SAH FOR NCC RESIDENTS

Aneurysmal Subarachnoid Hemorrhage

 Cause Aneurysm, dissection, trauma  Epidemiology 3% of all strokes Multiple aneurysms in 15-33%  Mortality 25-55%  Risk factors HTN, smoking, FH, cocaine, connective tissue disorders, polycystic kidney disease

Aneurysmal Subarachnoid Hemorrhage  Presentation “worst headache of life” neck stiffness, photophobia, low back pain, nausea/vomiting, seizure, diplopia, eye pain, visual loss  Physical exam findings Decreased level of consciousness, confusion Ptosis, dilated pupil from CN3 stunning Signs of increased ICP

Aneurysmal Subarachnoid Hemorrhage  Workup Noncon head CT Lumbar puncture (if CT nondiagnostic) CTA or cerebral angiography CTA sensitivity 85-98% Angiography is the “gold standard” 10-20% will have a negative angio Angiography complication rate ~1%

Aneurysmal Subarachnoid Hemorrhage Fisher Scale Clinical, associated with mortality Radiologic, associated with vasospasm

Aneurysmal Subarachnoid Hemorrhage  Clinical course and complications Aneurysmal rerupture Cerebral edema Hydrocephalus Vasospasm and delayed cerebral infarction (stroke) Cerebral salt wasting Seizures Myocardial stun Respiratory failure/neurogenic pulmonary edema Central Fever

Post-cardiac arrest brain injury treatment: the golden triangle Cerebral Oxygenation  PaO2 (normooxic)  Hemoglobin (>30) Cerebral Metabolism  Sedation  Seizure screening/rx  Thermoregulatory mgmt (hypothermia)  Shivering mgmt  Glucose mgmt Cerebral Perfusion  Blood pressure (MAP>65)  Cardiac output  Volume status (euvolemic)  ICP / CPP (ICP 60)  PaCO2 (normocarbic)

Aneurysmal Subarachnoid Hemorrhage

 Aneurysmal rerupture  Prevention SBP< , aneurysm precautions

Aneurysmal Subarachnoid Hemorrhage  Securing the aneurysm Coiling via endovascular approach Clipping via open surgical approach

Aneurysmal Subarachnoid Hemorrhage  Cerebral edema

Aneurysmal Subarachnoid Hemorrhage  Hydrocephalus

Aneurysmal Subarachnoid Hemorrhage  Vasospasm and delayed cerebral infarction !!STROKE!! -Leading cause of death and disability after aneurysmal rerupture -Highest risk: Day Occurs in 70% of patients -Symptomatic in 30% of patients -Signs: -Confusion->decreased LOC->focal deficit -Increasing BP Nimodipine Statin X

Aneurysmal Subarachnoid Hemorrhage  Vasospasm diagnosis Transcranial Doppler (TCD) CT Angiogram Cerebral Angiogram  Vasospasm treatment Keep pts at least euvolemic at all times Hypervolemia Permissive/Induced hypertension Transfusion Angioplasty / IA nicardipine

Hemoglobin in aneurysmal SAH  Is there an optimal hemoglobin concentration for patients with aSAH?  Should transfusion be used to maintain an optimal hemoglobin concentration for patients with aSAH?

Hemoglobin in aneurysmal SAH Role of hemoglobin in aSAH  Poor outcome after aSAH is associated with symptomatic Delayed Cerebral Ischemia (DCI)  DCI is caused by impaired CBF and DO2  DO2= CBF x arterial oxygen content  Arterial oxygen content = linearly related to Hb

Hemoglobin in aneurysmal SAH Anemia in aSAH  Hb drops to 80% of patients  Hb drops to <10 g/dl in ~ 50% of patients  Observational studies associate anemia with infarction, dependency, and death

Hemoglobin in aneurysmal SAH Kramer AH et al. Relationship between hemoglobin concentrations and outcomes across patients with aneurysmal subarachnoid hemorrhage. Neurocrrit Care 2009; 10(2): Hemoglobin levels throughout hospital stay in patients with favorable and unfavorable outcome after aSAH

Hemoglobin in aneurysmal SAH Hemoglobin threshold in aSAH  In normal brain, compensatory vasodilation occurs at Hb <10, brain hypoxia at Hb <6

Hemoglobin in aneurysmal SAH Oddo M et al. Hemoglobin concentration and cerebral metabolism in patients with aneurysmal subarachnoid hemorrhage. Stroke 2009 Apr; 40(4): Percentage of episodes of brain tissue hypoxia (PbtO2 40) according to different Hgb ranges. *P<0.05 for Hgb <9 g/dl  In aSAH, microdialysis and brain tissue oxygen monitoring associate Hb <9-10 with brain tissue hypoxia and metabolic distress

Hemoglobin in aneurysmal SAH Does transfusion change outcomes?  TRICC (1999): Hb 10 g/dL vs 7 g/dL trigger  7g/dL trigger improved mortality for <55yo and APACHE II <20  CRUSADE (2008): NSTEMI registry  Transfusing when Hct <25% assoc. with  mortality  Transfusing when Hct >27% assoc. with  mortality

Hemoglobin in aneurysmal SAH Does transfusion change outcomes in aSAH?  Does transfusion increase DO2/PbtO2?  Does transfusion decrease DCI?  Do the medical complications outweigh the benefits?

Hemoglobin in aneurysmal SAH Does transfusion increase DO2/PbtO2?  Smith 2005: SAH/TBI patients transfused at Hb 6-9 g/dL   PbtO2 in 75% of patients   PbtO2 in 25% of patients

Hemoglobin in aneurysmal SAH Dhar R et al. Red blood cell transfusion increases cerebral oxygen delivery in anemic patients with subarachnoid hemorrhage. Stroke. 2009;40:3039– Effect of fluid bolus, hypertension, and red blood cell transfusion on DO2 and PbtO2

Aneurysmal Subarachnoid Hemorrhage  Cerebral salt wasting diagnosis Usually around day 3-14 Declining sodium Urine output > 250cc/h  Cerebral salt wasting treatment Hypertonic saline / salt tabs Hourly cc / cc replacement to euvolemia using NS boluses Fludrocortisone

Aneurysmal Subarachnoid Hemorrhage  Seizures 19% of all SAH patients have seizures 70% of seizing patients are in nonconvulsive status epilepticus Antiepileptics are indicated on all patients until the aneurysm is secured, and will be continued if the patient is high risk for seizure (s/p craniotomy, sz activity) Continuous EEG monitoring x 24 hrs is a Class I, LOE B recommendation for all altered SAH patients

Aneurysmal Subarachnoid Hemorrhage  Myocardial stun Diastolic dysfunction in 71% of patients Systolic dysfunction in 30% of patients (Tako-Tsubo) Elevated troponin in 20-30% of patients  Respiratory failure/neurogenic pulmonary edema Onset minutes-hours Non-cardiogenic, 2/2 pulmonary HTN and capillary leak

Aneurysmal Subarachnoid Hemorrhage  Central fever Occurs in 40-70% of patients Associated with poor outcome Increases cerebral metabolic rate, ICP, and stroke risk Normothermia should be maintained and fever treated aggressively, using antipyretics and intravascular/surface cooling devices if needed (Class I, LOE B recommendation)