Acute Kidney Injury Flashcards

1
Q

What is the definition of acute kidney injury?

A

Increase in serum creatinine by at least 26.5 micromoles/litre within 48 hours

OR

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

OR

Urine volume less than 0.5 ml/kg/h for 6 hours

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2
Q

What are the immediately dangerous consequences of AKI?

A

Acidosis - can cause cardiac arrest

Electrolyte imbalance - can cause cardiac arrest (hyperkalaemia)

Intoxication TOXINS - opiates can cause respiratory and then cardiac arrest

Overload - with fluid and pulmonary oedema can cause cardiac arrest

Uraemic complications

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3
Q

What are the outcomes of AKI?

A

Short - term:

Death, dialysis, AEIOU

Intermediate:

Death, CKD, dialysis, CKD related CV events

Long term:

RRT, CKD

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4
Q

What are the divisions of causes of AKI?

A

Pre-renal (blood flow to the kidney)

Renal (intrinsic - damage to renal parenchyma)

Post - renal (obstruction to urine exit)

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5
Q

What are the pre-renal causes of AKI?

A
  • Reduced vascular volume : haemorrhage / hypovolemia
  • Reduced cardiac output: MI, cardiogenic shock
  • systemic vasodilation: sepsis, drugs
  • Renal vasoconstriction: drugs e.g. NSAIDs, ACE-I, hepatorenal syndrome
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6
Q

What are the intrinsic causes of acute renal injury?

A
  • Acute tubular necrosis
  • Toxin related: drugs, RADIOCONTRAST, Rhabdomyolisis (haem pigment)

Radiocontrast nephropathy: AKI could present after administration of the iodine dye

  • Acute intersistial nephritis
  • Acute glomerulonephritis
  • MYELOMA
  • Intra-renal vascular obstruction: vasculitis
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7
Q

What are the post - renal causes of AKI?

A
  • Intraluminal: calculus, clot
  • Intramural: malignancy, ureteric stricture, radiation fibrosis, prostate disease
  • Extramural: malignancy , retro-peritoneal fibrosis
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8
Q

What is the most common cause of AKI?

A

Poor perfusion - established tubule damage

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9
Q

What is the effect of myeloma on blood cells?

A

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

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10
Q

What are the investigations for AKI?

A

Urine dipstick

U and E’s

FBC (bicarb, LFT’s, Bone, clotting) - ANCA?

USS

Blood gas

Fancy blood tests if indicated

Renal Biopsy

Urine PCR?

Urine Bence Jones Protein - immunoglobulin light chain that may be suggestive of myeloma

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11
Q

What is the management of AKI?

A

Pre - renal - do they need fluid? BP support

Renal (intrinsic) - can you remove the precipitant

Post renal - do they need a catheter

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12
Q

STOPAKI

A
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13
Q

How do we manage fluid balance in AKI?

A

Volume resuscitation if volume deplete

Fluid restriction if volume overload

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14
Q

How do we optimise blood pressure in AKI?

A

Give fluid / vasopressors

Stop ACE i / antihypertensives

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15
Q

What are the sources of fluid intake?

A

Drinks

Food

Metabolic oxidation

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16
Q

What are the sources of fluid output?

A

Urine

Insensible losses (skin and lungs)

Faeces

17
Q

What is the ECG reading of hyperkalaemia?

A

Peaked T waves (usually the earliest sign of hyperkalaemia)

Tall tented T waves

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

18
Q

What is the treatment of hyperkalaemia?

A

Stabilise the myocardium - calcium gluconate

Shift potassium intracellularly - salbutamol, insulin -dextrose

Remove:

  • Diuresis, dialysis, anion exchange resins
19
Q

What are the antidotes of morphine and digoxin?

A

Morphine - naloxone

Digoxine - digibind

20
Q

What are the indications for dialysis in AKI?

A

Decreasedbicarbonate

Hyperkalaemia

Pulmonary oedema

Pericarditis