Depletion Of Coagulation Factors Research Articles

THE IMPACT OF HYPOTHERMIA ON DILUTIONAL COAGULOPATHY

The control of hemorrhage in hypothermic patients with platelet and clotting factor depletion is often impossible. Determining the cause of coagulopathic bleeding (CB) will enable physicians to appropriately focus on rewarming, clotting factor repletion, or both. To determine the contribution of hypothermia in producing CB and ascertain if simultaneous hypothermia and dilutional coagulopathy (DC) interact synergistically. Prothrombin time, partial thromboplastin time, and platelet function were determined at assay temperatures of 29 degrees to 37 degrees C on normal and critically ill, noncoagulopathic (NC) individuals. Dilutional coagulopathy was created using buffered saline and the assays repeated. Hypothermic assay at < or = 35 degrees C significantly prolonged coagulation times. The effect of hypothermia on NC and DC samples was not different. Assays performed at 37 degrees C underestimate coagulopathy in hypothermic patients. The effect of hypothermia on NC and DC is not different, indicating the lack of a synergistic effect. Normalization of clotting requires both rewarming and clotting factor repletion.

Management of Hemophilia Patients with Inhibitors

rFVIIa seems to offer an alternative in the treatment of hemophiliacs as well as nonhemophiliacs with antibodies against FVIII/FIX. The treatment can be given regardless of the inhibitor titer in those patients and is also hemostatically active in hemophilia B patients. It is easy to administer but seems to need a repeated dosing at 2- to 3-hour intervals, at least initially in severe bleedings. A dose of 70 to 100 micrograms/kg body weight seems to induce hemostasis. Depending on the severity of the bleeding, the dose intervals may then be prolonged to 3 hours for 1 to 2 days or until clinical improvement is observed. Thereafter, the dosage interval can be increased to 4 hours if continued therapy is indicated.

Assessment of thrombogenicity of prothrombin complex concentrates in a porcine model

Infusion of prothrombin complex concentrates into pigs resulted in evidence of disseminated intravascular coagulation manifested by positive fibrin monomer tests, depletion of coagulation factors and platelets, and the presence of fibrin in small blood vessels at autopsy. All of the nine prothrombin complex concentrates were found to be thrombogenic. The response appeared to be dose-related, and the two activated materials were more thrombogenic than the non-activated products. In contrast, a purified factor IX concentrate resulted in minimal transient changes in only 2 of 5 animals tested, and autopsy findings were negative for fibrin deposition in all. Four of these animals received 200 factor IX units/kg, which was twice the dose used for any of the other products. Control animals received human plasma or albumin with no evidence of coagulation changes or fibrin deposition at autopsy. The porcine model is more sensitive than other animal models for detection of the thrombogenic effects of prothrombin complex concentrates and may be useful for testing new products found to be non-thrombogenic in other test procedures.

The hemostatic system in children undergoing intensive plasma exchange

We report the effects on the hemostatic system of intensive plasma exchange therapy using replacement fluids devoid of plasma coagulation proteins. Five children were studied during ten exchanges. There were no hemorrhagic episodes clearly attributable to the plasma exchange, but one patient developed recurrent thrombosis of the vascular access used for the procedure. Plasma values of the various coagulation factors (II to XII) were decreased by 35 to 67% immediately following the plasmapheresis. The mean decrease in levels of antithrombin III antigen and activity and of plasminogen were 58, 60, and 66%, respectively. The recurrent thrombosis of the vascular access in one of the patients, and the decrease in antithrombin III and plasminogen values in plasma following plasmapheresis in all patients, suggest that there is increased potential for thrombosis in patients undergoing intensive plasmapheresis, despite the depletion of coagulation factors. At 24 hours following plasmapheresis the values for all factors were within normal limits, attesting to the ability of the synthetic mechanisms in children to replenish hemostatic factors rapidly.

The coagulation and fibrinolytic properties of peritoneal and venous blood in patients with ruptured ectopic pregnancy.

SummaryThe coagulation and fibrinolytic properties of peritoneal and venous blood were studied in ten African patients with ruptured ectopic pregnancy. The peritoneal blood showed marked depletion of coagulation factors and the level of fibrinfibrinogen degradation products (FDP) was grossly elevated. A slight but significant elevation of FDP was the only abnormality detectable in the venous blood. In the light of these findings the value and hazards of autotransfusion are discussed.

CARE OF THE CRITICALLY ILL CHILD: THE PROBLEM OF DISSEMINATED INTRAVASCULAR COAGULATION

A critically ill child should be suspected of the complication of disseminated intravascular coagulation when evidence of the following signs and symptoms are present: (1) the potential of a triggering substance or event such as endotoxin, tissue thromboplastin (damaged tissue), endothelial damage, or proteolysis; (2) multiple system involvement producing coma, renal shutdown, respiratory disease, and shock; (3) a bleeding diathesis; and (4) a hemolytic anemia associated with fragmented and burred red cells. Laboratory confirmation should include evidence for depletion of coagulation factors consumed during clotting (i.e., platelets, fibrinogen, and factors II, V, and VIII). Treatment consists of heparinization, replacement of depleted factors if needed, and supportive care, which includes removal of the triggering event.

Coagulation defects and metastatic neuroblastoma

The association of metastatic neuroblastoma and a fatal progressive depletion of coagulation factors is described in a 2-month-old male infant. The anemia observed may have been at least partly due to a hemolytic process. The mechanisms responsible for the observed findings were not conclusively defined.