Forensic Science International 144 (2004) 211–214
Asphyxia-related deaths$
Klaus Püschel*, Elisabeth Türk, Holger Lach
Institute of Legal Medicine, University of Hamburg, Butenfeld 34, 22529 Hamburg, Germany
Available online 17 June 2004
1. Introduction
In the 19th and early 20th century, questions concerning
the morphology and pathophysiology of asphyxial deaths
were almost a domain of German forensic medicine, and
still, continuous progress is achieved in asphyxia-related
scientific aspects. Consequently, a plethora of renowned
forensic specialists have contributed on the field.
2. Forensic aspects
Among fatalities that are subjected to medico-legal autop-
sies, asphyxia-related deaths account for a significant num-
ber of cases: according to experiences at the Institute of
Legal Medicine in Hamburg, Germany, one third of all
suicides, a one-fourth of all homicides and a significant
number of all fatal accidents can be attributed to asphyxia.
Qualitatively, the forensic pathologist often has to face
sophisticated questions regarding these fatalities. The inves-
tigating officers expect quick answers to questions like ‘‘is
this a suicidal or a homicidal manner of death?’’, ‘‘was the
victim hanged after strangling him or her to fake suicide?’’,
‘‘could the fatality be accidental, e.g. in an autoerotic
accident?’’, ‘‘can a natural death be assumed in cases with
suspicious death scene findings, e.g. deaths in connection
with sexual intercourse?’’, or ‘‘if instantaneous neurogenic
cardiac arrest is diagnosed, was it the result of manual
strangling or a short hit against the neck?’’. Answering these
questions may be especially difficult if—as it is often the
case, where there are no objective, witnesses and the forensic
pathologist has no information on the deceased’s history, and
has to give his expertise on the basis of the autopsy findings
alone.
$
Main focusses of German-language forensic medicine.
*
Corresponding author. Tel.: þ49 40 42803 2130;
fax: þ49 40 42803 3934.
E-mail address: pueschel@uke.uni-hamburg.de (K. Püschel).
0379-0738/$ – see front matter # 2004 Elsevier Ireland Ltd. All rights reserved.
doi:10.1016/j.forsciint.2004.04.055
3. Definition
There are almost as many different possibilities of group-
ing asphyxial deaths as there are authors, and there are
different definitions of the term ‘‘asphyxia’’ itself, too.
One possibility is to define asphyxia, all-ecompassingly,
as the failure of body cells to either receive or utilize oxygen;
more or less in parallel with an increase of the blood carbon
dioxide level. This led to the differentiation between ‘‘exter-
nal’’ and ‘‘internal’’ asphyxia. In medico-legal usage,
‘‘asphyxia’’ almost exclusively refers to forms of external
hypoxia and can be further divided into mechanical and
environmental asphyxia. In practice, environmental
asphyxia is of subordinate importance, as a deficiency of
oxygen in the environment demands a special constellation
of circumstances, e.g. entrapment in an air-tight enclosure.
Consequently, the present survey on research into asphyxia-
related fatalities shall focus on mechanical asphyxia.
4. Specificity of postmortem findings
The underlying pathophysiological mechanism in asphyxia-
related deaths is the lack of oxygen. Thus, it is justified to some
extent to talk about a common reaction pattern. This relates
to the agonal process as well as to autopsy findings.
For more than 100 years, the diagnosis of asphyxia has
been based upon the classical vital signs of asphyxia. They
have been reported in many textbooks on forensic medicine,
e.g. Puppe (1899), von Hofmann (1903), Haberda (1927) or
Walcher (1950). However, signs of asphyxia in a dead body
are, to a certain extent, something that ‘‘all causes of death
have in common’’, and the diagnosis of ‘‘asphyxia’’—if not
applied in the strict medico-legal sense—‘‘does not tell
much except that the examined person is dead’’ (Puppe,
1899). It has always been stressed that the signs of asphyxia
are non-specific and can be the sequel of a violent death as
well as of internal disease. As Kratter expressed it concisely
in 1921, ‘‘unless a proof of the cause of asphyxia is
furnished, the diagnosis of asphyxia is a meaningless word’’.
212 K. Püschel et al. / Forensic Science International 144 (2004) 211–214
It is in no way easy to establish the diagnosis of asphyxia
on the basis of autopsy findings. In the early 1940s, Walcher
(1943) stated: ‘‘The history of research into anatomical
findings in fatal asphyxia is to a great extent a history of
misconceptions. Nobody who knows the articles that have
been published on vital findings in asphyxia can help getting
this impression.’’ Repeatedly, the desire dominates in
research scientists to denote their own findings as specific
or at least highly significant for establishing the diagnosis of
fatal asphyxia. With equal regularity, critics came about to
entirely deny the discussed finding any significance in the
diagnosis and concerning vitality, until conciliating voices
established—at least for some of those findings—a certain
significance for the diagnosis of asphyxia or even for a
special form of asphyxia.
The number of unrecorded cases of homicide by asphyxia
is a special problem, Heinemann and Püschel (1996) [3].
Macromorphological signs of asphyxia may be weak or even
absent at autopsy, for instance in cases of physical super-
iority of the culprit over the victim, in ambush attacks or in
cases where the victims are children, disabled or elderly
people. Consequently, with ameliorating technical possibi-
lities, the question was aroused whether micromorphologi-
cal and biochemical investigations could contribute to
establishing the diagnosis of fatal asphyxia.
5. Etiology and pathophysiology of strangulation
There are three major mechanisms of mechanical
asphyxia, namely hanging, ligature strangulation, and man-
ual strangulation. In addition, asphyxia can be caused by
smothering, e.g. obstruction of the airways by a pillow, or by
thoracic compression which might occur in an accidental
manner of death, but also in homicides, e.g. thoracic com-
pression of the defenceless victim through the body weight
of the culprit, which has historically been termed ‘‘burking’’.
5.1. Compression of the neck arteries
In 1876, von Hofmann held a lecture in front of the
‘‘Association of Physicians of Lower Saxony’’ which
pointed the way ahead when he suggested that in strangula-
tion deaths, the mechanism of death is the compression of
the neck arteries. This view was confirmed in research
experiments by von Hofmann himself as well as by Haberda
and Reiner. Many articles on arterial compression in stran-
gulation have been published since those days. In the recent
literature, Brinkmann et al. (1981) have added to this knowl-
edge with experimental and reconstructional investigations.
It has become generally accepted in forensic pathology
that a minimum weight of 5 kg (carotid artery) and 35 kg
(vertebral artery) is necessary for the complete compression
of neck arteries. The same forces can cause complete arterial
compression in horizontal ligature strangling. In contrast,
complete compression of the neck arteries does usually not
occur in manual strangling, except for constellations where
the culprit’s hand is significantly bigger than the victim’s
neck or the pressure is aimed at the anterolateral neck region.
5.2. Airway obstruction
In 1870, Ecker impressively proved the airway obstruc-
tion in strangling when he sawed the frozen dead body of a
hanged individual to show how the tongue was pressed
against the posterior pharynx wall. The significance of this
airway obstruction for fatal outcome was, however, relati-
vized when hanging deaths were observed in individuals
who had undergone tracheotomy, which was verified by
experiments on rabbits (Reineboth, 1895).
In 1886, Langreuter used a special preparation method to
show that if the thumb and index are placed on both sides of
the thyroid cartilage in manual strangling, only a ‘‘very low
pressure’’ is sufficient for complete compression of the
larynx. Langreuter, too, could show that in hanging deaths,
the tongue and epiglottis are pressed against the posterior
pharynx wall. In suspension experiments on dead bodies in
1922, Strassmann demonstrated a complete airway obstruc-
tion when the point of suspension was located in the poster-
ior neck region or behind one ear, even in cases of
incomplete suspension through only parts of the body
weight. Also, in 1924, Strassmann found out that in ligature
strangulation, ‘‘moderate pressure’’ is sufficient to induce
complete airway obstruction. More recent experiments,
showed that an average pressure of 8–12 kg is necessary
to achieve complete airway obstruction in manual strangula-
tion of an adult (Koops et al., 1983).
5.3. Carotid sinus stimulation
Hering gained basic knowledge on death due to carotid
sinus stimulation in strangling in animal models and also
extensively discussed the problem in theory (1927), but apart
from some single experiments on human individuals, further
experiments were not performed. Since then, the problem
has repeatedly been discussed regarding hanging, ligature
strangling and manual strangling, especially in connection
with spectacular criminal cases, e.g. the case of Dielingen
(Esser, 1933) or Hetzel (Prokop, 1970). Since then, forensic
expert witnesses regularly have to face testimonies concern-
ing instantaneous neurogenic cardiac arrest due to carotid
sinus stimulation at court.
5.4. Spinal cord/brainstem injuries
It is a common misconception among the medico-legal
laity that fractures of the spine and consequent brainstem/
spinal cord lesions cause immediate death in hanged indi-
viduals, and this has even been proposed in research pub-
lications. It is, however, evident from a plethora of autopsy
cases that injuries of the cervical spinal column are very rare
in cases of strangulation. In an autopsy series from the
 K. Püschel et al. / Forensic Science International 144 (2004) 211–214
Institute of Legal Medicine in Hamburg over a ten-year
period, fractures of the cervical spinal column were only
found in six out of 821 hanging deaths. These fractures were
localized between the segments C5 and C6. Brainstem
lesions are exceptionally rare and almost exclusively occur
in falls from greater heights into the noose.
6. Morphologically detectable vital reactions in
asphyxial deaths
6.1. Direct lesions
The best overview of the old literature can be found in the
chapter on asphyxial deaths in volume I of the ‘‘Handbook of
Legal Medicine’’ (in German: ‘‘Handbuch Gerichtliche
Medizin’’) by Brinkmann and Madea (2003) [2]. Many of
the articles date from the 19th century; virtually all anato-
mical structures of the neck have been investigated regarding
injuries after strangling.
Many authors have dealt critically with the question of
vital versus postmortem origin of neck injuries. Some
particularly comprehensive, critical and precise investiga-
tions have been performed by Maxeiner (1987, 1995, 1999).
It has become generally accepted that all findings once taken
to be vital reactions have to be treated with considerable
caution regarding their value as evidence (overview in:
Püschel [5,1]). For example, hemorrhagic strips of skin
between two furrows in a double-looped noose have been
observed in postmortem suspension long ago.
6.2. Indirect lesions
Indirect lesions due to strangling include hemorrhages at
the origin of the sternocleidomastoid muscles, hemorrhages
in the auxiliary inspiratory muscles and trunk muscles as
well as stripe-like hemorrhages on the dorsal and ventral
surface of the intervertebral discs (Simon’s hemorrhages,
Simon, 1968). Fibre ruptures in the auxiliary inspiratory
muscles have already been observed by Reuter in 1922. All
these findings have been discussed critically regarding their
value as evidence for vital strangling.
7. So-called asphyxial hemorrhages
7.1. Petechiae in the head and neck region
Petechiae of the conjunctivae have always been attached
special importance to, as well as petechiae of the facial skin
and mouth mucosa. Less easily detectable, petechiae can also
be found at the root of tongue, in the pharynx, the laryngeal
mucosa, the salivary glands, the mucosa of the paranasal
sinuses, the galea, underneath the fasciae of the oculomotor
muscles and in the temporal muscles. All these hemorrhages
have the same underlying pathogenetic mechanism, which
213
has also been described for brain tissue, dura mater and
hypophysis (e.g. Reuter, 1902, 1922; von Hofmann, 1880,
1903; Liman, 1871; Lesser, 1880; Strassmann, 1898).
Considerable restraint should be exercised regarding the
specificity of these hemorrhages—especially the conjuncti-
val petechiae. This has already been demonstrated by earlier
authors (Liman, Lesser, von Hofmann and Strassmann).
More recently, the frequency with which these findings
can be observed in different causes of death has been
investigated (Prokop and Wabnitz, 1970; Jarosch, 1971;
Geserick and Kämpfe, 1990). Conjunctival petechiae are
regularly found in manual and ligature strangling, atypical
hanging and thoracic compression. They can, however, also
be found in sudden cardiac death. Moreover, they can be
inflicted postmortem by placing the body head-down, which
morphologically cannot be distinguished from vital pete-
chiae (von Hofmann and Haberda, 1898).
7.2. Subserous intrathoracic hemorrhages
According to Kratter (1895), ecchymoses in violent
asphyxial deaths were first described by Röderer in 1753.
These subpleural and subepicardial bleedings were first
considered eminently valuable for the diagnosis of
asphyxia-related deaths. Especially Liman criticized this
view in 1861, and other authors, too, doubted the overriding
value of those findings as evidence for asphyxia. This was
especially true for the differential diagnosis between
mechanical asphyxia of infants and sudden infant death
syndrome (SIDS). In 1898, Strassmann pointed out that
subpleural ecchymoses are of no practical value for the
determination of the cause of death. In 1861, Liman already
stated that subserous ecchymoses, namely of the thoracic
organs, can be a valuable symptom of an asphyxial death, but
their absence does not exclude an asphyxial death, nor do
they in any way allow to distinguish between self-infliction
and infliction by another person. Jarosch performed experi-
ments in 1971 to add to earlier theories on subserous
intrathoracic hemorrhages. According to his findings, these
hemorrhages occur due to the same underlying pathogenetic
mechanism as the hemorrhages in the head and neck region,
namely an increase of pressure in the arteriolae and venules.
It is today generally accepted that these subserous hemor-
rhages are a non-specific phenomenon.
8. Lung morphology
8.1. Macromorphology
Macromorphologic findings in the lungs have always
been considered especially important in asphyxial deaths,
e.g. subpleural ecchymoses, usually referred to as Tardieu-
spots. However, it was stressed by Liman as early as 1868
that no pathomorphologic finding is specific enough to serve
as a proof of an asphyxial death.
214 K. Püschel et al. / Forensic Science International 144 (2004) 211–214
Partial vesicular and interstitial emphysema adjacent to
areas of increased blood content and hemorrhages have
repeatedly been described (Puppe, 1907). According to
Schrader (1940), interstitial emphysema can be observed
especially in cases of smothering; this has also been reported
by other authors (Walcher, 1950; Mueller, 1953; Prokop,
1975; Brinkmann et al. [2]). Irregularly distributed venous
hyperemia and hemorrhages have, among many authors,
been described by von Hofmann (1903), Lochte (1905),
Maschka (1881), Böhmig (1930) and Reuter (1930, 1933).
Reuter suggested that focal hemorrhagic edema should be
typical especially of slow asphyxial deaths, which was later
corroborated by Schrader (1940), Walcher (1943), and more
recently by Pollack (1975). As a caveat it has to be noted,
however, that in patients who undergo resuscitation before
death, it is virtually impossible to distinguish between
asphyxia-related morphologic findings and resuscitation-
induced artifacts—a problems that increases in importance
with the development of modern emergency medicine.
8.2. Micromorphology
Earlier investigations on histopathology in asphyxial
deaths, Janssen (1977) [4], have almost completely fallen
into oblivion. They basically dealt with selected aspects like
interstitial emphysema (Leers, 1908; Puppe, 1907), hemor-
rhagic edema and microhemorrhages (Böhmig, 1930;
Reuter, 1930; Schrader, 1937, 1940). In animal experiments
performed in 1966, Wagner found focal interstitial and
alveolar edema, focal hemorrhagic edema and marked
hyperemia after 20–30 s of outer airway obstruction.
We owe it to Brinkmann that micromorphological inves-
tigations on the lungs have re-gained an adequate standing in
the diagnosis of asphyxia. In systematic histological inves-
tigations on the lungs of strangling fatalities he regularly
found signs of acute hemorrhagic dysregulation and
increased blood vessel permeability which can be inter-
preted as signs of a vital reaction. He also found that typical
alterations of lung parenchyma include pulmonary edema,
which is partly hemorrhagic and alveolar and partly septal
and perivascular. Furthermore, hydropic endothelial cell
degeneration, vascular leucocytosis, immature myeloic bone
marrow cells in the pulmonary vasculature and pulmonary
microembolisms can be observed. Other authors have rela-
tivized the significance of some of these findings; however,
the hemorrhagic-dysoric syndrome as characterized by
Brinkmann seems to be characteristic of violent asphyxial
deaths, particularly in cases with a longer survival time.
9. Biochemical vital reactions
The comprehensive understanding of those vital reactions
that are independent of localized morphological changes,
referred to as ‘‘biochemical vital reactions’’, is attributable
to Berg. First, the release of certain hormones—above all
adrenaline and noradrenaline, but also histamine—was dis-
covered. In 1963, Berg concluded that ‘‘if there is no
morphological sign of myocardial infarction, pulmonary
embolism or major blood loss, the detection of high adre-
nalin and histamine levels allow the diagnosis of acute
external asphyxia’’. These results have been relativized later
(Kauert, 1990).
In 1952, Berg already described a ‘‘vital reaction char-
acteristic of hanging’’, namely a relevant difference between
the phosphatid level of cardiac blood and the blood of the
cerebral venous sinuses. These results were later corrobo-
rated by Mueller (1961) in animal models as well as by
Weiler and Haarhoff (1972) and Saternus (1980) in inves-
tigations on hanging fatalities. The analysis of those bio-
chemical changes has, however, yet not become part of
routine diagnostic measures.
References
(Historical German-language citations are not listed;
they are all referred to in the following references.)
[1] B. Brinkmann, K. Püschel (Eds.), Ersticken, Fortschritte
in der Beweisführung. Springer, Berlin, Heidelberg, New York,
1990.
[2] B. Brinkmann, H.G. Bone, M. Booke, A. DuChesne, H.
Maxeiner, Ersticken, in: B. Brinkmann, B. Madea (Eds.),
Handbuch Gerichtliche Medizin, Springer, Berlin, Heidelberg,
New York, 2003, pp. 699–796.
[3] A. Heinemann, K. Püschel, Zum Dunkelfeld von Tötungsde-
likten durch Erstickungsmechanismen. Arch Kriminol, vol.
197, 1996, pp. 129–141.
[4] W. Janssen, Forensische Histologie, Schmidt-Römhild, Lü-
beck, 1977.
[5] K. Püschel, Vitale Reaktionen zum Beweis des Todes durch
Strangulation, Habilitationsschrift, Hamburg, 1982.
Reproduced with permission of the copyright owner. Further reproduction prohibited without permission.