1. Arteriovenous Malformation A Case Discussion on Presented by Ri 周伯翰 Ri 黃博浩 Supervised by R3 陳健宇 Date: 2003.02.24

2. Pre-operation ► 23 y/o female, HBV carrier, AVM s/p 5 times TAE, present with seizure since childhood and under anticonvulsant control (Aleviatin 100mg tid and Depakine 1# bid, no steroid use). ► In last January, a large AVM (85ml)over R’t frontal lobe was disclosed by MRI and angiography. After failure of Gamma knife, five times of TAE were performed for scheduled surgical intervention ► Seizure pattern : shivering of both hands as preictal presentation, followed by generalized tonic-clonic seizure for 10+ minutes with post-ictal confusion finally. ► No particular on P.E. or N.E. ► Seizure attack once before operation under Ativan control ► Blood sugar(84 mg/ml), Dilantin level(9.44 mg/dl), HB :11.7,Na:140 mmol/l, K:4.32 mmol/l

8. Peri-Operation ► 70.5kg,161 cm, ASA class 3 ► Supine position ► CVP (L’t femoral) remain 4~9 mm-Hg. ► PaCO2(36.6,32,29.8,26.9,30.7,27.3) ► Pre-op BP 110/60, peri-op BP 120/60 with few fluactuation; vasodilator (Trandate 5mg twice) ► 8hr neosynesin 0.1mg administered to keep SBP 130mmHg for Bp challenge ► Urine output 1500 cc ► No intracranial pressure monitor ► Blood loss 1500 ml; PRBC 8U+HAES 2 bottle+ mannitol 450ml+IVF 2800 ml ► Operation time: 12 hr

9. Post-operation ► Mannitol, Solumedrol, Zantac, Dilantin 500mg loading, Propofol titration ► Seizure attack controlled by Ativan in ICU ► Extubation next day in ICU ► E3M6V4 ► Dizziness, vertigo, none-correlated speech, stable C-V status ► Angiography: residual AVM become smaller ► 2nd operation

11. AVM-Introduction Vascular malformation: ► AVM ► Venous malformation ► Caverous malformation ► Capillary telangiectasia ► AVF

12. AVM-introduction ► Most dangerous vascular malformation ► Congenital lesion ► Abnormal collection of vessels wherein arterial blood flows directly wherein arterial blood flows directly into draining veins without the into draining veins without the normal capillary beds normal capillary beds ► Feeding arteries/ Nidus/ Draining veins ► Static/ Grow/ Regress

13. AVM-Presentation ► Hemorrhage(50%) ► Seizure ► Mass effect ► Ischemia; steal phenomenon ► Headache ► Bruit ► IICP ► Peds: hydrocephalus, heart failure

14. AVM-Hemorrhage ► Peak age: 15-20 y/o ► 10 % mortality; 30-50% morbidity ► ICH(80%)/IVH/SAH ► Risk of hemorrhage: High feeding a. pressure/V. outflow obstruction/Size/Location/Aneurysm/ Pregnancy High feeding a. pressure/V. outflow obstruction/Size/Location/Aneurysm/ Pregnancy

15. Hemorrhage related to AVM size ► Small AVMs are more lethal than larger ones ► Small AVMs tends to present more often as hemorrhage than do larger ones 1 ► Small AVMs are thought to have much higher pressure in feeding artery 1, 2 1. Crawford P M, West C R, et al: Arteriovenous Malformation: Natural History in Unoperated Patients. J Neurol Neurosuurg Psy 49:1-10,1986 2. Spetzler R F, Hargraves R W, et al: Relationship of Perfusion Pressure and Size to Risk of Hemorrhage from Arteriovenous Malformations. Neurosurgery 37: 851-5, 1995

16. Annual & Lifetime risk of Hemorrhage ► Lifelong risk of bleeding: 2-4% per yr ► A study of 166 symptomatic AVMs with 24 year follow-up found the risk of major bleeding was constant at 4% per year, independent of whether the AVM presented with or without hemorrhage 3 ► The AVM Study Group: Annual rate of rehemorrhage was 18% among pt who had hemorrhage at presentation; 2% among pt with no history of bleeding (306 cases) 4 Annual rate of rehemorrhage was 18% among pt who had hemorrhage at presentation; 2% among pt with no history of bleeding (306 cases) 4 ► Rebleeding rate significantly lower than aneuyrsm 3. Ondra SL, Troupp H, et al: The natural history of symptomatic cerebral arteriovenous malformation: A 24-year follow-up assessment. J Neurosurg 25:387-91, 1990

17. AVMs & Associated Aneurysms ► 7% of pts with AVMs have aneurysms ► 75% are located on major feeding artery; probably from increased flow 1 ► The symptomatic one is treated first ► Although 66% of related aneurysms will regress following AVM removal, this does not always occur 4 4. Cunha M J, Stein B M, et al: The Treatment of Associated Intracranial Aneurysm and Arteriovenous Malformations. J Neurosurg 77: 853-9, 1992.

18. Hemodynamic Effects of AVM Pre-op effects: ► Steal phenomenon ► AVM & aneurysm ► High-flow angiopathy 7 Post-op effects: ► Normal perfusion pressure breakthrough ► Occlussive hyperemia 7. Pile Spellman JM, Baker KF, et al: High flow angiopathy: cerebral blood vessel changes in chronic arteriovenous malformation. Am J Neuroradiol 1986; 7:811-5

19. Cerebral Steal Phenomenon ► Autoregulation curve shifts to left ► Despite cerebral arterial hypotension, focal neurological deficits are rare(<10%) ► More likely to be local mass effect

20. Normal perfusion pressure breakthrough (NPPB) ► Peri-/Post-op swelling or hemorrhage ► Loss of autoregulation 4 ? 5 ► Less than 5% ► Should be diagnosis of exclusion ► Mx: prevent post-op hypertension 4. Spetzler R F, Wilson C B, et al: Normal perfusion breakthrough theory. Clin Neurosurg 25: 651-72, 1978 5. Young W L, Kader A, et al: Pressure autoregulation is intact after arteriovenous malformation resection. Neurosurgery 32: 491-7, 1993

21. Evaluation-MRI ► Flow void on T1WI or T2WI or T2WI ► Feeding arteries ► Nidus ► Draining veins

22. MRI MRI

23. TAE

24. Evaluation-Angiography ► Tangle of vessels ► Large feeding artery ► Large draining veins ► Not all AVMs show up on angiography! Angiographically occult vascular malformation (AOVM) Angiographically occult vascular malformation (AOVM)

25. Evaluation-Grading ► Spetzler-Martin grade ► Outcome based on Spetzler-Martin grade: 100 consecutive cases operated by Spetzler 100 consecutive cases operated by Spetzler

26. Treatment ► Multidisciplinary approach ► Primary goal: decrease the risk of bleeding 1) Surgery: mainstay 2) Stereotactic Radiosurgery (SRS): high-risk for surgery high-risk for surgery 3) TAE: adjuct to 1) & 2)

27. Surgery American Stroke Association recommends: ► Low grade ( I & II )- surgery alone ► Higher grade(>III)-TAE before surgery ► Eliminates risk of bleeding immediately, seizure controls improves ► Invasive, risk of surgery

28. Surgery ► Pre-op propanolol 20mg po QIDx3d to minimize post-op normal perfusion pressure breakthrough (NPPB) ► Peri-op labetalol to keep MAP 70-80mmHg

29. Surgery ► Craniotomy ► Dural opening ► Identify the borders ► Cautery of feeding arteries

30. Surgery ► Deep dissection of the nidus ► Securing the ventricle ► Obliterate the draining veins ► Final removal of AVM ► Post-resection BP challenge Hemostasis/ Residual nidus/ Areas prone to NPPB Hemostasis/ Residual nidus/ Areas prone to NPPB ► Immediate post-op/ Peri-op angiography

31. Intra-Op Complication ► Premature division of venous drainage ► Extensive bleeding along the deep margin ► Post-resection NPPB/ Residual AVM ► Pack the wall with Avitene & Gelfoam ► Immediate removal of the entire AVM

32. Post-Op Complications ► Subgaleal fluid collection ► Sterile meningitis ► Wound infection ► Intracerebral hematoma

33. Post-op Deterioration ► Normal Perfusion Pressure Breakthrough 4 post-op swelling or hemorrhage post-op swelling or hemorrhage loss of autoregulation 4 ? 5 loss of autoregulation 4 ? 5 Mx: prevent post-op hypertension Mx: prevent post-op hypertension ► Occlusive Hyperemia 6 immediate: obstruction of venous outflow immediate: obstruction of venous outflow delayed: venous or sinus thrombosis delayed: venous or sinus thrombosis Mx: adequate post-op hydration Mx: adequate post-op hydration ► Rebleeding from a retained nidus ► Seizures

34. Radiation treatment ► Conventional radiation: effective in< 20% of cases effective in< 20% of cases ► SRS: for small (Nidus<3cm) & deep AVMs ► Radiation-induced endothelial cell proliferation → Obliteration, thrombosis ► Gamma knife/ Linac ► Non-invasive, gradual reduction of flow ► Takes 1-3 yrs to work, limited to small lesion

35. Endovascular Approach (TAE) ► Op inaccessible deep or dural feeding a. ► Usually inadequate if used alone for AVM; may recanalize ► Facilitates OP (less bleeding) & possibly SRS ► Can ’ t be used alone, acute hemodynamic change, multiple procedures

36. Endovascular Approach (TAE) ► Glue: N-butyl cyanoacrylate (nBCA), Lipiodol, tantalum powder, D5W tantalum powder, D5W ► Embolization of the nidus through the feeders without any significant glue entering the draining veins ► In general, only 2-3 vessels are embolized per session.

37. Endovascular Approach (TAE) ► Anesthesia: MAC/ GA ► Induced hypotension with vasoactive agents, general anesthesia, or even brief adenosine- induced cardiac pause at the time of embolization to allows the glue to set ► Provocation test: Sodium amytal & cardiac lidocaine injection to determine that embolization will not result in neurologic deficit Sodium amytal & cardiac lidocaine injection to determine that embolization will not result in neurologic deficit

38. Anesthesia-related Considerations for Cerebral AVMs ► Extensive blood loss ► Pharmacological brain protection ► Non-pharmacological brain protection Anesthesia-related considerations for cerebral arteriovenous malformations Hashimoto T, Young W L, et al Departments of Anesthesia and Perioperative Care, Neurosurgery, and Neurology, Center for Cerebrovascular Research, UCSF Neurosurg Focus 11 (5): Article 5, 2001

39. Monitor ► EKG/SpO 2 /ETCO 2 /BT/CVP ► Measurement of vascular pressure differentiate a. from v. differentiate a. from v. decision of whether a vein can be sacrificed decision of whether a vein can be sacrificed

40. Anesthetic Technique Choice of Agents ► Avoid cerebral vasodilators!!! ► General condition ► Isoflurane/N 2 0 ► Additional Barbiturate loading ► Metabolic suppression- propofol, etomidate

41. Non-pharmacological Cerebral Protection

42. Brain Relaxation ► Good head position ► CSF drainage ► Diuretics/Osmotherapy ► Avoid excessive cerebral vasodilator!!! ► Modest hypocapnia with hyperventilation

43. Euvolemia & Pressure Control ► Euvalemia ► Optimal cerebral perfusion pressure

44. Induced Hypotension ► Aneurysm/ AVM ► Large AVMs with deep a. supply ► Barbiturate therapy

45. Fluid and Electrolyte Management ► Isotonicity Stable cardiovascular status Stable cardiovascular status Prevention of cerebral edema Prevention of cerebral edema Aggressive isotonic crystalloids may worsen brain edema by decreasing colloid oncotic pressure. 6 Aggressive isotonic crystalloids may worsen brain edema by decreasing colloid oncotic pressure. 6 ► Euglycemia less than 200mg/dl less than 200mg/dl 6. Drummond JC, Patel PM, et al: The effect of the reduction of colloid oncotic pressure, with and without reduction of osmolarity, on post-traumatic cerebral edema. Anesthesiology 88:993-1002,1998

46. Toleration of Modest Hypothermia ► Mild hypothermia(34-35° C); cerebral protection cerebral protection ► SE: drug metabolism increased rate of myocardial ischemia increased rate of myocardial ischemia infection infection arrhythmia arrhythmia coagulopathy coagulopathy

47. Emergence & Recovery ► Post-resection BP challange; Hemostasis/ Residual nidus/ Areas prone to NPPB Hemostasis/ Residual nidus/ Areas prone to NPPB ► BP control: most important ► NE

48. Postoperative Management ► BP control SBP< 120mmHg x 2d SBP< 120mmHg x 2d ► BT control

49. Any Comment or Question?

50. Thanks for Your Attention & Have a Good Day!!!