Haemorrhagic conversion of infectious myelitis in an immunocompromised patient - PubMed (original) (raw)
Case Reports
Haemorrhagic conversion of infectious myelitis in an immunocompromised patient
Michael Stephen Pohlen et al. BMJ Case Rep. 2017.
Abstract
A 28-year-old man recently diagnosed with HIV (CD4 19 cells/mm3, viral load 3.6 million copies/mL, not on highly active antiretroviral therapy on initial diagnosis at outside hospital), disseminated histoplasmosis, shingles and syphilis presented with paraplegia developing over 3 days. Spine MRI demonstrated a longitudinally extensive cord lesion extending from C3 to the tip of the conus. Brain MRI was consistent with meningoencephalitis. Cerebrospinal fluid findings were notable for positive varicella zoster virus (VZV) and cytomegalovirus (CMV) PCRs as well as a Venereal Disease Research Laboratory titre of 1:2. Patient was started on treatment for VZV and CMV meningoencephalitis, neurosyphilis and high-dose steroids for infectious myelitis. Repeat spine MRI demonstrated subacute intramedullary haemorrhage of the cervical cord. He was ultimately discharged to a skilled nursing facility for long-term intravenous antiviral therapy and rehabilitation. After 59 days in the hospital, his neurological exam remained grossly unchanged, with flaccid paraplegia and lack of sensation to fine touch in his lower extremities.
Keywords: HIV / AIDS; infection (neurology); infections; radiology (diagnostics).
© BMJ Publishing Group Ltd (unless otherwise stated in the text of the article) 2017. All rights reserved. No commercial use is permitted unless otherwise expressly granted.
Conflict of interest statement
Competing interests: None declared.
Figures
Figure 1
**(**A) Axial T2 fluid-attenuated inversion recovery imaging on presentation demonstrated nodular foci of hyperintensity centred in the frontal and temporal lobes as well as the midbrain. Abnormal leptomeningeal hyperintensity is located in the interpeduncular and perimesencephalic cisterns (white arrowheads). These findings are altogether consistent with meningoencephalitis. (B) Repeat imaging performed 12 days later demonstrates increased number of abnormal hyperintense foci scattered throughout the brain parenchyma, most notably in the deep grey and right temporal lobe. (C) Imaging performed 1 month following the initial MRI demonstrates less conspicuous and near-complete resolution of the lesions within the brain parenchyma and leptomeninges.
Figure 2
(A) Sagittal T1-weighted imaging of the cervical spinal cord without contrast or fat saturation does not demonstrate high signal to suggest subacute intramedullary haemorrhage. (B) Sagittal T2-weighted imaging of the cervical spinal cord without fat saturation demonstrates intramedullary high signal extending greater than three contiguous vertebral levels, consistent with a longitudinally extensive cord lesion. Note the associated marked expansion of the cord due to underlying oedema.
Figure 3
(A) Sagittal T1-weighted imaging of the cervical spine without contrast or fat saturation demonstrates a linear and central focus of intramedullary high signal extending from approximately C2 to C4 (white arrow), suggestive of presence of either intracellular or extracellular methaemoglobin seen in the subacute stages of haemorrhage. (B) Axial T1-weighted imaging of the cervical spine without contrast or fat saturation demonstrates the high-signal abnormality located within the central cord (white arrowhead).
Figure 4
Sagittal T2-weighted imaging of the cervical spine without fat saturation continues to demonstrate high signal extending longitudinally throughout the expanded cord. The lack of low T2 signal suggests the absence of deoxyhaemoglobin (seen in the acute stage of haemorrhage) and, in combination with high signal on T1-weighted imaging, suggests that the intramedullary haemorrhage is within the late subacute stage.
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