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) 1 04/09/2015 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” 2 04/09/2015 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 3 04/09/2015 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 4 04/09/2015 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 5 04/09/2015 Subarachnoid Hemorrhage 6 04/09/2015 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 7 04/09/2015 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 8 04/09/2015 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 04/09/2015 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 10 04/09/2015 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 11 04/09/2015 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 12 04/09/2015 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 % 13 04/09/2015 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 14 04/09/2015 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 15 04/09/2015 Hunt & Hess Grade Correlates with clinical outcomes Fisher Grade Correlates with severity of vasospasm 16 04/09/2015 WFNS Grade Correlates with prognosis ICU Care 17 04/09/2015 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 18 04/09/2015 • 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 19 04/09/2015 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 20 04/09/2015 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 21 04/09/2015 “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 04/09/2015 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 – – – – – Amount of blood in subarachnoid space High clinical grade Smoking Cocaine Use Age < 50 23 04/09/2015 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. 24 04/09/2015 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! 25 04/09/2015 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 • • • • • • Retrospective study of 617 consectutive SAHs N= 87 patients Myocardial infarction: 47% Arrhythmia: 63% Congestive heart failure: 31% Mortality 23% 26 04/09/2015 Neurogenic Cardiomyopathy “Takotsubo Cardiomyopathy” 27 04/09/2015 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 04/09/2015 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 04/09/2015 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 30 04/09/2015 Neurogenic Pulmonary Edema • Catacholamine Mediated? • Increased pulmonary vascular permeability • Increased pulmonary vascular pressure • LV dysfunction • Inflammatory Cytokine Mediated? Electrolyte Abnormalities 31 04/09/2015 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 32 04/09/2015 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 33 04/09/2015 “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 34 04/09/2015 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 35 04/09/2015 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 36 04/09/2015 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 37 04/09/2015 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) 38 04/09/2015 Outpatient Modifiable Risk Factors 39 04/09/2015 • Cognitive Rehab • Depression VOMIT 40 04/09/2015 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 41 04/09/2015 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 04/09/2015 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 43 04/09/2015 • 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) 44 04/09/2015 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 45
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