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Renal (Year 2 GM) > Acute Kidney Injury > Flashcards

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 is the incidence of acute kidney injury?

A

Hospital admissions - 1 in 5 to 7

ITU admissions - more than half

Uncommon in the community

Incidence is higher or more corbidity

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3
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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4
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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5
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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6
Q

What are the pre-renal causes of AKI?

A

Reduction in effective circulation volume:

  • Volume depletion (haemorrhage/dehydration - diarrhoea and vomiting)
  • Hypotension and shock (sepsis )
  • Congestive heart failure / liver failure

Arterial Occlusion

Vasomotor

  • NSAIDS / ACE inhibitors (nsaids potentially reduce blood flow to the kidneys)
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7
Q

What are the intrinsic causes of acute renal injury?

A

Acute tubular necrosis (ischaemic)

Toxin - related:

  • Drugs (aminoglycosides/ amphotericin / NSAID)
  • Radiocontrast
  • Rhabdomyolysis (haem pigments) (happens as a result of muscle damage)
  • Snake venom / heavy metals - Pb, Hg
  • Mushrooms

Acute interstitial nephritis (many causes including drugs - PPI’s)

Acute Glomerulonephritis

Myeloma

Intra renal vascular obstruction

  • Vasculitis
  • Thrombotic microangiopathy
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8
Q

What are the post - renal causes of AKI?

A

•Obstruction

–Intraluminal (calculus, clot, sloughed papilla)

–Intramural (malignancy, ureteric stricture, radiation fibrosis, prostate disease)

–Extramural (RPF, malignancy)

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9
Q

What is the most common cause of AKI?

A

Poor perfusion - established tubule damage

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10
Q

What is the prognosis of radiocontrast nephropathy?

A

Common contributor to hospital acquired AKI

Usually transient renal dysfunction, resolving after 72 hours

May lead to permanent loss of function

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11
Q

What are the risk factors for radiocontrast nephropathy?

A
  • Diabetes mellitus
  • Renovascular disease
  • Impaired renal function
  • Paraprotein
  • High volume of radiocontrast
  • All of the above
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12
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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13
Q

How is diagnosis of myeloma made?

A

Bone marrow aspirate - >10% clonal plasma cells

Serum paraprotein ± immunoparesis

Urinary Bence-Jones protein (BJP)

Skeletal survey - lytic lesions

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14
Q

What are the clinical features of myeloma?

A

–Anaemia

–Back pain

–Weight loss

–Fractures

–Infections

–Cord compression

–Markedly elevated ESR

–Hypercalcaemia

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15
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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16
Q

How do we avoid AKI?

A

Avoid dehydration

Avoid nephrotoxic drugs

Give fluids

Treat Sepsis

17
Q

What are AKI risk factors?

A
18
Q

When patients at risk are experiencing a risk event? (sepsis, toxins, hypertension, hypovolaemia, major surgery) what is the management?

A
19
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

20
Q

STOPAKI

A
21
Q

How do we manage fluid balance in AKI?

A

Volume resuscitation if volume deplete

Fluid restriction if volume overload

22
Q

How do we optimise blood pressure in AKI?

A

Give fluid / vasopressors

Stop ACE i / antihypertensives

23
Q

What are the 5 R’s for IV prescribing?

A

Resuscitation - to restore circulation with hypovolaemia

Routine maintenance - when the patient cannot take anything orally or enterally

Replacement - don’t need urgent resuscitation but need additional maintenance to correct an existing defecit or ongoing abnormal external loss - diarrhoea or fever

Redistribution - Abnormal internal fluid as a result of sepsis, cardiac/liver/renal disease (tissue oedema) or GI tract/thoracic/ peritoneal collection

REASSESSMENT

24
Q

What are the sources of fluid intake?

A

Drinks

Food

Metabolic oxidation

25
Q

What are the sources of fluid output?

A

Urine

Insensible losses (skin and lungs)

Faeces

26
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

27
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
28
Q

What are the antidotes of morphine and digoxin?

A

Morphine - naloxone

Digoxine - digibind

29
Q

What are the indications for dialysis in AKI?

A

Decreasedbicarbonate

Hyperkalaemia

Pulmonary oedema

Pericarditis

30
Q

What is the difference between haemodialysis and haemofiltration?

A

Haemodialysis - solute removal by diffusion

Intermittent therapy - each session lasting 3 - 5 hours

Haemofiltration - solute removal by convection, larger pore size, continuous therapy

31
Q

What are the advantages of HD?

A

–Rapid solute removal

–Rapid volume removal

–Rapid correction of electrolyte disturbances

–Efficient treatment for hypercatabolic patient

32
Q

What are the disadvantages of HD?

A

Haemodynamic instability

Concern if dialysis associated with hypotension, may prolong AKI

Fluid removal only during short treatment time

33
Q

What are the advantages of CRRT? - continuous renal replacement therapy

A

–Slow volume removal associated with greater haemodynamic stability

–Absence of fluctuation in volume and solute control over time

–Greater control over volume status

34
Q

What are the disadvantages of CRRT?

A

Need for continous anticoagulation

May delay weaning / immobilisaation

May not have adequate clearance in hypercatabolic patient

35
Q

Explain the significance of the relationship between plasma creatinine and GFR.

A

Renal (Year 2 GM) (28 decks)

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