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.
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.
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.
PT or APTT is prolonged in a stable patient without current major bleeding.