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SAH FOR NCC RESIDENTS
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Aneurysmal Subarachnoid Hemorrhage
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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
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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
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Aneurysmal Subarachnoid Hemorrhage
WorkupNoncon head CTLumbar 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%
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Aneurysmal Subarachnoid Hemorrhage
Fisher Scale
Clinical, associated with mortality
Radiologic, associated with vasospasm
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Aneurysmal Subarachnoid Hemorrhage
Clinical course and complicationsAneurysmal reruptureCerebral edemaHydrocephalusVasospasm and delayed cerebral infarction (stroke)
Cerebral salt wastingSeizuresMyocardial stunRespiratory failure/neurogenic pulmonary edema
Central Fever
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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<20, CPP>60) PaCO2 (normocarbic)
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Aneurysmal Subarachnoid Hemorrhage
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Aneurysmal Subarachnoid Hemorrhage Aneurysmal rerupture
PreventionSBP<140-160, aneurysm precautions
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Aneurysmal Subarachnoid Hemorrhage
Securing the aneurysm
Coiling via endovascular approach
Clipping via open surgical approach
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Aneurysmal Subarachnoid Hemorrhage
Cerebral edema
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Aneurysmal Subarachnoid Hemorrhage
Hydrocephalus
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Aneurysmal Subarachnoid Hemorrhage Vasospasm and delayed cerebral
infarction
!!STROKE!!
-Leading cause of death and disability after aneurysmal rerupture-Highest risk: Day 3-14-Occurs in 70% of patients-Symptomatic in 30% of patients-Signs: -Confusion->decreased LOC->focal deficit -Increasing BP
NimodipineStatin
X
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Aneurysmal Subarachnoid Hemorrhage
Vasospasm diagnosisTranscranial Doppler (TCD)CT AngiogramCerebral Angiogram
Vasospasm treatmentKeep pts at least euvolemic at all timesHypervolemiaPermissive/Induced hypertensionTransfusionAngioplasty / IA nicardipine
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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?
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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
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Hemoglobin in aneurysmal SAH
Anemia in aSAH
Hb drops to <11 g/dl in >80% of patients Hb drops to <10 g/dl in ~ 50% of
patients
Observational studies associate anemia with infarction, dependency, and death
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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):157-65.
Hemoglobin levels throughout hospital stay in patients with favorable and unfavorable outcome after aSAH
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Hemoglobin in aneurysmal SAH
Hemoglobin threshold in aSAH
In normal brain, compensatory vasodilation occurs at Hb <10, brain hypoxia at Hb <6
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Hemoglobin in aneurysmal SAH
Oddo M et al. Hemoglobin concentration and cerebral metabolism in patients with aneurysmal subarachnoid hemorrhage. Stroke 2009 Apr; 40(4): 1275-81
Percentage of episodes of brain tissue hypoxia (PbtO2 <20 mm Hg) and cell energy dysfunction (LPR >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
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Hemoglobin in aneurysmal SAHDoes 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
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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?
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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
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Hemoglobin in aneurysmal SAH
Dhar R et al. Red blood cell transfusion increases cerebral oxygen delivery in anemic patients with subarachnoid hemorrhage. Stroke. 2009;40:3039–44. 173.
Effect of fluid bolus, hypertension, and red blood cell transfusion on DO2 and PbtO2
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Aneurysmal Subarachnoid Hemorrhage
Cerebral salt wasting diagnosisUsually around day 3-14Declining sodiumUrine output > 250cc/h
Cerebral salt wasting treatmentHypertonic saline / salt tabsHourly cc / cc replacement to euvolemia using NS boluses
Fludrocortisone
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Aneurysmal Subarachnoid Hemorrhage Seizures
19% of all SAH patients have seizures70% of seizing patients are in nonconvulsive status epilepticusAntiepileptics 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
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Aneurysmal Subarachnoid Hemorrhage
Myocardial stunDiastolic dysfunction in 71% of patientsSystolic dysfunction in 30% of patients (Tako-Tsubo)
Elevated troponin in 20-30% of patients
Respiratory failure/neurogenic pulmonary edema
Onset minutes-hoursNon-cardiogenic, 2/2 pulmonary HTN and capillary leak
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Aneurysmal Subarachnoid Hemorrhage
Central feverOccurs in 40-70% of patientsAssociated with poor outcomeIncreases cerebral metabolic rate, ICP, and stroke riskNormothermia should be maintained and fever treated aggressively, using antipyretics and intravascular/surface cooling devices if needed (Class I, LOE B recommendation)