Fibrinolytic response to trauma.

The fibrinolytic response to trauma was investigated in 23 patients. Patients were triaged upon arrival in the emergency center into three groups; group I-patients with significant trauma who maintained normal vital signs, had a good prognosis, and tolerated the trauma well (mean injury severity score 8, range 4 to 12); group II--patients with significant trauma and transient episodes of hypotension, hypoxia, or acidosis who recovered (mean injury severity score 22, range 9 to 38); and group III--patients with profound or continued hypoxia and hypotension who eventually died of the trauma (mean injury severity score 41, range 30 to 50). Serial measurements of prothrombin time, activated partial thromboplastin time, and platelet count; concentrations of fibrinogen, plasminogen, and fibrin degradation products; and assays of euglobulin fraction fibrinolytic activity on plasminogen-free and plasminogen-rich fibrin plates were obtained on all patients. Coagulation studies documented a trauma-related coagulopathy that correlated with the degree of trauma. Plasminogen concentrations were initially depressed in all three groups; however by 24 hours group III patients were noted to have significantly elevated plasminogen concentrations while group I and group II patients had normal plasminogen concentrations. Fibrinolytic activity measured on plasminogen-free and plasminogen-rich fibrin plates was initially increased in all three groups with group III patients demonstrating the greatest increase. Over the succeeding 14 hours fibrinolytic activity returned to baseline values in group I and group II patients while group III patients demonstrated no detectable fibrinolytic activity for the remainder of the study period. This absence of fibrinolytic activity and increase in plasminogen concentrations in group III patients is thought to be caused by depletion of the intravascular plasminogen activator with the subsequent development of a hypofibrinolytic state.

Heparin-induced thrombocytopenia, thrombosis, and hemorrhage.

Sixty-two patients with a heparin-induced thrombocytopenia are reported. Clinical manifestations of this disorder include hemorrhage or, more frequently, thromboembolic events in patients receiving heparin. Laboratory testing has revealed a falling platelet count, increased resistance to heparin, and aggregation of platelets by the patient's plasma when heparin is added. Immunologic testing has demonstrated the presence of a heparin-dependent platelet membrane antibody. The 20 deaths, 52 hemorrhagic and thromboembolic complications, and 21 surgical procedures to manage the complications confirm the seriousness of the disorder. Specific risk factors have not been identified; therefore, all patients receiving heparin should be monitored. If the platelet count falls to less than 100,000/mm3, while the patient is receiving heparin, platelet aggregation testing, using the patient's plasma, is indicated. Management consists of cessation of heparin, platelet anti-aggregating agents, and alternate forms of anticoagulation when indicated.

A new Cd-115 leads to In-115m radionuclide generator.

A new column-type Cd-115 leads to In- 115m generator has been developed by adsorbing CdI4(-2) on an anion-exchange resin and eluting the In-115m with 0.05 M HCl. The In-115m yield of the prototype column is 90% in a volume of 3 ml, with Cd-115 breakthrough of less than 3 X 10(-4)%. Over thirty generators with up to 40 mCi of activity have been produced using components of a commercial Mo-99 leads to Tc-99m generator system; they behaved like the prototype. In-115m oxine prepared from these generators has been used to label canine platelets and to image an induced canine thrombus in vivo.

Transcutaneous quantitation of arterial flow with ultrasound.

Arterial blood flow was measured in dogs simultaneously with electromagnetic flow probes and with ultrasonic "flow probes." The ultrasonic probes were used to determine transcutaneously the mean velocity of arterial flow and the cross-sectional area of the blood vessel. A 10 MHz probe was used for blood vessels 1 cm deep or less, while a 5 MHz probe was used for vessels between 1.0 and 2.5 cm deep. The correlation coefficient between the flow calculated with the ultrasound method and the flow measured with the electromagnetic flow probes was 0.966, p less than 0.01. Blood flow was also measured intraoperatively in five patients. There was a correlation coefficient of 0.999, p less than 0.01, between the flow obtained with the ultrasound method and that determined simultaneously by the electromagnetic flow probes. The coefficient of determination for the regression of electromagnetic-determined flow on ultrasound-determined flow was 0.99. Thus, accurate transcutaneous determination of blood flow is possible with slightly modified ultrasound equipment.

Populations with the Leriche syndrome.

Complete infrarenal aortic occlusion was found in 20 of 325 patients who underwent bypass for atherosclerosis of the distal aorta. Eleven had normal distal arteries as demonstrated by arteriography; the remaining patients had multilevel areas of stenosis and occlusion below the inguinal ligament. The two groups were significantly different in age, blood pressure levels, and duration of symptoms. The bypass relieved symptoms and restored flow in all the patients with normal distal vessels. There were four acute graft failures, two of which resulted in death, in the group with distally diseased vessels, and only two of these nine patients were symptomatically improved by the bypass. These data indicate that there are at least two distinct patient populations with the Leriche syndrome. Anatomic changes at the aortic bifurcation may be responsible for the clinical differences.

Heparin-induced thrombocytopenia, thrombosis, and hemorrhage.

Twenty-two patients developed significant thrombocytopenia (5,000 to 96,000/cu mm; mean, 29,000/cu mm) while receiving prophylactic or therapeutic heparin. Seventeen of them developed serious thrombohemorrhagic complications which accelerated the deaths of six and contributed to the late death of one. Cessation of heparin therapy led to an immediate remission of the thrombohemorrhagic complications and thrombocytopenia, with no patient who was not already moribund dying, once appropriate therapy had been instituted. Platelet-count monitoring is recommended for all patients receiving heparin for more than 6 days, with cessation of heparin therapy mandatory for the successful management of patients with this disorder. Evidence is presented for an immunologic etiology for this disorder.