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?

18
Q

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

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

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
What are the sources of fluid output?
Urine Insensible losses (skin and lungs) Faeces
26
What is the ECG reading of hyperkalaemia?
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
What is the treatment of hyperkalaemia?
Stabilise the myocardium - calcium gluconate Shift potassium intracellularly - salbutamol, insulin -dextrose Remove: - Diuresis, dialysis, anion exchange resins
28
What are the antidotes of morphine and digoxin?
Morphine - naloxone Digoxine - digibind
29
What are the indications for dialysis in AKI?
Decreasedbicarbonate Hyperkalaemia Pulmonary oedema Pericarditis
30
What is the difference between haemodialysis and haemofiltration?
Haemodialysis - solute removal by diffusion Intermittent therapy - each session lasting 3 - 5 hours Haemofiltration - solute removal by convection, larger pore size, continuous therapy
31
What are the advantages of HD?
–Rapid solute removal –Rapid volume removal –Rapid correction of electrolyte disturbances –Efficient treatment for hypercatabolic patient
32
What are the disadvantages of HD?
Haemodynamic instability Concern if dialysis associated with hypotension, may prolong AKI Fluid removal only during short treatment time
33
What are the advantages of CRRT? - continuous renal replacement therapy
–Slow volume removal associated with greater haemodynamic stability –Absence of fluctuation in volume and solute control over time –Greater control over volume status
34
What are the disadvantages of CRRT?
Need for continous anticoagulation May delay weaning / immobilisaation May not have adequate clearance in hypercatabolic patient
35
Explain the significance of the relationship between plasma creatinine and GFR.