Lobar intracerebral hemorrhage
Sudden onset of confusion and disorientated after cardiac angriogram procedure. Quickly deteriorated to GCS 5
Loading Stack -
0 images remaining
Large left sided intracerebral hematoma. It involves both deep and lobar structures (parietal & temporal lobes, thalamus & midbrain). Its epicenter is within the left temporal white matter. The hemorrhage extends into the subarachnoid and subdural spaces but there is no clear intraventricular hemorrhage. The hematoma is irregular but there are no finger-like projections.
Further small acute cortical hemorrhage in the right parietal lobe with adjacent subarachnoid hemorrhage.
There is significant mass effect relating to the hematoma and perihaematomal white matter edema causing midline shift, compression of the ipsilateral lateral ventricle and third ventricle and effacement of ipsilateral cortical sulci. There is dilatation of the temporal horns of the lateral ventricles in keeping with hydrocephalus.
Mild periventricular low attenuation probably in keeping with small vessel disease. Mild cortical atrophy.
Large left intracerebral hemorrhage. It involves both the deep and lobar structures, causes significant mass effect and extends into the subarachnoid space.
Identifying whether an ICH is lobar or deep is important as this in part determines the likely underlying etiology as well as the prognosis (deep ICH are usually related to hypertensive arteriopathy, whereas lobar ICH can be due to hypertensive arteriopathy or cerebral amyloid angiopathy, which has a higher recurrent ICH rate). In cases such as this one, establishing whether an ICH is lobar or deep is difficult.
The Cerebral Hemorrhage Anatomical RaTing inStrument (CHARTS) is a recently published research tool which aims to improve observer agreement. The epicenter of this hemorrhage (axial slice with the biggest ICH diameter) is within the left temporal white matter, so this hemorrhage would be classified as "uncertain but probably lobar".
The patient died the same day after the ICH and underwent a post mortem. This showed an acute, extensive left intracerebral hemorrhage with subarachnoid hemorrhage. There is extensive small vessel disease in the form of lipohyalinosis and arteriolosclerosis with several lacunar infarcts. There is parencyhmal and vascular (amyloid angiopathy) on immunohistochemistry, however the distribution of the hemorrhage and severity of small vessel disease suggests this hemorrhage is secondary to lipohyalinosis
- Charidimou A, Schmitt A, Wilson D, Yakushiji Y, Gregoire SM, Fox Z, Jäger HR, Werring DJ. The Cerebral Haemorrhage Anatomical RaTing inStrument (CHARTS): Development and assessment of reliability. (2017) Journal of the neurological sciences. 372: 178-183. doi:10.1016/j.jns.2016.11.021 - Pubmed
- Pantoni L. Cerebral small vessel disease: from pathogenesis and clinical characteristics to therapeutic challenges. (2010) The Lancet. Neurology. 9 (7): 689-701. doi:10.1016/S1474-4422(10)70104-6 - Pubmed