Publication

Encephalopathy in traumatic fat embolism syndrome

Journal Paper/Review - Oct 24, 2009

Units
Keywords
encephalopathy, stroke, fat embolism syndrome, trauma

Citation
Burkhardt C. Encephalopathy in traumatic fat embolism syndrome. S C H W E I Z E R A R C H I V F Ü R N E U R O L O G I E U N D P S Y C H I A T R I E 2009; 2009:162-169.
Type
Journal Paper/Review (Deutsch)
Journal
S C H W E I Z E R A R C H I V F Ü R N E U R O L O G I E U N D P S Y C H I A T R I E 2009; 2009
Publication Date
Oct 24, 2009
Pages
162-169
Brief description/objective

We describe a case of cerebral fat embolism
in a young man following a traumatic fracture
of the lower limb with symptoms of hypoxia
and an organic psycho-syndrome.
A previously healthy 20-year-old man
was admitted to the hospital with a closed
and undislocated fracture of the tibia and
fibula after a skiing accident and treated
conservatively by applying an above-knee
cast and analgetics. He was referred to us
one day later due to bilateral blindness. On
admission the patient was fully conscious, well
oriented with stable vital parameters, neurological
examination was completely normal
apart from the reported bilateral amaurosis.
After 2 h of admission he became irritable,
confused, was not obeying commands, showed
episodes of tachycardia and started to
desaturate (O2 saturation below 80%). He
was put on oxygen supplementation via facemask,
which improved his saturation. EEG
showed intermittent rhythmic delta activities
(IRDAs) and a diffuse slowing as an
unspecific sign of a cerebral dysfunction. Diffusion-
weighted brain imaging revealed multiple
bihemispheric hyperintense white-matter
lesions resembling a “starfield pattern”.
No petechial rash was seen. Blood tests, including
haemoglobin and platelet levels,
extra- and intracranial Doppler sonography
and transthoracic echocardiography gave
normal results.
During the next days the patient slowly
recovered from the state of confusion and
oxygen saturation reached normal levels.
Vision also became normal again.A follow-up
MRI 3 months after discharge showed postischaemic
border zone lesions without signs
of acute infarction.