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Yr 3 renal > Acute kidney injury > Flashcards

Acute kidney injury Flashcards

1
Q

definition of AKI

A

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.

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2
Q

cut offs for dx of AKI

A

rise creatinine >26umol/L within 48hrs

rise in creatinine >1.5x baseline within 7days

UO <0.5mL/Kg/h for >6 consecutive hours

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3
Q

commonest causes of AKI

A

sepsis

major surgery

cardiogenic shock

hypovolaemia

drugs

hepatorenal syndrome

obstruction

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4
Q

RF for AKI

A

pre-existing CKD

age

male

comorbidity - dm, CVS disease, malignancy, chronic liver disease, complex surgery

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5
Q

classifications of AKI

A

pre-renal

renal/intrinsic

post-renal

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6
Q

aetiology of pre-renal AKI

A

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
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7
Q

aetiology of renal AKI

A

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)
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8
Q

aetiology of acute tubular necrosis

A

ischemia

drugs and toxins - paracetamol, aminoglycosides, amphotericin B, NSAIDs, ACEi, lithium

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9
Q

aetiology of post-renal AKI

A

obstruction to urine

  • within renal tract - stone, malignancy, stricture, clot
  • extrinsic compression - pelvic malignancy, prostatic hypertrophy/malignancy, retroperitoneal fibrosis
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10
Q

epidemiology of AKI

A

common

up to 18% of hospital pts and approx 50% of ITU pts

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11
Q

sx of AKI

A
  • 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
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12
Q

signs of AKI

A

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

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13
Q

Ix for AKI

A

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

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14
Q

urine microscopy in AKI

A

red cell casts in glomerulonephritis

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15
Q

complications of AKI

A

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

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16
Q

predictors of CKD after AKI

A

older age,

lower baseline eGFR,

higher baseline albuminuria,

higher stages of AKI

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17
Q

Px of AKI

A

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

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18
Q

bloods for AKI

A

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

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19
Q

urine stick testing in AKI

A

haematuria

proteinuria - glomerulonephritis

20
Q

testing urine in AKI

A

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%.
21
Q

renal biopsy for AKI

A

acute tubulointerstitial nephritis: tubulitis and intense interstitial cellular infiltrate including eosinophils

22
Q

steps in Mx of AKI

A

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

23
Q

assessment of hydration and fluid balance in AKI

A
  • 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

24
Q

treating hyperkalaemia (AKI)

A

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
25
Q

Mx of metabolic acidosis

A

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

26
Q

mx of pulmonary oedema

A

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

27
Q

treating the causes of AKI

A

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

28
Q

indictations for haemofiltration/dialysis

A

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

29
Q

haemofiltration

A

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

30
Q

dialysis

A

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

31
Q

how do you decide whether dialysis of haemofiltration

A

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

32
Q

Mx of pigment nephropathy

A

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

33
Q

mx of myeloma cast nephropathy

A

thalidomide and dexamethasone to reduce light chain production

isotonic fluids (aim UO >=3L/day)

careful monitoring for fluid overload

34
Q

mx of urate nephropathy

A

allopurinol

loop diuretic and fluids - wash out obstructing uric acid crystals

haemodilaysis of diuresis cannot be induced

35
Q

limitations to use of creatinine for AKI dx

A

effects of muscle mass and dilution

but no biomarker has superseded it

36
Q

Approach to AKI

A

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
37
Q

principle of Mx of pre-renal AKI

A

correct volume depletion and/or increase renal perfusion via circ/cardiac support

treat sepsis

38
Q

principle of Mx for renal

A

refer for likely biospy and specialst treatment of intrinsic renal disease

39
Q

principle of mx for post-renal AKI

A

catheter

nephrostomy

urological intervention

40
Q

possible complications fo renal replacement therapy

A

risks of dialysis catheter insertion and maintenance

procedurla hypotension

bleeding due to the requirement for anticoag

alterned nutrition and drug clearance

41
Q

pathophysiology of pre-renal AKI

A
  • 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
42
Q

pathophysiology of intrinsic AKI

A

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

43
Q

pathophysiology of postrenal AKI

A

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

44
Q

4 phases of AKI

A
  1. initiating event = sx of underlying illness, hours/days
  2. oliguric/anuric = reduced UO, increased urea and creatinine retention - complications: pul oedema, high K, met acidosis, uraemia, lethargy, asterixis
  3. polyuric/diuretic phase = glomerular function returns to normal - polyuria, tubular resorption still disturbed - complications: loss of electrolytes and water - dehydration, low K, and Na
  4. recovery phase = normal
45
Q

Acute tubular necrosis

A

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

46
Q

hepatorenal syndrome

A

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

Yr 3 renal (18 decks)

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