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PubMedDate not supplied

The fibrinogenopathies.

This paper reviews the reported clinical, functional and biochemical abnormalities associated with abnormal fibrinogens. It appears from studies on fibrinogen Detroit that a single amino acid substitution in a critical part of the molecule can lead to major functional abnormalities and clinical consequences of either bleeding or thrombosis. Functional defects observed include: abnormal release of fibrinopeptide A or B or both after incubation with thrombin, abnormal polymerization and abnormal clot stabilization.

Adolescent↗
PubMed1987

Prognostic factors in severe accidental hypothermia: experience from the Mt. Hood tragedy.

The May 1986 Mt. Hood climbing disaster presented Portland area hospitals the opportunity to initiate a trial of extracorporeal rewarming using cardiopulmonary bypass in ten severely hypothermic patients (two survivors). The data from this experience as well as others previously reported can yield prognostic indicators of survival in cases of accidental hypothermia. These are demonstrated to include: the presence of underlying medical illness, duration of cold exposure, initial core temperature, mental status, the presence of spontaneous respirations, presenting cardiac rate and rhythm, and arterial oxygen tension. Profound hyperkalemia and markedly elevated serum ammonia levels indicate cell lysis; significant hypofibrinogenemia suggests intravascular thrombosis and each laboratory marker predicts a dire outcome. The treatment of choice for severe accidental hypothermia is felt to be rapid core rewarming on cardiopulmonary bypass.

Accidents↗
PubMed1986

Reversal of coagulopathy in Kasabach-Merritt syndrome with tranexamic acid.

An infant with a giant cavernous haemangioma developed a severe consumption coagulopathy and systemic bleeding. Replacement therapy with cryoprecipitate produced only a transient improvement in the abnormal clotting, but the addition of tranexamic acid resulted in sustained correction, permitting corrective surgery to be performed.

Afibrinogenemia↗
PubMed1985

Defibrination during warfarin therapy in a man with protein C deficiency.

A 57 year old man presented with apparently spontaneous lower extremity deep vein thrombosis and pulmonary embolism. He was treated in conventional fashion with intravenous heparin and oral warfarin. After 4 daily doses of warfarin the prothrombin and proconvertin (P+P) time was within therapeutic range, and heparin was stopped. Over the next six hours complete defibrination occurred, associated with severe bleeding complications. Functional protein C measured after normalization of routine coagulation tests averaged 40% of normal, and was only 3.5% of normal immediately prior to the episode of defibrination. We conclude that the very low functional protein C levels seen immediately prior to defibrination were caused by a combination of pre-existent protein C deficiency and warfarin therapy, and directly predisposed to defibrination once heparin was stopped, despite "therapeutic" warfarin anticoagulation. Exacerbation of intravascular coagulation should be considered a potential prothrombotic effect of warfarin therapy in protein C deficient individuals.

Afibrinogenemia↗