Anticoagulation of the Circuit

The contract between this chapter and the reader.

1. 1. Explain why the extracorporeal circuit must be anticoagulated.
2. 2. Describe systemic heparin anticoagulation and its monitoring.
3. 3. Describe low-molecular-weight heparin and its considerations.
4. 4. Describe regional citrate anticoagulation and its risks.
5. 5. Describe heparin-free dialysis with saline flushes.
6. 6. Choose an anticoagulation method by bleeding risk.
7. 7. Recognise and manage heparin-induced thrombocytopenia.
8. 8. Recognise and respond to circuit clotting.

A sixty-second reading. Each bullet stands alone.

• Blood contacting the circuit activates clotting, so the circuit is anticoagulated to stay patent while limiting the patient's bleeding risk.
• Systemic unfractionated heparin is standard — a bolus and infusion, cheap, reversible with protamine, monitored by ACT or aPTT.
• Low-molecular-weight heparin is given as a single bolus with less monitoring, but it is not easily reversed and accumulates.
• Regional citrate anticoagulates the circuit only — citrate chelates calcium pre-filter and calcium is replaced — sparing the patient, at the cost of monitoring.
• Heparin-free dialysis with periodic saline flushes is used in active bleeding, accepting a higher clotting risk.
• Choose the method by bleeding risk: standard risk uses heparin; high risk uses heparin-free or citrate.
• In heparin-induced thrombocytopenia, stop all heparin and use a non-heparin method.
• Under-anticoagulation shows as clots in the chamber and dialyzer and rising venous and transmembrane pressures.
• Over-anticoagulation shows as prolonged bleeding from needle sites after dialysis.
• Heparin is monitored to a moderate prolongation; citrate is monitored by ionised calcium and acid-base.
• Circuit clotting is managed by flushing, checking anticoagulation and flow, and changing the circuit if it clots.
• Good blood flow, adequate anticoagulation, and pre-dilution help prevent clotting.

The medical core. An expert should agree circuit anticoagulation is fully covered here.

Why it matters at the bedside

Every dialysis session is a contest between two failures: a circuit that clots and is lost, and a patient who bleeds. Anticoagulation sits exactly on that line. Choose and monitor it well — matched to the patient's bleeding risk — and the session runs cleanly; choose poorly and you lose the dialyzer or harm the patient.

Why anticoagulate

• Blood contacting the artificial surfaces of the circuit and dialyzer activates the clotting cascade and platelets; left to itself, the circuit thromboses, the dialyzer is lost, and the blood in it may not be returnable. Anticoagulation keeps the circuit patent — the aim is just enough to prevent clotting without anticoagulating the patient more than necessary.

Systemic heparin

• Unfractionated heparin is the standard method: a loading bolus followed by a continuous (or intermittent) infusion through the circuit, cheap, rapidly acting, and reversible with protamine. It anticoagulates the whole patient, so it carries a bleeding risk, and it is titrated by the activated clotting time or aPTT to a moderate prolongation.

Low-molecular-weight heparin

• Low-molecular-weight heparin offers convenience — often a single pre-dialysis bolus with little intradialytic monitoring — with efficacy comparable to unfractionated heparin. Its drawbacks are that it is not readily reversed by protamine and that it accumulates, so repeated dosing must be cautious.

Regional citrate

• Regional citrate anticoagulates the circuit alone: citrate infused pre-filter chelates the calcium the clotting cascade needs, halting clotting within the circuit, while calcium is replaced so the patient remains coagulable. It is the option when systemic anticoagulation is undesirable, at the cost of monitoring ionised calcium and acid-base and the risk of citrate accumulation (detailed for continuous therapy in the CRRT chapter).

Heparin-free dialysis

• When any anticoagulation is dangerous — active bleeding — dialysis can run heparin-free, kept patent by periodic saline flushes, a high blood-flow rate to limit stasis, and (where available) pre-dilution. It accepts a higher clotting risk and demands close attention to the circuit throughout.

Choosing by bleeding risk

• The choice is driven by bleeding risk. Standard-risk patients receive systemic heparin (or LMWH). High-risk patients — active bleeding, recent surgery, pericarditis, severe thrombocytopenia — receive heparin-free dialysis or regional citrate. The method follows the patient, not habit.

Monitoring

• Heparin is monitored by the activated clotting time or aPTT to a moderate prolongation, with visual inspection of the circuit; citrate is monitored by a low circuit ionised calcium with a normal systemic value and stable acid-base. The circuit itself is the simplest monitor — clots and rising pressures mean too little anticoagulation, prolonged needle-site bleeding means too much.

Heparin-induced thrombocytopenia

• Heparin can trigger an immune thrombocytopenia — HIT — with a falling platelet count and, paradoxically, thrombosis. It is a reason to stop all heparin (including LMWH and heparin locks) and switch to a non-heparin method such as citrate or a direct anticoagulant. Continuing heparin into HIT risks devastating thrombosis.

Recognising and managing circuit clotting

• Clotting announces itself as rising venous and transmembrane pressures, clots in the drip chamber and dark streaks in the dialyzer, and a shortening circuit life. The response is to flush and check that anticoagulation is adequate, that blood flow is good, and that the access is not the problem; a fully clotted circuit is changed, returning the blood if it can be done safely. Prevention is adequate anticoagulation, good flow, minimal stasis, and pre-dilution.

Five fully-built tables.

Table A — Anticoagulation methods

Table B — Choosing by bleeding risk

Table C — Monitoring

Table D — Complications and management

Table E — Circuit clotting: signs and prevention

Visualise & Map

Numbered rules. These numbers are the cross-reference handle for the cases and flowcharts.

Clinical Reasoning

Five cases. Each stops you at a decision before it answers it.

Exhaustive. Every rule in the chapter is here.

Safety & Evidence

Panel A — Red flags

Panel B — NEVER DO

Anti-patterns clinicians fall into. Each becomes a Level 22 distractor.

The grade reflects strength of evidence, not importance.

Patient Decisions

Outcomes as natural frequencies. Figures are representative; the direction of effect is given where precise numbers are uncertain.

Apply & Test

Copy-paste chart notes that map to the real decisions in this chapter.

Template 1 — Anticoagulation prescription note

• Bleeding-risk assessment: standard / high (reason) / HIT.
• Method: systemic heparin / LMWH / regional citrate / heparin-free.
• Dosing: heparin bolus + infusion ___ ; or LMWH dose ___ ; or citrate/calcium ___.
• Monitoring plan: ACT/aPTT target ___ ; or ionised calcium ___ .
• Heparin avoided if HIT/active bleeding: yes/no.

Template 2 — Circuit clotting / complication note

• Event: rising pressures / clots / HIT / over-anticoagulation bleeding.
• Pressures and circuit findings: venous ___ ; TMP ___ ; chamber/dialyzer ___.
• Action: flush / dose change / method change / circuit changed (blood returned? ).
• If HIT: all heparin stopped; non-heparin agent ___ .
• Prevention adjustments (flow, pre-dilution, access): ___.

Pre-rounds compression. Rules only.

Active recall. At least one card per objective.

Micro-teaching for rounds. Two scenarios, five steps each.

Eight items, each anchored in this chapter. At least one per objective.