AKI Flashcards
(23 cards)
What is AKI?
- Syndrome
- rapid decrease GFR
- accumulation nitrogenous waste products
- decrease/ urine output
What is criteria of AKI?
- increase SCr atleast 27mol/L within 48 hrs
- increase baseline SCr by 1.5 times / more within 7 days
- Urine output < 0.5ml/kg/h atleast 6 hrs
= ONLY ONE CRITERIA MET FOR DIAGNOSIS
What is Pre-renal?
Pre-renal:
- reduced BF to kidneys
- due volume depletion - haemorrhage, dehydration/ GI fluid loss
- reduce CO - CHF, MI, septic shock, hypotension - reduce renal BF + glomerular perfusion
What medications cause pre-renal? how to manage?
Nsaids - naproxen: - impair pg -mediated inhibit angiotensin II mediated efferent arteriole - vasoconstriction - ACE-I - enalpril -ARB -
= decrease intraglomerular pressure + GFR
= discontinue
with mild-moderate decrease in renal BF - intraglomerular pressure is maintained
- dilation afferent arterioles
- constriction efferent arterioles
- redistribution renal bf –> oxygen-sensitive renal medulla
early volume restoration to prevent progression needed before structural damage
What is intrinsic AKI?
- diseases affect structure nephron - tubules, glomerulus, intersititium, BV
- ATN = necrosis tubular epithelial cells - nephrotoxins (aminogl, constrast agents, amphotericin B) , sepsis / ischemia
- less commonly caused by glomerular , interstitial and BV diseases - glomerulonephritis, SLE , intersititial nephritis and vasculitis
Can pre-renal AKI progress to intrinsic AKI?
yes
What is postrenal AKI?
- obstruction urinary flow
- prostate disease / bladder tumour
- causes BPH, tumours, renal calculi
Clinical presentation and diagnosis
What is criteria for stage 1 and 3?
stage 1: increase SCr 27umol/L / increase
Stage 3: patients receive RRT
what is presentation of urinary output ?
sensitive marker than SCr in AKI
- Oliguria - production small vol urine - daily urine output < 400ml/day
- Anuria - failure to produce urine - daily urine output < 50ml/day
- Non-oliguria AKI - urrine output > 400ml/day
How to determine prerenal AKI using BUN and SCr?
- elevated SCr + BUN (> protein + GIT bleeding due to AA breakdown in gut)
- Urea product AA met
- BUN < sensitive marker than SCr
- increase blood urea reabs at lower urine flow rates
What is fractional excretion of Na and what drug affects it?
- measure of % Na excreted by kidney
- Loop diruetic - furosemide - increase FENa
What is rhe FENa in pre-renal AKI?
- enhanced Na reabs
- decreased FENa + urine [Na]
<1% = decreased renal perfusion + Na excretion - urine > concentrated in pre-renal than post and intrinsic due higher osmolality + urine-to plasma creatine ratio
symptoms of AKI
- weight gain
- N, V, D, anorxia
- fatigue
- shortness of breath
- pruritis
- PRE-RENAL - weight loss
- Postrenal - anuria alternating polyuria + clocky abdominal pain radiating from flank to groin
physical examination AKI
- increased BP
- peripheral odema
- change mental status
- JVD
- pulmonary oedema
- crackles
- asterixis
- pericardial or pleural friction rub
- hypotension/ orthostatic hypoyension - pre-renal
- rash - instrinsic due to acute intersitial nephritis
- bladder distention + prostatic enlargement - postrenal
what are treatment goals?
- find identifiable cause
1. hypovolaemia
2. nephrotoxic drugs
3. ureter obstruction
pre-renal + post-renal can be reversed
instrinc - supportive therapy
Hydration therapy
- Isotonic colloidal solns = 0.9% normal salinr
- expand extravascular vol
- return volume status
- neural fluid balance - euvolaemia
= ensure tissue perfusion - Crystalloids - normal saline / balanced solns - ringers lactate / plasma - lyte A
- preffered over colloidal - albumin, hydroxyethyl starch for fluid resucitation - 0.9% normal saline PREFFERRED over lower tonicity saline due smaller fraction of hypotonic fluid remains in intravascular space
- Dextrose 5% in water = isotonic = its absorbed ONLY H20 left intravascular space
= too much fluid = pulmonary oedema, increased postoperative complications, increased mortality
= excess chloride from 0.9% normal saline = hyperchloraemic metabolic acidosis
Loop diuretics
- bumetanide
- furosemide
- torasemide
MIDE
= worsen kidney function
- improved urine ouput
- no improvement in survival / need dialysis
- reserved treating volume overload
- NOT given prevent AKI/ hasten recovery of kidney func in euvolAEMIC/ HYPOVOlaemic individuals
Purpose RRT
- treat pulmonary oedema + volume overload = unresponsive diuretics
- minimize accum nitrogenous waste
- correct electrolyte + a-b balance - hyper + metabolic acidosis
Name 2 process and explain of solute removal in RRT
Diffusion - move from [high] to [low] in dalysate across SP dialysis membrane
Convection - removal solutes secondarily to fluid removal of ultrafiltration = solute drag
2 modalities of RRT
- intermittent haemodialysis - IHD
- higher efficiency form
- fluid removal by ultrafiltration
- solute removal by diffusion
several hrs - daily 3/5 times a week - continous renal replacement therapy - CRRT
- slow fluid/ solute removal on continous basis - 24hrs
what is continos venovenous haemodialfiltration
CVVH-DF?
type of CRRT allows for fluid removal + removal of solutes - small-large mol via diffusion
Advantage of CCRT
haemodynamic stability
better volume control in patients unable tolerate rapid fluid removal
disadvantage of CCRT
continous nursing requirements + anticoagulation
frequent clotting dialyzer
patient immobility
increase cost
