AKI Flashcards
Definition of AKI.
Rise in creatinine > 26 mcmol/L within 48h
Rise in creatinine > 1.5 base line within 7 days
Urine output < 0.5 ml/kg/h for > 6 hours.
Explain AKI.
Life-threatening biochemical disturbances with oliguria, fallling urine output and rising serum urea as well as creatinine.
In some cases urea and creatinine cannot be relied upon.
When?
Low protein intake, liver failure and sodium valproate treatment will decrease the concentration of serum Urea.
Corticosteroid treatment, tetracycline and GI bleed will increase the concentration of Urea.
Low muscle mass = low creatinine
High muscles mass, red meat ingestion, muscle damage and decreased tubular secretion = high creatinine
AKI classifications.
Pre-renal
Renal parenchymal
Post-renal
Give examples of risk factors for AKI.
Diabetes/Metformin
CKD
IHD/CCF
Liver disease
Elderly >75
Sepsis
Cognitive impairment
Medications like ACEi, ARBs, NSAIDs and antibiotics.
Contrast medium during CT scans
KDIGO stages of AKI.
1 - > 26.5 micromol/l increase or 1.5 - 1.9 times the baseline of creatinine. Also < 0.5 ml/kg/h for 6-12 hours urine output.
2 - 2.0 - 2.9 times baseline creatinine. < 0.5 ml/kg/h for > 12 hours urine output.
3 - 3.0 time the baseline of creatinine, or > 353.6 micromol/l or initiation of renal replacement therapy. < 0.3 ml/kg/h > 24 hours or Anuria for > 12 hours urine output.
Pre-renal causes of AKI.
Hypovolaemia
Decreased cardiac output
Decreased effective circulating volume (CHF and Liver failure)
Impaired renal autoregulation (NSAIDs, ACEi and calcineurin inhibitors)
Causes of hypovolaemia.
Dehydration
Reduced intake
Gut losses by vomiting, nasogastric tube lossess and diarrhoea.
Burns, sweating
Haemorrhage
Third space losses from pancreatitis, peritonitis and bower obstruction.
Systemic vasodilation
Cardiac failure or shock
Causes of renal parenchymal/intrinsic AKI.
Glomerulonephritis
Ischaemia
Sepsis/infection
Nephrotoxins such as iodinated contrast, aminoglycosides, cisplating and amphotericin B. Also haemolysis, rhabdomyolysis, myeloma and intratubular crystals.
Vasculitis
Malignant hypertension
TTP
HUS
Pre-eclampsia
Give post-renal causes of AKI.
Bladder outlet obstruction
Bilateral pelvoureteral obstruction
Give causes of bladder outlet obstruction.
Intraluminal - Calculi, blood clot, sloughed papilla and tumour.
Luminal - pelviureteric neuromuscular dysfunction, ureteric stricture, ureterovesical stricture, neuropathic bladder.
Extraluminal - Tumours, Diverticulitis, Aortic aneurysm, retroperitoneal fibrosis.
How can you distinguish between pre-renal and intrinsic AKI?
By clinical examination and by urine specfic gravity, urine osmolality, urine sodium and FEna.
Distinguishing causes of shock on clinical examination.
Hypotension, peripheries and JVP in;
Hypovolaemia, low cardiac output and vasodilation.
Hypovolaemia has postural hypotension, cool peripheries and low JVP.
Low cardiac output has hypotension, cool peripheries and raised JVP.
Vasodilation has hypotension, warm peripheries and low JVP.
Urine specific gravity, urine osmolality, urine sodium and FEna in pre-renal vs. intrinsic AKI.
investigations in AKI.
Urine dipstick always.
This checks for blood and abnormal protein.
Daily FBC, U&Es, LFTs, Bone profile, CRP and serum bicarb.
Urine PCR, Urine MC+S, USS KUB to rule out obstruction.
Perform c-ANCA (PR3) + p-ANCA (MPO) to look for vasculitis, anti-GBM, ANA C3 and C4 to look for SLE, serum immunoglobulins and electrophoresis to look for myeloma.
Anti-streptolysin if post-streptococcal.
What should you check for if you suspect HUS/TTP or DIC?
Blood film
LDH
Bilirubin
Reticulocytes
Haptoglobin
Call renal SpR urgently.
When should you check for cryoglobulins?
If unexplain rash, peripheral neuropathy, hypocomplementaemia, known Hep C, +ve RhF.
Commonest causes of AKI.
Sepsis
Major surgery
Cardiogenic shock
Other hypovolaemia
Drugs
Hepatorenal syndrome
Obstruction.
Management of AKI according to workbook.
Send off investigations
Discontinue nephrotoxic agents
Ensure volume status and perfusion pressure. Give IV fluids if dehydrated, IV furosemide if overloaded.
Consider function haemodynamic monitoring with central venous pressure line.
Monitor urine output and daily bloods
Avoid hyperglycaemia
Check for changes in drug dosing
Treat underlying cause
Refer to specialist for consideration of renal replacement therapy.
Consider ICU admission.
Clinical approach to AKI according to Oxford handbook.
Life-threatening complication such as NEWS, pulmonary oedema and hyperkalaemia refer.
Examine heart rate, BP, JVP, capillary refill and palpate the bladder.
Monitor fluid balance, K+, BLOs, lactate, daily creatinine.
Ix urine dipstick, USS, LFTs, platelets, ix for intrinsic renal disease.
Supportive treatment of AKI.
Treat sepsis
Stop nephrotoxic medication
Stop drugs that may cause complications such as K+ sparing diuretics, metformin and anti-hypertensives.
Check drug dosages
Consider gastroprotection
Avoid radiological contrast.
When to refer to renal team?
AKI not responding to treatment
AKI with complications such as hyperkalaemia, acidosis, fluid overload or overscoring NEWS.
AKI with difficult fluid balance such as hypoalbuminaemia, heart failure and pregnancy.
AKI due to possible intrinsic renal disease.
AKI with hypertension.
Management of AKI due to hypovolaemia.
Give 500 ml crystalloid over 15 min, e.g. plasmalyte or ringer lactate or Hartmann’s.
Reassess fluid state.
Further boluses of 250-500 ml crystalloid with clinical review after each.
Stop when euvolaemic or seek expert help when 2L has been given.
Why should 0.9% saline not be used in AKI?
Contains chloride and can cause hyperchloraemic acidosis.
