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SpM Renal > AKI > Flashcards

AKI Flashcards

1
Q

What is AKI and what two ways is it detected?

A

AKI is decreased renal function detected by an increase in creatinine or a decrease in urine output

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2
Q

What is the improving global outcomes (KDIGO) definition of AKI? (3 parts)

A

Rise in creatinine >26umol/L in 48 hours
Rise in creatinine 1.5 times baseline in 7 days
Decrease in urine output to <0.5ml/kg/h for more than 6 hours

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3
Q

What are the stages of AKI in creatinine rise and urine output?

A

Stage 1 - 1.5-1.9 x baseline creatinine, <0.5ml/kg/h for 6-12 hours
Stage 2 - 2.0-2.9 x baseline creatinine, <0.5ml/kg/h >12hours
Stage 3 - .3.0X baseline creatinine, <0.3ml/kg/h for >24hours

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4
Q

What are some presentations of AKI?

A

Some patients are asymptoatic but oligouria is commonest
Nausea, vomiting, dehydration and confusion
May have symptoms of UTI, exposure to nephrotoxic drugs or PMH of renal problems

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5
Q

How is fluid balance assessed in renal patients?

A

JVP, heart rate, blood pressure, urine output, peripheral and central oedema, capillary refill

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6
Q

What clinical sign can indicate obstruction?

A

A palapable bladder

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7
Q

What are the clinical signs of ureamia?

A

Hand flap, confusion, pericardial rub

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8
Q

How does glomerulonephritis typically present?

A

With haematuria or proteinuria

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9
Q

Which surgical patients are at increased risk of AKI?

A

Vascular or emergency surgery because of hypovolaemia
CKD patients, Diabetes or heart failure
If the patient is on nephrotoxic medication
Patients having contrast need to be carefully cosidered as this is renally cleared

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10
Q

What is the most common cause of AKI prerenal, renal or postrenal?

A

Prerenal

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11
Q

What are the causes of prerenal AKI?

A

Decreased vascular volome - Haemorrhage, D and V, burns
Decreased cardiac output - Cardiogenic shock, MI
Systemic vasodilation - sepsis, drugs
Renal vasoconstriction - NSAIDs, ACE-i, hepatorenal syndrome

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12
Q

What are the causes of renal AKI?

A

Glomerular - Glomerulonephritis, acute tubular necrosis (prolonged renal hypoperfusion causing intrinsic renal damage)
Interstitial - Drug reaction, infection, infiltration (sarcoid)
Vessels - Vasculitis, thrombocytopenic purpura

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13
Q

What are the post renal causes of AKI?

A

Within renal tract - stone, renal tract malignancy, clot, stricture
Extrinsic compression - Pelvic malignancy, prostatic hypertrophy, retroperitoneal fibrosis

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14
Q

What are the 4 main reasons to get renal team involved for dialysis?

A

Fluid overload that is not responding to treatment
Hyperkalaemia
Refractive acidosis
Ureamia

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15
Q

What investigations should be done for AKI?

A

Urine dip - look for protein/haematuria, nitrates for UTI
USS within 24 hours unless AKI cause obvious
Check liver function (hepatorenal function)
Check platelets - if low do blood flim to check for haemolysis
Investigate for intrinsic renal disease if indicated (ANA [SLE], ANCA [vasculitis], anti-GBM [goodpastures])

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16
Q

What does creatinine kinase in blood tests indicate?

A

It shows rhabdomyolysis

17
Q

How does urine output vary between pre renal and intirinsic renal AKI?

A

Pre renal is low

Intrinsic renal is initially high

18
Q

How does urine:plasma osmolality vary between pre renal and intirnsic renal?

A

Urine:plasma osmolality is >2:1 in pre renal and intrinsic renal is <1:1

19
Q

How does urine sodium concentration differ between pre renal and intrinsic renal?

A

In prerenal <15 in intrinsic renal >40

20
Q

How does plasma sodium vary between pre renal and intrinsic renal?

A

In prerenal plasma sodium is high, in intrinsic renal it is low

21
Q

How does elevation of Urea v Creatinine vary between pre renal and intrinsic renal?

A

Pre renal has Urea&raquo_space; Creatinine and intrinsic renal Urea = Creatinine

22
Q

Generally how to you treat pre renal, renal and post renal akis?

A

Pre renal - correct volume depletion and increase renal perfusion via circulatory/cardiac support
Renal - refer for biopsy and specilist support for intrinsic renal disease
Post renal - catheter, nephrostomy or urological intervention

23
Q

What are the signs of hypovolaemia?

A

Decreased JVP, decreased urine output, decreased BP, decreased tissue turgor, increased pulse, weight loss

24
Q

What are the signs of fluid overload?

A

Increased JVP, BP, peripheral oedema, lung crepitations, gallop rhythm

25
Q

How do you treat hypovolaemia?

A

Volume replacement (500ml crystalloid over 15 mins)
Examine before and after all fluid given
Care must be taken in cardiovascular disease not to volume overload heart
Seek expert help when 2L has been given if unresolved

26
Q

What solution is normally used to treat hypovolaemia?

A

0.9% saline or a buffered crystalloid such as hartmann’s

27
Q

What is the treatment in hypervolaemia?

A

Monitor weight daily, treat with:

  • oxygen supplementation if required
  • Fluid restriction, consider oral and IV fluids, give concentrated nutrition
  • Diuretics - only in symptomatic fluid overload - do not use in oliguria as ineffetive and potentially dangerous
  • Renal replacement therapy
28
Q

When does hypervolaemia occur in renal?

A

Due to aggressive fluid resucitation, increased vascular permeability in sepsis, oligouria

29
Q

How should acidosis be treated?

A

Treatment of the underlying disorder that is producing the acid

30
Q

What are the ECG changes in hyperkalaemia?

A

Tall tented T waves
Small or absent P waves
Widened QRS complex

31
Q

How should ECG changes hyperkalaemia be treated?

A
  • 30ml of 10% calcium gluconate IV over 5-10 minutes - this is cardioprotective but does not treat hyperkalaemia
  • IV insulin - 10u in 25g glucose - this increases cellular K+ uptake over 30-60 mins - monitor
  • Definitive treatment requires treatment of underlying pathology - if this cannot be achieved then renal replacement therapy

SpM Renal (8 decks)

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