Posttraumatic subarachnoid fat embolism: Case presentation and literature review

Abstract

Fat embolism in the subarachnoid space has a unique pathophysiology and clinical picture when compared to fat embolism syndrome. Lipid deposits in the subarachnoid space—most commonly the sequela of dermoid rupture in the neuraxis—can cause an inflammatory reaction leading to irritation of nearby neurovascular structures. Herein, we report the only case in the United States, to our knowledge, of a patient diagnosed with subarachnoid fat emboli secondary to sacral fracture who initially presented with a normal head CT and subsequently developed visual changes.

1. Introduction

Fat embolism (FE) occurs when fat globules enter the systemic microvasculature, a phenomena that typically follows either (1) a traumatic event, most commonly after fracture of long bones or pelvis, and certain elective and emergency orthopedic surgeries [1]; or (2) a stress-inducing event (e.g. acute pancreatitis, diabetes mellitus, liposuction, bone marrow transplantation, sickle cell disease, osteomyelitis, and corticosteroid administration) [2–6] leading to hormonal changes and subsequent degradation and release of free fatty acids from the bone marrow causing an inflammatory reaction [7,8]. Moreover, fat embolism syndrome (FES), although relatively rare with an incidence between 0.5 and 11% in long bone fractures and up to 30% in bilateral femoral fractures [9], occurs 12–72 h following such events and typically presents as three major clinical manifestations: petechial rash, respiratory symptoms, and/or central nervous system (CNS) signs [10–12]. Fat emboli reaching the cerebral cortex, via either right-to-left cardiac shunting (e.g. patent foramen ovale) or through an intact pulmonary capillary bed [7], results in cerebral fat embolism syndrome which can present with headache, confusion, focal neurological deficits, seizure, abnormal posturing, mental status change, or coma [7,13–15].

Subarachnoid fat embolism (SFE) is another subtype of FES affecting the CNS. Although this is most commonly related to rupture of a dermoid cyst in the neuraxis, a much less common cause is breach of the dura adjacent to a fracture; thereby, conceding bone marrow to enter the thecal sac [16]. SFE can also incite an inflammatory reaction, leading to irritation of neurovascular structures, hydrocephalus, aseptic meningitis, meningeal calcifications, and seizures [16–21]. Herein, we report the only case in the United States, to our knowledge, of a patient with SFE secondary to sacral fracture who initially presented with a normal head CT and subsequently developed visual changes possibly due to irritation by the suprasellar fat droplets adjacent to the optic chiasm.

2. Case report

An 86-year-old female was brought to the emergency department after an unwitnessed fall and complained of parieto-occipital and back pain. Although her Glasgow Coma Scale was 15 on admission, the history was obscured by the patient’s inability to recall the event. Her physical examination was remarkable for abrasions and a small posterior scalp hematoma. Initial CT of the head without contrast (Fig. 1a) showed no acute intracranial abnormality.

Fig. 1.

A Initial admission axial noncontrast head CT demonstrates no acute intracranial abnormality or fat droplets within the subarachnoid space. Note, the air under the right eyelid projecting into the orbit and the air in the frontal sinus should not be misdiagnosed as fat droplets. B and C Two days later, axial and sagittal noncontrast head CT demonstrates foci of macroscopic fat (arrows) within the subarachnoid space, including the suprasellar cistern and anterior interhemispheric fissure, consistent with SFE.

Two days after admission, the patient described a sensation of episodic whitening and curtaining in her left visual field. A repeat head CT without contrast was performed and demonstrated several new foci of fat density within the subarachnoid space, including the suprasellar cistern and middle cerebral artery and anterior interhemispheric fissures (Fig. 1b and c); moreover, there was no downward migration of the cerebellar tonsils or brainstem, obliteration of the basal cisterns, extra-axial collection, or ventricular collapse. The patient’s admission pelvic radiograph was reassessed for a possible explanation of SFE, but no obvious fracture could be identified. Ophthalmology was also consulted, and bedside examination showed age-related macular degeneration bilaterally. Based on these findings and continued back pain on physical exam, a CT of the lumbar spine and pelvis were recommended to evaluate for a radiographically-occult fracture; ultimately, an acute S3 vertebral body fracture with extension to the right sacral ala was diagnosed (Fig. 2) but did not require surgical intervention. The patient was subsequently discharged to a skilled nursing facility with neuro-ophthalmology and orthopedic surgery follow-up.

Fig. 2.

A Coronal and B reformatted images of the lower lumbar spine and pelvis, scanned in the supine position, demonstrate fractures (arrowheads) of S3 and the right sacral ala with nearby sacral perineural, so-called Tarlov, cysts (labeled “T”).

3. Discussion

SFE most frequently occurs after spontaneous rupture of a dermoid cyst/teratoma or surgical manipulation of the neuraxis [20]; trauma, as in our case, is a less commonly reported cause of SFE in the literature. It is understandable that our patient initially presented with a normal head CT, as the bone marrow likely attained entry via the sacral fracture with presumed dural violation with subsequent embolization to the cranial portion of the subarachnoid space via retrograde migration through the foramen magnum secondary to head position changes and CSF pulsations following trauma [21]. Our patient also had sacral perineural (so-called Tarlov) cysts, which are considered “extradural meningeal cysts with nerve root fibers” which may have connections to the subarachnoid space [22,23] and contribute to the development of SFE.

SFE can be easily diagnosed with noncontrast CT or MRI of the brain demonstrating foci of macroscopic fat within the subarachnoid space. Although CT is most often the initial imaging modality in trauma patients given its speed and availability, MRI has the advantage of also demonstrating potential concomitant cerebral FES with imaging findings including the starfield pattern on diffusion weighted imaging [24–26].

If FES—which may encompass SFE—is suspected, certain preventative measures can be implemented such as the administration of methylprednisolone, aspirin, albumin for volume resuscitation, and oxygen therapy [6,27,28] to decrease long-term neurological damage, while early surgical fixation of long-bone fractures may reduce FES severity; however, the mainstay of treatment involves support and lipid soluble drugs. Of note, symptoms caused by SFE—such as headache from hydrocephalus, focal neurological deficits, altered mental status, and seizures—can be transient with complete return to baseline [18].

In conclusion, this case highlights the importance of recognizing macroscopic fat droplets in the subarachnoid space, and this finding should raise clinical suspicion for the possibility of an axial skeleton fracture—that may be radiographically occult—in the setting of recent trauma.