Closed Head Injury
ANESTHESIA FOR NEUROSURGERY
Closed Head Injury
A patient is brought to the ER after having been in a motor vehicle accident. You are called to the trauma room as the patient just arrives.
Initial Assessment … ‘ABC, easy as 1,2,3’
What are we initially interested in? Our initial assessment is divided into two separate surveys: primary and secondary survey.
Primary Survey … first things first
The very first thing we assess during our primary surgery (of the initial assessment) is the patency of the patient’s airway. Why?! Well, without a patent airway your good as dead. Next we evaluate the respiratory status of the patient to ensure adequate ventilation and oxygenation. Thirdly, we evaluate the circulatory status of the patient to ensure adequate perfusion to the vital organs of the body.
Music to my ears
Its been a quiet trauma call until you are paged to the trauma bay as the patient who sustained a motor vehicle arrives. Entering into the ER, you hear the patient shouting at the top of her lungs, ” let me go you mother fucker asshole” as you turn the last corner to enter into the trauma bay. These words are like music to your ear. Not because you have any unresolved latent freudian issues with your mother but instead you know immediately the patient has a patent airway and is for the time being ventilating pretty damn well to be yelling that loud!
Not so musical
Suppose instead as you enter into the trauma bay the patient is quiet. You may think that the patients silence is far more appreciated, taking into consideration its nearly 3am and you have a scheduled 730am elective case. Don’t you hate having a line up of cases the following morning after having been up all night with a major trauma case? Anyways, you arrive to the trauma bay and the patient is silent. First concern? Patency of the airway! The patients airway is clearly obstructed preventing proper ventilation and requires immediate airway management! An oral airway and/or a nasopharyngeal airway just wont cut it this time and the patient requires an emergent ETT intubation.
What are some concerns when managing an airway of a trauma patient? Several concerns that should be racing in your mind are the ‘assumed C-spine injury’ that accompanies all trauma patients, the relative difficulty of the patients airway in the setting of a bloody mess. The patient may have mid-facial deformities or perhaps laryngeal trauma which turn what was a relatively simple airway into a nightmare, hellish condition in a heartbeat. Another major concern when establishing an airway (ex. ETT intubation) is that the patient is taken to be as a ‘full stomach’, therefore the goal would be to establish a secured airway RAPIDLY (RSI) in order to reduce the risk of aspiration. Of course, to make your hellish trauma call even more painful, the patient has sustained a closed head injury and therefore we are concerned of increased ICP (ex. cerebral edema, cerebral hmmg) which if increased any further (ex. during ETT intubation…buck buck buck) may result in HERNIATION (and we are not talking about an inguinal hernia, we are talking about brainstem herniation! )
We will talk about securing the airway of a patient with a closed head injury (increased ICP) later in this chapter. But before we move on with our primary surgery we have a million dollar question.
Who wants to be a millionaire anesthesiologist? … million dollar question
Q. Suppose are you attempt to secure the airway of the patient with a closed head injury and increased ICP, you are unable to visualize the glottic opening and therefore cannot intubate. The patient is quickly desaturating and now is clearly hypoxic. You are unable to ventilate the patient. As you are about to attempt a blind nasal endotracheal intubation you hear the ER doc behind you yelling she has a basilar skull fracture!… ‘Million dollar question’ is: Do you proceed with a blind nasal intubation? Even if the patient is about to die before you eyes?! Any other way to rapidly establish an airway before this patient is dead?!
After evaluating the patency of the airway, next in the primary survey is assessing the respiratory status of the patient: BREATHING. We want to ensure that the patient is adequately oxygenating and ventilating. Especially in a patient who has suffered from a closed head injury we have several concerns (such as cerebral ischemia, cerebral edema, intracranial hemorrhage) which can result in an Increased ICP and further worsened by hypoventilation!
Respiratory Gas Tensions (PaCO2) influence on CBF
PaCO2 has a very strong influence on the CBF. PaCO2 gas tensions (between 20-80mmHg) has a directly proportionate relationship with the CBF. Which means as the PaCO2 increases (ex. from hypoventilation) so does the CBF which can further increase the ICP of a patient who already has an increased ICP due to a closed head injury. As the PaCO2 gas tension increases 1mmHg, the CBF increases approximately 1-2 ml/100g/min.
So while performing the primary survey, the patient appears to be hypoventilating. Assuming a blood gas sample was miraculously obtained (which of course wouldn’t have and shouldn’t have been obtained because we are only within our primary survey within the initial assessment). But, lets assume for teaching purposes, that a blood gas was obtained and immediately the results reveal the PaCO2 to be 75mmHg.
Q. What might the CBF be assuming PaCO2 gas tensions (btw 20-80mmHg) maintain a directly proportionate relationship with CBF (an increase of 1-2 ml/100 g/min for every increase of 1mmHg PaCO2)
A. Change in PaCO2: 75mmHg – 40mmHg = 35mmHg PaCO2
Relationship: increase 1mmHg PaCO2 : increase 1-2 ml CBF/ 100 g/ min
35mmHg inc. PaCO2 x inc. 1-2 ml CBF/100 g/min = 35->70ml CBF/100g/m.
Lets assume prior to the closed head injury and hypoventilation the CBF was normal at 50 ml/100g/min and (after having sustained the CHI) with a PaCO2 now of 75mmHg (due to hypoventilation) the CBF is approximately [50 + (35 -> 70 ml/100g/min increase)] … 85 to 120 ml/100g/min !
This increase in CBF in the setting of an already increased ICP (ex. cerebral edema, cerebral hemorrhage) may lead to herniation!.
Therefore during the primary survey (of the initial assessment), focus has to be on ensuring adequacy of oxygenation and ventilation!
After having assessed the airway and breathing, next major concern is determining adequacy of “C”…Circulation! We need to ensure adequate perfusion and oxygen delivery to the vital organs therefore we evaluate the patient and the patients vital signs (ex. BP, HR). Our main concern here is hypotension example from hypovolemia due to bleeding.
Two wrongs make a right?…NO!
Suppose since its 3am and your still half asleep sleep walking with an overall state of unconscious awareness you did not properly assess the patient hypoventilating. Therefore the patient continues to increase the PaCO2, which increases the CBF, and worsening the already increased ICP. To make matters even worse the patient, being hypovolemic secondary to bleeding, is HYPOTENSIVE!
Q. How is the Cerebral Perfusion Pressure (CePP) affected by both HYPOTENSION and INCREASED ICP?!
A. Cerebral Perfusion Pressure (CePP) = MAP – ICP Therefore if the MAP is low (ex. HYPOTENSION) and ICP high (ex.cerebral edema) the Cerebral perfusion pressure will be severely LOW!
The decrease in Cerebral Perfusion Pressure (CePP) leads to a decrease in CBF which if severe enough can result in (worsening) CEREBRAL ISCHEMIA!. A vicious cycle begins to spiral out of control because cerebral ischemia then leads to increasing cerebral edema which leads to an (further) increase in ICP. This increase in ICP reduces the Cerebral Perfusion Pressure resulting in a decrease in CBF. The decrease in CBF leads to worsening cerebral ischemia which again promotes more chaotic cerebral edema and the vicious cycles spins out of control until … Bang! HERNIATION!
assume” … ‘ass of u and me’
Finally waking up to a relatively normal state of consciousness (whatever that may imply) you see the ER trauma physician moving onto the secondary survey. He had assumed you (the airway specialist extraordinaire) had assumed responsibility of ABC and he rushing moved onto the secondary survey.
side note: Never assume. It only makes an ASS out of you and me.
Secondary Survey: HEAD to TOE
head… shoulders knees and toes knees and toes, head….shoulders knees and toes knees and toes, eyes and ears and mouth and toes…head… shoulders knees and toes knees and toes…from ‘My baby can read DVD’
The patient is evaluated from head to toe:
-level of consciousness
“Belly”: …bleeding, etc
After having completing the Initial Assessment (both primary and secondary survey) our clinical picture becomes a little more clear. This patient who sustained a closed head injury has a decreased (LOST) level of consciousness with a GCS of 3. Pupils are sluggish at best…one step away from fixed and dilated indicating a severe increase in ICP. The airway is a bloody mess and still not secured. The patient is hypoventilating, increasing the PaCO2 by the minute resulting in a viscous cycle of worsening cerebral ischemia, cerebral edema, increasing ICP…. spiraling out of control…pending herniation!)
So, where to next?!
Amazingly the patient is sent for a CT for further diagnostic work up and guess what?!
Patient dies either in transport or in the CT scanner.
Theory of Relativity … ‘Ok Einstein’
Lets assume that after the Initial Assessment, the patient has obvious signs of increased ICP (after having sustained a closed head injury) and is “relatively stable” enough to go for a CT scan.
The patient is sent for a CT. While in the CT scanner the patient is moving and its difficult to obtain a good scan. The radiology technician thinks of a great idea and suggest sedating the patient so she will hold still.
Q. Do you sedate this patient? Why or why not?
concerned of hypoventilation? increased PaCO2 (decreased PaO2), increased ICP, worsening cerebral ischemia, worsening cerebral edema, worsening CePP, worsening CBF…viscous cycle spinning out of control…
A. You tell the technician he needs to CT scan his own brain, thats assuming he has one.
CT of the brain is finally complete. The study reveals evidence of INCREASED ICP:
– Cerebral Edema
– Midline Shift x > 0.5 cm
– Ventricular size/ compression
After the Initial Assessment and while the patient was sent for a CT, you headed back to your call room hoping to fall asleep, lose track of the nightmare call and float off into ‘dream land’. Fifteen minutes later (@ 4:05am) you are called to evaluate the patient for an emergency craniotomy. You see the patient (again) in the preoperative holding area and all the issues that were overlooked and unresolved are now very well present before your very own eyes.
What are your major concerns with this patient?
Neuro: S/P CHI with increased ICP
Airway: Laryngeal Trauma; bleeding…unprotected airway
Resp: Hypoventilation: (inc. PaCO2…inc. ICP, cerebral ischemia, cerebral edema)
CVS: Bleeding, hypovolemia, hypotension
Abd: “full stomach” …increased risk of Aspiration
Concerned about the SEVERITY of the CHI …digging a little deeper
Not knowing the results of the CT study, you are asked about factors which influence the severity and extent of injury to the brain after a closed head injury.
Generally speaking, the extent of injury depends on:
1. primary insult: the biomechanical damage upon impact
2. secondary insult: (ex. cerebral edema, cerebral ischemia, bleeding, inc. ICP)
3. factors which effect the secondary insults: (hypoxia, hypercarbia, hypotension, etc)
Taking a closer look at these insults …how insulting!
The primary insult which occurs upon impact is heavily determined by the blunt force the brain experiences. The biomechanical damage which occurs immediately upon impact is the first determinant (primary insult) influencing the extent of injury.
The secondary insults which follows the initial impact also are major determinants influencing the extent of injury after a closed head injury. Secondary insults (which can lead to increased ICP) consists of:
Factors which can promote secondary insults:
Concerns lead to goals which ironical lead to more concerns:
CHI: INCREASED ICP!
– cerebral ischemia
– cerebral edema
– intracranial hemorrhage
– intracranial HTN
Airway: (with INCREASED ICP + FULL STOMACH!)
hmm, my goals become a bit conflicting. Lets take a look at our goals.
Induction goals/plans for:
– increased ICP: avoid increase in ICP: therefore SCI
– difficult (bloody) airway: keep SV; therefore awake FOB (buck buck, and cant see)
– full stomach: avoid aspiration; therefore RSI
THIS IS WHAT THE WHOLE EXAM IS ABOUT!
hmm SCI vs RSI? …opposing goals, plan not clear…ADAPTABLE CLINICAL JUDGEMENT/ DECISIONS BASED ON SOUND CLINICAL KNOWLEDGE EXPRESSED (in an ORGANIZED fashion) PROFESSIONALLY!
Therefore this is a make it or break it (pass of fail) moment!…hmm equally important: This is a Life and Death situation which one can see any given day as an anesthesiologist!
– fluid restriction
– diuresis (osmotic: mannitol, loop: furosemide)
– +/- steroids
– +/- surgery
– head elevation
– diuresis (osmotic: mannitol, loop: furosemide)
– +/- hyperventilation
– +/- CSF drain
goals becoming another subset of concerns:
AIRWAY: C/Spine precaution: Inc ICP: Full stomach …
airway + inc. ICP: SCI + NDMR (avoid Sux?)
airway + full stomach: RSI with Sux? or RSI with NDMR
difficult (bloody) airway + inc. ICP + full stomach + hypotension: ???
– inc. MV = inc. TV? x inc. RR …hyperventilation
– inc. TV may lead to increased airway pressures, increasing CVP and not allowing proper cerebral venous drainage and resulting in an increase in ICP!
– inc. MV…hyperventilation effects oxygen-hb dissociation curve shifting to the left and therefore may lead to worsening cerebral ischemia.
Patient arrives to the OR already “intubated”
she’ll be coming around the corner when she comes…choo choo
As you rush off to the OR to set up, you get a call from the nurse stating the patient was intubated downstair in the ER. You have “all” your supplies (except your airway) prepared…after all why do you need airway supplies if the patient is “intubated”, RIGHT? …WRONG! Anyways, like most days in the OR…hurry up and wait. Your waiting for the patient to be transported from the ER to the OR…here she comes around the corner…”intubated” and being mechanically ventilated by the respiratory therapist (who happens to be the “hot shot” who “intubated” her downstairs in the ER)
Patient arrives in the OR and you connect the “ETT” to the anesthesia machine and begin controlled mechanical ventilation. You think for a second that the anesthetic circuit is missing the CO2 sampling line…and yell at the anesthesia technician on call. Pulse ox is placed and WTF…SpO2 60%, 50% and dropping!….
What do you do?! …HYPOXIC DRILL
– verify the reading (low pulse ox, no ETCO2) is real…ITS REAL!
– look at the patient…pink?…hell no…BLUE like papa smurf!
– auscultate the chest! : Ptx? bronchospam, ESOPHAGEAL INTUBATION!!!!!!
God damn Respiratory Therapist “INTUBATED” not the trachea but instead the esophagus…hypoxia, ischemia…cerebral edema …and distended “full stomach” abdomen …patient vomits and major pulmonary aspiration!
JUST THEN…you get a page waking you up from your nightmare dream. The nurse has paged you while you fell asleep in the call room. informing you the patient is in transport from the ER to the OR. You rush down ensuring all your supplies are set up…double, triple, and quadruple checking airway supplies! POINT TAKEN?!
The patient has sustained a closed head injury (s/p MVA) with severe increased ICP. The patient has a difficult airway complicated with facial deformity and lots of bleeding in the oral cavity. The patient is in respiratory distress, hypoventilating with inc. PaCO2 and hypoxemia! The patient has a C-spine collar on, neck has not been ‘cleared’ and the patient got into an accident immediately after eating at an ‘all you can eat buffet dinner’…full stomach!
The patient arrives to the OR, monitors are placed and the patient is hypotensive (50/30 mmHg) and hypoxic with SPO2 70%!
Induction of Anesthesia …How do you INDUCE?!
Its not what you use but how you use it?
Its not the size but how you use it… lies, lies and more lies!
You better choose your agents wisely and use it even more wisely!
Establishing an Airway with:
– increased ICP: SCI
– difficult airway (and Bloody) : …AWAKE FIBEROPTIC INTUBATION?!
Awake Fiberoptic Intubation … for real?!
You really going to attempt an awake fiberoptic intubation on a trauma patient with facial deformity who is bleeding extensively in the oral cavity?! The patient has severely increased ICP and is thrashing about uncontrollably as you attempt to direct the bronchoscope into the oral cavity. Hypoxia worsening and the patient begins coughing and then suddenly stops all movement. You put down the bronchoscope and gently open the patient’s eyes to see…yep, FIXED DILATED PUPILS.
Rapid Sequence Induction (RSI) … cowboy: prox sux tube
Its now 6:59: 55 am and your trauma call ends in 5 seconds. 7:00 am is here and your partner arrives eagerly to relieve you. You offer to stay and do the case because your not one to ‘dump’ on another. He insists on doing to case and you finally agree. As you leave the OR, you hear in the background, “Yeeehaaaw”. You have a knowing that the “cowboy” attending is up to no good.
Overlooking all the details which you stressed upon (CHI, Inc. ICP, cerebral edema, cerebral ischemia, etc)….he focuses only on the full stomach and decides to perform a rapid sequence induction.
preoxygenates the patient with 1.0 FIO2, “prop, SUX and Tube”…
looks at the monitor…HIGH BP, BRADY…looks at the pupils…FIXED DILATED!
Slow Controlled Induction (SCI)
Suppose you stayed to do the case. Being focused on the increased ICP you decide to perform a slow controlled induction of anesthesia. You slowly begin to administer you anesthetic drug of choice (ex. etomidate: to help maintain hemodynamic stability). A NDMR is given and gentle ‘cricoid pressure’ is placed while maintaining inline cervical stabilization. You attempt direct laryngoscopy and cannot visualize the glottic opening. You reach for the glidescope, still nothing but blood!. The saturation begins to fall and you attempt to ventilate the patient. Guess what?!. You can ventilate the patient! Now what?!
LOSING THE AIRWAY…going going going…..gone? AIRWAY DRILL!
– you call for help!
– attempt to reposition the patient
– oral pharyngeal airway
STILL CANNOT VENTILATE (not intubate), sats are dropping! … What do you do?!
Q. Would you perform a blind nasal endotracheal intubation knowing this patient has a basal skull fracture?!
too make matters worse …the patient aspirates! Oh, and the airway…gone!
Re-iterate: Hypoxic Drill
1. call for help: interesting phenomena occurs. All your anesthesia partner “buddies” will run the opposite direction.
Question you again: Losing the airway on a patient who sustained a closed head injury combined with a basal skull fracture…all other measures of establishing an airway have failed. Laryngeal trauma prevents any attempts for cricothyrotomy…would you attempt a blind nasal endotracheal intubation?
MAINTENANCE OF ANESTHESIA
Q. What is your anesthetic management for this patient who has sustained a closed head injury and now has increased ICP?
What are the pros / cons for both “TIVA” and “Balanced Anesthetics”?
” TIVA”: Total Intravenous Anesthesia:
– Pros: ?
– Cons: ?
“Balanced”: Balanced Anesthesia: volatile inh gas + opiod + NDMR?
– Pros: ?
– Cons: ?
Transition from Induction to maintenance…
Established a secure airway (ETT) and verified proper position by evaluating the presence of +ETCO2 and B/L breathe sounds.
MV = TV x RR
Avoiding increased airway pressure which may increase CVP and dec cerebral venous drainage resulting in worsening ICP
This patient who is bleeding and hypovolemic has a decrease in MAP. We are concerned about perfusion to the vital organs and more concerning in the setting of CHI and increased ICP is maintaining an adequate Cerebral Perfusion Pressure (CePP) to help prevent cerebral ischemia.
Intraoperative hypotension in a patient who has sustained a closed head injury often is related to other trauma related injuries. Therefore finding and correcting the cause (ex. intra-abdominal bleed) is crucial.
Hypovolemia … volume replacement … with what?!
what not to do:
Determining which fluid to infuse for volume replacement is often controversial (blood, crystalloid vs colloid etc), however, im sure we can agree not to infuse glucose-containing hypotonic solutions. This may worsen the neurological outcome further!
what to do:
This patient who has sustained a closed head injury with severely increased ICP is currently bleeding, hypovolemic and hypotensive and needs immediate correction. A concern we have to keep in mind when restoring intravascular volume is the possibility of worsening the cerebral edema associated with the closed head injury. Therefore for this patient, volume replacement may be best accomplished with a colloid solution and blood (opposed to strictly a crystalloid solution).
Blood … I want to suck your blood
Blood may be ideal in this setting were the patient is bleeding, hypovolemic and hypotensive. Blood allows for increased oxygen carrying capacity ([Hb]) and therefore helps to increase oxygen delivery to tissue helping to prevent tissue ischemia (ex. cerebral ischemia). Concerns with giving blood are the obvious blood transfusion reactions as well as possibility of actually decreasing cardiac output (by increasing blood viscosity and therefore SVR).
What is your goal with blood transfusion? … more is better?
As you transfuse blood a question should cross your mind. Well, a few questions should cross your mind but lets settle with one for now. How much blood to give and when to stop transfusing blood and begin replacing intravascular volume with another intravenous solution (ex. colloid, crystalloid). In this setting the goal for hematocrit should be kept above 30% and best perhaps between 30 – 33%.
If the blood pressure is still low despite volume resuscitation, an inotropic agent and/or vasopressor may be indicated.
Moments after surgical incision the patients blood pressure jumps to over 200mmHg systolic. In this clinical setting were the patient has sustained a closed head injury and now has a severely increased ICP, cerebral edema and intracranial hemorrhage tight blood pressure control is crucial.
First thought may be to increase the depth of anesthesia by providing an additional dose of an intravenous anesthetic (ex. proposal), opioid narcotic (ex. fentanyl), or by increasing the [inhalational anesthetic].
If not contraindicated, a beta blocker may be helpful to help control intraoperative hypertension.
Would you treat intraoperative hypertension for this patient with a vasodilators? Its best not to because this can lead to an increase in the CBF and worsen the already severely increased ICP. Its best to avoid vasodilators in the setting of a closed head injury at least until the dura has been opened.
Increased ICP … “tight brain”
Neurosurgeon keeps screaming that the brain is tight! How can we help to manage the intracranial hypertension and cerebral edema in the setting of a closed head injury?
First thing which should have been done in the beginning of the case is…Head elevation. The head of the patient should be elevated around 15 degrees which helps passive venous drainage.
Osmotic diuresis helps to lower the ICP by removing the intracellular water from normal brain tissue. Concerns that must be considered when administering mannitol are LV function, renal function, and electrolyte abnormalities.
Hyperventilation reduces the PaCO2 which has a direct and proportionate relationship with CBF. A decrease in 1mmHg PaCO2 will decrease the CBF 1-2ml/100g/min. Therefore hyperventilation helps to decrease the CBF which may help reduce the ICP.
Several concerns with hyperventilation arise. Increased MV may effect the peak airway pressures. Increased airway pressure may increase CVP which decreases the cerebral venous drainage worsening the already severely increased ICP.
Hyperventilation decreases the CBF which may also worsen the already apparent cerebral ischemia. Hyperventilation may also worsen the cerebral ischemia not only by reducing the CBF but instead by shifting the oxygen-hemoglobin dissociation curve to the left.
Taking a closer look at how hypertonic solutions help remove intracellular water from normal brain tissue. The infusion of a hypertonic solution within the intravascular space allows intracellular water within normal brain tissue to travel into the intravascular space through a process of osmosis. As a result the ICP is reduced and may increase the regional CBF. As the intravascular volume increases the blood pressure also may increase. Concerns of volume overload occur in patients with LV dysfunction and renal impairment.
Extubate? … hell to the No!
As the case nears an end, the neurosurgeon asks whether you plan to extubate. You clearly state, “Hell to the NO!” What concerns are we awaiting in the postoperative period for this patient who has sustained a closed head injury?
The patient as mentioned has a closed head injury associated with cerebral ischemia, cerebral edema, cerebral hemorrhage and increased ICP. We may anticipate postoperative pituitary dysfunction resulting in either increased ADH ( SIADH) or decreased ADH (DI).
The patient had an unprotected airway preoperatively for a relatively long period of time. The patient may have aspirated then or during the induction of anesthesia which may develop into aspiration pneumonia in the postoperative phase. With volume resuscitation and blood transfusion, the patient may develop pulmonary edema and even worse acute lung injury/ARDS.
As the patient continues to bleed and remains hypovolemic resulting in severe hypotension. As blood continues to be transfused the patient may become coagulopathic and may develop DIC.
Stress ulcers may lead to more bleeding and perhaps perforate.
Electrolyte and blood gas abnormalities with osmotic diuresis, blood transfusion, pituitary dysfunction, hyperventilation