Acute kidney injury Flashcards
How is AKI defined?
increase in S creatinine by >26.5 micromole in 48 hrs
increase in S creatinine by 1.5x in 7 days
urine volume <0.5ml/kg/hr for 6 hours
Immediately dangerous consequences of AKI (AEIOU)
acidosis electrolyte imbalance intoxication overload uraemic complications
Short term consequences of AKI
hospital stay, dialysis, death,
Long term consequences of AKI
CKD, death, dialysis, CKD related CVS events
Pre-renal causes of AKI
Hypovolaemia - diarrhoea and vomit, haemorrhage, dehydration
sepsis
hypotension
congestive cardiac failure/liver failure
arterial occlusion
vasomotor eg NSAIDS, ACEI
Renal causes of AKI
acute tubular necrosis - ischaemia
toxin related eg NSAIDS, aminoglycosides, contrast
acute glomerulonephritis
acute interstitial nephritis eg PPI’s
myeloma
intra-renal vascular obstruction eg vasculitis
Post renal causes of AKI
intraluminal eg clot, calculus
intramural eg malignancy, stricture, fibrosis, Prostate disease
extramural eg malignancy, RPF
Why does pre-renal causes lead to acute tubular necrosis?
poor perfusion and lack of circulation to provide sufficient plasma flow to maintain blood chemistry and fluid balance
Is the medulla hypoxic?why?
yes
receives 10-15% of renal blood flow
metabolically active
initiation of tubular necrosis
exposure to toxic/ischaemic insult
pre-renal parenchymal injury evolving but AKI preventable
Maintenance of tubular necrosis
established parenchymal injury and max. oliguric
1-2 weeks –> several months
Recovery of tubular necrosis
gradual increase in urine output and fall in serum creatinine
What happens if GFR recovers quicker than tubule resorptive capacity?
excessive diuresis
What is radiocontrast nephropathy?
hospital AKI following iodinated contrast agent
Risk factors for radiocontrast nephropathy
DM renovascular disease paraprotein impaired renal function high volume of radiocontrast
How is myeloma diagnosed?
bone marrow aspirate >10% clonal plasma cells
serum paraprotein and immunoparesis
urinary Bence-jonson protein
skeletal surrey-lytic lesions
Common features of myeloma
Anaemia, back pain, fractures, weight loss, infections, hypercalcaemia, increase ESR and cord compression
Myeloma kidney
cast nephropathy amyloidosis hypercalcaemia light chain nephropathy hyperuricaemia
History questions for AKI
PMH/systemic eg nose bleeds, rash, eyes, joint pain
drug exposure
uraemic symptoms
pre/post renal factors
Examination in AKI
vital sings eg bp, pulse
volume status
systemic illness eg rash, joints, eyes
obstruction - feel bladder
Blood test in AKI
FBC U+E bicarbonate clotting ANCA, Ig, C3 C4 dsDNA LFT bone
Other investigations in AKI
USS, blood gas, urine dipstick, renal function
Situations at risk of AKI
sepsis, toxins, hypotension, surgery, hypovolaemia
Risk factors for AKI
Age>75 previous AKI DM heart failure vascular disease
STOP AKI prevention
sepsis - suspect, investigate, treat
toxins = avoid eg NSAIDS, gentamicin, IV contrast
optimise bp and volume status
prevent harm - daily U+E, fluid balance
Treatment of AKI
avoid dehydration - give fluids optimise bp - stop antihypertensives and give vasopressin and fluids treat sepsis stop nephrotoxic drugs diagnose glomerulonephritis and treat
Hyperkalaemia on ECG
tall tented T waves p wave widen, flat and disappears PR segment lengthens prolonged QRS high grade AV block and conduction block sinus bradycardia or slow AF Sine wave appearance
Problems with hyperkalaemia
cardiac arrest
Progression of hyperkalaemia
asystole, VF and PEA
What hyperkalaemia treatments stabilises the myocardium?
calcium gluconate
What hyperkalaemia treatment shifts K+ intracellularly?
salbutamol
insulin-dextrose
What hyperkalaemia treatment removes K+?
diuresis, dialysis, anion exchange resins
Treatment of intoxication in AKI
antidote eg morphine, digoxin
may require RRT
4 indications for RRT in AKI
low bicarbonate
pulmonary oedema
hyperkalaemia
pericarditis
Advantages of haemodialysis
rapid solute and volume removal
rapid correction of electrolytes
Disadvantages of haemodialysis
Haemodynamic instability
concern if associated with hypotension
fluid removal only when being treated
Advantages of haemofiltration
slow volume removal - haemodynamic stability
absence of volume and solute fluctuations
greater control over volume status
Disadvantages of haemofiltration
Continuous coagulation
may delay mobilisation
