The case is a postpartum woman who starts bleeding two days after a normal delivery. Her APTT is long, her factor VIII level is only 10% of normal, but her PT and TT are both normal. We have to pick the diagnosis that explains this exact combination.
- Acquired factor VIII deficiency: An antibody made after delivery attacks factor VIII and lowers its activity. Since factor VIII sits only in the intrinsic pathway, APTT rises while PT and TT, which do not depend on factor VIII, stay normal. The sudden onset with no past bleeding history fits a new antibody rather than a lifelong defect.
- Hereditary factor VIII deficiency: This is present from birth and would usually have caused bleeding earlier in life, such as during childhood injuries. A first bleed only at this point in an otherwise healthy woman does not fit a hereditary cause.
- DIC: DIC uses up clotting factors from both pathways, so PT would also be raised, fibrinogen would fall, TT would lengthen, and platelets would drop. Here PT and TT are both normal, so DIC does not explain the picture.
- Antiphospholipid syndrome: This condition can raise APTT in the lab because the antibody interferes with the phospholipid used in the test, but the true factor VIII level stays normal, and the clinical problem it causes is clotting, not bleeding. A real drop in factor VIII to 10% does not match this diagnosis.
The pattern of an isolated raised APTT, a real drop in factor VIII activity, normal PT and TT, and a fresh onset after delivery points to an antibody against factor VIII that appeared after childbirth.
Let's summarize:
- APTT checks the intrinsic pathway, where factor VIII sits, while PT and TT do not depend on factor VIII.
- A new bleeding problem after delivery, with no childhood history, points to an acquired cause rather than a hereditary one.
So the likely diagnosis is acquired factor VIII deficiency from a postpartum antibody.