AKI Flashcards
Define AKI in serum creatinine levels.
Increase in serum creatinine >26umol/L within 48HR
1.5-x baseline within 7 days
Urine vol <0.5 ml/kg/h for 6 HR.
Pre renal causes of AKI
(decrease renal perusion, alterations in autoregulation of renal vasculature.
1. Hypovolaemic, cardiogenic or distributive shock
2. Sepsis
3. Renal artery stenosis
4. Drugs - NSAIDs, ACEi/ARBs
5. Haemorrhage
6. liver and cardiac failure.
Intrisinc causes of AKI
(Affects glomeruli, tubules, interstitium, renal vessels)
1. Nephrotoc syndrome, glomerulonephritis
Acute interstial nephritis
Acute tubular necrosis
Renal vein thrombosis,
TTP, vasculitis.
Post renal causes of AKI
(obstruction to urinary outflow anywhere along urinary tract)
* kidney stones
Tumour
Benign prostatic hypertrophy
Fluid overload signs
Oedema,
Hypertension
Puomonary oedema
Other signs of aki
Sepsis
Rashes
Fatigue
Vomiting
Nausea
Pruritis
Basic Inv of aki
- Urine dipstick
*bladder scan
*US KUB
ABG
BLOODS
ECG
CXR
Indications for acute dialysis or haemofiltration.
Uraemi
Electrolyte
Intoxication
Odeoma
Management of aki
ABCDE
1. Volume assesment
2. Sepsis screen
3. Toxins
4. Obstruction
5. Hyperkalaemia
6.Monitor
What drugs should be stopped in AKI
ACEi
ARBS
NSAIDS
AMINOGLYCOSIDE
DIURETICS
Metformin
Digoxin
Lithium
Pathology of pre renal cause of aki
Reduction in renal perfusion -> leads to decreased glomerular filtration -> triggering the release of renin, aldosterone, and antidiuretic hormone to conserve fluid and maintain perfusion pressure.
Prolonged prerenal states, progress to ATN, causing intrinsic renal damage.
Intrisinc causes pathology. (5) in aki
.
Glomerulopathies: Immune-mediated injury to the glomeruli results in inflammation filtering capacity of the glomerulus.
Interstitial Diseases: Inflammatory infiltration of the interstitium disrupts tubular function and can cause tubular atrophy.
Vascular Causes: renal vasculature damage -> ischaemic injury, inflammation, damaging the renal parenchyma.
Postrenal aki pathology
Obstruction results in increased intratubular pressure-> increases tubular reabsorption prolonged -> diminish (GFR).
Backflow of urine -> cause tubular damage -> expose the kidney to infection.
Presentation of pt w rhabdomyolysis
patient who had a fall or prologned sezuires
Rhabdomyolysis iv + Tx
AKI w raised creatinine
raised CK
hypocalecamia - myoglbin bind to Ca
Phosphate Increase
TX
IV fluids - maintain good urine output.