Introduction: Coagulation and fibrinolysis remain sparsely addressed with regards to acute respiratory distress syndrome (ARDS). We hypothesized that ARDS development might be associated with changes in plasma coagulation and fibrinolysis. Our aim was to investigate the relationships between ARDS diagnosis and plasma concentrations of tissue factor (TF), tissue plasminogen activator (t-PA) and plasminogen activator inhibitor-1 (PAI-1) in mechanically ventilated patients at increased risk of developing ARDS. Materials and Methods: We performed an ethically approved prospective observational pilot study. Inclusion criteria: patients with PaO2/FiO2 < 300 mmHg admitted to the intensive care unit (ICU) for mechanical ventilation for 24 hours, or more, because of one or more disease conditions associated with increased risk of developing ARDS. Exclusion criteria: age below 18 years; cardiac disease. We sampled plasma prospectively and compared patients who developed ARDS with those who did not using descriptive statistics and chi-square analysis of baseline demographical and clinical data. We also analyzed plasma concentrations of TF, t-PA and PAI-1 at inclusion (T0) and on third (T3) and seventh day (T7) of the ICU stay with non-parametric statistics inclusive their sensitivity and specificity associated with the development of ARDS using receiver operating characteristic (ROC) curve analysis. Statistical significance: p < 0.05. Results: Of 24 patients at risk, six developed mild ARDS and four of each moderate or severe ARDS, respectively, 3 ± 2 (Mean ± SD) days after inclusion. Median plasma concentrations of TF and PAI-1 were significantly higher at T7 in patients with ARDS, as compared to non-ARDS. Simultaneously, we found moderate correlations between plasma concentrations of TF and PAI-1, TF and PaO2/FiO2 and PEEP and TF. TF plasma concentration was associated with ARDS with 71% sensitivity and 100% specificity, a cut off level of 145 pg/ml and AUC 0.78, p = 0.02. PAI-1 displayed 64% sensitivity and 100% specificity with a cut off concentration of 117.5 pg/ml and AUC 0.77, p = 0.02. t-PA did not change significantly during the observation time. Conclusions: This pilot study showed that increased plasma concentrations of TF and PAI-1 might support ARDS diagnoses in mechanically ventilated patients after seven days in ICU.

Enhanced bleeding remains a serious problem after cardiac surgery, and fibrinolysis is often involved. We speculate that lower plasma concentrations of plasminogen activator inhibitor – 1 (PAI-1) preoperatively and tissue plasminogen activator/PAI-1 (t-PA/PAI-1) complex postoperatively might predispose for enhanced fibrinolysis and increased postoperative bleeding.

Background and Objective: Thrombosis due to inherited hypercoagulability is an issue that has been raised in microvascular flap surgery previously. We analyzed the association of a single nucleotide polymorphism (SNP) in rs2066865 in the fibrinogen gamma chain (FGG) gene, alteration in plasma fibrinogen concentration, and presence of microvascular flap thrombosis. Materials and Methods: A total of 104 adult patients with microvascular flap surgery were subjected to an analysis of the presence of SNP rs2066865 in the FGG gene. Alterations in plasma fibrinogen concentration according to genotype were determined as a primary outcome, and flap thrombosis was defined as a secondary outcome. Results: Flap thrombosis was detected in 11.5% of patients (n = 12). Successful revision of anastomosis was performed in four patients, resulting in a microvascular flap survival rate of 92.3%. We observed an increase in plasma fibrinogen concentration in genotype G/A and A/A carriers (G/G, 3.9 (IQR 4.76-3.04); G/A, 4.28 (IQR 5.38-3.18); A/A, 6.87 (IQR 8.25-5.49) (A/A vs. G/A, p = 0.003 and A/A vs. G/G, p = 0.001). Within group differences in microvascular flap thrombosis incidence rates were observed—G/G 6/79 (7.59%); G/A 5/22 (22.7%); A/A 1/3 (33.3%) (OR 0.30 95%; CI 0.044 to 0.57), p = 0.016; RR 3.2—when G/G versus G/A and A/A were analyzed respectively. Conclusions: A/A and G/A genotype carriers of a single nucleotide polymorphism in rs2066865 in the fibrinogen gamma chain gene had a higher plasma fibrinogen concentration, and this might be associated with an increased microvascular flap thrombosis incidence rate. Determined polymorphism could be considered as a genetic marker associated with microvascular flap thrombosis development. To confirm the results of this study, the data should be replicated in a greater sample size.

Microvascular free flap surgery, has become an important part of reconstructive surgery during the last decades, as it allows closure of various tissue defects and recovery of organs function. Despite surgical progress resulting in high rates of transferred tissue survival, the risk of pedicle vessels thrombosis still remains a significant problem. A total of 108 articles from Pubmed and Science Direct databases published in 2005–2015 were analysed. This review of the literature assessed the influence of patient-dependent risk factors and different perioperative management strategies on development of microvascular free flap thrombosis. Sufficient evidence for risk associated with hypercoagulation, advanced age and certain comorbidities was identified. Presently, rotational thromboelastometry allows early hypercoagulability detection, significantly changing further patient management. Identification of flap thrombosis promoting surgery-related aspects is also essential in preoperative settings. Choice of anaesthesia and postoperative analgesia, administration of different types and amounts of fluids, blood products and vasoactive agents, temperature control are no less important in perioperative anaesthesiological management. More attention should be focused on timely preoperative evaluation of patient-dependent risk factors, which can influence anaesthesiological and surgical tactics during and after microvascular free flap surgery. Perioperative anaesthesiological management strategy continues to be controversial and therefore it should be performed based on thrombotic risk assessment and patient individual needs, thus improving flap survival rates and surgical outcome.

Carriers of plasminogen activator inhibitor -1 (PAI-1) -675 genotype 5G/5G may be associated with lower preoperative PAI-1 plasma levels and higher blood loss after heart surgery using cardiopulmonary bypass (CPB). We speculate if polymorphisms of PAI-1 -844 A/G and angiotensin converting enzyme (ACE) intron 16 I/D also might promote fibrinolysis and increase postoperative bleeding. We assessed PAI-1 -844 A/G, and ACE intron 16 I/D polymorphisms by polymerase chain reaction technique and direct sequencing of genomic DNA from 83 open heart surgery patients that we have presented earlier. As primary outcome, accumulated chest tube drainage (CTD) at 4 and 24 h were analyzed for association with genetic polymorphisms. As secondary outcome, differences in plasma levels of PAI-1, t-PA/PAI-1 complex and D-dimer were determined for each polymorphism. SPSS® was used for statistical evaluation. The lowest preoperative PAI-1 plasma levels were associated with PAI-1 -844 genotype G/G, and higher CTD, as compared with genotype A/A at 4 and 24 h after surgery. Correspondingly, 4 h after the surgery CTD was higher in carriers of ACE intron 16 genotype I/I, as compared with genotype D/D. PAI-1 plasma levels and t-PA/PAI-1 complex reached nadir in carriers of ACE intron 16 genotype I/I, in whom we also noticed the highest D-dimer levels immediately after surgery. Notably, carriers of PAI-1 -844 genotype G/G displayed higher D-dimer levels at 24 h after surgery as compared with those of genotype A/G. Increased postoperative blood loss secondary to enhanced fibrinolysis was associated with carriers of PAI-1 -844 G/G and ACE Intron 16 I/I, suggesting that these genotypes might predict increased postoperative blood loss after cardiac surgery using CPB.

Dexmedetomidine prolongs the duration of regional block while its systemic sedative effect when administered perineurally is unknown. We aimed to evaluate the systemic sedative effect of perineural dexmedetomidine in patients after axillary brachial plexus block (ABPB). This single-blinded prospective randomized control trial included 80 patients undergoing wrist surgery receiving ABPB. Patients were randomized into two groups – Control group (CG, N = 40) and dexmedetomidine group (DG, N = 40). Both groups received ABPB with 20 ml of 0.5% Bupivacaine and 10 ml of 2% Lidocaine. Additionally, patients in DG received 100 mcg of dexmedetomidine perineurally. Depth of sedation was evaluated using Narcontrend Index (NI) and Ramsay Sedation Scale (RSS) immediately after ABPB and in several time points up to 120 min. Duration of block as well as patient satisfaction with sedation was evaluated using a postoperative survey. Our results showed that NI and RSS statistically differed between groups, presenting a deeper level of sedation during the first 90 min in DG compared to controls, P < 0.001. In the first 10 to 60 min after ABPB the median RSS was 4 (IQR within median) and median NI was 60 (IQR 44–80) in DG group, in contrast to CG patients where median RSS was 2 (IQR within median) and median NI was 97 (IQR 96–98) throughout surgery. The level of sedation became equal in both groups 90 and 120 min after ABPB when the median NI value was 98 (97–99) in DG and 97.5 (97–98) in CG, P = 0.276, and the median RSS was 2 (IQR within median) in both groups, P = 0.128. No significant intergroup differences in hemodynamic or respiratory parameters were found. Patients in DG expressed satisfaction with sedation and 86.5% noted that the sensation was similar to ordinary sleep. In DG mean duration of motor block was 13.5 ± 2.1 h and sensory block was 12.7 ± 2.8 h which was significantly longer compared to CG 6.3 ± 1.5 h, P < 0.001 and 6.4 ± 1.8 h, P < 0.001. We found that beside prolongation of analgesia, perineural administration of dexmedetomidine might provide rather safe and comfortable sedation with no significant effect on hemodynamic or respiratory stability and yields a high level of patient satisfaction.