SWI Pseudo-Subarachnoid Hemorrhage Sign in Hypoxic Ischemic Injury

A 14-year-old girl developed acute neuropsychiatric symptoms, such as increasing irritability, behavioral abnormalities, emotional instability, and had trouble performing her everyday activities. Her condition worsened over the next few days with episodes of confusion, agitation, and disorganized speech, prompting urgent hospital admission. Initial laboratory tests were within normal range. The cultures of cerebrospinal fluid, blood and urine showed no growth. However, the diagnosis of anti-N-methyl-D-aspartate (NMDA) receptor encephalitis was confirmed when the cerebrospinal fluid (CSF) autoimmune panel tested positive for anti-NMDA receptor antibodies. She received initial six sessions of therapeutic plasma exchange (PLEX) and started on standard first-line immunotherapy. While receiving treatment, she suffered an unanticipated cardiac arrest, attributed to the autonomic instability that can occur with NMDA receptor encephalitis. Quick and effective cardiopulmonary resuscitation (CPR) restored spontaneous circulation. However, her neurological condition remained poor after resuscitation. Magnetic resonance imaging (MRI) of the brain revealed extensive cerebral oedema, effacement of cortical sulci and basal cisterns, and loss of gray-white matter distinction. Furthermore, there were extensive blooming artefacts seen within the interhemispheric fissure, sulcal spaces, sylvian fissures and basal cisterns giving an appearance of blood within the subarachnoid spaces. However, this blooming artifact causing the pseudo-subarachnoid hemorrhage (pseudo-SAH) appearance is not due to blood. Hypoxia after events like cardiac arrest causes cerebral hypoperfusion and impaired oxygen delivery, leading to cytotoxic edema, ion pump failure and intracellular swelling.[1] As edema worsens, subarachnoid spaces compress, making superficial veins more prominent. Due to the susceptibility effects, elevated deoxyhemoglobin in these veins cause the blooming artefact on susceptibility-weighted imaging (SWI) as shown in Figure 1.[2]. This increase in deoxyhemoglobin, and vein prominence contribute to the appearance of pseudo-subarachnoid hemorrhage. This sign and its appearance have been described with CT scan.[3] This report highlights that the pseudo-SAH sign can also be seen in SWI sequence of MRI.Figure 1: MRI brain sagittal T2 Weighted image (a), axial diffusion weighted image (b), axial fluid attenuated inversion recovery (c) shows diffuse cortical swelling and hyperintensity with effacement of subarachnoid spaces and tonsillar herniation (arrow). Axial susceptibility weighted images (d-f) images show blooming within the suprasellar cisterns, sylvian fissure and interhemispheric fissure (arrowheads). This is due to increased concentration of deoxyhemoglobin within cerebral vessels giving pseudo-subarachnoid hemorrhage appearanceThe pseudo-subarachnoid hemorrhage (pseudo-SAH) sign in CT and MRI can easily be mistaken for true subarachnoid hemorrhage on the imaging especially in the acute post-arrest setting. Understanding this pattern helps clinicians avoid misdiagnosis and make the right treatment decision. Declaration of patient consent The authors certify that they have obtained all appropriate patient consent forms. In the form the patient(s) has/have given his/her/their consent for his/her/their images and other clinical information to be reported in the journal. The patients understand that their names and initials will not be published and due efforts will be made to conceal their identity, but anonymity cannot be guaranteed. Financial support and sponsorship Nil. Conflicts of interest There are no conflicts of interest.