Vitale Reaktionen in der Lungenstrombahn bei Tod durch Strangulation

Summary

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 HE-staining. 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, α-naphthole-esterase, naphtole-AS-D-Cl-esterase and toluidineblue on semi-thin-sections. 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.

Zusammenfassung

Histomorphologische Lungenuntersuchungen bei 34 Todesfällen durch Strangulation. Diverse Färbungen einschließlich Enzymhistochemie, Fettfärbung und Semidünnschnitt, z. T. frühpostmortale Probenentnahmen. Die wichtigsten Befunde: In 9 Fällen fand sich eine meist geringgradige pulmonale Fettembolie.

Fast alle Fälle wiesen Zeichen der akuten hämodynamischen Dysregulation und erhöhter Gefäßpermeabilität auf: z. T. hämorrhagisches alveoläres, teilweise auch septales und perivaskuläres Lungenödem. Gefäßwandverquellungen. Bei früher Probenentnahme auch hydropische Endothelzelldegeneration. Gefäßinhaltsveränderungen folgender Qualität: Knochenmarksembolie in drei Fällen. Disseminierte und aggregierte Zellembolien in allen Fällen, jedoch unterschiedlicher Zusammensetzung: Überwiegend handelte es sich um unreife Knochenmarkszellen der myeloischen Reihe, daneben auch jugendliche und gelapptkernige Granulocyten sowie andere mononukleäre Zellen. Weiterhin, meist in Kombination mit den aggregierten Zellen, Plättchenaggregate. Ätiologisch wird an ein Zusammenwirken mehrerer Pathomechansimen gedacht: Erstickungskrämpfe mit mechanischer Alteration des Knochenmarks; hypoxydotische Schädigung der Gefäßendothelien der Knochenmarkssinusoide; humorale Mediatoren des frühen Schocks mit direkter Knochenmarkswirkung. Die Befunde werden im Sinne einer vitalen Reaktion auf das Strangulationsgeschehen gedeutet.