Renal Physiology - AKI & RRT Flashcards
- PB_BK_55 Micturition - PB_BK_56 Pathophysiology of acute renal failure
What is AKI and how is it diagnosed?
An abrupt decrease in renal function resulting in:
Retention of urea and other waste products
Dysregulation of ECV and electrolytes
Dysregulation of acid-base balance
Measured through creatinine and urea (which lag behind renal function, and do not indicate prognosis)
Other markers
NGAL and IL-18 rise before any other markers of AKI
KIM-1, L-FABP
Diagnosis:
Increase of creatinine by 0.3mg/dl within 48hr, increase to >1.5x baseline within 7 days, or urine output <0.5ml/kg/hour for 6 hours.
AKI is up to 7 days
Acute kidney disease up to 90 days
Chronic kidney disease is beyond 90 days
What are the causes of AKI and how can they be differentiated?
Pre-Renal (Hypoperfusion)
Heart failure, Hypovolaemia (including dehydration), liver disease
Renal
ATN, Pyelonephritis, glomerulonephritis, rheumatic, diabetic, hypertensive, nephrotic syndrome
Post-Renal (Obstructive)
Ureteric stone, prostate, tumour, constriction, clot retention
Urinalysis can indicate pre-renal vs renal
Renal biopsy can identify renal causes
USS or CT KUB will demonstrate a post-renal cause
What is the management of AKI?
Fluid
Diuretics
Clearly indicated in cardiogenic pre-renal AKI
Unclear benefit in other situations
High dose furosemide is often given to kick start the kidney - higher dose needed, because a very small proportion actually reaches the loop of Henle
Albumin & diuretic infusion
Often used in liver failure, but strict caution against use in hepatorenal syndrome
Dopamine
Rarely used anymore, no benefit seen, especially in sepsis
Sodium bicarbonate
Controversial, as may make ECV acidaemia transiently better, however intracellular acidosis may worsen - can stimulate superoxide formation, and trigger pro-inflammatory cytokine release
Can be given in extreme acidosis to improve inotrope/vasopressor function as a bridge to RRT.
RRT
To allow for recovery of normal physiology and clear toxins
What are the indications for RRT in AKI?
Fluid overload refractory to diuretic medical therapy
Uraemia leading to encephalopathy
Acidosis or hyperkalaemia despite medical management
Specific toxin removal
Lithium
Methanol
Aspirin
Barbiturates
What are the different types of RRT
Continuous
CAVHD - Continuous arteriovenous haemodialysis
SCUF - Slow continous ultrafiltration
CAVH - Continuous arteriovenous haemofiltration
CVVHD - Continous venovenous haemodialysis
CVVHDF - Continuous venovenous haemofiltration
Intermittent
PD - Peritoneal Dialysis
IHD - Intermittent haemodialysis
SLED - Sustained low efficiency dialysis
SLEDF - Sustained low efficiency diafiltration
SCD - Slow continuous dialysis
6 hours of intermittent = 72 hours CRRT
CRRT is more haemodynamically stable
Combinations of ultrafiltration (fluid pushed against a filtering membrane), and dialysis (where dialysate fluid is used to generate osmotic/concentratiuon gradients across a membrane)
What are the indications for CRRT over IRRT, and what are its disadvantages?
Indications
Risk of disequilibrium syndrome with intermittent therapy
Raised ICP
High volume removal
Critically ill
Haemodynamically unstable
Disadvantages
Long period of immobility
Hypothermia
Labour intensive
Expensive
Requires continuous anticoagulation
Explain the difference between dialysis and ultrafiltration
Dialysis:
Separation of particles in a liquid determined by permeability through a membrane
Blood and dialysate pass each other on opposing sides of a semi-permeable membrane, allowing solutes to diffuse across, down their concentration gradient.
Usually counter-current exchange (blood and dialysate pass in opposite directions)
Ultrafiltration:
Hydrostatic pressure causes solvent to be pushed across a filter, leaving solute behind.
This can be used to remove only water during treatment of fluid overload
Determined by Starling forces in the same manner that occurs in the glomerulus.
What features of CRRT need to be prescribed?
Dose
Rate of blood clearance, or ‘effluent dose’
Usually 20-25ml/kg/hrDialysis rate (ml/hr) + predilution replacement rate (ml/hr) + postdilution replacement (ml/hr) + fluid removal (ml/hr) / weight in kg
Blood flow
100-300ml/hr, higher flow increases rate of filtration, but with more profound haemodynamic effect, and requiring more citrate which can lead to accumulation
Fluid removal
The net fluid balance after any fluid is added or removed.
Filtration factor
The fraction of water removed from the blood
FF (Ultrafiltrate flow rate/plasma water flow rate)
Target is < 20%, as increased risk of clotting if higher than this.
If FF is too high, then increasing blood flow or addition of pre-filter replacement can correct it.
Pre-filter replacement reduces clotting risk, but reduces efficacy of dialysis.
Anticoagulation
Citrate - Localises anticoagulant to the machine, as it can be deactivated before returning to the patient. Requires calcium monitoring, and alternative anticoagulation for DVT prophylaxis
Heparin - Requires all of the patient’s blood to be heparinised
Prostacycline
Not used frequently, can cause hypotension
None
If severe bleeding or coagulopathy such as severe hepatic failure
What complications are associated with RRT?
Access related
Thrombosis, bleeding, infection, recirculation
Circuit related
Clotting, disconnection, allergic reaction
Anticoagulation related
HIT, hypocalcaemia, thrombocytopaenia, bleeding
Other
Hypotension, hypothermia, electrolyte imbalance, air embolism, nutrient losses, drug doses may need modifying.