Download Aneurysmal Subarachnoid Hemorrhage (SAH)

04/09/2015
Non‐Operative Management of Subarachnoid Hemorrhage
William Humphries M.D., MPH
Assistant Professor,
Division of Neurological Surgery University of Missouri School of Medicine ‐
Columbia
Aneurysmal Subarachnoid Hemorrhage (SAH)
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Disclosure
• I have no funding sources or conflicts of interest to disclose. 48 yo AAM inpatient develops acute on‐set of the “worst headache of his life”
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Pre‐Test Question 1 • You receive a phone call indicating that a patient that you sent for a stat CTH has subarachnoid hemorrhage. You decide to transfer the patient to the ICU while awaiting neurosurgical consultation. What type of IV fluids are most appropriate assuming the patient has no renal dysfunction?
1) D5 ½ NS
2) D5 ¼ NS
3) ½ NS 4) NS w 20meq KCL Pre‐Test Question 2
• You are concerned that the patient may have some intracranial swelling/edema. What is the most appropriate agent for this setting?
1) Decadron
2) Methylprednisolone
3) Prednisone
4) 1 or 3
5) None of the above
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Pre Test Question 3 What type of cardiac complications are commonly encountered in patients with SAH?
1) Myocardial infarction
2) Stunned myocardium
3) Takotsubo’s Cardiomyopathy
4) 1 and 2
5) All of the above Pre Test Question 4
Which of the following is the most appropriate blood pressure goal until a decision is made regarding the most appropriate treatment?
1) SBP < 100
2) SBP 180‐220
3) SBP < 140
4) SBP 160‐180
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Pre Test Question 5
• In addition to the SAH the radiologist also informs you that there is marked hydrocephalus on the CTH. The nurse keeps calling you to inform you that Vicodin is not adequately addressing the patient’s headache and she is becoming agitated. What is the most appropriate alternative in the setting of hydrocephalus? 1) Dilaudid
2) Morphine
3) Add Ativan to the patient’s oral pain medication regimen
4) 2 or 3 5) None of the above
Objectives
• To review medical management of non‐
traumatic SAH
– Primary Focus on Aneurysmal SAH
• To review systemic pathophysiology of SAH
• To identify and review major systemic contributors to morbidity and mortality in SAH patients
• Provide a framework for appropriate triage and transfer of patients with SAH
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Subarachnoid Hemorrhage
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Traumatic SAH
• Single most common cause of SAH
• Seen in 33‐60% of traumatic brain injury
• Vasospasm can occur (low incidence)
– Angiography, TCD, CBF studies
– Ischemic brain injury considered rare
• Complicated by traumatic injury to brain
– No good evidence to support early treatment (e.g. nimodipine)
• American Stroke Association classifies non‐
traumatic SAH as a stroke
– Ischemic Stroke
– Hemorrhagic Stroke
• Subarachnoid Hemorrhage
• Intraparenchymal Hemorrhage
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Nontraumatic / Spontaneous SAH
• Aneurysmal SAH: ~80%
–
Van Gijn et al. Brain 2001
• Nonaneurysmal SAH: ~20%
–
–
–
–
AVM (intracranial or spinal)
Dural AVF (intracranial or spinal)
Arterial dissection
Angionegative SAH: ~7‐10%
•
•
•
•
•
Isolated/Benign Perimesencephalic SAH: 5‐10%
Coagulation disorders / iatrogenic coagulopathy
Cavernous malformation
Vasculitis
Tumor
Isolated/Benign Perimesencephalic
SAH
• 5‐10 % of SAH
– Low clinical grade • HH 1‐2
• Pt looks better than scan
– Location
• Perimesencephalic cisterns
• Negative cerebral DSA – Mechanism: Unknown • Venous source?
– Excellent outcome • Rarely rebleed
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48 y.o. woman with spontaneous severe headache and nausea
Further W/U Angionegative SAH
• MRI: evaluate for vascular malformation of brain, brain stem, or spinal cord
• Repeat angiogram (7 ‐ 14 days)
– Aneurysms can be obscured by hemorrhage, thrombosis or vasospasm
– Aneurysms can be detected on the second angiogram in 2‐24% of patients 9
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Aneurysmal SAH
• Incidence: 10.5 cases / 100,000 person‐years
– Increases with age, mean age at presentation‐ 55 yo
• Male: Female 1 : 1.6
• White: Black 1: 2.1
• Mortality 51%
–
–
–
–
Most within 2 weeks
10% before patients receive medical attention
Up to 25% within 24 hours after event
Up to 40 % at 30 days
Aneurysmal SAH
• Mortality 70‐80% if re‐hemorrhage
• Mortality higher for posterior circulation vs
anterior circulation
• 1/3 of survivors need lifelong care
Hop et al. Stroke 1997
• Major factors associated with poor outcome
– Level of consciousness / deficits on admission
– Amount of blood shown by initial CT
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SAH Risk Factors
• Modifiable Risk Factors
– Cigarette smoking (nicotine)
– Hypertension
– Drug use
• Cocaine
• Methamphetamines
– Heavy alcohol use
• Non‐Modifiable Risk Factors
– Family history
• 2 or more first degree relatives
– Heritable connective‐tissue disorders
• Polycystic kidney disease, Ehlers‐Danlos
(IV), pseudoxanthoma
elasticum, fibromuscular dysplasia
– Size and location of aneurysm
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Clinical Presentation
• Typical
– Headache
• “Worst headache of my life” (sudden, severe)
• “sentinel (warning) headache” up to 40%
– Weakness
– Vomiting
– Meningismus (6‐24 hrs)
– Photophobia
– Seizure
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Clinical Presentation
• Other
– CN dysfunction
• CN III‐ PCOM
• CN VI‐ increased intracranial pressure
– Seizures
– Syncope
– Altered consciousness or AMS
• High ICP, Decreased CBF
• Brain injury due to ICP or hemorrhage
• Hydrocephalus
– Ocular hemorrhage: pre‐retinal, retinal, vitreous humor
• hypertension due to high ICP
• Terson syndrome‐ Vitreous humor hemorrhage • Pre‐retinal and Terson syndrome associated with higher mortality rates
CT Findings
• CT Head w/o contrast
• Hyperdensity (blood) in the cisterns and fissures – Sensitivity
• 100 % (12 hours from onset)
• 93% (12‐24 hours from onset)
• 50 % (7 days from onset)
– False negative
2.5 – 7 %
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Lumbar puncture
• High clinical suspicion for SAH, but CT negative
– History: correlate timing of symptoms/presentation and test
• Differentiation from traumatic tap
– Opening pressure: High
– Bloody CSF (> 100,000 RBC /mm3) • SAH does not significantly clear with sequential tube
– Xanthochromia (spectrophotometry)
• Rare < 2hrs
• 70 % + by 6 hrs
• > 90 % + by 12 hrs
• 70 % + at 3 weeks
– If equivocal ‐> vascular study
MRI‐ Findings
• Sensitive to detect met‐Hb
– In particular in subacute to remote SAH
• Sensitivity of FLAIR image is even higher than that of CT
• MRA is not as sensitive as CTA and DSA to detect aneurysms
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CTA and Cerebral DSA
• Detecting source of SAH
• CTA: CT Angiography – Prospective evaluation‐ 97% Sensitivity
– Cheaper, safer, faster than DSA
– Provides bony anatomy, Helpful in surgical planning
• Cerebral DSA: Digital Subtraction Angiography – Gold standard for imaging aneurysms and planning treatment strategy
– Collateral flow
– Treatment in same setting
Grading Scales used in SAH
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Hunt & Hess Grade
Correlates with clinical outcomes
Fisher Grade
Correlates with severity of vasospasm 16
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WFNS Grade
Correlates with prognosis
ICU Care
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Chen S, Li Q, Wu H, Krafft PR, Wang Z, Zhang JH. The harmful effects of
subarachnoid hemorrhage on extracerebral organs. Biomed Res Int.
2014;2014:858496. doi: 10.1155/2014/858496. Epub 2014 Jul 7. PubMed PMID:
25110700; PubMed Central PMCID: PMC4109109.
• Organized by The Neurocritical Care Society
• International Multidisciplinary Conference – Neurocritical Care
– Neurologists – Neurosurgeons
– Anesthesiologists
– Neuroradiology
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• American Academy of Neurology
• American Association of Neurological Surgeons
• Congress of Neurological Surgeons
• Society of NeuroInterventional Surgery Rebleeding
• Rebleeding of untreated ruptured aneurysms
– 4%‐13.6% in the first 24 hours
– 5‐10% in the first 72 hours
– 1.5 % daily for 13 days: 20% cumulative at 2 weeks
– 50 % at 6 months
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Antifibrinolytic Therapy
• Amicar / Aminocaproic
acid • May reduce rebleeding
rate
• Prolonged use (>72hrs) complications: clotting, increased risk of hydrocephalus and vasospsam
• Discontinue 2 hours prior to endovascular procedure
Blood Pressure
• No randomized‐controlled trials
• Hypertension
– Concern for rebleeding in unsecured aneurysms
– SBP <140
• Cardene ggt
• Labetalol 10mg IV q2h prn for SBP<140
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Blood Pressure
• Hypotension
– Should be avoided – Concern for ischemic stroke in the setting of vasospasm/increased ICP
– CPP = MAP – ICP
– Permissive hypertension if aneurysm is secured and vasospasm is a concern.
• Be mindful of cardiac disease – Refractory hypotension: think about cardiogenic
shock/ MI
Hydrocephalus
• 20% mild ventriculomegaly or HCP at SAH presentation
• Ventriculostomy and CSF drainage prior to protection of aneurysms may increase rate of rebleeding
– Keep ICP 15 ‐ 25 mmHg
• Chronic hydrocephalus occurs in 8‐45% of cases
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“Remember: CSF has killed more people than blood”
• Hydrocephalus is a neurosurgical emergency!
• Limit sedatives –
–
–
–
Morphine
Oral Opiods
Fentanyl
Ativan
• Do not sedate
• Frequent neuro checks
• Transfer to ICU immediately
“Young doctor there a lot of things worse than a headache, like death”
 DO NOT SEDATE AN AGITATED PATIENT WITH HYDROCEPHALUS




Call for help
Transfer to the ICU
Stand your ground
They may hate you at that point but they will thank you later. 22
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Seizures
• Seizures after SAH in 6‐18%
• 90% of seizures occur within 24 hrs after bleed
• Seizure is not associated with an increased risk of rebleeding
• Routine seizure prophylaxis is not necessary
– If done, 1 week or less
• Incidence of epilepsy after SAH is 3‐8%
• Fewer seizure in patients with coiling compared to clipping (ISAT)
Cerebral Vasospasm
• Major cause of morbidity and mortality
• Pathogenesis not fully elucidated
– Red blood cell lysis in subarachnoid space ‐> release of various vasoconstrictive mediators – Oxyhemoglobin, free radicals, eicosanoids, endothelin, etc
• Days 4‐14 (Maximum frequency in 6‐8 days)
• Angiographic vasospasm: 70%, Symptomatic vasospasm: 20‐30%
• Risk factors
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–
–
–
–
Amount of blood in subarachnoid space
High clinical grade
Smoking
Cocaine Use
Age < 50
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Diagnosis of Vasospasm
(Delayed Ischemic Neurologic Deficit)
• Clinical presentation
– Altered mental status,
– Focal neurological deficits
• Radiological evaluation
– Transcranial Doppler (TCD)
– CTA
– CBF studies (CT perfusion, SPECT)
– Cerebral angiography (Gold Standard)
• Significant is > 25‐50% of normal caliber
Figure 2. Illustrative case no. 1.
Cerebral Vasospasm
Barth M et al. Stroke. 2007;38:330-336
Copyright © American Heart Association, Inc. All rights reserved.
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Prevention of Vasospasm
•
•
•
•
•
•
Avoid hypovolemia, hyponatremia and anemia
Nimodipine
Drain (EVD, LD)
Statin ?
Mg ?
Prophylactic hyperdynamic therapy ?
Treatment of Vasospasm
• Hyperdynamic therapy (HHH)
– Hypervolemia
– Hemodilution
– Hypertension
• Endovascular therapy
– Infusion of vasodilators
– Balloon angioplasty
• Be mindful of cardiac function!
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Cardiac abnormalities
• Caused by increased sympathetic tone, electrolyte alterations
• ST‐T wave inversions, QT prolongation,
• Arrhythmias
• Myocardial infarctions • Heart Failure
• Correlates with the severity of SAH • Usually disappear within a few days
• Cardiac monitoring, correction of electrolytes
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•
•
•
•
•
Retrospective study of 617 consectutive SAHs
N= 87 patients
Myocardial infarction: 47%
Arrhythmia: 63%
Congestive heart failure: 31%
Mortality 23%
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Neurogenic Cardiomyopathy
“Takotsubo Cardiomyopathy” 27
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Neurogenic Cardiomyopthy
• Etiology not completely understood
– Catecholamine Surge
– 20 times as high in SAH
• Higher prevalence in Females
• Left ventricular dysfunction with troponin elevation occurs
• Associated with increased sympathetic activation with coronary vasospasm 28
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Takotsubo Cardiomyopathy
• Also described as
–
–
–
–
–
“Apical Ballooning Cardiomyopathy”
“Stress Induced Cardiomyopathy”
“Broken Heart Syndrome”
“Stunned myocardium”
“Reversible Cardiomyopathy”
• LV dysfunction leads to apical ballooning – Resembles an octopus pot (Takot Subo)
CDiagnostic Hallmarks
• Diminished LV function
• Wall motion abnormalities on ECHO that involve more than one vascular territory
• Elevated cardiac enzymes and/or EKG changes
• Recovery of wall motion abnormalities with time. 29
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Neurogenic Pulmonary Edema
Neurogenic pulmonary edema
• Occurs in ～20‐25% of SAH
• Bimodal distribution
– Hours
– 3‐7 days
• Cardiogenic (Hours)
– Pulmonary vasoconstriction
– LV dysfunction
• Hydrostatic (Days)
– Damage to pulmonary endothelium
– Increased permeability
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Neurogenic Pulmonary Edema
• Catacholamine
Mediated?
• Increased pulmonary vascular permeability
• Increased pulmonary vascular pressure
• LV dysfunction
• Inflammatory Cytokine Mediated?
Electrolyte Abnormalities
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Hyperglycemia
• Occurs in 30% after SAH
• Caused by generalized stress response
• Independent predictor of poor outcome
– accelerates acidosis
– produces free radicals
– Increased risk of infection
• Control of serum glucose with insulin can reduce mortality
– Avoid Dextrose containing solutions
– Avoid Decadron
Hyponatremia
• > 30% pts after SAH
• > 80% of patients with hyponatremia have symptomatic vasospasm
• CSW > SIADH
• Difference between CSW and SIADH is volume status
CSW is hypovolemic; SIADH is normo‐hypervolemic
• Overcorrection and rapid correction should be avoided
< 0.7 mEq/l/h, 15 mEq/l/day
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Other electrolyte abnormalities associated with poor outcome
• Hypernatremia (20%)
– Caused by Mannitol, DI (rare; < 1% after SAH)
– Treat with hypotonic fluid, desmopressin
• Hypokalemia (20‐30%)
– can lead to EKG change (Ventricular arrhythmia)
• Hypomagnesemia (40%)
– Can lead to EKG change, vasospasm
Take Home Points
• SAH is a systemic and dynamic process
– Multisystem organ involvement
– Be mindful of the cardiac and pulmonary status
• Beware of hydrocephalus…. It kills
– Do not sedate these patients
• Avoid Dextrose and steroids
• Involve Neurosurgery early
• Outpatient follow up is key
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“You recognize what you know”
What does the neurosurgeon want to know at 3am?
• Where is the blood?
– Subdural – Epidural – Subarachnoid
– Intraparenchymal
•
•
•
•
Is there a history of trauma?
Is there Hydrocephalus or midline shift?
When in doubt ask the radiologist
Neuro exam, blood pressure
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What to do until the neurosurgeon arrives?
• Transfer to ICU
– NPO
• SBP goal <140
– Cardene ggt, Labetalol 10mg IV Q2h prn,
• Hydralazine, Vasotec
• Frequent (q1hour) neuro cheecks
• CBC, BMT, PT,PTT,INR, Type and Screen, cardiac enzymes, accuchecks
• EKG
• IVF: NS w/ 20meq KCL (euvolemic)
What NOT to order:
• Decadron (or any steroid)
• D5 anything
• Hyptonic fluids
– 1/2NS
– 1/4NS
• Sedatives when hydrocephalus is present
– Nail in the coffin
• Hold Lovenox, Coumadin, ASA, Plavix
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Posr‐Test Question 1 • You receive a phone call indicating that a patient that you sent for a stat CTH has subarachnoid hemorrhage. You decide to transfer the patient to the ICU while awaiting neurosurgical consultation. What type of IV fluids are most appropriate assuming the patient has no renal dysfunction?
1) D5 ½ NS
2) D5 ¼ NS
3) ½ NS 4) NS w 20meq KCL Post‐Test Question 2
• You are concerned that the patient may have some intracranial swelling/edema. What is the most appropriate agent for this setting?
1) Decadron
2) Methylprednisolone
3) Prednisone
4) 1 or 3
5) None of the above
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Post‐ Test Question 3 What type of cardiac complications are commonly encountered in patients with SAH?
1) Myocardial infarction
2) Stunned myocardium
3) Takotsubo’s Cardiomyopathy
4) 1 and 2
5) All of the above Post‐Test Question 4
Which of the following is the most appropriate blood pressure goal until a decision is made regarding the most appropriate treatment?
1) SBP < 100
2) SBP 180‐220
3) SBP < 140
4) SBP 160‐180
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Pre‐Test Question 5
• In addition to the SAH the radiologist also informs you that there is marked hydrocephalus on the CTH. The nurse keeps calling you to inform you that Vicodin is not adequately addressing the patient’s headache and she is becoming agitated. What is the most appropriate alternative in the setting of hydrocephalus? 1) Dilaudid
2) Morphine
3) Add Ativan to the patient’s oral pain medication regimen
4) 2 or 3 5) None of the above
University of Missouri Neurovascular Stroke Team
• Niranjan Singh, M.D., Stroke Director
• Ashish Nanda, M.D., Stroke Co‐Director, Interventional Neurology
• Brandi French, M.D., Vascular Neurology, NICU Director
• Vikas Gupta, M.D., Interventional Neurology
• William Humphries, M.D.,MPH Vascular/Endovascular Neurosurgery • Tami Harris, RN, CCRN, CNRN Stroke Coordinator • Dianne Hurt, RN
• Michelle Laas, RN ,CFRN Chief Flight Nurse
Admission Advice (573 882 6985)
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Outpatient Modifiable Risk Factors
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• Cognitive Rehab
• Depression
VOMIT
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Infundibulum
• Trangular in shape
– Vessel origin
– < 3 mm
– Vessel at apex
• In 7 ‐ 13 % of “normal” angiograms • Common site: P‐comm
• Incomplete remnants of fetal vessel
• Few documented bleeds from infundibula
SAH Treatment
• No treatment
– Generally not recommended
*If no good treatment option; temporizing
• Open microsurgical treatment
– Clip ligation (clipping)
• variants
• Endovascular / Interventional treatment
– Coil embolization
• variants
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SAH Treatment
• Prospective, randomized trials
– ISAT: International Subarachnoid Aneurysm Trial
• Multicenter, predominantly European, 2143 patients
• Published in 2005
– BRAT: Barrow Ruptured Aneurysm Trial
• Single Center, 471 patients treated
• Published in 2012
• Neurosurgeon & Interventionalist‐ had to agree
– Either clipped or coiled for randomization
• Primary endpoint
– Death or dependency (mRS 3‐6) at 1 year
• Secondary endpoints
– Seizures, rebleeding from treated aneurysm, death or dependency at later time points, follow‐up angiography findings 42
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ISAT Study
• Dead or dependent at 1 year
– Coiling (23.5%) < Clipping (30.9%)
• Absolute risk reduction 7.4% (p = 0.0001)
• 74/1000 pts will not be disabled or dead
• Seizure
– Clipping > Coiling
• Rebleeding of treated aneurysm
– Coiling > Clipping
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• Rebleeding from treated aneurysm
– Coil > Clip
• Rebleed risk in both groups is low • At similar level risk of SAH from another source
– pre‐existing or newly formed aneurysm
• Risk of death by 5 years
– Clip > Coil (p= 0.03)
• Functional independence at 5 years
– Clip = coil (p = 0.61)
• Pt randomly assigned to treatment group
– Physician decides to proceed or have pt crossover to other group
– “real world” experience
• Intent‐to‐treat analysis
• Primary endpoint
– Poor functional outcome at 1 year (mRS > 2)
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BRAT Study
• Dead or dependent at 1 year
– Coiling (23.3%) < Clip (33.7) p=0.02
– Patients assigned to coil who crossed over to clip
• Fared worse than remainder of patients who received coiling – Results still held true in “as‐treated” analysis (20.4 vs 33.9; p=0.01) and if cross‐over patients were excluded (18.4 vs 33.9; p= 0.005)
• No recurrent hemorrhages in coiling group
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