1 Anticoagulation in Hemodialysis

Anticoagulation in
hemodialysis
Dr.
Scope
Introduction
Coagulation cascade
Hemostatic abnormalities in renal insufficiency
Anticoagulation for hemodialysis
Unfractionated heparin
No heparin dialysis
LMWH
Regional anticoagulation
Newer developments
Conclusions
Introduction
Adequate anticoagulation in hemodialysis

procedures relies on
Knowledge
of the
Basic
principles of hemostasis and notably the

clotting cascade
Hemostatic abnormalities in renal insufficiency as
well as activation of clotting on artificial surfaces
Hemodialysis International 2007; 11:178189
Introduction
Hemostasis defined as a
Process of fibrin clot formation to seal a site of

vascular injury without resulting in total occlusion of
the vessel
Multiple processes including both cellular elements
and numerous plasma factors with enzymatic activity
is arranged
(1) to activate clotting rapidly,

(2) to limit and subsequently terminate this activation, and
(3) to remove the clot by fibrinolysis in the end
Introduction
The initial hemostatic response to stop bleeding

is the
Formation of a platelet plug at the site of vessel wall

injury
Platelets are activated by
Multitude of stimuli, the most potent of which are
Thrombin and collagen
Upon activation, platelets
Adhere to the subendothelial matrix, aggregate,

secrete their granule content, and expose
procoagulant phospholipids such as
phosphatidylserine
Introduction
Platelet-derived membrane microvesicles

Markedly
increase the phospholipid surface on

which coagulation factors form multimolecular
enzyme complexes with procoagulant activity
Hence, platelet activation also

Leads
to propagation of plasmatic coagulation
Coagulation Cascade
Coagulation Cascade
Complex,
multiply redundant and includes

intricate checks and balances
Coagulation Cascade
Intrinsic pathway
Activated by damaged or negatively charged surfaces

and the accumulation of kininogen and kallikrein
The activated partial thromboplastin time (APTT)
tends to reflect changes in the intrinsic pathway
Extrinsic pathway
Triggered by trauma or injury, which releases tissue
factor
The extrinsic pathway is measured by the
prothrombin test
Hemostatic abnormalities in
renal insufficiency
The accumulation of uremic toxins causes
complex disturbances of the coagulation
system
Uremia can lead to an increased bleeding
tendency, e.g.,
Due
to platelet dysfunction
which is further enhanced with use of
anticoagulants during extracorporeal blood
purification procedures
renal insufficiency
Clot formation and development of

thrombosis can also occur at increased
rates in dialysis patients
Pulmonary
embolism is more frequent in

dialysis patients than in age-matched controls
renal insufficiency
Patients on chronic intermittent

hemodialysis frequently suffer from
Vascular
access thrombosis, the risk of which

is increased in
Polytetrafluoroethylene
arteriovenous fistulas
grafts compared with
Anticoagulation for hemodialysis (HD)
Anticoagulation is routinely required to

prevent clotting of
The
dialysis lines and dialyser membranes,
In
both acute intermittent haemodialysis and

continuous renal replacement therapies
Field of anticoagulation is constantly

evolving
Important
to regularly review advances in

knowledge and changing practices in this area
Semin. Dial. 2009; 22: 1415
Anticoagulation for HD
The responsibility for

prescribing and delivering
anticoagulant for HD is
shared between the
Dialysis
doctors and nurses
Dialysis is a medical therapy

Must
be prescribed by an
appropriately trained doctor
Nephrology 2010;15:386392
The prescribing doctor usually determines

which
anticoagulant agent will be used and

the dosage range
The doctors prescription may include

broad instructions such as
no
heparin, low heparin or normal heparin
In a mature dialysis unit the dose and

delivery of anticoagulant is, however, the
responsibility of professional and
experienced dialysis nurses,
who
have latitude within parameters

determined by detailed written policies or
standing orders
Dosing regimens, while generally safe and
effective, are somewhat unscientific
In terms of monitoring
Most
units do not practise routine monitoring,

Although the anticoagulant effect of
unfractionated heparin (UF heparin) can be
monitored with some accuracy by the APTT or
the activated clotting time tests where
indicated
The dialysis nurses

Know
- too much anticoagulation if
The
needle sites continue to ooze excessively for a

prolonged period (e.g. more than 15 min) after
dialysis
Know
- too little anticoagulation if
streaking
in the dialyser, excessively raised

transmembrane pressure or evidence of thrombus
in the venous bubble trap indicated by dark
blood, swelling of the trap or rising venous
pressure
The nurses
Know
that patients dialysing with a venous

dialysis catheter are at greater risk of
thrombosis
With some trial and error,

The
right dose of anticoagulant for any

patient can be empirically determined
In normal circumstances effective and

safe anticoagulation for HD can be
delivered with
Low
risk and high efficiency
Constitute a mixture of anionic
glucosaminoglycans of varying molecular size
(540, mean 15 kDa)
Mechanism:
Indirect due to the binding to antithrombin (heparinbinding factor I)

Heparin enhances the activity of this natural
anticoagulant protein 1000 to 4000-fold
Antithrombin inactivates thrombin, factor Xa, and to a
lesser extent factors IXa, XIa, and XIIa
At high doses, heparin also binds to heparin-binding
factor II
Heparin can be directly procoagulant through
platelet activation and aggregation
However, its main effect is anticoagulant,
through its binding to anti-thrombin
(antithrombin III or heparin-binding factor I)
At high doses heparin can also bind to heparinbinding factor II which can directly inhibit
thrombin
When heparin binds antithrombin it causes a
conformation change, which results in a 1000
40 000 increase in the natural anticoagulant
effect of anti-thrombin
Heparin is ineffective against thrombin or

factor Xa
If
they are located in a thrombus or bound to

fibrin or to activated platelets
UFH has a narrow therapeutic window of

adequate anticoagulation without
bleeding,
Laboratory
testing (aPTT or as bedside test

activated clotting time, ACT) of its effect is
required
First isolated from liver (hepar) mast cells of dogs

Now commercially derived from porcine intestinal
mucosa or bovine lung
When administered intravenously
Half-life approx. 1.5 h
Highly negatively charged and binds non-specifically

to endothelium, platelets, circulating proteins,
macrophages and plastic surfaces
In addition to removal by adherence,

heparin is cleared by both renal and
hepatic mechanisms and is metabolized by
endothelium
Interestingly, UF heparin has both proand anti-coagulant effects
At high doses heparin can also bind to
heparin-binding factor II which can
directly inhibit thrombin
When heparin binds antithrombin it causes
a conformation change, which results in a
100040 000x increase in the natural
anticoagulant effect of anti-thrombin.
Heparin-bound anti-thrombin inactivates multiple
coagulation factors including covalent binding of
thrombin and Xa and lesser inhibition of VII,
IXa, XIa, XIIa.
By inactivating thrombin, UF heparin inhibits
thrombininduced platelet activation as well
Of note, UF heparinbound anti-thrombin
inactivates thrombin (IIA) and Xa equally
Only UF heparin with more than 18 repeating
saccharide units inhibits both thrombin and Xa,
whereas shorter chains only inhibit Xa.
For haemodialysis,
UF heparin can be administered, usually into the

arterial limb, according to various regimens, but
Most commonly is administered as a loading dose
bolus followed by either an infusion or repeat bolus at
23 h
The initial bolus is important to overcome the high
level of non-specific binding, following which there is
a more linear dose : response relationship
The loading dose bolus may be 500 units
or 1000 units and infusion may vary from
500 units hourly to 1000 units hourly,
depending on whether the prescription is
low dose heparin or normal heparin
Heparin administration usually ceases at
least 1 h before the end of dialysis
The most important risk of UF heparin is the HIT
syndrome (HIT Type II)
Other risks or effects attributed to UF heparin
that have been reported include hair loss, skin
necrosis, osteoporosis, tendency for
hyperkalaemia, changes to lipids, a degree of
immunosuppression, vascular smooth muscle
cell proliferation and intimal hyperplasia
Beef-derived heparin can be a risk for the
transmission of the prion causing Jacob
Creutzfeld type encephalopathy
Use of UF heparin is
Safe, simple and inexpensive and

Usually encounters few problems
However, there are risks with HD

anticoagulation which are important to be aware
of and include
The risk of bleeding

Some risks are not immediately obvious such as
inadvertent over-anticoagulation in high-risk patients
because of excessive heparin volume used to lock the
venous dialysis catheter at the end of dialysis
The disadvantages of UF heparin may

include
Lack
of routine or accurate monitoring of

anticoagulation effect
The need for an infusion pump and the costs
of nursing time
Perhaps the most important risk is that of

Heparin-induced
thrombocytopaenia (HIT
Type II), which is greatest with the use of UF
heparin
At times the routine anticoagulation
prescription needs to be varied
Additional choices include
no
heparin dialysis,
the use of low-molecular-weight heparin
(LMWH) instead of UF heparin, and
the use of regional anticoagulation
New agents and new clinical variations

appear in the literature continuously
No Heparin Dialysis
Dialysis without anticoagulation may be

indicated in patients with
High
risk of bleeding
Acute bleeding disorder
Recent head injury
Planned major surgery
Trauma
Acute HIT syndrome or
Systemic anticoagulation for other reasons
No Heparin Dialysis
The procedure involves

Multiple
flushes of 2550 ml of saline every

1530 min, in association with a high blood
flow rate
In some units the lines are pretreated with
20005000 U of UF heparin and then flushed
with 1 L of normal saline, to coat the lines
This form of dialysis anticoagulation is

Very
labour-intensive and
Usually only partially effective
No Heparin Dialysis
No Heparin Dialysis
Partial clotting still occurs in 20% of cases with

complete clotting of lines or dialyser, requiring
The risk of clotting may be exacerbated by
Line change in 7% of no heparin dialyses

Poor access blood flow, the use of a venous catheter,
hypotension or concomitant blood transfusion
Where a venous catheter is used, there is an increased risk
of catheter occlusion
No heparin dialysis may also provide less

effective dialysis and result in lower clearances
Low molecular weight heparin (LMWH)
Depolymerized fractions of heparin can be

obtained by
Anionic glycosaminoglycans but
Chemical or enzymatic treatment of UF heparin

have a lower molecular weight of 29 kDa, mostly @
5 kDa thus consisting of 15 saccharide units
The shorter chain length results in

Less coagulation inhibition, but
Superior pharmacokinetics, higher bioavailability, less
non-specific binding and longer half-life, all of which
help to make
LMWH dosage simpler and more predictable than UF
heparin
LMWH
LMWH
In addition
Less
impact on platelet function, and thus

may cause less bleeding
Binds anti-thrombin III and inhibits factor Xa,
But most LMWH (5070%) does not have the
second binding sequence needed to inhibit
thrombin
because
of the shorter chain length

LMWH
In most cases the affinity of LMWH for Xa
versus thrombin is of the order of 3:1
The anticoagulant effect of LMWH can be
monitored by the anti-factor Xa activity in
plasma
LMWH
LMWH
Cleared
by renal/dialysis mechanisms, so
dosage must be adjusted to account for this
When high flux dialysers are used, LMWH is
more effectively cleared than UF heparin
Often administered into the venous limb of
the dialysis circuit
Enoxaparin
One of the most commonly used LMWH

Has
the longest half-life

Predominantly renally cleared
Dose reduction need to be made in the
elderly, in the presence of renal impairment
and in very obese patients, to avoid lifethreatening bleeding
Enoxaparin
Generally does not accumulate in 3/week
dialysis regimens, but there is a risk of
accumulation in more frequent schedules
No simple antidote and in the case of
severe haemorrhage
Activated
required
factor VII concentrate may be
Enoxaparin
On the other hand patients dialysing with

a high flux membrane, as compared with
a low flux membrane,
May
require a higher dose because of dialysis

clearance
Effect and accumulation can be monitored

by the performance of anti-Xa levels
Enoxaparin
A common target range is

0.4
0.6 IU/ml anti-Xa but a
More conservative range

0.2
0.4 IU/ml is recommended in patients

with a high risk of bleeding
The
product insert should always be consulted
Enoxaparin
The use of LMWH such as enoxaparin for HD

anticoagulation is
Well supported in the literature
Enoxaparin can be administered as a
Single dose and generally does not require to be

monitored
Yet unclear whether enoxaparin can successfully
anticoagulate patients for long overnight (nocturnal)
HD
Against the utility of LMWH, the purchase price of
LMWH still significantly exceeds UF heparin
LMWH
The other available forms of LMWH e.g.

Dalteparin,
Nadroparin, Reviparin Tinzaparin

and newer LMWH vary somewhat, especially
in
Anti-Xa/anti-IIa
effect
The higher this ratio the more Xa selective the agent and
consequently the less effect protamine has on reversal
Enoxaparin
High
anti-Xa/anti-IIa ratio of 3.8, and is < 60%

reversible with protamine
Is LMWH better?
Significance is
Lower
incidence of HIT Type II, a devastating

and deadly complication, in patients exposed
to LMWH compared with UF heparin
Another advantage of LMWH is the
Longer
duration of action and predictability of

dosage effect, allowing the convenience of a single
subcutaneous injection at the start of dialysis
without the need for routine monitoring
Is LMWH better?
The use of LMWH is reported to cause

Less
dialysis membrane-associated clotting,

fibrin deposition and cellular debris
LMWH has less non-specific binding to
platelets, circulating plasma proteins and
endothelium
Is LMWH better?
UF heparin induces
Inhibition
of mineralocorticoid metabolim and

reduced adrenal aldosterone secretion, but
LMWH
has been shown to have less inhibition in

this regard
Other
deleterious effects associated with UF

heparin are also generally less common with
the use of LMWH including
The
risk of osteoporosis, hair loss, endothelial cell

activation and adhesion molecule activation
Is LMWH better?
A meta-analysis including 11 studies was

published in 2004 and showed that
LMWH
and UF heparin were similarly safe and

effective in preventing extracorporeal circuit
thrombosis, with
No
significant difference in terms of bleeding,

vascular compression time or thrombosis
J. Am. Soc. Nephrol. 2004; 15: 3192206.
Is LMWH better?
LMWH is however recommended as the agent of

choice for routine haemodialysis by the
European Best Practice Guidelines
The single factor weighing against the use of LMWH

as the routine form of anticoagulation for dialysis is
cost
More and more dialysis units are assessing the

cost/benefit ratio as in favour of the routine use
of LMWH for haemodialysis
Because of the potency, ease of administration,

predictable clinical effect and low rate of side effects
Anti-Xa monitoring
May be used for dosing adjustment of
LMWH, to ensure therapeutic dosing or to
exclude accumulation prior to a
subsequent dialysis
Because of the high bioavailability, doseindependent clearance by renal
mechanisms, and predictable effect, there
is generally no need to monitor routinely.
Regional anticoagulation for HD
Aim of regional anticoagulation is

To
restrict the anticoagulant effect to the

dialysis circuit and prevent systemic
anticoagulation,
For
instance in patients at increased risk of

bleeding
UF heparin/protamine
Historically, the use of UF

heparin/protamine was prototypical of
regional anticoagulation
UF
heparin is infused into the arterial line and

protamine into the venous line
Protamine
Basic
protein that binds heparin, forming a stable

compound and eliminating its anticoagulant effect
Full neutralization of heparin can be

achieved with
A
dose of 1 mg protamine/100 units heparin

Protamine has a shorter half-life than heparin
so
There
may be an increased risk of bleeding 24 h

after dialysis
Most authors agree that

Procedure
can be technically challenging and

No significant advantage over low-dose
heparin regimens
Reactions to protamine are not uncommon
and may be serious
As
all forms of heparin are absolutely

contraindicated in HIT Type II this form of regional
anticoagulation cannot be used in that syndrome
Citrate regional anticoagulation
Citrate binds ionized calcium and is a

Potent
inhibitor of coagulation
Regional citrate regimens generally

Utilize
isoosmotic trisodium citrate or

hypertonic trisodium citrate infusion into the
arterial side of the dialysis circuit
This methodology
Avoids
the use of heparin and

Limits anticoagulation to the dialysis circuit
Effects
which can be used for routine dialysis in

patients at increased risk of bleeding or for dialysis
anticoagulation in the stable phase of HIT Type II
The citratecalcium complex
The procedure may require, or be enhanced by,
Partially removed by the dialyser

Use of calcium and magnesium-free dialysate
A low bicarbonate dialysate is also

recommended to
Rreduce the risk of alkalosis,
Especially in the setting of daily dialysis, as citrate is

metabolized to bicarbonate
To neutralize the effect of citrate,

Calcium
chloride solution is infused into the

venous return at a rate designed to correct
ionized calcium levels to physiologic levels
Plasma calcium must be measured frequently,
e.g.
second
hourly, with prompt result turnaround
The procedure
Complex
and high risk

Requirement for two infusion pumps and
Point of care calcium measurement
Either high or low calcium levels in the patient
may risk severe acute complications
Hypertonic citrate may risk hypernatraemia
Metabolism of citrate generates a metabolic
alkalosis
Nevertheless, the technique has been

used with
Great
success in some hands, with
Few
bleeding complications and improved

biocompatibility with reduced granulocyte
activation and
Less deposition of blood components in the lines
or on the dialyser
Simplified protocols have been proposed

Prostacyclin regional anticoagulation
Utilizes prostacyclin as a
Vasodilator and platelet aggregation inhibitor
Very short half-life of 35 min

Infused into the arterial line
Of importance
Prostacyclin is adsorbed onto polyacrylonitrile

membranes
Side effects can include
Headache, light headedness, facial flushing,

hypotension and excessive cost
Heparin-induced thrombocytopaenia
(HIT)
There are two well-described syndromes

of HIT, the
First
relatively benign
Second potentially devastating
HIT Type I
HIT type I
1020% of patients treated with UF heparin

Mild thrombocytopaenia occurs (<100 000) as a
result of heparin activation of platelet factor 4 (PF4)
surface receptors, leading to platelet degranulation
Mechanism is non-immune and early in onset, after
the initiation of heparin
The syndrome generally resolves spontaneously
within 4 days despite the continuation of heparin
Generally no sequelae of clinical significance
HIT Type II
HIT Type II
Much
more serious and devastating than HIT

Type I
Generally occurs within the first 410 days of
exposure to heparin
Late onset is less common
Mechanism of HIT which results in both
platelet activation and activation of the
coagulation cascade
HIT Type II
Severe platelet reduction occurs rapidly,

Generally
platelet count remains > 20 000
Clinical HIT Type II is reported to occur in

215%
of patients exposed to heparin

More commonly in females and surgical cases
In dialysis patients the incidence varies
between 2.8% and 12%
HIT Type II
HIT Type II
Occurs
in incident patients or after reexposure to heparin after an interval

Of importance the incidence is 510 times
more common with UF heparin than with
patients receiving only LMWH
The risk with LMWH is reportedly very low, in
the order of <1%
HIT Type II
HIT Type II
Two clinical phases

Acute phase
Significant thrombocytopaenia and high risk of

thromboembolic phenomena
Avoidance of heparin and systemic anticoagulation are
essential
Second phase,
Signalled by recovery of platelet levels, heparin must still be

avoided (for a prolonged period if not forever) but systemic
anticoagulation is not required
Dialysis anticoagulation remains a challenge as all forms of
heparin must be avoided
HIT Type II
With the onset of HIT Type II, heparin must be

immediately discontinued, even before confirmatory
results are available
Available tests for HIT Type II include detection of
antibodies against heparinPF4 complex, detection of
heparin-induced platelet aggregation or platelet release
assays but none is totally reliable
HIT acute phase will not resolve while heparin is
continued and HIT will recur on rechallenge with either
UF heparin or LMWH
Once HIT is established after exposure to UF heparin,
there is a >90% cross-reactivity with LMWH
HIT Type II
Untreated, there is a major risk of venous

and arterial thrombosis, estimated at
>50%
within 30 days
Most of the clots are described as venous

Arterial
thrombi are often platelet-rich white

thrombi (white clot syndrome) which can
cause limb ischaemia and cerebral or
myocardial infarcts
HIT Type II
In patients with HIT Type II all heparin products

must be avoided, including
Topical preparations, coated products as well as

intravenous preparations
Systemic anticoagulation without heparin is

mandatory in the acute phase
For haemodialysis, patients may have
no heparin dialysis or anticoagulation with nonheparins

The available agents commonly used include
Danaparoid, Hirudin, Argatroban, Melagatran and
Fondaparinux
HIT Type II
Alternatively, regional citrate dialysis has proved

effective in this setting
Each approach or alternative agent provides its own
challenges and there may be a steep learning curve.
Both UF heparin and LMWH are contraindicated
Venous catheters must not be heparin locked, but can
be locked with recombinant tissue plasminogen activator
or citrate ( trisodium citrate 46.7%)
Other alternatives to consider may include switching the
patient to peritoneal dialysis or using warfarin
In the longer term it may be possible to cautiously
reintroduce UF heparin, or preferably LMWH, without
reactivating HIT Type II
Danaparoid
Currently, this agent remains drug of

choice in most Australian hospitals for HIT
Type II,
May
have unique features, which interfere

with the pathogenesis of HIT Type II
Extracted from pig gut mucosa

Heparinoid of molecular weight of 5.5 kDa
83%
heparan sulphate, 12% dermatan

sulphate and 4% chondroitin sulphate
Danaparoid
Danaparoid
Binds to antithrombin (heparin cofactor I) and

heparin cofactor II and has some endothelial
mechanisms, but
More selective for Xa than even the LMWH
Minimal impact on platelets and a low affinity for PF4
(Xa : thrombin binding : Danaparoid 2228 : 1;

LMWH 3:1 typically)
Low cross-reactivity with HIT antibodies (6.5

10%) although
Recommended to test for cross-reactivity before use

of Danaparoid in acute HIT Type II
Danaparoid
Danaparoid
Very
long half-life of about 25 h in normals
Longer
with chronic renal impairment (e.g. 30 h)
No reversal agent
Clinically, significant accumulation should
be tested by
Anti-Xa
estimation before any invasive

procedure
Hirudin
Originally discovered in the saliva of leeches
Binds thrombin irreversibly at its active site and
the fibrin-binding site
Recombinant or synthetic variants are also
available including
Lepirudin, Desirudin and Bivalirudin
Hirudin and its cogeners are
Polypeptides of molecular weight of 7 kDa with no

cross-reactivity to the HIT antibody
Hirudin
Hirudin
Prolonged
half-life
Renally cleared, so its half-life in renal
impairment is > 35 h
Studies have confirmed

Hirudin
HD
can be used as an anticoagulant for
Hirudin
Hirudin
No
cross-reactivity with UF heparin or LMWH;

however,
Hirudin
and its analogues are antigenic in their

own right, and up 74% of patients receiving
Hirudin i.v. can develop anti-Hirudin antibodies,
which can further prolong the half-life
Hirudin
Hirudin
Because of the tendency to form antibodies, difficult

to use, as anaphylaxis can occur with a second course
The APTT
May be used to monitor Hirudin anticoagulant effect

but
The relationship is not necessarily linear
No antidote to Hirudin, but
Removed to some extent by haemofiltration/

plasmapheresis but not HD
Argatroban
Synthetic derivative of L-arginine

Appears
to be the treatment of choice in the
USA
Acts as a direct thrombin inhibitor and
Binds irreversibly to the catalytic site
Short half-life of 4060 min

Not
effected by renal function

Hepatic clearance means prolonged duration
of action in patients with liver failure
Argatroban
Anticoagulant effect can be monitored by
a variant of the APTT the ecarin clotting
time
No available reversal agent
Melagatran
Direct thrombin inhibitor
Available orally as a prodrug, which is
taken twice a day
Renally cleared and has a prolonged halflife
No antidote
Melagatran
Reports of hepatotoxicity have impeded
further drug development
It has been suggested that Melagatran
may have a role in anticoagulation
between dialysis treatments in patients
with HIT Type II
Fondaparinux
Synthetic pentasaccharide of 1.7 kDa,

Copy
of an enzymatic split product of heparin

Synthetic analogue of the pentasaccharide
sequence in heparin that mediates the antithrombin interaction
High affinity for anti-thrombin III but

No
affinity for thrombin or PF4
Fondaparinux
Fondaparinux
Can
be administered i.v. or s.c.

Monitored by the use of anti-Xa testing
With a prolonged half-life it can be
administered alternate days
Renally cleared, it may accumulate in renal
failure
Removed
to some degree by high flux

haemodialysis or haemodiafiltration
Conclusions
Anticoagulation is an essential part of the

safe and effective delivery of HD
Physicians accredited to prescribe dialysis

must have a fundamental understanding
of anticoagulation therapy in different
dialysis settings
Conclusions
Essential for nephrologists to have a good

understanding of
The
relative merits of UF heparin and LMWH,

To develop an approach to the clinical
management of HIT Type II and other
important heparin-related complications
Conclusions
Continuous development of new

anticoagulant drugs and associated clinical
recommendations
This
is an area that dialysis clinicians should

revisit at timely intervals

1 Anticoagulation in Hemodialysis

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1 Anticoagulation in Hemodialysis

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Anticoagulation in

Anticoagulation for hemodialysis

Adequate anticoagulation in hemodialysis

principles of hemostasis and notably the

Hemodialysis International 2007; 11:178189

Process of fibrin clot formation to seal a site of

(1) to activate clotting rapidly,

Hemodialysis International 2007; 11:178189

The initial hemostatic response to stop bleeding

Formation of a platelet plug at the site of vessel wall

Platelets are activated by

Multitude of stimuli, the most potent of which are

Thrombin and collagen

Upon activation, platelets

Adhere to the subendothelial matrix, aggregate,

Platelet-derived membrane microvesicles

increase the phospholipid surface on

Hence, platelet activation also

to propagation of plasmatic coagulation

Hemodialysis International 2007; 11:178189

multiply redundant and includes

Hemodialysis International 2007; 11:178189

Activated by damaged or negatively charged surfaces

Hemodialysis International 2007; 11:178189

Clot formation and development of

embolism is more frequent in

Hemodialysis International 2007; 11:178189

Patients on chronic intermittent

access thrombosis, the risk of which

grafts compared with

Anticoagulation for hemodialysis (HD)

Anticoagulation is routinely required to

dialysis lines and dialyser membranes,

both acute intermittent haemodialysis and

Field of anticoagulation is constantly

to regularly review advances in

The responsibility for

doctors and nurses

Dialysis is a medical therapy

The prescribing doctor usually determines

anticoagulant agent will be used and

The doctors prescription may include

heparin, low heparin or normal heparin

In a mature dialysis unit the dose and

have latitude within parameters

units do not practise routine monitoring,

The dialysis nurses

- too much anticoagulation if

needle sites continue to ooze excessively for a

- too little anticoagulation if

in the dialyser, excessively raised

that patients dialysing with a venous

With some trial and error,

right dose of anticoagulant for any

In normal circumstances effective and

risk and high efficiency

Indirect due to the binding to antithrombin (heparinbinding factor I)

Heparin is ineffective against thrombin or

they are located in a thrombus or bound to

UFH has a narrow therapeutic window of

testing (aPTT or as bedside test

First isolated from liver (hepar) mast cells of dogs