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*Urinary System > Acute Kidney Injury > Flashcards

Acute Kidney Injury Flashcards

1
Q

Relationship between serum creatinine and GFR - graph

A
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2
Q

What is the current definition of AKI? (AKI 1) (3 options)

A

Increase in serum creatinine by 26.5µmol/l within 48 hours

OR

Increase in serum creatinine to 1.5 or more times baseline, which is known or presumed to have occurred within the prior 7 days

OR

Urine volume <0.5ml/kg/h for 6 hrs

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3
Q

Staging for AKI is AKI 1, 2 and 3; 3 being most severe

A
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4
Q

How many emergency hospital admission per year involve AKI?

A

1 in 5-7

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5
Q

What are the 5 immediately dangerous consequences of AKI? (AEIOU)

A

Acidosis

Electrolyte imbalance (hyperkalaemia)

Intoxication TOXINS

Overload

Uraemic complications

(can all lead to cardiac arrest)

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6
Q

What are the short-term outcomes of AKI?

A

Death

Dialysis (indications AEIOU)

Length of stay

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7
Q

What are the intermediate/long-term complications of AKI?

A

Death

CKD

Dialysis

CKD-related CVS events

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8
Q

What is the incidence of dialysis-requiring AKI?

A

45-75%

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9
Q

Example case - rise in serum creatinine >50% baseline

baseline = 80µmol/L; rises to 120µmol/L - may still be in ‘normal’ range

Is this the moment to act?

A

YES; it is too late when creatinine reaches 400

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10
Q

What are the 3 categories of causes for AKI?

A

Pre-renal (blood flow to kidney)

Renal (intrinsic) (damage to renal parenchyma)

Post-renal (obstruction to urine exit)

(often several causes will exist so think broadly)

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11
Q

What are the pre-renal cause of AKI? (3 broad headings)

A

Reduce effective circulation volume - Volume depletion (haemhorrage/dehydration; diarrhoea + vomiting); Hypotension/shock (sepsis); Congestive cardiac failure/liver failure

Arterial occlusion

Vasomotor - NSAIDs/ACE inhibitors (potentially reduce BF to kidneys)

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12
Q

What are the renal (intrinsic) causes of AKI? (6 broad headings)

A

Acute tubular necrosis (ATN) - ischaemic

Toxin-related - Drugs (aminoglycosides/amphotericin/NSAID); Radiocontrast; Rhabdomyolysis; Snake venom/heavy metals (Pb, Hg), mushrooms etc

Acute interstitial nephritis (many causes including PPIs)

Acute glomerulonephritis

Myeloma

Intra-renal vascular obstruction - Vasculitis; Thrombotic microangiopathy

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13
Q

What are the post-renal causes of AKI? (1 broad heading - 3 sub)

A

Obstruction:

  • Intraluminal (calculus, clot, sloughed papilla)
  • Intramural (malignancy, ureteric stricture, radiation fibrosis, prostate disease)
  • Extramural (RPF, malignancy)
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14
Q

What is the most common cause of AKI? What can it lead to if untreated?

A
  • Poor perfusion* leading to established tubule damage (pre-renal)
    e. g. hypotension, hypovolaemia (failure of circulation to provide sufficient plasma flow to maintain blood chemistry and fluid balance, due to loss of volume and/or pressure)

If promptly treated - can resolve; if sustained = Acute Tubular Necrosis (exacerbated by toxic injury e.g. drugs)

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15
Q

What is radiocontrast nephropathy?

A

AKI following administration of iodinated contrast agent; common contributor to hospital acquired AKI

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16
Q

How quickly does RCN usually resolve? Can it lead to permanent loss of function?

A

After 72hr usually resolves

Yes, it may lead to permanent loss of function

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17
Q

Give risk factors for RCN

A
  • Diabetes mellitus
  • Renovascular disease
  • Impaired renal function
  • Paraprotein
  • High volume of radiocontrast
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18
Q

What is myeloma in terms of plasma cells?

A

Monoclonal proliferation of plasma cells producing an excess of immunoglobulins and light chains

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19
Q

Some clinical features of myeloma? (also called multiple myeloma)

A
  • Anaemia
  • Back pain
  • Weight loss
  • Fractures
  • Infections
  • Cord compression
  • Elevated ESR
  • Hypercalcaemia
20
Q
A
21
Q

How is myeloma diagnosis made?

A
  • Bone marrow aspirate - >10% clonal plasma cells
  • Serum paraprotein +/- immunoparesis
  • Urinary Bence-Jones protein (BJP)
  • Skeletal survey - lytic lesions - shown below
22
Q

Investigations for AKI (basic terms)

A
  • History
  • Examination (fluid status; look for systemic illness e.g. rashes, joint tenderness)
  • Renal function etc
  • Urine dipstick
  • FBC
  • USS
  • Blood test
  • ‘Fancy’ blood tests if indicated
23
Q

What should be included when doing blood tests for AKI?

A

U+Es

Bicarb (for acidosis)

LFTs

Bone

FBC

Clotting

Blood gas

(fancier - ANCA, Ig, C3 C4 dsDNA)

24
Q

What should be done when AKI is found not to be pre-renal, post-renal and is not responding well to drugs?

A

Renal biopsy

25
Q

What is involved in urine dipstick for AKI?

A

Detecting blood/protein

?Urine PCR or ACR

?Urine Bence Jones Protein (indicates myeloma)

26
Q

How do we avoid AKI?

A

Avoid dehydration

Avoid nephrotoxic drugs

Give fluids

Treat Sepsis

27
Q

Risk factors for AKI?

A
28
Q

What are the AKI ‘risk events’?

A
29
Q

When patients have a risk event and one/more risk factors (therefore prob have AKI) what is the prevention care bundle that should be considered?

A

‘STOP-AKI‘

Sepsis - if suspected screen + treat (SEPSIS 6)

Toxins - avoid (e.g. Gentamicin, NSAIDs, IV iodinated contrast)

Optimise BP and volume status - avoid/correct hypovolaemia, review BP meds

Prevent harm - identify + investigate cause; daily U+Es, fluid balance + meds review

30
Q

What is the main question to ask in each of: pre-renal, renal (intrinsic), post-renal

A

Pre-renal: do they need fluid? BP support

Renal (intrinsic): can you remove precipitant?

Post-renal: do they need a catheter?

31
Q

How do we balance fluid in AKI?

A
  • Volume resuscitation if volume deplete
  • Fluid restriction if volume overload
32
Q

How do we optimisie BP in AKI?

A
  • Give fluid/vasopressors
  • Stop ACEI/anti-hypertensives
33
Q

What 2 nephrotoxic drugs should be stopped in AKI?

A
  • NSAIDs
  • Aminoglycosides
34
Q

What are the 5 Rs for IV prescribing?

A

Resuscitation - IV fluids urgently to restore circulation w hypovolaemia

Routine maintenance - IV fluids if cannot take orally or enterally to meet patient maintenance requirements

Replacement - IV addiitonal maintenance to correct exisitng deficit/ongoing abnormla external losses

Redistribution - some patients have abnormal internal fluid redistribution/abnormal fluid handling (i.e. in speis, cardiac, liver, renal disease)

REASSESSMENT

35
Q

What on the ECG is usually the earliest sign of hyperkalaemia?

A

Peaked (tall, tented) T waves

36
Q

What are other ECG changes seen in hyperkalaemia? (P wave changes; QRS changes; pathologies)

A

P wave widens and flattens; PR segment lengthens; P waves eventually disappear

Prolonged QRS

AV block - slow junctional and ventricular escape rhythms

Conduction block

Sinus bradycardia

Slow AF

Development of a sine wave appearance - a pre terminal rhythm

Cardiac arrest !!!

  • Aystole*
  • V fib*
37
Q

Treatment for hyperkalaemia? (SSR)

A
  • Stabilise* the myocardium - calcium gluconate
  • Shift* potassium intracellularly - salbutamol, insulin -dextrose
  • Remove -* diuresis, dialysis, anion exchange resins
38
Q

Intoxication - What are the antidotes for morphine and digoxin?

A

Morphine = naloxone

Digoxin = digibind

39
Q

What may be required in cases of intoxication AKI?

A

Renal replacement therapy

40
Q

What are the indications for dialysis in AKI?

A

Decreased bicarbonate (Acidosis)

Hyperkalaemia (Electrolytes)

Pulmonary oedema (Overload)

Pericarditis (Uraemia)

41
Q

Difference between haemodialysis and haemofiltration?

A

Haemodialysis = solute removal by diffusion; intermittent therapy (each session 3-5hrs)

Haemofiltration = solute removal by convection; larger pore size; continuous therapy

42
Q

What are the advantages of HD (intermittent)?

A
  • Rapid solute removal
  • Rapid volume removal
  • Rapid correction of electrolyte disturbances
  • Efficient treatment for hypercatabolic patient
43
Q

What ar the disadvantages of HD (intermittent)?

A
  • Haemodynamic instability
  • Concern if dialysis associated with hypertension, may prolong AKI
  • Fluid removal only during short treatment time
44
Q

What are the advantages of CRRT (continuous)?

A
  • Slow volume removal associated with greater haemodynamic stability
  • Absence of fluctuation in volume and solute control over time
  • Greater control over volume status
45
Q

What are the disadvantages of CRRT (continuous)?

A
  • Need for continuous anticoagulation
  • May delay weaning/metabolism
  • May not have adequate clearance in hypercatabolic patient
46
Q

Pre-renal = v common

Renal = less common but v important

Post-renal = v common and usually v curable

A

*Urinary System (26 decks)

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