SAH FOR NCC RESIDENTS
Aneurysmal Subarachnoid Hemorrhage
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
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%
Aneurysmal Subarachnoid Hemorrhage
Fisher Scale
Clinical, associated with mortality
Radiologic, associated with vasospasm
Aneurysmal Subarachnoid Hemorrhage
Clinical course and complicationsAneurysmal reruptureCerebral edemaHydrocephalusVasospasm and delayed cerebral infarction (stroke)
Cerebral salt wastingSeizuresMyocardial stunRespiratory 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<20, CPP>60) PaCO2 (normocarbic)
Aneurysmal Subarachnoid Hemorrhage
Aneurysmal Subarachnoid Hemorrhage Aneurysmal rerupture
PreventionSBP<140-160, 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 3-14-Occurs in 70% of patients-Symptomatic in 30% of patients-Signs: -Confusion->decreased LOC->focal deficit -Increasing BP
NimodipineStatin
X
Aneurysmal Subarachnoid Hemorrhage
Vasospasm diagnosisTranscranial Doppler (TCD)CT AngiogramCerebral Angiogram
Vasospasm treatmentKeep pts at least euvolemic at all timesHypervolemiaPermissive/Induced hypertensionTransfusionAngioplasty / 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 <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
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
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): 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
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
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;40:3039–44. 173.
Effect of fluid bolus, hypertension, and red blood cell transfusion on DO2 and PbtO2
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
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
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
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)