Synopsis
Interpret PT, APTT, fibrinogen and thrombin time as pathway tests, identify anticoagulant and pre-analytical effects, and recognise consumptive or factor-deficiency patterns that require urgent action.
- A coagulation screen is not a global bleeding-risk test. Normal PT and APTT do not exclude von Willebrand disease, platelet dysfunction, factor XIII deficiency or an anatomical bleeding source.
- Check sample quality first: underfilled citrate tubes, high haematocrit, heparin contamination, delayed processing and a clot in the tube can create misleading prolongation or consumption.
- PT mainly assesses the tissue-factor and common pathways and is used as INR for vitamin K antagonist monitoring; APTT assesses contact, intrinsic and common pathways but varies by reagent.
- An isolated prolonged APTT can reflect heparin, lupus anticoagulant, factor VIII, IX or XI deficiency, or non-bleeding contact-factor deficiency. Bleeding history determines significance.
- An isolated prolonged PT suggests vitamin K deficiency, early liver dysfunction, warfarin or factor VII deficiency, while combined prolongation raises common-pathway deficiency, severe liver disease, DIC or anticoagulant effect.
- A mixing study that corrects supports factor deficiency; failure to correct supports an inhibitor or drug effect. Time-dependent inhibitors may require incubation and specialist interpretation.
- Falling fibrinogen, thrombocytopenia, prolonged clotting and high D-dimer in the right clinical context supports DIC, but trends and the precipitating illness matter more than one borderline value.
- Direct oral anticoagulants can variably affect routine tests, and a normal PT or APTT does not reliably exclude clinically important drug concentration. Establish agent, dose and last administration time.
Key red flags
DIC, severe liver disease, marked vitamin K deficiency, common-pathway factor loss, massive dilution or anticoagulant effect can prolong PT and APTT together.
A falling platelet count and fibrinogen with rising D-dimer and prolonged clotting in sepsis, trauma, obstetric catastrophe or malignancy supports DIC.
Investigation priorities
Confirm the pattern on a correctly collected peripheral sample and assess common mechanisms.
Management branches
Active significant bleeding accompanies an abnormal screen or anticoagulant exposure.
- Use ABCDE, secure access, identify the bleeding source, send FBC, coagulation, fibrinogen, group and screen or crossmatch, renal and liver tests, and activate the major-haemorrhage pathway when indicated.
- Preferred haemostatic treatment is source control plus agent- and defect-specific reversal or component support advised by haematology and transfusion; an alternative empirical product is justified only within the major-haemorrhage protocol.
- Escalate intracranial, obstetric, postoperative or haemodynamically significant bleeding immediately and repeat clinical and laboratory endpoints after each major intervention.
PT or APTT is prolonged in a stable patient without current major bleeding.
- Verify the sample and medication history, repeat from a clean peripheral venepuncture and assess personal and family bleeding, previous surgery and thrombosis.
- For isolated APTT, the preferred next step is laboratory-guided thrombin time, anti-Xa or mixing assessment after drug exclusion; for isolated PT, review warfarin, vitamin K, liver and factor VII mechanisms.