Coagulation Screening
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Direct answer
Three tests screen haemostasis: prothrombin time (normal about 11-14 seconds) tracks the extrinsic and common pathways (factors VII, X, V, II, I); activated partial thromboplastin time (about 25-35 seconds) tracks intrinsic plus common (XII, XI, IX, VIII, X, V, II, I); and bleeding time (Ivy method, 2-7 minutes) tests the platelet plug and vessel wall. PT and aPTT prolong together in liver disease, disseminated intravascular coagulation and mixed anticoagulant therapy. Isolated aPTT prolongation suggests heparin contamination, haemophilia A or B, von Willebrand disease or a lupus anticoagulant; isolated PT prolongation appears early in vitamin K deficiency and liver failure because factor VII has the shortest half-life at 4-6 hours. The INR standardises PT for warfarin monitoring (target usually 2-3), and a mixing study separates factor deficiency, which corrects, from inhibitor, which does not.
What you must remember
- Normal ranges to quote: PT 11-14 s, aPTT 25-35 s, bleeding time 2-7 min (Ivy), platelets 150,000-400,000 per microlitre (1.5-4 lakh in Indian convention), fibrinogen 200-400 mg/dL, clotting time (Lee-White) 5-10 minutes.
- Vitamin K dependent factors: II, VII, IX, X plus proteins C and S; factor VII's 4-6 hour half-life makes PT the earliest abnormal test in deficiency — the physiological logic of the newborn's 1 mg intramuscular vitamin K.
- Warfarin numbers: INR target 2-3 for most indications, 2.5-3.5 for mechanical mitral valves; early protein C depletion explains the transient hypercoagulable window and skin necrosis.
- Heparin monitoring: aPTT roughly 1.5-2.5 times control for unfractionated heparin; anti-Xa assays for high-dose protocols; protamine reverses.
- Bleeding time logic: prolonged by thrombocytopenia, uraemic platelet dysfunction, aspirin and von Willebrand disease — but normal in haemophilia, the single most-quoted line in Indian practicals.
- Mixing study: 1:1 correction means factor deficiency; no correction means an inhibitor (heparin, lupus anticoagulant, acquired factor VIII inhibitor).
- DIC panel pattern: PT prolonged, aPTT prolonged, platelets low, fibrinogen low (relative to its acute-phase rise) and D-dimer high — all five together make the diagnosis.
Four panels, four diagnoses
Read them as patterns. A boy with haemophilia A: bleeding time normal, platelets normal, PT normal, aPTT markedly prolonged, corrected by mixing — factor VIII deficiency. A woman with menorrhagia since menarche: bleeding time prolonged, aPTT mildly prolonged, platelets normal, ristocetin assay abnormal — von Willebrand disease, where the plug fails and factor VIII is secondarily unstable. A patient on no anticoagulants with an isolated prolonged aPTT that does not correct on mixing, yet a history of thrombosis not bleeding: lupus anticoagulant, the paradox to name deliberately — an in vitro prolongation with in vivo thrombophilia. Finally, a jaundiced septic patient with all three screens deranged plus falling platelets and rising D-dimer: DIC, where consumption outruns production; the fibrinogen may read "normal" only because it is an acute-phase reactant that has fallen from an even higher baseline.
Where students slip
"Bleeding time is normal in haemophilia" is the line most often inverted — platelets and vessel wall are intact, so the plug forms; what fails is the fibrin reinforcement, hence the deep delayed bleeds of haemophilia against the immediate superficial bleeds of thrombocytopenia. The lupus anticoagulant paradox is the second trap: a prolonged aPTT that does not correct on mixing in a patient who clots, not bleeds. Third, the vitamin K question stops at "II, VII, IX, X" without proteins C and S, losing the explanation of warfarin-induced skin necrosis — transient protein C fall before factor X falls. And in Indian practical examinations, platelet counts are still commonly reported in lakhs; converting 1.5-4 lakh to 150,000-400,000 per microlitre on the spot is expected fluency.
Frequently asked questions
Which pathways do PT and aPTT evaluate?
PT screens the extrinsic (factor VII) plus common pathways; aPTT screens the intrinsic (XII, XI, IX, VIII) plus common pathways, and both use the common factors X, V, II and I.
Why does PT prolong before aPTT in early liver failure and vitamin K deficiency?
Factor VII has the shortest half-life (4-6 hours), so its level falls first, deranging the PT in isolation before other factors decline.
What is the purpose of a mixing study?
Mixing patient plasma 1:1 with normal plasma: correction indicates a missing factor, while persistent prolongation indicates an inhibitor such as heparin, a lupus anticoagulant or an acquired factor inhibitor.
Why is bleeding time normal in haemophilia?
Primary haemostasis — platelet adhesion and aggregation with vessel contraction — is intact; the defect is secondary haemostasis (fibrin clot formation), so the plug bleeds later rather than immediately.
What INR range is targeted on warfarin?
Two to three for most indications including atrial fibrillation and deep vein thrombosis, and 2.5-3.5 for high-risk mechanical mitral valves.