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732/21 Second Street, Manchester,
King Street, Kingston United Kingdom


Pi Fb In Fl


Cerebral Aneurysm


Cerebral Aneurysm

Preoperative Evaluation
A 45 year old female was at home spending “quality time” (if such a thing) with her (monster) mother-in-law and suddenly developed the worst headache of her life. At first the ego centric mother-in-law took offense as she felt she was the cause of such dismay. Suddenly the daughter-in-law (patient) developed increasing nausea and vomiting and EMS was called.

The patient arrives in the ER and a thorough history and physical examination is performed. The patient states having developed a sudden headache as she was talking to her mother-in-law, which she emphatically stated, ” as the worst headache of her life!”. Not being clear. you ask whether her mother-in-law is the worst headache of her life or the current headache?

Severity … how bad is bad? Bad or really really Bad?!
Immediately the patient is sent for a CT ‘angio’ of the brain which reveals an intracranial aneurysm. How do we determine the relative severity of this cerebral aneurysm?

Certain factors which help determine the severity of the cerebral aneurysm such as:
– classification (Hess and Hunt, WFNS)
– size of aneurysm (ex. x >7mm = !)
– location of aneurysm

ICU or OR …Now what? Where to next?
Gambling: wait and provide supportive care at risk of ‘delayed complications’ or go to the OR for surgical obliteration to help reduce the risk of ‘delayed complications’ but increase the risk of other surgical-related complications

After having evaluated the patient and reviewed the CT a decision must be made whether to observe and provide supportive treatment for the patient in the Neuro ICU or head off to the OR for early surgical obliteration in hopes of preventing ‘ delayed complications’.

Delayed Complications…whats wrong with delaying complications? (until I sign out)

The ‘delayed complications’ we are most concerned about following a ruptured cerebral aneurysm are:
– Rebleed
– Vasospasm
– Increased ICP
– Hydrocephalus

Suppose you are paged to evaluate a patient in the Neuro ICU who has had a recent rupture of a cerebral aneurysm. This patient is a 56 year old female with a medical history of HTN, IHD, CHF, DM, + cigarette smoking as well as recent cocaine use.

Any Concerns? … hell yeah!

1. Cerebral Aneurysm:

1a. Severity:
– classification: (Hess and Hunt, WFNS)
– size: (x > 7mm?!)
– location (location, location, location)

1b. Delayed Complications!:
– Rebleed
– Vasospasm
– increased ICP
– Hydrocephalus

2. Airway

2a. ‘Easy’ Airway: “easy” intubation + “full stomach” + cerebral aneurysm = ?
2a1. SCI with cricoid pressure?
2a2. modified RSI with cricoid pressure?
2a3. DMR vs NDMR?

2b. “Difficult” Airway: “difficult intubation” + “full stomach” + cerebral aneurysm = !
2b1. Awake FOB? patient uncooperative, BP increases… “pop!”
2b2. SCI with cricoid pressure? BP stable (no bleed) BUT cant intubate/ventilate: dead
2b3. RSI with cricoid pressure: BP unstable risk of cerebral ischemia, Bleed

3. Breathing

3a. Smoking
– increased mucous production
– decreased mucous clearance
– increased carboxyhemoglobin levels

3b. COPD

3b1. Severity?
– cough with exertion?
– sputum production?
– Pa02
– hyperinflation on CXR?
– Bronchospasm?

4. Circulation

4a. HTN
– duration
– tx/mx
– associated complications: ( CVA. MI, CHF, Renal impairment)
– severity

4b. IHD
– hx previous MI: (when, where, extent of damage)
– associated complications: ( dysrhythmias, conduction defects…)
– reversible myocardial ischemia?!

4c. CHF
– LV f(n)
– severity?!

5. Renal function
6. Labs: H/H

Taking a Closer Look at our Concerns: RUPTURE…BLEEDING!

Rupture of Cerebral Aneurysm …POP!
Our first main concern for this patient is (re)-rupture of the cerebral aneurysm which leads to a major intracranial bleed. What major factor is involved with that rupture of the cerebral aneurysm? Two words, ‘Transmural Tension’!

Transmural Tension = MAP – ICP
An increase in the transmural tension across the vessel wall of the cerebral aneurysm increases the risk of rupture. What increases the transmural tension? Well, according to the above equation we can see that either:
– A sudden increase in MAP increases the transmural tension…POP!
– A sudden decrease in ICP can also increase the transmural tension…POP!

Therefore, in order to prevent a (re)- rupture of the cerebral aneurysm our plan is to prevent sudden increase in transmural tension by preventing a sudden increase in MAP (and/or sudden decrease in ICP).

This concern becomes increasingly important during times of increased stimulation in the preoperative period for example during:
– direct laryngoscopy/ ETT intubation
– incision
– dural opening
– closure
– emergence
– postoperative conditions: (pain, anxiety, respiratory acidosis, volume overload, etc)

As you review the patients chart you begin developing a hell of a headache as well! Being concerned of:

1. (re)- rupture and bleeding you are anticipating:
– Blood transfusion
– Surgical hemostasis as the brain swell to the size of a pumpkin within a second

2. Periods of increased Transmural Pressure:
– direct laryngoscopy/ ETT intubation: SCI, +/- topicalization, skillful instrumentation
– incision: adequate depth of anesthesia, opioids, vasoactive meeds?
– dural opening: adequate depth of anesthesia
– emergence: SCE: deep extubation?

3. Treatment of Increased MAP?!
– increasing depth of anesthesia
– +/- vasodilators?
– +/- betablockers?

Goals for a particular concern can create a new set of concerns another can of worms
Preventing a sudden increase in transmural tension may be challenging. However, the true challenge occurs when the patient has other co-exiting conditions (for example, IHD,CHF) which limit the degree of hypotension the patient can tolerate before hemodynamic instability occurs.

Intracranial Aneurysm + IHD + CHF …Rupture vs MI ?
Suppose our patient has severe IHD with reversible myocardial ischemia. The degree of hypotension required intraoperatively during clipping of the aneurysm puts (what little amount of available) viable myocardium (the only few ‘healthy’ myofibers avaiable in this patient’s left ventricle) at risk of infarction. This in the setting of pre-existing severe LV dysfunction puts the patient at increased risk of decompensated heart failure, MI, ARF, CVA…and death!

Cerebral Vasospasm:
busy ‘spasming’ about rupture; time to spasm about vasospasm

Spasming over the not so distant (grim) future…
While evaluating the patient in the Neuro ICU, you spent the last 20 minutes spasming out about the risk of rupture and bleed from the cerebral aneurysm. Now its time to spasm out about the risk of cerebral vasospasm. After all cerebral vasospasm appears to be one of the major causes of morbidity and mortality for patients who have cerebral aneurysm. Generally speaking, cerebral vasospasm if it does occur (which does occur in about 30% of these patients with ruptured cerebral aneurysm), occurs most commonly after 4- 14 days after the initial bleed (rupture).

Treatment of Cerebral Vasospasm: “Triple H”
Generally speaking, its thought that a blood clot around the cerebral vessel leads to cerebral vasospasm. Prevention of cerebral vasospasm may be attempted with the use of a calcium channel blocker (ex. nimodipine or nicardipine). However, once cerebral spasm occurs treatment includes:
– hypervolelemia: intravascular volume expansion
– hypertension
– hemodilution

Treatment plan (for cerebral vasospam) creates a new set of concerns…
Suppose our patient has a significant cardiac history of:
-IHD ( recent myocardial infarction), with extensive CAD…reversible ischemia!
-CHF: LV dysfunction, EF 15%

How well do you think this patent will tolerate induced hypertension before developing myocardial ischemia, myocardial infarction and decompensated heart failure?

Induced- Hypertension (for example with Dopamine) leads to an increase in myocardial oxygen demand (with increased contractility, +/- increase in HR) along with increased risk of developing cardiac dysrhythmias.

Hypervolemia increases the risk of decompensated heart failure.



The patient is brought to the OR, monitors attached, and an A-line placed as the patient is preoxygenated with 1.0 FIO2.

What not to do!
Now being in private practice, I reflect back in my residency training days and realize I learnt a great deal of what not to do with various attendings. This is a classic example of what not to do…this is not a time to cowboy up nor is it a time to be stingy but instead respectfully proceed cautiously with a slow controlled induction.

Suppose during your preoperative evaluation, the patients blood pressure appeared relatively stable at a range of 105 – 120/ 70-80 mmHg. Upon arrival to the OR, the patients initial blood pressure is 110/75 mmHg. Being concerned of the patients poor LV function and ongoing myocardial ischemia.

You being a stingy miser give the patient midazolam 0.5 mg IV followed by fentanyl 50mcg and last but not least, a whole 2 mls of propofol. The patient yawns, and you go in for the kill…literally!

You enter the laryngoscope blade into the patients mouth and push the tongue off to the left. Fully concentrated on viewing the “cords”, you loose complete awareness of the patients blood pressure. That is, until you hear a “POP”. Desperately hoping that someone has just cracked their knuckles, you quickly look up at the monitor. The monitor shows a blood pressure of 210/105 mmHg and another second later 250 /115 mmHg with a heart rate of 35 beats per minute.

Rupture of the cerebral aneurysm, massive bleed and an acute severely increased ICP has lead to brain herniation…and the patient is DEAD.

So what the hell happened? … instant replay
The patient had an inadequate depth of anesthesia in relation to the amount of stimuli imposed during airway manipulation. Upon direct laryngoscopy and ETT intubation the patent was stimulated and initiated a sympathetic response which increased the blood pressure. The sudden increase in blood pressure created a sudden increase in the transmural tension across the cerebral vessel which lead to rupture (POP!) , massive intracranial bleed, sudden severe increase in ICP…and brain herniation!

Having just entertained a nightmare induction from hell in the previous example, the natural question to follow is… is there a better approach? Of course there is, its called a SLOW and CONTROLLED INDUCTION (of anesthesia)!

concerns and considerations:

– Intense stimulation w/ airway manipulation therefore consider blunting airway response (ex. ‘airway blocks’, topical 4% lidocaine)

– Intense sympathetic response to airway manipulation therefore consider first providing an adequate depth of anesthesia, consider a short acting antihypertensive medication (ex. esmolol; if not contraindicated) in order to maintain steady hemodynamics.

– hypotension (while attempting to provide a deep plane of anesthesia prior to airway manipulation) therefore consider judicious volume loading to help prevent hypotension upon induction. Small incremental dosing of hypnotic agents constantly watching changes in patients level of consciousness and changes in blood pressure.

Deepening the Plan of Anesthesia
Once you have reached a plane of anesthesia in which you think is deep enough to allow airway instrumentation without a sudden increase in blood pressure, you slowly open the patients mouth and gently glide the laryngoscope displacing the tongue to the left. As you do so, one eye is watching the monitor. The initial blood pressure of 110/75 mmHg increases to 125/80 mmHg should make you on edge. The point is you are in a process of THINKING while doing. You thought the patient was deep enough, and you have come to realize she is not. Therefore its not an all or nothing induction. Do not Enter! Do not proceed to enter a place you are unwelcome…trespassers will be PROSECUTED (in the court of law).

You may want to back off and consider further deepening the level of anesthesia. You may want to consider:
– additional doses of an intravenous sedative-hypnotic (ex. propofol)
– additional doses of an opioid narcotic (ex. fentanyl)
– ventilating the patient with an inhalational volatile anesthetic (ex. sevoflurane)

If concerned of increased ICP, you may want to consider hyperventilating the patient to help decrease the PaCO2 which will also help reduce the ICP.

Blunting the Hemodynamic Response to airway manipulation
After having provided additional doses of IV anesthetics, opioid narcotic, and have hyperventilated the patient with an inhalational volatile anesthetic for the last 3-5 minutes, the deepest plane of anesthesia has been reached before significant hypotension occurs. Again, you approach the airway skillfully gently gliding the laryngoscope blade into the patients mouth, slowly pushing the tongue off to the left. Glance at the monitor, the blood pressure increases from 90/50 mmHg to 100/60 mmHg. Things are looking pretty benign so you advance the ETT past the (already topicalized) glottic opening and down the trachea. Quickly looking up at the monitor, blood pressure again increases from 100/60 mmHg to 115/75 mmHg. Few seconds later the blood pressure continues to increase to 130/85 mmHg. Concerned of the current trend, you pick up an anti-hypertensive agent and slowly administer it. Blood pressure slowly decreases to 100/50 mmHg with HR 65 bpm.

Choice of Antihypertensive: (to blunt the hemodynamic response to ETT intubation)
– quick onset/ short acting BB ideal if not contraindicated


Maintenace of Anesthetics TIVA vs Balance Anesthetic?!
After having successfully secured the airway without ‘blowing up’ the ‘ticking time bomb’ cerebral aneurysm you take a deep breathe of celebration. Knowing this is only the first baby step of a monstrous case from hell, you tape the ETT tube securely and reach back automatically towards the sevoflorane vaporizer. Generally speaking, what are the effects of inhalation volatile anesthetics on cerebral physiology?

Volatile Inhalational Anesthetics
– increase CBF
– increase CBF
– decrease CMRO2

TIVA (ex. Propofol + Remifenail +/- NDMR)
– decrease CBF
– decrease ICP
– decrease CMRO2

TIVA may be more beneficial across the board

The OR table is turned, making sure none of your “lines” (intravenous, arterial, and CVP), and circuit don’t get disconnected. The paint is properly positioned.

Ensure ABC are well controlled

Airway will be out of reach for the most part during the remainder of the case therefore check, double check (triple and quadruple check) the ETT is secured without the risk of kinking.

Ensure adequate oxygenation and ventilation.
Planning to hyperventilate the patient to help reduce ICP. Generally speaking, hyperventilation is best avoided in order to reduce the risk of rupture/bleed.

Transmural Tension = MAP – ICP

If the ICP is suddenly reduced, this can in fact increase the transmural tension and increase the risk of rupture of the cerebral aneurysm.

For a ruptured aneurysm, hyperventilation and the sudden decrease in ICP (assuming the dura is not yet opened) can actually promote rebleeding by removing the tamponading effect on the ruptured aneurysm.

Tight blood pressure control in essence is the central focus for this case. In order to prevent (re) rupture of the cerebral aneurysm, or our goal is to prevent any sudden increases in the transmural tension which implies preventing any sudden increase in the MAP.

Increased ICP
Struggling to keep this ‘ticking time bomb’ cerebral aneurysm from (re) rupturing, the neurosurgeon keeps yelling over to you that “the brain is TIGHT and wants more SLACK!” The patient has increased ICP. How can we help to reduce the ICP?

Management of Increased ICP
– Hyperventilate: goal for PaCO2? , any additional concerns with hyperventilation?!
– Diuresis: osmotic vs loop diuretic
– Barbiturate (ex. Thiopental)
– CSF drain

(Re) Rupture of Cerebral Aneurysm …”how low can you go?”
The surgeon continues to yell as he dissects further exposing the cerebral aneurysm. Nearing the cerebral aneurysm, the surgeon asks for further reduction of the blood pressure. You are able to drop the blood pressure from 90/50 mmHg to 80/45 mmHg. The surgeon screams, “if the blood pressure doesn’t come down anymore, this fucking aneurysm is going to BLOW!” He demands that you reduce the blood pressure lower and lower and lower! Does this concern you?!

Assuming this patient also has a significant cardiac history of:
– IHD ( récent MI) with extensive CAD and ongoing myocardial ischemia
-CHF with significant LV dysfunction

Reducing the blood pressure will help prevent rupture of the cerebral aneurysm but instead lead to an acute MI, heart failure, acute renal failure and stroke!

When Push comes to shove!
The blood pressure at 80/45 mmHg shows ECG ST segment changes. The surgeon pushes you to further reduce the blood pressure to 50/30 mmHg. After all the neurosurgeon is God, and you being a faithful christian believing in God reduce the blood pressure to 50/30 mmHg. God, sorry I mean the Neurosurgeon, request for further reduction in the patients blood pressure! What do you do? Lose faith, become agnostic, atheist?!

CPB with Deep hypothermia/ Circulatory Arrest
How low you willing to Go? …All the F’ing Way!
This asshole Neurosurgeon, is screaming over the drapes that he wants the blood pressure reduced even further. You are put in a predicament. Continue to lower the blood pressure and let the patient stroke out, have a heart attack, develop acute renal failure for the sake of preventing a (re) rupture of the cerebral aneurysm. Instead maintain the blood pressure at risk of (re) rupture of the cerebral aneurysm causing the brain to swell up to the size of a beach ball in less than 3 seconds.

CPB pump time … You call in the other God complex surgeon
The Neurosurgeon continues to scream at the top of his lungs. You call in the cardiothoracic surgeon to initiate the cardiopulmonary bypass pump. CPB is initiated and the patients blood pressure drops from 50/30 mmHg to 40/20 mmHg. You still hear the neurosurgeon yelling…”lower, lower lower!”. The Blood pressure continues to drop to 20/5 mmHg…and the asshole is still yelling…”lower. lower, lower!”. Eventually you have achieved deep hypothermia circulatory arrest while on the CPB pump. The asshole is still yelling, “lower, lower, lower”. You look over the drapes and tell him to go fuck off!

Suppose you don’t budge. You keep the patients blood pressure at 100/50 mmHg despite the screaming from the neurosurgeon. He looks over the drapes and tells you that “if the blood pressure doesn’t decrease, this f’ing cerebral f’ing aneurysm is going to F’ing blow the F’up”! Being amazed that the use of the “f” word can be used as a non, adjective, verb, and pronoun all in one run on sentence, you still are not influenced by the neurosurgeons demand. Blood pressure remains at 100/50 mmHg. Nearly three seconds later you hear one of the most profound statements of your life.

“OH SHIT” means only one thing when clipping an aneurysm.

“POP!”. You look over the drapes and see the brain swell up to the size of a beach ball within 3 seconds. Feeling quite helpless knowing no way in hell is the surgeon going to be able to obtain surgical hemostasis.

Treatment Plan for Rupture of Cerebral Aneurysm
– prevent rupture with decreased transmural tension
– prevent rupture with decreased transmural tension
– prevent rupture with decreased transmural tension

(ok im sure you got the above redundant point)

1. Volume Resuscitation: Transfuse BLOOD!
2. Surgical Hemostasis: “good luck!”
3. +/- consider cerebral protection?…umm BP is 20/10 mmHg…giving thiopental?!
4. got on your knees and pray, then crawl up into a fetal position

Lets assume the case went relatively well. The cerebral aneurysm is clipped without any major complications. The patient has been relatively stable despite the underlying comorbidities.

What are our main concerns for this patient? Our concerns continue to be the major complications related to cerebral aneurysm (clipping):
– Bleeding
– Vasospasm
– Increased ICP
– Hydrocephalus
– Airway: +/- Extubation?! SCE…deep extubation?
– Breathing: +/- hyperventialtion
– Circulation: goal for MAP?!
– Renal: urine output? Oligura? Azotemia (pre, renal, post)…ARF?!
– labs: H/H, Electrolytes?!

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