An Unusual Cause of Fat Embolism Syndrome

Xavier Repesse, M.D.,* Laurent Bodson, M.D.,* Siu Ming Au, M.D.,* Bernard Page, M.D.,
Jean-Francois Cote, M.D., Ph.D., Cristi Marin, M.D., Mostafa El Hajjam, M.D.,
Cyril Charron, M.D., Antoine Vieillard-Baron, M.D., Ph.D.#

beats/min, respiratory rate was 25 per min, vesicular

breathing was abolished in the left lung field, oxygen
saturation was 98% with oxygen therapy of 6 l/min, and
Glasgow Coma Scale score was 14. Auscultation was consistent with the diagnosis of pneumothorax. There was no
external bleeding or circulatory instability. Chest radiograph revealed a left hemopneumothorax due to five rib
fractures without thoracic outlet, and a left clavicle fracture (fig. 1). Body scan showed a left pulmonary contusion and a right piriform muscle hematoma. No other
visceral or vascular lesion was noted. Brain computed tomography scan was normal. Hemoglobin concentration
at admission was 11.8 g/dL. Coagulation was normal and
platelet count was 202,000/mm3. Otherwise, the patient
presented with minor liver cytolysis (twice normal) and a
moderate increase in creatine kinase (277 U/L). The hemopneumothorax was safely drained with a 24 French
tube in the intensive care unit where the patient was then
followed up. Six hours after admission, she suddenly lost
consciousness (Glasgow Coma Scale score 3) and became
hypoxemic, requiring mechanical ventilation with a high
amount of oxygen. The patients hemodynamics remained normal. Her chest radiograph showed diffuse alveolar-interstitial infiltrates. Bronchoalveolar lavage fluid
revealed a high amount of lipid-laden macrophage-like
cells (47%) showing Oil red O staining with red intracellular lipid droplets (fig. 2). At the same time, the patients
platelet count fell to 62,000/mm3. Body temperature was
38.4C in the 4 h after the neurologic degradation. Brain
magnetic resonance imaging showed multiple cerebral
emboli on a diffusion-weighted sequence without abnormality on a T2 gradient echo sequence, attesting to the
absence of hemorrhagic axonal injury (fig. 3). Transesophageal echocardiography with bubble contrast demonstrated no evidence of a patent foramen ovale. No left
atrial thrombosis was found. Ocular fundus findings were
normal. Despite the initial severe neurologic presentation, the patient started to recover progressively 1 month
after admission and was transferred to a rehabilitation
center. Two months after transfer the patient had recovered the ability to walk with a cane. The patient was
oriented to time and location when last examined.

AT embolism syndrome (FES) is a combination of

respiratory, neurologic, cutaneous, and hematologic
symptoms associated with physical trauma to fat tissue
secondary to bone fracture or to medical or surgical softtissue injury.1 4 The incidence in patients with bone fractures is usually reported as low (0.510%),4 but can reach
more than 30%.2,5 Diagnosis is based on major or minor criteria
historically described by Gurd and Wilson.6 We report the case of a
67-yr-old female polytrauma patient who developed FES secondary to unusual bone fractures.

CASE REPORTS
A 67-yr-old woman was admitted to our intensive care
unit because of polytrauma after high-speed injury. Despite an initial loss of consciousness, neurologic findings
were normal on arrival. First clinical findings revealed left
thoracic trauma and clavicle fracture. Heart rate was 81

* Resident Head, Intensive Care Unit, Section Thorax-Vascular Disease-Abdomen-Metabolism, University Hospital Ambroise Pare, Assistance Publique-Hopitaux de Paris, Faculty of Medicine, Paris Ile-deFrance Ouest, University of Versailles Saint-Quentin en Yvelines,
France. Assistant Senior, Intensive Care Unit, Section Thorax-Vascular
Disease-Abdomen-Metabolism, University Hospital Ambroise Pare, Assistance Publique-Hopitaux de Paris. Assistant Senior, Faculty of Medicine, Paris Ile-de-France Ouest, University of Versailles Saint-Quentin
en Yvelines, Department of Anatomic Pathology, University Hospital
Ambroise Pare, Assistance Publique-Hopitaux de Paris, France. Assistant Senior, Department of Anatomic Pathology, University Hospital
Ambroise Pare, Assistance Publique-Hopitaux de Paris. Assistant Senior, Radiology Department, University Hospital Ambroise Pare, Assistance Publique-Hopitaux de Paris. # Professor, Intensive Care Unit,
Section Thorax-Vascular Disease-Abdomen-Metabolism, University
Hospital Ambroise Pare, Assistance Publique-Hopitaux de Paris, Faculty of Medicine, Paris Ile-de-France Ouest, University of Versailles
Saint-Quentin en Yvelines.
Received from the Intensive Care Unit, Section Thorax-Vascular Disease-Abdomen-Metabolism, University Hospital Ambroise Pare, Assistance Publique-Hopitaux de Paris. Submitted
for publication January 11, 2012. Accepted for publication April
11, 2012. Support was provided solely from institutional and/or
departmental sources.
Address correspondence to Dr. Repesse: Intensive Care
Unit, Section Thorax-Vascular Disease-Abdomen-Metabolism,
University Hospital Ambroise Pare, 9, Avenue Charles-de-Gaulle
92100 Boulogne-Billancourt. xavier.repesse@apr.aphp.fr. Information on purchasing reprints may be found at www.anesthesiology.org or on the masthead page at the beginning of this
issue. ANESTHESIOLOGYs articles are made freely accessible to all
readers, for personal use only, 6 months from the cover date of
the issue.

Discussion
The combination of neurologic signs confirmed by imaging,
respiratory symptoms with alveolar-interstitial infiltrate and
hypoxemia, thrombocytopenia, and a high amount of
lipid-laden macrophages in bronchoalveolar lavage fluid7

Copyright 2012, the American Society of Anesthesiologists, Inc. Lippincott

Williams & Wilkins. Anesthesiology 2012; 117:216 8

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EDUCATION

Fig. 1. Immediate chest x-ray after drainage showing

pulmonary infiltrates, secondary to fat embolism syndrome.

led us to the diagnosis of FES. The only missing symptom

was petechiae, which are absent in more than 40% of cases
of FES.13 FES is a rare complication of bone fractures
and soft tissue injury, generally associated with long bone
fractures1 4 and sometimes also caused by multiple fractures.2,3 In our case, FES was a quite unexpected complication of isolated rib and clavicle fractures. The absence of
patent foramen ovale in the current case, as well as in most
published studies,8 raises the key issue of the pathophysiology of FES. Explanations described thus far remain controversial and include the infloating theory, which holds
that high pressure on fat tissue leads to lipid embolism in
the systemic circulation via a transient patent foramen
ovale; the lipase theory, according to which lipid stores
could be saponified before embolizing; the free fatty acid
theory, in which these toxic molecules create vasculitis;
the coagulation theory, in which a procoagulant state is
generated by the contact of bone marrow fat with platelets; and the systemic embolization theory, which argues

Fig. 3. Brain magnetic resonance imaging. Disseminated

high-signal spots in a diffusion-weighted sequence secondary to fat embolism (A). Normal T2 gradient echo sequence excluding hemorrhagic axonal injury (B; same level
as A).

that the combination of the deformability of fat emboli

with the rise in pulmonary arterial blood pressure forces
the fat globules through the pulmonary capillary bed.3 In
the current case, one possible mechanism could be the
passage of fat droplets directly from bone marrow to injured pulmonary veins. The clinical improvement of our
patient despite the severe initial presentation illustrates
the potentially good prognosis of cerebrovascular accidents caused by fat embolism.

Conclusion
FES without long bone fracture is an authentic clinical
entity that should be considered in patients with polytrauma and soft-tissue injury or multiple fractures. This
case report highlights an unexpected complication
of rib and clavicle fractures. It also reemphasizes the
value of complementary examinations, such as magnetic
resonance imaging, bronchoalveolar lavage, and ocular
fundus examination, in typical presentations or in sudden
neurologic or respiratory distress without clear explanation. Physicians ought to be aware of such a complication
even in the absence of patent foramen ovale and of its
potential resolution even if the presentation is initially
severe.

Fig. 2. Bronchoalveolar lavage fluid. Oil Red O staining shows

high concentration of lipid-laden macrophages (47%) with
red intracellular lipid droplets.
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Repesse et al.

Case Reports

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The Boston Posts Obituary of Oliver Wendell Holmes, Sr.

Physician Oliver Wendell Holmes, Sr. (1809 1894) is widely regarded as one of Americas leading authors
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