"Muscular compartment syndrome and in vivo optical spectroscopy monitoring: a new model"

events in patients with acute coronary and III (23 ± 9.52 ms vs. 45.33 ± 15.97 ms vs. 58.66 ± 23.25 ms respectively, P <0.05 for QTd and 26 ± 11.63 ms vs. 52.66 ± 21.2 ms vs. 60.66 ± 23.25 ms respectively, P <0.05 for QTcd). QT and QTcd on admission were higher in patients who developed ventricular arrhythmias than patients who did not (90 ± 11.55 ms vs. 70 ± 24.54 ms; P = 0.05 regarding QTd and 110 ± 8.61 ms vs. 80.53 ± 28.78 ms with P = 0.028 regarding QTcd). Patients with early peaking of enzymes had more reduction in QTd and QTcd early after reperfusion (43.2 ± 11.44 vs. 60.5 ± 13.16, P <0.001 regarding QTd and 49.60 ± 15.93 vs. 68.5 ± 17.55, P <0.001 regarding QTcd). Conclusions QTd is higher in patients with acute MI (AMI) who developed ventricular arrhythmias. So QTd and QTcd on admission may be a helpful parameter that can detect patients with AMI who are at risk for development of ventricular arrhythmias. Reperfusion therapy with primary PCI or thrombolytic agents reduces QTd and QTcd in patients with AMI, however; QTd and QTcd are shorter with primary PCI compared with thrombolytic therapy. Measurement of specifi c enzymes has become an important clinical tool for the diagnosis and management of MI. The aim of this study was to demonstrate the role of arginase and adenosine deaminase (ADA) in patients suff ering from MI, and in a group of patients with chronic renal failure (CRF) with cardiovascular diseases (CVD). Methods In this prospective study including 90 consecutive subjects were included the MI group (GI) consisting of 30 patients with mean age = 51.7 admitted to critical care medicine (CCM) in Cairo University Conclusions According to our data, there is no diff erence in TEG parameters between severe sepsis and postoperative patients apart from the α-angle, which seems to be lower in the fi rst group. The α-angle is supposed to be high in the procoagulant state; our result could be thought of as linked to the late phase characterizing our severe sepsis group wherein factor consumption coagulopathy could occur. we investigated the eff ect of anemia on platelet function and plasmatic hemostasis with two diff erent point-of-care methods: the multiple elec trode aggregometry Multiplate® (MEA) and the rotational thrombelastometry ROTEM®. Blood was taken from 13 healthy volunteers to arrange in vitro anemia-series with 10, 7 and 3 g/dl hemoglobin. For the MEA we applied the agonists collagen, arachidonic acid, adenosine diphosphate (ADP), thrombin-receptor- activating peptide (TRAP) and ristocetin. For the ROTEM® analysis we used the tests EXTEM, INTEM and FIBTEM. Results The MEA showed signifi cantly increased velocity of platelet aggregation in anemic blood samples. The agonists TRAP and ADP demonstrated the highest eff ects. The Aggregation Units and the area under the curve were not infl uenced by anemia. The ROTEM® analysis displayed signifi cantly an amplifi ed maximum clot fi rmness (MCF), a shortened clot formation time (CFT) und an increased α-angle. The CFT and lysis index at 30 minutes did not show any changes through lowering hemoglobin. The calculated eff ect of platelets on ROTEM® coagulation (MCF platelet = MCF EXTEM – MCF FIBTEM ) was unchanged. Conclusions In our study platelet function in anemic blood was observed with the MEA for the fi rst time. Our results showed accelerated platelet aggregation through lowering hemoglobin. Our fi ndings of a hypercoagulable profi le in ROTEM® are in accordance with earlier observations. Future clinical studies are needed to evaluate risk of bleeding or hypercoagulability in anemic patients. In this in vitro study we evaluated the eff ects of pH levels (7.6, 7.4, 7.2, 7.0 and 6.8) on platelet aggregation and coagulation with human whole blood of healthy male volunteers. We used multiple electrode aggregometry (MEA) Multiplate® (tests: ADP, ASPI, TRAP) for platelet function testing. The global coagulation was evaluated at pH 6.8 and 7.4 with ROTEM®, which is a rotational thrombelastometry (tests: NATEM and APTEM). The pH levels of the blood samples were achieved by titration of HCl and NaOH. Results In MEA the AUC was signifi cantly reduced for pH 7.0 and pH 6.8 in all three tests (ADP, ASPI and TRAP), as well as aggregation and velocity. Platelet function was not infl uenced by alkalosis (pH 7.6). In ROTEM® the AUC, CT, CFT and MCF showed no signifi cant alterations. The α-angle and lysis index for 60 minutes were signifi cantly reduced at pH 6.8. NATEM values were signifi cantly diff erent from those measured with APTEM. Conclusions In our study we evaluated a signifi cant decrease of platelet function at pH 7.0 and 6.8 with MEA. The results of the analysis with the ROTEM® system showed a signifi cant reduction of thrombus formation at pH 6.8, as described in the literature. In the APTEM test, we could identify hyperfi brinolysis. by sepsis and in the second group complications in the form of sepsis not The groups of patients were balanced in age and severity of the disease. Sepsis was diagnosed on the basis of clinical, laboratory and bacteriological fi ndings, as well as confi rmed by morphological studies in casualties. The control group consisted of 130 apparently healthy people. Comparative analysis of hemostasis system disorders in severe burn patients with early sepsis and those without similar complication showed that the progress of generalized infection in the acute period of burn disease is accompanied by reliable decreased activity of antithrombin III, XIIa-dependent fi brinolysis, blood plate count, and prothrombin time prolongation. There were no diff erences revealed between the studied groups of severe burn when determining fi brinogen content, soluble fi brin monomeric complexes, activated partial thromboplastin time, thrombin clotting time and echitox time, and the test revealing fragmented erythrocytes. Correlation analysis showed that the most contingency between progress of sepsis and hemostasis system data was noted on the third to fourth days after burn (with decreased activity of XIIa-dependent fi brinolysis ( r = 0.58, P <0.0001), antithrombin III ( r = –0.57, P <0.0001), prothrombin time ( r = 0.49, P <0.0001) and thrombocytopenia ( r = –0.48, P <0.0001)). On the basis of a retrospective analysis of case histories of severe burns with verifi ed generalized infection, it was determined that the development of an acute form of DIC syndrome manifesting in a marked imbalance of coagulation and anticoagulative blood mechanisms as well as severe hepatorenal failure has a lead time of 1 to 8 days in revealing sepsis in the clinic. Conclusions Sepsis aff ects the venous component of microcirculation by decreasing venular compliance and volume of the venular bed. This might be caused by a real decrease of venular bed volume, due to microthrombosis, or by an increase of venular tone. However, the clinical relevance of our fi ndings is not known, and further studies are needed.

Introduction Acute ischemia alters action potentials and a ects myocardial repolarization. Dispersion of repolarization is arrhythmogenic.
QT dispersion has been suggested to give information about the heterogeneity of myocardial repolarization. Methods Our study included 60 patients presented with acute STEMI, the study populations were divided into two groups: Group I: 30 patients who underwent primary PCI. Group II: 15 patients who received streptokinase. Group III: 15 patients who did not receive reperfusion therapy. QTd and QTcd were measured and compared in the three groups on admission, after 24 hours and after 5 days. Results QTd and QTcd were signi cantly higher in patients with anterior compared with inferior MI (79.16 ± 25.67 ms vs. 62 ± 18.17 ms, P = 0.004 regarding QTd and 91.95 ± 28.76 ms vs. 68.33 ± 23.52 ms, P <0.001 regarding QTcd). After 24 hours, QTd and QTcd were signi cantly lower in group I than groups II and III (34.33 ± 13.56 ms vs. 48 ± 18.2 ms vs. 66 ± 24.43 ms respectively, P <0.05 as regards QTd and 39.33 ± 11.72 ms vs. 56 ± 23.84 ms vs. 74.60 ± 26.7 ms respectively, P <0.05 as regards QTcd). On the 5th day reduction in QTd and QTcd was statistically signi cantly lower in group I than groups II and III (23 ± 9.52 ms vs. 45.33 ± 15.97 ms vs. 58.66 ± 23.25 ms respectively, P <0.05 for QTd and 26 ± 11.63 ms vs. 52.66 ± 21.2 ms vs. 60.66 ± 23.25 ms respectively, P <0.05 for QTcd). QT and QTcd on admission were higher in patients who developed ventricular arrhythmias than patients who did not (90 ± 11.55 ms vs. 70 ± 24.54 ms; P = 0.05 regarding QTd and 110 ± 8.61 ms vs. 80.53 ± 28.78 ms with P = 0.028 regarding QTcd). Patients with early peaking of enzymes had more reduction in QTd and QTcd early after reperfusion (43.2 ± 11.44 vs. 60.5 ± 13.16, P <0.001 regarding QTd and 49.60 ± 15.93 vs. 68.5 ± 17.55, P <0.001 regarding QTcd). Conclusions QTd is higher in patients with acute MI (AMI) who developed ventricular arrhythmias. So QTd and QTcd on admission may be a helpful parameter that can detect patients with AMI who are at risk for development of ventricular arrhythmias. Reperfusion therapy with primary PCI or thrombolytic agents reduces QTd and QTcd in patients with AMI, however; QTd and QTcd are shorter with primary PCI compared with thrombolytic therapy. The main causal and treatable risk factors for MI include hypertension, hypercholesterolemia or dyslipidemia, diabetes mellitus, and smoking. Acute MI results in cellular necrosis with release of constituent proteins into the circulation. Measurement of speci c enzymes has become an important clinical tool for the diagnosis and management of MI. The aim of this study was to demonstrate the role of arginase and adenosine deaminase (ADA) in patients su ering from MI, and in a group of patients with chronic renal failure (CRF) with cardiovascular diseases (CVD). Methods In this prospective study including 90 consecutive subjects were included the MI group (GI) consisting of 30 patients with mean age = 51.7 admitted to critical care medicine (CCM) in Cairo University Introduction It is known that red blood cells are involved in hemo stasis. They can support and improve coagulation in di erent ways. Therefore recommendations are given for red blood cell transfusions in anemic patients with massive bleeding to reach a hemoglobin concentration of 8 to 10 g/dl. Although blood transfusions can be life-saving, a number of negative or even potentially life-threatening e ects are described. Methods In this study we investigated the e ect of anemia on platelet function and plasmatic hemostasis with two di erent point-of-care methods: the multiple electrode aggregometry Multiplate® (MEA) and the rotational thrombelastometry ROTEM®. Blood was taken from 13 healthy volunteers to arrange in vitro anemia-series with 10, 7 and 3 g/dl hemoglobin. For the MEA we applied the agonists collagen, arachidonic acid, adenosine diphosphate (ADP), thrombin-receptoractivating peptide (TRAP) and ristocetin. For the ROTEM® analysis we used the tests EXTEM, INTEM and FIBTEM.

Results
The MEA showed signi cantly increased velocity of platelet aggregation in anemic blood samples. The agonists TRAP and ADP demonstrated the highest e ects. The Aggregation Units and the area under the curve were not in uenced by anemia. The ROTEM® analysis displayed signi cantly an ampli ed maximum clot rmness (MCF), a shortened clot formation time (CFT) und an increased α-angle. The CFT and lysis index at 30 minutes did not show any changes through lowering hemoglobin. The calculated e ect of platelets on ROTEM® coagulation (MCF platelet = MCF EXTEM -MCF FIBTEM ) was unchanged. Conclusions In our study platelet function in anemic blood was observed with the MEA for the rst time. Our results showed accelerated platelet aggregation through lowering hemoglobin. Our ndings of a hypercoagulable pro le in ROTEM® are in accordance with earlier observations. Future clinical studies are needed to evaluate risk of bleeding or hypercoagulability in anemic patients.

Introduction
The combination of acidosis, hypothermia and coagulopathy is associated with high mortality in polytrauma [1]. Acidosis impairs coagulation [2]. Whether acidosis leads to a reduced platelet function has not so far been evaluated. Methods In this in vitro study we evaluated the e ects of pH levels (7.6, 7.4, 7.2, 7.0 and 6.8) on platelet aggregation and coagulation with human whole blood of healthy male volunteers. We used multiple electrode aggregometry (MEA) Multiplate® (tests: ADP, ASPI, TRAP) for platelet function testing. The global coagulation was evaluated at pH 6.8 and 7.4 with ROTEM®, which is a rotational thrombelastometry (tests: NATEM and APTEM). The pH levels of the blood samples were achieved by titration of HCl and NaOH. Results In MEA the AUC was signi cantly reduced for pH 7.0 and pH 6.8 in all three tests (ADP, ASPI and TRAP), as well as aggregation and velocity. Platelet function was not in uenced by alkalosis (pH 7.6). In ROTEM® the AUC, CT, CFT and MCF showed no signi cant alterations. The α-angle and lysis index for 60 minutes were signi cantly reduced at pH 6.8. NATEM values were signi cantly di erent from those measured with APTEM. Conclusions In our study we evaluated a signi cant decrease of platelet function at pH 7.0 and 6.8 with MEA. The results of the analysis with the ROTEM® system showed a signi cant reduction of thrombus formation at pH 6.8, as described in the literature. In the APTEM test, we could identify hyper brinolysis.
Introduction Among infectious complications in patients with serious heat injury, the most dangerous is sepsis developing in the early stages of burn disease. Sepsis is characterized by a fulminant, severe course, complex diagnostics, and a high case fatality rate. Hemostasis system disorders are one of the key pathogenic links of organ failure development in sepsis. Methods The hemostasis system condition was studied in 100 patients with over 20% of the body burned, from the rst to 12th day after burn. Examined patients were divided into two groups: in the rst group an acute period of burn disease was complicated by progress of sepsis (33 patients), and in the second group complications in the form of sepsis were not observed. The groups of patients studied were balanced in age and severity of the disease. Sepsis was diagnosed on the basis of clinical, laboratory and bacteriological ndings, as well as con rmed by morphological studies in casualties. The control group consisted of 130 apparently healthy people. Results Comparative analysis of hemostasis system disorders in severe burn patients with early sepsis and those without similar complication showed that the progress of generalized infection in the acute period of burn disease is accompanied by reliable decreased activity of antithrombin III, XIIa-dependent brinolysis, blood plate count, and prothrombin time prolongation. There were no di erences revealed between the studied groups of severe burn when determining brinogen content, soluble brin monomeric complexes, activated partial thromboplastin time, thrombin clotting time and echitox time, and the test revealing fragmented erythrocytes. Correlation analysis showed that the most contingency between progress of sepsis and hemostasis system data was noted on the third to fourth days after burn (with decreased activity of XIIa-dependent brinolysis (r = 0.58, P <0.0001), antithrombin III (r = -0.57, P <0.0001), prothrombin time (r = 0.49, P <0.0001) and thrombocytopenia (r = -0.48, P <0.0001)). On the basis of a retrospective analysis of case histories of severe burns with veri ed generalized infection, it was determined that the development of an acute form of DIC syndrome manifesting in a marked imbalance of coagulation and anticoagulative blood mechanisms as well as severe hepatorenal failure has a lead time of 1 to 8 days in revealing sepsis in the clinic. Conclusions Hemostasis system disorders corresponding to an acute form of DIC syndrome not only accompany the progress of sepsis in severe burn but can be an indirect predictor of its development. This is a rare but serious postoperative complication. In vivo optical spectroscopy (INVOS) monitors tissular oxygenation continuously and non-invasively. Our objective was to develop a model mimicking the physiopathology of MCS and to assess the interest of the INVOS in this case [1][2][3]. Methods After approval of the ethics committee, we in ated a tourniquet in nine healthy volunteers at a pressure equal to the mean arterial pressure (MAP), obtaining a model of slight venous congestion and arterial hypoperfusion. The INVOS monitoring was compared with sensory de cits, pain, motor activity, electromyography and invasive pressure. Results A profound motor nerve conduction block (>30% decrease in action potential amplitude from baseline) was observed in the seven volunteers completing the protocol, immediately reversible after releasing the external pressure. At baseline, the values of MAP, INVOS and intracompartmental pressure (ICP) were respectively 94.3 ± 6.5 mmHg, 73.3 ± 8.9% and 16.9 ± 8.6 mmHg. At the time of appearance of a signi cant block, the values of INVOS were 46.4 ± 10.9%; the absolute decrease of INVOS was 28.7 ± 10.6% and the ICP values were 70.0 ± 5.5 mmHg. The times to reach this signi cant block from baseline and from the time of an absolute INVOS decrease of 10% were respectively 33.0 ± 10.9 minutes and 27.43 ± 10.4 minutes ( Figure 1). Conclusions Our model is appropriate since it mimics perfectly MCS [3]. The time after achieving an absolute decrease of the INVOS value of 10% from baseline is as accurate as the time of intracompartmental hyperpression to predict MCS ( Figure 2). Introduction Sepsis has several e ects on microcirculation, including microthrombosis, interstitial edema and reduced reactivity of arteriolar tone leading to shunt areas [1]. Little is known about the e ects of sepsis on the venous component of microcirculation. Changes of venular compliance and volume of the venular bed may a ect cardiac preload, which has a key role in occurrence of cardiac failure. Near-infrared spectroscopy (NIRS) is a widely used, non-invasive technique that enables one to quantify the tissue oxyhemoglobin and deoxyhemoglobin (Hb) concentration, through which microvascular blood ow, compliance and oxygen consumption can be extrapolated [2]. The aim of our study was to evaluate the e ects of sepsis on venous compliance and volume of the venular bed. Methods Seven ICU patients with sepsis (according to ACCP/SCCM criteria [3]) and seven healthy subjects were studied. NIRS data were collected during several venous compressions at 20 to 30 to 40 mmHg. The venular bed volume increase at 20 mmHg was obtained from the total Hb concentration increase. Venular compliance was calculated as the volume increase and pressure in ated ratio. Results expressed as mean values ± SD for compliance and volume. The Mann-Whiney U test was performed to compare values in patients and controls. Results The mean venular bed volume increase in the sepsis group was 3.32 ± 0.90 ml while in controls it was 7.80 ± 4.24 ml (P <0.05). Venous compliance was signi cantly lower in the sepsis group compared with the control group (0.17 ± 0.06 ml/mmHg*l vs. 0.44 ± 0.10 ml/mmHg*l; P <0.05). Conclusions Sepsis a ects the venous component of microcirculation by decreasing venular compliance and volume of the venular bed. This might be caused by a real decrease of venular bed volume, due to microthrombosis, or by an increase of venular tone. However, the clinical relevance of our ndings is not known, and further studies are needed.
Introduction Seventy-ve percent of ICU mortality after the rst 72 hours following major trauma is due to multiple organ dysfunction syndrome (MODS) [1]. How to follow this evolution is not completely understood yet and new parameters are still needed. The aim of this study was to evaluate the e ects of polytrauma on sublingual microcirculation and to search correlations among it, Sequential Organ Failure Assessment (SOFA) score and biochemical markers and to use these factors for monitoring patients [2]. Methods This prospective study included 12 patients. Sublingual micro circulation has been registered using sidestream dark eld imaging and analysed with AVA software, searching for indices of