Neurosurgery in Stroke. When and How?

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1 artery endarterectomy. BOND et al. systematically reviewed the risk of carotid endarterectomy in relation to the clinical indication for, and timing of, surgery. 24 It included 383 studies, only 13 of which reported on urgent carotid surgery. The absolute risk of stroke and death resulting from urgent carotid endarterectomy was 19.2%. The combined relative odds ratio of the peri-operative mortality and morbidity resulting from surgery for urgent indications versus non urgent surgery was 4.9. There have been several studies published in the last 5 years, with very good results and outcomes. Risk-benefit analysis for each patient is important. Outcome of urgent carotid surgery : studies of recent years n Stable or better (after 1 month) Mortality Schneider et al (20) % 0% Brandl et al (21) % 0% Peiper et al (22) % 0% Gay et al (10) % 9.5% Huber et al (11) 67 76% 3% The principle of urgency after or during acute neurological ischemic events in patients with carotid disease has to be thoroughly investigated and outlined. Indications and timing of urgent CEA after recent neurological deficit are still not precisely defined. Urgent CEA seems safer and effective treatment option for patients with crescendo TIA and stroke in progression. References: 1. North American Symptomatic Carotid Endarterectomy Trial (NASCET) Investigations. Clinical alert: benefit of carotid endarterectomy for patients with high-grade stenosis if the internal carotid artery. Stroke 1991;22: European Carotid Surgery Trialists, Collaborative Group. MRC European Carotid Surgery Trial: interim results for symptomatic patients with severe (70 99%) or with mild (0 29%) stenosis. Lancet 1991;337: Mayberg MR, Wilson SE, Yatsu F, et al. Carotid endarterectomy and prevention of cerebral ischaemia in symptomatic carotid stenosis. Veterans Affair Cooperative Studies Program 309 Trialis Group. JAMA 1991;266: Golstone J, Moore WS. A new look at emergency carotid artery operations for the treatment of cerebrovascular insufficiency. Stroke 1976;9: Whittemore AD, Ruby ST, Couch NP, Mannick JA. Early carotid endarterectomy in patients with small fixed neurogical deficits. J Vasc Surg 1984;1: Piotrowski JP, Bernhard VM, Rubin JR, et al. Timing of carotid endarterectomy after acute stroke. J Vasc Surg 1990;11: Little JR, Moufarriji NA, Furlan AJ. Early carotid endarterectomy after cerebral infarction. Neurosurgery 1989;24: Mussa F, Aaronson N, Lamparello PJ, et al. Outcome of carotid endarterectomy for acute neurological deficit. Vasc Endovasc Surg 2009;43: Dorigo W, Pulli R, Nesi M, et al. Urgent carotid endarterectomy in patients with transient ischaemic attacks or acute stroke. Eur J Vasc Endovasc Surg 2011;41: Rerkasem K, Rothwell PM. Systematic review of the operative risks of carotid endarterectomy for recently symptomatic stenosis in relation to the timing of surgery. Stroke 2009;40: Karkos CD, Hernandez-Lahoz I, Naylor AR. Urgent carotid surgery in patients with crescendo transient ischaemic attacks and stroke-in-evolution: a systematic review. Eur J Vasc Endovasc Surg 2009;37: Radak DJ, Ilijevski NS, Nenezic D, et al. Temporal trends in eversion carotid endarterectomy for carotid atherosclerosis: single-center experience with 5,034 patients. Vascular 2007;15: Radak D, Tanaskovic S, Ilijevski N, et al. Eversion carotid endarterectomy versus best medical treatment in symptomatic patients with near total internal carotid occlusion: a prospective nonrandomized trial. Ann Vascr Surg 2009;24: Radak D, Davidovic L, Vukobratov V, et al. Carotid artery aneurysms: Serbian multicentric study. Ann Vasc Surg 2007;21: Ilijevski N, Gajin P, Neskovic V, Kolar J, Radak D. Postendarterectomy common carotid artery pseudoaneurysm. Vascular2006;14: Ilijevski N, Krivokapic B, Smiljanic B, et al. Carotid endarterectomy in cervical block anesthesia in patients with occluded contralateral internal carotid artery. Srp arh celok lek 2006;134: Radak D, Radevic B, Sternic N, et al. Single center experience on eversion versus standard carotid endarterectomy: a prospective non-randomized study. Cardiovasc Surg 2000;8: Radak D, Tanaskovic S, Matic P, Babic S, Aleksic N, Ilijevski N. Eversion carotid endarterectomy our experience after 20 years of carotid surgery and 9897 carotid endarterectomy procedures. 19.Goodney PP, Wallaert JB, Scali ST, et al. Vascular Study Group of New England. Impact of practice patterns in shunt use during carotid endarterectomy with contralateral carotid occlusion. J Vasc Surg 2012;55: Gay J. L., Curtil A., Buffiere S. et al. Urgent carotid artery repair : a retrospective study of 21 cases. Ann Vasc Surg, 2002,16 : Huber R., Müller B. T., Seitz R. J. et al. Carotid surgery in acute symptomatic patients. Eur J Vasc Endovasc Surg, 2003, 25 : Eckstein H. H., Schumacher H., Klemm K. et al. Emergency carotid endarterectomy. Cerebrovasc Dis, 1999, 9 : Gertler J. P., Blankensteijn J. D., Brewster D. C. et al. Carotid endarterectomy for unstable and compelling neurologic conditions: do results justify an aggressive approach? J Vasc Surg, 1994, 19 : Bond R., Rerkasem K., Rothwell P. M. Systematic review of the risks of carotid endarterectomy in relation to the clinical indication for, and timing of, surgery. Stroke, 2003, 34 : The theme for the next issue of Stroke talk will be on Stroke brain imaging. The Pandora s box. So kindly send your articles/experiences/related activity to: stroketalk.isa@gmail.com (As always your case studies on interesting cases of Stroke management are welcome too) Dear Friends, We welcome you to this new issue of Stroke talk in continuation with our last issue entitled Neurosurgery in Stroke: When & How? We were overwhelmed by the response from our readers from last issue where we discussed different neurosurgeries currently in practice to reduce mortality & risk of recurrent stroke. In this issue, we present to you expert articles describing ischemic stroke concerned with carotid lesions & their link with coronary heart disease, along with the pivotal role played by carotid endarterectomy in times of urgency. In order to improve neurological & functional outcomes & quality of life, preventive and therapeutic strategies must address both cerebral and systemic risk. Neurosurgeries like decompressive hemicraniectomy can produce good functional outcomes in such conditions with minimally compromising functional decline of the patient especially concerning disability & aphasia. We also present an interesting case study discussing brain swelling following stroke & its associated complications. We sincerely thank our readers for supporting us in this endeavour. We hope our readers find this issue as interesting as the previous one, helping doctors to take management & treatment of stroke to the next level. Regards Dr. S.M. Hastak Dr. Abhishek Srivastava Neurosurgery in Stroke. When and How? ISSUE-16 Dr. Dheeraj Khurana Dr. D. Nagaraja Dr. Ashok Uppal Dr. V.G. Pradeep Kumar Dr. Vinit Suri Dr. Anand Alurkar Dr. Jeyaraj D. Pandian Dr. Sunil K. Narayan Dr. P.N. Sylaja

2 SURGERY IN STROKE WHEN AND HOW? Dr. Anu Gupta, Dr. Dheeraj Khurana Department of Neurology, Postgraduate Institute of Medical Education and Research, Chandigarh Case vignette A 83 Yrs male, diabetic and hypertensive with chronic kidney disease and CAD, presented with weakness of right upper and lower limb of 1 hour duration. On examination his GCS was E4V2M6,NIHSS 28. His NCCT Head revealed a left dense MCA Sign (Figure 1a) with an ASPECT of 0/10. He was thrombolysed with alteplase (Dose 0.6 mg/kg due to nephropathy). His repeat CT scan at 24 hours showed an infarct in the left MCA territory (Figure 1b). He maintained a good general and neurological condition for the next 48 hours. On day 4 of stroke, he became drowsy to stuporose (GCS E2V2M5) NCCT now showed well formed Infarct with mass effect and midline shift to the right. A prompt neurosurgical consultation was sought for an emergency decompressive hemicraniectomy. While he was being prepared for surgery, his sensorium further deteriorated with a fall in saturation and after ~3.5 hours of his worsening, he sustained a cardiac arrest. Medical management of brain edema and increased ICP may not suffice in the event of significant swelling occurring in the cerebral or cerebellar hemisphere and the slightest of delays in recognition of decompensating cerebral edema is life threatning. Decompressive hemicraniectomy could be life saving and an efficacious surgical procedure and associated with good functional outcomes. Malignant cerebral infarction Brain swelling is a life-threatening consequence of a large-territory ischemic stroke. It occurs due to loss of function of membrane transporters, causing sodium and water influx into ischemic cell, leading to cytotoxic edema. The development of clinically significant cerebral edema can occur in 3 ways: a rapid and fulminant course (within hours), a gradually progressive course (over several days), or an initially worsening course followed by a plateau and resolution (about a week).1 The mass effect of the swollen hemisphere produces a decreased level of arousal due to compression of thalamus, brainstem and network projections to the cortex. Medical management alone in such situations may not be adequate to salvage these patients or change outcomes. The term malignant middle cerebral artery (MCA) infarction, introduced in 1996, was originally defined as infarction of the entire MCA territory appearing on computed tomography (CT) within 48 hours, with or without infarction in other vascular territories.2 Presently, the target population is defined as patients who are at high risk for or who ultimately suffer neurological deterioration attributable to cerebral swelling after ischemia % of all MCA territory ischemic strokes are hemispheric infarctions.4 Subsequent neurological deterioration and death occurs in 40-80%.5 It is typically seen in patients with ICA or mainstem MCA occlusions. Clinically the most common findings are hemiplegia, global or expressive aphasia, severe dysarthria, neglect, gaze preference, and a visual field defect. An initial National Institutes of Health Stroke Scale score of > 20 with dominant hemispheric infarction and >15 with nondominant hemispheric infarction is a sensitive but not specific marker.6 Pupillary abnormalities indicate significant brainstem compression and develop between 3 to 5 days. Acute carotid artery occlusion or dissection may present with an early Horner s syndrome. The most specific sign of significant cerebral swelling after stroke is a decline in the level of consciousness, usually occurring within hours.7 However combined MCA and ACA infarctions may have diminished responsiveness from the beginning. The presence of cerebral ptosis(in right MCA infarctions) may give a false suggestion of a decreased level of consciousness. The other clinical parameters associated with development of a malignant infarction include early nausea vomiting, younger age (intracranial compliance is less as compared to older patients), female sex, congestive heart failure and leukocytosis.3 Haemorrhagic conversion of the infarct may produce a new mass effect and lead to worsening. On neuroimaging progressive cerebral edema and mass effect is characterised by ipsilateral sulcal effacement, compression of the ipsilateral ventricular system, and then a shift of the midline structures such as the septum pellucidum and the pineal gland. The blockage of foramen of Monro or the third ventricle might lead to entrapment and dilatation of the contralateral lateral ventricle and obstructive hydrocephalus. Brainstem displacement may lead to widening of the ipsilateral ambient cistern. These cisterns become effaced when swollen tissue eventually fills the cisterns. Infarction in the territories of the anterior or posterior cerebral arteries may be seen in some patients. Serial CT findings in the first 2 days are thus useful to identify patients at high risk for developing symptomatic swelling. CT findings that predict malignant edema and poor prognosis include frank hypodensity on head CT within the first 6 hours, involvement of one third or more of the MCA territory and involvement of basal ganglia in the infarcted area (Figure 1b).8 The presence of a dense MCA sign8 or midline shift 5 mm9 within the first 2 days is also associated with neurological deterioration and early mortality. Angiographically a Tocclusion of the distal internal carotid artery10, 11 and an incomplete circle of Willis10 leading to involvement of multiple vascular territories is also predictive of development of malignant edema and worse outcome. On MRI, acute DWI volume (MRI done within 6 hours of stroke onset) of 80 ml3 and DWI volume of > 145 ml (MRI done 14 hours after stroke onset) is predictive of a progressive downhill course.12 Such patients should be managed in an intensive care or

3 stroke unit and an early neurosurgical consultation should be sought to plan surgery if patient deteriorates. Generally, deterioration in a supratentorial hemispheric infarct may present in 2 ways, either a gradually progressive rostrocaudal deterioration (development of midposition pupils, worsening of motor responses, and progression to irregular breathing and death) or more sudden deterioration with a unilaterally dilated pupil progressing to bilateral pupils followed by decreasing motor response. Figure 1A and B: Cranial Non contrast CT showing dense left MCA (A) and Early Malignant left MCA infarct (B) Surgical treatment of the swelling associated with cerebral infarctions is performed by removal of the skull and expansion of the dura is known as decompressive craniectomy with dural expansion. Three prospective, randomized trials (i.e., Decompressive Surgery for the Treatment of Malignant Infarction of the Middle Cerebral Artery [DESTINY] 13, Decompressive Craniectomy in Malignant Middle Cerebral Artery Infarction [DECIMAL] 14, and Hemicraniectomy After Middle Cerebral Artery Infarction With Life-threatening Edema Trial [HAMLET] 15 ) and 14 case series have studied patients with supratentorial infarctions treated with decompressive craniectomy within 48 hours of stroke onset. On the basis of a pooled analysis, it is recommended that patients <60 years of age with unilateral MCA infarctions who deteriorate neurologically within 48 hours despite best medical therapy, should undergo decompressive craniectomy with dural expansion. 16 The effect of later decompression is not known, but it should be strongly considered. The above trials have shown a significant reduction in mortality (22% versus 71% mortality, pooled analysis) with hemicraniectomy compared to medical management. The residual disability remains significant as only 14% of the survivors could look after their own affairs without assistance (mrs score 2). 16 All prior clinical trials involved patients <60 years of age (mean age, 45 years) and it remained unclear whether older patients would experience a similar effect until the results of DESTINY 2 became available. The trial concluded that early hemicraniectomy significantly increased the probability of survival even among patients older than 60 years of age with malignant middle-cerebral-artery infarction (proportion of patients who survived at 6 months without severe disability was 38% in the hemicraniectomy group, as compared with 18% in the control group), but majority required assistance with most bodily needs (7% had modified rankin score of 3, 32% had a score of 4 and 28% had a score of 5 compared to 3%, 15% and 13% respectively in the control group). 17 Postoperative concerns include wound dehiscence and requirement of tracheostomy and gastrostomy in the initial postoperative period. The timing of cranioplasty after decompressive craniectomy remains unknown with a wide variation in clinical practice. Early cranioplasty (within 10 weeks of craniectomy) results in higher chance of complications like hydrocephalus and infection, particularly in patients with a ventriculoperitoneal shunt at the time of cranioplasty. Late cranioplasty can produce a communicating hydrocephalus, requiring ventriculoperitoneal shunt placement. 3 Indian perspective In a prospective observational cohort study on 60 patients of large MCA infarcts, decompressive hemicraniectomy lead to markedly improved survival (45% risk reduction in death at 1 year compared to medical management alone) and better functional outcome (motor and language) at 1 year (20% patients achieved good outcome that is modified ranking score 3 as compared to none in the other group). The benefit of surgery in motor and aphasia recovery was progressive and sustained until 1 year. 18 Malignant cerebellar infarction Few, if any, reliable clinical signs and symptoms can serve to stratify cerebellar stroke patients across a continuum of clinical severity. Swelling after cerebellar infarction may result in pontine compression causing ophthalmoparesis, breathing irregularities, and cardiac dysrhythmias. It may produce acute hydrocephalus secondary to obstruction of the fourth ventricle. Often both pontine compression and hydrocephalus occur together. The most reliable clinical symptom of tissue swelling is decreased level of consciousness. Peak swelling occurs several days after the onset of ischemia. Effacement of the fourth ventricle is a key radiologic marker, followed by basal cistern compression, followed by brainstem deformity, hydrocephalus, downward tonsillar herniation, and upward transtentorial herniation. Predictive MRI based infarct volumes have not been clearly defined for cerebellar strokes. Decision of surgery (Bioccipital craniectomy) is based on a combination of clinical and radiologic worsening. The time interval to surgery does not seem to affect outcome. The value of preemptive surgery (that is when swelling and hydrocephalus progress on CT scan in a clinically stable patient) and the best neurosurgical approach (i.e., removal of necrotic tissue versus decompression alone versus decompression and ventriculostomy) are not known. Surgery in spontaneous ICH For most patients with ICH, the usefulness of surgery is uncertain. As per the 2010 AHA/ASA guidelines 19, patients with cerebellar hemorrhage who are deteriorating neurologically or who have brainstem compression and/or hydrocephalus from ventricular obstruction should undergo surgical removal of the hemorrhage as soon as possible. Initial treatment of these patients with ventricular drainage alone rather than surgical evacuation is not recommended. For patients presenting with lobar clots >30 ml and within 1 cm of the surface, evacuation of supratentorial ICH by standard craniotomy might be considered. The effectiveness of minimally invasive clot evacuation by stereotactic or endoscopic aspiration with or without thrombolytic usage is uncertain and considered investigational. Although intraventricular administration of recombinant tissue-type plasminogen activator in IVH appears to have a fairly low complication rate, efficacy and safety of this treatment is uncertain and is again considered investigational. Conclusion To conclude, brain swelling following stroke can cause secondary cerebral ischemia, herniation syndrome, and brain death. Aggressive surgical treatment is necessary to prevent detrimental outcomes. Important questions such as the acceptable degree of disability in survivors post surgery, long-term effect of chronic disability, the importance of aphasia and the best timing of surgery require further research. References 1. Wijdicks EF, Diringer MN. Middle cerebral artery territory infarction and early brain swelling: progression and effect of age on outcome. Mayo Clin Proc 1998; 73: Hacke W, Schwab S, Horn M, Spranger M, De Georgia M, von Kummer R. 'Malignant' middle cerebral artery territory infarction: clinical course and prognostic signs. Arch Neurol 1996; 53: Wijdicks EF, Sheth KN, Carter BS, Greer DM, Kasner SE, Kimberly WT, et al. Recommendations for the management of cerebral and cerebellar infarction with swelling: a statement for healthcare professionals from the American Heart Association/American Stroke Association. Stroke 2014; 45: Heinsius T, Bogousslavsky J, Van Melle G. Large infarcts in the middle cerebral artery territory. Etiology and outcome patterns. Neurology 1998; 50: Kasner SE, Demchuk AM, Berrouschot J, Schmutzhard E, Harms L, Verro P, et al. Predictors of fatal brain edema in massive hemispheric ischemic stroke. Stroke 2001; 32: Bardutzky J, Schwab S. Antiedema therapy in ischemic stroke. Stroke 2007; 38: Frank JI. Large hemispheric infarction, deterioration, and intracranial pressure. Neurology 1995; 45: Manno EM, Nichols DA, Fulgham JR, Wijdicks EF. Computed tomographic determinants of neurologic deterioration in patients with large middle cerebral artery infarctions. Mayo Clin Proc 2003; 78: Pullicino PM, Alexandrov AV, Shelton JA, Alexandrova NA, Smurawska LT, Norris JW. Mass effect and death from severe acute stroke. Neurology 1997;49: Jaramillo A, Góngora-Rivera F, Labreuche J, Hauw JJ, Amarenco P. Predictors for malignant middle cerebral artery infarctions: a postmortem analysis. Neurology 2006; 66: Kucinski T, Koch C, Grzyska U, Freitag HJ, Krömer H, Zeumer H. The predictive value of early CT and angiography for fatal hemispheric swelling in acute stroke. AJNR Am J Neuroradiol 1998; 19: Oppenheim C, Samson Y, Manaï R, Lalam T, Vandamme X, Crozier S, et al. Prediction of malignant middle cerebral artery infarction by diffusion-weighted imaging. Stroke 2000; 31: Jüttler E, Schwab S, Schmiedek P, Unterberg A, Hennerici M, Woitzik J, et al. Decompressive Surgery for the Treatment of Malignant Infarction of the Middle Cerebral Artery (DESTINY): a randomized, controlled trial. Stroke 2007; 38: Vahedi K, Vicaut E, Mateo J, Kurtz A, Orabi M, Guichard JP, et al. Sequential-design, multicenter, randomized, controlled trial of early decompressive craniectomy in malignant middle cerebral artery infarction (DECIMAL Trial). Stroke 2007; 38: Hofmeijer J, Kappelle LJ, Algra A, Amelink GJ, van Gijn J, van der Worp HB. Surgical decompression for space-occupying cerebral infarction (the Hemicraniectomy After Middle Cerebral Artery infarction with Life-threatening Edema Trial [HAMLET]): a multicentre, open, randomised trial. Lancet Neurol 2009; 8: Vahedi K, Hofmeijer J, Juettler E, Vicaut E, George B, Algra A, et al. Early decompressive surgery in malignant infarction of the middle cerebral artery: a pooled analysis of three randomised controlled trials. Lancet Neurol 2007; 6: Jüttler E, Unterberg A, Woitzik J, Bösel J, Amiri H, Sakowitz OW, et al. Hemicraniectomy in older patients with extensive middle-cerebral-artery stroke. N Engl J Med 2014; 370: Rai VK, Bhatia R, Prasad K, Padma Srivastava MV, Singh S, Rai N,et al. Long-term outcome of decompressive hemicraniectomy in patients with malignant middle cerebral artery infarction: a prospective observational study. Neurol India 2014; 62: Morgenstern LB, Hemphill JC 3rd, Anderson C, Becker K, Broderick JP, Connolly ES Jr, et al. Guidelines for the management of spontaneous intracerebral hemorrhage: a guideline for healthcare professionals from the American Heart Association/American Stroke Association. Stroke 2010; 41: Corresponding author Dr. Dheeraj Khurana Additional Professor Department of Neurology PGIMER, Chandigarh dherajk@yahoo.com

4 ISCHEMIC STROKES RELATED TO CAROT- ID LESIONS, AND LINK WITH CORONARY HEART DISEASE Dr. S. Ravikumar and Dr. K. Srinivasan Madurai Medical College and Apollo Hospitals It is now realized that Extracranial carotid disease (ECAD) as a cause of stroke is less common in the Tropics compared to the west. Intracranial (ICVD) and cardioaortic causes proved in more than 20-30% of patients. 1 In one recent study in South India, in 198 patients with Ischemic Stroke, who had DSA done ICAD was seen exclusively in 14% and along with ECVD in 42%. 2 Already reported that ICAD explains strokes in 10% of whites, 15-30% in Blacks and 30-50% in Asians Large numbers could be asymptomatic, since robust collaterals mitigate stroke evolution. 3 Link between Carotid (CVD) and Coronary HT diseases (CHD) C. Miller Fisher said earlier that for every cerebral vessel blocked, 2 coronaries are already blocked and 4 peripheral vessels may be blocked, asymptomatic because of collaterals. In a large P.M. Study, Atheroma was significant in Aortoiliac (952 patients) Femoropopliteal (772), ICA (256) ECA (9), CCA (16) Subclavian (29) vertebral (55), Innominate (16). Atherosclerosis is widespread. 4 In 184 patients with CHD, carotid stenosis over 50% seen in 28% and 48% of these were asymptomatic. In a study of 619 patients with asymptomatic carotid stenosis followed for 4 years, 45 had TIA, 29 had stroke, CHD in 132 (59 died of M.I.). Carotid strokes occur after CABG (2-9%), mostly within 48hrs after surgery. Similarly MI occurs after CEA. Perioperative stroke may occur in opposite carotid area, often due to Aortic causes during CABG, reflecting basic atherosclerosis risks 6, 7, 8 than blaming carotid disease!! Sever CHD greater than 50% stenosis in the Left mam (LAD) or 3 vessel disease is recorded in 18-38% of patients with recent stroke without prior angina. This is based CTA. This is 6, 7, 8 considered lower in Europeans (18-26%) than Asians 32-38%. Our data reviewing over 1000 CABG cases showed only less than 10% eligible for CEA. Posterior circulation, extracranial stenosis is even less strongly associated with CAD. 5 Morphology of carotid intimal lesions Non obstructive planques with more inflammatory ulceration (oxidized LP) lipid rich, than fibrous caps in carotid and coronary are more harmful than thick fibrous caps. TCD shows abundant microemboli to brain during CABG. Our studies show less frequent obstructive on atherogenic (unstable) carotid plaques compared to west (USG and Catheter angiography). Morphology studies in carotid is subjective with USG and controversial. It is better evaluated in CHD with IVUS, OCT etc. used before stenting coronaries but still far from wide acceptance. Our study: results - see table- Adult ischemic strokes (340pts). CABG 120 patients as a preliminary study. Carotids assessed by USG, MRA and in CABG cases by catheter, angiography. 1. Symptomatic ICA lesions with compelling need for CEA or CAS in only less than 10%. Significant carotid atheroma in only 20%. Carotids normal in 50-60% of Ischemic Strokes and CHD. 2. Link between carotid and coronary disease less strong than in the west. However carotid bruit should alert both the neurologist and cardiologist. 3. Less well studied but relevant: Morphology of plaques, (CIMT recorded), Haemodynamic factors, Haemorheology etc. 4. Common risk factors (RF). e.g. Diabetes, Hypertension, Lipids can be decisively blamed in only less than 50% of CVD or CHD. Especially with the causative intracranial and cardio embolic causes more common in the East than the west. 5. Patients asks. Why did I need CABG? Or why did I experience TIA or stroke. I do not have any RF, smoking, drinking, Diabetes, H.T., Lipids, etc. We blame Genes, Stress and Life style etc.! APPENDIX A B (Medical College) ISCHEMIC STROKE C.A.B.G Done (Another centre) 340 (M=260) 120 (M=105) ICA Stenosis >70% 10% <10% Normal 50% 50% I.H.D, EF <30 25% all R.F Ischemic Stroke CABG Cases Hypertension 35% 40% Diabetes 35% 45% Dyslipidemia 15% 30% Reference: 1. Nagaraja, D.Strokes in Tropics. Tropical Neurology, Landes Biosc pub. 2003, p Vanchilingam et al., Incidence of ECAD and ICAD in Ischemic stroke, in rural South India; TANCON conference, Homstedt CA et al, ICAS risk factors, Lancet Neurology, 2013, 12, Crawford, RS. et atl, Aortic atheroscerosis, Post Gr.Med, 1961, 29, Rima, MD, Risk of stroke after CABG, Neurol Clinics, 2006, 24, Guzman LA et al. Review of staged CAS with CABG, Stroke, 2008, 37, Venkatachalam S et al. Carotid disease with CABG, Current opinion cardiol. 2011, Lippincott pub Walki et al., Strokes after cardiac surgery and carotid stenosis, Arch. neurol, 2009, 66, Markquarath L.et.al VBI, Brain, 2009, 132, 982, Tauze et al. Risk of MI after stroke, Stroke 2005, 35, David calvet etal. Predicting asymptomatic CAD after stroke, Stroke, 2013, 44, Corresponding Address Dr. K. Srinivasan, 10, (41/158), Ramiah Thevar St, Nataraja Nagar, Madurai doctorks@icloud.com EXTRACRANIAL EMERGENCY CAROTID ENDARTERECTOMY Dr. Padma S. Veerapaneni Stroke Specialist and Consultant Neurologist, Director, KIMS. Carotid artery endarterectomy (CEA) aims to remove atherosclerotic plaque from the carotid artery, preventing thrombus forma tion on the plaque, which could otherwise lead to a stroke or transient ischaemic attack (TIA). Crescendo TIA is defined as two or more episodes within 24 hours, with complete recovery after each episode, while stroke in progression is defined as gradual deterioration of neurological deficit that took place for over at least six hours. CEA can be termed urgent only if done immediately after or during arising neurological ischemic event (within six hours or less). CEAs done several days after ischemic event (TIA, stroke) can be termed as early but not urgent. Natural course of carotid related ischaemic stroke is poor. Re-infarction rate is about 12% and mortality 19% within the first year after index event Images of Carotid Endarterectomy After the three large multicentric randomized trials, namely North American Symptomatic Carotid Endarterectomy Trial (NASCET), European Carotid Surgery Trial (ECST), and Veterans Affair Cooperative Studies Program Trial Group, published their results, it became evident that carotid endarterectomy (CEA) is beneficial for stroke risk reduction in symptomatic and asymptomatic patients with high-grade internal carotid artery (ICA) stenosis. 1-3 Earliest studies have described urgent CEA with a high rate of postoperative mortality in the range of 42 60%. 4 Later studies reported that urgent CEA showed decreased rate of postoperative complications. 5-7 Most recent studies demonstrated that urgent CEA performed in patients with crescendo transient ischemic attack (TIA) as well as in patients with stroke in evolution could have favorable outcome.8-9 Increased perioperative risk has been described in patients with crescendo TIA and stroke in evolution compared with the outcome after elective CEA After the publication of results from the North American Symptomatic Carotid Endarterectomy Trial (NASCET) and the European Carotid Surgery Trial (ECST), guidelines for stroke care in the USA, Europe and elsewhere recommended operating on patients with symptomatic carotid stenosis within 6 months of the presenting ischaemic event. In 2004, a pooled analysis of data from NASCET and ECST was conducted to deter mine the effect of surgery, including surgery timing, outcomes in various subgroups etc. The study concluded that patients benefitted most from an operation within 2 weeks of an ischaemic event, and thereafter, this benefit decreased with time from event to surgery. 4 As a consequence of the above findings, clinical guidelines were revised and widely implemented in clinical practice. A study was done by P Gajin, Dj Radak, S Tanaskovic, S Babic and D Nenezic to analyze the outcome of urgent CEA in patients with crescendo TIA and stroke in progression, and was performed within less than six hours after index event occurred. 58 urgent CEAs were done in all in 46 patients with crescendo TIA and 12 patients with stroke in progression. Carotid stenosis was estimated by the means of computed tomography angiography and color duplex scan according to ESCT criteria. Carotid stenosis was considered significant (>70%) if peak systolic velocity (PSV) was >150 cm/s and end diastolic velocity (EDV) >90 cm/s. Median follow-up was 42.1 ± 16.6 months. In the early postoperative period stroke rate was 0% for the patients in crescendo TIA group while in patients with stroke in progression group 3 patients (25%) had positive postoperative brain CT, yet neurological status significantly improved. In the early postoperative period there were no lethal outcomes, mid-term mortality was 8.3% in stroke in progression while in crescendo TIA group no bad outcomes were observed. All patients in crescendo TIA group and nine patients (75%) in stroke in progression group completely recovered. While three patients (25%) in stroke in progression group had brain CT positive for ischemia, yet neurological outcome significantly improved. Kaplan Meier curve depicts stroke-free rate in patients with crescendo TIA of 97% and for patients in stroke in progression group of 75%. Neuorological mortality free rate was 100% in patients with crescendo TIA and 89% in patients with stroke in progression. Surgical technique is based on fast and efficient carotid plaque removal with very short clamping time, which has been proved as good treatment option regarding very low rate of postoperative morbidity and mortality Selective shunt use (if not standard) could be associated with increased postoperative complications. 19 Absolute contra-indications for emergent carotid endarterectomy are cerebral coma, cerebral bleeding and extensive established infarction on CTscan (more than 1/3 of the middle cerebral artery territory) The danger of urgent carotid endarterectomy is the dysautoregulated cerebral vascular bed. This, in combination with the increased perfusion pressure postoperatively and anticoagulation required for surgery, means that there is a high risk of cerebral oedema and bleeding. The study of GERTLER et al. confirmed that when the operation was performed within 3 hours the outcome was satisfactory in 61%, unsatisfactory in 29.5% and fatal in 9.5% of cases. 23 When the procedure had a delay of more than 3 hours, the results were respectively 47%, 35% and 18%. Predictive factors for a good neurological outcome are the quality of collateral flow (patent circle of Willis and patent contra-lateral carotid artery) and the absence of embolism in the middle cerebral artery. There are no randomised controlled trials concerning the risks of urgent carotid surgery versus conservative measures and delayed carotid

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