Acute Kidney Injury

Question 1

Define Acute kidney Injury

Answer 1

Sperctum of damage from mild deterioration to severe injury (any raised Cr causes increase in mortality)

Usually defined as rise in Cr within 48h and/or drop in urine output for 6h

usually defined as 1.5x baseline Cr for 1
2)-2-2.9x baseline
3) 3x baseline Cr // >354umol/L

Urine output->0.5 for 6h for 1
2) 0.5 for 12 h
3) 0.3 cor 24H or 0 for 12h

causes are numerous

Question 2

Aetiology and Risk factors of AKI

Answer 2

Can be Pre-Kidney, Kidney or post Kidney

Pre-Kidney-anything decreasing Kidney perfusion-most common is hypovalemia (or CCF) -> activates RAS which retakes in a lot of water (physiological)

Kidney-can be multifactorial-most common cause is Acute tubular necrosis (severe ischemia, often due to poor kidney perfusion (pre-renal))

Post Kidney-obstruction-prostate cancer, stones-> increase pressure-> schema-> damage

Pre renal-40-70% due to renal hypotension (hypovalemia/sepsis/Renal stenosis+AceI)

Intrinsic renal-need renal bioposy- (10-50%)
ATN-tubular
Glomerular-SLE, drugs,
Interstitial-Drugs, infection
vascular-thrombus

Post Renal-10-25%
Stones and malignancy

risk factors–
Age>75, CKD, Cardiac failure, Liver disease, Diabetes, New drugs, Sepsis, Poor fluid intake/increased losses

Surgery, use of contrast, trauma, cancer

Question 3

Epidemology of AKI

Answer 3

Very very common
10-20% of people seen in emergencies

ATN is 45% of the cause of all AKI (and 20% of ATN is caused by sepsis)

Question 4

Symptoms of AKI

Answer 4

Check for risk factors!
and always assess fluid balance

check causes

Defines-
stage 1-1.5x Creatinine or UO <0.5 ml/kg/hr for 6h (roughly 40ml/hr)
stage 2-1.5-3x Crt or UO <0.5 ml/kg/hr for 12h
Stage 3- >3x Crt or UO<0.3 ml/kg/hr for 12h

Question 5

Signs of AKI

Answer 5

Hypotension if the biggest one-assess volume state (pre renal AKI)

assess volume status-
high-absent JVP, bp down, pulse up
Overload-ankle swelling, lung crepitation, gallop rhythm, BP high, JVP high

Blood in urine-Glomerular causes have blood/protein in urine
Tubular (ATN)-no blood
Pre-Renal-no blood

Question 6

Investigation for AKI

Answer 6

BLOODS
U&E-always, either to get baseline or too see a change
Potassium-hyper is common complications of AKI
FBC-WBC for sepsis
CRP
Urinanalysis
VBG

Question 7

Management of AKI

Answer 7

Main -find the cause-> treatment depends on it

Assess volume status (overload-oedema, swelling, lung crackle, or under)

Aim for Euvalemia–overloaded patients given diurteics
Underloaded are given V fluids (AVOID K+ containing fluids except if hypokal)

Stop any nephrotoxic drugs (NSAIDS, ACEi, Abx, metformin)
Monitor-fluid status, U&E’s
Nutrition-feed well

Treat cause—
Pre-renal-more fluids, treat sepsis with Abx
Post Renal-catheterise and consider CT–discuss with urology with stents
Intrinsic Renal-Refer early to nephrology if any signs of multi organ involvement/ dialysis

and manage complications
Hyperkalemia, Pulm oedema, Uremia, Academia

Question 8

Complications of AKI

Answer 8

Common:
Hyperphosphataemia (treat with binders-calcium acetate)
Hyperkaleamia-use K+ sparing fluids-check ECG for signs
Uremia-dialysis

CKD–AKI might damage and never return to baseline0be left with CKD
End stage Kidney issues-replace or die

Question 9

Prognosis for AKI

Answer 9

Depends on early recognition-longer it goes one the worse it gets
Mortality can be high (80%) in burns, trauma,
less in medical illness/poisoning (30%)

if recognised early, about 6%

if AKI needs dialysis, mortality is 50%

AKI is irreversible in about 5-7% of adults