1 Death Due to Hypothermia 13

(A) (B)

Fig. 1.5A,B Hemorrhagic infarction of the colon in a fatality due to hypothermia. A Gross
appearance. B Histology: hemorrhages into the colonic wall with thrombosis of the veins of
the submucosa and an acute inflammatory infiltrate

had always been present in the stomach, too. Besides ulcerations of the colon
and ileum, hemorrhagic infarctions of the colon have been described as well
(Fig. 1.5). These infarctions are due to rheologic and hemodynamic alterations
during hypothermia with sludge formation of red blood cells and subsequent
thrombosis of the veins of the submucosa (Table 1.6). They are very rare
findings; these authors have seen such infarctions of the large bowel in associa-
tion with fatal hypothermia in two cases; they were associated with an episode
of hemorrhagic shock prior to death [62].

1.3.5 Pancreas Changes

A variety of pancreas changes has been described in association with hypother-

mia: focal or diffuse pancreatitis, hemorrhagic pancreatitis, patches of fat necro-
sis over the organs surface, increased levels of serum amylase, hemorrhages, and
focal or diffuse interstitial infiltration of leukocytes [20, 29, 30, 32, 33, 35, 65,
66, 67] (Table 1.7). At autopsy, hemorrhages into the pancreas parenchyma as
well as under the mucosa of the pancreatic duct may be seen. In animal experi-
ments, Fisher et al. [66] were able to reproduce these pancreatic changes; they
found a nonhemorrhagic pancreatitis with fat necrosis in 10% of their cases. A
recent retrospective analysis of 143 cases of death due to hypothermia revealed
that pancreatic bleedings are of no diagnostic significance in deaths due to

Table 1.6 Hemodynamic and rheological response in phase III (paralysis) of hypothermia
Hemodynamic response Rheological response
Ý
ÝÝÝÝ

Heart rate Hematocrit

Ý

Blood pressure Plasma volume

ÝÝ

Blood pressure amplitude Viscosity

Venous pressure Red blood cells sludge-formation
Ý

Resistance
14 B. Madea et al.

Table 1.7 Pancreatic changes in hypothermia according to different authors

Pancreatic changes in Hypothermia Author
Focal or diffuse pancreatitis in 10% of patients (n = 50) who were Sano and Smith [67]
treated with hypothermia
Among 13 cases of hypothermia 2 cases of hemorrhagic pancreatitis, 3 Duguid et al. [28]
cases of pancreatitis with fat necrosis over its surface (38%)
Focal pancreatitis or hemorrhagic pancreatitis in 29 of 43 cases (67%) Mant [34]
Hemorrhage into the gland in 4 of 22 cases (18%) Hirvonen [20]
Raised serum amylase in 11 of 15 cases (73%) Duguid et al. [28]
Focal, non-hemorrhagic pancreatitis with patches of fat necrosis in Fisher et al. [66]
10% of animals in experimental hypothermia
Empty vacuoles in adenoid cells of the pancreas Preuß et al. [68]

hypothermia [68] – they are observed only very rarely and are seen in other causes
of death with the same frequency.
The high incidence of pancreatic changes described by Mant [32, 33, 34]
might be caused by the composition of his case material – mostly older people;
in such a biased autopsy population the delimitation of preexisting diseases may
be difficult.
Preuß et al. [68] found in 24 out of 62 cases of fatal hypothermia (38.7%) in
microscopic investigations seemingly empty vacuoles in the adenoid cells of
pancreas (Fig. 1.6). These vacuoles were not observed in a control group with-
out hypothermia prior to death and in a control group of chronic alcoholics.
Although these vacuoles seem to be diagnostically significant, their pathogen-
esis still remains unclear.

1.3.6 Hemorrhages into Core Muscles

Hemorrhages into muscles belonging to the core of the body, for instance
the iliopsoas muscle, as a diagnostic criterion of death due to hypothermia
were first described by Dirnhofer and Sigrist [69]. This morphological alteration

Fig. 1.6 Vacuoles in

pancreatic adenoid cells
1 Death Due to Hypothermia 15

seems to be known only in the German literature [70, 71]. Muscular hemor-
rhages in cases of hypothermia have, however, already been described in the
textbook of von Hofmann and Haberda [42], but it remained unclear whether
these hemorrhages developed during life as a response to hypothermia or post-
mortem as a resuscitation or transportation artefact. The observation of hemor-
rhages into core muscles especially in the iliopsoas muscle has been confirmed by
other authors but seems to be a rare finding. Histologically, a vacuolated
degeneration of subendothelial layers of the vascular walls with a lifting of
epithelial cells is seen. These changes were thought to represent a hypoxic damage
and the hemorrhages as due to diapedesis. The hypoxic damage of vessels of core
muscles is interpreted as a result of insufficient circulation due to hypothermia
induced vasoconstriction. However, compared to the muscles of the surface, the
oxygen requirement of the core muscles is not reduced. The misbalance of
reduced perfusion and normal oxygen requirement is thought to be the cause
of hypoxic damage of epithelial cells with resultant raised permeability [69].

1.3.7 Lipid Accumulation

Fatty changes in heart, liver, and kidneys have been described repeatedly in
fatalities due to hypothermia [46] but data on their diagnostic value and the
sensitivity of this finding are still missing. As fatty changes of the liver may have
many causes and are frequently found, they are of no diagnostic significance for
the diagnosis of death due to hypothermia.
Recent investigations show that lipid accumulation in epithelial cells of
proximal renal tubules seem to be of high diagnostic significance,
pointing towards hypothermia of the affected individual prior to death
[72, 73] (Fig. 1.7). This lipid accumulation is always seen at the base of the
epithelial cells; there are no concomitant changes of cell nucleus or plasma. The
fatty changes may be either a result of energy depletion after shock-induced
hypoxia or caused by tubular resorption after raised mobilisation of triglycer-
ides [72, 73]. There is a strong positive correlation between the grade of fatty
change with the occurrence of macroscopic signs of hypothermia (frost
erythema and Wischnewsky spots) [72]. In control cases, only slight fatty
changes can be found. The degree of fatty degeneration of renal tubules can
therefore be used as a very helpful marker for the diagnosis of death due to
hypothermia and has an equal value of diagnostic sensitivity compared to that
of Wischnewsky spots [72]. Also for the cardiac muscle, a fatty degeneration of
myocytes may be observed in cases of fatal hypothermia (Fig. 1.8) [74]. How-
ever, this fatty degeneration is only of diagnostic significance if a lipofuscin
staining is also carried out and a marked difference between lipid staining and
lipofuscin staining is obvious in the case in question (Fig. 1.9). There is also a
correlation between fatty degeneration of cardiac myocytes and Wischnewsky
spots. However, fatty degeneration of the cardiac muscle does not have the
diagnostic sensitivity of fatty degeneration of proximal renal tubules [72, 74].
16 B. Madea et al.

(A)

(B)

0 (×200) +1 (×200)

+2 (×200) +3 (×200)

Fig. 1.7A,B Lipid accumulation in renal proximal tubules. A The lipid stains are always
located the base of the cells. B Fatty changes in cells of in renal proximal tubules
1 Death Due to Hypothermia 17

grade 0 grade +1

grade +2 grade +3

Fig. 1.8 Fatty changes of cardiac myocytes in hypothermia

1.3.8 Endocrine Glands

Since endocrine glands are responsible for the maintenance of normal body
temperature, a decrease of body temperature activates the function of most
of the endocrine glands, especially the thyroid and adrenals [6, 10, 11, 75].

grade 0 grade +1

grade +2 grade +3

Fig. 1.9 Lipofuscin staining of cardiomyocytes

18 B. Madea et al.

However, morphological findings can be expected only in long-lasting

hypothermia, not after the usual exposition to cold ambient temperatures for
only a few hours [6]. In animal experiments, no morphologic changes have been
detected after exposure to cold temperatures for 49 h, but an activation of the
thyroid has been observed after long lasting exposure (5–9 days with tempera-
ture drops from 37.5 to 368C; morphologic changes: depletion of colloid, raise
of epithelial cells). Only after long lasting hypothermia has a lipid depletion of
adrenal cortex been found in animal experiments (10 days with core tempera-
tures of 338C) not after short exposures of 4–7 h [6].

1.4 Conclusions

Vital morphological alterations due to exposure to cold may be scarce in

hypothermia fatalities. Most of the findings are unspecific and clinically of no
relevance. However, external and internal findings are of diagnostic signifi-
cance, not only as the sole finding of frost erythema but especially when they
are found in combination like the presence of both frost erythema and
Wischnewsky spots. Although unspecific as an exclusive finding, frost erythema
and Wischnewsky spots are specific for hypothermia in combination. This is
also true for fatty changes of proximal renal tubules which have a strong
correlation with the aforementioned macroscopic signs of hypothermia. The
pathogenesis of morphologic alterations caused by hypothermia differs widely
(hypoxic changes, stress, disturbances of microcirculation with vasoconstric-
tion and increased hematocrit) due to the different organs and tissues affected.

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