotericin B, aminoglycosides)
types of AKI: prerenal- decreased cardiac output
requires a MAP of 65mmHg or higher to adequately perfuse the kidneys
2 mechanisms that alter CO:
1) intravascular volume depletion: absolute volume loss (through the body), relative volume loss (vascular bed is increased via vasodilation), translocation of fluid (third spacing, fluid shifts into compartment like peritonitis/ascites and doesn’t get used)
2) intravascular volume depletion leads to decreased cardiac output which causes kidneys to produce vasoconstriction = decreased perfusion to kidneys bc blood shunts away and goes to more vital organs
prolonged poor perfusion to kidneys causes ischemia of renal tubules = ATN
types of AKI: post renal (define + causes)
obstruction of urine outflow from the kidneys after it leaves tubules
occurs at urethra, bladder, bilateral ureters
causes: blood clots, calculi, tumors, prostate hypertrophy or cancer, urethral strictures, diabetic neuropathy, neurogenic bladder
types of AKI: intrinsic
problems that target the kidney issue causing damage (ATN is most common cause)
ATN- necrosis of renal tubule cells
other causes: rhabdomylosis (anything that causes this), prerenal injury (anything that causes prerenal injury to lead up to it) , obstruction in renal tubules, infections, glomerulonephritis, nephrotoxic agents, hepatorenal syndrome
phases of AKI
prodromal/initiation phase: injury occurred, urine output normal or slightly decreased, increase in BUN + creatinine
Oliguric phase: lasts 1-2 weeks, (some pt can skip this phase), low to no urine output (<400mL/day), volume overload (edema, weight gain), hyperkalemia (dysrhythmias), azotemia uremia (itching), neuro changes (confusion, delirium), metabolic acidosis (rapid RR), mild hyponatremia, hyperphosphatemia, hypocalcemia
Diuresis: lasts 1-3 weeks, voiding increases (lead to volume deficit= low BP), labs begin to normalize (may cause hypokalemia)
Recovery- some don’t make it to this step and get CKD, lasts 1-2 years, everything is normal for the most part
AKI- signs and symptoms
oliguria (low urine output)
encephalopathy causing confusion, delirium, coma (build up of toxins)
Cerebral edema causing ICP leading to ALOC (build up of fluid)
renal ischemia triggers RAAS causing HTN
Fluid volume excess can cause pulmonary/peripheral edema and HF
Accumulation of hydrogen ions can cause metabolic acidosis
Elevated ammonia levels cause gastric mucosal irritation leading to ulcerations
when kidney function decreases, so does erythropoietin (which makes RBC) = anemia
Platelet function (adhesion) decreases due to uremic molecules that build up = easily bruising
increased melanin can cause pale yellow skin
high phosphorus causes itchy and dry skin
uremic frost (uremic crystals form causing white layer on skin) occurs later in CKD
hypocalcemia occurs due to high phosphorus leading to hyperparathyroidism
decreased kidney function leads to poor vitamin D hydroxification = poor bone growth
hyperkalemia occurs from poor excretion leading to dysrhythmias
Glucose intolerance
risk for infection due to diminished leukocyte count
AKI: important lab values to consider and findings
BUN (Urea) -(end-product of protein metabolism) — elevated
Creatinine (end-product of muscle metabolism) —- elevated
Bun-to-creatinine ratio —- higher (20:1) ratio = reduced blood flow, glomerular disease, azotemia. lower (<10:1) ratio = ATN
creatinine clearance- decreased = decrease in glomerular function
What is azotemia?
accumulation of nitrogenous waste products
S+S: nausea, vomiting, hiccups, increased bleeding, confusion, irritability & twitching
skin/mouth ulcers, oliguria, hyperkalemia, metabolic acidosis, pericarditis
AKI Fluid overload (how, causes, treatment)
occurs due to stimulation of SNS and RAAS causing retention of water and sodium
can lead to HF, peripheral edema, pulmonary edema, intra abdominal HTN (pressure)
Fluid restriction, diuretics, RRT (lastly)
May give IV fluid bolus to flush out kidney wastes and try to kick start the kidneys, once pt is stable then you treat overload
AKI metabolic imbalances (how, causes, treat)
AKI patients develop hypermetabolism due to stress/injury
causes muscle breakdown, impaired amino acid transport, supression of protein synthesis, depletion of body energy reserves, insulin resistance = malnourished
parenteral/enteral feeding with amino acid intake 10-15g/day
Restrict K, mg, PO4, protein (0.8g/kg/day)
high calories with minerals and vitamins
AKI electrolyte imbalances (how, causes, treatment)
hyperkalemia: build up bc of decreased in kidneys ability to excrete it
stabalize cardiac membrane by Caclium gluconate/chloride IV (if ECG changes present)
Drive K back into cells by nebulized albuterol, sodium bicarbonate, combination insulin
and glucose
Removal of excess K through digestive tract by kayexelate
Removing a large amount rapidly by dialysis
Sodium levels (differ)
if high - diuretics, Na restriction
AKI metabolic acidosis treatment
IV fluids, dialysis, bicarbonate infusion
AKI infection
prevention control measure
Be cautious with antibiotic use due to nephrotoxic
