sah for ncc residents. aneurysmal subarachnoid hemorrhage

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


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%


Fisher Scale

Clinical, associated with mortality

Radiologic, associated with vasospasm


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 rerupture

PreventionSBP<140-160, aneurysm precautions


Securing the aneurysm

Coiling via endovascular approach

Clipping via open surgical approach


Cerebral edema


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


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?


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


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


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 threshold in aSAH

In normal brain, compensatory vasodilation occurs at Hb <10, brain hypoxia at Hb <6


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


Does transfusion change outcomes in aSAH?

Does transfusion increase DO2/PbtO2?

Does transfusion decrease DCI?

Do the medical complications outweigh the benefits?


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


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


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


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


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)

sah for ncc residents. aneurysmal subarachnoid hemorrhage

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