Haemofiltration in the Intensive Care Unit - PowerPoint Presentation

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Haemofiltration in the Intensive Care Unit

Mairi

Mascarenhas

Clinical Educator ICU

Department of Critical Care

2018

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Introduction Acute kidney injury (AKI) with or without the need for continuous renal replacement therapy (CRRT) is a frequent problem in the ICU.

AKI has been described as a rapid onset deterioration of the function of the kidneys, impairing their ability to maintain fluid homeostasis and electrolyte and acid base balance.

Patients presenting with AKI and multi-organ failure have been reported to have mortality rates of over 50%.

If CRRT required the mortality rate rise further to as high as 80%.

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Classic renal indications for CRRTRapidly rising U/Es. Hyperkalaemia

unresponsive to medical management.

Severe metabolic acidosis.

Diuretic-resistant pulmonary oedema.

Oliguria

or

anuria

.

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Non-renal indications for CRRT:Management of fluid balance e.g. cardiac failure.Clearance of ingested toxins.Correction of electrolyte abnormalities.

Temperature control.

Removal of inflammatory mediators in sepsis.

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Implications of AKI:AKI follows from a rapid deterioration in renal function – especially in glomerular filtration rate (GFR) resulting from ischaemic or toxic injury to the kidney.

Loss of urine excretion –

anuria

. Raised levels of urea and

creatinine

; metabolic acidosis and electrolyte imbalances.

The inability to remove toxic metabolites is often associated with fluid overload – leading to pulmonary oedema and hypoxia as well as an increase in interstitial water.

May last days or weeks. Early correction is crucial.

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Diagnosing of AKI:KDIGO guidelines define AKI as:Increase in serum Creatinine by ≥ 0.3mg/dl (≥ 26.5µmol/l) within 48 hours or

Increase in serum

Creatinine

to ≥ 1.5 times baseline, which is known or presumed to have occurred within the prior 7 days or

Urine volume ≤ 0.5ml/kg/hr for 6 hours.

Kidney Disease: Improving Global Outcomes (KDIGO) 2012

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Staging of AKI:

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Pathophysiology of AKI:The kidneys are particularly susceptible to damage as the renal parenchyma and the nephrons

are exposed to particularly high concentrations of toxins as water is

reabsorbed.

Additionally, there are regions in the kidney where oxygen supply is already

scarce under physiological conditions.

Any impairment of oxygen supply/perfusion could result in tissue damage.

Even though tubular necrosis may occur, regeneration of epithelial cells is

possible if the tubular basement membrane is damaged then the

nephron

will not

regain its function.

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Aetiology:

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Pre-renal: Results from decreased blood flow to the kidneys. There is no structural damageto the kidney in the early phase of pre-renal failure, but decreased oxygen supplycould result in tubular necrosis i.e. additional intrinsic renal failure.

Causes include

:

Dehydration due to poor fluid intake or excess fluid loss

Haemorrhage

Congestive heart failure

Sepsis

Poor systemic vascular tone

Poor renal vascular tone due to NSAIDS, ACE inhibitors or

hepatorenal

syndrome.

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Intrinsic renal failure:Involves direct injury to the renal parenchyma and often includes the development of acute tubular necrosis (ATN).Causes include

:

Acute or rapidly progressive

glomerunephritis

Acute tubular necrosis caused by

ischaemia

or

nephrotoxic

drugs such as ACE inhibitors, acyclovir, high dose NSAIDs

Septic AKI mediated e.g. by inflammatory mediators or changes in intra-renal

haemodynamics

.Allergic or idiopathic interstitial nephritis Micro-vascular diseases such as

vasculitis

, disseminated intravascular coagulation (DIC), thrombotic thrombocytopenic

purpura

.

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Post-renal failure:Results from obstruction of urine flow out of the kidney. Back-flow and backpressure result in increased intra-tubular pressure and a decreased filtration gradient.

Causes include:

Renal calculi

Tumours – these may be within the bladder or external to the renal system but apply pressure/obstruct outflow to the bladder,

ureter

or urethra.

Enlarged prostrate

Congenital malformations

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Goals of treatment:Prevent further damage by treating the precipitating cause.Restore adequate cardiac output.Correction of electrolyte imbalance.

Correction of acid-base balance.

Removal of inflammatory mediators.

Prevention of fluid overload/access for nutritional support.

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Overdose with a dialysable drug or toxin:Some drugs are removed by RRT but some are not.Drugs are cleared if they are water-soluble.

Drugs that are highly protein-bound are not cleared.

National Poisons Information Service

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RRT techniques used in ICU:Treatment may be intermittent or continuous.Intermittent haemodialysis (IHD) or conventional renal dialysis involves renal unit nursing staff.

IHD method of solute clearance is by diffusion.

Continuous renal replacement therapy (CRRT) is used the most frequently involving ICU nursing staff.

CRRT method of solute clearance can is by convection (CVVH) or can be combined with diffusion (CVVHDF).

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Filter anatomy:Thousands of fine capillaries.Blood flows through the fibres.Fluid surrounds the fibres.

Fibres are semi-permeable.

Similar to

glomerular

filtration.

Depending on the molecular weight,

various weight products can be filtered.

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Solute clearance and molecules: Molecular weights up to 50,000 daltons are removed.The larger the molecule the slower the rate of transfer across the membrane.

E.G. urea (60) is cleared more efficiently than

creatinine

(113).

Small molecules <500 are cleared efficiently by diffusion but as molecule size increases diffusion becomes less effective

.

Middle molecules > 500 are cleared efficiently by convection

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The smaller the molecule, the greater the clearance by

dialysate

/blood flow increases.

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Drug prescribing:Drug adjustment is often required.Access to a pharmacist is advisable.Drug levels should be measured where possible.

Care is needed not to under-dose patients

especially

when using antibiotics to treat sepsis.

Refer to ‘The Renal Drug Handbook’ , online calculators or apps

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Methods of clearance:ConvectionDiffusion

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Convection:Relies on a pressure gradient.Solute removal is by solvent drag across the semi-permeable membrane.Convection extremely efficient at middle molecule clearance (>500

Da

).

Less efficient at small molecule clearance (<500

Da

)

but capable

of clearance – just takes longer.

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Advantages of CVVH convection:Best suited for haemodynamically unstable patients.Creates less

haemodynamic

disturbance.

Gentler means of lowering urea and electrolytes.

Prevents large fluid shifts over short time.

Better control of fluid balance.

More flexibility for drugs and nutrition.

Clearance of molecules > 500 Da.

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Disadvantages of CVVH (convection):Slower at small molecule clearance (<500 Da).Anticoagulation may be needed.

Heat loss.

Patient immobility.

More labour intensive and more expensive than IHD.

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Dialysis (diffusion):Relies on a concentration gradient.Solutes move across membrane from an area of HIGH concentration to an area of

LOW

concentration.

High concentration = blood. Low concentration = replacement fluid.

Replacement fluid flows counter-current to direction of blood flow.

Replacement fluid (

dialysate

) is pumped from the green scale on the

prismaflex

.

Diffusion more efficient at small molecule clearance (<500

Da

).

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Advantages of Renal Unit dialysis:Intermittent treatment.Short treatment ~ usually 3 to 4 hours ~ 3 times a week.Rapid removal and clearance of toxins (<500

Da

).

Rapid removal of fluid.

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Disadvantages of Renal Unit dialysis:Poorly tolerated by haemodynamically unstable patients.Hypotension.

Arrhythmias.

Muscular complications.

Disequilibrium syndrome.

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Pre Dilution:

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Benefits of Pre Dilution:Dilutes blood before it comes in to contact with the hollow fibres.Dilutes the blood in the filter fibres.Reduces concentration of clotting factors.

Prolongs the life of the filter.

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Post Dilution:

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Benefits of Post Dilution:Enhanced clearance of toxins > 15%.Speedier clearance of potassium; urea; creatinine; acidosis and inflammatory mediators.

Possible earlier reduction in

vasoactives

.

Possible reduced length of treatment time.

Possible earlier enhanced recovery and earlier discharge from ICU.

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Vas-cath or dual-lumen catheter:Right internal jugular or right subclavian ~ a 15cm length catheter may be used

Left internal jugular or left

subclavian

~ a 20cm catheter may be inserted the full length or to the black guide mark.

Femoral access: 25cm length may be used and inserted to the black guide mark. Bio-patch is used for femoral sites.

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Insertion Procedure:As per CVC insertion.Trendelenburg.CVC insertion sticker needs to be completed and filed in medical notes.

Vascath

maintenance sheet needs to be completed.

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When to change the filter:End of filter life i.e. at 72 hours.If blood appears in the waste collection bag (turns pink) → triggers the ‘blood leak detected’ alarm.Blood in waste bag indicates filter leak/rupture and treatment needs to be terminated immediately

.

If filter leak/rupture occurs – complete

datix

form and inform Gambro

If BLD alarm occurs – check that the front panel of the machine is not in direct sunlight

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Catheter patency:20ml sodium chloride 0.9% via each port.Heparin lock (1000 units per ml vial) → Lock with volume indicated on the catheter ports

→

Use red caps.

Always remove the

same volume

from

vascath

prior to recommencing treatment.

This ensures residual heparin is removed from the dead space.

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Anticoagulation via the haemofiltration circuit: 1. Citrate

2. Heparin

“For anticoagulation in CRRT, we suggest using regional citrate

anticoagulation rather than heparin in patients who do not have

contraindications for citrate” KDIGO guidelines 2012

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Coagulation cascade

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Citrate – is metabolised in liver, skeletal muscle and the kidney into bicarbonate releasing the chelated calcium

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Approximately 50% calcium is lost in the effluent

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Citrate dose to prevent clotting:Concentration of citrate required to inhibit extracorporeal coagulation has been estimated at approximately between 2.5 and 5.0 mmol/L blood in pharmacodynamic studies.

No clotting factors if ionised calcium level of the extracorporeal circuit is maintained between 0.25 and 0.35

mmol

/L.

Prismaflex

administers citrate solution into the circuit at a dose to maintain circuit ionised calcium levels between 0.25 and 0.35mmol/L

post filter

– default starting dose is 3.00mmol/L blood.

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Net loss of calcium: blood returning to the patient combines with venous blood in body normalising the ionised calcium and preventing systemic anticoagulation but there is a net loss of calcium-citrate complex into the effluent.

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The prismaflex syringe driver compensates for the net loss:Citrate anticoagulation is only regional – returning extracorporeal blood mixes with systemic blood; calcium (therefore clotting) normalises instantly.

However, there is a loss of calcium-citrate complex into effluent through convection and/or diffusion.

Calcium needs to be infused into the patient to replace the loss to the effluent.

The syringe pump automatically delivers calcium to the patient at a dose to replace calcium lost into the effluent – default 100%. The rate will adjust automatically when other flow rates are altered to maintain percentage.

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Solutions for use during Citrate Anticoagulation in CRRT

Doesn’t contain K+ 4mmol/litre K+ 4mmol/litre K+

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Equipment needed:ST150 Prismaflex® kit CA250 calcium line

50 ml Luer lock syringe

5 litre bag of

Prismocitrate

® 18/0 (citrate used as pre-dilution)

5 litre bag of Prism0cal® B22 (calcium-free

dialysate

solution)

5 litre bag of Prismasol4® (post-dilution replacement solution)

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Equipment needed:2 x 1 litre bags of 0.9% sodium chloride (priming solution) 3 ampoules of calcium chloride diluted to total volume of 50ml using 0.9% sodium chloride. Sterile dressing pack and trolley

2 x 2 ml syringes to withdraw hep-lock, 2 x 20 ml syringes to check flow (20 ml in 6 seconds), 2 x 10 ml syringes for sodium chloride flush.

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Setting up and Priming:Switch the machine on, input the patient details, ensure accurate patient weight and haematocrit is entered. Choose the CVVHDF option

→

Choose citrate-calcium via the

Prismaflex

®

syringe pump.

Follow the on-screen step-by-step installation instructions.

Install

Prismocitrate

® 18/0 on the white scale (PBP = pre-blood pump).

Install Prism0cal® B22 on the green scale (

dialysate).Install

Prismasol

4 on the purple scale (replacement)

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Setting up and priming:Prime the ST150 with 2 litres of 0.9% sodium chloride (no heparin required).Install the calcium chloride syringe into the Prismaflex® syringe pump. This should be a 50ml

Luer

Lock syringe.

Leave the calcium line unclamped for priming by the

Prismaflex

® machine.

Ensure fluid loss/gain limit is set to 400 ml/3 hours, this is a default setting do not change.

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Starting parameters:Mode: CVVHDF Starting citrate dose: 3.0 mmol/L blood

Starting calcium compensation: 100%

Flow settings: Based on actual body weight

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Connection:Using a sterile pack and sterile gloves to access the vascath, ensure flow test isperformed –

1. Withdraw 5 ml blood from the red

vascath

port to remove hep-lock and discard onto gauze (observe for clots).

2. Withdraw and replace 20 ml blood. Flow should be sufficient to withdraw 20 ml blood from the

vascath

in 6 seconds or less.

3. Flush with 10 ml 0.9% sodium chloride.

4. Repeat on the blue

vascath

port.

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Monitoring example:Measure serum electrolytes and ABGS before initiation.At one hour

measure

(1) post filter ionised calcium to check circuit calcium

(2) patient ionised calcium to check systemic calcium

Adjust citrate dose or calcium concentration according to table.

Make adjustments as required and repeat measurement after

one

hour.

Once ideal values/steady state reached measure 6 hourly

Once a day total calcium to check ratio.

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Example monitoring table – clinical decision support

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Treatment adjustments:

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