Pseudo-Subarachnoid Hemorrhage on Computed Tomography after Resuscitation from Cardiopulmonary Arrest.

A 64-year-old woman with dyspnea called the ambulance service. When an ambulance arrived at her home, she was experiencing cardiopulmonary arrest. She was resuscitated and transferred to the emergency department. Her Glasgow coma score was 3/15, and her pupils were dilated at 7 mm bilaterally. Although the immediately performed non-enhanced head computed tomography (CT) revealed no abnormalities (Fig. 1), she continued to be in a comatose state. On the second day of admission, laboratory tests revealed a markedly elevated white cell count (21,400/µL), C-reactive protein (11.72 mg/dL; reference value, <0.2 mg/dL), aspartate aminotransferase (478 U/L; reference value, 13-30 U/L), alanine aminotransferase (272 U/L; reference value, 7-23 U/L), lactate dehydrogenase (1,847 U/L; reference value, 124-222 U/L), and creatinine phosphokinase (3,212 U/L; reference value, 41-153 U/L) and follow-up non-enhanced head CT revealed diffuse brain edema, poor gray-white matter differentiation, and increased attenuation of the subarachnoid spaces (Fig. 2). Three-dimensional CT angiography was performed for excluding subarachnoid hemorrhage (SAH) due to a ruptured cerebral aneurysm, but no cerebral aneurysms were found. The patient was diagnosed with pseudo-SAH associated with anoxic encephalopathy. She did not recover from a deep coma and passed away on the eighth day of admission.

FIG. 1

Non-contrast head computed tomography (CT) on admission revealed no abnormalities.

FIG. 2

Non-contrast head CT on the second day revealed diffuse brain edema, loss of gray-white matter contrast, and increased attenuation of the subarachnoid spaces of the basal and Sylvian cisterns (arrows) and the sulci of the frontal lobes (arrowheads) with a mean CT value of 39.8 Hounsfield unit.

Pseudo-SAH might be seen on CT scans of the patients with hypoxic-ischemic brain injury. Although the mechanism for the development of pseudo-SAH has not been fully elucidated, the pseudo-SAH appearance is likely to result from a combination of low attenuation of brain parenchyma, loss of gray-white matter differentiation, narrowing and effacement of the subarachnoid spaces, and engorgement of superficial pial veins.1 Severe brain edema causes the compression of dural sinuses, the blockage of the venous drainage of the brain, and pial vein congestion.2 The differential diagnosis between pseudo-SAH and true SAH is important because of the different treatment strategies. Yuzawa et al.3 reported that the CT values of high-attenuation areas in pseudo-SAH ranged from 30 to 42 Hounsfield unit (HU) and were significantly lower than those in true SAH, in which CT attenuation values typically range from 60 to 70 HU. Another differentiating point may be the presence or absence of intraventricular high attenuation. Cerebrospinal fluid examination by lumbar puncture may be utilized to differentiate between true SAH and pseudo-SAH.4 However, this procedure is generally contraindicated in patients with severe brain edema. Pseudo-SAH is a rare neuroradiologic finding and suggests severe brain damage and a poor prognosis.5 Clinicians should be aware that recognition of pseudo-SAH is important to avoid unnecessary clinical investigations and inappropriate treatments.