*50mL/100g/min

*750mL/min or 15-20% of cardiac output

*15-20mL/100g/min= Impairment

*6-15mL/100g/min= isoelectric EEG

*<6mL/100g/min= neuronal death

What is a normal CPP?

Where are neurological changes seen with decreases in CPP?

*80-100mmHg

*50mmHg is acceptable low

*<50mmHg slowing EEG

*25-50mmHg flat EEG

*<25mmHg brain damage

*Keeps CMRO2 between 3-5mL O2/100gm/min

*Maintains cerebral blood flow at 50mL/100gm/min (15-20% of CO)

*Keeps cerebral perfusion pressure approximately 80-100mmHg

*Luxury flow is caused by high CO2 levels throughout the brain could steal blood flow from areas that require extra oxygen and produce metabolites.

*Bad

*Cause by deliberate hyperventilation leading to hypocapnea; cerebral vasoconstriction and improved blood flow to ischemic areas

*Gets more blood flow to all areas not just dilated areas, good effect

*Hypothermia vasoconstricts and decreases CBF by 57% for each 1 degree celcius

*Hyperthermia vasodilates and increases CBF by 5-7% for each 1 degree celcius

Describe the make up of the blood brain barrier.

Which substances are permeable and which are impermeable?

*BBB are vascular endothelial cells made up of tight junctions.  This type of lipid barrier allows for the selective passive of molecules

*Permeable substances: oxygen, carbon dioxide, water, and lipid soluble molecules like anesthetic agents.

*Impermeable solutions are proteins, ionic compounds and high molecular weight substances such as Mannitol

*Severe HTN

*Tumor

*Trauma

*Stroke

*Infection

*Hypoxia

*Hypercapnea

*Sustained Seizure

*Women

*40-60

*Congenital/developmental defect

*Brain trauma

*Infection

*Atherosclerosis

*Abnormal rapid cell growth (neoplastic disease)

*Certain rare diseases of the connective tissue: 

-Marfan's Syndrome

-Psuedoxanthoma Elasticum

-Ehlers-Danlos Syndrome

-Fibromuscluar dysplasia

-Polycystic Kidney Disease

*Increased risk is caused by an increase in the transmural pressure (TMP) inside the aneurysm.

*Transmural pressure is the difference between the MAP and the ICP.  A liner relationship exists, any significant change that increases the difference can lead to rupture. (increase in MAP or decrease in ICP).

*Increase in transmural pressure

*Aneurysm size 2.5cm or larger in diameter although smaller aneurysms also rupture

*Cigarette smoking

*Excessive alcohol consumption

*Recreational drug use

*Pupil dilation

*Drooping eyelid

*Pain above or behind the eye

*Headache

*unsteady gait

*a temporary problem with sight

*Double vision

*numbness in the face

*Photophobia

*Sudden, extremely severe headache typically described as the worst headache of the victims life

*N/V

*Short loss of consciousness or prolonged coma

*25% experience specific neurological problems linked to specific areas of the brain

*Hydrocephalus (d/t decreased CSF absorption in arachnoid villi)

*Seizure

*Intracranial HTN

*Rebleed

*Vasospasm

*Hydrocephalus

*H&P

*CT, MRI

*LP

*Angiography

*

*Grade O: Unruptured aneurysm

*Grade I: Asymptomatic, or minimal headache and slight nuchal rigidity

*Grade II: Moderate to severe headache, nuchal rigidity, no neurologic deficit other than cranial nerve palsy

*Grade III: Drowsiness, confusion, or mild focal deficit

*Grade IV: Stupor, moderate to severe hemiparesis, early decerebration, vegetative disturbance

*Grade V: Deep coma, decerebrate rigidity, moribund 

*Early diagnosis

*Airway management d/t disordered breathing that can occur from cerebral compromise

*Control of ICP

*Hemodynamic stabilization

*Seizure prophylaxis (Dilantin, Phenobarbital)

*Intubation

*Mannitol

*Corticosteroids (Decadron)

*Beta Blockers

*Ca Channel blockers (Nimodipine)

*Early surgical intervention following a major rupture ahd been found to improve outcome

*Less change of rebleed

*Removal of subarachnoid blood

*Secure aneurysm

*Less bed rest with associated complications (earlier mobility)

*Operating on a freshly injured brain with impaired autoregulation (often why surgery is delayed)

*May not have a good H&P and subsequently may not be as "tuned-up" as they could be for surgery

*Recovery from SAH

*Vasospasm resolved

*Co morbidities can be identified and managed

*Cerebral vasospasm is the spasm of affected or associated arteries close to the rupture site.

*Believed to be caused by the oxyhemoglobin portion of blood

*Symptoms are caused by cerebral ischemia and infarction

*Occurs in 30% of patients

*4-14 days after bleed

*Change in LOC

*Hemodynamic instability (HTN)

*Lethargy

*Coma

*Prevention is taking Nimodipine (a CCB).  Nimodipine is not effective in treating a vasospasm

*Treatment with triple H therapy (Goal is to treat ischemia with an increase in CPP)

*Hypertension (pressors if needed)

*Hemodilution (33% hematocrit)

*Hypervolemia volume expansion with

-Crystalloids 0.9NS (avoid dextrose and LR)

-Colloids

-Aim for PAWP of 12-18 and

-CVP 10-12

*Thorough neurological assessment

*Identify and document neurological deficits

*Hung and Hess classification of SAH

*Identify coexisting diseases that may be aggravated by induced hyper/hypotension (Ex: carotid stenosis)

*Other Co Morbidities (CVA, DM, Respiratory impairments)

*EKG (Arrhythmias are common with elevated ICP, SAH)

*Electrolyte abnormalities (D/t diuretic administration, volume status)

*Diuresis

*Hyperventilation

What are some important preoperative considerations for the patient undergoing a cerebral aneurysm clipping?

*Line placed in Preop as patient tolerates, may need to postpone until after induction for CVP/PA cath.

*Best to have arterial line for induction

*2 large bore IVs

*T&C 2 units PRBCs

*Prepare to be far away from the head of the patient

-Long circuit

-IV extensions

-Plenty of body padding

*A massive adrenergic response to intubation stimulus, followed by a long non stimulating shave/prep time

*BP should be 15-20% below baseline

*Avoid tachycardia

*Pentothol 3-5mg/kg

*Propofol however is an appropriate choice 2-3mg/kg (being used as first choice d/t pentothol shortage)

*Vecuronium 

*Pancuronium if HR stable

*Succinylcholine should be avoided due to increased ICP associated with its use.  Precurarize if necessary.

*Short acting beta blocker- Esmolol 0.5mg/kg

*Nicardipine 0.5-1.0mg boluses to effect

*Lidocaine 1.0-1.5mg/kg

* Opioids (Fentanyl 7-10mcg/kg front-loaded to blunt effects of laryngoscopy)

-Sufenta bolus of 0.5-1.0mcg/kg/hr throughout case. 

*Foley catheter

*CVP 

-To treat VAE, monitor fluid status

*Pulmonary artery catheter

*Arterial line

*Precordial dopplar (2nd-3rd ICS righ of the sternum)

*PNS

*Temperature with warming modalities

What inhalational agent should be used for maintenance and why?

*Isoflurane 0.7-1.0% (around a MAC).  Iso is shown to provide slightly more decrease in CMRO2 with less cerebral vasodilation than the others 

*75-100mcg/kg/min

*To decrease CMRO2, cerebral blood volume and metabolism

*Similar to barbiturates but not as cerebroprotective

*Offers cerebral effects similar to barbiturates but to a lesser degree.

*Offers hemodynamic stability

*NDMRs do not cross BBB

*Vec, Pav, Roc are a safe choice (lack histamine release)

*To prevent vasospasm

*Decrease EBL

*Allow for surgical exposure and visualization

*Mannitol 1gm/kg

*Loop diuretics Lasix 0.5mg/kg

*Nitroprusside

*NTG

*May ask for temporary increase in MAP to 80-100mmHg if a feeder vessel is clamped for a short period to allow for clipping of aneurysm

*Increased MAP during clipping will increase tributary perfusion

*Mild hypothermia around 33 degrees will

-Decrease CMRO2

-Brain size

-increase the brain's ability to tolerate ischemia

*1 degree decrease will decrease CMRO2  7%

*4-5mL/kg/hr plus losses (urine and blood)

*Fluids must be given to avoid further hypovolemia and hypotension, sudden boluses should be avoided

*Glucose, which increases osmolarity, has a large volume of distribution pysiologically, and glucose- containing fluids are hypotonic and very likely to cause brain edema in regions where the blood brain barrier is impaired.  

*Glucose at the time of neurologic insult correlates strongly with a poor outcome.

*Vasospasm

*The amount of blood in the subarachnoid space and the extent of vessel narrowing are closely correlated.

*Triple H 

-Hypertension

-Hemodilution (33% Hct)

-Hypervolemia

*Nimodopine (CCB)

*CT

*STP, airway management tools, resuscitation drugs

*Endovascular Therapy (Guglieimi Detachable Coil- GDC)

*Goal of treatment is to prevent the flow of blood into the aneurysm sack by filling the aneurysm with coils and thrombus. Interruption of flow will prevent rupture.

*A standard cerebral arteriogram is performed to locate the aneurysm

*Another catheter is passed though the first up to the aneurysm neck.

*A platinum coil is advanced into the aneurysm and coils until the aneurysm is completely occluded

*Low voltage is passed into the tip of the coil to release it into the aneurysm

*A post procedure arteriogram is completed to verify complete occlusion of the aneurysm. 

*Shorter hospital stay

*Less anesthetic requirements

*Fewer surgical complications, minimally invasive

*Uncomplicated positioning, supine without external fixation of head (head fixed with tape instead of tongs)

*Aneurysm rupture

*Vasospasm

*Stroke

*SAH

*Supture

*Reexpansion of original aneurysm

*Incomplete coiling requiring more coil to be placed

*Long-term follow up of aneurysm is suggested at this time.  (The aneurysm is not clipped so there is a chance of expansion or bleed).

*GA with complete muscle paralysis to allow for a completely still patient

*minimal narcotic, painless procedure requiring fast wake up and assessment

*Short duration 2-3 hours

*Arterial line perfered

*Induction and emergence same as clipping

*Isoflurane/NDMR maintenance (need to be completely still)

*Minimal to no blood loss

*Heparin may be used (ACT 200-250)

*Intravascular embolization alone or followed by surgical excision

*Surgical excision

*Radiation

Who is more at risk for AVM?

*Males>Females

*Present at any age but bleeding most common in age 10-30

*Usually healthy without comorbidities 

*Loss of cerebral autoregulation leading to hyperemia and swelling.

*Tight hemodynamic control

*Beta blockers, SNP, NTG, Phenylephrine

*Neurological deficits

*Cerebral edema 

*Increased ICP

*Intracerebral hemorrhage