Book Rev Intracerebral Hemorrhage.pptx...

ich

1. Chapter 66 Intracerebral Hemorrhage Presenter : dr. Raisa Cleizera Rembulan Supervisor : Prof. Dr. dr. Suroto , Sp.N ., Subsp. NIIOO(K)., FAAN Book Review

2. Outline Introduction Summary 2

3. Introduction Intracerebral hemorrhage (ICH) accounts for approximately 10%–20% of strokes. Its clinical importance derives from its high frequency and 30-day mortality, which is close to 50%. Greater among middle-aged Blacks and Hispanics than in Whites 3

4. Mechanisms of Intracerebral Hemorrhage

5. Non Traumatic Traumatic Mechanisms of Intracerebral Hemorrhage See Chapter 62 5

6. 1. Hypertension The main cause of ICH is hypertension. The primary role of hypertension in ICH is supported by a high frequency (72%–81%) of history of hypertension, significantly higher blood pressure measurements at admission in comparison with patients with other stroke subtypes The vascular lesion produced by chronic hypertension that leads to arterial rupture and ICH is probably lipohyalinosis of small intraparenchymal arteries/small penetrating arterioles The role of microaneurysms of Charcot and Bouchard is uncertain, although their anatomical location at sites preferentially affected by ICH supports their causal importance It is recommended to target a long-term blood pressure of less than 130/80 mm Hg for the secondary prevention of ICH, (Hemphill et.al., 2015) 6

7. 2. Vascular Malformations Due to AVM and cavernous angiomas ICHs associated with small vascular malformations generally tend to occur in younger patients than those with hypertensive ICH AVM cause by direct connection between cerebral arteries and veins. ( Arterial system brings the high pressure of blood and without intercapillary network the vessels can easily rupture) Cavernous angiomas are often recognized by MRI as a cause of ICH in the subcortical portions of the cerebral hemispheres and in the pons (the “popcorn” pattern ) 7

8. 3. Intracranial Tumors Relatively rare, less than 10% of the cases. Most likely to lead to this rare complication are glioblastoma multiforme or metastases from melanoma, bronchogenic carcinoma, choriocarcinoma, or renal cell carcinoma Clinical and imaging characteristics that should suggest an underlying brain tumor, including: The presence of papilledema on presentation The location of ICH relatively rare such as the corpus callosum Multiple sites simultaneously CT scan characterized by a ring of high-density hemorrhage surrounding a low-density center in a noncontrast study Enhancing nodules adjacent to the hemorrhage on contrast CT or MRI A disproportionate amount of surrounding edema and mass effect associated with the acute hematoma. 8

9. 4. Bleeding Disorders, Anticoagulants, and Fibrinolytic Treatment Bleeding disorders: Hemophilia caused by factor VIII deficiency (2.5% to 6.0% of patients) ITP idiopathic thrombocytopenic purpura (approximately 1% of patients) Acute lymphocytic variety, is a common cause of ICH that favors the lobar white matter of the cerebral hemispheres 9

10. Anticoagulants (account for 9% to 14% of ICH) Treatment with oral vitamin K antagonists (VKA) 2-4 times higher, ( Pezzini et al., 2014) Oral anticoagulation in patients with cerebrovascular disease should aim at an INR of 2–3 to reduce the frequency of this complication, (SPIRIT Study Group, 1997) DOACs (Direct oral anticoagulants) including dabigatran, rivaroxaban, apixaban, now is more favorable profiles because it has lower ICH rates than warfarin in management of nonvalvular atrial fibrillation ( Tsivigoulis et al, 2018) rtPA leads to improved clinical outcomes in acute ischaemic stroke but is associated with ICH. These hemorrhages occur at the site of the preceding cerebral infarct, are generally large and carry a worse prognosis, (NINDS rtPA Stroke Study Group., 1997). 10

11. 5. Cerebral Amyloid Angiopathy CAA is characterized by selective deposition of β-amyloid in the walls of cerebral vessels, primarily small and medium-sized arteries of the cortex and leptomeninges.  vessels becomes weak This is the most common angiopathy in age > 55 yo , and usually associated with dementia CT/MRI show multiple lobar and deep microhemorrhages 11

12. 6. Granulomatous Angiitis of the Central Nervous System and Other Vasculitides Granulomatous angiitis of the CNS, also referred to as isolated angiitis of the CNS , is characterized by mononuclear inflammation with giant cell formation in the media and adventitia of small and medium-sized intracranial arteries and veins. An associated element of intimal hyperplasia leads frequently to cerebral infarcts and occasionally to ICH. 12

13. 7. Sympathomimetic Agents Sympathomimetic agents can cause ICH after IV, oral, or intranasal use The hemorrhages usually occur within minutes to a few hours after drug use , and the majority are located in the subcortical white matter of the cerebral hemispheres Cocaine has become the most common sympathomimetic agent associated with ICH The decongestant and appetite-suppressant phenylpropanolamine has been associated with ICH in young patients. ( Kernan et al., 2000) 13

14. 8. Hemorrhagic Infarction Hemorrhagic infarction is pathologically and pathogenically different from ICH in that it results from restoration of blood flow to infarcted tissue that had previously ensued from arterial or venous occlusion. As a result, its pathological aspect is one of multifocal petechial hemorrhagic staining of an area of the brain primarily affected by ischemic necrosis 14

15. 15

16. Clinical Features of Intracerebral Hemorrhage

17. CLINICAL FEATURES OF ICH Effect of Intracranial Hypertension Location of Hematoma SYMPTOMPS Headache Vomitus Depress LOC * Symptomps varies depends on size of hematoma and associated with mortality PUTAMEN (35%) CAUDATE (5%) THALAMIC (10-15%) LOBAR (25%) CEREBELLAR (5-10%) PONTIN (5%) MESENCEPHALIC (rare) MEDULLA (rare) INTRAVENTRICULAR (3%) 17

18. The presence of the spot sign (Fig. 66.10) correlates with a frequency of hematoma enlargement in up to 77% of patients, compared to only 4%–22% in patients without the sign ( Demchuk et al., 2012; Wada et al., 2007) 18

19. Another marker in head CT scan that show the risk of expansion No High Risk (A) High risk (B-F) A B C D F E 19

20. MRI can be a good diagnostic tool for ICH especially in determining the time elapsed between onset and time of MRI examination as shown on the table above The type of signal intensity change depicted by T1- and T2-weighted MRI sequences can be correlated with the hyperacute, acute, subacute, and chronic stages of evolution of an intracerebral hematoma (Table 66.4). 20

21. CLINICAL FEATURES BASED ON THE LOCATION OF THE HEMATOMA 21

22. ICH Etiology Determines Hemorrhage Location Deep/Posterior Fossa ICH Etiologies Arteriolosclerosis Penetrating arteriole lipohyalinosis due to HTN, DM, dislipidemia Lobar ICH Etiologies Arteriolosclerosis Non hypertensive mechanism including: AVM Sympatomimethic agent (young patients) Cerebral Amyloid Angiopathy ( Amyloid deposition in vessel walls) Diagnostic Reasoning: CAA typically causes only lobar (or superficial cerebellar) hemorrhages. Arteriolosclerosis may cause both deep and lobar hemorrhages. 22

23. Treatment of Intracerebral Hemorrhage

24. Hypertension Seizure Location, size for determine the plan further management Complete blood count, a toxicology screen, serum glucose, coagulation studies) Stabilization of vital sign and airway protection (Intubation, sedation) Decompression EVD Manitol Hypertonic saline Reversal Therapy 24

25. Prevention of Further Elevation of Intracranial Pressure 25

26. Drug of choice 26

27. Specific Treatment of Increased Intracranial Pressure 27

28. Surgical 28

29. Patient with ICH on anticoagulant treatment STOP immediately. START Reversal Therapy Heparin Warfarin DOACs e.x dabigatran Factor Xa -Inhibitors rTPA Protamine Sulfate PCC, IV Vit K Cryoprecipitate and 1 g of tranexamic acid Idarucizumab Andexanet alfa If not available PCCs If not available PCCs Hemostatic Therapy of Intracerebral Hemorrhage The benefits of tranexamic acid in major trauma have increased interest in its potential benefits in spontaneous ICH. In the TICH-2 trial ( Sprigg et al., 2018), the use of tranexamic acid (1 g bolus, followed by 1 g infused over 8 hours) was shown to be safe and seemed to reduce hematoma expansion and early deaths, but ultimately did not improve functional outcomes at 90 days in spontaneous ICH patients treated within 8 hours of symptom onset. 29

30. SUMMARY ICH continues to be a major public health problem, its clinical importance derives from its high frequency and 30-day mortality, which is close to 50%. Although hypertension is still the most common cause of ICH, there are many differential diagnoses that can cause intracranial bleeding such as vascular malformations, CAA, tumors, bleeding disorders, anticoagulants, and fibrinolytic treatment, sympathomimetic agents, vasculitides , until hemorrhagic infarction. Every patient who experiences increased intracranial pressure due to ICH not limited to one or two modalities, but there are many variations according to the main cause. The acute management of ICH entails treatment of elevated intracranial pressure (ICP), prompt blood pressure lowering, reversal of coagulopathies, and, less frequently, surgical hematoma evacuation. 30

31. THANK YOU