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NEW Added to close a syllabus gap — coagulation appears twice in the EDAIC syllabus, as physiology and as measurement.

Coagulation & transfusion

The cascade, the tests that interrogate each half of it, anticoagulants and their reversal, and blood products with their reactions.

The cascade

PathwayFactorsTest
IntrinsicXII → XI → IX → VIIIAPTT (30–40 s)
ExtrinsicTissue factor → VIIPT / INR (12–15 s)
CommonX → V → II (thrombin) → fibrinogen to fibrin → XIII cross-linksBoth PT and APTT; thrombin time tests fibrinogen
  • PT = extrinsic = warfarin. APTT = intrinsic = heparin. That pairing answers most questions.
  • Factor VII has the shortest half-life (4–6 h) — so the PT/INR rises first in liver failure and on starting warfarin.
  • Vitamin K dependent: II, VII, IX, X plus proteins C and S. Because protein C also falls, warfarin is transiently prothrombotic at initiation.
  • Factor VIII is NOT made in the liver (endothelium) — so it is preserved or raised in liver disease.

Anticoagulants and reversal

DrugMechanismMonitorReversal
Unfractionated heparinPotentiates antithrombin III ~1000×APTTProtamine 1 mg per 100 units
LMWHMainly anti-XaAnti-Xa levelProtamine — partial only
WarfarinInhibits vitamin K epoxide reductaseINRVitamin K + PCC (or FFP)
Apixaban / rivaroxabanDirect factor Xa inhibitorsAnti-Xa (specific)Andexanet alfa; PCC
DabigatranDirect thrombin inhibitorThrombin timeIdarucizumab
Aspirin / clopidogrelCOX-1 / P2Y12 platelet inhibitionPlatelet function testsPlatelet transfusion
  • Heparin-induced thrombocytopenia (HIT) — immune, 5–10 days after exposure, causes thrombosis not bleeding. Stop all heparin; use argatroban or fondaparinux.
  • Protamine itself causes hypotension, pulmonary hypertension and anaphylaxis — give slowly.

Thromboelastography

The trace is symmetrical about a baseline: the wider it opens, the stronger the clot. Read it left to right in time — initiation, then rate of build-up, then strength, then breakdown.

2 mm 20 mm α MA platelets LY30 lysis at 30 min R time factors → FFP K K & α: fibrinogen → cryo time R → K → α → MA → LY30, in the order the clot forms and breaks down
ParameterRepresentsIf abnormal, give
R timeTime to clot initiation — clotting factorsFFP
K time / α angleRate of clot build-up — fibrinogenCryoprecipitate or fibrinogen concentrate
MA (maximum amplitude)Clot strength — plateletsPlatelets
LY30Fibrinolysis at 30 minTranexamic acid

The abnormal traces

Six shapes worth recognising on sight. Compare each against the normal in the top left — what has changed is the width, the delay, or the tail.

NORMAL Normal R · normal width · no tail ↑ R TIME Long R — heparin / factors → FFP (or protamine) ↓ MA Narrow — weak clot, low platelets → platelets FIBRINOLYSIS Tapering tail — clot dissolves LY30 > 7.5% → tranexamic acid HYPERCOAGULABLE Short R, wide MA → consider thromboprophylaxis DIC (late) Long R AND narrow MA factors AND platelets consumed Width = clot strength · delay before opening = R time · tapering tail = lysis

Reading an abnormal trace in three steps

  • 1. How long before it opens? A long delay is a prolonged R — factors are lacking or heparin is on board. Give FFP.
  • 2. How wide does it get? A narrow trace means a weak clot — low or dysfunctional platelets (low MA, give platelets), or poor fibrinogen if the angle is also shallow (give cryoprecipitate).
  • 3. Does it close again? A tapering tail is fibrinolysis — LY30 above about 7.5%. Give tranexamic acid.
  • DIC is the combination: long R AND narrow MA, because both factors and platelets are being consumed. Early DIC can look hypercoagulable before it becomes the classic hypocoagulable picture.
  • The mirror-image opposite — short R with a wide MA — is the hypercoagulable trace, and points to thrombotic rather than bleeding risk.

Blood products & transfusion

ProductContainsStorageIndication
Packed red cellsRBC, Hct ~0.62–6 °C, 35 daysHb <70 g/L (80 in ACS)
FFPAll clotting factors−30 °C, 12–36 months12–15 ml/kg for factor deficiency
CryoprecipitateFibrinogen, VIII, XIII, vWF−30 °CFibrinogen <1.5 g/L
PlateletsPlatelets20–24 °C, agitated, 5 days<50 with bleeding; <100 in neuro/eye surgery

Storage lesion & reactions

  • Stored red cells: ↓2,3-DPG (curve shifts LEFT), ↑K⁺, ↓pH, ↓ATP, microaggregates.
  • Acute haemolytic — ABO incompatibility, usually a clerical error. Fever, hypotension, haemoglobinuria, DIC. Stop immediately.
  • TRALI — non-cardiogenic pulmonary oedema within 6 h, donor antibodies. Commonest cause of transfusion death.
  • TACO — circulatory overload; distinguished from TRALI by raised JVP and response to diuretics.
  • Massive transfusion: hypothermia, hypocalcaemia (citrate), hyperkalaemia, dilutional coagulopathy, acidosis.

Major haemorrhage

  • Balanced ratio ~1:1:1 red cells : FFP : platelets · tranexamic acid within 3 hours · calcium replacement · keep warm · definitive source control.
  • Lethal triad: hypothermia, acidosis, coagulopathy (+ hypocalcaemia = "lethal diamond").