Intracranial spontaneous hemorrhage mechanisms, imaging and management

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1 Intracranial spontaneous hemorrhage mechanisms, imaging and management Dora Zlatareva Department of Diagnostic Imaging Medical University, Sofia, Bulgaria

2 Intracranial hemorrhage (ICH) ICH 15% of strokes 25 per 100,000 pt/year Mortality -40% in 1 mo Multiple intracranial compartments By diverse pathology Neuroimaging Identify the cause of hemorrhage location and severity of hemorrhage To guide patient treatment

3 Mechanisms Hypertensive damage to blood vessels Rupture of ananeurysm Rupture of AVM Cerebral amyloid angiopathy Altered hemostasis (thrombolysis & anticoagulation) Hemorrhagic necrosis (like tumor and infection) Substance abuse (cocaine)

4 Location Basal ganglia Lobes of cerebrum Thalamus Pons Cerebellum Other brainstem sites

5 Causes Hypertension Cerebral amyloid angiopathy Hemorrhagic conversion of ischemic infarction Cerebral aneurysms Cerebral AVM Dural AV fistula Vasculitis Venous sinus thrombosis

6 Imaging CT first modality-acute blood-hyperdense CTA- vascular underlying cause (SAH, IPH) CT venography dural venous sinuses MRI r/o tumour Depend on time, sequence, size, location Cerebral DSA suspected vascular abnormality, CTA is either normal or equivocal, or to treat

7 AHA/ASA Guideline(2010) Guidelines for the Management of Spontaneous Intracerebral Hemorrhage Recommendations for Neuroimaging in ICH Rapid neuroimaging with CT or MRI is recommended to distinguish ischemic stroke from ICH CT angiography and contrast-enhanced CT may be considered to help identify patients at risk for hematoma expansion CTA, CT venography, CeCT, CeMRI, MRA and MRV can be useful to evaluate for underlying structural lesions including vascular malformations and tumors when there is clinical or radiologic suspicion Class I, Level of Evidence A (Unchanged from the previous) Class IIb, Level of Evidence B Class IIa, Level of Evidence B(New recommendation).

8 ICH: CT appearance Acute phase: Hyperdense mass (50-80 HU) Subacute phase (1-6 weeks) Peripheral edema Attenuation falls1.5 HU / day from the periphery chemical breakdown of globin Hb < 8-10g/dl isodense hematoma

9 ICH: CT appearance Chronic phase Hypodense lesion Sequelae gliosis Hemosiderin!!

10 ICH: CT appearance Still bleeding hematoma Swirl sign Due to semiliquid unretracted clot

11 Parizel, Eur Radiol 2001

12 IPH due to hypertension 60ies -70ies, 30-50% mortality Acute-BG, cerebellum, occipital lobes IPH cerebral cortex -consider other Dg Younger than 50 -?other causes -Tu or vascular malformation

NCCT -predict outcome Worse prognosis Initial size of the hematoma

13 IPH due to hypertension Complications Intraventricular hemorrhage Hydrocephalus Herniation Rebleeding Initial hemorrhage different size NCCT -predict outcome Worse prognosis Initial size of the hematoma intraventricular extension of the hemorrhage expansion of the hematoma on serial imaging

14 IPH due to hypertension Management Surgical treatment contoversial Hematoma >3cm Benefit of surgery?? External drainage for hydrocephalus? Treatment of systemic HT

15 IPH-Cerebral amyloid angiopathy Cerebral microhemorrhages Sulcal SAH DD from vasculitis AGE >60 Other areas of ICH Large cerebral IPH -DD hypertensive Subcortical WM Spares BG, posterior fossa, brainstem

16 Linn, AJNR, 2008

17 Hemorrhagic transformation of ischemic stroke Risk post i.v./i.a. vessel recanaliza on Petechial hemorrhage in margin (HI1) Confluent PH in infarcted tissue (HI2) Parenchymal hematoma <30% infarcted tissue, slight mass effect (PH1) >30% + significant mass effect (PH2) clin. significant

18 Antithrombotic or thrombolytic Th

19 Cerebral aneurysms CT -100% sensitivity for acute SAH in the first 6-24H SAH in basal cisterns or diffusely through SA space Ventricles and brain parenchyma (lobar hematoma) Surgical clipping, endovascular coiling/embolization

20 SAH

21 SAH

23 Cerebral AVM ICH -most common presentation of cerebral AVM IPH -(young pt or child suspect AVM) Intraventricular hemorrhage (IVH) SAH CTA, MRI,MRA, DSA Heit et al, J stroke 2017

24 Management Embolization, Surgery, Radiosurgery

25 Dural AV fistula

26 Vasculitis Primary, SLE, Behcet ICH or ischemic lesion Sulcal SAH near convexity -most common CT -hyperdensity within cerebral sulci MRI -sulcal hyper FLAIR, hypo GRE or SWI Sulcal SAH +NO trauma -DSAin negative CTA to r/o vasculitis or vasculopathy Immunosuppressive Th

27 CNS vasculıtıs Multiple chronic hemorrhages Perivascular enhancement Irregular vessel walls

28 Venous thrombosis Cortical vein or dural venous sinus Cord sign (hyperdense cortical vein on NCCT), empty delta sign (CT venography) Cerebral edema, parenchymal hemorrhages, ischemic and hemorrhagic infarcts SAH -uncommon, cerebral convexities or Sylvian fissures, sparing the basal cisterns

29 Venous thrombosis Uncommon and often clinically confusing entity Imaging plays an essential role in Dg Secondary to skull base infections, dehydration, hypercoagulable states, compression from meningiomas or other dural tumors

30 Superior sagittal sinusthrombosis

surgery, Radio, Chemotherapy Choi, ET AL.

31 Underlying tumors Primary Tu-hemorrhage inside the Tu Metastasis- at the periphery Management-Tutherapy, surgery, Radio, Chemotherapy Choi, ET AL., Glioma Mimicking a Hypertensive Intracerebral Hemorrhage, JKNS 2013

32 Tumors, cavernoma

33 Substance abuse (cocaine) Hemorrhagic or ischemic strokes IPH or SAH -twice as common as ischemic strokes 40% 50% -an underlying AVM or aneurysm Hematoma in BG, thalamus

Management Initial medical stabilization Neuroimaging - establish Dg and elucidate etiology Neurologic exam - determine baseline severity

34 Management Initial medical stabilization Neuroimaging - establish Dg and elucidate etiology Neurologic exam - determine baseline severity Prevent hematoma expansion (BP management, reversal of coagulopathy) Consideration of early surgical intervention Prevention of secondary brain injury

35 Management Hemostatic agents (factor VIIa) early-reduce hematoma expansion, clinical effectiveness has not been shown Anticoagulation reversal with prothrombin concentrates + Vit K - in VitK antagonist-related ICH Ongoing trials for minimally invasive approaches or hemicraniectomy, role of surgery in ICH to be defined BP control, antithrombotic prevention after ICH - consider the risk of recurrent bleeding and ischemia

36 Take home messages Elderly patient with HT, BG hematoma Hypertensive hemorrhage Do SWI to see other microbleeds Eldery normotensive patient, lobar hematoma Amyloid angiopathy / tumor Do +C MRI, SWI, MRA? DSA? Enhancing lesion Tm Subcortical microbleeds on SWI Amyloid angiopathy

37 Take home messages Young patient with ICH (ALERT!!!) Do +C MRI, MRA / CTA / DSA, SWI Angio abnormal Vasc. Malf, Vasculitis, DVST Enhancing single lesion Tm Enhancing multiple lesions Met, Vasculitis, Septic emboli Multiple black dots on SWI Vasculitis, Cavernomas Patient of any age with associated SAH Aneurysm Patient of any age with ICH, you still cannot decide the etiology Refer to the clinician,short time FUpscan

38 I would like to thank to Cem Calli for ideas and cases

39 Thank you for your kind attention!

ISCHEMIC STROKE IMAGING

ISCHEMIC STROKE IMAGING ผศ.พญ พญ.จ ร ร ตน ธรรมโรจน ภาคว ชาร งส ว ทยา คณะแพทยศาสตร มหาว ทยาล ยขอนแก น A case of acute hemiplegia Which side is the abnormality, right or left? Early Right MCA infarction