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Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_885_Библиотеки_им_академика_М_И_Перельмана.pdf
48 M. D. Richardson and K. Beauchamp
• Clinical symptoms of acute intracranial hypertension may include headache,
nausea, vomiting, Cushing’s triad, coma, signs of herniation, cerebral ischemia,
and ultimately death.
• Treatment of intracranial hypertension depends on a variety of factors
including etiology of intracranial hypertension, clinical neurologic examination, clinical comorbidities.
• The ultimate goal in treating intracranial hypertension is both the reduction of
pressure (which may have an independent effect on the central nervous
system independent of its effect on cerebral perfusion) and the maintenance
of cerebral perfusion.
• The normal value of ICP is less than 20 mmHg in adult patients.
• Pathological elevation of ICP can result from many different intracranial
processes (hydrocephalus, intracranial bleeding, cerebral edema).
• Treatment of intracranial hypertension is determined by the pathophysiologic
process underlying the etiology of the intracranial hypertension.
• The neurologic examination is currently the best known measure of neu-
rologic function. Maintenance of the neurologic exam is preferred (when
possible) to measurement of intracranial pressure, which is an adjunct to
neurologic exam and a very indirect surrogate for neurologic function —
ultimately, maintaining function is the goal of treatment regardless of
intracranial pressure.
Main Body
• Normal value of ICP
{ The Monro-Kellie hypothesis asserts that the intracranial contents are
contained within a rigid bony calvarium and that the brain is relatively
non-compressible. Therefore, the volume of blood and cerebrospinal
fluid within the intracranial space is directly proportional to the intracranial pressure. If the intracranial pressure is to remain constant, an
increase in the volume of one of the intracranial contents must lead to a
decrease in the volume of another of the intracranial contents. The addition of a foreign body or lesion (e.g., subdural hematoma) that occupies
intracranial space will therefore result in an increase in the ICP if there is
no concurrent decrease in the volume of one or more of the normal
intracranial contents.
{ Normal ICP has been suggested to be less than 15–20 mmHg, though
several studies have produced different threshold pressures.
Intracranial Hypertension 49
• Pathological elevation of ICP
{ In practice, any lesion which causes and expansion of the intracranial
contents can lead to intracranial hypertension.
An increase in the intracranial volume of cerebrospinal fluid is defined
as hydrocephalus.
An increase in cerebral intravascular blood volume is defined as
hyperemia.
Ö In general, cerebral autoregulation maintains the intravascular
volume of the cerebral vasculature, but in severe TBI, cerebral
autoregulation can be lost allowing a direct correlation between
ICP and blood pressure.
{ Extravascular intracranial bleeding
Epidural hematoma — a hematoma resulting from bleeding in the
potential space between the skull and the dura mater.
Subdural hematoma — a hematoma resulting from bleeding in the
potential space between the dura propria and the arachnoid membrane.
Subarachnoid hemorrhage — a hematoma resulting from bleeding
into the subarachnoid space.
Intracerebral hematoma — a hematoma that forms within the brain
parenchyma; it can be spontaneous or traumatic.
Intraventricular hemorrhage — a hematoma that is the result of bleed-
ing within the ventricular system of the brain.
In addition to forming a mass lesion, intraventricular bleeding may
also result in obstruction of CSF flow pathways resulting in obstructive hydrocephalus.
{ Mass lesions — a mass lesion in any form (tumor, vascular malformation,
etc.) will result in increased ICP unless a concomitant decrease in another
intracranial content has occurred.
{ Cerebral edema
Vasogenic edema — the result of disruption of the blood brain barrier.
Intravascular proteins extravasate into the extracellular space in the
brain which results in expansion of the extracellular space.
Cytotoxic edema — the result of disruption of cellular metabolism
which leads to a decrease in the ability of a cell to maintain its ionic
equilibrium potential and a consequent increase in intracellular volume.
In traumatic brain injury, both mechanisms are present in most cases.
50 M. D. Richardson and K. Beauchamp
• Clinical signs and symptoms of elevated ICP
{ Elevation of ICP can produce a variety of symptoms ranging from
headache to coma. In the awake patient, elevated ICP produces headache,
nausea, and vomiting in the setting of intracranial trauma. The association
between these clinical indicators after traumatic brain injury has been
found to correlate with increased odds of requiring neurosurgical intervention after a minor head injury and should prompt CT scanning when
being evaluated in the emergency department.
{ Intracranial hypertension is also classically associated with Cushing’s
triad, which is the clinical syndrome of hypertension, bradycardia, and
respiratory irregularity. In practice, the full Cushing’s triad is only
observed in approximately 33% of cases of elevated ICP.
{ Elevated ICP may result in brain herniation. The brain herniation
syndromes include:
Subfalcine herniation — the cerebral hemisphere is forced under the
inferior edge of the falx cerebri, which is rigidly attached. The anterior
cerebral arteries course parallel with the falx and can be occluded with
subfalcine herniation resulting in cerebral infarction in an anterior
cerebral artery distribution.
Transtentorial herniation — the medial temporal lobe (uncus) is
forced medially and inferiorly through the tentorium cerebelli. The
third nerve courses just medial to the medial temporal lobe, so when
the medial temporal lobe is forced medially, it compresses the third
nerve resulting in its dysfunction. This is most commonly seen as a
unilateral mydriasis.
Central herniation — Generally this occurs in a superior to inferior
direction and is the result of a supratentorial force that causes the
diencephalon and supratentorial contents through the tentorial notch.
The posterior cerebral arteries (PCA) are at risk for compression thus
resulting in an ischemic stroke risk for the cerebral PCA distribution.
Downward central herniation may also result in stretch being applied
to the paramedian pontine perforating vessels, which can result in
duret hemorrhages in the ventral pons.
Tonsillar herniation — lesions of the posterior fossa may result in
upward herniation of posterior fossa contents through the tentorium
into the middle fossa or, more commonly, result in downward herniation of the cerebellar tonsils through the foramen magnum.
Intracranial Hypertension 51
• Treatment of intracranial hypertension
{ In accordance with the most recent brain trauma foundation guidelines,
we recommend initiation of treatment for intracranial hypertension above
a threshold of 20–25 mmHg.
{ Treatment options for intracranial hypertension should proceed in a
stepwise fashion as listed below:
Patient positioning — patients suspected of intracranial hypertension
should be positioned with the head elevated 30–45° with the head in a
neutral position without compression of the major draining veins of
the neck. Other injuries should be noted and positioning of the patient
should be determined accordingly (e.g., spine fractures).
Normalize vital signs and metabolic factors — patients should be
maintained with normal blood pressure to prevent both cerebral
ischemia and hyperemia/expansion of hemorrhage following traumatic brain injury. Patients with an indication should be intubated and
mechanically ventilated. PaCO2 should be maintained at the lower
limit of normal (35 mmHg). Hyperglycemia should be corrected.
Normothermia should be maintained.
Sedation
Ö Fast-acting agents such as propofol in combination with a fast-
acting synthetic narcotic agent such as fentanyl are preferred for
neurologically injured patients as they can be rapidly titrated to
allow for neurologic examination.
Ö In situations where patients will require maintenance of sedation
for long periods of time and propofol is not feasible, a continuous
benzodiazepine infusion is initiated.
Hyperosmolar therapy
Ö Mannitol — 0.25–1 g/kg bolus. This treatment likely improves
rheological properties of blood which results in reduced hematocrit, decreased viscocity and increases in cerebral blood flow.
There is also an osmotic effect which may draw fluids from the
brain into the intravascular space. Caution should be exercised
because mannitol may ultimately result in arterial hypotension.
Additionally, mannitol opens the blood brain barrier and may
result in rebound intracranial hypertension.
Ö Hypertonic saline — increases serum sodium and promotes a
redistribution of fluids from the brain into the intravascular space.
52 M. D. Richardson and K. Beauchamp
We currently recommend maintaining normonatremia and do not
recommend driving serum sodium higher than 150 as it may result
in rebound intracranial hypertension over time.
Ö Furosemide — may be used as an adjunct therapy along with man-
nitol — may result in decreases in cerebral edema and decrease in
CSF production (see Greenberg for references).
CSF diversion
Ö External ventricular drainage should be considered in patients not
otherwise requiring neurosurgical intervention if the above therapies have not resulted in control of intracranial pressure. At the
discretion of the clinician, an external ventricular drain (EVD)
may be inserted at the initiation of the process of treatment of
intracranial hypertension both as a diagnostic and therapeutic
measure.
Pharmacologic paralysis
Ö Initiation of a paralytic drip may be considered following the ini-
tiation of the above measures if intracranial hypertension persists.
Barbiturate coma
Ö Barbiturate coma can be instituted if the patient has persistent
intracranial hypertension following initiation of the above measures. In general, dosage is titrated to EEG findings consistent with
burst suppression and blood levels are measured to ensure that
therapeutic/non-toxic levels are maintained.
Hypothermia
Ö There is some evidence that hypothermia initiated prophylactically
may reduce mortality. Currently, the evidence supporting its use is
insufficient to make strong recommendations.
Decompressive surgery
Ö This maximally invasive approach results in removal of the calva-
rium and duraplasty to allow for expansion of the brain through a
cranial defect. This may be performed as the initial step in management of a traumatic brain injury at the discretion of the
neurosurgeon. Indications for decompressive craniectomy range
from the presence of a mass lesion to post-ischemia edema with
brain shift. Though a recent trial of decompressive surgery did not
demonstrate a benefit for this procedure compared with maximal
medical therapy, its methodology does not permit broad application.
Intracranial Hypertension 53
Practical Algorithm(s)/Diagrams
Fig. 1. Example of different intracranial pathologies suffered as a result of trauma.
(a) is an epidural hematoma, (b) is a subdural hematoma, (c) is a cerebral contusion/
intraparenchymal hemorrhage, (d) is a traumatic subarachnoid hemorrhage. Note how the
blood tracks the gyri and sulci into the sylvian fissure and along the insular cortex. All
forms of traumatic hemorrhage occupy intracranial space, thereby displacing other intracranial contents and/or causing an elevcation of intracranial pressure.
54 M. D. Richardson and K. Beauchamp
Fig. 2. Examples of different types of herniation.
Intracranial Hypertension 55
Fig. 3. Generalized stepwise algorithm for treatment of intracranial hypertension. Note
that this represnts a generalized approch, but depending on the clinical situation and etiology
of intracranial hypertension, one or more steps may be omitted or left out entiredly.
Review of Current Literature with References
• Guidelines for the management of severe traumatic brain injury. VIII.
Intracranial pressure thresholds. Brain Trauma Foundation; American
Association of Neurological Surgeons; Congress of Neurological Surgeons;
Joint Section on Neurotrauma and Critical Care, AANS/CNS, Bratton SL,
Chestnut RM, Ghajar J, McConnell Hammond FF, Harris OA, Hartl R,
Manley GT, Nemecek A, Newell DW, Rosenthal G, Schouten J, Shutter L,
Timmons SD, Ullman JS, Videtta W, Wilberger JE, Wright DW. J Neurotrauma.
2007; 24 Suppl 1:S55–58. PMID: 17511546.
{ Review of most current literature regarding the threshold at which treat-
ment for intracranial hypertension is indicated.
{ Consensus among this group of experts based on the literature review
performed indicate that treatment for intracranial hypertension should be
initiated at values of 20–25 mmHg.
56 M. D. Richardson and K. Beauchamp
• Guidelines for the management of severe traumatic brain injury. IX. Cerebral
perfusion thresholds. Brain Trauma Foundation; American Association of
Neurological Surgeons; Congress of Neurological Surgeons; Joint Section on
Neurotrauma and Critical Care, AANS/CNS, Bratton SL, Chestnut RM,
Ghajar J, McConnell Hammond FF, Harris OA, Hartl R, Manley GT,
Nemecek A, Newell DW, Rosenthal G, Schouten J, Shutter L, Timmons SD,
Ullman JS, Videtta W, Wilberger JE, Wright DW. J Neurotrauma. 2007; 24
Suppl 1: S59–64.
{ Review of the most current literature regarding the goal cerebral perfusion
pressure which should be maintained following severe traumatic brain
injury.
{ Cerebral ischemia likely begins at cerebral perfusion pressures less than
50–60 mmHg
{ Maintaining a goal cerebral perfusion pressure of 60 mmHg is likely ideal
for most patients.
{ Artificially elevating cerebral perfusion pressure above 70 mmHg may be
toxic and does not lead to improved outcomes.
{ Ancillary monitoring of brain tissue oxygenation may aid in tailoring
treatment to individual patients’ needs.
Chapter 4-(iii)
Spine Trauma: Diagnosis, Clearance,
and Mobility
Todd F. VanderHeiden, MD* Samuel E. Smith, MD
and Philip F. Stahel, MD
* Chief, Orthopaedic Spine Surgery, Denver Health Medical Center
†
Orthopaedic Spine Surgeon, Denver Health Medical Center
‡
Director of Orthopaedics, Denver Health Medical Center
Take Home Points
• Assume a serious spinal injury exists until proven otherwise.
• Maintain strict log-roll precautions and cervical rigid-collar immobilization
until spinal injury can be confirmed absent or definitive spinal treatment is
provided.
• Critically injured patients need total spinal evaluation: occiput to coccyx. This
includes physical examination and advanced imaging studies. Computed
Contact information: (Todd F. VanderHeiden), Department of Orthopaedic Surgery, Spine
Surgery Division, Rocky Mountain Regional Trauma Center, Denver Health Medical
Center, 777 Bannock Street, Mail-Code 0188, Denver, CO 80204, USA; Tel.: 303-6021848, Fax: 303-436-3123, email: Todd.VanderHeiden@DHHA.Org
†
‡
57