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International Journal of Legal Medicine | 1976

[Fat embolism of the lungs as the cause of death. Etiology, pathogenesis and reasoning (author's transl)].

Bernd Brinkmann; Michael Borgner; Margrit von Bülow

SummaryA comprehensive survey is given of the most important theories of etiology, pathogenesis and pathophysiology of pulmonary fat embolism. Autopsy and microscopic examinations were performed on 26 corpses with different causes of death. The total contents of fat of the lungs was analyzed by chloroform extraction. Death due to pulmonary fat embolism was diagnosed in three cases. In those with whole fat contents of about 20 g or more the histological degree was equivalent to occlusion of half of all vessels. The histological feature resembled that of shock; hemorrhage and microthrombosis were regular findings. The functional and morphological relationships with shock are discussed. It is concluded that, at least in the initial stage, fat embolism is due to mechanical injury. This mechanism is possibly altered or enhanced by biochemical changes in later phases. Pulmonary fat embolism is a disease which may cause death if mechanical, toxic and shock-inducing effects lead to insufficiency of the cardio-respiratory system. In forensic cases death due to fat embolism should be diagnosed only after exclusion of other lethal factors. Posttraumatic cases often show competition with shock due to hemorrhage. It is important to relate the degree of fat embolism to preexisting diseases.ZusammenfassungDarstellung der Literatur zur Ätiologie, Pathogenese und Pathophysiologie der Fettembolie. Die Pathomorphologie der pulmonalen Fettembolie zeigt Ähnlichkeiten mit jener der Schocklunge. Besonders die wechselwirkenden Faktoren zwischen Fettembolie und Schock werden erörtert. Die Wirkungen der pulmonalen Fettembolie werden unterteilt in: mechanische, toxische und Schockinduzierende Wirkungskomponenten. Verfasser kommen zu der Ansicht, daß die pulmonale Fettembolie ein eigenständiges Krankheitsgeschehen darstellt. Es werden 26 Todesfälle mit und ohne Fettembolie untersucht. Die Fettembolie wird morphologisch und gravimetrisch quantifiziert. Bei geringen Graden der Fettembolie besteht eine schlechte Korrelation zwischen mikromorphologischem Grad und gravimetrischem Ergebnis. Bei hohem Grad der Fettembolie besteht scheinbar eine engere Korrelation. Zusätzlich finden sich bei hohen Fettemboliegraden Mikrohämorrhagien, Mikrothromben.Die todesursächliche Bedeutung der pulmonalen Fettembolie wird eingehend besprochen. Verfasser kommen zu dem Schluß, daß eine eingehende individuelle Beurteilung meist erforderlich sein wird. Die Diagnose „Tod durch pulmonale Fettembolie” ist eine Diagnose per exclusionem.A comprehensive survey is given of the most important theories of etiology, pathogenesis and pathophysiology of pulmonary fat embolism. Autopsy and microscopic examinations were performed on 26 corpses with different causes of death. The total contents of fat of the lungs was analyzed by chloroform extraction. Death due to pulmonary fat embolism was diagnosed in three cases. In those with whole fat contents of about 20 g or more the histological degree was equivalent to occlusion of half of all vessels. The histological feature resembled that of shock; hemorrhage and microthrombosis were regular findings. The functional and morphological relationships with shock are discussed. It is concluded that, at least in the initial stage, fat embolism is due to mechanical injury. This mechanism is possibly altered or enhanced by biochemical changes in later phases. Pulmonary fat embolism is a disease which may cause death if mechanical, toxic and shock-inducing effects lead to insufficiency of the cardio-respiratory system. In forensic cases death due to fat embolism should be diagnosed only after exclusion of other lethal factors. Posttraumatic cases often show competition with shock due to hemorrhage. It is important to relate the degree of fat embolism to preexisting diseases.


International Journal of Legal Medicine | 1981

Zur Pathophysiologie der Atmung und des Kreislaufs bei Tod durch obstruktive Asphyxie

Bernd Brinkmann; K. Pschel; Hans-Werner Bause; Manfred Doehn

SummaryThe pathophysiology of respiration and hemodynamics during the agonal period of death by obstructive asphyxia was investigated. Experiments were carried out on ten dogs that were strangulated by ligature (seven cases) or asphyxiated by occlusion of the intubation tube (three cases). The following parameters were registered: Blood pressure in the arteria femoralis and arteria pulmonalis, electrocardiogram, endotracheal pressure, respiratory frequency, electroencephalogram. These were the most important findings:(a) An excessive and distinctly biphasic hypertonic reaction takes place after strangulation by ligature whereas occlusion of the intubation tube results in a slight increase of arterial blood pressure. (b) After occlusion of the tube more than after strangulation the endotracheal pressure becomes deeply negative during the inspiration trials. (c) After cessation of respiration a distinct pulmonary arterial hypertension develops in both forms of obstructive asphyxia. (d) The paralyzation of the respiratory center takes place after about 4 min at the same time when the circulatory breakdown develops. The final cardiac failure occurs after about 9–10 min.The dysregulation of respiration and hemodynamics in the agony of obstructive asphyxia can be differentiated from other shock models. This results in special morphological alterations of the lung tissue which have been described elsewhere.ZusammenfassungDer pathophysiologische Ablauf der Agonie bei obstruktiver Asphyxie (einerseits Strangulation durch Drosselung — andererseits Verschluß eines endotrachealen Tubus) wurde tierexperimentell an 10 Hunden untersucht. Gemessen wurde das Verhalten von verschiedenen Parametern des Kreislaufs (systemarterieller Druck, pulmonalarterieller Druck, Herzfrequenz) und der Atmung (endotrachealer Druck, Atemfrequenz). Außerdem wurde das EKG und das EEG registriert. Der Vergleich der beiden Modellformen der obstruktiven Asphyxie ergibt folgende herausragende Aspekte:a) Bei der Strangulation findet eine excessive hypertonische Krise statt mit deutlich biphasischem Verlauf, während es bei der Tubusblockade lediglich zu einem mäßigen Blutdruckanstieg kommt; b) Atemmechanisch wird ein Inspirationsversuch ausgewiesen durch tiefe negative endotracheale Drucke, welche bei Tubusblockade deutlich stärker ausgebildet waren als bei der Strangulation; c) Bei beiden Formen der obstruktiven Asphyxie entwickelt sich etwa zeitlich mit dem Nachlassen der Atmung eine ausgeprägte pulmonalarterielle Hypertonie; d) In allen Fällen beginnt die Lähmung des Atemzentrums nach ca. 4 min gleichzeitig mit dem Beginn des Kreislaufzusammenbruchs; der endgültige Kreislaufstillstand erfolgt nach 9–10 min.Die festgestellte Atem- und Kreislaufdysregulation bei Tod durch obstruktive Asphyxie zeigt gegenüber anderen Schockformen ein abgrenzbares Muster. Dementsprechend sind insbesondere im Lungenparenchym spezielle morphologische Veränderungen zu erwarten.The pathophysiology of respiration and hemodynamics during the agonal period of death by obstructive asphyxia was investigated. Experiments were carried out on ten dogs that were strangulated by ligature (seven cases) or asphyxiated by occlusion of the intubation tube (three cases). The following parameters were registered: Blood pressure in the arteria femoralis and arteria pulmonalis, electrocardiogram, endotracheal pressure, respiratory frequency, electroencephalogram. These were the most important findings: (a) An excessive and distinctly biphasic hypertonic reaction takes place after strangulation by ligature whereas occlusion of the intubation tube results in a slight increase of arterial blood pressure. (b) After occlusion of the tube more than after strangulation the endotracheal pressure becomes deeply negative during the inspiration trials. (c) After cessation of respiration a distinct pulmonary arterial hypertension develops in both forms of obstructive asphyxia. (d) The paralysis of the respiratory center takes place after about 4 min at the same time when the circulatory breakdown develops. The final cardiac failure occurs after about 9-10 min. The dysregulation of respiration and hemodynamics in the agony of obstructive asphyxia can be differentiated from other shock models. This results in special morphological alterations of the lung tissue which have been described elsewhere.


Annals of Human Genetics | 1972

Inherited partial deficiency of the PGM1 gene: biochemical and densitometric studies

Bernd Brinkmann; E. Koops; O. Klopp; K. Heindl; H. W. Rüdiger

Venous blood samples of the two propositi and of three other individuals with apparently normal PGM patterns were examined 36 hr. after they were drawn. Horizontal starch-gel electrophoresis was performed using the original method (Spencer, Hopkinson & Harris, 1964). A horizontal polyacrylamide gel technique was employed too using a technique similar t o that described for acid phosphatase (Hennig, Hoppe & Kaifie, 1968) but with different buffers (Brinkmann & Fritz, 1968). Five pl. of a concentrated haemolysate (previously adjusted to a haemoglobin concentration of 20g %) were inserted on filter papers Schleicher & Schull No. 598. Electrophoresis and staining was performed as described by Spencer et al. (1964). Densitometric investigations were performed on formazan-stained polyacrylamide gels by recording the absorbance at 580 nm. with a Zeiss Chromatogram Spectrophotometer. The individual peaks were cut out from the recording paper and the relative isozyme activities were calculated by weighing the sheets. The sum of all PGM, isozymes was compared with that of PGM, isozymes. Quantitative enzyme essays were performed on each sample three times on the basis of the following reaction sequences : PGM 7G-6-P, G1 -P--


International Journal of Legal Medicine | 1981

Halskompression und arterielle Obstruktion

Bernd Brinkmann; E. Koops; F. Wischhusen; M. Kleiber

SummaryLiterature dealing with the obstruction of neck arteries induced by strangulation is referred to. Two types of strangulation are applied to ten human corpses, i.e., hanging and strangulation by ligature. The neck arteries are isolated at their origins from the thoracic vessels. After removal of the brain the arterial openings at the skull base are observed of their flow through. Tap water is perfused through the vessels under four pressures, i.e., 100, 200, 300, and 170 mm Hg. By using strangulation tools of three different diameters, various strangulation experiments are performed under controlled conditions imitating strangulation by ligature as well as atypical hanging. The most relevant results were:(1)In strangulation by ligature with the rope running horizontally round the neck it is possible to bring about obstruction to the carotid arteries by the same forces as in experimental hanging. Depending on the tool and on the arterial pressure, these forces vary between 2.5 and 10 kg. There are relations between the necessary forces, the diameter of the strangulation tools and the arterial pressures. Even by applying tractive forces in the range between 30–40 kg or by enhancing with a manual draw we did not succeed in bringing about an obstruction of the vertebral arteries. With the rope running obliquely round the neck as it does in typical hanging it is possible by minor tensile forces (between 8 and 17 kg) to obstruct these vessels as well.(2)In experimental hanging using a typical position of the tool, obstructions of all arteries occur between 5 and 15 kg. In types of hanging with an anterior suspension point above the level of the chin it was possible to occlude at least two vessels by application of intermediate forces.(3)In strangulation by ligature, the site of the appliance seems to have some influence. Infralaryngeal strangulation need somewhat greater tensile forces than a supralaryngeal course of the rope.(4)An additional longitudinal extension of the neck (maximal 80 kg) does not influence the obstruction forces in horizontal strangulation. Extreme bending of the neck does not impede the free passage of water, whereas with rotation and lateral flexion there could very well result obstructions of the arterial passage of the neck if physiological move of the head is reached or slightly overstepped.Some individual parameters of the corpses used (neck girth, rigor mortis, arteriosclerosis) did not have any influence on the powers obstructive to the carotid arteries.ZusammenfassungDie Literatur über die Behinderung der arteriellen Kopfdurchblutung bei Strangulation wird referiert. In eigenen Experimenten werden die isolierten Halsarterien von zehn Leichen unter verschiedenen Drucken perfundiert. Die experimentelle Strangulation erfolgt mit verschiedenen Strangwerkzeugen und in unterschiedlicher Lokalisation. Dabei werden die zum Gefäßverschluß erforderlichen Kräfte bestimmt. Weiterhin werden verschiedene atypische supracervicale Erhängungsformen simuliert und der Einfluß verschiedener Kopfhaltungen untersucht.Die wesentlichen Ergebnisse sind:(1)Bei horizontaler Drosselung gelingt es unter Anwendung der gleichen Zugkräfte wie beim Erhängen, die Carotiden zu verschließen. Es bestehen direkte Beziehungen zwischen Strangwerkzeugdurchmesser, intraarteriellem Druck und zum Verschluß erforderlichem Kraftaufwand. Es gelingt auch mit mehr als 40 kg Zugkraft nicht, die Vertebralarterien zu verschließen. Bei schräger Drosselung dagegen erfolgt der Verschluß beider Gefäßgruppen mit den gleichen Kräften wie bei typischer Stranglage beim Erhängen.(2)Bei den Experimenten mit supracervicaler Stranglage gelingt auch bei kleinem oder mittlerem Kraftaufwand der Verschluß zumindest von zwei Gefäßen. Diese experimentellen Ergebnisse entsprechen denen Rauschkes (1957).(3)Auch eine maximale Halsextension (80 kg) ist ohne Einfluß auf die bei horizontaler Drosselung ermittelten Werte. Extreme Beugung allein ist nicht geeignet, einen Durchblutungsstopp zu verursachen, während bei Rotation und Lateralflexion sehr wohl Behinderungen der arteriellen Kopfdurchblutung bei Überschreiten der physiologischen Kopfhaltung erfolgen. Individuelle Parameter wie Halsumfang, Arteriosklerose und Leichenstarre sind ohne erkennbaren Einfluß auf die zum Verschluß der Carotiden erforderlichen Kräfte.Die Literatur uber die Behinderung der arteriellen Kopfdurchblutung bei Strangulation wird referiert. In eigenen Experimenten werden die isolierten Halsarterien von zehn Leichen unter verschiedenen Drucken perfundiert. Die experimentelle Strangulation erfolgt mit verschiedenen Strangwerkzeugen und in unterschiedlicher Lokalisation. Dabei werden die zum Gefasverschlus erforderlichen Krafte bestimmt. Weiterhin werden verschiedene atypische supracervicale Erhangungsformen simuliert und der Einflus verschiedener Kopfhaltungen untersucht. Die wesentlichen Ergebnisse sind: Individuelle Parameter wie Halsumfang, Arteriosklerose und Leichenstarre sind ohne erkennbaren Einflus auf die zum Verschlus der Carotiden erforderlichen Krafte.


Virchows Archiv | 1978

Heat injuries to the respiratory system

Bernd Brinkmann; Klaus Püschel

A steam-tube of the main boiler exploded on a ship lying in the harbour of Hamburg. The steam temperature was 283‡ C. Cutaneous and severe inhalational scalding occured in the 27 fatalities, the men dying after different intervals. This paper deals with the pathological findings in the respiratory passages and the lung, describing the topographical extent of direct thermal injury and the temporal course of tissue reactions. In cases of instantaneous death coagulation necrosis of the tracheal and bronchial wall was found to extend to alveolar ducts in central parts of the lung. The lung parenchyma showed marked congestion, alveolar edema and desquamation of alveolar epithelial cells. Death occured due to acute pulmonary dysfunction and shock. Lethal complications following the period of primary shock consisted of fulminant confluent bronchopneumonia, the hyaline membrane syndrome or the onset of desquamative interstitial pneumonia. These changes rendered it difficult to evaluate the effects of the heavy cutaneous scalding on the pathological course of inhalational injuries in those surviving for longer periods.


Human Heredity | 1971

Red Cell Enzyme Polymorphisms in a Northern German Population

Bernd Brinkmann; H.H. Hoppe; W. Hennig; E. Koops

From a random northern German sample, gene frequencies of five red cell enzyme polymorphisms are calculated. For acid phosphatase (n = 7,059) the gene frequencies are estimated to be: pa =


International Journal of Legal Medicine | 1981

Die Lunge als Erfolgsorgan der Strangulationsagonie

Bernd Brinkmann; Klaus Püschel

SummaryIt was investigated by animal experiments (50 rats, 15 rabbits) if histomorphological vital reactions can be found in the lung after strangulation and how far these findings differ from other violent causes of death with comparatively short survival period. Besides strangulation by ligature the animals were killed by overdose of ether, chloroforme, pentobarbitone, and ketaminhydrochlorid; gasing with propane and nitrogen; suffocation in a small closed box; thoracic compression; injection of KCN i.p.; decapitation; blunt force; electric current; cardiac injection of KCL.In comparison with the controls the striking findings after strangulation consisted of a qualitatively and quantitatively considerable hemorrhagic syndrome and an edema of all compartments of the lung which was frequently hemorrhagic, too. The authors award specific significance to the alveolarseptal edema which was found in semithin sections (and electron-micro-scopically)—which never occurred in the controls.ZusammenfassungTierexperimentell wurde untersucht, ob nach Strangulation histomorphologisch vitale Reaktionen in der Lunge feststellbar sind, die eine von anderen Todesarten mit entsprechend kurzer Überlebenszeit abgrenzbare Prägung aufweisen. Verwendet wurden 50 Ratten sowie 15 Kaninchen. Neben der Strangulation wurden die Tiere folgenden Todesarten unterworfen: Überdosierung von Äther, Chloroform, Nembutal, Ketanest; Ersticken in Propangasatmosphäre bzw. durch Begasung mit Stickstoff; Rückatmungsversuch, Thoraxkompression, KCN-Injektion intraperitoneal, Dekapitation, stumpfe Gewalt, Stromschlag, KCL-Injektion intrakardial.Die im Vergleich zu den Kontrolltodesarten qualitativ und quantitativ herausragenden Befunde bei Strangulation waren ein ausgeprägtes hämorrhagisches Syndrom und ein sich über alle Kompartimente der Lunge erstreckendes, häufig hämorrhagisches Ödem. Besondere Bedeutung kommt bei Strangulation dem im Semidünnschnitt (und elektronenmikroskopisch) vorgefundenen deutlichen alveolär-septalen Ödem zu, welches bei den untersuchten Kontrolltodesarten mit sehr kurzer Agonie im Minutenbereich nicht auftrat.


Human Genetics | 1972

Gene frequencies of soluble glutamic-pyruvic-transaminase in a northern German population (Hamburg)

Bernd Brinkmann; P. Krukenberg; M. Brinkmann; H. H. Hoppe

SummaryA random population sample of Northern Germany (Hamburg), consisting of 2026 individuals, has shown a GPT1 frequency of 0.53. There is a good agreement with other results reported before.ZusammenfassungEine zufällige Bevölkerungsstichprobe aus Norddeutschland (Hamburg), die aus 2026 Individuen bestand, zeigte eine GPT1-Häufigkeit von 0,53. Dieses Ergebnis steht in guter Übereinstimmung mit anderen Ergebnissen.


Human Genetics | 1971

Phosphoglucomutase (PGM) and 6-phosphogluconate dehydrogenase (PGD) isozymes in human sperm cells.

Bernd Brinkmann; E. Koops

SummaryThis is report about the PGM and PGD isozymes that are present in sperm cells. 4 isozymes that are controlled by the PGM1 alleles can be detected regularly. Only one isozyme is identified as a product of the PGM21gene. The isozymes that are controlled by the PGM3 locus are detected at regular intervals. PGD patterns differ only slightly from those of red cells.ZusammenfassungEs wird über die PGM- und PGD-Isoenzyme, die in Spermatozoen vorkommen, berichtet. Als Produkte der PGM1-Allele lassen sich regelmäßig 4 Isoenzyme erkennen. Nur ein Isoenzym ist erkennbar, welches dem PGM21-Gen zugeordnet werden kann. Weiterhin lassen sich regelmäßig die Isoenzyme des PGM3-Locus erkennen. Die PGD-Muster in Spermapherogrammen ähneln denen aus Erythrocytenhämolysaten.


American Journal of Forensic Medicine and Pathology | 1985

Ultrastructural alterations of skeletal muscles after electric shock

Klaus Püschel; Bernd Brinkmann; Klaus Lieske

The existence of tracks of electric current in the skeletal muscles was checked by electron-microscopic investigations in animal experiments on rats. Hypercontraction bands alternating with dilated sarcomeres and tumefaction of tubular apparatus and mitochondria with cristiolysis were established. The most severely expressed alterations were found in the vicinity of the electrodes and adjacent to the joints; they are thought to be caused by electrically induced tetanus and local hyperthermia. The forensic aspects of these findings are discussed

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E. Koops

University of Hamburg

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K. Pschel

University of Hamburg

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