- About this Journal ·
- Abstracting and Indexing ·
- Aims and Scope ·
- Article Processing Charges ·
- Articles in Press ·
- Author Guidelines ·
- Bibliographic Information ·
- Citations to this Journal ·
- Contact Information ·
- Editorial Board ·
- Editorial Workflow ·
- Free eTOC Alerts ·
- Publication Ethics ·
- Reviewers Acknowledgment ·
- Submit a Manuscript ·
- Subscription Information ·
- Table of Contents
Radiology Research and Practice
Volume 2012 (2012), Article ID 475497, 11 pages
Differentiating between Hemorrhagic Infarct and Parenchymal Intracerebral Hemorrhage
1Stroke and Ageing Research Group, Neurosciences Program, Southern Clinical School, Monash Medical Centre, Monash University, Level 5, Block E, 246 Clayton Road, Clayton, Melbourne, VIC 3168, Australia
2Department of Diagnostic Radiology, Monash Medical Centre, Southern Health, 246 Clayton Road, Clayton, Melbourne, VIC 3168, Australia
Received 17 July 2011; Revised 11 November 2011; Accepted 8 December 2011
Academic Editor: David Maintz
Copyright © 2012 P. M. C. Choi et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
Differentiating hemorrhagic infarct from parenchymal intracerebral hemorrhage can be difficult. The immediate and long-term management of the two conditions are different and hence the importance of accurate diagnosis. Using a series of intracerebral hemorrhage cases presented to our stroke unit, we aim to highlight the clues that may be helpful in distinguishing the two entities. The main clue to the presence of hemorrhagic infarct on computed tomography scan is the topographic distribution of the stroke. Additional imaging modalities such as computed tomography angiogram, perfusion, and magnetic resonance imaging may provide additional information in differentiating hemorrhagic infarct from primary hemorrhages.
In acute stroke, the differential diagnosis of hemorrhage detected on computed tomography (CT) scan ranges from hemorrhagic infarct (HI), primary intracerebral hemorrhage (ICH) to hemorrhage from venous infarction. The differentiation between the first two conditions can be difficult, and there are currently no radiological criteria to assist in this regard. It is, therefore, not surprising that previous investigators have found poor agreement in making a diagnosis of HI or ICH .
HI, or hemorrhagic transformation of an infarct, occurs in approximately one-third of cases of ischaemic stroke . When an infarct is immediately followed by the occurrence of petechial hemorrhage in the same arterial territory, the diagnosis of HI is easily made. However, when brain imaging is delayed after the onset of the patient’s stroke symptoms, an erroneous diagnosis of ICH may be made if the hemorrhage appears confluent on CT. This issue of misdiagnosing HI has been recently raised by other investigators and may also be partly responsible for the overestimation of the prevalence of ICH . Correct assignment of diagnosis is critical in guiding both acute and long-term management and also estimating prognosis. Patients with ischaemic stroke are more likely to develop recurrent ischaemic stroke than ICH. Antiplatelet is the mainstay therapy for this group of patients. Likewise, the finding of HI and atrial fibrillation suggests that the stroke mechanism is cardioembolism and anticoagulation needs to be considered. Furthermore, it has also been suggested that some cases of “ICH” in patients on anticoagulants may in fact be HI and thus represent “failure of anticoagulation” rather than anticoagulant-induced ICH .
2. Clinical Factors and Mechanism of HI
HI occurs more commonly in elderly patients and those with larger infarcts . Among patients receiving thrombolytic therapy, it occurs more commonly in patients with diabetes and hypertension [7, 8]. It has also been associated with carotid endarterectomy  and carotid artery stenting.
HI typically happens within 1-2 weeks after stroke onset, less commonly (~9%) in the first 24 hours . The occurrence of dense hematoma complicating HI may be even lower at approximately 3% . The mechanism of HI has been postulated to be due to breakdown of the basal lamina of microvessels related to activity of matrix metalloproteinase . This may be a consequence of prolonged ischaemia and exacerbated by recanalisation of the occluded artery. It has been suggested that tissue plasminogen activator (tPA) may exacerbate this process, but spontaneous intrainfarct hematoma can also occur in the absence of thrombolysis .
3. Recognition of HI on CT Scans
A classification of HI based on the topography and intensity of hemorrhage on CT has previously been proposed by Moulin et al. in 1993 : type 1, a multifocal or pethechial hemorrhagic infarction and type 2, an intra-infarct hematoma. The appearance of the latter can mimic ICH on CT scans. Careful observation of the deep structures involved by the stroke lesion and the topography of the surrounding hypodensity may help in reaching the correct diagnosis.
ICH involving the caudate nucleus is uncommon [12, 13] (Figures 1 and 2) and involvement of both the caudate nucleus and putamen may suggest embolism affecting the lenticulostriate arteries and hemorrhagic infarction of the striatocapsular region (Figures 3, 4, and 5). Petechial hemorrhage after intravenous thrombolysis is easily recognized given there is always a baseline CT scan done prior to thrombolysis. The initial CT scan may also show coexisting signs of ischaemia such as the hyperdense middle cerebral artery (MCA) sign and the loss of insula ribbon (Figure 6).
The hypodense region of oedema surrounding the hematoma in ICH usually radiate centripetally, and it does not follow the topography of an arterial territory. Similar pattern of oedema is seen in hemorrhages resulting from venous infarction (Figures 7 and 8). In patients with HI, the hypodense regions surrounding the hematoma may reach the cortical surface and spread far from the centre of the hematoma (Figures 9, 10, and 11). The topography of this hypodense region usually follows the affected vascular territory. Maps of the MCA  and the posterior cerebral artery (PCA) infarct territory  have been recently published and can be used to aid assignment of territorial membership of the stroke. The centre of the hematoma in cases of HI seems to correspond to regions at highest risk of infarction on the infarct map. For example, in the MCA territory, the region at risk is the striatocapsular region and in the PCA territory, the medial temporal and occipital lobes.
4. MR Imaging Features of HI
The magnetic resonance (MR) imaging features of HI on diffusion weighted imaging (DWI) sequence have a mixed appearance. Within the hemorrhagic area, the appearance between HI and ICH is indistinguishable. However, the presence of an ischaemic process may be evidenced by discrete regions of restricted diffusion remote from the hemorrhagic area (Figures 12–14). These lesions further strengthen the possibility of the primary lesion being a HI.
Time-of-flight MR angiography can show the presence of occlusive intracranial disease and hence aids in confirming the diagnosis of HI (Figures 13-14). Although not widely available, MR perfusion imaging may help in diagnosing HI if it shows the presence of a perfusion deficit extending beyond the region of hematoma. In ICH, the region of perfusion deficit does not extend beyond the ICH .
The presence of “microbleeds” on gradient-echo (GRE) or susceptibility weighted imaging (SWI) sequence suggests the presence of blood product but does not necessarily indicate that the lesion in question is HI or ICH . In elderly patients, it has been recognised that some patients with ischaemic stroke may also have evidence of silent microbleeds. Lobar ICH tend to be located posteriorly, corresponding to the distribution of microbleeds and the location of binding of amyloid tracer in PET studies .
5. Role of CT Angiography and Perfusion
CT angiography (CTA) is often used as a screening tool to exclude the possibility of aneurysmal bleed. It can also be used to concurrently evaluate the possibility of arterial occlusion and potential intra-arterial therapy. Given the additional risk of radiation exposure and iodinated contrast agents, further studies are required to evaluate the usefulness of this modality for determining arterial occlusion in patients with isolated putaminal or thalamic hemorrhage.
CT perfusion (CTP) with cerebral blood flow, cerebral blood volume, and mean transit time is usually performed at the same time as CTA in tertiary stroke centres. When this is available, it can help with differentiation between HI and ICH. In contrast to ischaemic stroke, a large perfusion defect around an ICH has not yet been reported. The presence of such a mismatch may point to the possibility of HI.
Differentiating HI from ICH can be difficult. Careful examination of the topography of the stroke on the initial CT in different sections may distinguish the two conditions. Signs compatible with an infarct such as dense artery sign and insular ribbon sign should be actively looked for. Advanced imaging technique such as CTA, CTP, and MR imaging may be particularly helpful in difficult cases, looking for perfusion deficit, arterial occlusion, and diffusion restriction remote from the site of hemorrhages. Distinguishing HI from ICH is important given the difference in acute and long term management.
- T. Moulin, T. Crepin-Leblond, J. L. Chopard, and J. Bogousslavsky, “Hemorrhagic infarcts,” European Neurology, vol. 34, no. 2, pp. 64–77, 1993.
- C. E. Lovelock, P. M. Rothwell, P. Anslow et al., “Substantial observer variability in the differentiation between primary intracerebral hemorrhage and hemorrhagic transformation of infarction on ct brain imaging,” Stroke, vol. 40, no. 12, pp. 3763–3767, 2009.
- R. G. Hart and J. D. Easton, “Hemorrhagic infarcts,” Stroke, vol. 17, no. 4, pp. 586–589, 1986.
- J. Bogousslavsky, F. Regli, A. Uske, and P. Maeder, “Early spontaneous hematoma in cerebral infarct: is primary cerebral hemorrhage overdiagnosed?” Neurology, vol. 41, no. 6, pp. 837–840, 1991.
- R. D. Bailey, R. G. Hart, O. Benavente, and L. A. Pearce, “Recurrent brain hemorrhage is more frequent than ischemic stroke after intracranial hemorrhage,” Neurology, vol. 56, no. 6, pp. 773–777, 2001.
- M. Paciaroni, G. Agnelli, F. Corea et al., “Early hemorrhagic transformation of brain infarction: rate, predictive factors, and influence on clinical outcome: results of a prospective multicenter study,” Stroke, vol. 39, no. 8, pp. 2249–2256, 2008.
- A. K. Gilligan, R. Markus, S. Read et al., “Baseline blood pressure but not early computed tomography changes predicts major hemorrhage after streptokinase in acute ischemic stroke,” Stroke, vol. 33, no. 9, pp. 2236–2242, 2002.
- A. M. Demchuk, L. B. Morgenstern, D. W. Krieger et al., “Serum glucose level and diabetes predict tissue plasminogen activator- related intracerebral hemorrhage in acute ischemic stroke,” Stroke, vol. 30, no. 1, pp. 34–39, 1999.
- R. D. Henderson, T. G. Phan, D. G. Piepgras, and E. F. M. Wijdicks, “Mechanisms of intracerebral hemorrhage after carotid endarterectomy,” Journal of Neurosurgery, vol. 95, no. 6, pp. 964–969, 2001.
- G. F. Hamann, Y. Okada, R. Fitridge, G. J. Del Zoppo, and J. T. Povlishock, “Microvascular basal lamina antigens disappear during cerebral ischemia and reperfusion,” Stroke, vol. 26, no. 11, pp. 2120–2126, 1995.
- G. J. del Zoppo, R. von Kummer, and G. F. Hamann, “Ischaemic damage of brain microvessels: inherent risks for thrombolytic treatment in stroke,” Journal of Neurology Neurosurgery and Psychiatry, vol. 65, no. 1, pp. 1–9, 1998.
- C. S. Chung, L. R. Caplan, Y. Yamamoto et al., “Striatocapsular hemorrhage,” Brain, vol. 123, part 9, pp. 1850–1862, 2000.
- E. Kumral, D. Evyapan, and K. Balkir, “Acute caudate vascular lesions,” Stroke, vol. 30, no. 1, pp. 100–108, 1999.
- T. G. Phan, G. A. Donnan, P. M. Wright, and D. C. Reutens, “A digital map of middle cerebral artery infarcts associated with middle cerebral artery trunk and branch occlusion,” Stroke, vol. 36, no. 5, pp. 986–991, 2005.
- T. G. Phan, A. C. Fong, G. Donnan, and D. C. Reutens, “Digital map of posterior cerebral artery infarcts associated with posterior cerebral artery trunk and branch occlusion,” Stroke, vol. 38, no. 6, pp. 1805–1811, 2007.
- P. D. Schellinger, J. B. Fiebach, K. Hoffmann et al., “Stroke MRI in intracerebral hemorrhage: is there a perihemorrhagic penumbra?” Stroke, vol. 34, no. 7, pp. 1674–1679, 2003.
- H. C. Koennecke, “Cerebral microbleeds on MRI: prevalence, associations, and potential clinical implications,” Neurology, vol. 66, no. 2, pp. 165–171, 2006.
- J. V. Ly, G. A. Donnan, V. L. Villemagne et al., “11C-PIB binding is increased in patients with cerebral amyloid angiopathy-related hemorrhage,” Neurology, vol. 74, no. 6, pp. 487–493, 2010.