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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
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
What is involved in urine dipstick for AKI?
Detecting blood/protein ?Urine PCR or ACR ?Urine Bence Jones Protein (indicates myeloma)
26
How do we avoid AKI?
Avoid dehydration Avoid nephrotoxic drugs Give fluids Treat Sepsis
27
Risk factors for AKI?
28
What are the AKI 'risk events'?
29
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?
**'STOP-**AKI**'** **S**epsis - if suspected screen + treat (SEPSIS 6) **T**oxins - avoid (e.g. Gentamicin, NSAIDs, IV iodinated contrast) **O**ptimise BP and volume status - avoid/correct hypovolaemia, review BP meds **P**revent harm - identify + investigate cause; daily U+Es, fluid balance + meds review
30
What is the main question to ask in each of: pre-renal, renal (intrinsic), post-renal
Pre-renal: *do they need fluid? BP support* Renal (intrinsic): *can you remove precipitant?* Post-renal: *do they need a catheter?*
31
How do we balance fluid in AKI?
- Volume resuscitation if volume deplete - Fluid restriction if volume overload
32
How do we optimisie BP in AKI?
- Give fluid/vasopressors - Stop ACEI/anti-hypertensives
33
What 2 nephrotoxic drugs should be stopped in AKI?
- NSAIDs - Aminoglycosides
34
What are the 5 Rs for IV prescribing?
**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
What on the ECG is usually the earliest sign of hyperkalaemia?
Peaked (tall, tented) T waves
36
What are other ECG changes seen in hyperkalaemia? (P wave changes; QRS changes; pathologies)
**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
Treatment for hyperkalaemia? (SSR)
* Stabilise* the myocardium - calcium gluconate * Shift* potassium intracellularly - salbutamol, insulin -dextrose * Remove -* diuresis, dialysis, anion exchange resins
38
Intoxication - What are the antidotes for morphine and digoxin?
Morphine = *naloxone* Digoxin = *digibind*
39
What may be required in cases of intoxication AKI?
Renal replacement therapy
40
What are the indications for dialysis in AKI?
Decreased bicarbonate (Acidosis) Hyperkalaemia (Electrolytes) Pulmonary oedema (Overload) Pericarditis (Uraemia)
41
Difference between haemodialysis and haemofiltration?
Haemodialysis = solute removal *by diffusion*; *intermittent* therapy (each session 3-5hrs) Haemofiltration = solute removal *by convection*; larger pore size; *continuous* therapy
42
What are the advantages of HD (intermittent)?
- Rapid solute removal - Rapid volume removal - Rapid correction of electrolyte disturbances - Efficient treatment for hypercatabolic patient
43
What ar the disadvantages of HD (intermittent)?
- Haemodynamic instability - Concern if dialysis associated with hypertension, may prolong AKI - Fluid removal only during short treatment time
44
What are the advantages of CRRT (continuous)?
- Slow volume removal associated with greater haemodynamic stability - Absence of fluctuation in volume and solute control over time - Greater control over volume status
45
What are the disadvantages of CRRT (continuous)?
- Need for continuous anticoagulation - May delay weaning/metabolism - May not have adequate clearance in hypercatabolic patient
46
Pre-renal = v common Renal = less common but v important Post-renal = v common and usually v curable

*Urinary System (26 decks)

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