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


Pi Fb In Fl


Cerebral Mass


Mass Lesion


You are called to evaluate a patient in the ER. The patient was brought in by the EMS after the patient had a seizure. The patient has been suffering the last several weeks with a progressively worsening headache. Last few days the patient had severe nausea/vomiting according to the caregiver. Today the patient had a seizure and was immediately brought to the ER. The caregiver is unable to provide any more useful information; isn’t that the usual case?

Being concerned of a cerebral mass you attempt to perform a thorough history and physical examination. The patient has an altered state of consciousness and is not helpful in providing any useful information. The caregiver is nearly as useful (useless is a more descriptive word) as the altered patient. Having said that, the caregiver was actually able to provide some helpful information regarding signs and symptoms the patient complained of before becoming altered.

Location, Location, Location

common presentation
When you have something growing in your brain it makes perfect sense to have a general decline in cognitive and neurological function. Patients with intracranial mass may generally also have a progressively worsening headache associated with increased nausea and vomiting.

Intracranial Mass Location … Real Estate: location, location, location

The clinical presentation of the patient may vary depending on the location of the intracranial mass. In addition to the common presentation ( general decline in cognitive function +/- headache, N/V) the patient may present with signs and symptoms which may help identify the location of the intracranial mass.

Supratentorial Mass: often is associated with the ‘common presentation’ along with:
– seizure
– hemiplegia
– aphasia

Infratentorial Mass: often is associated with the ‘common presentation’ along with:
“cerebellar dysfunction” which manifests as:
– ataxia
– dysarthria
– nystagmus

Brainstem Mass: often is associated with the ‘common presentation’ along with:
-altered mental status
-cranial nerve palsy
-abnormal respirations

Continuing to obtain a thorough history (well, at least attempting to, or pretending to) its important to investigate into what medications the patient normally takes along with medications which have been administered while in the ER. The medications which the patient normally takes will provide an insight into the patients past medical history.

Special considerations for certain medications which may have been administered for example within the ER include:
– corticosteroids: which can lead to hyperglycemia; worsen neurological outcome
– diuretics: (osmotic,loop) which may lead to electrolyte abnormalities
– anticonvulsants: which may be sub- therapeutic and allow for another seizure.

Therefore as mentioned, its important to evaluate the patients laboratory values.
Chem 7 , hematology, cogs…any concerns?

sometimes if you want it done right, right to do it yourself
The patient is sent off for a CT of the brain. As the patient is being scanned, the radiologist confirms a cerebral mass and rushes back to his office to…drink coffee. You chase him down for his interpretation of the CT scan. He rushingly says, “yeah, yeah, this is a mass”. Again, you ask for a more detailed interpretation. He says, “the patient has an intracranial mass”. This is getting no where.

You take a look at the CT scan of the brain and look for any evidence of:
– cerebral edema
– midline shift x > 0.5 cm
– ventricular size/ +/- compression

Your essentially wanting to know whether there is an increase in the ICP, and if so, how severe is the increase?!

Severity of Increased ICP … how the hell do I know?
By properly evaluating the patient and obtaining a thorough history and physical examination as well as reviewing the CT of the brain, we are able to determine the relative severity of increased ICP.

Suppose our patient presented with mild cognitive impairment and low grade headache which just began a few days ago. The patient denies any nausea or vomiting. The patient is alert and oriented x3, no focal neurological deficit, and the CT of the brain has no evidence of edema, midline shift nor change in ventricular size. The patient is not demonstrating any significant signs or symptoms of severely increased ICP

Now suppose our patient presents to the ER with an altered state of consciousness after having had a seizure an hour ago. According to the caregiver, the patient had been complaining of a progressively worsening headache associated with severe nausea and vomiting. The patient clearly has a change in mental status and with obvious focal neurological deficit. The CT of the patients brain reveals a large intracranial mass with evidence of cerebral edema, midline shift x > 0.5 cm with compression of the ventricles. This patient is clearly demonstrating signs and symptoms of severely increased ICP!

One of those million dollar questions…will you premeditate the patient. The answer depends on the level of consciousness of the patient and the severity of increased ICP you feel the patient has.

example 1: No evidence of severely increased ICP
For a patient who has no evidence of severely increased ICP (ex. alert oriented x 3, no nausea/vomiting, no focal neurological deficit, CT reveals small mass with no evidence of cerebral edema, midline shift, nor any changes with the ventricle size) and the patient is adequately ventilated, I would consider preoperative sedation if the patient were extremely anxious.

example 2: Strong evidence for severely increase ICP!
Would you premedicate a patient who has obvious signs/ symptoms of increased ICP? Obviously not. You answer should be ‘hell to the no”!

Whats wrong with providing sedation to a patient with increased ICP?
A patient who has severely increased ICP we are generally concerned with:
-further increasing the ICP which will further reduce the cerebral perfusion pressure
-decreasing the MAP which will further reduce the cerebral perfusion pressure

From the above statement we can clearly say that one of our main concerns is to maintain an adequate cerebral perfusion pressure to allow for adequate CBF to prevent cerebral ischemia.

Cerebral Perfusion Pressure (CePP) = MAP – ICP

Suppose you give midazolam 2mg IVP to our clinical example 2 patient who has obvious signs (well, not so obvious to you) of severely increased ICP. The patients airway becomes obstructed and begins to hypoventilate. What happens to the PaC02? The PaCO2 naturally increases which will eventually result in a further increase in ICP!
This further increase in ICP will worsen the Cerebral perfusion pressure and may lead to worsening cerebral ischemia.

Also, depending on the patients cardiac reserve, premedication with a sedative-hypotic agent may decrease the MAP which would also decrease the Cerebral Perfusion Pressure resulting in worsening cerebral ischemia!


The patient is just about to be transferred to the OR. After having properly evaluated the patient our main concerns are:

The obvious intracranial mass with evidence of severely increased ICP!

Airway: … this dilemma always “sux” !
This patient has a difficult airway in the setting of increased ICP and ‘full stomach’…the patient has increased nausea and vomiting.

SCI vs RSI?! hmm: things that make you say “hmm”

SCI: ensuring adequate depth of anesthesia prior to direct laryngoscopy and ETT intubation making sure not to further increase the ICP…at the expense of “losing the airway” (not being able to intubate nor ventilate) and risk of aspiration!

RSI: To ensure the ETT tube is placed in the airway as quickly as possible to avoid aspiration and as a ‘safety’ factor of having “sux” wear off and patient resume spontaneous ventilation in case you are unable to intubate nor ventilate the patient BUT at the expense of theoretically increasing the ICP with “sux” or severely reducing the MAP. Both the decrease in MAP and increase in ICP may lead to a major reduction in cerebral perfusion pressure resulting in severe cerebral ischemia!

Although not the major concern for this chapter, the patient may very well have severe obstructive disease (ex. Asthma, COPD) with a severe bronchospatic element. This would also influence your perioperative management. A deeper plan of anesthesia may be required upon induction not only to prevent any straining/’bucking’ (which would increase the ICP) but to help prevent severe bronchospasm!

This patient could also very well have severe cardiac disease such as hypertension, IHD, CHF with EF 15%

All the above concerns sure do make a wonderful ‘clinical case from hell’ which can be presented to anyone of us on any given day…life of an anesthesiologist; not for the faint at heart.

Goal for Induction of General Anesthesia … maintaining adequate CePP!
The patient arrives and is placed on the OR table, monitors placed, A-line quickly inserted while being preoxygenated with 1.0FIO2. Baseline BP is 100/50 mmHg.

You plan of induction is a slow controlled induction in order to maintain an adequate cerebral perfusion pressure by tight control of MAP and preventing any further increase in ICP.

You slowly administer (apparently not slow enough) a small dose (apparently not small enough) of propofol and the patient suddenly becomes hypotensive! The blood pressure suddenly drops from 100/50 mmHg to 50/30 mmHg!

Q. How do you think this sudden hypotension effects the cerebral perfusion pressure?

A. Lets assume for the fun of it, that the patients ICP before (and during induction) was (is) nearly 30mmHg. We know what Cerebral Perfusion Pressure is:


After the induction of anesthesia the blood pressure drops from 100/50 to 50/30 mmHg. The MAP (of 50/30 mmHg) is approximately 36 mmHg
Therefore the CePP = 36 – 30 = 6 mmHg. We can boldly state that the end result is Cerebral Ischemia!

TREATMENT OF HYPOTENSION upon induction of anesthesia:
phenylephrine, ephedrine preferred over fluids.

Direct laryngoscopy/ ETT intubation …stingy miserly anesthesiologist
The complete opposite concern of hypotension upon administering the anesthetics is hypertension upon direct laryngoscopy and ETT intubation. You slowly (very very slowly) administer a small dose (very very small dose) of propofol (a whole whopping 2mls!). You very proudly point out to the nurse the patients stable BP and mumble the importance of maintaining hemodynamic stability. She, not knowing what an idiot you truly are, is impressed and states what a great doc you are.

You go for direct laryngoscopy and ETT intubation… go in for the “KILL”!
As you not so gently (shove!) the laryngoscope blade into the patients mouth and jam the ETT down the patients throat the BP sky rockets out of control. The patients blood pressure jumps from 100/50 mmHg to 270/160 mmHg. The patient bucks several times which probably sky rockets the ICP into another orbit as well. The increased BP promotes cerebral edema which further worsens the ICP until finally the patient herniates! You secretly take a look at the patients pupils without having the nurse see…blown out fixed and dilated pupils!. You tell the nurse everything is fine and she again flatters you with greatness.

deep plane of anesthesia, BB (if not contraindicated) preferred to vasodilators (ex. NTP, CCB, etc) until the dura has been opened


Airway has been secured, you connect the ETT to the circuit and set the mode of ventilation.

Controlled mechanical ventilation obviously but what settings for TV and RR? Do you plan to hyperventilate the patient in attempts to lower the ICP. Hyperventilation (which perhaps is out-dated) by decreasing the PaCO2 also decreases the CBF and eventually the ICP.

Its crucial to ensure adequate cerebral perfusion in the setting of increased ICP. Therefore its critical to maintain tight control of the patients BP.
-plan to use an osmotic diuretic? Patients LV function, renal function?
-starting H/H? …planning to transfuse the patient?
-electrolytes need correction?

Concerns with hyperventilation:
– the decrease in CBF may further worsen focal cerebral ischemia
– increased airway pressures may inc. CVP, dec. venous drainage and inc. ICP!
– hyperventilation…respiratory alkalosis, shift ODC to left…worsen cerebral ischemia

Concerns with hypoventilation:
Inadequate ventilation can also worsen the clinical situation. Hypoventilation will lead to an increase in PaCO2. PaCO2 and CBF have a directly proportionate relationship between a PaCO2 20 – 80 mmHg. For every 1mmHg increase in PaCO2 leads to approximately 1-2 ml/100g/min increase in CBF.

Suppose that the patients PaCO2 increased from 40 to 60 mmHg because of inadequate ventilation. How would the increase in PaCO2 effect the overall CBF?
The CBF would increase.

Increase 20 mmHg => 20-40 ml/100g/min increase in CBF

50 + (20 to 40 ) ==> 70 to 90 ml/100g/min CBF in the setting of severely increased ICP may lead to HERNIATION!

ICP Management during maintenance of anesthesia
concern is obviously dealing with the patients severely increased ICP.
goal is to decrease the ICP and to make sure no sudden increases in ICP.

plan is:
– to promote venous drainage with head elevation and to avoid increases in CVP
– diuresis either with an osmotic or loop diuretic
– consider placement of CSF drain
– consider hyperventilation

Anesthetic Management during maintenance of anesthesia
After having connected the ETT to the circuit and set the vent setting, almost automatically your right hand reaches back to crank on some ‘sevo’. As you do so, you think to yourself, “hmm” <--- profound thought huh?! What might be a more beneficial anesthetic plan for this patient who has severely increased ICP due to a intracranial mass? Keep in mind that the neuro-monitoring team will be bugging the hell out of you as their SSEP signals become whacky. TIVA vs. Balanced Anesthesia?! TIVA (ex. propofol + remifentanil +/- NDMR +/- phenylephrine) The benefits of the above TIVA infusion is the reduction across the board. Decrease in CBF, ICP and CMRO2!. The rate at which propofol may need to be infused in order to provide an adequate depth of anesthesia may lead to hypotension. The hypotension has its obvious effects on CePP and would have to be treated. Phenylephrine infusion may help maintain stable hemodynamics with this anesthetic plan. Balanced Anesthesia Volatile anesthetics may appear to be a messy style of anesthesia for a patient with intracranial mass and severely increased ICP. Volatile anesthetics increase both CBF and ICP in a dose-related fashion and decreases the CMRO2 Volatile anesthetics also effect the measurement of evoked potentials (ex. SSEP) and if used, often is limited to 0.5 MAC. Glucose Management Perioperative glucose management in the setting of neurosurgery is crucial. Hyperglycemia has been associated with worsen neurological outcome. Likewise, hypoglycemia has its own obvious concerns. Frequent and diligent monitoring of glucose is imperative. Emergence Thankfully (who to thank? God or the neurosurgeon who thinks he is God?) the case is nearing an end. The patient has just had a large intracranial mass resected and left with a huge 'whole' within his brain, any concerns?! Your immediate answer should be, "uh, yes". Several concerns Several concerns upon the emergence of this case (resection of intracranial mass with severely increased ICP) are: Neuro: - formation of hematoma/ bleeding - cerebral edema - delayed emergence - pain Airway/ Breathing: - able to protect airway - adequate ventilation - are we going to extubate?! Circulation: MAP - hypertension: leads to worsening cerebral edema, bleeding/ hematoma, inc. ICP - hypotension: decreases CePP, CBF and may lead to severe cerebral ischemia! Extubation Lets assume you attempt to extubate at the end of this case. What special concerns do you have in regards to extubation? concerns: … rough extubation done by a complete moron As the patient emerges from anesthesia, the blood pressure is likely to increase. This increase in MAP increases the risk of bleeding and formation of a hematoma. The increased blood will also increase the CePP and CBF resulting in increased ICP. As the patient becomes 'light' she begins to buck uncontrollably on the ETT. This 'bucking' (this word "bucking" can so easily be a typo into a whole other word…which probably increases the ICP equally as much…next research project for someone) dramatically increases the ICP and in combination with a severely increased BP ( ex. 240/120 mmHg: MAP 160 mmHg!) can result in brain herniation!. goals/ plan … Smooth extubation done by a stud Neuro: Goal: avoid increase in ICP Plan: head elevation, diuresis, +/- hyperventilation, slow controlled emergence! Airway: Goal: smooth extubation. Therefore: either blunt airway reflexes or deep extubation Plan: ex. +/- lidocaine 1.5 mg/kg IV, deep extubation Breathing: Goal: ensure adequate oxygenation/ventilation Plan: pray, or keep intubated with CMV Circulation: Goal: hemodynamic stability (SCE); avoiding inc. or dec. MAP Plan: treat inc BP with quick onset/ short acting BB (if not contraindicated): esmolol Delayed Emergence Case was finished 20 - 30 minutes ago. Scrub tech has removed all the drapes, head wrapped like a turban, patient cleaned up, transport bed brought into the room next to the OR table, transport monitors applied, and all eyes watching are watching YOU as YOU watch the patient NOT WAKE UP! 30 minutes now approaches 35 minutes…and a little neuron fires within your brain and becomes concerned of… concerns with delayed emergence: - Neuro: cerebral hematoma/ bleed, cerebral edema leading to increased ICP! - 'Drugs': muscle relaxant, opioid, residual volatile/ intravenous anesthetics - Metabolic: ex. hypoglycemia - Hypothermia When do you call the Neurosurgeon? When do you race off to get a CT? Postoperative Concerns Patient is transferred to the Neuro ICU. Any concerns with postoperative management of this patient who has had resection of an intracranial mass with increased ICP? concerns Neuro: - as mentioned 1000 times; hemotoma/bleed, inc ICP…blah blah blah - +/- sedation - +/- analgesia Airway: - +/- extubation Breathing: - +/- hyperventilation Circulation: - MAP Renal: - diuresis? Labs: - electrolyte abnormalities - h/h - renal function - anticonvulsant therapeutic

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