Acute Kidney Injury Flashcards
Relationship between serum creatinine and GFR - graph
What is the current definition of AKI? (AKI 1) (3 options)
Increase in serum creatinine by 26.5µmol/l within 48 hours
OR
Increase in serum creatinine to 1.5 or more times baseline, which is known or presumed to have occurred within the prior 7 days
OR
Urine volume <0.5ml/kg/h for 6 hrs
Staging for AKI is AKI 1, 2 and 3; 3 being most severe
How many emergency hospital admission per year involve AKI?
1 in 5-7
What are the 5 immediately dangerous consequences of AKI? (AEIOU)
Acidosis
Electrolyte imbalance (hyperkalaemia)
Intoxication TOXINS
Overload
Uraemic complications
(can all lead to cardiac arrest)
What are the short-term outcomes of AKI?
Death
Dialysis (indications AEIOU)
Length of stay
What are the intermediate/long-term complications of AKI?
Death
CKD
Dialysis
CKD-related CVS events
What is the incidence of dialysis-requiring AKI?
45-75%
Example case - rise in serum creatinine >50% baseline
baseline = 80µmol/L; rises to 120µmol/L - may still be in ‘normal’ range
Is this the moment to act?
YES; it is too late when creatinine reaches 400
What are the 3 categories of causes for AKI?
Pre-renal (blood flow to kidney)
Renal (intrinsic) (damage to renal parenchyma)
Post-renal (obstruction to urine exit)
(often several causes will exist so think broadly)
What are the pre-renal cause of AKI? (3 broad headings)
Reduce effective circulation volume - Volume depletion (haemhorrage/dehydration; diarrhoea + vomiting); Hypotension/shock (sepsis); Congestive cardiac failure/liver failure
Arterial occlusion
Vasomotor - NSAIDs/ACE inhibitors (potentially reduce BF to kidneys)
What are the renal (intrinsic) causes of AKI? (6 broad headings)
Acute tubular necrosis (ATN) - ischaemic
Toxin-related - Drugs (aminoglycosides/amphotericin/NSAID); Radiocontrast; Rhabdomyolysis; Snake venom/heavy metals (Pb, Hg), mushrooms etc
Acute interstitial nephritis (many causes including PPIs)
Acute glomerulonephritis
Myeloma
Intra-renal vascular obstruction - Vasculitis; Thrombotic microangiopathy
What are the post-renal causes of AKI? (1 broad heading - 3 sub)
Obstruction:
- Intraluminal (calculus, clot, sloughed papilla)
- Intramural (malignancy, ureteric stricture, radiation fibrosis, prostate disease)
- Extramural (RPF, malignancy)
What is the most common cause of AKI? What can it lead to if untreated?
- Poor perfusion* leading to established tubule damage (pre-renal)
e. g. hypotension, hypovolaemia (failure of circulation to provide sufficient plasma flow to maintain blood chemistry and fluid balance, due to loss of volume and/or pressure)
If promptly treated - can resolve; if sustained = Acute Tubular Necrosis (exacerbated by toxic injury e.g. drugs)
What is radiocontrast nephropathy?
AKI following administration of iodinated contrast agent; common contributor to hospital acquired AKI
How quickly does RCN usually resolve? Can it lead to permanent loss of function?
After 72hr usually resolves
Yes, it may lead to permanent loss of function
Give risk factors for RCN
- Diabetes mellitus
- Renovascular disease
- Impaired renal function
- Paraprotein
- High volume of radiocontrast
What is myeloma in terms of plasma cells?
Monoclonal proliferation of plasma cells producing an excess of immunoglobulins and light chains
Some clinical features of myeloma? (also called multiple myeloma)
- Anaemia
- Back pain
- Weight loss
- Fractures
- Infections
- Cord compression
- Elevated ESR
- Hypercalcaemia
How is myeloma diagnosis made?
- Bone marrow aspirate - >10% clonal plasma cells
- Serum paraprotein +/- immunoparesis
- Urinary Bence-Jones protein (BJP)
- Skeletal survey - lytic lesions - shown below
Investigations for AKI (basic terms)
- History
- Examination (fluid status; look for systemic illness e.g. rashes, joint tenderness)
- Renal function etc
- Urine dipstick
- FBC
- USS
- Blood test
- ‘Fancy’ blood tests if indicated
What should be included when doing blood tests for AKI?
U+Es
Bicarb (for acidosis)
LFTs
Bone
FBC
Clotting
Blood gas
(fancier - ANCA, Ig, C3 C4 dsDNA)
What should be done when AKI is found not to be pre-renal, post-renal and is not responding well to drugs?
Renal biopsy
What is involved in urine dipstick for AKI?
Detecting blood/protein
?Urine PCR or ACR
?Urine Bence Jones Protein (indicates myeloma)
How do we avoid AKI?
Avoid dehydration
Avoid nephrotoxic drugs
Give fluids
Treat Sepsis
Risk factors for AKI?
What are the AKI ‘risk events’?
When patients have a risk event and one/more risk factors (therefore prob have AKI) what is the prevention care bundle that should be considered?
‘STOP-AKI‘
Sepsis - if suspected screen + treat (SEPSIS 6)
Toxins - avoid (e.g. Gentamicin, NSAIDs, IV iodinated contrast)
Optimise BP and volume status - avoid/correct hypovolaemia, review BP meds
Prevent harm - identify + investigate cause; daily U+Es, fluid balance + meds review
What is the main question to ask in each of: pre-renal, renal (intrinsic), post-renal
Pre-renal: do they need fluid? BP support
Renal (intrinsic): can you remove precipitant?
Post-renal: do they need a catheter?
How do we balance fluid in AKI?
- Volume resuscitation if volume deplete
- Fluid restriction if volume overload
How do we optimisie BP in AKI?
- Give fluid/vasopressors
- Stop ACEI/anti-hypertensives
What 2 nephrotoxic drugs should be stopped in AKI?
- NSAIDs
- Aminoglycosides
What are the 5 Rs for IV prescribing?
Resuscitation - IV fluids urgently to restore circulation w hypovolaemia
Routine maintenance - IV fluids if cannot take orally or enterally to meet patient maintenance requirements
Replacement - IV addiitonal maintenance to correct exisitng deficit/ongoing abnormla external losses
Redistribution - some patients have abnormal internal fluid redistribution/abnormal fluid handling (i.e. in speis, cardiac, liver, renal disease)
REASSESSMENT
What on the ECG is usually the earliest sign of hyperkalaemia?
Peaked (tall, tented) T waves
What are other ECG changes seen in hyperkalaemia? (P wave changes; QRS changes; pathologies)
P wave widens and flattens; PR segment lengthens; P waves eventually disappear
Prolonged QRS
AV block - slow junctional and ventricular escape rhythms
Conduction block
Sinus bradycardia
Slow AF
Development of a sine wave appearance - a pre terminal rhythm
Cardiac arrest !!!
- Aystole*
- V fib*
Treatment for hyperkalaemia? (SSR)
- Stabilise* the myocardium - calcium gluconate
- Shift* potassium intracellularly - salbutamol, insulin -dextrose
- Remove -* diuresis, dialysis, anion exchange resins
Intoxication - What are the antidotes for morphine and digoxin?
Morphine = naloxone
Digoxin = digibind
What may be required in cases of intoxication AKI?
Renal replacement therapy
What are the indications for dialysis in AKI?
Decreased bicarbonate (Acidosis)
Hyperkalaemia (Electrolytes)
Pulmonary oedema (Overload)
Pericarditis (Uraemia)
Difference between haemodialysis and haemofiltration?
Haemodialysis = solute removal by diffusion; intermittent therapy (each session 3-5hrs)
Haemofiltration = solute removal by convection; larger pore size; continuous therapy
What are the advantages of HD (intermittent)?
- Rapid solute removal
- Rapid volume removal
- Rapid correction of electrolyte disturbances
- Efficient treatment for hypercatabolic patient
What ar the disadvantages of HD (intermittent)?
- Haemodynamic instability
- Concern if dialysis associated with hypertension, may prolong AKI
- Fluid removal only during short treatment time
What are the advantages of CRRT (continuous)?
- Slow volume removal associated with greater haemodynamic stability
- Absence of fluctuation in volume and solute control over time
- Greater control over volume status
What are the disadvantages of CRRT (continuous)?
- Need for continuous anticoagulation
- May delay weaning/metabolism
- May not have adequate clearance in hypercatabolic patient
Pre-renal = v common
Renal = less common but v important
Post-renal = v common and usually v curable
