What is the definition of acute kidney injury?
Increase in serum creatinine by at least 26.5 micromoles/litre within 48 hours
Increase in serum creatinine to 1.5 times the baseline, which is known or presumed to have occured within the prior 7 days
Urine volume less than 0.5 ml/kg/h for 6 hours
What is the incidence of acute kidney injury?
Hospital admissions - 1 in 5 to 7
ITU admissions - more than half
Uncommon in the community
Incidence is higher or more corbidity
What are the immediately dangerous consequences of AKI?
Acidosis - can cause cardiac arrest
Electrolyte imbalance - can cause cardiac arrest (hyperkalaemia)
Intoxication TOXINS - opiates can cause respiratory and then cardiac arrest
Overload - with fluid and pulmonary oedema can cause cardiac arrest
What are the outcomes of AKI?
Short - term:
Death, dialysis, AEIOU
Death, CKD, dialysis, CKD related CV events
What are the divisions of causes of AKI?
Pre-renal (blood flow to the kidney)
Renal (intrinsic - damage to renal parenchyma)
Post - renal (obstruction to urine exit)
What are the pre-renal causes of AKI?
Reduction in effective circulation volume:
- Volume depletion (haemorrhage/dehydration - diarrhoea and vomiting)
- Hypotension and shock (sepsis )
- Congestive heart failure / liver failure
- NSAIDS / ACE inhibitors (nsaids potentially reduce blood flow to the kidneys)
What are the intrinsic causes of acute renal injury?
Acute tubular necrosis (ischaemic)
Toxin - related:
- Drugs (aminoglycosides/ amphotericin / NSAID)
- Rhabdomyolysis (haem pigments) (happens as a result of muscle damage)
- Snake venom / heavy metals - Pb, Hg
Acute interstitial nephritis (many causes including drugs - PPI's)
Intra renal vascular obstruction
- Thrombotic microangiopathy
What are the post - renal causes of AKI?
–Intraluminal (calculus, clot, sloughed papilla)
–Intramural (malignancy, ureteric stricture, radiation fibrosis, prostate disease)
–Extramural (RPF, malignancy)
What is the most common cause of AKI?
Poor perfusion - established tubule damage
What is the prognosis of radiocontrast nephropathy?
Common contributor to hospital acquired AKI
Usually transient renal dysfunction, resolving after 72 hours
May lead to permanent loss of function
What are the risk factors for radiocontrast nephropathy?
•Impaired renal function
•High volume of radiocontrast
•All of the above
What is the effect of myeloma on blood cells?
Monoconal proliferation of plasma cells producing an excess of immunoglobulins and light chains
How is diagnosis of myeloma made?
Bone marrow aspirate - >10% clonal plasma cells
Serum paraprotein ± immunoparesis
Urinary Bence-Jones protein (BJP)
Skeletal survey - lytic lesions
What are the clinical features of myeloma?
–Markedly elevated ESR
What are the investigations for AKI?
U and E's
FBC (bicarb, LFT's, Bone, clotting) - ANCA?
Fancy blood tests if indicated
Urine Bence Jones Protein - immunoglobulin light chain that may be suggestive of myeloma
How do we avoid AKI?
Avoid nephrotoxic drugs
What are AKI risk factors?
When patients at risk are experiencing a risk event? (sepsis, toxins, hypertension, hypovolaemia, major surgery) what is the management?
What is the management of AKI?
Pre - renal - do they need fluid? BP support
Renal (intrinsic) - can you remove the precipitant
Post renal - do they need a catheter
How do we manage fluid balance in AKI?
Volume resuscitation if volume deplete
Fluid restriction if volume overload
How do we optimise blood pressure in AKI?
Give fluid / vasopressors
Stop ACE i / antihypertensives
What are the 5 R's for IV prescribing?
Resuscitation - to restore circulation with hypovolaemia
Routine maintenance - when the patient cannot take anything orally or enterally
Replacement - don't need urgent resuscitation but need additional maintenance to correct an existing defecit or ongoing abnormal external loss - diarrhoea or fever
Redistribution - Abnormal internal fluid as a result of sepsis, cardiac/liver/renal disease (tissue oedema) or GI tract/thoracic/ peritoneal collection
What are the sources of fluid intake?
What are the sources of fluid output?
Insensible losses (skin and lungs)
What is the ECG reading of hyperkalaemia?
Peaked T waves (usually the earliest sign of hyperkalaemia)
Tall tented T waves
P wave widens and flattens
PR segment lengthens
P waves eventually disappear
AV block - slow junctional and ventricular escape rhythms
Development of a sine wave appearance - a pre terminal rhythm
What is the treatment of hyperkalaemia?
Stabilise the myocardium - calcium gluconate
Shift potassium intracellularly - salbutamol, insulin -dextrose
- Diuresis, dialysis, anion exchange resins
What are the antidotes of morphine and digoxin?
Morphine - naloxone
Digoxine - digibind
What are the indications for dialysis in AKI?
What is the difference between haemodialysis and haemofiltration?
Haemodialysis - solute removal by diffusion
Intermittent therapy - each session lasting 3 - 5 hours
Haemofiltration - solute removal by convection, larger pore size, continuous therapy
What are the advantages of HD?
–Rapid solute removal
–Rapid volume removal
–Rapid correction of electrolyte disturbances
–Efficient treatment for hypercatabolic patient
What are the disadvantages of HD?
Concern if dialysis associated with hypotension, may prolong AKI
Fluid removal only during short treatment time
What are the advantages of CRRT? - continuous renal replacement therapy
–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?
Need for continous anticoagulation
May delay weaning / immobilisaation
May not have adequate clearance in hypercatabolic patient
Explain the significance of the relationship between plasma creatinine and GFR.