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HYPERDENSITY SUGGESTIVE OF HEMORRHAGE AFTER STENTING OF PCA

HYPERDENSITY SUGGESTIVE OF HEMORRHAGE AFTER STENTING OF PCA. Anil Karapurkar, Nishant Aditya, Rakesh Singh, Vishwanathan Iyer Sir H N Hospital Mumbai. Mr S P. Right handed 48 years old policeman Sudden onset severe vertigo with blurred vision whilst doing his morning exercises

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HYPERDENSITY SUGGESTIVE OF HEMORRHAGE AFTER STENTING OF PCA

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  1. HYPERDENSITY SUGGESTIVE OF HEMORRHAGE AFTER STENTING OF PCA Anil Karapurkar, Nishant Aditya, Rakesh Singh, Vishwanathan Iyer Sir H N Hospital Mumbai

  2. Mr S P • Right handed 48 years old policeman • Sudden onset severe vertigo with blurred vision whilst doing his morning exercises • No loss of consciousness • On Exam: Large left homonymous visual field defect • No other deficit

  3. 03.12.08

  4. Focal stenosis PCA Dec 2009

  5. Mr S P • Severe focal stenosis of right PCA • Stenting suggested after 4 weeks in view of large infarct • Patient had recurrent transient episodes of blurred vision lasting for few minutes especially after exertion

  6. Dec 2009 30.03.2009

  7. Xience Coronary DES stent 2.5mmx14mm

  8. Pre Post

  9. Immediate Post Stenting

  10. Mr S P • CT Scan thought to show h’age • Clinically patient very well • Vision better than before • No additional deficit • Mild headache, no vomiting • Carefully monitor patient • Repeat CT Scan 6 hours later

  11. 6 hrs. later…… Most of the contrast has disappeared

  12. Immediate Post Stenting 03.12.08 6 hrs. later…… 150ml I 350 contrast used

  13. S.S F/43 Y Sudden Onset Severe Headache followed by multiple episodes of Vomiting. Lt. Arm weakness- CT & MRI had shown ICH and possible AVM Treated conservatively Completely recovered at the time of presentation 3 weeks later

  14. CT 10.02.10

  15. MR 13.02.10

  16. CT 03.03.10 Pre-treatment

  17. Rt. ICA Pre Rx 08.03.10

  18. SELEC

  19. Post Rt. ICA

  20. Came out of anesthesia without any deficit Had mild headache Post –op CT done

  21. Imm. Post CT 08.03.10

  22. Next Day CT 09.03.10

  23. Imm. Post CT 08.03.10 Next Day CT 09.03.10

  24. What is this hyperdensity

  25. 1.CONTRAST ENHANCEMENT (CE)2.CONTRAST EXTRAVASATION (CEX)3.PARENCHYMAL HEMORRHAGE(PH)4.CEREBRAL HYPERPERFUSION SYNDROME(CHS)

  26. Literature • Hyperdensity seen on NECT after cerebral interventions may be contrast extravasation or contrast  enhancement or ICH • ICH can be due hemorrhagic transformation or CHS or traumatic injury to vessel wall due wire or stent

  27. ENHANCEMENT V/S EXTRAVASATION • Contrast enhancement: pattern gyral or focal,periventricular . contrast enhancement is caused by leakage of contrast medium from vessels into the extracellular spaces as a result of increased permeability of the blood–brain barrier. Contrast agents can induce injury to the blood–brain barrier. • Contrast extravasation: results from potential contrast toxicity on basal lamina, a structural barrier where loss of integrity is associated with disruption of the blood–brain barrier. It results in cellular blood element extravasation from microvessels

  28. Enhancement v/s extravasation • Contrast enhancement is characterized by rapid clearance of a hyperdense lesion on follow-up CT scans without remaining mass effect or cavity. Contrast enhancement of hyper acute infarct and chronic infarct on CT is different • Contrast enhancement was defined as a hyperdense (HU<90)lesion that disappeared on a 24-hour follow-up CT scan • Contrast extravasation is commonly present as a mixture of blood and contrast material and is noted by its extremely high density on CT scans. Contrast extravasation usually persists within the hematoma cavity on subsequent CT scans.  • Contrast extravasation was defined as a hyperdense lesion with maximum Hounsfield unit >90 that persisted on a follow-up CT scan

  29. Contrast enhancement :Hyperacute infarct A 68-year-old woman presented with acute ischemic stroke. A, Nonenhanced CT scan just after intra-arterial thrombolytic therapy shows hyperdense lesion (arrow) in posterior part of lentiform nucleus. B, Follow-up CT scan obtained 24 hours after completion of intra-arterial thrombolytic therapy shows disappearance of hyperdense lesion and development of acute infarction involving right basal ganglia (arrows).

  30. Contrast extravasation Immediate post 24 hrs post

  31. HEMORRHAGIC TRANSFORMATION • Hemorrhagic transformation of infarcts divided into two types as per European Cooperative Acute Stroke Study I (ECASS I) proposed criterion (3) HI- hemorrhagic infarcts- HI was defined as a petechial infarction without space-occupying effect . HI type 1 (HI-1)=small petechiae along the margins of the infarct; HI type 2 (HI-2)=more confluent petechiae within the infarcted area but without space occupying effect PH-parenchymal hemorrhage-PH was defined as a homogeneous hemorrhage (coagulum) with mass effect PH type 1 (PH-1)=hematoma in ≤30% of the infarcted area with some slight space occupying effect; PH type 2 (PH-2)=dense hematoma in more than 30% of the infarcted area with substantial space occupying effect or as any hemorrhagic lesion outside the infarcted area

  32. Hemorrhagic transformation • HI-H’agic Infarct has been often explained as a result of reperfusion of the vascular bed of the infarct, such as would occur after fragmentation and distal migration of an embolus or after early reopening of a large vessel occlusion in the setting of a large infarction; the full pressure of arterial blood into hypoxic capillaries results in a diapedesis of red cells through their hypoxic walls.

  33. HI-petechial hemorrhage

  34. Hemorrhagic transformation • PH-pathogenesis of PH may involve "ischemic necrosis resulting in the rupture of small penetrating vessels analogous to hypertensive hemorrhage, leading to massive bleeding rather than the multifocal diapedesis of blood through capillary walls, as seen in HI

  35. PH

  36. Cerebral hyperperfusion syndrome:Large homogenous with dissection into IVH • Hypertension • Barorecptor DEFECT • Free radical INJURY • Decreased Cerebro Vascular Reserve • Impaired autoregulation • Contralateral occlusion of opening of highgrade stenosis

  37. Cerebral Hyperperfusion Syndrome Pre stenting Post stenting

  38. Microcath Inj: Contrast Enhancement :Parenchymal H’age • Microcatheter injections were directly proportion to CEx---PH Hence minimize MCIs during acute stroke therapy

  39. Overlap between mechanisms of Contrast Extravasation and Parenchymal h’age and Cerebral hyperperfusion syndrome

  40. Identical NECT findings CHS CEx PH

  41. Present Cases • 150ml total contrast • At least 10 microcath. Inj as distal catheterization was difficult in first case • Multiple microcath. injections to get good position in 2 nd case

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