Pressure reactivity as a guide in the treatment of cerebral perfusion pressure in patients with brain trauma (original) (raw)
Related papers
Critical Care Medicine, 2002
C erebrovasCular pressure reactivity reflects the capability of smooth muscle tone in the walls of cerebral arteries and arterioles to react to changes in transmural pressure (cerebral vessels constrict in response to an increase in CPP, and vice versa). Cerebro-vascular pressure reactivity represents a key element of cerebral autoregulation, although the two terms should not be used interchangeably because vascular responses can occur outside the range of cerebral autoregulation. 7,25 With increasing ABP, intact cerebrovascular pressure reactivity will lead to vasoconstriction and a reduction of cerebral blood volume. Under the condition of a finite pressure-volume compensatory reserve, this reduction of cerebral blood volume will produce a decrease in ICP, a condition that is usually not met in patients after a decompressive craniectomy or in those with an external ventricular drain. When cerebrovascular pressure reac
Continuous determination of optimal cerebral perfusion pressure in traumatic brain injury*
Critical Care Medicine, 2012
S urvival after traumatic brain injury (TBI) is dependent on the control of intracranial hypertension and the provision of hemodynamic support to achieve an "adequate" cerebral perfusion pressure (CPP). However, the idea of a single value (or even a single range) of CPP being adequate for the diverse group of TBI patients is an oversimplification (1-3). Age and premorbid arterial blood pressure (ABP) are examples of factors likely to influence individual CPP targets, with elderly, hypertensive patients requiring a higher CPP compared with young, normotensive patients. Although multimodal brain monitoring, including continuous brain-tissue oxygenation, near infrared spectroscopy, transcranial Doppler ultrasonography, and microdialysis provide valuable information at the bedside regarding the adequacy of CPP, these technologies are costly and restricted to a relatively small number of specialized neurocritical care units. The 2007 Brain Trauma Foundation guidelines advocated randomized controlled trials to verify the feasibility and the impact on outcome of strategies based on individualized CPP management following severe TBI (4). A method for individualization of CPPoriented management based on determination of cerebrovascular reactivity Objectives: We have sought to develop an automated methodology for the continuous updating of optimal cerebral perfusion pressure (CPP opt ) for patients after severe traumatic head injury, using continuous monitoring of cerebrovascular pressure reactivity. We then validated the CPP opt algorithm by determining the association between outcome and the deviation of actual CPP from CPP opt .
JAMA Neurology, 2020
IMPORTANCE Intracranial pressure (ICP) elevation is a compartment syndrome that impairs blood flow to the brain. Despite the importance of ICP values in neurocritical care, normal ICP values and the precise ICP threshold at which treatment should be initiated remain uncertain. OBJECTIVE To refine our understanding of normal ICP values and determine the ICP threshold most strongly associated with outcome. DESIGN, SETTING, AND PARTICIPANTS Prospective observational study (2004-2010), with outcomes determined at hospital discharge. The study included neurocritical care patients from a single level I trauma center, San Francisco General Hospital. Three hundred eighty-three patients had a traumatic brain injury with or without craniectomy; 140 patients had another indication for ICP monitoring. Consecutive patients were studied. Data analyses were completed between March 2015 and December 2019. EXPOSURES Five hundred twenty-three ICP-monitored patients. MAIN OUTCOMES AND MEASURES A computer system prospectively and automatically collected 1-minute physiologic data from patients in the intensive care unit during a 6-year period. Mean ICP was calculated, as was the proportion of ICP values greater than thresholds from 1 to 80 mm Hg in 1-mm Hg increments. The association between these measures and outcome was explored for various epochs up to 30 days from the time of injury. A principal component analysis was used to explore physiologic changes at various ICP thresholds, and elastic net regression was used to identify ICP thresholds most strongly associated with Glasgow Outcome Scale score at discharge. RESULTS Of the 523 studied patients, 70.7% of studied patients were men (n = 370) and 72.1% had a traumatic brain injury (n = 377). A total of 4 090 964 1-minute ICP measurements were recorded for the included patients (7.78 years of recordings). Intracranial pressure values of 8 to 9 mm Hg were most commonly recorded and could possibly reflect normal values. The principal component analysis suggested state shifts in the physiome occurred at ICPs greater than 19 mm Hg and 24 mm Hg. Elastic net regression identified an ICP threshold of 19 mm Hg as most robustly associated with outcome when considering all neurocritical care patients, patients with TBI, and patients with TBI who underwent craniectomy. Intracranial pressure values greater than 19 mm Hg were associated with mortality, while lower values were associated with outcome in surviving patients. CONCLUSIONS AND RELEVANCE This study provides insight into what normal ICP values could be. An ICP threshold of 19 mm Hg was robustly associated with outcome in studied patients, although lower ICP values were associated with outcome in surviving patients.
Critical Care Medicine, 2002
Background: Impaired cerebral autoregulation is frequent after severe traumatic head injury. This could result in intracranial pressure fluctuating passively with the mean arterial pressure. Objective: This study examines the influence of autoregulation on the amplitude and direction of changes in intracranial pressure in patients with severe head injuries during the management of cerebral perfusion pressure. Design: Prospective study. Setting: Neurosurgical intensive care unit Patients: A total of 42 patients with severe head injuries. Interventions: Continuous recording of cerebral blood flow velocity, intracranial pressure, and mean arterial pressure during the start or change of continuous norepinephrine infusion. Measurements and Main Results: Cerebrovascular resistance was calculated from the cerebral perfusion pressure and middle cerebral artery blood flow velocity. The strength of autoregulation index was calculated as the ratio of the percentage of change in cerebrovascular resistance by the percentage of change in cerebral perfusion pressure before and after 121 changes in mean arterial pressure at constant ventilation between day 1 and day 18 after trauma. The strength of autoregulation index varied widely, indicating either preserved or severely perturbed autoregulation during hypotensive or hypertensive challenge in patients with or without intracranial hypertension at the basal state (strength of autoregulation index, 0.51 ؎ 0.32 to 0.71 ؎ 0.25). The change in intracranial pressure varied linearly with the strength of autoregulation index. There was a clinically significant change in intracranial pressure (>5 mm Hg) in 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. It seemed to be caused by a loss of cerebral autoregulation in the remaining two tracings for one patient. Conclusion: Cerebral perfusion pressure-oriented therapy can be a safe way to reduce intracranial pressure, whatever the status of autoregulation, in almost all patients with severe head injuries.
Pressure Reactivity-Based Optimal Cerebral Perfusion Pressure in a Traumatic Brain Injury Cohort
Acta neurochirurgica. Supplement, 2018
Retrospective data from patients with severe traumatic brain injury (TBI) indicate that deviation from the continuously calculated pressure reactivity-based "optimal" cerebral perfusion pressure (CPPopt) is associated with worse patient outcome. The objective of this study was to assess the relationship between prospectively collected CPPopt data and patient outcome after TBI. We prospectively collected intracranial pressure (ICP) monitoring data from 231 patients with severe TBI at Addenbrooke's Hospital, UK. Uncleaned arterial blood pressure and ICP signals were recording using ICM+ software on dedicated bedside computers. CPPopt was determined using an automatic curve fitting procedure of the relationship between pressure reactivity index (PRx) and CPP using a 4-h window, as previously described. The difference between an instantaneous CPP value and its corresponding CPPopt value was denoted every minute as ΔCPPopt. A negative ΔCPPopt that was associated with impair...
Measurement and Management of Increased Intracranial Pressure
The Open Critical Care Medicine Journal, 2013
Increased intracranial pressure (ICP) is a serious complication of a variety of neurologic injuries and is a major challenge in intensive care units. The most common causes of increased ICP are: traumatic brain injury (TBI), stroke, neoplasms, hydrocephalus, hepatic encephalopathy, CNS venous return impairment, encephalitis, and abscesses. Prompt diagnosis and intensive monitoring and therapy of this condition are essential for successful management of this potentially devastating condition. Recent technical innovations in neuromonitoring may allow for improvement in morbidity and mortality rates attributable to elevated ICP. Normal ICP ranges from 3-15 mmHg. In routine intensive care unit (ICU) practice, the goal of ICP management is to maintain levels below 20 mmHg. Noninvasive and metabolic monitoring of ICP including imaging-clinical examination has been studied and suggested to be as efficient as the care based on invasive ICP monitoring; however its application in clinical practice is to be established. Raised intracranial pressure correlates with decreased survival and is often the only remediable element of brain pathology. While elimination of the cause of elevated ICP remains the definitive approach, there are maneuvers that should be used to decrease ICP urgently. Surgical decompression of mass effect may rapidly improve ICP elevation. Osmolar therapy, maintenance of euvolemia, cerebral metabolic suppression, and temperature control are part of the advanced management of elevated ICP.
Intracranial pressure monitoring
Anaesthesia, Pain, Intensive Care and Emergency Medicine — A.P.I.C.E.
Brain injury is the result of both primary and secondary damage, yielded by a complex range of factors including ischemia, biochemical changes and inflammatory cascade. Secondary brain injury may be caused by systemic or intracranial mechanisms including oligaemia due to low cerebral perfusion pressure (CPP) or increased cerebral vascular resistance (vascular distortion or cerebro-vascular narrowing), hypoxemia (airway obstruction, pulmonary pathology or anaemia), intracranial hypertension and changes of brain metabolic rate. Furthermore, secondary insults cause tissue damage according to their nature, severity and duration, making their early detection and correction an essential step of management. Several neuroprotective agents have been introduced in the past two decades, but, despite their potential effectiveness, the results have been disappointing; therefore, the current basis for prevention of secondary brain damage remains prevention and correction of secondary insults. While nowadays several techniques are available for monitoring severely head-injured patients, monitoring intracranial pressure (ICP) still plays a key role, providing essential information for further decision making.