Acute kidney injury Flashcards
definition of AKI
syndrome of decreased renal func - measured by serum creatinine or urine outputs occuring over hours to days
Impairment of renal function over days or weeks, which often results in high plasma urea/creatinine and oliguria (<400 mL/day)
usually reversible.
The term AKI represents the full spectrum of acute kidney dysfunction.
cut offs for dx of AKI
rise creatinine >26umol/L within 48hrs
rise in creatinine >1.5x baseline within 7days
UO <0.5mL/Kg/h for >6 consecutive hours
commonest causes of AKI
sepsis
major surgery
cardiogenic shock
hypovolaemia
drugs
hepatorenal syndrome
obstruction
RF for AKI
pre-existing CKD
age
male
comorbidity - dm, CVS disease, malignancy, chronic liver disease, complex surgery
classifications of AKI
pre-renal
renal/intrinsic
post-renal
aetiology of pre-renal AKI
reduced perfusion to kidney
- reduced vascular vol - haemorrhage, D&V, burns, pancreatitis
- reduced CO - cardiogenic shock, MI
- systemic vasodilation - sepsis, drugs
- renal vasoconstriction - NSAIDs, ACEi, ARB, hepatorenal syndrome
aetiology of renal AKI
intrinsic renal disease
- glomerular - glomerulonephritis, ATN (prolonged renal hypoperfusion causing intrinsic renal damage)
- acute interstitial nephritus - drug reaction, NSAIDs, penicillins, sulphonamides, infection, leptospirosis, infiltration eg sarcoid
- small/large vessel obstruction - vasculitis, HUS, TTP, DIC, renal artery/vein thrombosis, cholesterol emboli
- light chain - myeloma
- urate - lympho- or myeloproliferative disorders - particularly after chemo/radio induced cell lysis
- pigment - haemolysis, rhabdomyolysis, malaria
- nephropathy
- accelerated phase HTN (eg pre-eclampsia)
aetiology of acute tubular necrosis
ischemia
drugs and toxins - paracetamol, aminoglycosides, amphotericin B, NSAIDs, ACEi, lithium
aetiology of post-renal AKI
obstruction to urine
- within renal tract - stone, malignancy, stricture, clot
- extrinsic compression - pelvic malignancy, prostatic hypertrophy/malignancy, retroperitoneal fibrosis
epidemiology of AKI
common
up to 18% of hospital pts and approx 50% of ITU pts
sx of AKI
- may be asymptomatic
- oliguria/anuria
- anorexia
- malaise
- nausea/vomiting
- pruritis
- incomplete voiding
- changes to urine colour
- fatigue, confusion, lethargy, drowsiness
- seizure, coma - because of uraemia
signs of AKI
signs of vol depletion - orthostatic/frank hypotension and tachycardia, reduced skin turgor, low UO, hypotn, non-visible JVP, daily wht loss
signs of fluid overload - peripheral and pul oedema, hypertension, HF, SOB, high BP, high JVP, lung crep, gallop rhythm
signs of uremia - encephalopathy, asterixis. pericarditis, platelet dysfunction
signs of renal obstruction - distended bladder, pain over bladder/flanks
signs of complications
Ix for AKI
bloods
urine dipstick pre-catheter and quantification of any proteinuria - haematuria/proteinuria indicate intrinsic renal disease
USS within 24hrs, small kidneys <9cm suggest CKD. Asymmetry suggest renal vascular disease. To exclude obstructive cause
check liver func - hepatorenal
check platelets - if low need bloodfilm to check for haemolysis (HUS/TTP)
investigate for intrinsic renal disease if indicated, Ig, paraprotein, complement, autoAb (ANA, ANCA, anti-GBM)
CXR - look for fluid overload
ECG - check for hyperkalaemia (tented t waves, increased PR, small/absent P, wide QRS, sine wave, asystole)
renal US
renal biopsy
urine microscopy in AKI
red cell casts in glomerulonephritis
complications of AKI
because of impairment of excretory, endocrine and metabolic actions:
risk of complications is related to the stage of AKI
common and life threatening:
- hyperkalaemia - asymptomatic until severe = muscle weakness, paralysis, cardiac arrhythmias or cardiac arrest
- sepsis
- metabolic acidosis - alter level of consciousness, circulatory collapse and hypervent
- volume overload - peripheral and pulmonary oedema - tachypnoea, tachycardia, cyanosis, and lung crepitations. often from excessive IV fluids
- HTN
high Mg and phos, low Na and Ca
gastric ulceration
bleeding - platelet dysfunction
muscle wasting - hypercatabolic state
uraemia - confusion, lethargy, altered consciousness - need dialysis (uraemic encephalopathy and uraemic pericarditis)
acute cortical necrosis
CKD and end-stage renal disease - high risk of hypertension and CKD
predictors of CKD after AKI
older age,
lower baseline eGFR,
higher baseline albuminuria,
higher stages of AKI
Px of AKI
important consequences even in mild, reversible cases
early detection improves prognosis
depends on clinical setting, comorbidities and cause
mortality increases with increasing stages of AKI
higher mortality in community than hospital acquired
ATN biphasic recovery - oliguria the polyuria as tubular cells regenerate - Px depends on number of organs involved - many recover
Acute cortical recrosis - may cause HTN and chronic renal failure
bloods for AKI
ABG
FBC
UE - urea, creatinine, K, Na
LFT
ESR or CRP
Ca
clotting
culture
blood film - red cell fragmentation in HUS/TTP
CK - rhabdomyolysis
urate
serum electrophoresis
autoAb
urine stick testing in AKI
haematuria
proteinuria - glomerulonephritis
testing urine in AKI
culture and sensitivity
bence-jones protein (exclude myeloma)
urine osmolarity/Na:
- pre-renal
- increased urine osmolarity,
- low urine Na
- low fractional excretion of Na <1%
- renal
- low urine osmolarity/specific gravity (as a result of low renal conc ability)
- high urine Na - low resporpative ability
- high fractional excretion of Na - (PCr.UNa/ PNa.UCr): >2%.
renal biopsy for AKI
acute tubulointerstitial nephritis: tubulitis and intense interstitial cellular infiltrate including eosinophils
steps in Mx of AKI
assess hydration and fluid balance
mx acidosis
treat the complications
treat the cause
optimise nutritional support
identify and treat bleeding tendency - prophylaxis with PPIs or H2 antagonist, transfuse if required, avoid aspirin
haemofiltration
dialysis
treatment of pigment/light chain/urate nephropathy
assessment of hydration and fluid balance in AKI
- pulse rate
- lying and standing BP
- JVP
- skin turgor
- chest auscultation
- peripheral oedema
- CVP
- fluid and weight charts
if hypovolaemic - renal perfusion improve with volume replacement - use Hartman’s or plasmalyte less likely to get hypercholeraemic acidosis than with saline
if hypervolaemic - fluid restriction, ox, diuretics if sx
treating hyperkalaemia (AKI)
if ECG change or K >7mmol/L
- 10mL of 10% calcium gluconate IV (protect the myocardium) and ECG monitoring
- 50ml of 50% dextrose with 5U actrapid insulin over 15mins - drive K into cells
- nebulised salbutamol can lower K
- Ca/Na resonium PO/PR - reduce bowel absorption
- contact renal team and arrange for dialysis if appropriate
Mx of metabolic acidosis
if pH <7.2
50-100mL of 8,4% bicarbonate via central line over 15-30mins
will generate CO2 so need adequate ventilation to stop resp acidosis making it worse
sodium bicarb can alsoe ppte a fluid overload in a vulnerable patient
mx of pulmonary oedema
ox - consider CPAP
IV GTN 2-10mg/h
IV furosemide - 250mg over 1hr followed by infusion 5-10mg/h
IV diamorphine - single doe of 2.5mg - relieves anxiety and breathlessness
treating the causes of AKI
IV fluids if volume depleted - 500ml colloid or 0.9% saline over 30mins - assess response (ie UO or CVP) - continue until CVP 5-10cm
inotropes if hypotension persists in spite of CVP >10cm
treatment of infection - dose in view of the renal impairment
stop the nephrotoxic drugs (eg ACEi and NSAIDS) and non-essential drugs
idenyify intrinic renal disease and treat
relieve the obstruction eg urinary catheter, nephrostomies
indictations for haemofiltration/dialysis
persistant hyperkalaemia >7mmol/L
fluid overload - refractory pulmonary oedema
pericarditis
acidosis - arterial pH <7.1, bicarb <12
symptomatic uraemia (tremor, cognitive impairment, coma, fits, urea typically >45mmol/L) - encephalopathy or pericarditis
haemofiltration
continuous arteriovenous or venous-venous
filtration of plasma water across the membrane
induced by the hydrostatic pressure gradient and convective transport of solutes in the same direction as water
substitution fluid is needed to prevent excessive fluid removal
dialysis
intermittent haemodialysis (using central venous catheters or arteriovenous fistulae)
or peritoneal dialysis (using a double cuff straight Tenckhoff catheter)
solutes passively diffuse down their concentration gradient (urea, creatinine, and K more from blood to dialysate; ca and bicarb move from dialysate to blood
venesect 250-500ml if delay for dialysis
how do you decide whether dialysis of haemofiltration
depends on availability, expertise, haemodynamic stability, vascular access and whether primary need is for fluid and/or solute removal
haemofiltration is preferred if hypotensive or haemodynamically unstable - because rate of fluid and solute removal is slow
Mx of pigment nephropathy
isotonic saline to maintain diuresis of 200-300ml/h
careful monitor for fluid overload
if diuresis is established - switch to alkaine soln (bicarb)
increasing urine pH to >6.5 may reduce release of free iron from myoglobin and intratubular pigment deposition and cast formation
if desired diuresis is not established with adequate volume replacement alone - loop diuretics or mannitol
mx of myeloma cast nephropathy
thalidomide and dexamethasone to reduce light chain production
isotonic fluids (aim UO >=3L/day)
careful monitoring for fluid overload
mx of urate nephropathy
allopurinol
loop diuretic and fluids - wash out obstructing uric acid crystals
haemodilaysis of diuresis cannot be induced
limitations to use of creatinine for AKI dx
effects of muscle mass and dilution
but no biomarker has superseded it
Approach to AKI
is there a life threatening complication:
- NEWS
- pul oedema
- hyperkalameia
examine - HR, BP, JVP, cap refill, palpate for bladder
treat hypovolaemia
monitor:
- fluid balance - catheter
- K
- obs
- lactate if signs of sepsis
- daily creatinine until it falls
Ix
support
- treat sepsis
- stop nephrotoxic med - NSAIDs, ACEi, ARB, aminoglycosides
- stop drugs that increase complications - diuretic (esp K sparing), metformin, antiHTN
- check all doses appropriate
- gastroprotection and nutritional support
- avoid radiological contrast
principle of Mx of pre-renal AKI
correct volume depletion and/or increase renal perfusion via circ/cardiac support
treat sepsis
principle of Mx for renal
refer for likely biospy and specialst treatment of intrinsic renal disease
principle of mx for post-renal AKI
catheter
nephrostomy
urological intervention
possible complications fo renal replacement therapy
risks of dialysis catheter insertion and maintenance
procedurla hypotension
bleeding due to the requirement for anticoag
alterned nutrition and drug clearance
pathophysiology of pre-renal AKI
- decreased blood supply to kidneys
- = failure of renal vascular autoregulation to maintain renal perfusion
- = reduced GFR
- = activation of RAAS
- = increased aldosterone release
- = increased absorption of Na and water
- = increased urine osmolarity
- = secretion ADH
- = increased resporption of water and urea
- creatinine still secreted in the proximal tubule so the blood BUN:creatinine ratio increases
pathophysiology of intrinsic AKI
damage to vascular or tubular component of nephron
= necrosis or apoptosis of tubular cells
= decreased resorption capacity of electrolytes (Na, water, and/or urea)
= increased Na and water in urine
= decreased urine osmolarity
pathophysiology of postrenal AKI
bilateral urinary outflow obstruction
= increased retrograde hydrostatic pressure in renal tubules
= decreased GFR and compression of the renal vasculature
= acidosis, fluid overload, increased BUN, Na, K
normal GFR can be maintained as long as one kidnye functions normally
4 phases of AKI
- initiating event = sx of underlying illness, hours/days
- oliguric/anuric = reduced UO, increased urea and creatinine retention - complications: pul oedema, high K, met acidosis, uraemia, lethargy, asterixis
- polyuric/diuretic phase = glomerular function returns to normal - polyuria, tubular resorption still disturbed - complications: loss of electrolytes and water - dehydration, low K, and Na
- recovery phase = normal
Acute tubular necrosis
caused by ischemia or nephrotoxic substances
- eg hypotn, thromboembolism, thrombotic microangiography, cholesterol embolism
- contrast, aminoglycosides, cisplatin, myoglobinuria due to rhabdomyolysis, haemoglobinuria associated with haemolysis, acute uric acid nephropathy
necrotic prox tubular cells fall into the tubular lumen - debris obstructs tubules - decreased GFR - pre-renal AKI
hepatorenal syndrome
deterioration of kidney function in patients with advanced liver disease
cirrhosis/portal HTN = increase in splanchnic vasodilators eg nitric oxide = low arterial blood flow = activation of RAAS = renal vasoconstriction = low GFR
features of advanced liver disease, oliguria -> anuria with progressive kidney failure, hypotension with a wide pulse pressure
