Forensic Science, Medicine and Pathology

https://doi.org/10.1007/s12024-018-0053-0

IMAGES IN FORENSICS

An unusual case of pulmonary fat embolism following blunt trauma

Danica Cvetković 1 & Vladimir Živković 1 & Slobodan Nikolić 1

Accepted: 5 November 2018

# Springer Science+Business Media, LLC, part of Springer Nature 2018

Abstract
Fat embolism is markedly underdiagnosed, even though it is a well-known phenomenon following fractures of the long bones,
injury to subcutaneous fat tissue, rupture of a fatty liver, surgical operations on fatty tissues, septicemia, burns and barotrauma.
Forensic pathologists tend to “simplify” autopsy report conclusion in cases with multiple injuries where fat embolism and
exsanguination could be considered to be the concomitant causes of death. Herein we present a case of 24-year-old male who
was beaten with a metal rod by several persons. On admission to hospital his vital signs and laboratory findings indicated
hemorrhagic shock with gradual respiratory failure; he died 17 h after injury. On internal autopsy examination the subcutaneous
tissue of the limbs and back was severely bruised, corresponding to about 35% of the body surface area. He had fractures of
several small bones. Injuries of the internal organs were absent, there was no free blood in the body cavities, and all other autopsy
findings were unremarkable but suggestive of a significant blood loss. Microscopic examination showed a massive pulmonary fat
embolism (grade III according to Sevitt), without systemic fat embolism. The cause of death was attributed to pulmonary fat
embolism combined with severe blood loss, following extensive and severe bruising of the subcutaneous tissues and bone
fractures.

Keywords Autopsy . Fat embolism . Pulmonary fat embolism . Nonfracture-associated . Blunt trauma . Subcutaneous tissue

Case report His conscious state deteriorated gradually and he died 17 h

A 24-year-old male was intercepted by three strangers while
he was riding his scooter. They pushed him into a vehicle and
drove into the nearest woods. After beating him with a metal
rod, they left him on a city street. On admission to the hospital,
he was conscious, pale, confused, somnolent, but did not
show any other neurological signs. After diagnostic investiga-
tions, no internal organ injuries or blood effusions were found.
However, his vital signs and laboratory findings were indica-
tive of hemorrhagic shock (blood pressure 80/50 mmHg,
pulse 115/min, hemoglobin 84 g/L, erythrocyte count 2.87 ×
1012/L, hematocrit 25.6%) with gradual respiratory failure
(pH 7.28, pCO2 4.5 kPa, pO2 8.4 kPa, lactate 5.6 mmol/l).
* Slobodan Nikolić
bobanvladislav@yahoo.com; slobodan.nikolic@med.bg.ac.rs
1
Institute of Forensic Medicine, University of Belgrade – School of
Medicine, 31a Deligradska str, Belgrade 11000, Serbia
after the asault. The police found the perpetrators along with a
long, heavy metal rod in the trunk of their car matching the
description given by the victim (Fig. 1a).
An autopsy was performed the following day. On external
examination, the body was of average physique (weight
76 kg, height 181 cm) with multiple injuries: lacerations of
the head, forearms (with typical defense patterns), and lower
legs; numerous bruises, some of them with a “tramline” shape,
abrasions and skin contusions (Fig. 1b, c). There were no
petechial hemorrhages on the skin. On internal examination,
the subcutaneous tissue of the limbs and back, which
corresponded to about 35% of the body surface area (BSA),
was severely bruised (on average, the bruising was 2 cm thick;
Fig. 2), and on the left leg a traumatic avulsion of the skin and
subcutaneous fat tissue was evident (Fig. 2c). Fractures were
present of the nasal bones, one rib, the upper part of the ulnas,
the middle portion of the right fibula, and one metatarsal bone.
There was no evidence of pneumothorax. The lungs were firm
and heavy (weight 1900 g), with signs of acute respiratory
distress syndrome. The brain was edematous (weight
1500 g). No injuries were found to the internal organs and

Fig. 1 a The metal rod used by the assailants. b and c Multiple external
injuries on the victim’s body
there was no free blood in body cavities. All other autopsy
findings were unremarkable but suggestive of significant
blood loss. The foramen ovale was closed. The clinical course
and autopsy findings suggested the possibility of a fat embo-
lism. To evaluate the presence and the degree of fat embolism,
samples taken from the lungs and kidneys were stained with
Sudan III. Microscopic examination showed massive pulmo-
nary fat embolism (grade III according to Sevitt [1]; Fig. 3).
There were, however, no microscopic signs of systemic fat
embolism. Toxicological analyses were negative for both al-
cohol and psychoactive substances. The cause of death was
attributed to pulmonary fat embolism combined with severe
blood loss, following extensive and severe bruising of the
subcutaneous tissues with bone fractures.
Discussion
The topography of the victim’s injuries (mostly limbs, and
notably forearms and lower legs) indicates that the assail-
ants’ main goal was not to kill the victim, but rather to
intimidate or punish him – the background involved fraud
Forensic Sci Med Pathol
Fig. 2 Diffuse subcutaneous bruising on: a the left arm, b the right arm,
and c the left leg
and gambling. For this reason the victim presented to hos-
pital conscious, able to describe the details of the event to
the police. Although organ damage with hemorrhage was
excluded, he gradually developed signs of hemorrhagic
shock. Since there were no sources of significant external
hemorrhage, it could be concluded that he was bleeding into
the severely bruised subcutaneous tissues. Some authors
state that exsanguination into contusions in subcutaneous
fat tissue could be the cause of death, if more than 50% of
the body surface is injured (using “the rule of nine” by
Wallace) [2]. Herein, BSA of the deceased was 1.96m2
[3], and the bruised subcutaneous tissue affected about
35% of the BSA or 0.69m2; the subcutaneous hematoma
was on average 2 cm thick, which in our opinion could also
be an important factor in the estimation of blood loss. In
addition, we have to keep in mind that blood loss accom-
panies bone fractures (every fractured rib involves about
150 mL of blood [4]). The frequent use of hematocrit (and
hemoglobin concentration) to evaluate the presence and se-
verity of acute blood loss is often not appropriate [5]. On the
other hand, the changes in the pulse rate and blood pressure
that occur with acute hypovolemia have a good sensitivity-
Forensic Sci Med Pathol
Fig. 3 Histological appearance of the lungs, showing orange, drop-,
sausage-, and branching-shaped fat emboli (the most severe, grade III,
Sudan III staining) a magnification 4x. b magnification 10x
specificity ratio when estimating severe blood loss [6]. A
loss of 30–40% of the blood volume (20–30 mL/kg [7])
causes a measurable decrease in systolic blood pressure,
because peripheral vasoconstriction fails to compensate for
the increasing loss [4]; clinical consequences can include
supine hypotension, evidence of impaired organ perfusion
(e.g. cool extremities, oliguria, depressed consciousness),
and evidence of anaerobic metabolism (i.e. lactate accumu-
lation in the blood) [8]. This clinical course corresponds to
the one described in this case (before resuscitative measure-
ments were taken), and if the weight of the deceased is taken
into account, it could be concluded that he lost approximate-
ly 1.5–2.25 l of blood. Still, he did not die only because of
the severe blood loss.
For fat to appear in the bloodstream, three conditions
must be fulfilled: 1) damage to fat tissue stores (e.g. frac-
ture of a long bone or subcutaneous bruising; 20-30 g of
fat can result in a fatal embolism); 2) rupture of surround-
ing veins; 3) increase in the local interstitial tissue pres-
sure, which allows fat globules to access the circulation
[4, 9–11]. Veins within the marrow cavity are held apart
by their osseous attachments, allowing fat globules to en-
ter with relative ease [11], while the veins in the subcuta-
neous tissues tend to collapse. Therefore, fat embolism
following bone fractures is more frequent and clinically
more severe [11–13]. Herein, massive contusion of subcu-
taneous fat tissues and fractures of smaller bones were
evident reservoirs of fat globules. Only a short period of
cardiac pumping is required to move a droplet of fat from
any part of the body into the pulmonary circulation [7]. In
this case, tachycardia occurred due to concomitant blood
loss, speeding up fat dissemination.
There is usually a delay between trauma and cerebral
fat embolism while fat builds up in the lungs, so that a
“lucid interval” occurs, which in polytraumatized pa-
tients may be confused with the development of an
extradural or subdural hemorrhage [7]. Some authors
suggest that the presence of a patent foramen ovale
(PFO) is a risk factor for developing more severe man-
ifestations of FES [14], while others argue that the pres-
ence of PFO associated with a systemic fat embolism
(SFE) should be less emphasized and propose that arte-
riovenous shunts and anastomosis between the function-
al and nutritive circulation of lungs play a more impor-
tant role in developing SFE [15]. In this case, the fora-
men ovale was closed and fat globules were not detect-
ed in the kidneys. Under the normal conditions of ho-
meostasis, shunts between the bronchial and pulmonary
arteries are the cause of a small right-to-left leakage (up
to 5%) [16]. We can assume that the flow through these
anastomoses became even greater during the initial stage
of hypovolemic shock, as some authors propose [16].
However, this was not enough to cause systemic dis-
semination in the presented case, probably due to a
short period from injuring to death.
In cases of blunt trauma injury without bone fracture,
when a significant area of subcutaneous tissues has been
involved and other autopsy findings are unremarkable,
fat embolism should be regarded as the possible cause
of death. Careful analysis of medical documentation is
important (if available), while microscopic examination
with the use of special staining for oil (e.g. Sudan III)
is essential.
Funding This work was supported by the Ministry of Science of the
Republic of Serbia, Grant No. 45005.
Compliance with ethical standards
Conflict of interest The authors hereby declare that they have no con-
flict of interest. The paper has been presented as poster presentation (P6)
at 26th Alpe-Adria-Pannonia International meeting on Forensic Medicine
that has been held in Pula, Croatia, from 30 May until 02 June 2018.
Ethical approval This article does not contain any studies with human
participants or animals performed by any of the authors.

References
1. Sevitt S. Fat embolism in patients with fractured hips. Br Med J.
1972;2:257–62.
2. Hiss J, Kahana T, Kugel C. Beaten to death: why do they die? J
Trauma. 1996;40:27–30.
3. Mosteller RD. Simplified calculation of body-surface area. N Engl J
Med. 1987;317:1098.
4. Madea B. Handbook of forensic medicine. Chichester: Wiley
Blackwell; 2014.
5. Marino P. The ICU book. 4th ed. Philadelphia: Wolters Kluwer
Health/Lippincott Williams & Wilkins; 2014.
6. Sinert R, Spektor M. Clinical assessment of hypovolemia. Ann
Emerg Med. 2005;45:327–9.
7. Saukko P, Knight B. Knight’s forensic pathology. 4th ed. Boca
Raton: CRC Press; 2016.
8. American College of Surgeons. Advanced trauma life support man-
ual. 7th ed. Chicago: American College of Surgeons; 2004.
9. Li S, Zou D, Qin Z, Liu N, Zhang J, Li Z, et al. Nonfracture-
associated pulmonary fat embolism after blunt force fatality: case
Forensic Sci Med Pathol
report and review of the literature. Am J Forensic Med Pathol.
2015;36:61–5.
10. Levy D. The fat embolism syndrome. Clin Orthop Relat Res.
1990;261:281–6.
11. Hulman G. The pathogenesis of fat embolism. J Pathol. 1995;176:3–9.
12. Nikolić S, Micić J, Savić S, Gajić M. Factors that could influence
the severity of post-traumatic lung fat embolism – a prospective
histological study. Srp Arh Celok Lek. 2003;131:244–8.
13. Nikolić S, Micić J, Savić S, Uzelac-Belovski Z. Post-traumatic
pulmonary and systemic fat embolism in forensic practice – a pro-
spective histological study. Srp Arh Celok Lek. 2000;128:90–3.
14. Riding G, Daly K, Hutchinson S, et al. Paradoxical cerebral embo-
lisation. An explanation for fat embolism syndrome. J Bone Joint
Surg. 2004;86:95–8.
15. Nikolić S, Zivković V, Babić D, Djonić D, Djurić M. Systemic fat
embolism and the patent foramen ovale – a prospective autopsy
study. Injury. 2012;43:608–12.
16. Barzdo M, Berent J, Markuszewski L, Szram S. A coronary
artery crossed embolism of bone-marrow origin: proof of
connections between pulmonary arteries and veins. Forensic
Sci Int. 2005;49:47–50.