Hemorrhagic Lesions as seen on CT/MRI

1. Hemorrhagic Lesions as seen on CT/MRI Ryan Hakimi, DO, MS Associate Professor Director, Critical Care Neurology Emmaculate Fields, APRN-CNP Clinical Instructor Department of Neurology The University of Oklahoma Health Sciences Center

2. DISCLOSURES • FINANCIAL DISCLOSURE • Nothing to disclose • UNLABELED/UNAPPROVED USES DISCLOSURE • Nothing to disclose • Some of the slides have been adapted from teaching materials used at the University of Oklahoma Health Sciences Center • Some slides are from the National Stroke Association (denoted NSA)

3. LEARNING OBJECTIVES Upon completion of this course, participants will be able to: • Describe the significance of neuroimaging in the management of patients presenting with hemorrhagic stroke • Identify the various neuroimaging tools available to clinicians to aid in the management of patients with hemorrhagic stroke • Distinguish the common neuroimaging findings in patients with hemorrhagic stroke that help identify the underlying etiology • Identify different hemorrhagic lesions (IPH/SAH, EDH, SDH)

4. Hemorrhagic lesions • Hemorrhagic stroke 15-20% of all strokes (CDC) • ICH/IPH 59% • SAH 41% • 30 day mortality rate 55%-61% • 20% of survivors achieving full functional independence at six months & approx. 55% at 12 months • Structural neuroimaging modalities; • CT, MRI, transcranial color coded Duplex • Vascular neuroimaging modalities • (CTA, MRA, DSA, and transcranial Doppler ultrasound) • Optimal window for hemorrhagic lesions is +60 to 80

5. Hemorrhagic lesions • Epidural hematoma: over brain convexity, confined by suture lines, thus does not cross suture lines, lens shaped (biconvex) • Subdural hematoma: over brain convexity, interhemipespheric, along the tentorium, SDH will cross suture lines and it’s crescent shaped • Intraparenchymal/Intracerebral hemorrhage: within the brain matter, sizes/shape varies dependent on etiology can be regular or irregular. • Intraventricular hemorrhage: inside ventricles, can be isolated and or secondary to SAH, ICH. • Subarachnoid hemorrhage: blood within the subarachnoid spaces (sulci, sylvian fissure, cisterns). Usually assumes shape of the surrounding cerebral structure.

6. Hemorrahgic lesions • Density/age of blood on CT • Hyperdense: Acute hemorrhage which is bright white usually < 4 days old • Isodense: Sub acute Hemorrhage will be same density as the brain usually 4 days to 2 weeks old • Hypodense: Old hemorrhage will be darker than brain tissue usually > 2-3 weeks • Blood on MRI • Mnemonic       Stage                    T1                              T2------------------------------------------------------------------------------------It BeHyperacute           isointense (I)                  hyperintense (B) IdDy         Acute                    iso to hypointense (I)      hypointense (D) BiDdy         Early Subacute     hyperintense (B)          hypointense (D) BaBy       Late Subacute      hyperintense (B)           hyperintense (B) Doo Doo    Chronic                hypointense (D)              hypointense (D)

7. Appearance of intracerebral hemorrhage on non-contrast CT and MRI by stages

8. Cerebral amyloid angiopathy as seen on CT/MRI Image 1 • Images 1 and 2 with an acute spontaneous lare the CT and MRI MRI images of an 84-year-old woman who presented eft parietal intracerebral hemorrhage (cortical location). MRI images show the characteristic microbleeds suggestive of CAA as the underlying of spontaneous ICH. • Image 3, 4, & 5 are MRI images from a 94 year old man who presented with a very small spontaneous left frontal hemorrhage. The gradient recall and susceptibility weighted MR images demonstrated significant microbleeds in bilateral cortical regions indicating CAA as the cause of spontaneous ICH. Image 2 Image 5 Image 3 Image 4

9. ICH/IPH ICH Facts • Medical emergency, clinical deterioration early on after initial symptoms • Approx 20%Mortality – Overall case-fatality 40% despite aggressive treatment • Morbidity – Return to independence after 1 year • 12-39% • National Burden: $34 billion Source 2015 American Heart Association

10. ICH Risk factors ICH score GCS Age ICH volume Location of the clot Intraventricular blood Predictor of 30 day mortality, the higher the score = Increased Mortality ICH score provides a reasonable guide for prognostication of patients with large hemorrhagic strokes and help in making challenging decisions such as comfort care or withdrawal of care • Coagulopathy secondary to anticoagulation, liver dysfunction • Uncontrolled HTN • Smoking • Alcohol use • Hyperlipidemia • Vascular disorders: Amyloid Angiopathy –

11. Calculating the ICH Volume (Slide adapted from National Stroke Association). For standard 0.5 cm slice thickness CT: ICH volume = A X B XC/4

12. Prognostication of ICH based on the ICH score (Slide adapted from National Stroke Association). The ICH score comprises of two patient related factors (age and GCS) and three neuroimaging findings (size of hematoma, location, intraventricular component).

13. CTA use in hemorrhagic lesions • Approximately, one-third of patients will have hematoma expansion on follow up head CT within the first three hours of symptoms onset • Presence of a spot sign on CTA head is indicative of active hemorrhage, predictive of hematoma growth, and may favor admit to intensive care unit even if the patients is not intubated and appears to be clinically stable • The use of CTA head or a contrast enhanced head CT (when CTA is not available) can allow for earlier identification of such patients via the “spot sign” wherein contrast is identified within the hemorrhage suggesting active bleeding • A “dynamic spot sign” has also been reported on CT perfusion imaging with a higher predictive value. However, the utility of CT perfusion imaging in a patient with hemorrhagic stroke is unclear at this time. • A CTA head can further identify underlying vascular lesions that would then guide therapy and influence the patient’s outcome.

14. Common sites of spontaneous intraparenchymal hemorrhage

15. Subarachnoid Hemorrhage • Blood within the subarachnoid spaces (sulci, sylvian fissure, cisterns). • Usually assumes shape of the surrounding cerebral structure. • Approx. 30,000 cases a year in US • 60 % mortality rate, 50% of survivors unable to go back to prehospital status • Excluding trauma, aneurysmal rupture is the most common cause of subarachnoid hemorrhage (SAH). • Potential underlying etiologies of SAH include arteriovenous malformation or fistula, intracranial dissection, cerebral venous thrombosis, reversible cerebral vasoconstriction syndrome, vasculitis, and use of sympathomimetic drugs.

16. Subarachnoid • Neuroimaging plays a key role in management of these patients including the identification of SAH, guiding the etiology and treatment of SAH, as well as prognostication. • A non-contrast head CT is highly sensitive in detecting subarachnoid blood, especially within 6 hours of hemorrhage • In a patient with clinical history highly suggestive of SAH but negative head CT, further options include lumbar puncture to assess for xanthochromia

17. Imaging in SAH • Imaging helps when SAH happens in the setting of trauma. For example, if the SAH is located over frontal poles and patient was found to have a basilar apex aneurysm that would indicate that the aneurysm is an incidental finding and SAH is from trauma itself. These determinations for SAH in the setting of trauma have significant ramifications in determining the urgency of treatment. • MRI to assess for subarachnoid hemorrhage, and a CTA or DSA to identify the presence of an aneurysm or other etiology. • CTA is slowly replacing digital subtraction angiography as the first-line technique for the diagnosis and treatment planning of cerebral aneurysms, but digital subtraction angiography is still required in patients with diffuse SAH and negative initial CTA. • Recently the SAH literature has described, perfusion imaging to assess for delayed cerebral ischemia and functional MRI/ positron emission tomography to assess the physiological, functional, and cognitive sequelae after SAH. • DSA continues to be the best modality to assess for aneurysms smaller than 3 mm, intracranial dissections, and reversible cerebral vasoconstriction syndrome.

18. SAH scales • Hunt and Hess –mortality predictor the higher the scale the worse the mortality • WFNS-Prognosis • Fischer-Vasospasm incidence

19. SAH SCALES • Fisher CM, Kistler JP, Davis JM. Relation of cerebral vasospasm to subarachnoid hemorrhage visualized by computerized tomographic scanning. Neurosurgery. 1980 Jan;6(1):1-9.

20. SAH SCALES • Claassen J, Bernardini GL, Kreiter K, et al. Effect of cisternal and ventricular blood on risk of delayed cerebral ischemia after subarachnoid hemorrhage: the Fisher scale revisited. Stroke 2001 Sep;32(9):2012-20.

21. Epidural Hematoma • 20% will have a lucid period before clinical worsening • Note the soft tissue swelling adjacent to the hematoma explaining the mechanism of the injury

22. Epidural hematoma • Surgical emergency if clinically symptomatic and > 1cm thickness • Epidural hematoma: over brain convexity, not crossing suture line, lens shaped (biconvex). • Less common in comparison to SDH • Mostly due to trauma, injury to middle meningeal artery • Other uncommon causes- vascular abnormalities of the dura, skull base infectious etiology & metastasis, coagulopathies

23. Subdural Hematoma (SDH) • Differentiate between acute, subacute, chronic, or acute on chronic • Acute SDH • Bright white on CT • Can only be removed with a craniotomy • Doesn’t always require surgery, depends on the patient’s neurological examination and comorbidities • Usually related to shearing of bridging veins between the dura and brain

24. Subdural hematoma • Subdural hematoma: over brain convexity, interhemipespheric, along the tentorium, SDH will cross suture lines & it’s crescent shaped. • Acute • Acute on Chronic

25. Acute and Chronic Subdural Hematoma • Patient may be asymptomatic until the event leading to the acute component • Chronic component can be drained using a bedside burr hole device such as the Subdural Evacuation Port System (SEPS) http://www.hakeem-sy.com/main/files/subdural%20hematoma.jpg, accessed on 3/31/10

26. Traumatic Intracerebral hemorrhage • Occurs at the time of impact • Diffuse axonal injury • Inertial forces cause deformation of the white matter, aka shear injuries • Most commonly leads to acute coma • CT (not very sensitive) may reveal petechial hemorrhages in the central 1/3 of the brain (subcortical white matter, corpus collosum, basal ganglia, brainstem, cerebellum) • MRI to evaluate extent of injury Gennarelli, et al J. Trauma 1994

27. Focal parenchymal contusions Coup, contra coup, intermediate coup CT: hemorrhagic core surrounded by low density edema Variable CBF in and around contusion Traumatic Intracerebral hemorrhage

28. Intraventricular hemorrhage • Found inside ventricles, can be isolated and or secondary to SAH, ICH • Isolated IVH in the absence of an identifiable parenchymal or subarachnoid component is an uncommon presentation of ICH, accounting for approximately 3% of ICH . • The diagnostic neuroimaging evaluation of such patients is variable and only described in case series. • In a pooled meta-analysis performed by Flint and colleagues, of isolated IVH patients who underwent a DSA, cerebral angiography identified a secondary bleeding source in 56%. • In contrast, DSA is of limited diagnostic utility in the evaluation of parenchymal ICH except in younger, non-hypertensive patients, with atypical hemorrhage locations on CT head.

29. ICH secondary to cerebral venous thrombosis (CVT) • CVT is thrombosis of the venous sinuses and veins in the brain. • Cortical vein thrombosis refers to CVT involving only a small cortical vein as opposed to venous or lateral sinus thrombosis, which implies involvement of one of the large cerebral venous sinuses. • The appearance of the thrombus on MRI is time specific: • Isointense on T1 and hypointense on T2 in the acute phase • Hyperintense on T1 and T2 in the subacute phase • Isointense on T1 and hyperintense on T2 in the chronic phase ( 34) • MR and CT venography techniques can further aid in diagnosing CVT. • While the CT venogram involves administration of iodinated contrast medium, the MR venography can be performed without the need for contrast using 2D/3D time of flight as well as 2D and 3D phase contrast techniques.

30. T1 G+ T1 G- Sagittal Coronal Coronal CVT ON MRI WITH CONTRAST:DELTA SIGNT1 WITHOUT & WITH GADOLINIUM Parenchyma: often paramedian, gyral enhancement Sinovenous system: G- no flow; G+ delta/empty triangle sign

31. CVT: RECANALIZATION ON MRI MAXIMAL BY 4 MONTHS Admission: SSS thrombosis Two months later: Recanalization

32. T2 T1 CVT: PARENCHYMAL LESIONS DWI FLAIR DWI 1. Lack of hyperintense area suggests vasogenic edema • Hypointense area suggests acute hemorrhage (when considered with T1 findings)

33. References • Brain Aneurysm Foundation. Understanding Brain Aneurysm Statistics and Facts. Retrieved from: http://www.bafound.org/Statistics_and_Facts • Claassen J, Bernardini GL, Kreiter K, et al. Effect of cisternal and ventricular blood on risk of delayed cerebral ischemia after subarachnoid hemorrhage: the Fisher scale revisited. Stroke 2001 Sep;32(9):2012-20. • Fisher CM, Kistler JP, Davis JM. Relation of cerebral vasospasm to subarachnoid hemorrhage visualized by computerized tomographic scanning. Neurosurgery. 1980 Jan;6(1):1-9. • Gean AD, Fischbein NJ, Purcell DD, et al. Benign anterior temporal epidural hematoma: indolent lesion with a characteristic CT imaging appearance after blunt head trauma. Radiology. 2010 Oct. 257(1):212-8. [Medline]. • Kremer, P. C., Jolink, W. T., Kappelle, L. J., Algra, A., Klijn, C. M., & null, n. (2015). Risk Factors for Lobar and Non-Lobar Intracerebral Hemorrhage in Patients with Vascular Disease. Plos ONE, 10(10), 1-10. doi:10.1371/journal.pone.0142338 • Hemphill, C. et al. Guidelines for the Management of Spontaneous Intracerebral Hemorrhage. Stroke. 2015 July 46(7): 2032-60 • Sander Connolly, E. et al. Guidelines for the Management of Aneurysmal Subarachnoid Hemorrhage. Stroke 2012. 43: 1711-37 • van Asch CJ, Luitse MJ, Rinkel GJ, van der Tweel I, Algra A, Klijn CJ. Incidence, case fatality, and functional outcome of intracerebral haemorrhage over time, according to age, sex, and ethnic origin: a systematic review and meta-analysis. Lancet Neurology. 2010 Feb; 9(2):167-76 2. • Ying-Ming, Y., Xiao-Huan, Y., Min-Dong, H., Wei-Qiang, C., & Wang-An, L. (2007). Efficacy of subdural saline injection during surgery for acute epidural haematomas. Brain Injury, 21(12), 1303-1306. doi:10.1080/02699050701727478

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