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Changes in Intracranial Pressure and Cerebral Autoregulation in Patients with Severe Traumatic Brain Injury *

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Changes in Intracranial Pressure and Cerebral Autoregulation in Patients with Severe Traumatic Brain Injury * Ovid: Changes in intracranial pressure and cerebral autoregulation in patients with severe traumatic brain injury *. Main Search Page Ask A LibrarianDisplay Knowledge BaseHelpLogoff Full Text Save Article TextEmail Article TextPrint Preview 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
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