Acute Kidney Injury Flashcards

1
Q

Define AKI

A

-> Reversible! renal dysfunction

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2
Q

What is the KDIGO Classification of AKI ?

A

KDIGO Classification of AKI;

Increase in serum creatinine by ≥ 26 umol/L within 48 hrs

Increase in serum creatinine to ≥ 1.5 times baseline within the preceding 7 days

Urine volume < 0.5 ml/kg/hr for 6 hours

SO NOTICE; Changes in creatinine are a MASSIVE hint to kidney malfunction!

KDIGO stands for; Kidney disease, Improving global outcomes

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3
Q

`Recognise the presenting symptoms of AKI

A

Depends on underlying CAUSE ;
Whether it is pre-renal, intrinsic, or post-renal

  1. Oliguria/anuria (reduced or no urine output)

NOTE: abrupt anuria suggests post-renal obstruction

  1. Nausea/vomiting
  2. Dehydration
  3. Confusion
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4
Q

Recognise the signs of AKI on physical examination

A
  1. Hypertension
  2. Distended bladder
  3. Dehydration - postural hypotension
  4. Fluid overload (in heart failure, cirrhosis, nephrotic syndrome) - Raised JVP, pulmonary and peripheral oedema
  5. Pallor, rash, bruising (vascular disease)
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5
Q

Name Pre-Renal causes of AKI

A

Pre-Renal ( accounts for 90% of AKIs);

Hypovolaemia (e.g. haemorrhage, Diuresis, Diarrhoea, Dehydration, severe vomiting)

Heart failure

Cirrhosis

Nephrotic syndrome

Hypotension (e.g. shock, sepsis, anaphylaxis)

Renal hypoperfusion (e.g. NSAIDs, ACE inhibitors, ARBs, renal artery stenosis)

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6
Q

Name intrinsic causes of AKI?

A

Glomerular - glomerulonephritis, haemolytic uraemic syndrome

Tubular - acute tubular necrosis

Interstitial - acute interstitial nephritis (e.g. NSAIDs, autoimmune)

Vasculitides (e.g. Wegener’s granulomatosis)

Eclampsia

Anything/ drug that wil cause nephrotoxicity so; Cisplatin, Vancomycin. So if the patient is on chemo… red flag -> intrinsic!

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7
Q

Name causes of Post-Renal AKI?

A

(due to obstruction)

Calculi

Urethral stricture

Prostate hypertrophy or malignancy

Bladder tumour

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8
Q

Name risk factors for AKI?

A

Age

Chronic kidney disease

Comorbidities (e.g. heart failure)

Sepsis

Hypovolaemia

Use of nephrotoxic medications ; chemotherapy, infections etc

Emergency surgery

Diabetes mellitus

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9
Q

Summarise the epidemiology of AKI

A

15% of adults admitted to hospital will develop an AKI

Most common in the ELDERLY

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10
Q

Identify appropriate investigations for AKI

A

All with aim to identify which subtype and then the casusative mechanism.

Bloods - all including clotting
Urinalysis - presence of blood indicates intrinsic cause?
Virology - hepatitis and HIV
Immunology
Ultrasound -Check for post-renal cause + Look for hydronephrosis

Imaging; cxr (if you find pulm oedema, then you can say, heart failure cause the aki)
CT KUB - look for renal calculi

Renal biopsy - if you have ruled out pre-renal and post renal causes and are certain it’s a renal parenchymal disease

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11
Q

What very notable systemic disease causes aki?

Is it a pre-renal intrinsic or post-renal cause

A

SLE

It damages the glomerulus so it is an intrinsic cause

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12
Q

What things do we look out for in immunology investigations in AKI? (considering the last card)

A

Serum immunoglobulins and protein electrophoresis - for multiple myeloma

Also check for Bence-Jones proteins in the urine

ANA - associated with SLE

Also check anti-dsDNA antibodies (high in active lupus)

Complement levels - low in active lupus

Anti-GBM antibodies - Goodpasture’s syndrome

Antistreptolysin-O antibodies - high after Streptococcal infection

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13
Q

Generate a management plan for AKI

A
Treat the cause
• FOUR main components to management:
○ Protect patient from hyperkalaemia (calcium gluconate)
○ Optimise fluid balance
○ Stop nephrotoxic drugs
○ Consider for dialysis
  • Monitor serum creatinine, sodium, potassium, calcium, phosphate and glucose
  • Identify and treat infection
  • Urgent relief of urinary tract obstruction
  • Refer to nephrology if intrinsic renal disease is suspected
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14
Q

When is Renal replacement therapy considered?

A

Renal Replacement Therapy (RRT) considered if:

○ Hyperkalaemia stubborn to medical management
○ Pulmonary oedema resistant to medical management
○ Severe metabolic acidaemia
○ Uraemic complications; seizure, coma, cardiac arrest, death

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15
Q

Identify possible complications of AKI

A
  • Pulmonary oedema
  • Acidaemia
  • Uraemia
  • Hyperkalaemia; palpitations, numbness and tingling, weakness and tiredness etc
  • Bleeding
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16
Q

What is the prognosis of aki?

A
Inpatient mortality varies depending on cause and comorbidities
• Indicators of poor prognosis:
○ Age
○ Multiple organ failure
○ Oliguria
○ Hypotension
○ CKD
• Patients who develop AKI are at increased risk of developing CKD
17
Q

what are the 2 overaching ways AKI is diagnosed?

A
  1. Fall in urine output

2. Rise in creatinine

18
Q

when does AKI progress to CKD?

A

Last for more than 3 months

Doesnt reverse

19
Q

mnemonic for most common causes of AKI?

A

S - sepsis
T - toxins eg amikacin
O - obstruction
P - parenchymal renal disease

20
Q

what counts as rhabdomyolysis?

A

creatinine 5x of upper limit of normal for age so eg 175x5 = 875