AKI Flashcards

1
Q

What is the definition of acute kidney injury?

A

A rapid decline in kidney function within a short period of time.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What criteria is used to stage AKI?

A

KDIGO criteria

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Stages of serum creatinine in KDIGO criteria?

A

Stage 1: Increase >/= 26 micromol/l within 48 hours or increase >/= 1.5 to 1.9 baseline serum creatinine.

Stage 2: Increase 2-2.9 baseline serum creatinine

Stage 3: Increase >/= 3x baseline serum creatinine or is commenced on renal replacement therapy regardless of stage.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Stages of urinary output in KDIGO criteria?

A

Stage 1: less than 0.5ml/kg/hour for 6-12 hours

Stage 2: less than 0.5ml/kg/hour for more than/equal to 12 hours

Stage 3: less than 0.3ml/kg/hour for more than 24hrs or anuria (lack of urine production) for more than 12 hours.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Commonest form of AKI in hospital setting?

A

Renal AKI, specifically acute tubular necrosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What is acute tubular necrosis?

A
  • Tubular cell death
  • Commonest form of AKI in hospital
  • Occurs due to a number of factors resulting in decreased renal perfusion.
  • Common causes include: sepsis and severe dehydration
    *Other important causes include: Rhabdomyolysis and drug toxicity
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Examples of drugs causing acute tubular necrosis

A

NSAID’s
Antibiotics I.e. aminoglycosides, vancomycin etc.
Radiocontrast agents

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What is acute interstitial nephritis?

A
  • Another type and cause of renal AKI
  • Characterised by inflammatory infiltrate in the kidney interstitium.
  • Associated with medications, infections and systemic diseases.
  • Associated with: NSAID’s, antibiotics i.e. penicillins (amoxicillin), ciprofloxacin
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What is hyperkalaemia?

A

High serum potassium; associated with cardiac arrhythmias.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Causes of hyperkalaemia

A

AKI (acute kidney injury)
CKD (chronic kidney disease)
Rhabdomyolysis
Adrenal insufficiency (Addison’s disease)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Medications associated with hyperkalaemia

A

ACE inhibitors
Aldosterone antagonists (spironolactone and epleronone)
ARB’s (angiotensin receptor blockers)
NSAID’s
Potassium supplements

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Symptoms of hyperkalaemia

A

Non-specific symptoms - mainly relating to cardiac or muscular function, such as:
* Fatigue
* Muscle weakness
* Palpitations/chest pain

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Investigations for hyperkalaemia

A

Bloods
- U and E’s (potassium, creatinine, urea and eGFR)

ECG

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Appearance of hyperkalaemia on ECG

A

Tall peaked T-waves
Flattened or absent p waves
Broad QRS complexes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Management of hyperkalaemia

A
  • Cardiac monitor and IV access
  • Treat with insulin and dextrose infusion and IV calcium gluconate (calcium chloride used if calcium gluconate is unavailable).
  • 10ml 10% calcium gluconate (2-3 min) - to protect myocardium.
  • Insulin with 50ml 50% dextrose (30 mins) - moves K+ back into the cell from the ECF (extracellular fluid).
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What is Rhabdomyolysis?

A

Condition where skeletal muscle tissue breaks down and releases breakdown products into the blood. Usually triggered by an event that causes the muscle to break down e.g. extreme underuse or extreme overuse or a traumatic injury.

17
Q

Main causes of Rhabdomyolysis

A

Anything that can cause significant damage to the muscle cells. This can include:
* Prolonged immobility, particularly frail patients that fall and spend time on the floor before being found.
* Extremely rigorous exercise beyond person’s fitness level (e.g. ultramarathon etc).
* Crush injuries
* Seizures

18
Q

What is the pathophysiology of Rhabdomyolysis?

A

Muscle cells (myocytes) undergo apoptosis resulting in the release of myoglobin, phosphate, creatine kinase and potassium (the most dangerous breakdown product as it can lead to arrhythmias).

These products are filtered through the kidney in high concentrations - resulting in AKI.

19
Q

Clinical presentation for rhabdomyolysis

A

Muscle aches and pains
Oedema
Brown-red urine
Fatigue
Confusion (especially in older frail patients).

20
Q

Investigations for rhabdomyolysis

A

Creatine kinase (raised)

Urine: will be red-brown in colour due to myoglobinuria (will be positive for blood)

Urea and electrolytes for AKI and hyperkalaemia

ECG is important in assessing the hearts response to high potassium levels.

21
Q

What are the types of AKI?

A

Pre - renal (occurring before the kidneys) - lack of perfusion to kidneys.

Renal aka intrinsic (occurring within the kidneys) - affects components of nephron directly.

Post - renal (occurring below the kidneys) - obstruction to urinary flow beyond kidney.

22
Q

Causes of pre - renal AKI

A

1) Hypovolaemia: low blood volume
- GI loss e.g. vomiting, diarrhoea.
- Haemorrhage
- Burns

2) Hypotension: low blood pressure
- Cardiogenic
- Distributive i.e. anaphylaxis, sepsis.
- Obstructive i.e. pulmonary embolism.

23
Q

Causes of intrinsic AKI

A

1) Drugs - NSAID’s, ACEi’s/ARB’s.

2) Acute tubular necrosis

3) Acute interstitial nephritis

4) Glomerular disease i.e. anti-GBM disease, post-streptococcal glomerulonephritis.

5) Vascular events i.e. thrombosis/embolism.

24
Q

Causes of post - renal AKI

A

1) External (outside the urinary system) i.e. BPH, tumour.

2) Internal (within the urinary system) i.e. stricture, renal stones (more uncommon as will only affect one kidney), urinary tract tumours.

25
Q

Treatment of AKI

A

1) IV fluid resuscitation

2) Stop nephrotoxic medications i.e. diuretics, ACE inhibitors, metformin and NSAID’s.

3) Correct the electrolyte imbalance. Hyperkalaemia treat with IV calcium gluconate + Insulin + Dextrose

4) Urinary catheter - monitor urine output and monitor weight.

5) Renal replacement therapy
- Haemodialysis is indicated for: AEIOU
* Severe Acidosis (despite treatment)
* Electrolyte abnormalities i.e. Hyperkalaemia (despite treatment)
* Drug Intoxications
* Oedema (overload of fluid)
* Ureamic pathology (encephalopathy, pericarditis, anorexia, neuropathy and asterisix)

26
Q

What are the indications for dialysis

A

Remember: AEIOU

A - Acidosis pH > 7.20
E - Electrolyte abnormalities includes K+ over 7 mmol/l
I - Intoxication
O - Oedema
U - Ureamic pathology i.e. encephalopathy, pericarditis.