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160
J. D. Harms et al.
22.1.2 Habitat
Stoneshes are found on coral reefs, muddy
waters or sandblasters of the Indian Ocean, Red
Sea, Indonesia, Australia, New Caledonia and the
Pacic [5].
22.1.3 Venomous Apparatus
22.1.3.1 Thorns andGlands
withVenom
The stonesh has 13 thorns on its dorsal n,
which rise in case of danger. Every thorn is covered with a verrucose tegumental envelope and
has a pair of glands with venom in its base. Every
gland has a canal lled with poison leading to the
top of the thorn. If someone walks on or tries to
seize the stonesh, its thorns penetrate into the
skin and the tegumental envelope is then pushed
downward causing the compression of the gland,
which if sufcient will launch the release of the
poison. The stinging and poisoning are a defensive mechanism.
The venom: its composition is complex: substances such as histamine, adrenalin, norepinephrine and dopamine as well as enzymes such as
hyaluronidase, protease and lipase. The main
toxin is the verrucotoxin: it inhibits the calcic
canals, and it activates the potassium canals. The
venom is myotoxic, neurotoxic and haemolytic.
It is inactivated at 54°C [3].
22.2 Stings by Stonesh
22.2.1 General Ideas
Stoneshes were notorious for being among
the most venomous animals of the world, and
its stings were thought to be lethal. In fact, the
sting by stonesh provokes an extremely
intense pain that can possibly result in a faint
t. Also, if it happens to a scuba diver, it may
cause an accident if the diver is unable to control his ascent (barotraumatism) or to make the
required decompression stops (desaturation
accident).
22.2.2 Circumstances
The stonesh is a sedentary and benthic sh. It
favours rocky areas or lays buried under sand or
mud. It feeds on small shes and shrimps, which
it swallows with its mouth. The stonesh can survive several hours out of the water, and its venom
remains active from 24 to 48h after its death.
Stings by stoneshes mostly occur during activities such as bathing, shing, snorkelling and
scuba diving.
22.2.3 Wound Location
The wounds are mainly seen on the feet of people
who accidentally walked on a stonesh. They can
also be seen on hands due to an attempt to touch
or seize the sh.
22.2.4 Clinical Evidence
The pain is immediate and very intense. It can
cause a person to faint. The pain is quoted
between 8 and 10 on the visual analogic pain
scale. It often results in restlessness and
aggressiveness.
There are one or several wounds, mostly in the
foot or in the hand.
An oedema quickly develops, sometimes limited around the wound, often wider and spreading.
Not rarely, it might extend to the whole limb up
to its base.
General symptoms are often noticed: sweats,
nauseas, arterial hypotension, tachycardia, heart
rhythm disorders, myasthenia and pulmonary
oedema.
22 Stonesh Necrosis
161
22.2.5 Diagnosis
The diagnosis is easy when the victim saw the
sh and clearly identied it. It is often the case
with shermen and scuba divers. In many other
cases, it is about a person who was bathing and
suddenly felt an excruciating pain without seeing
the cause of such pain. Thus, there is a doubt that
it could also be a wound by a piece of coral or
shell or a sting by another marine animal (Pterois
volitans, ray, poisonous shell, etc.).
The diagnosis is then based on assumption. If
the stonesh is not clearly identied, the elements which allow to incriminate the stonesh
are the following:
• The pain which is of maximum intensity at
once and resists to painkillers, including level
3 analgesics. The pain remains at highest
intensity during 12–18 h and then gradually
decreases within 2–3days.
• The examination of the wound allows identi-
fying the origin of the sting: if there are sev-
eral stings by several thorns, they are
distributed at equal distance. Every sting pres-
ents a small wound with clear edges from 1 to
2mm in length with an inammatory area and
a bluish halo (Fig. 22.3) and sometimes a
small blood and uid ow.
Often, the delay is more important and thus
the inammation has further extended with
oedema and phlyctenas around the wound.
Fig. 22.3 Typical aspect of a sting with punctiform
lesion and bluish halo
The association of a sudden, intense pain and
these local aspects allows evoking the diagnosis
of sting by stonesh.
22.2.6 Severity oftheWound
Depends onSeveral Factors
The size of the sh: the bigger the stonesh is,
the more venom is injected and the more serious
is the wound.
The wound: the number and depth of the
stings.
The victim: his (or her) age, weight and medical history.
The time period until medical care is given.
22.2.7 Medical Complications
Presence of a foreign body which will have to be
removed: a piece of thorn that would have broken
into the wound. Medical imaging might be necessary if there is a doubt, though this is rare since
the Synanceia verrucosa thorns are very
resistant.
Superinfection of wounds: the marine environment is rich in bacteria of all kinds, and any
wound by marine animals may become infected.
Extended infection: the risk of a spread infection is real, possibly leading to cellulitis, fasciitis
or gas gangrene.
Thromboembolic complications are also
possible.
The necrosis of wounds is the most frequently
met complication, though rather infrequent. If
necrosis is observed, medical supervision of the
wound and its course is required. The bluish halo
around the sting usually evolves within a few
days towards a small lesion: a supercial necrosis
which only requires simple dressing. However,
the necrosis sometimes extends reaching the dermis, hypodermis and the muscle and tendon
underneath. This necrosis continues to extend in
spite of local care, and from the initial, limited
lesion, the wound extends to its neighbouring
structures. This is serious and worrisome for both
the patient and physician.
162
J. D. Harms et al.
22.2.8 Treatment
Treatment of the pain from the beginning is an
absolute priority due to its intensity:
• Grade 1 (paracetamol) or 2 (tramadol) analgesics are often ineffective. Morphine must be
tried, but in a number of cases and in spite of
important doses, it remains ineffective too.
• Heat is used because the venom is inactivated
at 54°C. It is necessary to dip the limb in a
45°C water tub and let it soak until the pain
decreases. This “hot-water technique” is
sometimes very effective, sometimes not. The
duration of the soaking is important which
exposes the patient to a risk of burn. It seems
that the sooner the technique is used, the better
the result is. However, the disparities observed
in the results are important. In all, some disadvise this technique because of the potential
burns, whereas others use it. In our personal
experience, we used it with sometimes dramatic results and often failures or poor
improvements, in particular the outbreak of
the pain as soon as the hot water is removed
[1, 2].
• The equimolar gas oxygen/nitrous oxide
(Entonox®) can be used, but it is often insufcient since the relief only lasts while the gas
is given and it cannot be given for a prolonged
duration. It can be helpful then while waiting
for the analgesics to become efcient.
• The local injection of lidocaine can be used.
• Locoregional anaesthesia is the most effective
method for the treatment of the pain. We
implemented an epidural anaesthesia using
bupivacaine and continuous administration
through a catheter during 12 h for a patient
whose pain was unbearable and resistant to
the drugs. C.Maillaud in New Caledonia successfully realised several truncal locoregional
anaesthesias on patients [6]. This requires
anaesthesiologist availability, and in our hospital, we have set up a protocol for locoregional anaesthesia made by anaesthesiologists
in our operating unit preparation room: “single shot” (no indication of nervous catheter)
with naropeine in a sciatic block in the lower
limb or axillary, infraclavicular or humeral
block in the upper limb. The patient must stay
at hospital for 1day.
22.2.9 Other Used Treatments
The antivenom serum for stonesh is made by
the Commonwealth Serum Laboratories in
Australia by immunisation of horse with some
venom of Synanceia trachynis and would be
effective according to its manufacturer on the
venom of Synanceia verrucosa. This serum is
expensive; it must be kept between 2 and 8°C,
and its duration of use is limited. It is not available in Réunion Island, but it is in Mauritius.
S. Hansrod, in her report of interuniversity
diploma of physiology and hyperbaric and
underwater medicine, studied the Mauritian
experience: the injection of “serum anti-stonesh” would have a very fast effect on the
decrease of pain especially if the intramuscular
injection can be prematurely made. The intravenous route can be exceptionally used. The risk
of anaphylactic shock and serum disease must
be taken into account [1–3].
Steroids as anti-inammation medication:
their efcacy has not been demonstrated by any
study, and their effect is not recommended
because of the risk of infection.
The antibiotic therapy is often prescribed,
especially if one or several wounds were not prematurely disinfected. Amoxicillin/clavulanate
potassium or a third-generation cephalosporin is
prescribed for 3in 5days [3].
The tetanus prevention must be considered
and implemented depending on the vaccine status of the subject.
Low-molecular-weight heparins are prescribed if there is an important oedema or to
patients at risk.
The treatment of the wound requires the earliest possible disinfection and dressings.
The surgery is sometimes necessary, secondly,
for the treatment of complicated wounds.
The hyperbaric oxygen therapy (HBOT) is
used for the treatment of wounds evolving unfavourably as an adjuvant therapy to improve the
22 Stonesh Necrosis
healing. It becomes essential in case of infection
such as cellulitis or gas gangrene [2].
22.3 Our Experience inRéunion
Island
In 2008, we made a retrospective study in
Réunion Island. We had listed the suspicions of
sting by stonesh in the Emergency Unit of the
Groupe Hospitalier Sud Réunion from 2000 until
2005: 51 cases had been counted. It was 11
females and 40 males (average age 30, 6years/
extremes: 3 and 63years). The stings concerned
the feet in 78% of the cases and the hands in 22%.
In all the cases, we found a very intense pain, a
local oedema (57%) or extended (in cases involving the whole limb) (16%), an ecchymosis (16%),
an inammation (20%) and an early local necrosis (16%). Analgesics were used in 70% of the
cases with an association of different grades in
33% and using morphine in 43%. The hot-water
soaking was used in 65% of the cases and the
local injection of lidocaine in 9%. An antibiotic
therapy was prescribed in 43% of the cases. The
patients were hospitalised in 46% of the cases.
The extension of the necrosis occurred in four
cases, and the surgery was necessary in two
cases. HBOT was used in three cases [2].
163
Fig. 22.4 Case 1: Pulp necrosis of the nger the day after
the sting
22.4 Clinical Cases
22.4.1 Case 1
It is an old report from 2001. A 63-year-old sherman caught a stonesh of a beautiful size, estimated at 2 kg. By picking it up, his right-hand
middle nger got wounded. He came to the emergency unit to consult a physician only the next
day. Figure 22.4 was taken on the 13th of
February 2001 at his admission in the emergency
unit. There is a necrosis of the pulp of the third
phalanx, while there was initially a phlyctena.
Figure22.5 was taken on the 21st, and later evolution of the wound is seen in Fig. 22.6: the
Fig. 22.5 Case 1: Aspect after 3weeks
Fig. 22.6 Case 1: Later evolution
164
Fig. 22.7 Case 2: Typical early aspect with three points
of sting
examination of the wound suggested the necessity of a distal amputation. This patient was
treated by dressings and HBOT sessions
(Fig.22.6). The healing of a good quality will be
obtained after 5months of care.
22.4.2 Case 2
It is about a 12-year-old boy who was stung while
bathing in a rocky area. We saw him approximately half an hour after the sting (Fig. 22.7).
The pain was extreme with a state of agitation.
The aspect is characteristic because we see three
stings made by three thorns: they are regularly
spaced out. We clearly distinguish the stings,
with blood and an ecchymosis which is spread on
the most external lesion. The internal injury has a
small halo: the penetration of the thorn was
supercial at this level. The soaking associated
with analgesics was effective and the course
simple.
22.4.3 Case 3
An 8-year-old girl was stung, and we saw her a
month later. Her mother was very worried. We gave
her explanations onto the usual evolution of these
wounds and our project for dressings with stop of
the daily use of povidone-iodine disinfection, and
use of dressings changed all the 3 or 4days. The
evolution was quickly positive, and healing was
obtained a month and a half later (Fig.22.8).
J. D. Harms et al.
Fig. 22.8 Case 3: Intermediate aspect after use of hydrocolloid dressings
The stings by stonesh are frequent in all the
tropical zones of Indian and Pacic seas because
of the presence of the sh in shallow water. The
severe pain monopolises the immediate care. The
risk of evolution in extensive necrosis, difcult
and long to be treated, should impose a particular
surveillance after initial care.
Acknowledgements Thanks to Elodie Couture for
help in translation.
References
1. Hansrod. Utilisation du sérum anti-stonesh dans les
accidents par piqûre de poisson-pierre (Expérience
mauricienne). Mémoire du DIU de physiologie et
médecine hyperbare et subaquatique Université de
Lille II Session de la Réunion 06 novembre 2001.
2. Harms JD, D’Andréa C, Grandcolas N, Staïkowsky
F.Piqûres par poisson-pierre à la Réunion. J Plaies et
Cicatrisations. 2009;68(XIII):66–8.
3. Leuteritz A.La piqûre de poisson-pierre : quoi de neuf
en 2009? Mémoire du DIU de physiologie et méde-
cine hyperbare et subaquatique. Université de Lille II,
Session de la Réunion, 03 mars 2010.
4. Levêque Y. Risques naturels des récifs coralliens de
l’archipel des Mascareignes. Thèse de doctorat en
médecine. Université de Poitiers. 2001.
5. Louis-François C, Mathoulin C, Halbswahs C, Grivois
JP, Bricaire F, Caumes E.Complications cutanées des
envenimations par poisson-pierre chez 6 voyageurs au
retour de la région maritime indo-pacique. Bul Soc
Pathol Exot. 2003;96(5):415–9.
6. Maillaud C, Maillard A.Prise en charge des envenima-
tions par poissons-pierres et autres scorpénidés. Intérêt
de l’anesthésie locorégionale JEUR. 2004;17:192–7.
22 Stonesh Necrosis
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165
Skin Necrosis fromComa Blister
MasayukiKashiwagi andShin-ichiKubo
23
23.1 Introduction
Skin lesions in forensic autopsy cases are mainly
injuries such as skin discoloration, subcutaneous
hemorrhage, and epidermal exfoliation. Pressure
ulcers are often experienced as skin necrosis. In
addition, there are many cases of death due to
sepsis caused by decubitus ulcers.
On the other hand, in forensic autopsy cases,
skin lesions may be useful to know antemortem
conditions and causes of death. A typical example is coma blister. Coma blisters, as the name
suggests, are skin lesions observed associated
with coma. Therefore, the nding of this skin
lesion at autopsy or postmortem examination
suggests that the deceased had coma prior to
death and that an overdose of sleeping pills was
the cause. Coma blisters are important skin
lesions in forensic autopsies and autopsies.
However, the details of the generating mechanism of the coma blister, such as drug eruption,
necrosis, or some other mechanism, are still
unclear.
This chapter introduces the coma blister.
In forensic autopsy cases, when there are spiloplaxia and vesicles on the body surface, those
regions are suspected as having thermal trauma
or frostbite congelation [1]. Although tradition-
ally associated with barbiturate overdose, they
can be seen in the setting of coma due to other
etiologies. The vesicles observed by Holzer in
cases of barbiturate intoxication have been
known for a long time [2].
The erythematous patches and vesicles that
are observed in coma patients, usually from an
overdose of medication, are known in the dermatology eld as coma blisters [3–5]. Recently, it
had been reported that a similar spiloplaxia and
vesicles are also observed in non-coma cases [6,
7]. Therefore, the pathogenesis of those skin
lesions is unclear. It is unknown whether the
degenerated sweat gland is a necrosis or
apoptosis.
We examined the skin lesions such as spiloplaxia and vesication histologically and immunohistochemically, observed in forensic autopsy
cases, to investigate the characteristics and pathogenesis of the coma blister. We also investigated
the histological and immunohistological characteristics of the coma blister, especially sweat
gland degeneration.
In our study, the apoptosis might be involved
in the sweat gland degenerations of coma blisters. There are not so many forensic autopsy
cases of the coma blister. Further prospective
studies would be useful to further elucidate the
underlying pathogenesis.
M. Kashiwagi · S.-i. Kubo (*)
Department of Forensic Medicine, Faculty of
Medicine, Fukuoka University, Fukuoka, Japan
e-mail: kuboshin@fukuoka-u.ac.jp
© The Author(s) 2024
L. Téot et al. (eds.), Skin Necrosis, https://doi.org/10.1007/978-3-031-60954-1_23
167
168
23.2 Case Examination
Skin samples: Skin region samples of bullae and/
or discoloration from a forensic autopsy case and
normal skin were collected from other autopsy
cases, as follows:
Case outline: A female in her 30s was caring
for her bedridden mother. One day in November,
the mother’s care manager visited their house;
however, there was no response, and none of the
doors were locked. The care manager notied the
police, and the policeman entered the house and
found the daughter dead on her back in her
bedroom. Autopsy ndings: The decedent was
159.7 cm in height and 43.0 kg in weight.
Postmortem lividity was intense on the back.
Spiloplaxia with excoriation and spiloplaxia with
a red halo were observed in the precordial region.
The spiloplaxia with the red halo was observed in
the left femoral region. Blisters surrounded by
rims of erythema were observed in the left femoral region, the lower left thigh, and the right knee
(Fig. 23.1). The blister on the right knee was
1.0 cm in diameter (Fig. 23.2). Obvious abnormalities, such as hemorrhages, were not observed
in the subcutaneous region of these wounds. Five
hundred and fty milliliters of urine had been
collected in the bladder. There was no fatal
M. Kashiwagi and S.-i. Kubo
Fig. 23.2 Blister surrounded by rims of erythema on the
right knee
trauma or disease observed. Autopsy also
revealed that postmortem interval (PMI) was suspected for 4days.
Toxicological analysis: Caffeine, ibuprofen,
bromovalerylurea, bromoisovaleric acid, and ethoxybenzoic acid were detected in the blood.
Caffeine, ibuprofen, bromovalerylurea, ethenzamide, ethoxybenzoic acid, and salicylamide were
detected in the urine. Quantitative analysis
revealed that ibuprofen, bromovalerylurea, and
caffeine were 26, 11, and 52μg/g in the blood,
respectively.
Fig. 23.1 Blisters surrounded by rims of erythema were
observed in the left femoral region, the lower left thigh,
and the right knee
23.2.1 Immunohistochemical
Examinations
Histological and immunohistochemical examinations of the skin lesions were performed. The
samples were xed in 10% phosphate-buffered
23 Skin Necrosis fromComa Blister
Table 23.1 Immunoreactivities in the degenerated sweat
glands
Antigens Lesion Control
Inammatory cell markers
CD3
CD8
CD45RO +
Keratin markers
CK-W + +
CK-H + +
CK-L ± +
Stress markers
HSP70
Fig. 23.3 In the secretory cells of the eccrine sweat
glands, eosinophilic homogenization of the cytoplasm and
pyknosis or absence of nuclei were observed (right knee).
Length of bar indicates 50μm
Ub
ORP150
Apoptosis markers
M30 +
TUNEL
formalin and embedded in parafn. Sections of
4μm thickness were stained with hematoxylineosin (HE). Immunohistochemically, CD3
(Dako, Japan); CD8 (Leica Microsystems,
Germany); CD45RO (Dako, Japan); Cytokeratin,
triphosphate nick end labeling (TUNEL) method
with ApopTag peroxidase in situ Apoptosis
Detection Kit (Takara Bio Inc., Japan), also
according to the manufacturer’s instructions.
Wide Spectrum Screening (CK-W) (Dako,
Japan); Cytokeratin, High Molecular Weight
(keratin 34βE12) (CK-H) (Dako, Japan);
Cytokeratin 8, Low Molecular Weight (CK-L)
(Dako, Japan); 70 kD heat-shock protein (HSP70)
(Amersham, USA); ubiquitin (Ub) (DAKO,
Japan); 150 kD oxygen-regulated protein
(ORP150) (Abcom, UK); and caspase-cleaved
keratin 18 neo-epitope M30 (M30) (Previa AB,
Sweden) were observed using a labeled streptavidin biotin (LSAB)/horseradish peroxidase (HRP)
technique (Histone SAB-PO kit, Nichirei,
Japan), following the manufacturer’s instructions. Staining specicity was checked using
negative control slides omitting the primary antibody. Additionally, tissue specimens other than
positive control tissues were used in a negative
control study. To detect the apoptosis, skin samples were stained by the terminal deoxynucleotidyl transferase-mediated deoxyuridine
from the right knee showed necrosed keratinocytes and the epidermis was thin in some areas.
Subepidermal vesicles were observed in the blister. In the secretory cells of the eccrine sweat
glands, eosinophilic homogenization of the cytoplasm and pyknosis or absence of nuclei were
observed (Fig.23.3). Summary of the immunoreactivities in the degenerated sweat glands is
shown in Table 23.1. The degenerated sweat
glands showed good immunoreactivities for
CK-W and CK-H just like the control. However,
the typical immunoreactivity for CK-L decreased
(Figs. 23.4). Weak CD45RO immunoreactivity
was observed (Fig.23.5). However, no immunoreactivities for HSP70, Ub, or ORP 150 were
observed. Further, apoptosis was not detected by
the TUNEL method. Otherwise, mild degenerated sweat glands showed partial M30 immunoreactivity (Fig.23.6).
169
− −
− −
−
− −
− −
− −
−
− −
Histological examination of the skin lesions
170
M. Kashiwagi and S.-i. Kubo
CK-W
Fig. 23.5 The degenerated eccrine sweat glands showed
weak CD45RO immunoreactivity (right knee). Length of
bar indicates 50μm
CK-H
CK-L
Fig. 23.4 The degenerated sweat glands showed good
immunoreactivities for CK-W and CK-H just like the control, but decreased the typical immunoreactivity for CK-L
Fig. 23.6 The mild degenerated sweat glands showed
partial M30 immunoreactivity (chest). Length of bar indicates 50μm
23.3 Features ofComa Blister
Skin blisters with underlying sweat gland necrosis
were rst reported by Larrey in 1812 occurring in
comatose patients after carbon monoxide intoxication [8]. Since then, most previously reported