A unique complication of autologous fat graft migration

A 70-year-old man with a right vestibular schwannoma underwent right retrosigmoid craniotomy and excision of the lesion. He later developed paradoxical CSF rhinorrhea for which right re-exploration mastoidectomy with CSF leak repair was performed. He presented with acute loss of left finger grip three months after the re-exploration surgery.

MR imaging showed fat graft in the surgical bed of right cerebello-pontine angle cistern and mastoid part of the temporal bone. Multiple rounded and ovoid extra-axial fat signal intensity globules were seen in right cerebello-pontine angle, quadrigeminal, prepontine, perimesencephalic, interpeduncular and suprasellar cisterns, anterior interhemispheric fissure, right sylvian fissure and right frontal sulcal spaces.  CT imaging also showed fat-density globules in the cerebral sulcal spaces and basal cisterns.

Acute infarcts were seen in right precentral gyrus and posterior aspect of right insular cortex extending to corona radiata involving right middle cerebral artery territory. No abnormal leptomeningeal enhancement was seen. On MR angiography, attenuated flow was seen in Sylvian segment of right middle cerebral artery at the level of fat globules and no flow was seen in distal cortical segments. Brain stem and cerebellum were normal. Ventricles were normal with no hydrocephalus or intraventricular haemorrhage.

Background

Vestibular schwannomas are typically benign, slow-growing tumours that most commonly originate from the vestibular division of the vestibulocochlear nerve sheath. The three main surgical routes employed for vestibular cranial nerve tumour resection include translabyrinthine, retrosigmoid (suboccipital) and middle cranial fossa approaches [1]. The post-surgical complications include recurrent tumour, CSF leakage, graft necrosis, infection, venous sinus thrombosis, cerebral infarction, haemorrhage, endolymphatic fluid loss, temporal lobe and cerebellar contusions [2]. CSF leaks are commonly repaired with autologous fat grafts, given less risk of infection. The complications following fat graft repair include fat necrosis, local fistula formation, sterile wound discharge, fat migration and lipoid meningitis[3].

Clinical perspective

Autologous fat graft migration is a recognized postoperative complication following skull base and lumbar spinal surgeries, causing complications such as brainstem compression, cervical cord compression, recurrent sciatica and cauda equina syndrome [4-6]. Fat products can induce vasospasm, vasculitis or cause mechanical compression of the adjacent vessel. This results in headache (the most common symptom), seizure, cerebral ischemia or aseptic meningitis [7].

Imaging perspective

Magnetic resonance imaging is the investigation of choice after resection to assess for residual or recurrent tumors and suspected complications. In the case of autologous fat graft migration, fat globules in CSF spaces appear hypodense with mean fat attenuation values on CT images. Fat globules are hyperintense on T1 and T2 sequences with signal loss on fat-saturated images on MRI. Fat necrosis appears as fragmentation of the fat graft and striated bands of fluid traversing the fat graft which is hyperintense on T2WI [2].

Outcome

Lipoid meningitis is differentiated from other forms of meningitis by delayed onset more than two weeks after surgery, allowing sufficient time for fat liquefaction. It usually follows a chronic or intermittent course taking several weeks to resolve, respond poorly to steroids, and antibiotics have no role in treatment [3].

Our patient was managed conservatively with low molecular weight heparin, anti-platelets and other supportive medications. As his condition improved, he was discharged and advised to follow up.

Take home message

Cerebral ischemia following rupture of intracranial dermoid cyst is well documented [7,8]. This is the first report of a patient with an autologous fat graft migration with secondary aseptic chemical meningitis and cerebral arterial vasospasm leading to acute infarction.  Clinicians and radiologists should be aware of this entity for early diagnosis and to prevent further complications.

‘Written informed patient consent for publication has been obtained.’