Ueber Knochenmarkgewebs-Embolie

Lubarsch, O.

doi:10.1007/bf01982042

Cited by 23 publications

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“…In verschiedenen Publikationen fallt eine Gruppe yon Todesfiillen auL welche als gemeinsames Merkmal agonale Kr~impfe aufweisen. Es handelt sich um unterschiedliche Todesursachen wie Tetanus, Eklampsie, Elektroschock und Stromunfall (Lubarsch, 1898;Rappaport et al, 1951;Woodruff und Benninghoff, 1959). -In Abwesenheit anderer Erkl~imngsm6glichkeiten wie extrathorakale Herzmassage ist es in /itiologischer Sicht naheliegend, einen gleichartig wirkenden Pathomechanismus ftir unsere KME-positiven F~ille in den Erstickungskonvulsionen zu suchen.…”

Section: Intraalveoldres Und Septales Lungenodem Mikrohdmorrhagien unclassified

Vitale Reaktionen in der Lungenstrombahn bei Tod durch Strangulation

Brinkmann

1978

Z Rechtsmed

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Vital Reactions of the Pulmonary Circulation in Fatal StrangulationSummary. Morphological examinations in 34 fatal strangulations. Thirty cases were caused by hanging, 2 by strangulation by ligature, 2 by throttling. The age of the victims ranged between 6 and 86. Extensive documentation of pathological findings with special contribution to signs of strangulation and suffocation. Histological examinations of the lungs in each case. In a first series of ten cases 5 to 7 tissue specimens from different lobes were investigated after routine HEstaining. In the second series of 24 cases 10 to 15 tissue samples were subjected to Giemsa-dyeing. Additional special stains were performed on about 30 % of all paraffin blocks in a second step. These included: Pappenheim, HE or Giemsa (depending on the series' routine stainings), PTAH, Mallory, Masson-Goldner, ~-naphthole-esterase, naphtole-AS-D-Cl-esterase and toluidineblue on semi-thinsections. Furthermore 3 to 6 specimens per case were subjected to sudan-staining. The most important results were: Nearly all cases showed intraalveolar edema and hyperemia usually combined with micro-hemorrhages as well as unequal emphysema of the lungs. The contents of the small arteries and arterioles were regularly altered in varying degrees and patterns. All cases showed an increase of intravascular bone marrow cells either scattered diffusely between erythrocytes or arranged to aggregates. Most of the mononuclear cells gave strongly positive N-AS-D-Cl-esterase reactions, showing that they belonged to the myelopoetic system. Additional admixtures of young and adult leucocytes were also encountered in the altered vessels as well as platelet aggregates. Three cases showed pulmonary embolism of small tissue pieces consisting of bone marrow. There were minor degrees of fat embolism in nine cases usually with fat droplets only in a few vessels. With regard to the small number of cases it is tentatively suggested, that the degree of microembolism is diminishing in the elderly age groups. The vascular walls show edema and swelling and vacuolar degeneration of the endothelial cells. The observed changes are considered to have resulted from vital reactions to strangulation. Since skeletal injuries were carefully excluded it is suggested, that bone marrow embolism was due to marrow fractures following the suffocation convulsions. The release of immature and young bone marrow cells could be partly due to intramedullary pressure changes and to hypoxic damages of the endothelial cells of the sinusoids and to direct effects of humoral substances that are increased in shock.

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Section: Intraalveoldres Und Septales Lungenodem Mikrohdmorrhagien unclassified

Vitale Reaktionen in der Lungenstrombahn bei Tod durch Strangulation

Brinkmann

1978

Z Rechtsmed

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“…So war sie yon den Erstbeschreibern (Lubarsch 1898, Lengemann 1901) tierexperimentell nach Injektion yon Organhomogenaten und auch bei an Eklampsie verstorbenen Frauen gesehen worden. So war sie yon den Erstbeschreibern (Lubarsch 1898, Lengemann 1901) tierexperimentell nach Injektion yon Organhomogenaten und auch bei an Eklampsie verstorbenen Frauen gesehen worden.…”

Section: Zur Pathomorphologie Und Pathophysiologieunclassified

Zur Pathophysiologie und Pathomorphologie bei Tod durch Druckstauung

Brinkmann

1978

Z Rechtsmed

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A literature review of traumatic asphyxia is given. The most important presuppositions for the development of traumatic asphyxia are: a) thoracic compression, b) warning of impending disaster just prior to trauma leading to inspiration and closing of the glottis.These mechanisms result in an increase of the intrathoracic pressure with subsequent reflow of blood into the cranio-cervical veins which are not protected by valves. -Independently the prevention of thoracic breathing leads to severe asphyxia. Death occurs only in prolonged thoracic compression and is either due to pulmonary congestion or to asphyxia.Morphological and biochemical examinations were performed systematically with four fatalities of asphyxia and three cases who had died of both, asphyxia and polytraumao The autopsy findings corresponded to the well-known picture of traumatic asphyxia: edema, cyanosis and hemorrhages in the region of the upper v. cava, excessive pulmonary congestion and signs of suffocation.Histological changes were felt to be due to three major pathomechanisms: a) Changes of hypoxidosis due to asphyxia: vacuolisation and edema of hepatocytes, the renal tubular epithelium and the heart muscle cells, mobilization of alveolar cells with formation of multinucleated giant-cells, b) Intermediate or severe degrees of pulmonary microembolism mainly consisting of fat droplets and bone marrow and additionally of smaller quantities of free megacaryocytes, c) Interstitial and intraalveolar edema of the lungs and interstitial edema of the heart muscle mainly due to the haemodynamic disturbances. Biochemically the serum catecholamine concentrations were moderately or strongly elevated pointing to asphyxial pathomechanisms. -Fatal termination is supposed to be due to a combined action of haemodynamic dysregulation, asphyxia and pulmonary microembolism.

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Bindegewebe und blutbildende Gewebe

Maximow¹

1927

Die Gewebe Teil Epithel- Und Drüsengewebe · Bindegewebe Und Blutbildende Gewebe · Blut

168

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Ueber Knochenmarkgewebs-Embolie

Cited by 23 publications

References 0 publications

Vitale Reaktionen in der Lungenstrombahn bei Tod durch Strangulation

Vitale Reaktionen in der Lungenstrombahn bei Tod durch Strangulation

Zur Pathophysiologie und Pathomorphologie bei Tod durch Druckstauung

Bindegewebe und blutbildende Gewebe

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