Traumatic brain injury is one of the leading causes of mortality and morbidity among
children and young adults in western developed countries. Subsequently to the direct
effects, secondary injury is characterized by the activation of different pathophysiologic
pathways; intracranial compensatory mechanisms initiate immediately as the secondary
injury progresses. Furthermore, intracranial hypertension leads to the development
of physiologic events that are crucial for patients’ clinical outcomes.
The intracranial hypertension phenomenon is of clinical significance in patients with
brain injury. Brain elastance is defined based on the intracranial pressure (ICP)
per volume unit, added to the cranial compartment, whereas compliance is the inverse
of the elastance, defined by the change of pressure over the change of volume. Additionally,
the elastance curve can be graphically expressed as the lateral changes in the ICP
compared with the volume changes within the cranial compartment.
The initial phase (also known as compensatory) is characterized by low elastance and
high compliance. Posteriorly, a phase of high elastance and low compliance occurs
when the compensatory reserves are depleted.
Intracranial Pressure and Hypertension
Intracranial pressure (ICP) is the pressure existing in the interior of the cranial
cavity, being directly related to three components:
-
Parenchymal brain structures.
-
Cerebrospinal fluid (CSF) located in the ventricular cavities and subarachnoid space.
-
Blood circulating in the intracranial compartment at a given time, as described by
the Monro-Kellie hypothesis.[1]
The Monro-Kellie hypothesis defines an equilibrium state, where the fixed volume of
the cranium, and its constituents, defines the incompressibility of the compartment.
Therefore, differential volume increases must be compensated by the intracranial constituents.[1]
Moreover, intracranial hypertension is the leading cause of death in patients with
traumatic brain injury, and it contributes to the secondary brain injury if handled
incorrectly. Any additional volume, such as bruising, swelling of the neural tissue,
or hydrocephalus, will result in increased ICP when the compensatory changes of the
primary volumes have been exceeded. As we have discussed elsewhere[2], derivation of, up to, 150 mm3 of intracranial venous blood into the systemic circulation, is the first compensatory
mechanism for preventing the increase of ICP; complementarily, CSF shifting-out depends
on disease progression and patient's age. Elders tend to exhibit cerebral atrophy,
and in this sense, rearranging high volumes results in a demanding task in the context
of slow expansions. Abnormal brain volumes and blood flow self-regulation and cerebral
edema persist as causes of raised ICP. It is important to highlight that the relationship
between the intracranial volume and pressure is depicted as a sigmoidal function rather
than linear. Nonetheless, any physiological or pathological processes, and most uncompensated
variations in the volume of any component, will be evident in the values of ICP.
Clinical studies have shown that patients with cranial trauma and ICP greater than
20 mm Hg have worse clinical prognosis and are more likely to experience brain herniation
syndrome, particularly in cases with treatment-refractory injury.[3]
Recent studies have found brain hypoxia in the settings of a cerebral perfusion pressure
less than 70 mm Hg.[4] Hypoxia is as well associated with the onset of aberrant metabolic routes and an
increase of mortality. Neuromonitoring guides treatment preventing this sequence by
maintaining brain homeostasis.
As a mass grows inside the skull, a proportional amount of CSF is withdrawn from it.
During this period, the ICP does not rise. After the extrusion of the entire CSF volume,
a linear relationship is expected between the intracranial pressure and volume. However,
this curve actually shows an exponential trend.[5]
Specifically, Langfitt curve (ICP vs. displaced volume) can be categorically divided
into four phases ([Fig. 1]):
Fig. 1 Hemodynamic phases of Langfitt curve. ICP, intracranial pressure (based on concepts
from Turner).[6]
Phase 1 (Initial): In this phase, intracranial expansive process promotes proportional changes in CSF
input and output, without an increased ICP. There is no activation of the vasodilator
cascade.
Phase 2 (Decompensation): There is virtually no more CSF in the intracranial compartment. The expansion process
modifies the regional perfusion causing lactic acidosis, activation of the vasodilator
cascade, and increasing the blood volume within the cranium.
Phase 3 (Exponential): At this stage, there is an exponential increase in cerebral blood volume, certainly
due to the vasodilator cascade effect. The cerebral blood volume increases the ICP
until it equals the mean arterial pressure (MAP), tending the cerebral blood flow
to 0.
Phase 4 (Final): Phase of vasoplegia. The compensatory reserve of the brain elastance (pressure/volume)
curve can be estimated using a linear correlation (LC) coefficient obtained from comparing
the fundamental component of amplitude of ICP pulse wave with an average volume assessed
by data mining techniques and based on 40 consecutive intervals of 6 to 10 seconds.
An LC coefficient close to 0 indicates that there is no correlation between the fundamental
component of amplitude of ICP pulse wave and the average volume. This represents the
ideal compensatory damages when the values of ICP are lower; in other words, changes
in the volume produce little or no variation in pressure. On the contrary, an LC coefficient
close to 1 corresponds to a perfect correlation between the fundamental component
of amplitude of ICP pulse wave and the mean volume. For this compensatory reserve,
changes in the volume produce evident changes in pressure. If the ICP keeps increasing,
the fundamental component of the pulse wave will be reduced because the capacity to
direct flow from dilated capillaries into arterioles will be diminished as well. Therefore,
passive collapse of vessels occurs and then the LC coefficient tends to 0.[7]
[8]
[9]
[10]
In the fourth phase, the end of the exponential curve, the cerebral blood volume is
low, the ICP is equal to the mean arterial pressure, and perfusion pressure and blood
flow to the brain are equivalent to 0. That is the brain death.
