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Pseudo Subarachnoid Hemorrhage in Meningeal Leukemia

2012, The Journal of Emergency Medicine

The Journal of Emergency Medicine, Vol. 42, No. 5, pp. e109 – e111, 2012 Copyright © 2012 Elsevier Inc. Printed in the USA. All rights reserved 0736-4679/$–see front matter doi:10.1016/j.jemermed.2010.04.006 Visual Diagnosis in Emergency Medicine PSEUDO SUBARACHNOID HEMORRHAGE IN MENINGEAL LEUKEMIA Sun-Wung Hsieh, MD,*†‡ Gim-Thean Khor, MD,* Chau-Nee Chen, MD,§ and Poyin Huang, MD* *Department of Neurology, Kaohsiung Medical University Hospital, and †Department of Master’s Program in Neurology, Faculty of Medicine, College of Medicine, Kaohsiung Medical University, Kaohsiung, Taiwan, ‡Department of Neurology, Fooyin University Hospital, Pingtung, Taiwan, and §Division of Neurology, Department of Internal Medicine, Yuan’s General Hospital, Kaohsiung, Taiwan Reprint Address: Poyin Huang, MD, Department of Neurology, Kaohsiung Medical University Chung-Ho Memorial Hospital, No. 100, Tzyou 1st Road, Kaohsiung 807, Taiwan delirium. The patient was admitted to our Neurological Intensive Care Unit (NICU) for further management of SAH. During hospitalization at NICU, brain computed tomographic angiography (CTA) was arranged, but it failed to demonstrate aneurysms or vascular malformations causing relapsing SAH. This patient had neither meningism nor fever. Although SAH was suspected initially, the atypical clinical presentation and negative results in CTA raised suspicion of the diagnosis. Thus, brain magnetic resonance imaging (MRI) and cerebrospinal fluid (CSF) studies were obtained. Brain MRI revealed signal hypointensities along the sulci of bilateral temporal and parietal lobes on fluid-attenuated inversion-recovery (FLAIR) images and T2-weighted images (Figure 1, C and D). Post-enhanced T1-weighted FLAIR images showed hyperintensities along the sulci of bilateral temporal and parietal lobes (Figure 1E). CSF studies were performed on days 2 and 5 during hospitalization, and both revealed lymphocytic pleocytosis (92 cells/uL, 98% lymphocytes and 230 cells/uL, 99% lymphocytes, respectively), elevated protein (139.4 mg/dL and 152.0 mg/dL, respectively), and normal sugar (69 mg/dL and 78 mg/dL, respectively). The CSF was clear without appearance of xanthochromia, and no blood was detected in these two studies. CSF cytology showed plenty of blast cells with a very high nuclear/cytoplasmic ratio (Figure 2). Thus, SAH was reasonably excluded INTRODUCTION The characteristic finding of subarachnoid hemorrhage (SAH) is the increased attenuation in the basal cisterns and subarachnoid spaces on brain computed tomography (CT) scan. The appearance of SAH in imaging without true subarachnoid blood has become known as pseudoSAH and it often leads to misdiagnosis initially. Here we report a case of pseudo-SAH in a patient with meningeal leukemia. CASE REPORT A 68-year-old man was sent to our Emergency Department (ED) due to delirium. He had past history of acute myeloid leukemia (AML-M3) and was under treatment. Before this event, he had been admitted twice for the same clinical presentation of acute confusion state (10 months and 4 months before this admission) with the diagnosis of SAH on the basis of imaging finding. This time, SAH was impressed again by emergent brain CT scan, which demonstrated bilateral subarachnoid spaces filling with faint hyperdensities (Figure 1, A and B). There was no head injury, nor fever in this patient. Vital signs were also stable. The laboratory data, including complete blood count and blood biochemistry profiles, were all within normal limits so that we could exclude concurrent infection or metabolic disturbance leading to RECEIVED: 18 August 2009; FINAL ACCEPTED: 4 April 2010 SUBMISSION RECEIVED: 14 November 2009; e109 e110 S.-W. Hsieh et al. Figure 1. (A, B) Noncontrast brain computed tomography scan showed hyperdensities along bilateral subarachnoid spaces of temporal and parietal lobes (arrow). Hypointensities along the sulci of bilateral temporal and parietal lobes were noted on fluid-attenuated inversion-recovery (FLAIR) imaging (C) and T2-weighted brain magnetic resonance imaging (MRI) (D) (arrows). These hypointensities indicated possible hemosiderin deposition. (E) Post-enhanced T1-weighted FLAIR brain MRI revealed hyperintensities covering the sulci of bilateral temporal and parietal lobes (arrow). These images suggested meningeal metastases or meningitis. and the diagnosis of meningeal leukemia was made. Although nimodipine was administered initially for prevention of vasospasm, it was discontinued later due to the complication of low blood pressure and exclusion of SAH. Consciousness level improved during hospitalization, and the patient was transferred to the hematological ward for AML. He received chemotherapy and his condition improved. Figure 2. Cerebrospinal fluid (CSF) cytology shows plenty of blast cells with a very high nuclear/cytoplasmic ratio (arrow). The diagnosis of meningeal leukemia was confirmed by CSF cytology. DISCUSSION The most common cause of SAH is rupture of the intracranial aneurysm. It is a devastating event owing to its high mortality rate and severe complications, such as rebleeding, vasospasm, hydrocephalus, cerebral edema, and seizures (1). Brain CT scan should be the first tool in establishing the diagnosis of SAH for its availability and ease of interpretation (2). It can clearly demonstrate the characteristic finding of increased attenuation in the basal cisterns and subarachnoid spaces. But imaging findings resembling SAH without true subarachnoid blood, described as pseudoSAH, may occur in some special clinical conditions. In the literature review, pseudo-SAH could be seen in patients with brain edema, contrast leakage, hypoxic encephalopathy, cerebellar infarction, polycythemia, and spontaneous intracranial hypotension (3–7). The imaging finding of post-enhanced T1-weighted FLAIR brain MRI revealed hyperintensities covering the sulci of bilateral temporal and parietal lobes. It suggested meningeal metastases or meningitis. To explain the origin of the appearance of pseudo-SAH in association with meningeal leukemia, we speculated that meningeal leukemia caused chronic oozing of the pial vessels, resulting in hemosiderin deposition. The hyperdensities on brain Pseudo-SAH in Meningeal Leukemia CT and hypointensities on T2-weighted and FLAIR brain MRI could be explained by the above speculation. CONCLUSION Hyperattenuations in the basal cistern and subarachnoid space in brain CT do not always indicate SAH. 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