Approach to bleeding Flashcards
What are the features of primary haemostasis pathology?
Epistaxis not stopped by 10 mins compression or requiring medical attention/ transfusion
Cutaneous haemorrhage or bruising without apparent trauma (esp. multiple/large) / spontaneous; Distribution
- Eg: bruising over the limbs may point to a less significant bruising! Since we often bruise our limbs
- If on the trunk 🡪 more likely significant as we rarely get bruises there
Prolonged (>15 mins) bleeding from trivial wounds, or in oral cavity
What are the features of 2’ haemostasis pathology?
Bleeding recurring spontaneously in 7 days after wound
Muscle / Joint bleeds
What are features of significant bleeding diathesis?
Spontaneous GI bleeding leading to anaemia
Menorrhagia requiring treatment or leading to anaemia, not due to structural lesions of the uterus
Heavy, prolonged or recurrent bleeding after surgery or dental extractions
How do you take a bleeding history from a child patient?
Is child crawling? – bruising rare in infants before they crawl. Remember to think about abuse
History at birth: e.g. bruising and bleeding from birth, from umbilical stump, haematoma after intramuscular vitamin K given from birth, bleeding from heel prick neonatal blood test
- Heel prick done to check for congenital diseases (congenital hyperthyroidism in jaundiced babies, phenylketonuria)
What is the physical exam performed for a bleeding patient?
Record the appearance, distribution, number, site, and size of bruising together with any petechiae, ecchymosis, and haematomas
Pattern of bruising
Look out for non-accidental injury (signs of abuse)
Other associated signs (connective tissue disease)
What are the haematological causes of a bleeding patient?
Platelet disorder (quantitative e.g. ITP/qualitative e.g. MDS. Inherited/acquired)
Clotting factor deficiencies (inherited /acquired)
Malignancy (e.g. acute leukaemia, MDS, BM infiltration from 2nd malignancy with ↓Plt)
Disseminated Intravascular Coagulation (DIC)
Drugs e.g. warfarin, heparin, NOACs, antiplatelet
Vitamin K / C deficiency, Malnutrition
MAHA (microangiopathic haemolytic anaemia)
Rarer: HELLP, eclampsia, malaria, dengue fever, heparin induced thrombocytopenia, post transfusion purpura – all cause thrombocytopenia
What are the non haematological causes of a bleeding patient?
Senile purpura
Purpura simplex
Abuse
- NAI – non-accidental injury
- Not just in neonates but also elderly!! May be due to Caregiver Stress
Alcohol abuse
- Causes decreased platelet count
- Esp in pt who have low platelet count to begin with 🡪 may ppt brusing
Metabolic Disorders (e.g. Cushing’s Syndrome) Inherited disorders (Marfan’s, Ehlers-Danlos, Hereditary haemorrhagic telangiectasia)
Connective Tissue / Autoimmune Disorders
What is senile purpura and what is it caused by?
Purpura from increased vessel fragility due to connective tissue damage by chronic sun exposure, aging, and drugs
- Drugs: corticosteroids, warfarin, aspirin, clopidogrel
Senile purpura typically affects elderly patients (mainly extensor areas of hands and forearms)
What is HHT?
bnormal angiogenesis in the skin, mucous membranes, causing nosebleeds and BGIT
How does Cushing syndrome affect risk of bleeding?
Causes increased thromboembolic events due to glucocorticoid-induced increases in clotting factors and von VWF, and decreases in fibrinolytic activity
However also causes loss of subcutaneous connective tissue due to the catabolic effects of glucocorticoid 🡪 senile purpura
What are the investigations required in a bleeding patient?
FBC: anaemia, iron deficiency, whether defect is across all cell lines
Blood film:
- Platelet clumping (platelet clumping due to chemical in blood tube, resulting in falsely low platelet count OR due to inherent platelet defect)
- Platelet defects
- MDS (e.g. pelger-huet)
Clotting: PT, APTT, - Fibrinogen, D-dimers, FDPs
D-Dimers are much more specific to Fibrinogen breakdown
- PT looks at extrinsic pathway
- APTT looks at intrinsic pathway
- TT looks at common pathway
Biochemistry: urea, LFTs, albumin, inflammatory markers
Further Investigations: PT/APTT mixing studies, von Willebrand antigen and function, factor and inhibitor assays, platelet function testing, anti-Factor Xa for LMWH, NOAC assays
[APTT/PT 50% Correction Test – aka Mixing Studies]
Used to distinguish factor deficiencies from factor inhibitors, such as lupus anticoagulant or antibodies directed against factors
Principle: normalizing the patient’s plasma with pooled normal plasma; as long as Coag factors >50% of normal, will give normal PT/APTT results
- If PT and APTT are corrected: __________________
- If PT and APTT NOT corrected, but patient not bleeding: ____________
- If PT and APTT NOT corrected, but patient is bleeding: __________________
Factor deficiencies in patient’s plasma;
lupus anticoagulant;
inhibitors of FVIII, IX, XI (e.g. antibodies in acquired haemophilia)
What are the causes of prolonged PT only?
Factor VII deficiency (rare)
- Congenital
- Acquired (Vitamin K deficiency, Liver disease)
Factor VII inhibitor: Warfarin
What are the causes of prolonged APTT only?
Factor 8 Deficiency
- Von Willebrand Disease
- Haemophilia A (presents at birth)
Factor 8 Inhibitor
- Lupus anticoagulant is a type of APLS (the others being anti-cardiolipin Ab & Anti-β2-glycoprotein) causes a global inhibition of all APTT coag factors
Factor 9 Deficiency
- Haemophilia B (presents at birth)
F12 Deficiency – will have NO BLEEDING Hx despite prolonged aPTT!
How does Von Willebrand disease cause APTT prolongation?
APTT prolongation is 2° to low levels of FVIII as vWF functions to protect FVIII from degradation.
Haemostatic tests may be normal in the presence of a mild but significant bleeding diathesis such as VWD – consider vWF Ag, Ristocetin Cofactor
