AKI Flashcards
What is the definition of acute kidney injury?
A rapid decline in kidney function within a short period of time.
What criteria is used to stage AKI?
KDIGO criteria
Stages of serum creatinine in KDIGO criteria?
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.
Stages of urinary output in KDIGO criteria?
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.
Commonest form of AKI in hospital setting?
Renal AKI, specifically acute tubular necrosis
What is acute tubular necrosis?
- 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
Examples of drugs causing acute tubular necrosis
NSAID’s
Antibiotics I.e. aminoglycosides, vancomycin etc.
Radiocontrast agents
What is acute interstitial nephritis?
- 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
What is hyperkalaemia?
High serum potassium; associated with cardiac arrhythmias.
Causes of hyperkalaemia
AKI (acute kidney injury)
CKD (chronic kidney disease)
Rhabdomyolysis
Adrenal insufficiency (Addison’s disease)
Medications associated with hyperkalaemia
ACE inhibitors
Aldosterone antagonists (spironolactone and epleronone)
ARB’s (angiotensin receptor blockers)
NSAID’s
Potassium supplements
Symptoms of hyperkalaemia
Non-specific symptoms - mainly relating to cardiac or muscular function, such as:
* Fatigue
* Muscle weakness
* Palpitations/chest pain
Investigations for hyperkalaemia
Bloods
- U and E’s (potassium, creatinine, urea and eGFR)
ECG
Appearance of hyperkalaemia on ECG
Tall peaked T-waves
Flattened or absent p waves
Broad QRS complexes
Management of hyperkalaemia
- 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).
What is Rhabdomyolysis?
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.
Main causes of Rhabdomyolysis
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
What is the pathophysiology of Rhabdomyolysis?
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.
Clinical presentation for rhabdomyolysis
Muscle aches and pains
Oedema
Brown-red urine
Fatigue
Confusion (especially in older frail patients).
Investigations for rhabdomyolysis
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.
What are the types of AKI?
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.
Causes of pre - renal AKI
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.
Causes of intrinsic AKI
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.
Causes of post - renal AKI
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.
Treatment of AKI
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)
What are the indications for dialysis
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.
