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Neuromonitoring in Head Trauma 891

53 Neuromonitoring in Head Trauma

53.1 General information

This section considers neuromonitoring instrumentation that can be done primarily at the patient’s
bedside, and therefore does not include CT perfusion studies, PET scans…. The bulk of neuromonitor-
ing literature deals with intracranial pressure (ICP). Other parameters that can be monitored include:
jugular venous oxygen monitoring (p. 899), regional CBF (p. 90 1), brain tissue oxygen tension
(p. 90 0 ), and brain metabolites (pyruvate, lactate, glucose…) (p. 90 1).
The role of adjunctive monitoring is currently unknown. Unanswered questions include: should
neuromonitoring be disease specific (e.g. is SAH different from TBI), which monitors provide addi-
tional unique information, what are the critical values of the monitored entity, and what interven-
tions should be undertaken to correct abnormalities?

53.2 Intracranial pressure (ICP)

53.2 .1 Background
Intracranial pressure (ICP) is discussed in this section on trauma because of the close relationship
between elevated ICP and brain damage from head injury. However, factors involved in diagnosing
and treating intracranial hypertension (IC-HTN) also may pertain (with modifications) to brain
tumors, dural sinus thrombosis, etc.

53.2 .2 Cerebral perfusion pressure (CPP) and cerebral autoregulation

Secondary brain injury (i.e., following the initial trauma) is attributable in part to cerebral ischemia;
see Secondary injury (p. 858). The critical parameter for brain function and survival is not actually
ICP, rather it is adequate cerebral blood flow (CBF) to meet CMRO2 demands; see discussion of CBF &
CMRO2 (p. 1330 ). CBF is difficult to quantitate, and can only be measured continuously at the bed-
side with specialized equipment and difficulty.1 However, CBF depends on cerebral perfusion pres-
sure (CPP), which is related to ICP (which is more easily measured) as shown in Eq (53.1).

fcerebral perfusion pressureg ¼ fmean arterial pressure" g # fintracranial pressureg

or; expressed in symbols ð5 3:1Þ
53
CPP ¼ MAP" # ICP

*note: the actual pressure of interest is the mean carotid pressure (MCP) which may be approxi-
mated as the MAP with the transducer zeroed ≈ at the level of the foramen of Monro.2

As ICP becomes elevated, CPP is reduced at any given MAP. Normal adult CPP is > 50 mm Hg.
Cerebral autoregulation is a mechanism whereby over a wide range, large changes in systemic BP
produce only small changes in CBF. Due to autoregulation, CPP would have to drop below 40 in a
normal brain before CBF would be impaired.
In the head injured patient, older recommendations were to maintain CPP ≥ 70 mm Hg due to
increased cerebral vascular resistance.3 However, recent evidence suggests that elevated ICP
(≥ 20 mm Hg) may be more detrimental than changes in CPP (as long as CPP is > 60 mm Hg4)5 (higher
levels of CPP were not protective against significant ICP elevations5).

53.2 .3 ICP principles

The following are approximations to help simplify understanding ICP (these are only models, and as
such are not entirely accurate):
1. normal intracranial constituents (and approximate volumes):
a) brain parenchyma (which also contains extracellular fluid): 140 0 ml
b) cerebral blood volume (CBV): 150 ml
c) cerebrospinal fluid (CSF): 150 ml
2. these volumes are contained in an inelastic, completely closed container (the skull)
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892 Head Trauma

3. pressure is distributed evenly throughout the intracranial cavity (in reality, pressure gradients
exist6,7)
4. the modified Monro-Kellie doctrine8 states that the sum of the intracranial volumes (CBV, brain,
CSF, and other constituents (e.g. tumor, hematoma…)) is constant, and that an increase in any
one of these must be offset by an equal decrease in another. The mechanism: there is a pressure
equilibrium in the skull. If the pressure from one intracranial constituent increases (as when that
component increases in volume), it causes the pressure inside the skull (ICP) to increase. When
this increased ICP exceeds the pressure required to force one of the other constituents out
through the foramen magnum (FM) (the only true effective opening in the intact skull) that other
component will decrease in size via that route until a new equilibrium is established. The cranio-
spinal axis can buffer small increases in volume with no change or only a slight increase in ICP. If
the expansion continues, then the new equilibrium will be at a higher ICP. The result:
a) at pressures slightly above normal, if there is no obstruction to CSF flow (obstructive hydro-
cephalus), CSF can be displaced from the ventricles and subarachnoid spaces and exit the
intracranial compartment via the FM
b) intravenous blood can also be displaced through the jugular foramina via the IJVs
c) as pressure continues to rise, arterial blood is displaced and CPP decreases, eventually produc-
ing diffuse cerebral ischemia. At pressures equal to mean arterial pressure, arterial blood will
be unable to enter the skull through the FM, producing complete cessation of blood flow to
the brain, with resultant massive infarction
d) increased brain edema, or an expanding mass (e.g. hematoma) can push brain parenchyma
downward into the foramen magnum (cerebral herniation) although brain tissue cannot
actually exit the skull

53.2 .4 Normal ICP

The normal range of ICP varies with age. Values for pediatrics are not well established. Guidelines
are shown in ▶ Table 53.1.

53.2 .5 Intracranial hypertension (IC-HTN)

General information
Traumatic IC-HTN may be due to any of the following (alone or in various combinations):
1. cerebral edema
53 2. hyperemia: the normal response to head injury.10 Possibly due to vasomotor paralysis (loss of
cerebral autoregulation). May be more significant than edema in raising ICP (p. 936)11
3. traumatically induced masses
a) epidural hematoma
b) subdural hematoma
c) intraparenchymal hemorrhage (hemorrhagic contusion)
d) foreign body (e.g. bullet)
e) depressed skull fracture
4. hydrocephalus due to obstruction of CSF absorption or circulation
5. hypoventilation (causing hypercarbia → vasodilatation)
6. systemic hypertension (HTN)
7. venous sinus thrombosis
8. increased muscle tone and Valsalva maneuver as a result of agitation or posturing → increased
intrathoracic pressure → increased jugular venous pressure → reduced venous outflow from
head
9. sustained posttraumatic seizures (status epilepticus)

Table 53.1 Normal ICP

Age group Normal range (mm Hg)
adults and older childrena < 10 –15
young children 3–7
term infantsb 1.5 –6
atheage of transition from “young” to “older” child is not precisely defined
bmay be subatmospheric in newborns9