Traumatic Hemothorax Blood Contains Elevated Levels of Microparticles that are Prothrombotic but Inhibit Platelet Aggregation.

OBJECTIVES: Autotransfusion of shed blood from traumatic hemothorax is an attractive option for resuscitation of trauma patients in austere environments. However, previous analyses revealed that shed hemothorax (HX) blood is defibrinated, thrombocytopenic, and contains elevated levels of D-dimer. Mixing studies with normal pooled plasma demonstrated hypercoagulability, evoking concern for potentiation of acute traumatic coagulopathy. We hypothesized that induction of coagulopathic changes by shed HX blood may be due to increases in cellular microparticles (MP) and that these may also affect recipient platelet function. METHODS: Shed HX blood was obtained from 17 adult trauma patients under an Institutional Review Board approved prospective observational protocol. Blood samples were collected every hour up to 4 h after thoracostomy tube placement. The corresponding plasma was isolated and frozen for analysis. The effects of shed HX frozen plasma (HFP) and isolated HX microparticles (HMP) on coagulation and platelet function were assessed through mixing studies with platelet-rich plasma at various dilutions followed by analysis with thromboelastometry (ROTEM), platelet aggregometry (Multiplate), enzyme-linked immunosorbent assays, and flow cytometry. Furthermore, HFP was assessed for von Willebrand factor antigen levels and multimer content, and plasma-free hemoglobin. RESULTS: ROTEM analysis demonstrated that diluted HFP and isolated HMP samples decreased clotting time, clotting formation time, and increased α angle, irrespective of sample concentrations, when compared with diluted control plasma. Isolated HMP inhibited platelet aggregation in response to adenosine diphosphate, arachidonic acid, and collagen. HFP contained elevated levels of fibrin-degradation products and tissue factor compared with control fresh frozen plasma samples. MP concentrations in HFP were significantly increased and enriched in events positive for phosphatidylserine, tissue factor, CD235, CD45, CD41a, and CD14. von Willebrand factor (vWF) multimer analysis revealed significant loss of high molecular weight multimers in HFP samples. Plasma-free hemoglobin levels were 8-fold higher in HFP compared with fresh frozen plasma. CONCLUSION: HFP induces plasma hypercoagulability that is likely related to increased tissue factor and phosphatidylserine expression originating from cell-derived MP. In contrast, platelet dysfunction is induced by HMP, potentially aggravated by depletion of high molecular weight multimers of vWF. Thus, autologous transfusion of shed traumatic hemothorax blood may induce a range of undesirable effects in patients with acute traumatic coagulopathy.

Prognostic value of hepatocyte proliferative activity after transjugular intrahepatic portosystemic shunt.

OBJECTIVES: Previous data indicated that the proliferating cell nuclear antigen-labeling index (PCNA-LI) reflects the liver functional reserve in human liver cirrhosis. The aim of the study was to evaluate the hepatocyte proliferative activity as a marker for the outcome of patients after transjugular intrahepatic portosystemic shunt (TIPS). METHODS: Twenty-eight consecutive patients were electively treated with TIPS for recurrent variceal bleeding (n = 14), refractory ascites (n = 12), or hydrothorax (n = 2). PCNA immunostaining was analyzed on methanol-fixed, paraffin-embedded liver biopsies. RESULTS: After TIPS, six patients died within the first 3 months, eight other patients died later, two were transplanted, and 12 were alive at the time of analysis. Early death occurred in patients with refractory ascites (5/12) and/or in Child C patients (3/6). Among the evaluated variables, there was a statistical trend for the PCNA-LI to be lower in patients who died early after TIPS than in those having long term survival (1.55% vs 2.65%, p = 0.07). After TIPS insertion, the probability of remaining alive during the first 6 months of follow-up was significantly higher in patients with a preprocedural PCNA-LI > 2.9%. CONCLUSIONS: The PCNA-LI measured on liver biopsy before the TIPS procedure might be a pre-TIPS marker to discriminate those patients for whom TIPS is likely to be beneficial.

[Fibrinolytic activity in traumatic hemothorax fluids]. / Etude de l'activité fibrinolytique dans les liquides de ponction d'hémothorax traumatique.

Twenty-nine patients, 15 to 85-year-old (mean: 50 years) who presented with a pleural effusion after trauma were studied. The blood content of pleural fluid was confirmed by thoracocentesis. None of the patients had been taking anticoagulant drugs during the fortnight preceding the trauma. Thoracocentesis was always carried out less than 90 min after the trauma. The following parameters were measured in the haemothorax liquid samples: clotting fibrinogen fraction (Fg C), fibrin degradation D-dimers, functional plasminogen, alpha 2-antiplasmin, alpha 2-macroglobulin, plasminogen tissue activator (tPA Ag), type 1 tPA plasma inhibitor (PAI), and haematocrit. Haemothorax liquid haematocrit values ranged from 13 to 35% (25 +/- 7%, with a mean peripheral venous haematocrit of 34 +/- 6%). Only three patients had some Fg C (0.05-0.13 g.l-1). The D-dimer level was very high (0.23 +/- 0.22 g.l-1). The other factors involved in fibrinolysis were also present. Moreover, there was a statistically significant inverse correlation between D-dimer and alpha 2-macroglobulin levels (r = -0.64, p less than 0.0025). These data suggest two possible mechanisms to explain the fibrinogen levels: coagulation is activated, followed by an important fibrinolytic reaction elicited by the large amounts of plasminogen and tPA present in the haemothorax liquid.