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Aquarius System

Nikkiso Educational

Framework

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Aquarius System
Continuous Renal

Replacement Therapy

(CRRT)

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Agenda Morning

 Theoretical perspectives
 Kidney Anatomy & Physiology
 Acute Kidney Injury
 Acute Blood Purification
 Transport Mechanisms
 Treatment Modalities
 Treatment Dose

 Practical
 Aquarius Overview
 Lining and Priming
 Recirculation

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Agenda Afternoon

 Theoretical
 Filtration Fraction
 Filtration Ratio
 Vascular Access

 Practical
 Programming
 Connection
 Alarms
 Troubleshooting
 Disconnection
 Safe Disposal

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Aquarius System
Renal Anatomy

and

Physiology

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Renal Anatomy and Physiology

 The kidneys are two bean shaped organs, located just below the inferior
boundary of the rib cage.

 Each kidney can function independently of the other.

 Each adult kidney weighs approximately 110 – 170 grams and is about the
size of a human fist.

 The adult kidneys receive 1200 millilitres of blood (25% of cardiac output)
every minute. That is 72 litres per hour or 1728 litres per day.

 Normal kidney function is measured in terms of glomerular filtration rate


(GFR). Normal GFR is typically 90-120 millilitres per minute. An estimation
of Glomerular Filtration Rate (eGFR) can be calculated based on age and
serum creatinine
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Component of the Kidney

Consists mainly of 3 parts:


Cortex contains 80% of the
Medulla contains 20% of the nephrons to filter the blood
nephrons that filter the continuously to maintain fluid
blood and concentrate urine. balance.
An important diagnostic tool.

Renal pelvis is the


start of the collecting
system, containing the
collecting tubules and
the ureter.
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Components of the Kidney

 The kidney functions using three principles:


• Ultrafiltration
• Excretion
• Re-absorption

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Components of the Kidney – The Nephron

Nephron – Is the functional unit of the kidney. Each kidney has


about one million nephrons

Each nephron contains a


glomerulus, which
functions as an individual
filtering unit
The nephron also
contains tubules for
secretion and
absorption of
substances

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Components of the Kidney

 The Glomerulus;
 The glomerulus consists of a group of cells with
selective permeability.
 Selective permeability means that certain
substances will cross the membrane and
others will not be allowed to cross.
 Through selective permeability, the kidney
regulates fluid and electrolyte balance.
 In an adult, the kidneys produce approximately
180 litres of filtrate per day.
 Only 1.5 - 2 litres are excreted as urine. The tea filter is a
 The remaining 178 litres are reabsorbed by the good example of a
semi-permeable
kidney.
membrane

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Functions of the Nephron

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Functions of the Kidney

 Fluid balance
Through ultrafiltration and reabsorption.
 Electrolyte balance
Through reabsorption and excretion.
 Acid-base balance
Through reabsorption and excretion.
 Excretion of drugs and by-products of metabolism
Nitrogen, urea, creatinine.
 Synthesis of erythropoietin
Stimulates bone marrow to produce mature red blood cells.
 Regulation of blood pressure
Through the secretion of renin.
 Maintenance of calcium-phosphate balance
Through the activation of vitamin D production.
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Aquarius System

Acute Kidney Injury

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Acute Kidney Injury

 Acute Kidney Injury (AKI) results from the sudden loss of kidney
function. AKI in the setting of critical care patients is defined as
“..an abrupt decline in glomerular filtration rate.”
Jefferson et al (2007)
 Waste products will start to accumulate in the blood.

 AKI may be accompanied by metabolic, acid-base and electrolyte


disturbances and fluid overload.

 AKI may affect other organ systems.

 AKI may require immediate treatment.

Jefferson JA, Schrier RW. Pathophysiology and Etiology of Acute Renal Failure. In: Comprehensive Clinical Nephrology.
3rd ed. Philadelphia, PA: Mosby Elsevier; 2007:755-770.

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RIFLE Criteria

The Acute Dialysis Quality


Improvement Initiative
(ADQI)
Recommends the
Classification
of AKI based on the RIFLE
criteria.

2 Ricci et al - The RIFLE criteria and mortality in acute kidney injury: A systematic review. Kidney International (2008) 73, 538–
546
Summary of Classifications of AKI

Kristensen et al (2014) ESC/ESA Guidelines on non-cardiac surgery: cardiovascular assessment and management The Joint Task Force on
non-cardiac surgery: cardiovascular assessment and management of the European Society of Cardiology (ESC) and the European Society of
Anaesthesiology (ESA). European Heart Journal 35 (35) 2383–2431
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Acute Kidney Injury Classification

 There are 3 types of Acute Kidney Injury Classification

Pre-Renal

Renal (Intra-Renal)

Post-Renal

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AKI Classification: Pre-Renal

 Pre-renal failure typically results from decreased blood flow to the kidneys.
The reduction in glomerular filtration enables the solutes in the blood to
accumulate but does not cause any structural damage to the kidney itself.
Examples of situations leading to pre-renal failure may include:
– dehydration
– haemorrhage
– congestive heart failure Pre renal 30-60%
– sepsis (think „p‟ for pressure)
– embolism/thrombosis
• Volume depletion
• Decreased circulating volume
• Reduced cardiac output
• Renal vascular disease

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AKI Classification: Renal (Intra-Renal)

 Renal (Intra-renal) failure typically involves direct injury to the kidney itself.
The most common cause is Acute Tubular Necrosis (ATN). Some causes of
ATN are:
– Ischaemia
– Hypertension
– Nephrotoxins
– Some systemic vascular diseases such as lupus.

.
Intra-Renal 20-40%
(think “I” for infection)
• Glomerular infection
• Vascular
• Nephritis

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AKI Classification: Post Renal

 In post-renal failure, the underlying cause is typically a bilateral obstruction


below the level of the renal pelvis. Causes for this may be:
– Tumour development
– Thrombi
– Urinary tract obstruction
– Hypertrophic prostate.
Post renal 1 – 10%
(think „o‟ for obstruction)

• Obstruction
• Ureters
• Bladder
• Urethra

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Nephrotoxic Drugs

 Nephrotoxicity is the poisonous effect on the kidneys caused by toxic


chemicals and medication.
 Drug-induced AKI is common in critical illness and accounts for 15% to 25%
of all cases of renal failure seen in this population.
 The medications implicated in causing drug-induced AKI can be classified
based on their mechanism of renal injury; pre-renal, intra-renal and post-
renal.
 The mechanisms of toxicity are complex and, in many cases, affect more
than one aspect of kidney function.
 All NSAIDs have been associated with AKI, and consideration should be
given to either avoid their use or, when indicated, use with extreme caution.

Bentley, M.L., Corwin H.L., Dasta J. (2010) Identification and Prevention of Common Adverse Drug Events in the Intensive Care
Unit. (Supplement in) Critical Care 38 S169-174
Ricci Z., Ronco C., (2008) The RIFLE criteria and mortality in acute kidney injury: a systematic review. Kidney International 7 (5)
538-546
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Nephrotoxic Drugs - Nonsteroidal anti-
inflammatory drugs

 Volume contraction from any cause or other forms of pre-renal AKI (cirrhosis,
congestive heart failure) will increase the incidence of and severity of
nephrotoxicity due to nonsteroidal anti-inflammatory drugs (NSAIDs).
 Conditions such as
a. Congestive heart failure
b. Hypotension
c. Volume depletion
d. 3rd spacing

 These conditions all decrease effective arterial volume.


 These are conditions that predispose the patient to NSAID-induced
nephrotoxicity.

Bentley, M.L., Corwin H.L., Dasta J. (2010) Identification and Prevention of Common Adverse Drug Events in the Intensive Care Unit. (Supplement in)
Critical Care 38 S169-174

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Nephrotoxic Drugs- ACE Inhibitors & others

 ACE inhibitors
ACE inhibitors are commonly prescribed drugs used for hypertension,
congestive heart failure and chronic kidney disease. These drugs affect renal
haemodynamics through an decrease in efferent arteriolar tone and
intraglomerular capillary pressure. The use of these drugs under normal
circumstances when renal perfusion is adequate poses very little problem.
However when these drugs are used in states of prerenal azotemia, renal artery
stenosis or concomitantly with other drugs such as NSAIDs, renal failure may
occur.
 Other drugs that cause altered glomerular haemodynamic instability
Drugs such as cyclosporine and tacrolimus, belong to a class of commonly
used immunosuppressant's for organ transplantation referred to as calcineurin
inhibitors. Calcineurin inhibitors are associated with early prerenal oliguria due
to vasoconstriction

Bentley, M.L., Corwin H.L., Dasta J. (2010) Identification and Prevention of Common Adverse Drug Events in the Intensive Care Unit. (Supplement
in) Critical Care 38 S169-174
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Phases of Acute Kidney Injury

Begins when urine

Polyuric phase
Oliguric phase

Maylast several

Recovery phase
Low urine output output begins to rise months following
(less than 400 Has variable time the onset of the
mL/24 hrs) frames, sometimes Acute Kidney Injury
Possibly protein in occurring as little as
24 hours after the During this period,
the urine onset of renal failure kidney function
Electrolyte gradually returns to
Associated with
imbalances potassium and
normal and proper
sodium loss in the urine
Metabolic acidosis urine concentrations and
volumes are
Enhanced urine
output may not reflect achieved
restored kidney
function but rather
may be the result of
accumulating serum
urea and creatinine,
which have an
osmotic diuretic effect

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Management Goals for Acute Kidney Injury

 Fluid balance.

 Correction of electrolyte abnormalities.

 Restoration of acid-base balance.

 Removal of waste products.

 Haemodynamic stabilisation.

 Nutritional support.

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Treatment options for AKI

Peritoneal Pharmacological
dialysis and fluid
Information and management
support

Acute Kidney
Injury Relieve
urological
Intermittent obstruction
haemodialysis
(IHD)
Continuous Renal
Replacement Monitoring
Therapy
(CRRT)
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Aquarius System
Continuous Renal

Replacement Therapy

(CRRT)

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Indications for commencing CRRT

Renal Indications: Non Renal indications:


 Rapidly rising serum urea and  Management of fluid balance e.g.
creatinine or the development in cardiac failure.
of uraemic complications.  Clearing of ingested toxins.
 Hyperkalaemia unresponsive  Correction of electrolyte
to medical management. abnormalities.
 Severe metabolic acidosis.  Temperature control.
 Diuretic resistant pulmonary  Removal of inflammatory
oedema. mediators in sepsis.
 Oliguria or anuria.

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Some Indications for CRRT

Pre & Post Cardiac Haemodynamic


Surgery Instability

Shock Fluid Overload

Sepsis – Lactate Drug Overdose


Acidosis

ARDS / /
ARDS Shock
Acute Multi-Organ VAP
VAP
Trauma -
Failure Rhabdomylosis
29
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Continuous Renal Replacement Therapy Goals

Clean the blood

Manage Intravascular volume

Wastes are cleaned from the blood by diffusion and convection.

Water is removed by ultrafiltration.

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Defining The Therapy

 Early application of Continuous Renal Replacement Therapy (CRRT) may prove


to be beneficial to the patient.

 CRRT is a therapy indicated for continuous solute removal in the critically ill
patient.

 CRRT allows for continuous, slow and isotonic fluid removal that results in
better haemodynamic tolerance even in unstable patients with shock and severe
fluid overload.

 CRRT can be modified at any time of the day and night to allow adaptation to
the rapidly changing haemodynamic situation of critically ill patients.

 CRRT therapy indications may be renal, non-renal, or a combination of both. It is


the treatment of choice for the critically ill patient requiring renal support and/or
fluid management.
Kellum J, Ronco C, Joannidis M (2012) An emerging consensus for AKI ICU Management 12 (1) 38-40
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Aquarius System
Treat ment M odal i t i es

&

Transport M echani sms

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Treatment Modalities

 CRRT includes several treatment modalities.

 All of these modalities use veno-venous access.

 The choice will depend on the needs of the patient and the preferences of
the physician.

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CRRT Treatment Modalities

SCUF CVVH
.
Slow Continuous
Diffusive & Continuous
Diffusive
Ultrafiltration
Convective Veno-Venous
Therapy
Haemofiltration
Therapy

CVVHDF CVVHD
Continuous Veno- Continuous Veno-
Convective Therapies
Venous Venous
HaemoDiaFiltration Haemodialysis
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Slow Continuous Ultrafiltration (SCUF)

Primary therapeutic goal: Safe management of fluid removal

Primary indications: Fluid overload

Principle used: Ultrafiltration (removal of water)

Therapy characteristics: • No dialysate or substitution solutions.


• Fluid removal only.

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Transport Mechanism: Ultrafiltration

Ultrafiltration is
the movement of
fluid through a
semi-permeable
membrane along a
pressure gradient.

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Slow Continuous Ultrafiltration (SCUF)

Graphics will become visible in presenter


mode.

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Continuous Veno-Venous Haemofiltration
(CVVH)

Primary therapeutic goal: Solute removal and safe management


of fluid volume.

Primary indications: Uremia, acid/base and/or electrolyte


imbalances, fluid overload.
Principle used: Ultrafiltration (removal of water)
Convection (clearance of solutes)

Therapy characteristics: • Requires substitution solution with a


buffer to drive convection.
• No dialysate solution
• Used to achieve solute removal
(small, medium and large sized
molecules) and fluid balance.

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Transport Mechanism: Convection

Convection is the
one-way movement
of solutes through
a semi-permeable
membrane with a
water flow.
Sometimes it is
referred to as
solvent drag.

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Continuous Veno-Venous Haemofiltration
(CVVH)

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Continuous Veno-Venous Haemodialysis
(CVVHD)

Primary therapeutic goal: Solute removal and safe management


of fluid volume.

Primary indications: Uremia, acid/base and/or electrolyte


imbalances, fluid overload.
Principle used: Diffusion

Therapy characteristics: • Requires substitution solution with a


buffer to aid the diffusive process.
• No substitution solution.
• Used to achieve solute removal
(small and medium sized molecules)
and fluid balance.

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Transport Mechanism: Diffusion

Diffusion is the
movement of
solutes through a
semi-permeable
membrane from an
area of higher
concentration to an
area of lower
concentration.

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Transport Mechanism: Diffusion

 Solutes move from a higher concentration to a lower concentration

 In CRRT, diffusion occurs when blood flows on one side of the


membrane, and dialysate solution flows counter-current on the other
side

 The dialysate does not mix with the blood

 Efficient for removing small and medium molecules but not large
molecules

 Molecular size and membrane type can affect clearances

 Diffusion occurs during haemodialysis

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No Counter Current Principle

3 3 3 3.5 3 4 2.5 2

3 3 3 4 4.5 5 6 6.5

3 3 3 3.5 3 4 2.5 2

Anaesthesia UK (2003) Acute renal failure and renal replacement therapy in the ICU
http://www.frca.co.uk/article.aspx?articleid=100367#
Accessed 10th August 2015 10:10

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Counter current principle (Diffusion)

2 2.5 3 3.5 4 4.5 5 5.5

2.5 3 3.5 4.0 4.5 5 6 6.5

2 2.5 3 3.5 4 4.5 5 5.5

Anaesthesia UK (2003) Acute renal failure and renal replacement therapy in the ICU
http://www.frca.co.uk/article.aspx?articleid=100367#
Accessed 10th August 2015 10:10

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Continuous Veno-Venous Haemodialysis
(CVVHD)

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Continuous Veno-Venous Haemodiafiltration
(CVVHDF)

Primary therapeutic goal: Solute removal and safe management


of fluid volume.

Primary indications: Uremia, acid/base and/or electrolyte


imbalances, fluid overload.
Principle used: Diffusion and Convection

Therapy characteristics: • Requires dialysate solution and


substitution solution, both contain a
buffer that drives the convection and
diffusion processes.
• Used to achieve solute removal
(small, medium and large sized
molecules) and fluid balance.

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Continuous Veno-Venous Haemodiafiltration
(CVVHDF)

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Treatment Modality Summary
Continuous Renal Replacement Therapy : A Summary
Fluids
Molecules
Modes Principles
Cleared
Pumps In Use
SCUF UltraFiltration No Fluid (for fluid removal only)
Slow Continuous UltraFiltration Movement of fluid through a
semi-permeable membrane Nil Pre-dilution pump
along a pressure gradient. Post-dilution pump
Filtrate Pump

CVVH Convection (active) Substitution fluid (pre/post)


Continuous Veno-Venous Haemofiltration One-way movement of solutes
Small
(can be pre or post dilution) through a semi permeable Pre-dilution pump
Medium
membrane with a water flow – Post-dilution pump
Large
sometimes referred to as „solvent Filtrate Pump
drag‟.
CVVHD Diffusion (passive) Dialysate fluid
Continuous Veno-Venous HaemoDialysis Movement of solutes through a
semi-permeable membrane from Small Dialysate pump
an area of high concentration to Medium Filtrate pump
low concentration.

Combined Mode: Substitution / Replacement Fluid


Convection Dialysate
CVVHDF • Haemofiltration Small
Continuous Veno-Venous • Active – convection Medium Post dilution pump
HaemoDiaFiltration Diffusion Large Dialysate pump
• Haemodialysis Filtrate pump
• Passive - diffusion
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Molecular Weights

Ashley et all. The Renal Drug Handbook, 2nd Ed. 2004, Medical Press, Abingdon, UK. ISBN: 1857758730

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Adsorption

Adsorption
is the adherence
of solutes and
biological matter to
the surface of a
membrane

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Transport Mechanism: Adsorption

 High levels of adsorption can cause some filters to clog and become
ineffective

 Membrane type affects adsorption tendencies/effectiveness

 Adsorption may also limited removal of some solutes (eg. β2 microglobulins)


from the blood

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Replacement Fluid

 Accusol 35 is a bicarbonate based solution primarily intended for use in


patients with hyperkalaemia.

 Accusol 35 solution gives health care providers a convenient and easy-to-


use solution for the patient‟s CRRT needs. It is completely lactate-free, with
a 100% bicarbonate buffer that provides all the necessary electrolytes.
Accusol solution comes in ready-to-mix formulations with varying potassium
levels

 Substitution fluid in haemofiltration and haemodiafiltration and a diaylsis


solution in haemodialysis and haemodiafiltration.

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Accusol 35

 Accusol 35 purifies blood of waste products; it corrects acidity or alkalinity


the level of salts in the blood.

 Accuosl 35 solutions are supplied in a non PVC bag with two chambers
containing bicarbonate and calcium. The chambers need to be spilt and
mixed before use. Once mixed the solution lasts for 24 hours.

 Accusol 35 works closely with the body‟s


natural chemistry to maintain electrolyte
balance during therapy and restore
haemodynamic stability

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Aquarius System

Tr e a t m e n t D o s e

6.02.08 Software Education Module

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Measurement of therapy dose

 Therapy dose is a measure of the quantity of blood purification achieved.

 The concept of clearance represents the volume of blood cleared of a given


solute over time.

 Commonly used solute markers to quantify clearance are serum Urea and
Creatinine.

 Best clinical practices combine clearance and dosing effectiveness using a


weight-related dosage of therapy

 On Aquarius, therapy dose is defined by the total ultrafiltration rate and is


expressed as millilitres (therapy amount) per kilogramme (patient weight)
per hour (time) or ml/kg/hr

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Prescribed vs Delivered Dose

Prescription should exceed that calculated to be adequate


because of the known gap.

8ml/kg/hr less

 Prescribed dose of therapy should be assessed daily to


account for any measured shortfalls in delivered dose.

 Delivered dose of therapy should be assessed to ensure the


adequacy of the prescription. According to Vesconi et al
(2009) in practice the delivered therapy dose was on
average 8ml/kg/hr less.

Vesconi et al (2009) Delivered dose of renal replacement therapy and mortality in critically ill patients with
acute kidney injury. Critical Care 13 (2);r57

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Where does that 8mls/kg/hr go?

 Why might we „lose‟ significant amounts of therapy dose?

• Recirculation in vascular access


• High filtration fractions
• Filter clogging and clotting
• Troubleshooting skills
• Changing of circuits
• Filter down time

Vesconi et al (2009) Delivered dose of renal replacement therapy and mortality in critically ill patients with
acute kidney injury. Critical Care 13 (2);r57

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Clinical Evidence for Therapy Dose

 Landmark studies suggest that increasing therapy dose improved survival1

 Recent studies find no difference in survival between 25 and 40 ml/kg/hr


therapy dose2,3

 Higher therapy doses (40 ml/kg/hr) did not alter mortality in the subgroup of
sepsis patients.

 How may clinicians use the evolving evidence base to choose an


appropriate therapy dose?

1. Ronco et al Effects of different doses in continuous veno-venous haemofiltration on outcomes of acute renal failure:
a prospective randomised trial Lancet 2000; 355: 26–30
2. Bellomo et al Intensity of Continuous Renal-Replacement Therapy in Critically Ill Patients n engl j med 2009 361;17
3. Palevsky et al Intensity of Renal Support in Critically Ill Patients with Acute Kidney Injury n engl j med 2008 359;1

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Study Comparison

AUTHORS STUDY POPULATION CRRT UFR EFFECTS PATIENT


NUMBERS TECHNIQUE (ML/HR) WEIGHT
Sander et al 26 SIRS CVVH 1000 No effects 70 kg

John et al 30 SEPSIS CVVH VARIABLE Increase in MAP 70 kg

De Vriese 15 SEPSIS/ CVVH 2700 Increase in SVR 70 kg


ARF

Increase in MAP
Wakabayashi 6 SIRS/ CVVH VARIABLE N/A
and
MOF
Oxygenation

Increase in MAP
Matamis 20 SEPSIS CVVH 1500 70 kg
and
MOF
Oxygenation

Grootendorst Improved
26 SEPSIS/ CVVH 4500 70 kg
Haemodynamics
MOF
and Survival

Improved
Honore 20 SEPTIC CVVH 9000 74 kg
Haemodynamics
SHOCK
and survival
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Pedrini et al (2000) The comparison of mixed pre and
postdilution compared to traditional infusion modes.

300

250

200 PostDilution
150 Mixed
Pre-Dilution
100

50

0
Urea Creatinine Phosphate

Pedrini LA1, De Cristofaro V, Pagliari B, Samà F. (2000) Mixed predilution and postdilution online hemodiafiltration compared
with the traditional infusion modes. Kidney Int Nov; 58 (5):2155-56.

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Predilution and middle molecule clearances.

 Bellomo et al (2001)
100
preliminary experience
Clearance (ml/min)

80 with high volume


60 haemofiltration in human
septic shock.
40
 6 litre exchange.
20
 Effects of predilution on
0 clearance of Vancomycin
0 1 2 4 5 6 (middle sized molecule).
Amount of Predilution (Litres)

Bellomo R, Tipping P, Boyce N (1993) Continuous veno-venous hemofiltration with dialysis removes cytokines from the circulation of
septic patients. Crit Care Med 21:522–526

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Aquarius- Renal Dose display

 Renal Dose display on Aquarius


6.02- during treatment, patient
weight can be entered and
modified at any time.

 At the start of treatment or after a


programmed value change, the
programmed renal dose is
displayed for the first 2 minutes.

 After 2 minutes of uninterrupted


therapy, the delivered renal dose
is displayed based on the actual
pump rates.

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Aquarius System

Vascul ar Access

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Overview

 Vascular access is required to


perform all CRRT therapies.

 Central venous catheters provide


rapid and easy vascular access
permitting immediate use

 The most common catheter now in


use is the large-bore, double-
lumen catheter.

 A practical understanding of
vascular access contributes to
optimal delivery of CRRT therapies

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Insertion Sites - Choices

 Internal Jugular

 Femoral

 Subclavian

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Considerations

 Diameter, length and types of catheters (II)

 Type: Material features


 Silicone elastomer catheters have lower thrombogenicity and better
flexibility.
 Biocompatible and kink resistance
 Conform to vessel anatomy, therefore reduce risk of trauma
 Diameter and blood flow:
 11 French : 250-300 ml/min Blood Flow
 13.5 French : 450-500 ml/min Blood Flow

 Recirculation- up to 20%
 Especially if femoral access is less than 20 cm
 Avoid reverse AV connection

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Patient Preparation

 Patient body status


 Coagulation and Intravascular filling
 Mobility influences
 Presence of other central lines
 Influences on catheter choice
 Clinician choice
 Availability of ultrasound guidance

 Assessment of catheter patency


 Connection techniques
 Special circumstances

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Catheter Characteristics

 Ease of insertion: to avoid vessel


trauma

 Good flow characteristics: to optimise


blood flow

 Kink resistant: to avoid access


pressure problems

 Biocompatible: to reduce complication


risks

 Amenability to guide wire change: to


optimise therapy

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Side-by-Side Polyurethane Catheters

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Coaxial Polyurethane Catheters

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Triple lumen Catheters

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Silicone Catheters

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Reversing the Lines

1 Lewington A, Kanagasundaram S. Acute Kidney Injury. Renal Association guidelines: Guideline 8.1 – AKI: Vascular access for RRT. Guideline 8.2,
Page 45 of 59, Para 3 ‘Rationale for 8.1-8.9’ lines 7-9 http://www.renal.org/Clinical/GuidelinesSection/AcuteKidneyInjury.aspx

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Vascular Access

 Vascular Access is continuously tested during CRRT treatment

 Practical understanding about vascular access is necessary for optimal


treatment

 Catheter site, size, type and patient preparation may be considered

 Inadequacies in vascular access may limit delivered therapy

 Troubleshooting choices

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Vascular Access Troubleshooting

 Starting blood flow


 Gradual increase
 Optimising blood flow rates
 Starting treatment

 Using Aquarius History


 Using Recirculation
 Troubleshooting choices

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Access Is KING

 Vascular Access is continuously tested during CRRT treatment.

 Catheter site, size, type and patient preparation should be considered.

 Practical understanding about vascular access is necessary for optimal


treatment.

 Inadequacies in vascular access may limit delivered therapy.

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Aquarius System

Other Considerations

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Choices of Anticoagulation

 Low Molecular Weight


Heparin (LMWH)

 Unfractioned Heparin

 Regional Heparinisation

 Regional Citrate

 Adjunctive anticoagulation
methods

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Introduction to Anticoagulation

 In CRRT, the anticoagulation is a challenge for physicians. The target is to


limit the risk of circuit coagulation and at the same time to limit the
Hemorrhage risk for the patient .

The coagulation activation is due to:

 Exogenous causes: extracorporeal circuit i.e. lines and the filter that
is in contact with the blood.

 If no anticoagulation is used the thrombosis is ineluctable with the


following consequences:
 Renal dose reduction
 Blood loss and loss of the coagulation factors
 Increase of the workload and the cost of the therapy

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Anticoagulation

 Systemic

 Regional

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How does Heparin work?

 Heparin inhibits reactions that lead to the clotting of blood and the formation of fibrin
clots.

 Heparin acts at multiple sites in the normal coagulation system.

 Small amounts of heparin in combination with antithrombin III (heparin cofactor) can
inhibit thrombosis by inactivating activated Factor X and inhibiting the conversion of
prothrombin to thrombin.

 Heparin prevents the formation of a stable fibrin clot by inhibiting the activation of the
fibrin stabilizing factor.

 Bleeding time is usually unaffected by heparin.

 Clotting time is prolonged by full therapeutic doses of heparin.

 Heparin does not have fibrinolytic activity; therefore, it will not lyse existing clots.
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Advantages & Disadvantages related to the use of
Heparin

Advantages:
 Easy to administer and monitor.
 Low cost of drug 2
 Short half life, Heparin can be antagonized.

Disadvantages:

 Results in systemic anticoagulation and potential risk of bleeding3


 Heparin induced thrombocytopenia (HIT) around 1% to 5% in patients given
heparin for 5 days leading to increased risk of central venous thrombosis
within the catheter4

2 Regional Citrate Versus Heparin Anticoagulation for Continuous Renal Replacement Therapy: A Meta-Analysis of Randomized Controlled Trials Mei-Yi Wu, MD
Am J Kidney Dis. 2012;59 810-818.
3 Regional citrate anticoagulation in continuous venovenous hemofiltration in critically ill patients with a high risk of bleeding Runolfur Palsson and John L Niles
Kidney International (1999) 55, 1991–1997; doi:10.1046/j.1523-1755.1999.00444.
4Heparin-induced thrombocytopenia during renal replacement therapy Andrew DAVENPORT Center for Nephrology, The Royal Free Hospital, Pond Street,
London, United Kingdom Hemodialysis International 2004; 8: 295--303

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How does Regional Citrate Anticoagulatin
(RCA) work?

 Citrate is added to the extracorporeal circuit pre-filter.

 It chelates or combines with ionized Calcium (free Calcium) in the filter by


forming Ca-Citrate complexes, thus removing Ca needed in coagulation
cascade, anticoagulant effect.

 Majority of these complexes are removed in the filter, some pass on to the
systemic circulation.

 Ca gets infused post-filter to restore iCa.

 Ca-Citrate complexes get metabolized in liver, muscle & kidney (Krebs cycle;
aerobic) releasing Ca & forming Bicarbonate (1:3), buffer effect.

 Anticoagulant effect is limited to the filter.


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Advantages related to Citrate

 Citrate is safer than nadroparin anticoagulation in CRRT.

 Citrate is recommended in patients who require CRRT but are at high risk of
bleeding (Only the extracorporeal circuit is anticoagulated).

 Monitoring can be performed to tightly control infusion rates.

 Can be performed in combination with standard CRRT equipment.

5 Citrate anticoagulation for continuous venovenous hemofiltration: Heleen M. Oudemans-van Straaten Crit Care Med 2009 Vol.
37, No. 2
6 Regional Citrate Versus Heparin Anticoagulation for Continuous Renal Replacement Therapy: A Meta-Analysis of
Randomized Controlled Trials Mei-Yi Wu, MD Am J Kidney Dis. 2012;59 810-818.

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Aquarius System

Questions and Discussion

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T h a n k Yo u

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