SAH for NCC residentsAneurysmal Subarachnoid Hemorrhage
2Aneurysmal Subarachnoid HemorrhageCauseAneurysm, dissection, traumaEpidemiology3% of all strokesMultiple aneurysms in 15-33%Mortality25-55%Risk factorsHTN, smoking, FH, cocaine, connective tissue disorders, polycystic kidney disease
Although subarachnoid hemorrhage is frequently caused by trauma and dissection, we wont talk about that here. Subarachnoid hemorrhages caused by aneurysms are what we are going to talk about here, and those aneurysms generally occur at branch points in the circle of willis, which sits right here around your brainstem, which is why when they blow, you get blood around your brainstem. Aneurysmal SAH counts for 3% of all strokes, with a mortality of 25-55%, which doubles if theyre not taken care of at high volume centers, like a comprehensive stroke center, that see more than 40 a year, because the clinical care makes such a difference in their outcome. Fortunately were one of those high volume centers and should become more high volume if we get our comprehensive stroke center designation. Risk factors are3Aneurysmal Subarachnoid HemorrhagePresentationworst headache of life neck stiffness, photophobia, low back pain, nausea/vomiting, seizure, diplopia, eye pain, visual loss
Physical exam findingsDecreased level of consciousness, confusionPtosis, dilated pupil from CN3 stunningSigns of increased ICP
4Aneurysmal Subarachnoid HemorrhageWorkupNoncon head CTLumbar puncture (if CT nondiagnostic)CTA or cerebral angiographyCTA sensitivity 85-98%Angiography is the gold standard10-20% will have a negative angioAngiography complication rate ~1%
5Aneurysmal Subarachnoid Hemorrhage
Fisher ScaleClinical, associated with mortalityRadiologic, associated with vasospasm6Aneurysmal Subarachnoid HemorrhageClinical course and complicationsAneurysmal reruptureCerebral edemaHydrocephalusVasospasm and delayed cerebral infarction (stroke)Cerebral salt wastingSeizuresMyocardial stunRespiratory failure/neurogenic pulmonary edemaCentral FeverSo the clinical course of a subarachnoid hemorrhage patient is complicated, and long. The average length of stay for these patients in the unit is 2 weeks, because of these complications that frequently happen. Here are the things that will harm or kill your subarachnoid hemorrhage patient, so I want you to be on the lookout for them.7Post-cardiac arrest brain injury treatment: the golden triangle Cerebral OxygenationPaO2 (normooxic)Hemoglobin (>30) Cerebral MetabolismSedationSeizure screening/rxThermoregulatory mgmt (hypothermia)Shivering mgmtGlucose mgmt
Cerebral PerfusionBlood pressure (MAP>65)Cardiac output Volume status (euvolemic)ICP / CPP (ICP60)PaCO2 (normocarbic)
The principles behind Preventing this secondary brain injury after cardiac arrest is no different than any other brain injured state, where therapy rests on optimizing the energy balance of the neuron. Its all about supply and demand, cerebral perfusion and oxygenation on the supply side, and metabolsim on demand side, and youre trying to balance it so those neurons that have been injured and are deciding whether to die or not, can be coaxed back into staying alive and healthy. The recommendations from the AHA in treating postcardiac arrest syndrome, maintaining . All fall into this paradigm.8Aneurysmal Subarachnoid Hemorrhage
Of note, all the management if youd like to know where it comes from, is based on the 2011 neurocritical care guidelines for subarachnoid hemorrhage9Aneurysmal Subarachnoid HemorrhageAneurysmal rerupture
PreventionSBPdecreased LOC->focal deficit -Increasing BP
The next thing that can happen is vasospasm, which is the second most deadly complication that happens after subarachnoid hemorrhage. It occurs in 70% of patients and is symptomatic in 30% of patients. What happens is when that blast pressure wave goes through the head, it sets of this cascade of neurohormonal dysregulation, causing vasoconstrictors to be released, and causing inflammation to build slowly and thicken the vessel over the course of a few days. So thats why the peak vasospasm time is days 3-14. Of note, the role of inflammation is why nimodipine and statins are given to all SAH patients, because they are both thought to decrease mortality by decreasing inflammation. So this is what vasospasm looks like--You can see here that this vessel here, see how thick it is here, and see how thin it becomes there? And that compromises the blood flow to whatever part of the brain that vessel supplies. So what youll see is often the pt is just a little off, a little weird, as the little vessels start to spasm down all over the head. They might get a little sleepy or confused. And then when a big vessel spasms down, then they get a focal deficit; weakness, visual field cut, what have you. Often, youll also see their blood pressure just start to creep up a bit, so its important not to jump on treating blood pressure if someones in vasospasm, since it could stroke them out. So thats why were watching soo carefully in these patients for any change in their neuro exam. 14Aneurysmal Subarachnoid HemorrhageVasospasm diagnosisTranscranial Doppler (TCD)CT AngiogramCerebral AngiogramVasospasm treatmentKeep pts at least euvolemic at all timesHypervolemiaPermissive/Induced hypertensionTransfusionAngioplasty / IA nicardipine
What we do when we detect a change in exam and suspect vasospasm, what do we do? The standard of care is to screen for vasospasm with daily TCDs, which is a little portable ultrasound that looks at the velocity of blood going through the blood vessels, and well have that soon here. But if we suspect vasospasm based on a clinical change, we can do a few things. We can do a CTA, if were not too suspicious, or a formal angiogram, if our suspicion is high, because we can also treat vasospasm during an angio. Sometimes well just go ahead and treat, if our suspicion is high enough, because even 30 minutes or an hour in vasospasm can cause someone to stroke. So how do we treat. There are a few therapies that have been proven to work. The first thing we ensure is that even when a pt isnt in vasospasm, they are euvolemic, because we know that if a pt goes into vasospasm when theyre dry, their mortality doubles. So youll see that we will want our patients to be euvolemic to positive every day, no matter what. When theyre actually in vasospasm, we will make them hypervolemic by bolusing them a couple liters so as to increase their cerebral blood flow. If theyre still symptomatic, we may hypertense them, using pressors to get their MAP up by 20 points, usually using phenylephrine. Last is transfusion, which works by increasing the oxygen carrying capacity of the blood so even though theres less blood getting through, the blood that is, is carrying more red blood cells and oxygen to the tissue. Angioplasty is the definitive therapy, so thats why youll see some patients go back to the angio suite multiple times during their hospital stay. And sometimes, youll see a magnesium drip on some patients, because it may decrease vasospasm, but the evidence for that is 50/50.15Hemoglobin in aneurysmal SAHIs there an optimal hemoglobin concentration for patients with aSAH?
Should transfusion be used to maintain an optimal hemoglobin concentration for patients with aSAH?
Now I know that the title refers to hematocrit, but since hematocrit is a function of both hemoglobin and volume status, I want to discuss hemoglobin and transfusion first, and then address volume status separately. So what are the questions surrounding hemoglobin in aneurysmal subarachnoid hemorrhage? First, is there an optimal hb concentration for these patients, and second, should transfusion be used to maintain an optimal hemoglobin concentration?16Hemoglobin in aneurysmal SAHRole 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
But first, a little physiology. Why do we care about hemoglobin levels in SAH anyway? Because of its relationship to delayed cerebral ischemia or DCI. Numerous studies have associated poor outcomes after sah with symptomatic DCI, which occurs in 30% of patients. DCI is caused by impaired cerebral blood flow and oxygen delivery. Although the cerebral circulation can compensate up to a point for reduced CBF by increasing its oxygen extraction fraction, when that compensation fails or if oxygen delivery falls further, infarction may occur. Cerebral oxygen delivery, in turn, is determined by the product of CBF and arterial oxygen content, which is linearly related to hemoglobin concentration.
17Hemoglobin in aneurysmal SAHAnemia in aSAH
Hb drops to 80% of patientsHb drops to