ma_attari@med.mui.ac.ir
A and B, The sitting position. The patient is typically semirecumbent rather than
sitting. In A, the head holder support is correctly positioned such that the head can be
lowered without the need to detach the head holder first. The configuration in B, with
the support attached to the thigh portion of the table, should be avoided.
Venous Air Embolism
The common sources of critical VAE are the major
cerebral venous sinuses, in particular, the transverse,
the sigmoid, and the posterior half of the sagittal
sinus, all of which may be noncollapsible because of
their dural attachments.
Venous Air Embolism
The most common situation involve tumors
Most often parasagital or falcin meningiomas and
craniosynostosis.
Pin sites and trappped gas can lead to VAE.
The common sources of critical VAE are the major
cerebral venous sinuses.
Detection of Venous Air Embolism
The monitors employed for the detection of VAE should
provide
(1) a high level of sensitivity,
(2) a high level of specificity,
(3) a rapid response,
(4) a quantitative measure of the VAE event,
(5) an indication of the course of recovery from the VAE
event.
The combination of a precordial Doppler and expired CO2
monitoring meet these criteria and are the current standard
of care.
Detection of Venous Air Embolism
Doppler placement in a left or right parasternal location
between the second and third or third and fourth ribs
has a very high detection rate for gas embolization,
and when good heart tones are obtained, maneuvers to
confirm adequate placement seem to be unnecessary.
TEE is more sensitive than precordial Doppler to VAE
and offers the advantage of identifying right-to-left
shunting of air.
The relative sensitivity of various monitoring techniques to the occurrence of
venous air embolism (VAE). BP, blood pressure; CO, cardiac output; CVP, central
venous pressure; ECG, electrocardiogram, ET-CO2, end-tidal carbon dioxide;
PAP, pulmonary arterial pressure; physiol, physiological; T-echo,
transesophageal echo.
Venous Air Embolism
Rate of occurrence:
1. Procedure
2. Position
3. Detection method
Posterior fossa
Sitting
Doppler precordial 40%
TEE
76%
In cervical spine procedure 25%
Posterior Fossa, Doppler, Nonsitting
12%
VAE in nonsitting Position has Smaller volume.
Management Of Acute Air Embolic Events
1. Prevent further air entry
Notify surgeon (flood or pack surgical field)
Jugular compression
Lower the head
2. Treat the intravascular air
Aspirate via a right heart catheter
Discontinue N20
FI02: 1.0
(Pressors/ inotropes)
(Chest compression)
Electrocardiogram (ECG) configurations observed at various locations when a central
venous catheter is used as an intravascular ECG electrode. The configurations in the
figure are observed when “lead II” is monitored and the positive electrode (the leg
electrode) is connected to the catheter. P indicates the sinoatrial node. The heavy black
arrow indicates the P wave vector. Note the equi-biphasic P wave when the catheter tip
is in the mid right atrial position.
Right Heart Catheter
Essentially all patients who undergo sitting posterior
fossa procedures should have a right heart catheter.
Although catastrophic, life-threatening VAE is relatively
uncommon, a catheter that permits immediate
evacuation of an air-filled heart occasionally is the sine
qua non for resuscitation.
Which Vein Should Be Used for
Right Heart Access?
Although some surgeons may ask that neck veins not be
used, a skillfully placed jugular catheter is usually
acceptable.
Positioning the Right Heart
Catheter
A multi-orificed catheter should be located with the tip
2 cm below the superior vena caval–atrial junction, and
a single-orificed catheter should be located with the tip
3 cm above the superior vena caval–atrial junction.
Paradoxical Air Embolism
There has been much concern about the possibility of
the passage of air across the interatrial septum via a
patent foramen ovale (known to be present in
approximately 25% of adults).
Fluid Therapy
The intraoperative fluid management of neurosurgical
patients presents special challenges for the
anesthesiologist. Neurosurgical patients often
experience:
1. Rapid changes in intravascular volume caused by
hemorrhage
2. The administration of potent diuretics
3. Or the onset of diabetes insipidus.
Intravenous Fluid Management

The general principles
1.Maintenance of normovolemia
2.Avoidance of a reduction in serum osmolarity.


Half-normal saline is probably a reasonable choice for
maintenance fluid
To replace blood and third-space loss: Normal
saline(308 mOsm/L ) and lactated Ringer's solution
(273 mOsm/L) [plasma (295 mOsm/L)].
Intravenous Fluid Management (cont.)
 In situations: multiple trauma, aneurysm rupture,
cerebral venous sinus laceration, fluid administration
to support filling pressure during barbiturate coma,
combination of isotonic crystalloid and colloid may be
appropriate. (Albumin to be a reasonable choice as
a colloid solution)
Fluid Therapy
Intracranial hypertension secondary to cerebral
edema is now known to be one of the most common
causes of morbidity and mortality in the intraoperative
and postoperative periods.
Fluid Therapy
We examine:
1. Some of the physical determinants of water
movement between the intravascular space and the
central nervous system.
2. Specific clinical situations and make suggestions for
the types and volumes of fluids to be administered.
Fluid Therapy
For physiologic solutions, osmolality is commonly
expressed as milliosmoles (mOsm) per kilogram of
solvent, whereas the units of measure for osmolarity
are milliosmoles per liter of solution.
Fluid Therapy
Water has a tendency to move from the solution of lower
osmolality, across the membrane, and into the
solution of higher osmolality.
All act to draw fluid from the capillaries and into the
extracellular space of the tissue:
1. Capillary pressure
2. Tissue pressure (negative in nonedematous tissues)
3. Tissue oncotic pressure.
In peripheral tissues, the only factor that serves to
maintain intravascular volume is the plasma oncotic
pressure, which is produced predominantly by
albumin and to a lesser extent by immunoglobulins,
fibrinogen, and other high-molecular-weight
(HMW) plasma proteins.
The clinical effects of altering one or more of the
variables in the Starling equation may frequently be
observed in the operating room. Many patients who
have been resuscitated from hemorrhagic
hypovolemia with large volumes of crystalloid
solutions demonstrate pitting edema, caused by a
dilution of plasma proteins.
Fluid Movement between
Capillaries and the Brain
The brain and spinal cord are unlike most other
tissues in the body in that they are isolated from the
intravascular compartment by the blood-brain
barrier. Morphologically, this barrier is now thought
to be composed of endothelial cells that form tight
junctions in the capillaries supplying the brain and
spinal cord.
Fluid moves in and out of the central nervous system
according to the osmolar gradient (determined by
relative concentrations of all osmotically active
particles, including most electrolytes) between the
plasma and the extracellular fluid.
Administration of large volumes of iso-osmolar
crystalloid results in peripheral edema caused by
dilutional reduction of plasma protein content but
does not increase brain water content or
intracranial pressure (ICP).
Osmolarity is the primary determinant of water
movement across the intact blood-brain barrier.
The administration of excess free water (either
iatrogenically or as a result of psychogenic polydipsia)
can result in an increased ICP and an edematous
brain.
Hyperosmolar solutions are used daily in operating
rooms throughout the world as standard therapeutic
agents to treat intracranial hypertension.
What occurs when the brain is injured with disruption
of the barrier?
In patients at risk for intracranial hypertension. The
infusion of colloids is often recommended to maintain
intravascular volume in such patients, implying that
maintaining or increasing plasma oncotic pressure
reduces cerebral edema.
In the case of the intact blood-brain barrier, neither
theoretical nor experimental evidence suggests that
colloids are more beneficial than crystalloids for either
brain water content or ICP.
SOLUTIONS FOR INTRAVENOUS USE
These fluids may be categorized conveniently on the
basis of:
Osmolality
Oncotic pressure
Dextrose content.
Osmolarity of Commonly Used Intravenous Fluids
Fluid
Osmolarity
(mOsm/L)
Oncotic Pressure
(mm Hg)
Lactated Ringer’s solution
D5 lactated Ringer’s solution
0.9% saline
D5 0.45% saline
0.45% saline
20% mannitol
Hetastarch (6%)
Dextran 40 (10%)
Dextran 70 (6%)
Albumin (5%)
Plasma
273
525
308
406
154
1098
310
≈300
≈300
290
295
0
0
0
0
0
0
31
169
69
19
26
The term colloid denotes solutions that have an oncotic
pressure similar to that of plasma. Some commonly
administered colloids are:
6% hetastarch (Hespan)
5% and 25% albumin
The dextrans (40 and 70)
Plasma
Dextran and hetastarch are dissolved in normal saline,
so the osmolarity of the solution is approximately 290
to 310 mOsm/L with a sodium and chloride ion
content of about 145 mEq/L.
Hyperosmolar Solutions
Although an acute beneficial effect has been
demonstrated, the longer-term (24-48 hours) effect of
such hyperosmotic fluid therapy remains unknown.
Acute increases to values that exceed 170 mEq/L sodium
are likely to result in a depressed level of consciousness
or seizures.
30 mL of 23.4% saline brought prompt and sustained
decreases in ICP.
Despite these impressive results, it is unclear why
hypertonic saline should be more effective than
mannitol.
In clinical studies, hyperglycemia has been associated
with worsened neurologic outcome after traumatic
brain injury (glucose > 200 mg/dL), acute ischemic
stroke, and subarachnoid hemorrhage.
Pediatric
Neuroanesthesia
Intraoperative Fluid and
Electrolyte Management
Because CBF constitutes 55% of total cardiac output in
2- to 4-year old patients, sudden blood loss or venous
air embolus can rapidly deteriorate to cardiovascular
collapse.
Normal saline is commonly used as the maintenance
fluid during neurosurgery because it is mildly
hyperosmolar (308 mOsm/kg) and should minimize
cerebral edema. However, rapid infusion of large
quantities of normal saline (>60 mL/kg) can be
associated with hyperchloremic acidosis.
Estimated Blood Volume in Children
Age
Preterm neonate
Full-term neonate
≤1 year
1-12 years
Adolescents and adults
Estimated Blood Volume
(mL/kg)
100
90
80
75
70
Decision to transfuse should be dictated by:
The type of surgery
Underlying medical condition of the patient
Potential for additional blood loss both intraoperative
and postoperative.
Pediatric Neuroanesthesia
Hematocrit values of 21% to 25% should provide some
impetus for blood transfusion. Packed red blood cells
(10 mL/kg) will raise the hematocrit by 10%. Initially,
blood losses should be replaced with 3 mL of normal
saline for each 1 mL of lost blood or a colloid solution
such as 5% albumin equal to the blood loss.
Additional fluid administration at 3 to 10 mL/kg/hr may
be necessary.
Pediatric Neuroanesthesia
Pediatric patients, particularly infants, are at particular
risk for hypoglycemia. Small premature infants, who
have limited reserves of glycogen and limited
gluconeogenesis, require continuous infusions of
glucose at 5 to 6 mg/kg/min to maintain serum levels.
Pediatric Neuroanesthesia
Surgery elicits a stress response, and children are
generally able to maintain normal serum glucose levels
without exogenous glucose administration
Pediatric Neuroanesthesia
In any case hyperglycemia is always best avoided,
because it may exacerbate neurologic injury if
ischemia occurs.
follow a conservative approach that keeps randomly
measured serum glucose levels below 180 mg/dL.
Pediatric Neuroanesthesia
Mannitol can be given at a dose of 0.25 to 1.0 g/kg IV.
This agent will transiently alter cerebral
hemodynamics and raise serum osmolality by 10 to 20
mOsm/kg.
Furosemide prevent the rebound swelling due to
mannitol.
Daily Water Loss for an Adult
Type/Location
Insensible losses:
Skin
Lungs
Urine
Sweat
Feces
TOTAL
Amount (mL/day)
350
350
1400
100
200
2400
PERIOPERATIVE MANAGEMENT OF ADULT
PATIENTS WITH SEVERE HEAD INJURY
During fluid resuscitation of the head-injured patient,
the goals are to maintain:
1. Serum osmolality
2. Avoid profound reduction in colloid oncotic pressure
3. Restore circulating blood volume.
PERIOPERATIVE MANAGEMENT OF ADULT
PATIENTS WITH SEVERE HEAD INJURY
Immediate therapy is directed at preventing
hypotension and maintaining cerebral perfusion
pressure (CPP) above 60 mm Hg.
PERIOPERATIVE MANAGEMENT OF ADULT
PATIENTS WITH SEVERE HEAD INJURY
Hypertonic saline solutions (3%, 7.5%) can be very
useful for low-volume resuscitation in the headinjured patient because they lower ICP, raise blood
pressure, and may improve regional cerebral blood
flow (CBF).
PERIOPERATIVE MANAGEMENT OF ADULT
PATIENTS WITH SEVERE HEAD INJURY
A minimum hematocrit value between 30% and 33% is
recommended to maximize oxygen transport.
Intraoperative Fluids
Intraoperative maintenance fluid administration usually
consists of lactated Ringer’s or normal saline solution.
These fluids are crystalloids and are approximately
equiosmolar to normal plasma. As a general rule, hypoosmolar solutions and dextrose-containing solutions
should be avoided.
Intraoperative Fluids
Iso-osmolar crystalloids are given at a rate sufficient to
replace the patient’s urine output and insensible losses
milliliter for milliliter. Blood loss is replaced at about a 3:1
ratio (crystalloid/blood) down to a hematocrit value of
approximately 25% to 30%.
Mannitol may have a biphasic effect on ICP.
Concomitant with the infusion.
ICP may transiently increase, presumably because of
vasodilation of cerebral vessels in response to the
sudden increase in plasma osmolality.
Subsequent reduction in ICP is achieved by the
movement of water from the brain’s interstitial and
intracellular spaces into the vasculature.
Medium MW Hydroxyethyl Starch
Products
Voluven is an equally effective volume expander
compared to hetastarch or HES 200/0.5 in the patient
populations described.
Plasma and Red Blood Cells
Red blood cells should be given only to keep hematocrit at a
“safe” level. This level varies from patient to patient; and
even in a specific circumstance, it may be difficult to
objectively define what constitutes “safe”.
In general, healthy individuals easily tolerate hematocrits
in the 20% to 25% range.
SPECIFIC NEUROSURGICAL
CHALLENGES
Fluid Management in Patients with Cerebral
Aneurysms
Fluid Management of Diabetes Insipidus
Fluid Management of the Trauma Patient with Head
Injuries
Fluid Management in Patients
with Cerebral Aneurysms
Volume loading may be accomplished by infusing isoosmolar crystalloids, colloids, or red blood cells in
order to achieve hemodilution to a hematocrit of
approximately 30%.
Fluid Management in Patients
with Cerebral Aneurysms
Frequent assessment of pulmonary function with
arterial blood gas measurements, chest radiographs,
and physical examination is essential.
Fluid Management of Diabetes
Insipidus
The patient should be vigorously rehydrated with 0.45%
saline until euvolemia is established. Because of the
preexisting hyperosmolar/hypernatremic state,
normal saline should not routinely be used for the
initial rehydration of these patients.
Fluid Management of the Trauma
Patient with Head Injuries
The ideal resuscitation fluid for patients who are
hypovolemic with ongoing blood loss is fresh whole
blood. Because whole blood is a colloid rather than a
crystalloid.
Fluid Management of the Trauma
Patient with Head Injuries
Smaller volumes of whole blood are required to restore
intravascular volume, thus producing a more rapid
resuscitation. Whole blood replaces clotting factors and
platelets that have been lost and may therefore prevent
the emergence of a dilutional coagulopathy.
Hypothermia
 Mild hypothermia (32-34°C) in reducing the
neurologic injury
 Mild hypothermia is perceived to hazards:
 Coagulation dysfunction
 Increased postoperative wound infection rate
 Hypertension on emergence
 Modest overshoot in temperature
Emergence from Anesthesia
To the prevention of coughing and straining:
 Narcotic
 N2O
 N2O + propofol (either bolus increments or infusion at
rates in the range of 25-100 μg/kg/min)
 Lidocaine
Emergence from Anesthesia
 Most practitioners of neuroanesthesia believe that
a premium should be placed on "smooth"
emergence, that is, one free of coughing/straining
and arterial hypertension.
 Avoidance of arterial hypertension is seen as
desirable because of the belief that arterial
hypertension can contribute to intracranial
bleeding and increased edema formation.
Emergence from Anesthesia
 In the face of a poorly autoregulating
cerebral vasculature, hypertension also has
the potential, through vascular
engorgement, to contribute to elevation of
ICP.
 Much of the concern with
coughing/straining has a similar basis.
Emergence from Anesthesia
 The sudden increases in intrathoracic
pressure are transmitted to both arteries and
veins, and the transient increases produced
in both cerebral arterial and venous pressure
have the same potential consequences:
edema formation, bleeding, and elevation of
ICP.
Emergence from Anesthesia
 Coughing is a specific concern with certain
individual procedures.
 In the circumstances of transsphenoidal pituitary
surgery in which the surgeon has opened and
subsequently taken pains to close the arachnoid
membrane to prevent leakage of CSF, it is believed
that coughing has the potential to disrupt this
closure because of sudden and substantial
increases in CSF pressure.
Emergence from Anesthesia
 Opening a pathway from the intracranial space to
the nasal cavity conveys a substantial risk of
postoperative meningitis.
 In other procedures, notably those that have
violated the floor of the anterior fossa, there is also
the potential for air to be driven into the cranium
and, in the event of a flap valve mechanism, cause
a tension pneumocephalus.
 This latter event can take place only when
coughing occurs after the endotracheal tube has
been removed.
Emergence from Anesthesia
 A common method for the management of systemic
hypertension during the last stages of a craniotomy is
the expectant or reactive administration (or both) of
vasoactive drugs, most commonly labetalol and
esmolol.
 Other drugs, including enalapril and diltiazem, have
been used to good effect.
Emergence from Anesthesia
 Administration of dexmedetomidine during the
procedure and up to 30 to 60 minutes before
conclusion of the procedure has also been
reported to lessen the requirement for
antihypertensives during emergence.
 There are also many approaches to the prevention
of coughing and straining.
 We encourage trainees to include in their
anesthetic technique
"as much narcotic as is consistent with
spontaneous ventilation at the conclusion of the
procedure."
Emergence from Anesthesia
 That practice is based on the same physiologic effect
that justifies the administration of codeine and related
compounds as antitussive medication, specifically, the
depression of airway reflexes by narcotics.
Emergence from Anesthesia
 A common practice among neuroanesthetists near the
conclusion of a craniotomy is the relatively early
discontinuation of the volatile anesthetic and
supplementation of residual nitrous oxide with
propofol by either bolus increments or infusion at
rates in the range of 25 to 100 g/kg/min.
Emergence from Anesthesia
 An additional principle relevant to emergence from
neurosurgical procedures that practitioners will learn
either from a book or by bad experience is that
emergence should be timed to coincide, not with
the final suture, but rather with the conclusion of
the application of the head dressing.
Emergence from Anesthesia
 Another nuance of our practice has been to
withhold the administration of
neuromuscular antagonists as long as
possible as a hedge against misjudgment while
lightening anesthesia in a patient in the later
stages of the procedure.
 An additional popular and apparently effective
technique for reducing airway responsiveness and
the likelihood of coughing/straining while
reducing the depth of anesthesia is the
administration of lidocaine.
Emergence from Anesthesia
 Bolus doses on the order of 1.5 mg/kg, often given as
application of the head dressing begins, are
appropriate for this purpose.
Emergence from Anesthesia
 In some instances, one may be tempted to
extubate patients before complete recovery of
consciousness.
 This practice may be acceptable in some
circumstances.
 However, it should be undertaken with caution
when the circumstances of the surgical procedure
make it possible that neurologic events may have
occurred that will delay recovery of consciousness
or when lower cranial nerve dysfunction may be
present.
Emergence from Anesthesia
 In these circumstances, it will generally be best to wait
until the likelihood of the patient's recovery of
consciousness is confirmed or until patient
cooperation and airway reflexes are likely to have
recovered (or until both)
Supratentorial Tumors
 Hypertension (due to irritation of the hypothalamus)
 Disturbances in consciousness varying from lethargy to
obtundation.
 Diabetes insipidus
 Cerebral salt-wasting syndrome (after 12-24 hrs)
Supratentorial Tumors (cont.)
 Frontal lobey:
1) Retraction and irritation of the inferior surfaces
of the frontal lobes can result in a patient who is
lethargic and does not awaken “cleanly,” and who
may exhibit delayed emergence .
2) The phenomenon is more likely to be evident
when there has been bilateral subfrontal retraction
than when it occurs only unilaterally.
Aneurysms and AV Malformations
 Fluid management
1) SIADH
2) Cerebral salt wasting syndrome (Na↓, volume ↓, urine
Na>50 mmol/lit)
 management of both is simple: administration of
isotonic fluids using intravascular normovolemia as the
end point.
Aneurysms and AV Malformations (cont.)
 Vasospasm
 Drowsiness is a common initial clinical sign.
 Administration of Nimodipine has been shown to
decrease the incidence of Vasospasm.
 Treatment: (triple H)
Hypervolemia
 Hemodilution(Hct≤ 30)
 Hypertension(20-30 mmHg)
(Phenylephrine and Dopamine are the most commonly
employed pressors )

Aneurysms and AV Malformations (Cont.)
 ECG abnormalities
 Canyon T waves
 Nonspecific T-wave changes, QT prolongation,
 ST-segment depression and U waves
 QT>550 msec → Torsades de pointes
Anesthetic Technique
 Important considerations include the following:
 Avoidance of acute hypertension
 Brain relaxation
 Maintenance of high-normal MAP
 Preparedness to perform precise manipulations of MAP as
the surgeon attempts to clip the aneurysm or control
bleeding from a ruptured aneurysm (or both)
Head Injury
 Intubating a Head-Injured Patient
 GCS of 7 to 8
 Trauma-related cardiopulmonary dysfunction
 Uncooperative, to facilitate diagnostic procedures
Factors that may be relevant during
intubation of a head-injured patient
 Full stomach
 Uncertain cervical spine
 Uncertain airway:
 Blood
 Airway injury (larynx, cricoarytenoid cartilage)
 Skull base fracture
 Uncertain volume status
 Uncooperative/ combative
 Hypoxemia
 Increased intracranial pressure
The Cervical Spine
Head Injury: Anesthetic Technique
 Choice of anesthetics
 All of the IV anesthetics, except Ketamine, cause some
cerebral vasoconstriction and are reasonable choices,
provided that they are consistent with hemodynamic
stability.
 All of the inhaled anesthetics (N20 and all of the vapors)
have some cerebral vasodilatory effect.
Blood Pressure Management
 Careful maintenance of a CPP of 60-70 mmHg in the
first 72 hours after TBI will be appropriate and is
common practice in a head-injured adult.
 A CPP target of 45 mm Hg has been recommended for
children.
Posterior Fossa Procedures
 Procedures involving dissection on the floor of the
fourth ventricle can result in loss of control and
patency of the upper airway
 The cardiovascular responses:
 Bradycardia and hypotension
 Tachycardia and hypertension
 Bradycardia and hypertension
 Ventricular dysrhythmias
Transsphenoidal Hypophysectomy
Preoperative Evaluation
 Hypocortisolism with associated hyponatremia
 Hypothyroidism
 Hypertension, diabetes, and central obesity (Cushing's
disease).
 Acromegaly: enlarged tongue and a narrowed glottis,
and the airway should be evaluated .
Transsphenoidal Hypophysectomy
 Diabetes insipidus (DI)
 DI usually develops 4-12 hours postoperatively and very




rarely arises intraoperatively.
Urine specific gravity is a useful bedside test.(<1.002)
Fluid management regimen is hourly maintenance fluids
plus 2/3 of the previous hour's urine output. (An
acceptable alternative is the previous hour's urine
output -50mL plus maintenance.)
Half-normal saline and 5% dextrose in water are
commonly used as replacement fluids .
If the hourly requirement exceeds 350-400 mL,
Desmopressin (DDAVP) is usually administered.
Cerebrospinal Fluid Shunting Procedures
 Hydrocephalus is particularly common after SAH.
 The ventriculoperitoneal shunt is the most commonly
employed device.
 Ventriculoperitoneal shunts are done supine.
Anesthetic Management
 Invasive monitoring is generally not required.
 Moderate hyperventilation (Paco2 25 to
30 mm Hg) is customary.
 Blood pressure may decrease abruptly (as
brainstem pressure is relieved) when the ventricle
is first cannulated. Infrequently, brief pressor
support is required.
 Burrowing the subcutaneous tunnel can produce a
sudden painful stimulus.
Parkinson's Disease
 Management of anesthesia is based on an understanding
of the treatment of this disease.
 Levodopa therapy should be continued during the
preoperative period (administered 20min before
induction) .
 Orthostatic hypotension, cardiac dysrhythmia and
hypertension must be considered.
 Droperidol, Alfentanil and Ketamine should not be used.
Multiple Sclerosis
 Management of anesthesia
 SCh should not be used (in GA)
 Spinal anesthesia has been implicated in postoperative
exacerbation of MS (vs EA and nerve block)
 Efforts must be made during the perioperative period to
recognize and prevent even modest increases in body
temperature (>1°C), as this change might lead to
deterioration of nerve tissue.
Protection of cervical spine
 cervical spine Injury
Awake fiberobtic intubation
Three providers are required to:
ventilate the patient,
hold cricoid pressure, and
provide in-line cervical stabilization;
 a fourth provider to administer anesthetic medications
Traumatic Brain Injury
 Brain injury after trauma is classified as mild,
moderate,
 or severe, depending on the GCS score on admission.
 Mild: GCS=13-15
 Moderate: GCS=9-12
 Severe: GCS≤8
Airway and Ventilatory Management
With adequate volume resuscitation, PEEP does not increase
ICP, nor does lower cerebral perfusion pressure (CPP)
Hyperventilation therapy, long a mainstay in the management
of patients with TBl, is no longer an appropriate treatment
unless signs of imminent herniation are present.
Current guidelines suggest maintenance of PaCO2 at 35 mmHg
with hyperventilation to 30 mmHg only for episodes of
elevated ICP that cannot be controlled with sedatives, CSF
deranging, neuromuscular blockage, osmotic agents, or
barbiturate coma.
Circulation
 Patients with severe TBI should have systolic SBP higher
than 110 mmHg with a goa1 of achieving MAP greater
than 90 mmHg (to allow for a minimum CPP of 70
mmHg) until ICP monitoring is instituted and CPP can be
directly targeted.
 Correction of anemia from blood loss is the first priority,
with a goal of maintaining hematocrit greater than 30%
Management of Intracranial and Cerebral
Perfusion Pressure
Most authors support treatment of ICP greater than 20 to 25
mmHg.
Patients with sever head injury (defined as a GCS <8) and
abnormal head CT findings (hematoma, contusions, edema,
or compressed basal cisterns) should be managed with the
aid of ICP monitoring.
In addition, patients should be monitored if they have severe
TBI, normal head CT findings, and any of the following: age
> 40 years, motor posturing, or SBP< 90 mmHg.
Escalating therapy for severe traumatic brain injury.
Spinal Cord Injury
Cervical spine injuries causing quadriplegia are
accompanied by significant hypotension because of
inappropriate vasodilatation and loss of cardiac inotropy
(neurogenic shock).
Autonomic hyperreflexia develops in 85%, of patients
with a complete injury above T5 because of excessive
sympathetic response to stimuli below the level of injury,
absent the brain's normal damping effect.
Early Supportive Care
Focused on preservation of adequate perfusion. Hypoxemia
must be avoided at all costs, and MAP should be maintained
at a normal to high level.
Emergency intubations are performed, with inclusion of
manual in-line axial stabilization.
In the acute setting (< 24 hours from the moment of injury),
succinylcholine can be safely used in patients with SCI.
Ventilatory support is absolutely required for patients with a
deficit above C4 because they will lack diaphragmatic
function.
Patients with deficits from C4 to C7 will still need support,
because of lost chest wall innervation, paradoxical
respiratory motion, and inability to clear secretions.
Intraoperative Management of
Spinal Cord Injury
 Direct laryngoscopy with in-line stabilization is
appropriate in the emergency setting and in
unconscious, combative, or hypoxemic patients when
the status of the spine is not known.
 In the OR, an awake, alert, and cooperative patient can
be intubated by a number of different methods known
to produce less displacement of the cervical spine and
presumably less risk of worsening an unstable SCI.
 Awake fiheroptic intubation (the most common technique)
 Blind nasal intubation
 Intubating LMA
 Bullard laryngoscope