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Changes in intracranial pressure and cerebral autoregulation in patients with severe traumatic brain injury *
Ter Minassian, Aram MD; Dubé, Laurent MD; Guilleux, Anne Marie MD; Wehrmann, Nina MD; Ursino, Mauro PhD; Beydon, Laurent ISSN: Author(s): MD 0090- 3493 Issue: Volume 30(7), July 2002, pp 1616-1622 Accession: Publication Type: [Neurologic Critical Care] 00003246- Publisher: © 2002 Lippincott Williams & Wilkins, Inc. 200207000- From the Département d’Anesthésie Réanimation, CHU, Angers Cedex, France (ATM, LD, AMG, NW, LB); and the Dipartimento 00036 di Elettronica, Systemistica e Mathematica, Universita degli studi Bologna, Italy (MU). Full Despite the correlation we find between the status of autoregulation and the direction and magnitude of changes in Institution(s): Text intracranial pressure, our data indicate that an alteration of autoregulation does not generally cause a significant change in the (PDF) expected qualitative relationship between intracranial pressure and mean arterial pressure during cerebral perfusion pressure 561 K management of patients with severe head injury. Email Keywords: head injury, cerebral autoregulation, intracranial pressure, cerebral perfusion pressure, cerebral blood flow velocity Jumpstart Find Citing Table of Contents: Articles ≪ Prognostic factors, clinical course, and hospital outcome of patients with chronic obstructive pulmonary ≪
disease admitted to an intensive care unit for acute respiratory failure. Table ≫ Antioxidant protection against iron in children with meningococcal sepsis. of Contents About Abstract Links this Background: Impaired cerebral autoregulation is frequent after severe traumatic Journal http://ovidsp.tx.ovid.com/spb/ovidweb.cgi (1 of 17) [6/11/2008 5:32:34 PM] Ovid: Changes in intracranial pressure and cerebral autoregulation in patients with severe traumatic brain injury *.
Abstract head injury. This could result in intracranial pressure fluctuating passively with ≫ Complete Reference the mean arterial pressure. ExternalResolverBasic Objective: This study examines the influence of autoregulation on the amplitude Outline and direction of changes in intracranial pressure in patients with severe head injuries during the management of cerebral perfusion pressure.
● Abstract Design: Prospective study. ● MATERIAL AND METHODS
❍ Materials. Setting: Neurosurgical intensive care unit ■ Changes in Systemic Arterial Pressure. Patients: A total of 42 patients with severe head injuries. ■ Statistical Analysis.
Interventions: Continuous recording of cerebral blood flow velocity, ● RESULTS intracranial pressure, and mean arterial pressure during the start or change ● DISCUSSION of continuous norepinephrine infusion. ❍ Validity of Transcranial Doppler Measurements and Measurements and Main Results: Cerebrovascular resistance was calculated from Assessment of the cerebral perfusion pressure and middle cerebral artery blood flow velocity. Autoregulation. The strength of autoregulation index was calculated as the ratio of the percentage ■ Hypotensive of change in cerebrovascular resistance by the percentage of change in Challenge. cerebral perfusion pressure before and after 121 changes in mean arterial pressure ■ Hypertensive at constant ventilation between day 1 and day 18 after trauma. The strength Challenge. of autoregulation index varied widely, indicating either preserved or severely perturbed autoregulation during hypotensive or hypertensive challenge ● CONCLUSION in patients with or without intracranial hypertension at the basal state (strength ● ACKNOWLEDGMENT
● FOOTNOTES of autoregulation index, 0.51 ± 0.32 to 0.71 ± 0.25). The change in
● REFERENCES intracranial pressure varied linearly with the strength of autoregulation index. There was a clinically significant change in intracranial pressure (>=5 mm Hg) in Graphics the same direction as the change in mean arterial pressure in five tracings of three patients. This was caused by the mean arterial pressure dropping below the identified lower limit of autoregulation in three tracings for two patients.
● Table 1 It seemed to be caused by a loss of cerebral autoregulation in the remaining
● Figure 1 two tracings for one patient.
● Figure 2
● Figure 3 Conclusion: Cerebral perfusion pressure–oriented therapy can be a safe way to
● Figure 4 reduce intracranial pressure, whatever the status of autoregulation, in almost all patients with severe head injuries. http://ovidsp.tx.ovid.com/spb/ovidweb.cgi (2 of 17) [6/11/2008 5:32:34 PM] Ovid: Changes in intracranial pressure and cerebral autoregulation in patients with severe traumatic brain injury *.
The continuous infusion of catecholamines is commonly used to increase the mean arterial pressure (MAP) during management
of the cerebral hemodynamics of patients with severe head injury (1). It is intended to preserve cerebral blood flow
when intracranial hypertension (ICHT) compromises the cerebral perfusion pressure (CPP) and exposes the patient to the risk
of cerebral ischemia. Maintaining a high CPP can also help stabilize intracranial pressure (ICP) and prevent the so-
called vasodilatory cascade when the CPP is close to the lower limit of the autoregulation plateau (2, 3). An elevated CPP
generates an autoregulatory vasoconstriction that reduces cerebral blood volume and thereby ICP.
However, cerebral autoregulation is frequently altered after severe traumatic brain injury (4–8). Cerebral blood flow and
volume could thus fluctuate passively with changes in the MAP in these cases, and ICP should have the same profile.
Previous studies have shown a trend toward a passive increase in ICP when MAP increases in patients with disturbed
autoregulation (7). This deleterious effect on ICP could have important clinical consequences as the outcome for patients
with presumably perturbed autoregulation, hyperhemia, and ICHT is poor (9).
Patients may show different autoregulation profiles during postraumatic ICHT. The “optimal” MAP for the status of the patient
at any given time should therefore be regularly reconsidered. This is especially important when therapeutic systemic
hypertension is used to reduce ICP. This study was done to prospectively test autoregulation to verify the negative
correlation between changes in MAP and in ICP during the management of ICHT. We have also identified those cases in which such
a relationship was not verified, suggesting that increasing MAP would be detrimental.
MATERIAL AND METHODS Materials.
This study was approved by our local ethics committee and informed consent was obtained by the patients’ next of kin. We
studied 42 patients (31 male patients; age, 32 ± 17 yrs) with severe closed head injuries (Glasgow Coma Scale score, <=8)
and multifocal contusions or diffuse brain swelling confirmed by computed tomographic scans. Ten patients also had
multiple trauma. Any cerebral hematomas causing a significant mass effect were evacuated. ICP monitoring was performed
either via an intraventricular catheter or by intraparenchymal transducer (Codman, France). All patients laid supine with the
head tilted upward at 30 degrees. They were sedated with midazolam and morphine and were ventilated mechanically to
http://ovidsp.tx.ovid.com/spb/ovidweb.cgi (3 of 17) [6/11/2008 5:32:34 PM] Ovid: Changes in intracranial pressure and cerebral autoregulation in patients with severe traumatic brain injury *. achieve 100% arterial oxygen saturation and moderate hypocapnia (around 35 mm Hg). According to our routine
management protocol, patients who had a CPP of <70 mm Hg were given a continuous infusion of norepinephrine to maintain
their CPP above this threshold. Second-range therapy included mannitol and thiopental infusion.
The blood flow velocity of the middle cerebral artery (MCAv) was recorded unilaterally by pulsed Doppler ultrasound (2 MHz
probe, TC 2020 EME) on the side of the most injured hemisphere. The probe was secured in a special helmet placed in front of
the temporal window to obtain a constant angle. The following variables were recorded at 200 Hz (LabVIEW 5.0,
National Instrument, Austin, TX) and averaged every 4 secs: ICP, MAP (radial catheter), end-tidal CO2, and MCAv. All signals
were stored for off-line analysis.
Changes in Systemic Arterial Pressure.
Recordings were made during a formal test of cerebral autoregulation, which is a component of our routine evaluation of
patients treated for severe head injury in our intensive care unit. This test was performed as follows. Starting from a period
of steady state (T0), MAP was altered by introducing norepinephrine if the patient had not received this drug before or by
changing the norepinephrine infusion (increasing or decreasing the rate of infusion, depending on the CPP at T0). Once the CPP
had reached a new plateau, a second steady state period (T1) was maintained for 3 mins. The rate of norepinephrine infusion
was then maintained or modified, depending on the effect on ICP and CPP. However, if CPP decreased below 50 mm Hg
or increased over 150 mm Hg, steady state was abandoned and the CPP was promptly restored to around 70 mm Hg by adjusting
the norepinephrine infusion rate. One to three tests were carried out on each patient, waiting at least 1 day between tests.
Among the patients with multiple trauma, five were hemodynamically unstable. In them, we monitored ICP, MAP, and
MCAv continuously until stabilization was achieved.
Statistical Analysis.
Data were assigned to one of two groups, depending on the presence or absence of ICHT at the time of measurement, because
the intracranial volume storage capacity of patients may vary, which could dump changes in ICP during autoregulation tests.
The group labeled ICHT+ was defined by an ICP of >=20 mm Hg at T0, and the group named ICHT- was defined by an ICP of <20
mm Hg at T0.
An index of cerebrovascular resistance (CVRi) was calculated from MCAv as follows: CVRi = CPP/MCAv (10). The strength
http://ovidsp.tx.ovid.com/spb/ovidweb.cgi (4 of 17) [6/11/2008 5:32:34 PM] Ovid: Changes in intracranial pressure and cerebral autoregulation in patients with severe traumatic brain injury *. of autoregulation index (SARi) was then calculated as the ratio between the percentage of change in CVRi and the percentage
of change in CPP between T0 and T1 (SARi = [delta]CVRi %/[delta]CPP %) (11, 12).
Results are expressed as means ± sd. Differences between means were assessed by two-way analysis of variance for
repeated measurements. Linear regressions and statistical comparisons between slopes, Student’s t-test or the Mann-Whitney
rank-sum test were used as required (Sigma Stat, Jandel Scientific, Sausalito, CA). Individual ICP values at T0 and T1 were
plotted against MAP to define patients whose ICP varied significantly (>=5 mm Hg) in the same direction as the CPP change.
RESULTS
A total of 121 autoregulation tests were performed on 42 patients between day 1 and day 18 after trauma. Thirty-eight
patients were tested three times, three were tested twice, and one was tested once. In five patients, data provided
corresponded with the measurement of spontaneous changes in MAP in response to instability caused by the clinical condition of
the patient. Levels of MAP of <70 mm Hg required norepinephrine bolus in emergency and fluid loading. Apart from these
emergent cases, in all other patients, tests were performed formally by modulation of the dose of norepinephrine. The data
were split into 56 tests classified as ICHT+ and 65 as ICHT-. The groups were not different for the day of measurement, even
if there was a trend toward a measurement made earlier in the group ICHT+ (ICHT+: median, 4 days [quartiles, median, 25% to
75%; range, 2–7 days]; ICHT-: median, 7 days [25% to 75%; range, 3–10 days]). However, there was no difference in SARi
between groups, and we found no correlation between SARi and time (days after trauma). The number of hypertensive
and hypotensive challenges in the two groups were quite similar. SARi and mean values of the main variables at T0 and T1
during hypertensive and hypotensive challenges are shown in Table 1.
Table 1. Mean values ± sd of the variables measured before (T0) and after (T1) hypotensive and hypertensive challenge and
the corresponding calculated strength of autoregulation (SARi)Etco2, endtidal CO2; ICP, intracranial pressure; MAP, mean arterial pressure; CPP, cerebral perfusion pressure; MCAv, middle cerebral artery blood flow velocity; ICHT, group without [Help with image viewing] intracranial hypertension at T0 (ICP <20 mm Hg); ICHT+, group with intracranial hypertension at T0 (ICP >=20 mm Hg). [Email Jumpstart To Image]
For group ICHT-, [delta]ICP was correlated with SARi during both hypotensive and hypertensive challenges (n = 29, r2 = .14, and
p = .05 for hypotensive challenge; n = 36, r2 = .13, and p = .05 for hypertensive challenge). Similarly, in group ICHT+, [delta]ICP http://ovidsp.tx.ovid.com/spb/ovidweb.cgi (5 of 17) [6/11/2008 5:32:34 PM] Ovid: Changes in intracranial pressure and cerebral autoregulation in patients with severe traumatic brain injury *.
was correlated with SARi during both hypotensive and hypertensive challenges (n = 26, r2 = .56, p = .001; and n = 30, r2 = .26,
p = .01; respectively) (Fig. 1). The slopes of the regression lines between [delta]ICP and SARi in the ICHT+ and ICHT- groups
differed significantly during both the hypotensive challenge (p = .01) and the hypertensive challenge (p = .05). Only five tracings
in three patients showed a significant [delta]ICP of >=5 mm Hg in the same direction as the MAP change (Fig. 2). All these
patients had increased MCAv of over 100 cm/sec, suggesting a vasospasm or hyperhemia (13). The MAP range explored in
three tracings of two of these patients was below the lower limit of cerebral vascular reactivity, as assessed by the decrease in
ICP when MAP was raised during the hypertensive challenge (Fig. 3). We could define no MAP threshold for cerebral
vascular reactivity in the remaining two tracings of one patient (Fig. 4).
Figure 1. Cerebral autoregulation tests: correlation between intracranial pressure variations ([delta]ICP) and the strength of autoregulation index (SARi). Top left, group without intracranial hypertension at basal state (ICHT-), hypotensive challenge ([delta]ICP = 6.37 SARi - 0.47). Top right, group without intracranial hypertension at basal state (ICHT-), hypertensive challenge ([delta]ICP = -3.68 SARi + 1.20). Bottom left, group with intracranial hypertension at basal state (ICHT+), hypotensive challenge ([delta]ICP = 24.4 SARi - 11.2). Bottom right, group with intracranial hypertension at basal state (ICHT+), hypertensive challenge ([delta]ICP = -10.1 SARi + 1.11). Solid lines, linear regressions;inner dashed lines, 95% confidence intervals of the regression;outer dashed lines, 95% predictions intervals. [Help with image viewing] [Email Jumpstart To Image]
Figure 2. Cerebral autoregulation tests: plots of absolute intracranial pressure (ICP) against mean arterial pressure (MAP) before and after changes. Points with low MAP values correspond to the recording of unstable patients. Top graphs, group without intracranial hypertension at basal state (ICHT-). Lower graphs, group with intracranial hypertension at basal state (ICHT +). Left graphs, hypotensive challenge. Right graphs, hypertensive challenges. Filled circles and dashed lines, autoregulation test with a change in ICP of >=5 mm Hg in the same direction as the MAP change;unfilled circles and solid lines, autoregulation tests with opposite MAP and ICP change or ICP changes of <5 mm Hg.
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Figure 3. Unstable patients. Identification of the lower cerebral perfusion pressure for cerebral vasoreactivity in two of the three patients having an intracranial pressure (ICP) change of >=5 mm Hg in the same direction as the change in mean arterial pressure (MAP). In hypertensive challenge, the correlation between ICP and MAP has a curvilinear relationship; above a given MAP, ICP decreases with increasing MAP, indicating restitution of cerebral autoregulatory vasoreactivity.
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Figure 4. Unstable patient. Relationship between intracranial pressure (ICP) and mean arterial pressure (MAP) in the single patient for whom no lower cerebral perfusion pressure limit for cerebral vasoreactivity was identified. Top, hypotensive challenge;bottom, hypertensive challenge. The relationship between ICP and MAP was linear during both challenges, indicating a passive change in ICP with MAP variations up to a CPP of about 75 mm Hg.
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DISCUSSION
Our findings confirm that the direction and amplitude changes in ICP caused by a change in MAP seemed to depend on the status
of autoregulation when MAP changes in patients with or without basal state ICHT. This is in agreement with the findings reported
by Bouma et al (7). They found a trend to an opposite change in ICP and MAP during an autoregulation test in patients with
intact and impaired autoregulation. They recommended that therapeutic hypertension should only be attempted after a
thorough assessment of the cerebrovascular status of autoregulation. Perturbations of autoregulation are common in patients
with head trauma (4–8), and CPP therapy could be theoretically extended to a large number of patients. Our study confirms
this paradigm. Some methodologic issues warrant additional comment.
Validity of Transcranial Doppler Measurements and Assessment of Autoregulation.
Cerebral autoregulation is generally defined as the maintenance of constant CBF over a wide range of CPP by active changes in
the diameter of the pial and cortical arteries (14, 15). However, the lower limit of autoregulation does not necessarily
correspond to the state of maximal vasodilation but rather to a fall in CPP that is larger than that of CVR. This imbalance results http://ovidsp.tx.ovid.com/spb/ovidweb.cgi (8 of 17) [6/11/2008 5:32:34 PM] Ovid: Changes in intracranial pressure and cerebral autoregulation in patients with severe traumatic brain injury *.
in a decreased CBF, as demonstrated by MacKenzie et al (15). They showed that the maximal vasodilation and decreased
CVR occurred below the lower limit of autoregulation. Thus, variations in CBF parallel to changes in CPP do not necessarily
mean the loss of cerebrovascular reactivity. This is the theoretical justification for quantifying autoregulation by the
formal percentage of change in CVR per percentage of change in CPP, rather than describing it as defective or intact, as
proposed by several authors. We chose to use SARi, which derives from the static cerebral autoregulation index proposed by
Tiecks et al (12). According to these authors and also to Lee et al. (16), when the static cerebral autoregulation equals zero,
there is no autoregulation. The value of 1 corresponds to a “perfect” autoregulation. Values of >0.7 indicate an
intact autoregulation. These authors did not include ICP in equations used to assess of autoregulation and only relied on MAP,
thus accepting to neglect the potential role of ICP on CPP variations. However, in patients with head injury with
increased intracranial elastance, one expects ICP to vary in response to changes in MAP as a consequence of the
autoregulatory modification of cerebral vascular resistance and volume. Enevoldsen and Jensen (5) were the first authors
who reported on the “false autoregulation.” They clearly stated that in patients with acute head inury, autoregulation is
measured as paradoxically preserved in some patients. This results from a rise in ICP, which dumps CPP-induced variations after
a rise in MAP. This is one reason why we chose to include in our study CPP in equations accepting the possibility of
mathematic coupling between ICP variations and SARi. In this way, we followed Bouma et al. (7) and Rosner et al. (1),
who suggested that changes in ICP after variations of MAP can depend on the status of autoregulation. This concept, although
not formally demonstrated, includes mathematic coupling per se. We aimed to purposely assess this issue by adapting
previous static cerebral autoregulation index to include CPP, thus anticipating the possible confounding effect of coupling for
the sake of avoiding the false autoregulation principle. The magnitude of error resulting from coupling cannot be modeled.
Raw data shown in Figures 2–4 allow analysis of the two main variables, namely ICP and MAP, which are not coupled.
We have used transcranial Doppler (TCD) measurement of MCAv instead of true CBF measurements to calculate CVRi. Variations
in flow velocity remain proportional to variations in flow as long as the cross-sectional area of the insonated artery
remains constant. This is generally believed to be true, as pial and cortical arteries—the effectors of autoregulation—are
located downstream of the circle of Willis. Several authors have compared variations in internal carotid blood flow and MCAv
during nonpharmacologic alterations in MAP (17, 18). The correlation was very close, indicating that any change in MCA
cross-sectional area must have been minor. It has also been shown by comparison of TCD with CBF measurement (Fick) that TCD
is valid for static measurement of cerebral autoregulation (19).
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However, we caused pharmacologic changes. The norepinephrine could have caused a direct constriction of the cerebral
arteries and arterioles and thus invalidated our TCD measurements. The intracarotid infusion of epinephrine and
norepinephrine does not influence the regional CBF in humans nor do these drugs change the diameter of the larger arteries
as shown by angiography (20). Furthermore, norepinephrine is unlikely to have a direct effect on the cerebral vasculature
because catecholamines do not cross the blood-brain barrier (21). The estimates of autoregulation from changes in MCAv caused
by pharmacologic and nonpharmacologic variations in MAP were shown to be identical (11, 12). However, the question of
the integrity of the blood-brain barrier after traumatic brain injury is important when using catecholamines; as in the case of
a broken blood-brain barrier, catecholamines could act, in theory, on cerebral vasculature. There are few published data, but
some recent studies indicate that the blood-brain barrier is not broken down a few hours after trauma (22–25), so
pharmacologic vasoconstriction is unlikely to affect our TCD estimation of SARi in patients with head injury. Hence, the mean
value and the wide range of SARi in our patients agree with the studies demonstrating that autoregulation could be either
preserved or severely impaired after severe head injury.
It is noteworthy that autoregulation of our patients may have been enhanced by hypocapnia (4), but possibly with differences
in magnitude among patients. Indeed, we could not disclose possible differences in the level of “effective
hyperventilation” between patients because the pH of cerebrospinal fluid is known to normalize after several days
of hyperventilation (26) and because we performed measurements in the acute period, but at times that were not standardized,
as did Rosner et al (1).
The physiopathology of cerebral hemodynamics after severe head injury is time dependent if one considers the whole
clinical evolution from injury to the resolution of cerebral edema (5). The question of knowing if our study was performed
between the first and the 18th day after trauma could disclose time-dependent differences in cerebrovascular status may be
raised. There was no difference between groups (ICHT+ and ICHT-) for the days of measurement, and we did not find
any correlation between SARi and time after trauma. Thus, groups are to be comparable in terms of time dependency,
and therefore, it was logical to stratify data on ICP, which is believed to reflect clinical severity, rather than on time
(27). Considering the number of tests performed in each patient, 90% of patients were studied three times. Thus,
the interdependency of results from multiple measurement in a single patient is probably minimal.
There are several reasons why cerebral vasoreactivity should be impaired. First, hypotension or increased ICP could decrease http://ovidsp.tx.ovid.com/spb/ovidweb.cgi (10 of 17) [6/11/2008 5:32:35 PM] Ovid: Changes in intracranial pressure and cerebral autoregulation in patients with severe traumatic brain injury *.
CPP below the lower limit of autoregulation. The cerebral hemodynamic phases of hyperhemia and possibly vasospasm that
follow an initial posttraumatic hypoperfusion state (28) are generally accompanied by altered autoregulation (29–31). Hyperhemia
is common and is primarily observed in structurally normal brain tissue adjacent to a contusion (32); it could be caused by
cerebral hyperglycolysis (33). The status of cerebral vascular reactivity during hyperhemia remains unclear. It has been
postulated that hyperhemia is caused by increased cerebral metabolic demand in a state of intact vasoreactivity in the majority
of patients (34).
Vasospasm caused by a traumatic subarachnoid hemorrhage is also frequent in patients with severe head injury, and it is
associated with defective autoregulation. However, autoregulation is not abolished in vasospasm, but its lower limit is
shifted toward higher values of CPP, as reflected by the finding that CO2 reactivity reappears when MAP is increased above
the lower limit of the autoregulation plateau (35). Thus, all qualitative or quantitative analyses of the status of
autoregulation should be done bearing in mind that findings within a finite range of CPP do not necessarily reflect the
cerebral vasculature capacity to react to changes in transmural pressure in another range of CPP. In the same way, the
SARi calculated from a range of CPP that includes the autoregulation limits will not reflect the cerebral vasoreactive
capacity within the optimal range of CPP.
In contrast to the correlation we find between [delta]ICP and SARi, clinically significant changes in ICP of >=5 mm Hg in the
same direction as the change in MAP caused by impaired autoregulation seem to be rare. Rapid changes in ICP in response
to changes in MAP depend on changes in cerebral blood volume. As the venous blood volume is believed to be the largest
cerebral vascular compartment (36), a small percentage of change in cerebral venous blood volume could critically
influence changes in ICP. Reciprocal changes in cerebral venous blood volume could be damped by simultaneous changes in
ICP caused by autoregulatory change in arteriolar blood volume as a consequence of a Starling resistor mechanism within
the bridging veins (37). This mechanism tends to keep the venous transmural pressure and the venous blood volume more or
less constant over a wide range of ICP.
Autoregulation could also be unevenly affected in patients with severe head injury when there are areas of intact parenchyma
and others with disturbed autoregulation. Lastly, the magnitude of changes in ICP is not affected by the absolute change in
cerebral blood volume alone, but also by the intra-cranial storage capacity that buffers blood volume and then damps changes
in ICP and by the cerebrospinal fluid outflow resistance (38). Increased cerebrospinal fluid outflow resistance is common in http://ovidsp.tx.ovid.com/spb/ovidweb.cgi (11 of 17) [6/11/2008 5:32:35 PM] Ovid: Changes in intracranial pressure and cerebral autoregulation in patients with severe traumatic brain injury *.
head trauma (39, 40) and can contribute to an increase in ICP at stable state (38) or to the generation of ICP plateau waves (2)
via an autoregulatory mechanism similar to the vasodilatory cascade described by Rosner et al (1).
As all these factors interact in a nonlinear fashion, changes in ICP during changes in MAP when autoregulation is disturbed
are unlikely to be predictable. This makes it reasonable to routinely assess autoregulation in patients with severe head trauma.
We find a weaker correlation between [delta]ICP and SARi in patients in group ICHT- than in group ICHT+ during both
hypotensive and hypertensive challenge. As the magnitude of the changes in MAP and SARi values in the two groups were
similar, the main difference between the ICHT- and ICHT+ groups is probably caused by a greater intracranial storage capacity
and a lower cerebrospinal fluid outflow resistance in the patients in group ICHT-.
Hypotensive Challenge.
Although the patients classified as ICHT- probably had a greater intracranial storage capacity and lower cerebrospinal fluid
outflow resistance, a hypotensive challenge caused a significant ICHT of >=20 mm Hg in nine patients (Fig. 2). This value of ICP
is generally the threshold that requires therapeutic intervention. There was no significant reduction in ICP (>=5 mm Hg) in
this subgroup, whatever the status of autoregulation (Fig. 1). Similarly, a hypotensive challenge caused a dramatic increase in
ICP in those ICHT+ patients with the greatest SARi, whereas there was no significant increase in ICP when SARi was <0.7 (Fig. 1).
In contrast, there was a significant reduction in ICP (>=5 mm Hg) in three patients in the ICHT+ group during hypotensive
challenge (Fig. 2). The SARi varied widely in these patients (from 0 to 0.68). However the absolute CPP fell to <40 mm Hg. Such
a low value of CPP is generally considered to be associated with cerebral hypoperfusion. Crossing the lower CPP limit
of cerebrovascular reactivity also occurred after restitution of CPP in two of these patients. This threshold was found for a CPP
of 40–60 mm Hg and a MAP of around 100 mm Hg in the two cases (Fig. 3, middle and bottom). Thus, the observed reduction in
ICP obviously cannot be considered to be an indicator of improved cerebral hemodynamics. The decrease in ICP in these
situations indicates a collapse of the cerebral vascular bed, and this reduces cerebral blood volume and improves
intracranial storage capacity before cerebral circulatory arrest (41). ICP was not reduced when CPP fell far below 70 mm Hg in
all the other cases in which SARi values indicated a disturbed autoregulation to <0.5. This supports the fact that there are
probably few if any variations in cerebral venous blood volume caused by the Starling resistor mechanism, even
when autoregulation is disturbed. In these cases, the modest decrease in the resistances of pial and cortical arteries is probably
the main factor contributing to changes in CBV and ICP. http://ovidsp.tx.ovid.com/spb/ovidweb.cgi (12 of 17) [6/11/2008 5:32:35 PM] Ovid: Changes in intracranial pressure and cerebral autoregulation in patients with severe traumatic brain injury *.
Hypertensive Challenge.
There was no significant increase in ICP in the ICHT- patients during hypertensive challenge. The change in ICP were more
sustained in patients in the ICHT+ group, and the ICP increased by >=5 mm Hg in two patients with poor autoregulation.
However, the lower limit of cerebral vascular reactivity to increasing CPP was 55 mm Hg in one patient, as assessed by the
decrease in ICP over this threshold (Fig. 3, top). We were unable to identify a threshold for vascular reactivity up to a MAP of
110 mm Hg and a corresponding CPP of 75 mm Hg in one patient (who also showed a decrease in ICP during hypotensive
challenge) (Fig. 4). This does not mean that a further increase in MAP should not have reached such a threshold. However,
we maintained a CPP of 60–70 mm Hg in this patient because of the linear relationship between ICP and MAP and because it
was impossible to further increase MAP. We saw no significant rise in ICP in any of the other patients with SARi values of <0.5.
These results are in accordance with those of Rosner et al. (1), who showed that autoregulation is damped and shifted to
higher CPP values in the majority of patients with head trauma. They support the view that a passive response of ICP to MAP
is mainly limited to CPP values at which cerebral autoregulation has not yet become effective.
CONCLUSION
Despite the correlation we find between the status of autoregulation and the direction and magnitude of changes in ICP, our
data indicate that an alteration of autoregulation does not generally cause a significant change in the expected
qualitative relationship between ICP and MAP during CPP management of patients with severe head injury. Hypotension
can especially induce a large rise in ICP, even in patients with poor autoregulation and without ICHT at the basal state. On
the other hand, the systematic performance of a hypertensive challenge can identify patients whose threshold for
cerebrovascular reactivity is shifted toward higher values. CPP management over the range we explored can thus be a safe way
of reducing ICP in almost all patients with severe head injury, whatever their status of autoregulation. Data indicate that
an alteration of autoregulation does not generally cause a significant change in the expected qualitative relationship between
ICP and MAP during CPP management of patients with severe head injury.
ACKNOWLEDGMENT
We thank Dr. Bruno Vielle, Department of Biostatistics, CHU d’Angers, France, for his methodologic support.
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*See also p. 1671. [Context Link]
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Key Words: head injury; cerebral autoregulation; intracranial pressure; cerebral perfusion pressure; cerebral blood flow velocity
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