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What are the determinants of intracranial pressure?

The intracranial cavity is a rigid structure with minimal compliance. The structures within this cavity
can be conceived of as belonging to one of three compartments:

The parenchymal compartment, which is made up of two subcompartments. The cellular


compartment, consisting of the neuronal, glial, and tumor cells, and the fluid
compartment, consisting of intracellular and extracellular fluid
The cerebrospinal fluid compartment
The blood compartment, consisting of the arterial and venous subcompartments

If the volume of any one of these compartments increases, there is limited compensatory potential.
Initially, cerebrospinal fluid can drain to the spinal cerebrospinal reservoir, and venous blood to the
extracranial veins. Therefore, during the early phase of intracranial volume expansion, only a
minimal increase in intracranial pressure may occun. However, at a critical point these
compensatory mechanism are exhausted, and even small increases in intracranial volumes will
result in significant increases in intracranial pressure. As intracranial pressure increases, the
pressure gradient may eventually lead to herniation of brain tssue through a noncompliant space,
rapidly resulting in often irreversible injury. Normal intracranial pressure is 5 to 15 mmHg,. Normal
adult brain tissue volume is aproximately 1400 ml, intracranial cerebrospinal fluid volume is 75 to
100 ml, and cerebral vascular volume is approximately 150 ml.

How does the presence of a mass alter the intracranial pressure in this patient?

As the intracranial cavity is essentially of fixed volume, the volume of any intracranial mass must be
accommodated by reduction in the volume of other intracranial contents. The neurological sequele
of the mass will be determined largely by its anatomic location and the rapidity of growth. Elevated
intracranial pressure in the presence of supratentorial masses is usually the result of their direct
space occupying effects. This may also be true of masses in the posterior fossa, but in addition ,
these masses may obstruct cerebrospinal fluid outflow at the fourth ventricle, resulting in a
noncommunicating hydrocephalus and elevated intracranial ppressure. Slow growing tumors, such
a meningiomas, can become astoundingly large without causing substantial increases in intracranial
as volume remodeling occurs, this is especially true of supratentorial hemispheric tumors.
Conversely, even small fast growing tumors in critical neuroanatomic locations in the posterior
fossa may rapidly lead to symptoms of elevated intracranial pressure. Especially if cerebrospinal
fluid outflow is obstructed. It is important to remember that while compensatory mechanisms may
be able to maintain a normal or near-normal intracranial pressure, the patient with an intracranial
mass will always have diminished reserve to accommodate increases in the volume of other
intracranial contents. In this patient, a slow-growing meningioma has been able to attain a large
size before becoming symptomatic. The patient is demonstrating early signs and symptoms of
elevated intracranial pressure, which most likely results from the combination of mass effect and
obstruction of cerebrospinal fluid outflow at the fourth ventrcle. This patient would have very little
volume reserve, even small further increases in volume, such as an increase in cerebral blood
volume, would likely cause a precipitous spike in intracranial pressure.
If the patient had presented with intracranial hypertension, what management may have already
been initiated preoperatively, and what are the implication for anesthetic management?

a patient with evidence of intracranial hypertension will be aggressively monitored and treated
preoperatively, it is likely that your preoperative assesment will occur in an intensive care setting.
The anesthesiologist should be aware of the implication of preoperative management of
intracranial hypertension. A likely hierarchy of management, and some common implications for
anesthetic management, is a follows. A likely hierarchy of management, and some common
implications for anesthetic management is as follows

Corticosteroids. May have resulted in hyperglicemia, which should be aggressively treated.


Head elevation. Care should be taken to avoid rapidly lowering the head during trasnport.
Diuretics (mannitol, furosemid). May result in electrolyte or acid-base abnormalities.
Decreased preload may increase the risk of hypotension in the peri-induction period.
Isotonic or hypertonic saline therapy. May have resulted in hypernatremia, or a
hyperchloremis, on-anion gap metabolic asidosis.
Intubation and institution of hyperventilation. If prolonged, cerebral blood flow response
may be diminished or absent, with risk of increase in cerebral blood flow and intracranial
pressure if hyperventilation is rapidly ceased. Can lead to underlying compensatory
metabolic acidosis. Care should be taken to avoid hypoventilation during transport.
Ventriculostomy. Should be clamped during transport, because of difficulty in maintaining
appropriate level. Should be attented to on arrival to operating room, as even relatively
short periods of clamping can result in elevations of intracranial pressure
Manipulation of systemic pressures to cerebral perfusion pressure. Care should be taken to
ensure drug infusions are maintained duruing transport to avoid rebound hypertension or
hypotension.
Drug induced cerebral vasoconstriction and/or coma. Thiopental is ussualy used. This
signifies a critical neurological status. The therapy is often continued as the primarry
anesthetic.
Deliberate hypothermia. Signifies a critical neurological status. Requires discussion of
intraoperative temperature management goals with the neurosurgein, as the
neuroprotectibe benefits may be countered by hypothermia-induced coagulopathy.

How would you approach the management of CO2?

A reduction of PaCO2 results in decreased cerebral blood flow and cerebral blood volume within
minutes. Therefore, hyperventilation is a rapidly effective measure that can be instituted to
decrease intracranial pressure or to improve surgical exposure. However, hyperventilation has
substantial limitations. At PaCO2 value less than 25 mmHg cerebral ischemia may result from a
critical reduction in cerebral blood flow combined with a larg left shift of oxyhemoglobin
dissociation, preventing oxygen unloading. Prolonged hyperventilation may result in the
development of an underlying metabolic acidosis through normal compensatory mechanisms,
which may result in a decreases in pH if hyperventilation is rapidly terminated. Further, prolonged
hyperventilation may result in a decrease in ionized Ca2+ , leading to hemodynamic difficulties and
prolonged emergence from effects on synaptic function.
It is important to remember that the difference between PaCO2 and end tidal carbon dioxide
(ETCO2) Can very greatly. Therefore, an arterial blood gas should be taken as soon as possible after
induction to establish the arterial end tidal gradient in CO2 partial pressure. We initially aim for a
PaCO2 of approximately 35 mmHg unless there is elevated intracranial pressure. If, once the bone
plate is removed, the surgeons determine that their exposure is suboptimal, we hyperventilate to a
PaCO2 +of 30 mmHg. Further hyperventilation is reserved for situations in which establishing
adequate exposure is extremely difficult. To avoid postoperative acid-base instability,
hyperventilation n be gradually reduced throughout the closure, permitting a steady
reestablishment of bicarbonate and Ca2+ equilibrium.

How would you approach diurethic therapy?

The purpose of diuretic therapy in intracranial procedures is to dehydrate the brain, thereby
leading to a reduction in the volume of the fluid compartment. This facilitates surgical exposure
and reduces the requirement for brain retraction. Through the same principal, mannitol is used as
therapy for elevated intracranial pressure states when the craniumm is closed. Manitol is an
osmotic diuretic that is usually prepared in a 20% solution (20g/100 ml), and should initially be
given in a dose of 0,5 to 1,0 per kg, the total dose can be increased to 1,5 g per kg if initial efforts
are ineffective. Higher doses have been reported to lead to cardiac arrest from disruption of
cardiac cellular function. Because manitol initially draws water into the vascular space before it is
excreated, rapid dosing can cause a transient increase in intracranial pressure, and so it should be
infused over 20 to 30 minutes. If there is very little intracranial compliance reserve, aggresive
dosing should be synchronized with the removal of the bone plate.If manitol does not provide
adequate surgical conditions, the loop diuretic furosemide can be used. In a naive adult patient, a
dose as low as 5 mg may be adequate. Furosemide does not have the problem of an initial increase
in vascular volume, and somay preferred in patients with marginal cardiac function who can
develop congestive heart failure with a large mannitol load. However, the combination of mannitol
and furosemide can cause electrolyte abnormalities and severe systemic dehydration, necessitating
fluid resuscitation. Because mannitol therapy alone is often adequate, we do not administer
furosemide routinly, and instead reserve its use for situations when surgical exposure is
suboptimal. In cases of extreme cerebral edema, hypertonic saline, in concentrations up to 7,5%,
can be used. This can be effective in refractory intracranial hypertension, but is limited by the
development of severe hypernatremia.

How will you approach maintenance fluid management?

If the blood brain barrier is intact, the principal determinant of brain tissue water is rhe osmotic
gradient across the blood brain barier. It is this principal that guides the use of hypertonic solutions
such as mannitol or hypertonic saline to reduce interstitial water and reduce intracranial pressure
or optimize surgical exposure. Under the same principal, the use of hypotonic solutions, such as
lactated ringer solution, favor the transport of water into the brain interstitium, and thereby the
development of edema. In regions where the blodd brain barrier is not intact, due to pathology
and surgical tissue injury, osmotic particles will be able to cross from the capillaries into the
interstitial tissue. Therefore, the benefits of hypertonic solutions are lost in these areas. It follows
that the benefit obtained from the use of hypertonic solutions is because of an overall effect on the
brain, and not from a specific effect in localized regions of brain injury. The above considerations
favor the use of isotonic normal (0,9%) saline as maintenance fluid in craniotomies. More
controversial is the approach to volume. Historically, craniotomy patients have been kept
deliberately hypovolomic in the belief that this will increase the passage of free water from the
brain in situations involving a disrupted blood brain barrier. However, recent evidence suggests
that there is in fact very little reduction in interstitial water, and that it comes at the price of
significant systemic hypoperfusion and hypotension. Therefore, the favor approach to fluid
management is now maintenance of isovolemia with normal saline. In prolonged cases, the
chloride loading may result in a mild hyperchloremic non-anion gap metabolic asidosis. Dextrose-
containing solutions should never be used unless for specifically treating hypoglycemia. 5% albumin
can be used when volume expansion is a requirement. Albumin has a plasma half life of 16 hours,
and little is known about how the passage of albumin molecules across a damaged blood brain
barrier influences interstitial water movements over these time periods. Therefore, its routine use
is not recomnended.

Management of head injury

A. Pathophysiology and differential diagnosis

A.1 What types of intracranial injuries are most likely to have occured in this patient?

in a patient without obvious sign of localizing neurologic deficits, the most probable intracranial
injury is cerebral contusion. This is usually a diffuse or multifocal process that results in disruption
of the blood brain barier, causing widespread brain swelling due to edema. The diagnosis can be
made with certainty only after ruling out other focal injuries, such as intracranial hematoma.
Traumatic intracranial hematomas includes epidural hematoma, subdural hematoma, and cerebral
hematoma. The clinical hallmark signifying a mass lesion is the presence of generalized elevated
intracranial pressure in conjunction with focal defisit. Interestingly, most patients who were able to
talk and then deteriorate into coma had a mass lesion requiring surgery, indicating the importance
of quickly diagnosing mass lesion with CT scanning. Epidural hematomas, located between the skull
and dura, are almost always caused by skull fractures. Most epidural hematomas occur in the
temporoparietal region as skull fractures in this area cross the path of the middle meningeal artery.
Consequently, epidural menatomas can rapidly expand in the presence of a lacerated meningeal
artery. The classic presentation of an epidural hematoma is a patient who appears lucid but then
deteriorates into a comatose state, with a fixed dilated pupil ipsilateral to the skull fracture and
contralateral hemiparesis. Subdural hematoma are located between the inner surface of the
duramater and the pial surface of the brain. In contrast to epidural hematomas, subdural
hematomas are caused by lacerations of the vnous sinuses (lateral sinus or sagittal sinus) and tend
to develop more insidiously. Intracerebral hematomas are collections of blood ranging from
petechial hemmorrhages to large collections usually in the temporal or frontal lobes. Some lession
are pure hematomas or hemorrhagic contusions. Often, these hemorragic areas can be managed
medically with follow up CT scans. Indications for surgical evacuaton of intracerebral hematomas
include rapid mental deterioration, mass effect, and marked elevations in intracranial pressure.
A.2 What is the difference between primary and secondary injury? What factors contribure to
secondary injury?

Primary injury represents neurologic damage that occurs at the time of impact. Secondary injury is
the cinsequence of ischemic insults to the brain that occur subsequent to the primary injury.
Prevention of further hypoxemia and hypotension are the mainstay of managing head injury
patients. Pathophysiological processes contributing to secondary injury include (a)alterations in the
balance between cerebral blood flow and metabolism, (b) disruption of cerebral autoregulation (c)
loss of cerebral vascular reactivity to carbon dioxide and (d) vasogenic fluid accumulation leading to
bran swelling. Unfortunately, many patients with severe head trauma arrive to the hospital after
having episodes of hypotension and hypoxemia. Improvement in outcomes depend on trauma
centers having emergency teams that provide rapid treatment in the field and direct transport to
the hospital. Initial management entails oxygenation by early intubation and maintenance of
cerebral perfusion pressure with rapid resuscitation to treat hemorragic or hypovolemic shock.
However, the difficulty with fluid administration is that brain swelling increases intracranial
pressure and lowers the treshold of the systemic blood pressure for cerebral ischemia. Elevation in
intracranial pressure, which heralds cerebral herniation, leads to further brain damage and
increased morbidity. The use of intacranial pressure monitoring has been important in decreasing
secondary injury as a means to quantify and treat cerebral hypoperfusion. Improved outcome in
patients with severe head trauma has been attributed to the approach of squeezing oxygenated
blood through a swollen brain.

A.3 What are risks and benefits of administering mannitol?

Manitol is an osmotic diuretic that has been a mainstay in decreasing intracranial pressure.
Traditionally, it was thought that mannitol could aggravate elevated intracranial pressure by
crossing a disrupted blood brain barrier and inducing additional edema. Following mannitol
administration, cerebrospinal fluid pressure transiently increases in normal patients but
immediately decreases in the presence of intracranial hypertension. Mannitol is effective in
reversing brain swelling and is recommended for the treatment of traumatic intracranial
hypertension. Indications for administering mannitol before intracranial pressure monitoring
include transtentorial herniation and progressive neurologic deterioration. The standard adult dose
has been 1 g per kg as a rapid itravenous infusion. However, in one study involving patients with
severe traumatic brain injury, patient receiving hig dose mannitol (1.4 g / kg) had improved
recovery of pupillary response and 6 month outcome parameters compared to patients receiving
0.7 g per kg.

A.4 What is the effect of hyperglicemia on neurologic outcome following head trauma?

The release of cathecholamines and hyperglycemia are manifestations of the stress response to
severe head injury. Patients with moderate and minor injury. Postoperative glucose levels above
200 mg per dL have been associated with a worse neurologic outcome. Early hyperglycemia is a
significant indicator of severity of injury and a predictor of outcome. Nevertheless, hyperglycemia
should be treated aggressively, especially when the risk of cerebral ischemia is present. Elevated
plasma glucose levels provide a substrate for anaerobic metabolism, allowing increased production
of lactate during ischemia. The approach to glucose control in traumatic brain injury patients is a
subject to debate as the downside of aggresive therapy is hypoglycemia and cerebral glucopenia.
In one study, intense insulin therapy, with the goal of maintaining blood glucose levels at 80 to 100
mg per dL, was associated with increased microdialysis levels of glutamate, which is a marker for
cellular distress

A.5 What alteration in sodium and pottasium balance can occur in head injury patients?

Neurologically injured patients are at risk for electrolyte imbalance. Perioperative fluid
administration, mannitol administration, syndrome of inappropriate antidiuretic hormone
secretion (SIADH), and cerebral salt wasting syndrome are potential causes of hyponatremia.
Severe hyponatremia (Na <120 mEg/L) may be associated with cerebral edema and seizures. The
correction of hyponatremia must be gradual to avoid precipitating central pontine myelinolysis.
Hypernatremia can occur as a result of enteral tube feedings, diuresis with mannitol, and diabetes
insipidus. Basilar skull fractures may predispose to the development of diabetes insipidus as a
consequence of shearing of the pituitary stalk. Treatment of diabetes insipidus entails
administration of 1-desamino-8-D-arginine-vasopressin (DDAVP) in conjunction with hypoosmolar
fluids. Hypokalemia may result from potasium loss secondary to polyuresis with diuretic
administration and high urine output states such as SIADH and cerebral salt wasting syndrome.
Concurrent hypomagnesemia, as seen with alcoholic and diabetic patients, can aggravate
hypokalemia. The loss of cellular magnesium depletes intracellular potassium, making hypokalemia
more difficult to treat if magnesium supplementation is not given. In addition, serum pottasium
levels may decrease despite normal total body stores. Common causes of intracellular shifts of
potassium include hyperventilation and insulin administration.

A.6 In addition to sodium and pottasium, what other electrolyte abnormalities can be present
after head trauma?

Potasium and sodium levels are routinely checked perioperatively. However, magnesium and
phospate levels are not routinely ordered so low levels ot these electrolytes are more likely to
remain undectected. Hypomagnesemia has been associated with cardiac arrhytmia such as
torsades de pointes, sudden death, seizures, and neuromuscular irritability. Hypophosphatemia has
been asociated with weakness of the respiratory muscles and respiratory infection.

A.7 What are the neuroprotective effects of administering magnesium?

Magnesium homeostasis is altered after traumatic brain injury because magnesium falls on the
order of 50%, in addition to treating hypomagnesemia, administration of magnesium affords
meuroprotection. Magnesium is an N-methyl-D-aspartate (NMDA) antagonist that supresses
excitotoxic mechanisms. Excitatory amino acids such a glutamate and aspartate are released after
traumatic injury, which initiates a cascades of events leading to secondary injury. Glutamate
induced ionic depolarization leads to calcium influx and cell death. Magnesium works at the
postsynaptic receptor to reduce the neurotoxic effect of glutamate. In animal models, traumatic
brain injury decreases intracellular free concetrations of magnesium. Magnesium crosses the blood
brain barrier. Repeated administration of magnesium attenuates brain edema and improves
neurologic recovery. Although prophylactic magnesium administration has received some
enthusiasm in the management of stroke, its clinical use in the treatment of head injury remains to
be seen.
A.8 What role does gender and female sex hormones have in the pathophysiology of traumatic
brain injury?

Women account for approximately 20% to 30% of the head injury population. Laboratory evidence
indicates that estrogen and progesterone mediate neuroprotection by decreasing lipid
peroxidation and reducing production of inflammatory cytokines. Compared to women, increases
on cerebrospinal fluid levels of glutamate, lactate, and F2-isoprostane (marker for lipid
peroxidation) are observed in men after traumatic brain injury. However, there appears to be a
paradox between the acute neuroprotective properties of femalu sex hormones and actual
recovery for women as functional outcome has been worse for women. It has been suggested that
female sex hormones may be detrimental to neuroplasticity and recovery. In addition to gender
differences, the effect of hormonal status in females in the pathophysiology of head injury remains
unclear. Consequently, gender selection and the relation of hormonal status at time of injury
become important un the design of clinical trials involving therapeutic interventions in brain
trauma patients.

B. Preoperative evaluation and preparation

B.1 What is the GCS? What is the significance of a GCS of five in this patient?

The GCS is the most widely used method to asses neurological status and severity of brain
dysfunction following head trauma. The scale, which ranges from 3 to 15, is based on evaluating
the best motor response, the best verbal response, and eye opening. Of the patients who initially
survive traumatic brain injury, 80% have minor injury (GCS 13 to 15), 10% have moderate injury
(GCS 9 to 12), and 10% have severe injury (GCS <9). Serial determination of GCS is essential to
monitor the patients condition as patient GCS can change in a rapid or delayed manner. Decreases
in the GCS of three or more points are indicative of catastrophic neurologic deterioration.

B.2 In addition to ehe GCS, what other assessments can be done to evaluate neurologic function?

The glasgow coma score assesses spontaneous activity. Further neurological evaluation includes
pupillary examination, checking for brainstream reflexes in unconscious patient, and looking for
lateralizing signs. Fixed bilateral enlarged pupils may signify an ominous prognosis whereas
unilateral papillary enlargement occurs in the presence of an expanding hematoma. Deeply
comatose patients lacking spontaneous eye opening should have evaluation of the brainstem
reflexes. The oculocephalic reflex or dolls eye maneuver is elicited by rotating the head
horizontally to one side. In the intact brainsteam, the eyes deviate conjugately to the other side.
This maneuver should be performed only when the cervical spine has been cleared. If the dolls eye
response is abnormal, then testing of the oculovestibular reflex (cold caloric test) is another
method to evaluate brainstem function. The cold caloric test entails irrigation of the external
auditory canal with ice water. In the intact brainstream, the eys should deviate to the side of cold
stimulation. Abnormal oculocephalic and oculovestibular signify severe brainsteam dysfunction
extending to the pons. However, other causes for abnormal responses need to be ruled out, which
include drugs (phenytoin), nerve injuries (oculomotor, abducens, vestibular), and labyrinthine
disease. Additional lateralizing sign include asymmetric posturing, hemiparesis, and facial
weakness. The presence of these findings could indicate the possibillity of a mass lession.

B.3 What is the role of CT scanning in the initial evaluation of the head injured patient?

If there has been aloss of consciousness or if the glasgow coma scale is less than 15, a head CT scan
should be obtained. Evidence of an intracranial hematoma that causes compression of the
ventricles or a midline shift of greater than 5 mm is an indication for surgical intervention.
Conversely, absence of a mass lesion or compression of the ventricles is an indication for
conservative management. In a patient whose neurological condition is deteriorating, prompt
intubation, ventilation, and mannitol administration usually provides sufficient time to obtain a
preoperative CT scan. In rare circumstances, the surgeon may need to initiate emergency surgical
exploration of an expanding intracranial hematome without CT scanning. In acute situations,
urgent partial surgical decompression through a burr hole close to the fracture may be requred.

B.4 What is the role of intracranial pressure monitoring in the management of head injury?

Life threatening emergencies such as impending herniation or hemorrhagic wounds in the


abdomen/thorax require rapid surgical intervention. Definitive surgery for non life threatening
injuries should be delayed until the patient is hemodynamically stabel to minimize hypotension,
hypovolemia, and cerebral hypoxemia. If the patient is not emergently taken to the OR, ICP
monitoring becomes helpful in optimizing blood pressure management because cerebral perfusin
pressure (CPP) can be calculated by measuring mean arterial pressure (MAP) and ICP. Patients with
head trauma often substain other injuries requring nonneurological surgery. The decision to have
an ICP monitor placed before nonneurological surgery includes neurologic status in conjunction
with CT finding, the nature and duration of the surgical procedure, and surgical procedures
requiring occlusion of the aorta. Although there have been no prospective, randomized, clinical
trials to establish the clinical efficacy of intracranial pressure monitoring, intracranial pressure
monitoring has become widely used for the management of intracranial hypertension. Intacranial
pressure monitoring helps in early detection of expanding hematomas and can be useful in
reducing intracranial pressure by cerebrospinal fluid drainage. In this patient, intracranial pressure
monitoring is appropiate because this patient has severe brain injury and an abnormal CT scan. In
patients with severe head injury but a normal CT scan, intracranial pressure monitorng is indicated
when systolic blood pressure is less than 90 mmHg and there is motor posturing. Intracranial
pressure monitoring is rerely indicated in patients with mild to moderate injury.

B.6 How can your clear this patients cervical spine?

Two percents of patients presenting to trauma units following closed head injury have a
concomitant cervical spine fracture. Adequate cervical spine x-rays, especially in the uncooperative
patient, are very difficult to obtain following many traumas. Furthermore, injuries in the
atlantooccipital region are especially difficult to identify radiographically, and up to 26% of lstersl
radiographs failed to shown fractures. Even in the face of normal radiographic studies, patients
may still have significant ligamentous injuries with cervical instability necessitating particular care
during airway management. Typically, patients are examined carefully, their cervical spine is
palpated, and tenderness or weakness is identified. In the uncooperative or unconscious patient,
the cervical spine should be considered not cleared, even in light of normal x-rays. On the other
hand, if the cervical spine is cleared radiographically, the mental status is normal, and the patient is
asymptomatic, then the examination can be considered cleared.

B.7 What are the benefits of early endotracheal intubation in this patient?

Endotracheal intubation not only provides a secure airway in a patient with an altered ability to
protect his airway, but also allows for the ability to hyperventilate the patient, providing a rapid
tool for lowering intracranial pressure if necessery. Also, atient with facial trauma can oftenn have
progressive swelling ang anatomic distortion, making subsequent intubation attempts more
difficult.

B.8 What is your plan for airway management in this patient? How would it change if the patient
were combative? How would it change had facial fractures with significant swelling of the head
and neck?

Patient with a glasgow coma scale of less than 8 often require intubation and controlled ventilation
to lower the intracranial pressure and protect the airway. Direct laryngoscopy following
introduction and musle relaxation should be accompanied by in line stabilization by an assistant,
with many authors recommending leaving the posterior portion of the rigid collar in place, so that
it can act as a stabilizier to prevent further movement. Earlier recommendations for in line traction
are no longer popular due to concerns for spinal cord damage in patients with gross instability.
Emergency airway equipment should always be available in case of the inability to intubate with
direct laryngoscopy. Another option is awake fiberoptic intubation, however, a compliant patient is
a necessity, as thrashing and fighting can cause more harm to the unstable spine than laryngoscopy
itself. A combative patient would make one lean more towards rapid sequence induction and
intubation with in-line stabilization, whereas a patient with facial fractures and facial swelling
would lead one to fiberoptic intubation. Mid face and basilar skull fractures should preclude
attempts at nasal intubation due to concerns for entering the cranial vault inadvertently. Blood in
the airway can complicate fiberoptic intubation in these patients, and alternate intubation devices
and plans should be readily available. In any event, the goals of preoxygenation and securing an
airway with a minimun of cervical spine motion should be observed, while being cognizant of the
risk of regurgitation and aspiration in a patient with a full stomach

B.9 What are the effects of succinylcholine on inracranial pressure? What is the significance of
the effect, If any?

Succinylcholine has been shown in animal and human studies to increase intracranial pressure
through increased muscle spindle activation with depolarization. The effect, however, can be
avoided by using a defasciculating dose of nondepolarizing drug before succinylcholine
administration. It is important to remember that the elevation in intracranial pressure from
succinylcholine will be much less than the elevation during intubation attempts in awake struggling
patients.
B.10 What coagulation abnormalities are present after traumatic brain injury? What treatment
modalities can be used to provide hemostasis and reduce intracranial hematome expansion?

Abnormalities in blood clotting occur in the setting of traumatic brain injury, which is further
aggravated in patients taking anticoagulant medication. The presentation of coagulopathy is
diverse, ranging from abnormalities in clotting studies to clinically significant bleeding diathesis.
Disseminated intravascular coagulation is a consequence of traumatic brain injury, presumably
related torelease of tissue thromboplastins. One explanation for secondary brain injury after
intracranial bleeding is ischemia secondary to cerebral herniation. Increased intracranial pressure,
and direct blood vessel occlusion by the hematoma. An alternative explanation is intravascular
microthrombosis secondary to disseminated intravascular coagulation. Traditionally, the
administration of fresh frozen plasma and clotting factors has been used in correcting coagulation
abnormalities after head injury. Early hemostatic therapy for acute hemorrhage has been proposed
to reduce the growth of hematoma expansion. Recombinant activated factor VII has been
administered to promote hemostasis in patients with acute intracerebral hemorrhage. One
randomized trial showed that factor VIIa given within 4 hours after onset of intracerebral
hemorrhage limited the growth of hematoma and improved functional outcome. However in this
trial, only patients with spontaneous intracerebral hemorrhage were studies whereas traumatic
brain injury patients were excluded. Moreover, the exclusion criteria also included (a) patients with
glasgow coma scale less than 5 (b) patient the underwent surgical evacuation within 24 hours after
admission, and (c) patients taking oral anticoagulants or with known coagulopathy. Given these
study limitation, further research is needed to evaluate the role of factor VIIa in traumatic brain
injury patients that undergo surgical intervention and may have concomitant abnormalities in
coagulation.

C. Intraoperative Management

C.1. What is appropriate hemodynamic monitoring during computed tomography (CT) scanning
and during craniotomy for evacuation of a subdural hematoma?

It is axiomatic that hemodynamic monitoring should be commensurate with the anticipated


changes in cardiovascular status during the planned procedure. Assuming there is no evidence of
occult blood loss or major intrathoracic injury, the most aggresive monitoring during CT scaniing
should consist of direct arterial pressure assessment. This is based on the requirement for arterial
blood gas analysis and the possible need to administer vasoactive drugs to control blood pressure.
Conversely, if there is evidence of occult bleeding or a major thoracic injury, placement of a central
venous pressure (CVP) or pulmonary arterial (PA) catheter may be required in guiding fluid
management before CT scanning. If no invasive monitors were placed during CT scanning, an
arterial line is needed before craniotomy surgery. Placement of a CVP or PA catheter inf the OR is
helpful in managing blood pressure in conjunction with fluid administration. If cardiac confusion is
a consideration, placement of a PA catheter would be more preferable than placement of a CVP
catheter, because both cardiac output and right ventricular pressures can be measured. Cardiac
confusion is most often associated with right ventricular dysfunction.

C.2. Should hyperventilation be used in this patient?

The theoretical advantages of hyperventilation are control of intracranial pressure (ICP) and
reversal of acidosis in brain tissue. However, cerebral blood flow in head-injured tissue is low and
vasocontriction can result in ischemia. In areas of severe injury (e.g., subdural hematomas, diffuse
contusions), there is local variability in perfusion as well as loss of autoregulation and CO2
reactivity. A randomized, clinical trial has shown hyperventilation is potentially deleterious,
suggesting that prophylactic hyperventilation (PaCO2 < 35 mmHg) should be avoided. It has been
suggested that the use of monitors such as jugular venous hemoglobin oxygen saturation
monitoring and cerebral oximeters may help determine the effects of hyperventilation on cerebral
oxygenation. Measures of cerebral metabolism may predict which patients benefit from
hyperventilation. Curently, it has been recommended that hyperventilation be used on a selective
rather than, on a routine basis. Hyperventilation may be necessary to lower ICP for brief periods in
which there is acute neurologic deterioration or intracranial hypertension that is refractory to
other treatment modalities such as mannitol and cerebrospinal fluid (CSF) drainage. If ICP
monitoring is present in the OR, hyperventilation could be used to lower ICP to less than 20 mmHg.
Other goals such as facilitating surgical access and minimizing surgical retraction are still important
considerations in the intraoperative management of head injury

C.3. What are the implications of arterial hypertension in head-injured patients? How should
blood pressure be managed?

Hypertension is a common feature of head injury in patients who do not have massive blood loss
associated with their injuries. The etiology of hypertension appears to be catecholamine related.
Some experts believe that cerebral perfusion is optimized when there is a high arterial pressure
opposing the effects of elevated intracranial pressure (ICP). Others fell that in the presence of a
disrupted blood-brain barrier, arterial hupertension contributes to extravasation of edema fluid
and aggravation of brain swelling. Although some experts advocate maintaining cerebral perfusion
pressure (CPP) above 60 mmHg, proponents of high CPP recommend maintaining CPP greater than
70 mmHg with the use of volume expansion and vasoactive drugs. Several clinical studies have
suggested improved outcomes when systemic arterial pressure is raised to keep CPP at 60 to 90
mmHg, but they were not controlled, blinded, or randomized. Other studies have questioned the
necessity of vasopressors to maintain cerebral perfusion above 70 mmHg and the role of CPP as a
determinant of cerebral blood flow. The majority impression at this time is to maintain arterial
pressure at normal to slightly elevated levels. Above all, arterial hypotension is to be avoided,
because it profoundly increases neuronal damage in the presence of elevated ICP.
C.4. What should be done about intravenous fluid replacement? Should cortocosteroids be given
empirically?

Often, many head-injured patients sustain multiple injuries, which require aggresive resuscitation
with crystalloid, plasma expanders, and blood. Once the patient arrives to the operating room (OR),
packed red blood cells should be administered to maintain normal central venous pressure (CVP)
along with crystalloid or colloid solutions in quantities sufficient to replace blood loss. The problem
with aggresive ressucitation is tha excessive crystalloid administration may exacerbate brain
edema. Rapid formation of brain edema is a common reaction associated with most
neuropathological processes, including intracranial hematomas. Although crystalloid administration
decreases colloid oncotic pressure (COP), the reduction of COP does not cause edema in normal or
injured brain tissue. It is the administration of free water and the decrease in osmolality that
appears to be important in edema formation. In experimental studies, D5 W solutions increase
edema, increase blood glcose, and worsen neurologic outcome. Isotonic solutions such as Ringers
lactate and 0,9% saline have no adverse effect on edema formation, blood glucose, and neurologic
outcome. The worsening of neurologicoutcome with D5 W has been attributed to edema formation
rather than hyperglycemia. Corticosteroids have been shown to be effective in reducing cortical
edema associated with brain tumores and abscesses, but prospective studies evaluating their
efficacy in head trauma have failed to demonstrate any benefit and are occasionally associated
with iatrogenic complications suc as sepsis. Glucocorticoids do not lower intracranial pressure (ICP)
and its routine use in not recommended for head injury. Moreover, their potential for raising
plasma glucose make their use less desirable in the setting of traumatic brain injury

C.5. Should hypertonic saline be administered to this patient? How is hypertonic saline
administered?

The rasionale for hyperosmolar therapy is to decrease cerebral edema by creating an osmolar
gradient between the intravascular space and cerebral tissue. Water moves from the cells and
interstitial spaces into the capillaries, to decrease cerebral water content and intracranial pressure
(ICP). Hypertonic saline and mannitol are the modalities for hyperosmolar therapy. Hypertonic
saline has been shown to decrease ICP even when other conventional measures such as
barbiturates and mannitol have been exhausted. Hypertonic saline is a volume expander in the
systemic circulation and does not impair renal function as seen with mannitol administration.
Often, with hypertonic saline administration, the goal is to maintain normovolemia with the help of
central venous pressure (CVP) or pulmonary arterial catheter monitoring. Typically, a 3% saline
solution is administered at a rate of 75 to 150 mL per hour whereas a bolus of 250 mL may be given
for aggresive therapy. Of further note, the use of 7.5% hypertonic saline has been reported.
Preliminary evidence supports the use of hypertonic saline in reducing ICP, suggesting that
controlled clinical trials should be performed to determine if hypertonic saline improves outcome.
Currently, the human data is still inconclusive to recommend the use of hypertonic saline as a
standard of management. In one study, patients receiving 2 mL per kg pf 7.5%saline had better
control of ICP compared to patient receiving mannitol, but no changes in mortality and neurologic
outcome were observed. In another study involving the prehospital administration of hypertonic
saline for resuscitation in hypotensive traumatic brain injury patients, ICP control was better in the
hypertonic saline patients, but again no differences in outcome were demonstrated.

C.6. The patient under went a craniotomy for a bifrontal craniectomy for evacuation of the
anterior frontal lobe and a frontal intracerebral hematoma. Are there anesthetic agents that
should be avoided in this situation? Which ones? What agents might be preferred in this
situation?

The principles of anesthetic management for patients with rapidly expanding intracranial mass
lessions are based on the idela of maximizing intracranial compliance by minimizing the volume
within the intracranial compartment. This means that any maneuver that increases cerebral blood
volume should be avoided. All intravenous induction agents (e.g., thiopental, etomidate, and
propofol) except for ketamine are known for their vasoconstrictive effects and are reasonable
choices provided that the hemodynamic stability is maintained. Ketamine has been out of favor in
the neurosurgical setting because early studies showed that it increases cerebral metabolic rate,
cerebral blood flow, and intracranial pressure (ICP). However, a more recent study allowed that in
ventilated patients receiving propofol sedation, ketamine actually decreased ICP and did not
adversely alter cerebral hemodynamics. These authors surmised that when ketamine is added to a
background anesthetic, the central nervous excitation effects of ketamine are blunted and
increases the depth of anesthesia. Because ketamine is an NMDA antagonist, with possible
neuroprotective effects, it has beed suggested that the use of ketamine in head injury warrants
reevaluation. All the volatile inhalation agents and nitrous oxide have some cerebral vasodilatory
effects. Caution must be exercised in using inhalation agents in patients with rapidly expanding
intracranial mass lessions. When the surgical field is tight, eliminating inhalation agents and going
with a total intravenous anesthetic (TIVA) technique may be appropriate. For example, a propofol
or thiopental infusion may render the patient sufficiently anesthetized for a craniotomy. Finally,
there is a concern tha opioids may act as cerebral vasodilators and raise ICP. Several stuides have
shown that sufentanil increases by autoregulatory compensation when meal arterial pressure
(MAP) decreases. Direct cerebral vasodilatation has been implicated in the increase in ICP seen
after morphine and fentanyl administration.

C.7. Should hypothermia be employed in this patient?

In experimental models, hypothermia has been shown to decrease the amount of edema and
necrosis volume after cerebral damage. A temperature of 320C (89.6oF) has been considered to be
the safe limit for patients with head injury. Several clinical trials, involving less than 100 patients,
have shown that inducing moderate (32oC to 33oC [89.6oF to 91.4oF]) or mild hypothermia (33oC to
35oC[91.4oF to 95oF]) in patients with severe head trauma (GCS <8), improves neurologic outcome.
However, a multicenter phase III head injury trial, involving almost 400 patients, showed that
inducing hypothermia in patients who already arrived to the hospital normothermic did not
improve outcome. In general, enthisiasm for the application of hypothermia in neurosurgical
patients has faded as another multicenter trial of hypothermia involving cerebral aneurysm
patients also demonstrated negative findings in improving neurologic outcome. Despite, negative
findings from the most recent comprehensive trials on hypothermia, various researchers contend
that the complete abandoment of hypothermia is premature that newer technologies which induce
hypothermia (e.g., intravascular cooling) should be further investigated.
D. Postoperative Neurointensive Care Management

D.1. What are the postoperative ventilation considerations in this patient?

If the patient had normal consciousness preopratively, early extubation would be preferable once it
is confirmed that the patient is able to follow commands and move extremities. Efforts should be
made to avoid bucking and coughing on the endtoracheal tube and to treat hypertension that
occurs on emergence. Intravenous lidocaine is a useful drug to smooth te coughing associated with
emergence. Short acting opiates, particularly remifentanil, can provide a patient that is
hemodynamically stable, tolerating the endotracheal tube, amd fp;;pwomg cp,,amds. However,
many traumatic brain injury patients undergoind emergency surgery remail intubated
posoperatively due to severity of the brain injury. In that case, blood pressure control to prevent
hypertension is needed to prevent further hemorrhage. In some patients, sedatives and muscle
relaxants may be administered on transport to prevent changes in intracranial pressure (ICP)
associated with stimulation and agitation. In ventilated patients, the use of a cerebral oxygen
monitor mau be useful in optimizing brain O2 delivery in relation to arterial carbon dioxide (PaCO2).

D.2. What specific measures should be used to control the patients intracranial pressure (ICP)?
What type of monitoring devices can be used to monitor ICP?

After removal of an intracranial hematoma, control of ICP is of paramount importance in the


patients recovery. Brieftly, those patients whose ICP can be maintained below 20 to 25 mmHG
tend to have significantly better outcomes that do patients whose ICP remain elevated. It has
become common practice, therefore, to monitor ICP in the posoperative perio in these patients.
This enables the intensivist to adjust treatment with hyperventilation, mannitol, cerebrospinal fluid
(CSF) drainage, and head-up tilt, to the desired ICP response. If these maneuvers fail, the next
intervention is to maintain barbiturate coma to a level where the electroencephalogram (EEG),
shows burst suppression. This is continued until it is no longer required to control intracranial
hypertension. After weaning, from barbiturate therapy, the patient can be weaned from diuretics
and/or hyperventilation, as appropirate. As aforementioned, the use of hyperventilation in head-
injury patients must be used on selective basis because hyperventilation has potentially deleterious
effects on cerebral perfusion. The classic intraventricular catheter or ventriculostomy was
introduced by Lundberg in 1960 and has been the gold standard for ICP monitoring and CSF
drainage. Placement of an intraventricular catheter has been associated with the potential for
infection and brain parenchyma injury. Placement of a subarachnoid bolt used to be a less invasive
modality but limitations included accuracy and stabillity. Subarachnoid bolts have been supplanted
by a variety of implantable pressure transducer devices. Curret ICP monitoring systems utilize a
twist drill for bolt placement in the skull to allow a catheter to be rapidly placed in the parenchyma
or subarachnoid space. Some system allow CSF drainage in which a catheter containing a
transducer at the tip is placed intto the ventricles
D.3. What is neurogenic pulmonary edema? Would you avoid positive end-expiratory pressure
(PEEP) in a patinet with increased intracranial pressure (ICP)?

Neurogenic pulmonary edema is a commonly seen disorder-following head injury or intracranial


bleed. The mechanisms are unclear, but are thought to be due to combination of increased
pulmonary pressures due to massive catecholamine release with increased ICP (Cushings
response) and altered pulmonary capillary permeability from as-yet undescribed neurogenic
fantors. The onset can be immediate or delayed, and treatment consist of supportive care as with
other cases of pulmonary edema, including PEEP. Positive pressure ventilation, PEEP, and increased
ICP have been studied in animal and human models, and although there is a slight increase in ICP
with higher levels of PEEP (10 to 12 cm H2O) in patients with normal ICP, patients with elevated ICP
do not seem to demonstrate a clinically significant change in ICP with event high levels of PEEP. On
the other hand, avoidance of PEEP, in such setting may lead to hypoxemia that, in turn, can
exacerbate cerebral ischemia.

D.4. What is the role of antiseizure prophylaxis in the perioperative management of head
trauma?

Seizures may cause secondary injury as a result of increases in intracranial pressure (ICP), changes
in oxygen suplly and demand, and increases in neurotransmitter release. Early posttraumatic
seizures (PTS) occur in the first week after injury, mostly within the first 24 hours. Late PTS occurs
after the first week. Often early PTS occurs within hours after injury, especially in patients with
depressed or open skull fractures and hemorrhagic brain contusions. Short-term prophylactic
administration of anticonvulsant drugs (e.g., phenytoin, carbamazepine) for early PTS is
recommended. Administration of anticonvulsant medicines, however, has not been shown to
prevent late PTS. Therefore, routine antiseizure prophylaxis is not recommended later that 1 week
following head injury.

D.5. How can cerebral oxygenation monitoring be used in the clinical management of traumatic
brain injury?

An indwelling parenchymal device that measures local oxygenation can be used to gain information
regarding tissue oxygenation in real time at the bedside. In a severely injured brain autoregulatory
mechanisms fail. As a result various areas of the brain will be ischemic. Use of an oxygen sensor
allows for more precise management to optimize oxygen delivery and eliminate progression of
ischemia. A cerebral oxygen monitor is placed either intraoperatively or at the bedside, much like a
ventriculostomy. Many studies have shown it to be equally as useful a jugular bulb catheter. The
device can either be placed in an ischemic penumbra of a lesion or in an uninjured area of the
brain. In the first case, the monitor will yield information that can be used to prevent further
ischemia and cell death in the second case, the device is used as a global indicator of cerebral
oxygenation and may be useful in guilding ventilatory management. Cerebral oxygenation
monitoring also offers the ability to measure parenchymal temperatures simultaneous to oxygen
content. This is of critical importance when using hypothermia or maitaining normothermia. By
definition, brain oxygen tension or partial pressure (PbO2) is not adequate if it drops below a value
of 20 mmHg. In recent studies, values of less than 20mmHg for short intervals of the time have
correlated with worse neurologic outcome. A value of greater than 30 mmHg is optimal. Curently,
there are several devices on the market that measure oxygen content.

D.6. What methods can be used in the neurointensive care unit to prevent hyperthermia?

Fever continues to be a problem in critically ill neurosurgical patients. One retrospective study
noted that greater than 50% of closed head injury patients had one febrile episode in the
neurointensive care unit. Fever and hyperthermia accentuate excitotoxic release of
neurotransmitters, increases production of free radicals, and accelerates cytoskeletal protein
degradation. Although the enthusiasm to induce perioperative hypothermia for neuroprotection
has waned, interventions are neede to coll patients to prevent hypothermia. Conventional water
circulating cooling blankets have been considered to be ineffective due to poor surface contact
with the skin. A newer external cooling device has been developed which utilizes self-adhesive,
hydrogel-coated pads that circulate temperature-controlled water under negative pressure.
Intravascular central venous catheters have been developed for both place for cooling and
rewarming. These catheters contain special built-in balloons through which cooled or warmed
saline is circulated in a closed loop design. The patients temperature is continuously compared
with a user-defined target temperature and the controller system is qeuipped with a safety system
that alarm when the temperature is above or below programmed levels or when there is a system
malfunction. Fig 25.2 shows a comparison of brain and rectal temperatures after intravascular
cooling through femoral catheter. Intracranial temperature measurements were obtained through
an indwelling cerebral oxygen catheter placed into the brain parenchyma of the left frontal region.
In view of the recent advances in technologies to lower temperature, experts contend that it is
premature to completely abandon the use of hypothermia. Future avenues of research include : (a)
evaluating the impact of fever and hyperthermia on neurologic outcome, (b) treating refractory
elevations in intracranial pressure (ICP) with hypothermia, and (c) exploring methods for
intraventricular or lumbar irrigation for rapid brain cooling