Pathologic Hemorrhage

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Every clinician sees at times patients who bleed without injury or who bleed excessively from a minor injury, and hence are subject to pathologic hemorrhage. The proper treatment of this condition depends on the correct classification of the homorrhagic disease and, if possible, recognition of the underlying cause. All pathologic hemorrhage is the result of an abnormal permeability of the capillaries, an increased tendency of the blood to penetrate the vessel walls, or a disturbed coagulation of the blood.

Normally, as we know, the blood does not penetrate the endothelial barrier of the capillaries, and when vessel injury occurs, a clot is quickly formed, preventing an abnormal loss of blood. According to Howell, the factors in blood coagulation are as follows: (1) prothrombin, the precursor of thrombin, is held neutral in the blood plasma by antiprothrombin (heparin); (2) on adding zymoplastic substances (tissue juice, platelets) to blood, the thromboplastin (cephalin) which these substances contain neutralize the antiprothrombin leaving the prothrombin in an active state; (3) prothrombin combines with ionized calcium to form thrombin; (4) thrombin unites with fibrinogen to form fibrin, the clot. A disturbance in any factor in the chain may lead to abnormal hemorrhage.

The important factors in blood coagulation, then are: (1) pro-thrombin, derived partly, but not solely, from platelets; (2) anti-prothrombin, formed probably in the liver; (3) calcium, derived from calcium salts in the blood plasma; (4) fibrinogen, a globulin formed principally in the liver; and (5) thromboplastin, a phos-pholipin derived from tissue juices or platelets.



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