No abstract

The objective was to diagnose a hypercoagulative state or "pre-DIC" with new laboratory tests. APACHE II score was used as a measure of primary illness. Ventilator time was used as a reflexion of secondary complications. Twenty-three ICU patients were divided into two groups depending on time on the ventilator: Group 1 > 7 days and Group II < or = 7 days. If, after admittance patients deteriorated or complications occurred, new quantitative coagulation tests were done: soluble fibrin, prothrombin fragment 1 + 2, thrombin-antithrombin complex, D-dimer and elastase. We found a positive correlation between SF levels, the APACHE II score and the ventilator time. Diagnostic efficacy for SF was 87%, sensitivity 91%, specificity 83%, the predictive value of a positive result was 87% and the predictive value of a negative result 91%. The levels of the other new tests were also generally higher in the clinically worse group, although not significantly. Prothrombin complex, APTT, platelet count and AT III were pathologic to the same extent in both groups. The patients who developed most secondary complications, resulting in longer ventilator treatment (Group I), were also hypercoagulative. Soluble fibrin, in particular, seems to be valuable in the diagnosis of "pre-DIC" and possibly of predictive value for organ system complications.

This article describes the outcome of 1,508 patients with traumatic brain injuries (TBI) treated in a single neurosurgical unit over an 8-year period. Our aim has been to compare those outcomes with our previous results and with other large patient series. Another important goal was to evaluate the effect of the introduction of a 4-year ongoing study initiated in January 1993 using a new strategy of prehospital care on postresuscitation Glasgow Coma Score (GCS) and Glasgow Outcome Score (GOS). Results from the 1,508 patients showed good recovery or moderate disability in 69%, severe disability or vegetative state in 11%, and a mortality rate of 20%. When outcome of the most severely injured patients (GCS < or = 8) was compared with those of our previous and other large international patient series, more favorable outcome figures were shown in the present study. To evaluate the impact of the improved prehospital care after half of the study period, a logistic regression analysis showed after January 1993 a significantly increased expected odds/ratio for a postresuscitation GCS 8-15 rather than a GCS 3-4 (odds/ratio: 2.2; p < 0.001). For patients with postresuscitation GCS 5-7 and 8-15, the expected odds/ratio for a GOS 4-5 instead of GOS 1 increased significantly (odds/ratio: 2.2 and 1.7, respectively; p < 0.05-0.01). For patients with GCS 3-4, an increased expected odds/ratio (2.0; p < 0.05) for a GOS 2-3 rather than a GOS 1 was seen. The principal conclusion is that outcome for the severely injured patients in the present study is more favorable than in other large series of TBI. We posit that the introduction of effective prehospital care most likely contributed to the improved postresuscitation neurological status and consequently to the better outcome observed after January 1993.

This study will determine if early administration of antithrombin concentrate to patients with traumatic brain injury (TBI) can inhibit or significantly shorten the time of coagulopathy. The progress of brain injury monitored by computed tomographic scan (CT) was also assessed, as was the time needed for intensive care and outcome related to Glasgow outcome scale (GOS). Twenty-eight patients with isolated brain trauma verified with CT were included in either of two parallel groups. The Glasgow coma score (GCS) was mean 7.5, and median 7.0; signifying a moderate to severe traumatic brain injury but with a mortality of only 3.5%. The patients randomized to antithrombin treatment received a total of 100 U/kg BW during 24 hours. To measure hypercoagulability, soluble fibrin (SF), D-dimer (D-d), and thrombin-antithrombin complex (TAT) were assessed together with antithrombin (AT) and routine coagulation tests. Before treatment, SF, D-d, and TAT were markedly increased in both groups. Soluble fibrin and D-dimer (measured after treatment began) appeared to decrease faster in the AT group, and there was a statistically significant difference between the groups at 36 hours for SF and at 36 hours, 48 hours, and at Day 3 for D-d. Thrombin-antithrombin complex levels were very high in both groups but, surprisingly, showed no significant difference between the groups. The authors conclude that antithrombin concentrate administered to patients with severe TBI resulted in a marginal reduction of hypercoagulation. We could not detect any obvious influence by antithrombin on brain injury progress, on CT, or on outcome or time needed for intensive care.

No difference between fixation with and without cementThe acrylic bone cement has been regarded as a very potent activator of the hemostatic mechanisms. A battery of coagulation, fibrinolytic. and kallikrein variables were studied perioperatively in 21 patients undergoing hip arthroplasty with fixation of the prosthesis either with (Charnley) or without (HP-Garches) cement. Epidural analgesia was used and dextran 6 per cent as thromboprophylaxis. The HP-Garches procedure was shorter and caused less blood loss. No differences were found between the two surgical procedures regarding the activation of the cascade systems. The coagulation and fibrinolytic systems were activated early, but a week postoperatively the latter seems to predominate. A marked activation of the kallikrein system was apparent.Our study shows that despite thromboprophylaxis a marked activation of the coagulation, fibrinolytic, and kallikrein systems occurs in relation to hip arthroplasty irrespective of the use or nonuse of cement and irrespective of the volume of blood loss during surgery. It may be the reaming of the bone marrow that initiates the activation of the cascade systems.