AKI Flashcards

1
Q

Define AKI

A

A sudden decline in renal function (GFR) significant enough to produce uraemia, and also often oliguria – a urine output of <400ml/day.
It normally occurs over hours/days or week
- often reversible. Diagnosis is usually based on serum urea and/or creatinine levels.

Severe Acute Kidney Injury is defined as a creatinine level of >500umol/L

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2
Q

Appropriate investigations of AKI and what should results be?

A

Urine dipstick
Urine microscopy – look particularly for the presence of red cell casts and red cells.
Blood tests – U+E’s (particularly Cr and K+, FBC, free haemoglobin and myoglobin.
Kidney function is monitored through urine output analysis and creatinine clearance monitoring – creatinine clearance monitoring is the ideal, i.e. it is a more precise indication of GFR than serum urea monitoring alone!
Check if the patient is on any nephrotoxic drugs.

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3
Q

What are the defining criteria of AKI?

A
  • Increase in serum urea > 26 μmol/L within 48 hrs
  • Increase in serum creatinine to > 1.5 times baseline within preceding 7 days
  • Urine volume < 0.5 ml/kg/hr for 6 hours
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4
Q

Broadly speaking what how can the causes of AKI be classified?

A

Pre-renal
Renal
Post-renal

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5
Q

Aetiology of AKI

A

• Usually occurs in context of catastrophic illness
o Hypotension, sepsis, orthopaedic surgery
o Common in critical illness
o 45% are ATN
o 21% are pre-renal
• 48% are hospital acquired

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6
Q

Describe what causes a pre-renal AKI

A

Inadequate perfusion of kidneys

  1. Hypovolaemia due to diuretics (renal loss), NSAIDS, ACEi, diarrhoea, DKA, vomiting (dehydration - extrarenal loss)
  2. Systemic vasodilation due to sepsis
  3. Decreased CO due to HF/MI
  4. Intrarenal vasoconstriction (cardiorenal syndrome)
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7
Q

Describe what causes a renal AKI

A

Intrinsic kidney damage

eg. acute tubular necrosis, glomerulonephritis, small vessel vasculitis/thrombosed renal artery

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8
Q

Describe what causes a post-renal AKI

A

Obstruction of urine flow

Most commonly stones, clots, blocked catheters, malignancies (bladder, prostate etc), fibrosis

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9
Q

Which type of AKI is most common in hospital?

A

Pre-renal

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10
Q

RF for AKI

A
  • Advanced age*
  • Underlying renal disease* eg CKD
  • Malignant hypertension
  • DM*
  • Sodium retaining states
  • Radiocontrast
  • Nephrotoxin* exposure: NSAIDs, chemotherapy, aminoglycosides
  • Trauma, haemorrhage
  • Sepsis*
  • Surgery
  • Cardiac arrest
  • Fluid loss
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11
Q

Epidemiology of AKI

A

Greater incidence in ICU (20-50%) – mainly caused by sepsis

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12
Q

Presenting symptoms of AKI

A
•	Symptoms of uraemia
o	Nausea, vomiting, anorexia, confusion
•	Features of underlying disease
o	Pre-renal
	Hypovolaemia: thirst, dizziness, vomiting, confusion
o	Intrinsic
	Glomerular: nephritic syndrome (haematuria, proteinuria, hypertension)
	Tubular: hypovolaemia
o	Post-renal
	Flank pain, haematuria
	Urgency, frequency and hesitancy
•	Oliguria/anuria - decreased urine output
•	Complications
o	Salt and water retention
	Orthopnoea
	Pulmonary oedema
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13
Q

Presenting symptoms of acute interstitial nephritis

A

Oliguria + triad (of drug side effect): rash, fever, eosinophilia +/- painful joints

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14
Q

Signs of AKI

A

Asterixis

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15
Q

Signs of pre-renal AKI

A

 AF
 Hypotension + tachycardia, dry mucous membranes
 CCF -> JVP, ascites

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16
Q

Signs of intrinsic AKI

A

 Butterfly rash (SLE?)
 Nephrotic syndrome -> pulmonary + peripheral oedema, raised JVP
 Vascular obstruction -> petechiae/purpura/bruising + pallor + tiredness

17
Q

Signs of post-renal AKI

A

 Costovertebral angle tenderness
 Prostatic hypertrophy
 Bladder enlargement

18
Q

What investigations would you do for AKI

A
Urinalysis
Bloods
Renal US
AXR
CXR
ECG
Venous blood gas
19
Q

What might you find in urinalysis indicative of AKI

A

o RBCS, WBCs, cellular casts, proteinuria, bacteria, nitrites, leucocyte esterase, glucose, urine osmolality

20
Q

What might you find in bloods indicative of AKI

A
In a metabolic profile:
	Acutely elevated serum creatinine
	Hyperkalaemia
	Metabolic acidosis
o	Serum urea:creatinine ratio >20:1 = pre-renal

FBC
 Anaemia, thrombocytopenia -> intrinsic AKI
 Infection -> pre-renal + intrinsic AKI

Blood film - could look for schistocytes = small vessel disease = intrinsic AKI

Serology
 Auto-antibodies – Anti-GBM, ANA (SLE), anti-streptolysin-O
 Immunoglobulins - IgA
 Protein electrophoresis (multiple myeloma)

21
Q

What might you see on renal US?

A

o Dilated renal calyces (hydronephrosis) – post renal

22
Q

What might you see on AXR

A

renal stones

23
Q

What might you see on CXR

A

Pulmonary oedema

Cardiomegaly

24
Q

What might you see on ECG

A

Severe hyperkalaemia
Peaked T waves
Widened QRS
Increased PR interval

25
Q

What might you see on venous blood gas

A

metabolic acidosis

26
Q

Management of pre-renal AKI

A

o Volume expansion +/- blood transfusion
o Vasopressor
o Treat infection

27
Q

Management of renal AKI

A

o Treat underlying condition
o Stop nephrotoxic agents
o Treat infection

28
Q

Management of post-renal AKI

A

o Bladder catheterisation

o Relief of obstruction above bladder neck

29
Q

What things should you monitor in all AKI patients?

A
Creatinine
K+
Na+
Phos
Ca
glucose
30
Q

What do you give to a patient who’s volume overloaded

A

Loop diuretic

31
Q

What do you give to a patient who is hyperkalaemic and why?

A

Calcium gluconate - reduces ventricular fibrillation
Insulin and glucose - insulin drives K+ into cells via the sodium potassium ATP pump
Salbutamol nebuliser

32
Q

In what cases would you use renal replacement therapy?

A
  • Hyperphosphataemia - asymptomatic
  • Uraemia -> affects all systems -> buzzword = pericarditis, pruritis, skin colour changes, peripheral weakness (loads of others, refer to 1st page)
  • Volume overload -> HTN, pulmonary oedema, peripheral oedema
  • Hyperkalaemia -> muscle weakness, tingling/numbness, n&v, chest pain, palpitations, arrhythmias
  • Metabolic acidosis -> tachypnoea
  • CKD
  • ESRD (end stage renal failure)
33
Q

Prognosis of AKI

A

• Recovery depends on cause, severity and duration
o Increased mortality
• 6% of ICU patients need RRT
• Irreversible in >5%