Flashcards in Acute Kidney Injury Deck (21):
What is the definition of acute kidney injury?
Decline of renal excretory function over hours/days
Recognised by the rise in serum urea and creatinine
What is the RIFLE criteria?
- serum creatinine by 1.5 or GFR decrease of 25%
- increased SCr by 2 or GFR decrease of over 50%
- increased SCr by 3 or greater than 353
- or GFR decrease of 75%
- persistent ARF (complete loss of kidney function for more than 4 weeks)
- end stage kidney disease
What are the diagnostic criteria of acute kidney injury?
- circulatory failure
- shock (lack of blood to the kidney)
- injury to the cells of the kidney
Name some of the causes pre-renal failure.
Hypovolaemia and hypotension
- Inadequate fluid intake
- Blood loss through trauma
Reduced effective circulating volume
- cardiac volume
- septic shock (vasodilation)
Renal artery stenosis
Name some causes of intrinsic renal disease.
- ischaemic ATN
- nephrotoxic ATN
- myeloma cast nephropathy
- drugs (gentamicin)
- small and large vessels
Name some causes of post-renal failure.
Renal papillary necrosis
Carcinoma of the cervix
What is the cause of acute tubular necrosis?
Underperfusion of the tubules and/or direct toxicity
Can be all three
Which toxins can cause acute tubular necrosis?
- drugs (NSAIDs, gentamicin, ACEI)
- poisons (e.g. metals and antifreeze)
- myoglobin (rhabdo)
- haemoglobin (sickle cell)
What happens to glomerular filtration as pressure falls?
Prostaglandins dilate the afferent arteriole to increase flow as the MAP falls towards 80mmHg
How do NSAIDs affect renal perfusion?
NSAIDs inhibit prostaglandins (which naturally dilate the afferent arteriole), so the flow of blood into the glomeruli of the kidneys keeps falling
- affernet arteriole remains constricted
- should be taken off it in renal failure
How do ACEI affect renal perfusion?
Efferent arteriole extra-vasodilated, which decreases the pressure within the glomerulus when a person is on ACEI
What do you need to know to manage acute kidney injuries?
- urea and creatinine
- potassium increased
Urine output less than 400ml/day
Clinical assessment of fluid status
- BP, JVP, oedema and heart sounds
Underlying diagnosis (history, exam and medication)
What do you need to treat with acute kidney injuries?
Airway and breathing
Circulation (shock) to restore renal perfusion
- pulmonary oedema
Describe the diagnostic procedure behind acute kidney injuries.
History and exam (septic, rashes, haemoptysis, rhabdomyolysis)
Drugs (prescribed, OTC, supplements, radio-contrast and abuse)
Renal ultrasound (small kidney indicates chronic condition)
GN screen - ANCA, ANA, Igs, EP, complement, aGBM, urine bence jones protien
Blood films - LDH, CK
How would you exclude obstruction in AKIs?
- small size
- loss of cortico-medullary differentiation
Describe ECG changes seen in hyperkalaemia.
Suppression of impulse generation by the SA node
- prlonged PR interval
Decreased conduction by the AV node
- prolonged QRS
- junctional and ventricular escape rhythms
Peaked T waves
Progression to VF and VT possible
What are the immediate problems associated with hyperkalemia?
<6 - no immediate concern
6-6.4 - risk of arrhythmia (needs treatment)
>6.5 - medical emergency
How is hyperkalemia treated?
Reduced absorption from the gut used to stablise the patient
- calcium resonium
Movement of potassium into cells
- insulin and 50% dextrose
Cardiac membrane stabiliser
- calcium gluconate
How is acidosis associated with hyperkalemia treated?
(Raised potassium and bicarbonate below 16)
- IV sodium-bicarbonate 1.26%
Name the absolute indicators for dialysis.
Refractory potassium at 6.5mmol/l or above
Refractory pulmonary oedema (and not passing urine)