Backspatter from experimental close-range shots to the head

Backspatter is the ejection of biological material from a gunshot entrance wound against the line of fire. This phenomenon was investigated experimentally in transverse gunshots to the heads of calves (n = 9) using two types of 9 mm Parabellum ammunition from shooting distances of 0–10 cm. The resulting bloodstains were documented on white paper placed horizontally 60 cm below the impact site. In this report the analysis was restricted to stains with a diameter > 0.5 mm. Backspatter was documented after every gunshot. The number of stains varied from 31–324 per gunshot and appeared to be independent of the shooting distance. The maximum distance droplets travelled varied from 72–119 cm. The majority of droplets accumulated between 0 and 50 cm. The number of droplets and the distances travelled should be higher in man for anatomical reasons. The direction a single droplet can take comprises every possible angle between the most tangential ones to the skin surface. This resulted in a semi-circle of 180° covered with stains. Skin ruptures of the entrance wound were not observed. The succession of events was documented on high speed film and started with the recoil of the firearm, immediately followed by a blow-out effect of the skin. Large droplets exited approximately 0.7–4 ms after the bullet impacted the skin. The calculated minimum initial velocity of these droplets was 13–61 m/s. Backspatter from gunshots to the head likely is caused by the hot gases expanding subcutaneously and by cavitation-related intracranial overpressure and tail splashing. In three out of nine gunshots, secondary backspatter additionally occurred as a result of droplets produced by a stream of blood from the entrance wound impacting the paper surface.     

Der vorzeitige Blasensprung am Termin — wann ist der günstigste Zeitpunkt zur Geburtseinleitung?

Zusammenfassung unsere Studie soll verdeutlichen, da? bei vorteitigem Blasensprung am Termin ein 12-stündiges Abwarten vor Geburtseinleitung mit Prostaglandin durchaus gerechtfertigt ist. Mit dem expektativen Verhalten kommen wir auf der einen Seite der Erwartung des Paares auf eine natürliche Geburt ohne Risikoerh?hung entgegen, auf der anderen Seite ist es aufgrund des reduzierten Medikamenteneinsatzes und der erniedrigten Sectiofequenz ein Beitrag zur Kostensenkung im Krankenhaus.     

Giant fusiform aneurysm of the vertebro-basilar artery presenting with stroke

The authors describe a case of giant fusiform aneurysm of the basilar artery presenting with ischemic symptoms. Angiography and CT revealed vertebro-basilar fusiform aneurysmal dilatation. Fusiform vertebro-basilar ancurysm is associated with various complications particularly brain stem infarction. Similar lesions in the literature are reviewed and the relationship between this clinical entity and cerebral ischemia, particularly brainstem infarction are discussed.     

Laparoscopic findings in serosal eosinophilic gastroenteritis. Report of two cases

This report describes the laparoscopic features of two patients with serosal eosinophilic gastroenteritis. In one case only hyperemia of the peritoneal serosa was found. In the other the laparoscopic picture resembled peritoneal carcinomatosis. We show that laparoscopy and peritoneal biopsy may permit diagnosis of the disease without the need for laparotomy.     

Ventricular late potentials in acute myocardial infarct

Ventricular late potentials are regarded as an expression of delayed impulse conduction in an area of myocardial ischemia and, accordingly, indicative of a preformed reentry circuit. Late potentials can be detected in chronic, stable coronary artery disease and their presence correlates closely with impairment of ventricular function and with the probability of future occurrence of tachyarrhythmic events or sudden cardiac death. While repetitive ventricular arrhythmias in the chronic stage of coronary artery disease result almost invariably from circling intraventricular wavefronts, tachyarrhythmias associated with acute myocardial infarction appear attributable to differing pathomechanisms. According to experimental studies, in acute myocardial infarction, three phases of arrhythmogenesis can be differentiated: phase 1 encompasses the first hours after vessel occlusion which generally corresponds with the prehospital phase. Due to the difference in potential of up to 25 mV between ischemic and nonischemic cardiac muscle areas, an injury current is called into existence which leads to depolarization of normal cardiac muscle tissue. The ectopic impulses so precipitated, the conduction of which is supported by the functional inhomogeneity of the infarcted region, are capable of initiating reentry tachycardia. During phase 2, a few hours to days after the ischemic event, only the subendocardial Purkinje fibers in the infarcted region exhibit focal arrhythmogenicity. In contrast to the working myocardial cells, the latter survive due to their immediate proximity to the cardiac chamber and show, ischemia-induced, a propensity to high-frequency impulse formation in terms of abnormal automaticity. Similar to the experimental findings, the cause of the frequently-observed ventricular arrhythmias in the early hospital phase appears predominantly attributable to a focal arrhythmia mechanism. During phase 3, several days to weeks after the acute myocardial ischemic event, reentry mechanisms again are in the foreground in which the electrophysiologic changes in the Purkinje fibers, in terms of increasing desynchronization, together with conduction barriers arising through the infarct scar, pave the way for reentry phenomenon. After abrupt restoration of patency of a previously occluded vessel the very frequent "reperfusion arrhythmias" are also attributable primarily to reentry mechanisms due to inhomogeneous improvement of the conduction properties in the region of the reperfused myocardium. Ventricular late potentials can be registered both invasively by means of epi- or endocardial leads as well as noninvasively from the body surface.(ABSTRACT TRUNCATED AT 400 WORDS)     

The influence of molsidomine on myocardial ischemia and ventricular dynamics an in-vivo study in anesthetized dogs by means of computer tomography

Summary In six anesthetized dogs with myocardium partially damaged by ischemia (LAD occlusion), the effect of an i.v. bolus injection of 0.05 mg molsidomine/kg body weight followed by a 6-h i.v. infusion of 0.5 g molsidomine/kg/min on the volume of myocardial ischemia, the relative remaining blood flow in the ischemic area, and the dynamics of the left ventricle were examined by means of computer tomography.The extent of the ischemic volume in the group treated with molsidomine was by far lower than in the control group; this difference was significant if one takes into account the individual heart size. The relative remaining blood flow in the ischemic region was not influenced by molsidomine. The reduction of preload and afterload resulted in corresponding changes in left ventricular areas, segments of these areas, the long axis, thickness of myocardium, ejection fraction and stroke volume. Aortic pressure was lowered insignificantly, heart rate remained nearly unchanged. Plasma analyses of molsidomine, SIN 1 and SIN 1C show that the applied dosage was sufficient to reach a constant concentration over the whole period of observation in the dog.Corvaton^®, Cassella-Riedel Pharma GmbH, Frankfurt/M.     

Acetylsalicylic acid pseudoallergy: an anomaly of thrombocyte function?

After a short historical review, the clinical symptomatology of the pseudoallergic reactions (PAR) after intake of acetylsalicylic acid (ASS) is examined. An intolerance to ASS mostly becomes manifest as bronchial asthma--sometimes up to a status asthmaticus: it is frequently combined with vasomotoric rhinopathia and nasal polyps (so-called "aspirin triad") or as urticaria and angio-edema, seldom as a shock reaction. These symptoms can - in contrast to an allergy--appear at the first intake of the drug. Changes in the arachidonic acid metabolism are of pathogenetic importance, as all substances that inhibit the cyclooxygenase pathway [e.g., most of the nonsteroidal anti-inflammatory drugs (NSAIDs)] are not tolerated by ASS-sensitive patients. Generally, a typical clinical history is sufficient for the diagnosis. Due to the fact that the ASS and NSAID pseudoallergy so far cannot be proved by in vitro methods, oral or inhalative provocation tests are needed when the tolerance situation to the drugs is unknown. However, these tests present high risks. A research group working with Capron (Lille) has recently been able to prove that washed platelets from patients with an analgetic asthma syndrome show an abnormal in vitro response to ASS or NSAID - like indomethacin and fluriprufen - which is characterized by liberation of cytocydal supernatants against parasites, as well as of free O2 radicals, which can be detected by chemiluminescence. Therefore, a platelet anomaly of arachidonic acid metabolism seems to be pathognomonic for ASS asthma. It is not yet known whether or not this is also related to ASS urticaria.(ABSTRACT TRUNCATED AT 250 WORDS)