A Mexican male in his mid-30s with a past medical history of atrial septal defect presented with sudden onset of left lower extremity weakness and a two-week history of fever, headache, and purulent rhinorrhea. On examination, his only neurological deficit was mild weakness in his left lower extremity. CT head showed two right frontal hypodense lesions with surrounding edema, mass effect and subfalcine herniation.  Given recent sinusitis and the radiologic features described above, cerebral abscess was considered as the most likely diagnosis.

He was started on broad-spectrum antimicrobials and steroids. However, the next day, he suddenly deteriorated losing all cortical and brainstem function. Measures for intracranial pressure control were started without improvement. MRI showed ring enhancement of the lesions but no new herniation. He had no improvement in examination, and the next day a cerebral perfusion study revealed no perfusion. He was pronounced brain dead.

Autopsy confirmed the presence of two abscesses, with the most anterior extending to the superficial surface of the frontal lobe. Exudate was found in the subarachnoid space resulting in meningeal inflammation. Given no worsening of mass effect, herniation, or evidence of rupture into intraventricular space, rupture of abscess into subarachnoid space was considered the cause of deterioration and brain death. 

Although rare, this complication has been described before. He was not immunosuppressed, but his sinusitis and atrial septal defect predisposed him to cerebral abscess by local spread and paradoxical embolism, respectively.  Little is known about risk factors for rupture into the subarachnoid space, but multiloculation and proximity to the ventricles increase risk for intraventricular rupture. Further research should be done to see if these factors influence the risk of rupture into the subarachnoid space and to determine what patients are at risk for this complication to facilitate early medical and surgical treatment.