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496 P R I N C I P L E S A N D P R A C T I C E O F C R I T I C A L C A R E

TABLE 18.3 Commonly used anti-clotting agents for CRRT

Drug Benefits Precautions
Heparin Inexpensive, wide experience, Sensitivity reactions, heparin-induced thrombocytopenia, to be effective means
easily reversed, easily increased risk of bleeding systemically
monitored, short half-life
Low-molecular-weight Moderately inexpensive, Difficult to monitor, not easily reversed, longer half-life, dosing varies between
heparin (LMWH) increasing experience, less likely types of LMWH
to result in sensitivity reactions
Prostacyclin Very short-acting, has a Expensive, no measure of effectiveness, narrow dose range with associated
physiological role in inhibiting hypotension, individual patients sensitive to haemodynamic effects, unstable
platelet activity, does not in solution
exacerbate other drug reactions
Citrate-based Limit anticlotting effect to EC – Substantial metabolic effect if not adequately managed (serum ionised calcium
solutions ‘Regional anticoagulation’; must be monitored closely); requires additions to extracorporeal circuit to
results suggest very effective in administer and reverse and use of specialised replacement/dialysate solutions.
prolonging circuit life Not useful when liver failure present, citrate is converted to bicarbonate by the
liver providing the necessary buffer for RRT. Acidosis may occur in liver failure
No anti-clotting agent No side effects, no exacerbation of May encounter very short circuit life that consumes remaining haematological
(with saline flushes) unstable haematological status, components, risk of fluid overload if saline flushes not part of fluid balance.
liver failure No evidence saline flushes have any benefit

monitoring line. It is advised that the blood level be visual inspection for clotting in the EC is undertaken,
adjusted to near full but allow for visual inspection of particularly noting the venous bubble trap.
incoming blood flow and to ensure that any air bubbles
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are trapped here. As this creates a gas–blood interface Citrate is another popular anticoagulant for CRRT as an
within the venous chamber there is a potential source of alternative to heparin. Citrate buffers pH and chelates
venous chamber clotting and hence circuit failure. 42,69,80 calcium inducing anticoagulation of blood by reducing
Addition of replacement fluids into this chamber when serum ionised calcium level. For anticoagulation, the
using post-dilution fluid administration can cause a dose and dose rate of citrate is commonly set to achieve
plasma fluid layer to develop above the blood level and a reduction in the CRRT circuit blood ionised calcium
87-89
may reduce clotting by stopping blood foaming on its level to <0.3 mmol/L. As ionised calcium is essential
surface and eliminates air or gas contact with the blood. 81 for the progression of the coagulation cascade to form a
stable clot, an anticoagulant effect is achieved when the
Anticoagulation calcium is bound or chelated. A continuous infusion of
88
There are several different drugs utilised to prevent blood citrate is administered into the CRRT circuit, as patient
clotting in the EC; heparin, prostacyclin and sodium citrate blood enters the circuit similar to heparin administra-
have been used separately or in various combinations (see tion. A new approach in Australia includes citrate as an
Table 18.3). 82-84 As blood comes into contact with the additive to commercially-prepared CRRT replacement
90
plastic tubing and the polymer fibres of the filter, various fluids. When circuit blood returns to the patient circula-
clotting systems are activated. This is a normal action of tion, it mixes with systemic blood and the calcium con-
blood when exposed to non-biological surfaces. The aim centration is restored to normal; free citrate not binding
of anti-clotting drugs is to delay clot formation while the to calcium is metabolised by the liver to provide carbon
87-89
blood is outside the body, particularly when within the dioxide and bicarbonate as a necessary buffer.
densely-packed fibres of the filter. As calcium, blood plate- However, citrate-bound calcium is lost in the waste fluid
80
let cells or thrombin are vital in clot formation, these removed and requires replacement by a separate calcium
drugs are targeted to one of these elements. This targeting infusion to maintain serum calcium levels to normal; at
87
must not be too pronounced, as the patient may begin to 1.0–1.3 mmol/L. With this method, the circuit is anti-
bleed when the blood returns from the EC to the body. 80 coagulated, but the patient is not (also called a ‘regional’
method of anticoagulation) as the patient blood calcium
Heparin is the most commonly-used agent for the level is restored to normal making this approach safer
prevention of clotting, as it is inexpensive, widely avail- compared to heparin use and can be applied in auto-
82
able and easily reversed by another drug, protamine. anticoagulated patients where premature circuit clotting
91
Heparin is commonly administered into the EC before continues to occur. Due to the complex nature of the
the blood enters the filter, although the optimal place to citrate-based anticoagulation approach a number of dif-
administer any anticoagulant drug during CRRT is not ferent protocols have been proposed to aid in manage-
92
agreed upon. 85,86 A bolus is often given prior to circuit ment. Not all methods will be applied in the one ICU,
connection, either in the circuit prime or via the venous and local expertise development of one method and an
access catheter. A maintenance dose (5–15 units/kg/h) is alternative is common. Recent reviews provide a good
then adjusted against the relevant laboratory tests and a synopsis of each method. 93