Pseudo-subarachnoid Hemorrhage Sign

CLINICAL DESCRIPTION OF THE CASE

A 34-year-old male with past medical history of drug abuse was admitted secondary to a cardiac arrest following heroin overdose. Paramedics on arrival gave intranasal Narcan, and cardiopulmonary resuscitation was initiated. The down time was unknown as the patient was found alone without any family around. The patient reportedly was in pulseless electrical arrest. In the field, patient was intubated emergently and did receive multiple doses of epinephrine. Computerized tomography (CT) head done following admission showed diffuse cerebral edema with loss of gray-white differentiation along with effacement of ventricles and basal cisterns with crowding of posterior fossa along with pseudo-subarachnoid hemorrhage (SAH) sign [Figure 1]. The Hounsfield units (HU) of the pseudo-SAH area was 32 HU while the surrounding brain parenchyma was 44 HU. On examination, the patient was comatose, pupils were 4 mm fixed not reacting to light, and the patient did not have any protective brainstem reflexes such as gag, corneal, or conjunctival reflexes, but he had spontaneous respiratory drive when switched to continuous positive airway pressure mode on the ventilator. The patient eventually became brain dead within 48 h of the event which was also confirmed by a positive apnea test.

Figure 1.

Computerized tomography scan head showing diffuse axonal injury with cerebral edema following cardiac arrest with pseudo-subarachnoid hemorrhage sign

DISCUSSION

SAH-like findings were first described by Spiegel et al. in 1986.[1] Avrahami et al. had initially proposed the term pseudo-SAH sign in 1998.[2] Yuzawa et al. reported that the incidence of pseudo-SAH in patients with traumatic cardiac arrest was 20%.[3] Pseudo-SAH sign is thought to result from basal cistern effacement associated with engorgement of the venous structures with adjacent brain hypoattenuation increasing the contrast difference.

Lee et al. recently reported that the prevalence of pseudo-SAH sign was about 8% in their study population.[4] The authors also concluded that pseudo-SAH occurred more commonly seen in unwitnessed asystole arrest as occurred in our case. Given et al. reviewed seven cases of generalized cerebral edema accompanied by increased basal cisternal attenuation but none of those patients had true SAH on lumbar puncture or autopsy.[5] It has been shown in the studies that pseudo-SAH sign correlates with extremely poor prognostic outcome.[3,4]

The most common cause of pseudo-SAH sign is anoxic brain injury secondary to cardiopulmonary arrest. In anoxic brain injury, there is diffuse cerebral edema which leads to loss of gray-white differentiation. Pseudo-SAH sign results from basal cistern effacement, increased intracranial pressure as well as engorgement of the superficial venous structures. The increased intracranial pressure associated with diffuse cerebral edema in anoxic brain injury as well as seen in other causes as discussed below leads to engorgement and dilatation of the superficial venous structures.[6] This leaves the subarachnoid space devoid of cerebrospinal fluid that would normally lead to hypoattenuation; but instead, there is increased fraction of meninges and dilated blood vessels that leads to higher attenuation areas on the CT head, but due to dilated vessels, the attenuation value decreases. And also, attenuation of the brain parenchyma decreases with the development of cerebral edema.[7]

Other causes of pseudo-SAH sign could include severe meningitis, venous sinus thrombosis, bilateral large subdural hemorrhage, and intrathecal contrast. In true SAH, there is higher attenuation of the basal cisterns. The attenuation value of blood in the CT head in a healthy individual corresponds to the normal hematocrit of 45% and is around 42 HU.[8] In true SAH, the blood that has leaked from the vessel or formed a hematoma has a higher attenuation value due to the absorption of plasma and has higher attenuation values ranging between 60 and 70 HU. However, in pseudo-SAH, the attenuation values within the basal cistern range between 30 and 40 HU due to the speculation that the finding reflects dilated vessels rather vasculature rupture as seen in true SAH.[9] Higher attenuation of the falx and tentorium can also be seen in association with cerebral edema.[10] These lower attenuation values, in association with signs of diffuse cerebral edema, should permit the prospective recognition of pseudo-SAH to avoid more invasive testing which given the grave prognosis might turn out to be cost-effective. Furthermore, awareness of pseudo-SAH sign will help avoid over investigation of such critical patients as possible SAH.

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Conflicts of interest

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