Free thoracodorsal,perforator-scapular flap based on the angular artery (TDAP-Scap-aa): Clinical experiences and description of a novel technique for single flap reconstruction of extensive oromandibular defects

PurposeThe reconstruction of oromandibular defects can be challenging, particularly when considerable amounts of bone and soft tissues are lost. In such cases, the use of a single flap may be unsatisfactory and a concomitant free flap is needed. Here we present a chimeric, thoracodorsal perforator-scapular free flap based on the angular artery of the subscapular system (TDAP-Scap-aa) as an alternative technique for single flap reconstruction of extensive oromandibular defects.Materials and methodsThe authors studied patients who underwent reconstructions of extensive oromandibular defects with a TDAP-Scap-aa free flap. The operative technique and the clinical experiences are described. Postoperatively, surgical complications were classified with the Clavien-Dindo Classification.ResultsFive male patients (59.4 ± 8.8 years) were treated with the TDAP-Scap-aa. Average sizes for harvested hard and soft tissue components, which are both included in the flap and completely independently from each other, were 10.4 ± 1.5 cm of bone length, 2.6 ± 0.3 cm of bone height, 11.6 ± 4.8 cm of skin paddle length and 8.4 ± 1.7 cm of skin paddle width. The overall mean operation time (cut-suture) was 14.6 ± 0.9 h. The postoperative follow-up was 6 months. No complications requiring surgical treatment as well as donor site nerve damages were observed.ConclusionsIn comparison to other double free flaps, the TDAP-Scap-aa offers several advantages such as higher amounts of hard and soft tissues without prolonged operation times, and provides satisfying aesthetic outcomes and little donor site morbidity due to the preservation of muscle and nerve structures. Therefore, the TDAP-Scap-aa constitutes a clinically reliable alternative in extensive oromandibular defect reconstruction.     

Long-term amelioration of rat adjuvant arthritis following systemic elimination of macrophages by clodronate-containing liposomes

Objective. To determine whether systemic elimination of macrophages by means of clodronate-containing liposomes counteracts inflammation and joint destruction in rats with established adjuvant arthritis (AA). Methods. Rats with AA received a total of 2.7 mg of clodronate encapsulated in liposomes in 3 intravenous doses on days 10, 11, and 12 of arthritis. Phosphate buffered saline (PBS), PBS-laden liposomes, or free clodronate were used as negative controls. Clinical, hematologic, and histopathologic signs of AA were monitored, and depletion of macrophages by clodronate-liposomes was evaluated both in the synovial membrane (SM) and in organs of the mononuclear phagocyte system (MPS). Results. Clodronate-laden liposomes led to significant, long-term amelioration of the clinical signs of AA, a reduction in the erythrocyte sedimentation rate (ESR), and counteraction of joint destruction, not only immediately after treatment, but also for 2 weeks thereafter. Free clodronate induced moderate clinical improvement and a significant decrease in the ESR, but only during the late phase of AA. Drug-free vesicles even aggravated the joint destruction. Clodronate-laden liposomes did not induce significant depletion of resident macrophages in the SM, but rather, in the paracortical region of popliteal lymph nodes, in the liver, and in the marginal zone and periarteriolar lymphatic sheaths of the spleen. Conclusion. Clodronate-laden liposomes induce long-term amelioration of AA, even if administered for a brief period during the florid phase of the disease. The amelioration is paralleled by the elimination of macrophages in immunocompetent areas of the spleen and draining lymph nodes, but not locally in the SM. This suggests an influence of the treatment on the immunoregulatory rather than effector, functions of macrophages.     

Risk Factors for Dysphagia and the Impact on Outcome After Spontaneous Subarachnoid Hemorrhage

Neurocritical Care - Despite the tremendous impact of swallowing disorders on outcome following ischemic stroke, little is known about the incidence of dysphagia after subarachnoid hemorrhage (SAH)...     

Oxidative modification of tropomyosin and myocardial dysfunction following coronary microembolization.

AIMS: We addressed a potential mechanism of myocardial dysfunction following coronary microembolization at the level of myofibrillar proteins. METHODS AND RESULTS: Anaesthetized pigs underwent intracoronary infusion of microspheres. After 6 h, the microembolized areas (MEA) had decreased systolic wall thickening to 38 +/- 7% of baseline and a 2.62 +/- 0.40-fold increase in the formation of disulphide cross-bridges (DCB) in tropomyosin relative to that in remote areas. The impairment in contractile function correlated inversely with DCB formation (r = -0.68; P = 0.015) and was associated with increased TNF-alpha content. DCB formation was reflected by increased tropomyosin immunoreactivity and abolished in vitro by dithiothreitol. Ascorbic acid prevented contractile dysfunction as well as increased DCB and TNF-alpha. In anaesthetized dogs, 8 h after intracoronary microspheres infusion, contractile function was reduced to 8+/-10% of baseline and DCB in MEA was 1.48+/-0.12 higher than that in remote areas. In conscious dogs, 6 days after intracoronary microspheres infusion, myocardial function had returned to baseline and DCB was no longer different between remote and MEA. Again contractile function correlated inversely with DCB formation (r = -0.83; P = 0.005). CONCLUSION: Myofibrillar protein oxidation may represent a mechanistic link between inflammation and contractile dysfunction following coronary microembolization.     

A novel bioartificial liver with culture of porcine hepatocyte aggregates under simulated microgravity

An extracorporeal bioartificial liver device could provide vital support to patients suffering from acute liver failure. We designed a novel, customized bioreactor for use as a bioartificial liver (patent pending). The Innsbruck Bioartificial Liver (IBAL) contains aggregates of porcine hepatocytes grown under simulated microgravity. The culture vessel rotates around its longitudinal axis and is perfused by two independent circuits. The circuit responsible for exchange of plasma components with the patient consists of a dialysis tube winding spirally around the internal wall of the culture vessel. IBAL was evaluated in vitro. Viability tests showed sufficient viability of hepatocytes for up to 10 days. Cytologic examination of samples from the bioreactor showed liver cell aggregates. These were also examined by electron microscopy. A number of biochemical parameters were analyzed. In conclusion, cell culture is possible for at least 10 days in the IBAL system, organoid hepatocyte aggregates are formed and synthetic activity of the hepatocytes was demonstrated.     

Verbesserte Strukturidentifizierung mittels Gewebe-Doppler-Echokardiographie

Tissue Doppler echocardiography (TDE) has been shown to be of particular value in patients with impaired myocardial function. Recently, the technique was successfully employed to localize the ventricular insertion of accessory atrioventricular pathways. The identification of abnormal cardiac structures is coming up now as a new field of clinical interest. The purpose of this study was to differentiate anomalous cardiac and aortic from native structures by physical properties of tissue motion using transesophageal TDE. Characteristic motion patterns of anomalous structures have not been described in detail and tissue Doppler findings have not been associated with clinical features up to now. Forty consecutive patients were included after anomalous cardiac or vascular structures had been detected by conventional transesophageal echocardiography (TEE). A control group consisted of 20 subjects. Rapidity of diagnosis in anomalous structures was divided into 3 categories, and TDE signals were related to particular pathology by a blinded, 2nd observer.Three different motion patterns could be defined: incoherent motion due to free oscillation of an anomalous structure which is independent of the surrounding tissue (Figure 1b); coherent motion with a phase difference meaning that motion depends on the motion of the surrounding tissue but is out of phase (Figure 2); concordant motion showing no difference in direction, velocity, or phase of motion compared with the surrounding tissue. Incoherent motion was present in endocarditic vegetations, 4th degree aortic plaques, Chiari network, valvular prolapse, intracavitary tumors, and freely oscillating thrombi as well as in normal valve leaflets and papillary muscles. Especially if endocarditic vegetations are present its incoherent motion facilitates to recognize these small structures. The colorcode of this motion pattern demarcates the vegetation reliably from the surrounding tissue (Figure 1b). Within 15 seconds vegetations could be detected in 9 (82%) vs 2 (18%) patients employing only conventional imaging. Using conventional echocardiographic approaches detection of vegetations is frequently hindered by their small size and minor echo intensity (Figure 1a). In contrast, size and echo intensity do not affect the tissue Doppler signal. Normal papillary muscles and distal portions of the mitral and tricuspid valves were demonstrated to regularly meet the criterion of incoherent tissue motion in the control group. In part, this was also observed with respect to the aortic and pulmonary valves. In valvular tissue incoherent motion was caused by passive floating, whereas papillary muscles show an active inverse motion for short time intervals. Nevertheless, physiologic incoherent motion did not lead to any false differential diagnosis. The phase difference of coherent motion results from damped oscillation. This phenomenon was visualized by tissue Doppler M-mode in 5 thrombi of the left atrial appendage (LAA) (100%) and in 1 ventricular thrombus (50% of all clots). Concordant motion was shown in 3rd degree aortic plaques and postrheumatic and calcified vegetations. These structures were found to be completely embedded or closely attached, so that their passive motion corresponded to the motion of the surrounding regular tissue. Detection and assessment of anomalous structures are based on their motion patterns which can be synchronous or asynchronous in comparison with the surrounding tissue. Another goal of this investigation was to test if the sensitivity of TEE to spontaneous echo contrast can be improved using TDE. In 21 patients presenting with left atrial dilation (left atrial diameter > 44 mm) due to mitral stenosis (n = 8), mitral regurge (n = 5), arterial hypertension (n = 5) and multiple valvular disease (n = 3) fundamental multiplane TEE and transesophageal TDE were performed with standardized gain setting. The control group consisted of 20 randomized individuals with normal left     

Coronary Microembolization—Its Role in acute coronary syndromes and interventions

The diagnosis coronary artery disease is classically based on patient's symptoms and morphology, as analyzed by angiography. The importance of risk factors for the development of coronary atherosclerosis and disturbance of coronary vasomotion is clearly established. However, microembolization of the coronary circulation has also to be taken into account. Microembolization may occur as a single or as multiple, repetitive events, and it may induce inflammatory responses. Spontaneous microembolization may occur, when the fibrous cap of an atheroma or fibroatheroma (Stary i.v. and Va) ruptures and the lipid pool with or without additional thrombus formation is washed out of the atheroma into the microcirculation. Such events with progressive thrombus formation are known as cyclic flow variations. Plaque rupture occurs more frequently than previously assumed, i.e. in 9% of patients without known heart disease suffering a traffic accident and in 22% of patients with hypertension and diabetes. Also, in patients dying from sudden death microembolization is frequently found. Patients with stable and unstable angina show not only signs of coronary plaque rupture and thrombus formation, but also microemboli and microinfarcts, the only difference between those with stable and unstable angina being the number of events. Appreciation of microembolization may help to better understand the pathogenesis of ischemic cardiomyopathy, diabetic cardiomyopathy and acute coronary syndromes, in particular in patients with normal coronary angiograms, but plaque rupture detected by intravascular ultrasound. Also, the benefit from glycoprotein IIb/IIIa receptor antagonist is better understood, when not only the prevention of thrombus formation in the epicardial atherosclerotic plaque, but also that of microemboli is taken into account. Microembolization also occurs during PTCA, inducing elevations of troponin T and I and elevations of the ST segment in the EKG. Elevated baseline coronary blood flow velocity, as a potential consequence of reactive hyperemia in myocardium surrounding areas of microembolization, is more frequent in patients with high frequency rotablation than in patients with stenting and in patients with PTCA. The hypothesis of iafrogenic microembolization during coronary interventions is now supported by the use of aspiration and filtration devices, where particles with a size of up to 700 microns have been retrieved. In the experiment, microembolization is characterized by perfusion-contraction mismatch, as the proportionate reduction of flow and function seen with an epicardial stenosis is lost and replaced by contractile dysfunction in the absence of reduced flow. The analysis of the coronary microcirculation, in addition to that of the morphology and function of epicardial coronary arteries, and in particular appreciation of the concept of microembolization will further improve the understanding of the pathophysiology and clinical symptoms of coronary artery disease.