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  • 1. CLINICAL STUDIESGregory M. Weiner, BADepartment of Neurosurgery,University of Pennsylvania School ofMedicine,Philadelphia, Pennsylvania Decompressive Craniectomy for ElevatedMichelle R. Lacey, PhDDepartment of Mathematics,Tulane University, Intracranial Pressure and Its Effect on theNew Orleans, Louisiana Cumulative Ischemic Burden and TherapeuticLarami Mackenzie, MDDepartment of Neurology,University of Pennsylvania School of Intensity Levels After Severe Traumatic Brain InjuryMedicine,Philadelphia, Pennsylvania BACKGROUND: Increased intracranial pressure (ICP) can cause brain ischemia and com-Darshak P. Shah, BA, BS promised brain oxygen (PbtO2 ≤ 20 mm Hg) after severe traumatic brain injury (TBI).Department of Neurosurgery,University of Pennsylvania School of OBJECTIVE: We examined whether decompressive craniectomy (DC) to treat elevated ICPMedicine, reduces the cumulative ischemic burden (CIB) of the brain and therapeutic intensity level (TIL).Philadelphia, Pennsylvania METHODS: Ten severe TBI patients (mean age, 31.4 ± 14.2 years) who had continuousSuzanne G. Frangos, RN, CNRN PbtO2 monitoring before and after delayed DC were retrospectively identified. PatientsDepartment of Neurosurgery,University of Pennsylvania School of were managed according to the guidelines for the management of severe TBI. The CIB wasMedicine, measured as the total time spent between a PbtO2 of 15 to 20, 10 to 15, and 0 to 10 mm Hg.Philadelphia, Pennsylvania The TIL was calculated every 12 hours. Mixed-effects models were used to estimate changesM. Sean Grady, MD associated with DC.Department of Neurosurgery,University of Pennsylvania School of RESULTS: DC was performed on average 2.8 days after admission. DC was found to imme-Medicine, diately reduce ICP (mean [SEM] decrease was 7.86 mm Hg [2.4 mm Hg]; P = .005). TIL, whichPhiladelphia, Pennsylvania was positively correlated with ICP (r = 0.46, P ≤ .001), was reduced within 12 hours afterAndrew Kofke, MD surgery and continued to improve within the postsurgical monitoring period (P ≤ .001).Department of Anesthesiology and The duration and severity of CIB were significantly reduced as an effect of DC in this group.Critical Care,University of Pennsylvania School of The overall mortality rate in the group of 10 patients was lower than predicted at the timeMedicine, of admission (P = .015).Philadelphia, Pennsylvania CONCLUSION: These results suggest that a DC for increased ICP can reduce the CIB of theJoshua Levine, MD brain after severe TBI. We suggest that DC be considered early in a patient’s clinical course,Departments of Neurosurgery, Neurology,and Anesthesiology and Critical Care, particularly when the TIL and ICP are increased.University of Pennsylvania School of KEY WORDS: Craniectomy, Ischemia, TraumaMedicine,Philadelphia, Pennsylvania Neurosurgery 66:1111-1119, 2010 DOI: 10.1227/01.NEU.0000369607.71913.3E www.neurosurgery-online.comJames Schuster, MD, PhD TDepartment of Neurosurgery,University of Pennsylvania School of raumatic brain injury (TBI) is a leading ment to maintain ICP ≤ 20 mm Hg, to optimizeMedicine, cause of death and disability among people cerebral perfusion pressure (CPP), and to pre-Philadelphia, Pennsylvania of all ages. Intracranial hypertension, par- vent secondary cerebral injury—is central to TBIPeter D. Le Roux, MD ticularly when it does not respond to maximal management.8-10 Today, many neurointensiveDepartment of Neurosurgery, medical management, increases the risk of mor- care units (NICUs) also use multimodality mon-University of Pennsylvania School ofMedicine, tality and poor outcome. 1-7 Marmarou et al 4 itoring, eg, brain oxygen (PbtO2), continuousPhiladelphia, Pennsylvania observed a significant association between poor electroencephalogram, or microdialysis, to helpReprint requests: outcome and the number of hourly intracranial prevent secondary brain injury. In addition,Peter D. LeRoux, MD, pressure (ICP) values that were > 20 mm Hg. advances in computer technology and the use ofDepartment of Neurosurgery, Consequently, ICP control—-specifically treat- derived ICP indexes suggest that ICP is a complexClinical Research Division,University of Pennsylvania Medical Center, ABBREVIATIONS: APACHE II, Acute Physiology and parameter that, when carefully analyzed, con-Philadelphia, PA 19104. Chronic Health Evaluation; CIB, cumulative ischemic tains information about cerebral compensatoryE-mail: mechanisms and mechanisms that contribute to burden; CBF, cerebral blood flow; CPP, cerebral per-Received, March 12, 2009. fusion pressure; DC, decompressive craniectomy; cerebral blood flow (CBF) regulation.11-14Accepted, December 5, 2009. ICP, intracranial pressure; NICU, neurointensive care The concept of cerebral compensatory reserve unit; TBI, traumatic brain injury; TIL, therapeutic is important. We have observed that cerebralCopyright © 2010 by the intensity levelCongress of Neurological Surgeons infarction and poor outcome may occur even ifNEUROSURGERY VOLUME 66 | NUMBER 6 | JUNE 2010 | 1111
  • 2. WEINER ET ALelevated ICP is successfully treated after severe TBI15 and that this Intracranial Monitoringdepends in part on the cerebral arteriovenous difference of oxygen. ICP (Camino®, Integra Neurosciences, Plainsboro, NJ), brainDerived ICP indexes, eg, cerebrovascular reactivity and cere- temperature, PbtO2 (LICOX®, Integra Neuroscience), and bloodbrospinal compensatory reserve, provide an insight into a patient’s pressure (arterial line) were monitored continuously. CPP wasreserve or how sick the brain is.11-14 A patient with an ICP of 20 calculated (CPP = MAP − ICP, where MAP is mean arterial pres-mm Hg and impaired cerebrospinal compensatory reserve or cere- sure). Intraparenchymal probes (ICP, brain temperature, andbrovascular reactivity index is at much greater risk than a patient PbtO2) were inserted at the bedside in the NICU through a burrwith the same ICP but normal indexes and ICP waveform. These hole into the frontal lobe and secured with a triple-lumen bolt.pathophysiological differences may be reflected in the therapeu- The monitors were placed into white matter that appeared normaltic intensity level (TIL), a quantitative measure of the manage- on admission head computed tomography (CT) and on the sidement required to control ICP.16 The greater the TIL is, the more of maximal pathology. When there was no asymmetry in braintherapy is required and the more complex the therapy needs to pathology on CT, the probes were placed in the right frontalbe to control ICP (ie, the “sicker” the patient). This information region. Follow-up head CT scans were performed in all patientsis important because every aspect of ICP or CPP management within 24 hours of admission to confirm correct placement of thehas potential deleterious side effects.7,17-22 Thus, selecting a ther- various monitors, eg, not in a contusion or infarct. Probe func-apy for elevated ICP or impaired CPP that does not cause extracra- tion and stability were confirmed by an appropriate PbtO2 increasenial complications, eg, lung injury, is critical.19 after an oxygen challenge (FIO2 of 1.0 for 5 minutes; final PbtO2 When cerebral compensation is impaired, an escalating cycle value after 5–10 minutes > 20 mm Hg). To allow for probe equi-of energy failure, edema, reduced substrate delivery, and further libration, data from the first 3 hours after PbtO2 monitor insertionICP increase may occur despite optimal medical management. In were discarded. ICP and PbtO2 monitors were removed once thethese patients, decompressive craniectomy (DC) is frequently used ICP was normal (≤ 20 mm Hg) without treatment (other thanto control elevated ICP.23-31 In recent years, there has been a resur- sedation for ventilator management) for > 24 hours or care was with-gence in the use of DC after severe TBI, and currently, 2 random- drawn because of injury severity.ized trials to examine its efficacy are underway (RescueICP32 andDECRA33). It is well known that DC can reduce ICP,28,29,34-37 but General Clinical Managementthe exact timing of when to perform DC is only beginning to be All patients were managed in the NICU according to a localelucidated. In addition, it is hypothesized that DC interrupts the algorithm consistent with the Brain Trauma Foundation TBI guide-cascade of ICP elevation, leading to cerebral ischemia and delayed lines.8,26,43 Each patient was fully resuscitated according to advancedneuronal injury. However, the relationship between ICP and cere- trauma life support guidelines, intubated, and mechanically ven-bral ischemia is not straightforward.15,38-42 In this study, we exam- tilated with the head of bed initially elevated approximately 20°ined how DC influenced the TIL and PbtO2. We used PbtO2 to 30°. FIO2 and minute ventilation were adjusted to maintainvalues to estimate a cumulative ischemic burden (CIB). We hypoth- SaO2 > 93%, PaO2 of 90 to 100 mm Hg, and PaCO2 of 34 to 38esized that DC would decrease ICP and TIL while reducing the mm Hg. Volume resuscitation was achieved with 0.9% normalCIB in a sustained manner. saline and albumin for a target central venous pressure of 6 to 10 cm H2O. Therapeutic targets were adjusted to avoid ICP > 20MATERIAL AND METHODS mm Hg and CPP ≤ 60 mm Hg. After adequate fluid resuscitation, phenylephrine (10–100 μg/min) was administered when CPP wasPatients ≤ 60 mm Hg and ICP was normal. A standard stairstep approach Approval for the study was obtained from the Institutional was used to treat intracranial hypertension. Initial managementReview Board at the University of Pennsylvania. Patients with consisted of head of bed elevation, sedation (lorazepam), analge-severe nonpenetrating TBI admitted to the Hospital of the University sia (fentanyl), neuromuscular blockade (vecuronium), and inter-of Pennsylvania, a level I trauma center, who had ICP and PbtO2 mittent cerebrospinal fluid drainage with an external ventricularmonitoring for at least 12 hours in the NICU were studied as part drain. If ICP remained > 20 mm Hg for > 10 minutes despite theof a prospective observational database. Patients were monitored initial management, osmotherapy (mannitol) was started, providedif their admission Glasgow Coma Scale was ≤8 or they later dete- that serum osmolarity was ≤ 320 mosm/L and serum sodium wasriorated to that level. Patients in this study were retrospectively ≤ 155 mmol/L. Other second-tier therapies for refractory intracra-identified from the database between January 2003 and December nial hypertension included optimized hyperventilation, barbitu-2007 and met the following inclusion criteria: (1) required no rates, and DC. Induced hypothermia was not used.immediate surgical intervention (ie, no space-occupying lesion),(2) had medically intractable intracranial hypertension, (3) under- Decompressive Craniectomywent a delayed DC for elevated ICP, and (4) had multimodality DC was performed at the discretion of the treating neurosur-brain monitoring before and after DC. Patients who underwent geon and neurointensivist. In general, DC occurred when otherprophylactic DC at the time a space-occupying lesion was evac- methods to control ICP or CPP failed. Medically refractory ele-uated were not included in this analysis. vated ICP was defined as an ICP of > 20 mm Hg for > 15 minutes1112 | VOLUME 66 | NUMBER 6 | JUNE 2010
  • 3. DECOMPRESSIVE CRANIECTOMY AND BRAIN OXYGENin a 1-hour period. Patients had either a bifrontal or unilateral DC,depending on the clinical indication and the injury distribution. TABLE 1. Classification ScoreFor a hemicraniectomy, a wide unilateral frontotemporoparietal Radiographic Conditions Scorecraniectomy was performed and included a subtemporal craniec- Marshall47 scoretomy to the middle cranial fossa floor. The medial margin was about1 cm lateral to the midline, and the anterior-posterior diameter was Normal 1 (Diffuse injury I)at least 12 cm in length. For a bifrontal DC, a coronal skin inci- Abnormal without 2 (Diffuse injury II)sion was used, and a large bifrontal bone flap from the superior Midline shift >5 mmorbital ridge to the coronal suture was made. Bilateral subtemporal Cistern compressiondecompressions also were performed. The ICP and PbtO2 moni- Mass >25 cm3tors were placed at the coronal suture on the same side that the Mass evacuationmonitor was before DC with either a bolt or tunnelable device. In Cistern compression without 3 (Diffuse injury III)all cases, the dura mater was opened as part of the operation, and Midline shift >5 mmthe dural defect was covered with DuraGen (Integra Neurosciences).A subgaleal drain was placed. The same intensive care management Mass >25 cm3protocol was followed after DC, and therapy was tailored to achieve Mass evacuationthe same ICP and CPP targets. Midline shift >5 mm but without 4 (Diffuse injury IV) Mass >25 cm3Patient Evaluation Mass evacuationClinical Surgically evacuated mass 5 (Evacuated mass lesion) At admission, the patient’s postresuscitation Glasgow Coma of any sizeScale44 score and Acute Physiology and Chronic Health Evaluation Mass lesion >25 cm3, no 6 (Nonevacuated(APACHE II45) score were recorded. An Internet-based APACHE surgical evacuation mass lesion)II calculator46 was used to derive both the score and the predic- Rotterdam48 scoretor rate of death for each patient. Multiple variables are required No abnormalities 0to calculate the APACHE score; for this study, the highest and Basal cisterns Maximum 2lowest values for each category (other than organ failure) during Abnormal but not effaced 1the first 24 hours of intensive care unit care was used for this cal-culation. Effaced 2 Midline shift Maximum 1Radiographic >5 mm 1 The Marshall47 and Rotterdam48 scores based on the initial Absence of epidural hematoma 1head CT scan were calculated on all patients (Table 1). In addi- Traumatic subarachnoid and/or 1tion, we calculated a basal cistern score (0 if normal, 1 if com- intraventricular hemorrhagepressed but not effaced, and 2 if effaced) based on the CT scan Bonusa +1obtained before DC. Maximum 6Therapeutic Intensity Level a For numerical consistency with Glasgow Coma Score grading and Marshall com- The TIL modified from Maset et al16 was calculated every 12 puted tomography classification.47hours for 2 days before and after DC. The number of calculatedTILs in some patients therefore depended on the interval betweenadmission and DC. There are 6 medical management categories as a Pbt O 2 between 15 and 20 mm Hg; moderate ischemia/(hyperventilation, pressor administration, hyperosmolar therapy, hypoxia, between 10 and 15 mm Hg; and severe ischemia/hypoxia,ventricular drainage, paralysis, and sedation) in the TIL. The max- PbtO2 ≤ 10 mm Hg.8,35,55-59 Individual episodes of PbtO2 ≤ 15 min-imum score is 18 (Table 2). utes in duration in each category were not used in analysis. CIB was estimated by the sum (in minutes) of PbtO2 recordings in each cat-Cumulative Ischemic Burden egory during each 12-hour interval for 2 days before and after DC. Several studies demonstrate that PbtO2 is influenced by a wide If a patient had severe ischemia/hypoxia, its duration was not usedrange of parameters49-54 and may reflect the product of CBF and in calculating whether there was mild or moderate ischemia/hypoxia;the arteriovenous difference in oxygen tension, ie, PbtO2 = CBF × ie, each patient was analyzed in 3 distinct potential PbtO2 categories.AVTO2.52 Although a PbtO2 monitor is not simply an “ischemia”or CBF monitor, we used PbtO2 values as a surrogate for cerebral Outcomeischemia associated with elevated ICP. To do this, we calculated the Outcome was recorded as survival (dead or alive) at 30 daysCIB based on 3 PbtO2 ranges. Mild ischemia/hypoxia was classified after TBI.NEUROSURGERY VOLUME 66 | NUMBER 6 | JUNE 2010 | 1113
  • 4. WEINER ET AL admission (range, 0.55 to 10.5 days). Two patients had a bifrontal TABLE 2. Modified Therapeutic Intensity Level Calculation16 and 8 patients a unilateral decompressive hemicraniectomy. The Therapy Score effect of DC on ICP was immediate; the average decrease in ICP from the 3 hours before surgery to the 3 hours after surgery was Hyperventilation Maximum 4 7.86 with a standard error of 2.40 mm Hg (P = .005). Fitted mixed- Intensive (PCO2 <30 mm Hg) 4 effects models for the entire time period not only showed a signif- Moderate (PCO2 = 30-35 mm Hg) 2 icant decrease in ICP associated with surgery overall (P ≤ .001) Pressor administration Maximum 4 but also demonstrated time-based trends, with ICP significantly Intensive (cerebral perfusion pressure 3 increasing in the 96-hour window before surgery (P = .02) and >80 mm Hg or mean arterial pressure >100 mm Hg) decreasing in the 96-hour window after surgery (P = .03; Table 4). Moderate (cerebral perfusion pressure 2 ≤80 mm Hg or mean arterial pressure ≤100 mm Hg) TIL and DC Hyperosmolar therapy Maximum 3 The TIL reflects the amount of medical therapy (eg, hyperven- –1 Intensive mannitol (>1 g•h •kg )–1 3 tilation, osmotherapy, sedatives, muscle blockades, and pressers) delivered to the patient to control ICP. Therapeutic values were cal- Intensive mannitol (≤1 g•h–1•kg–1) 2 culated in 12-hour blocks up to 4 times before and after the DC. Intensive hypertonic saline solution (≥2 L) 3 A reduction in TIL was observed after DC (Figure 1). A mixed- Intensive hypertonic saline solution (<2 L) 2 effects model confirmed these findings statistically, with a signif- Ventricular drainage Maximum 2 icant time-based increase in TIL before DC (P ≤ .001), an immediate Intensive (≥4 cm3/h) 2 decrease associated with surgery (P ≤ .001), and a continued time- Moderate (<4 cm3/h) 1 based decrease after DC (P ≤ .001). The mean estimated TIL Paralysis induction 1 reduction associated with surgery was 3.56 (95% confidence inter- Sedation 1 val, 1.63—5.5; Table 4). All 10 patients experienced a reduction in TIL (on average > 33%) from 12 hours before surgery to 48 Maximum total score 18 hours after DC, with a median decrease of 5.5 (P = .003). TIL and ICP were positively correlated (r = 0.46, P ≤ .001).Statistical Analysis CIB and DC Data were analyzed with the R software package.60 Data are The CIB was classified as mild, moderate, or severe, dependingrecorded as the mean and standard deviation unless otherwise on whether PbtO2 was 15 to 20, 10 to 15, or ≤ 10 mm Hg, respec-stated. A value of P ≤ .05 was considered statistically significant. tively. Nine of the 10 patients experienced PbtO2 ≤ 20 mm Hg atMixed-effects models51 were fit for PbtO2, ICP, and TIL to esti- some point during the observation period. Of these, 4 experiencedmate changes associated with DC while accounting for the random only mild hypoxia, 1 experienced mild to moderate hypoxia, and thevariation associated with individual patients and the varying lengths remaining 4 patients experienced at least 1 period of severe hypoxia.of time for which they were monitored. Nonparametric Wilcoxon At 12 hours before surgery, 7 of the 10 patients had positive CIB val-signed-rank tests61 were used to evaluate differences at specific ues (spent time with PbtO2 ≤ 20 mm Hg). For these 7 patients, wetime points and to analyze the CIB data, and an exact probabil- considered the total time spent with PbtO2 ≤ 20 mm Hg (denotedity calculation was used to analyze the outcome data with respect as the total CIB) during this period and observed a significantto predicted mortality rates. decrease in this time in the 12 hours after surgery (P = .02). The 5 patients with moderate to severe ischemia in the 12 hours beforeRESULTS DC experienced a significant post-DC reduction in the time spent with PbtO2 ≤ 15 mm Hg (P = .03), and the number of patientsPatient Characteristics experiencing severe CIB (PbtO2 ≤ 10 mm Hg) decreased from 4 Ten patients, 8 male and 2 female patients (mean age, 31.4 ± before DC to 1 after DC. Overall, as shown in Figure 2, the mean14.2 years), met the inclusion criteria for this study. Individual total CIB per patient was significantly reduced in the postsurgicalpatient clinical and radiological characteristics, outcome, and expected period (P = .02), and the greatest severity level of CIB also was sig-outcome are listed in Table 3. All patients had an admission Glasgow nificantly reduced (P = .05). Furthermore, a fitted mixed-effectsComa Scale ≤ 7. The median (range) Rotterdam and Marshall scores model suggested that the average PbtO2 levels also increased by abased on the initial head CT scan were 4 (3–6) and 3 (3–5), respec- small (9.83 mm Hg; 95% confidence interval, 3.6–16.1) but sig-tively. The median (range) APACHE II score was 25 (16–33). nificant amount after surgery (P = .003; Table 4).ICP and DC Outcome Delayed DCs for persistently elevated ICP that was refractory to The predicted mortality for all patients based on the individ-medical management were performed on average 2.8 days after ual APACHE II Scores ranged from 23.5 to 78.6, with a median1114 | VOLUME 66 | NUMBER 6 | JUNE 2010
  • 5. DECOMPRESSIVE CRANIECTOMY AND BRAIN OXYGEN TABLE 3. Patient Demographics and Admission Clinical and Radiographic Scoresa Predictive 30-Day Case/Age, Marshall Rotterdam MOI Pathology GCS Apache II Mortality BCS DC Time, d Outcome y/Sex Score Score Rate, %b (Survival) 1/24/M ATV CHI 6 24 49.7 3 3 1 10.5 A 2/43/M MVC SDH 3 24 49.7 5 6 2 0.66 D 3/37/M Fall CHI 6 25 53.3 3 4 1 1 A 4/24/M Fall DAI 5 33 78.6 5 5 2 0.55 A 5/21/F Fall SDH 7 27 60.5 3 4 1 2 A 6/22/M Fall CHI 5 25 53.3 3 4 1 4 A 7/18/M A vs P CHI 3 26 56.9 3 4 1 3 A 8/47/M M vs P DAI 7 16 23.5 3 4 1 4 A 9/19/F MVC IPH 3 23 46 3 4 1 1.4 A 10/59/M A vs P CHI 3 25 53.5 5 5 2 1 Aa MOI, mechanism of injury; GCS, Glasgow Coma Score44; APACHE II, Acute Physiology and Chronic Health Evaluation; BCS, basal cistern score; DC time, time from hospitaladmission to decompressive craniectomy; ATV, all-terrain vehicle; CHI, closed-head injury/contusions; A, alive; MVC, motor vehicle collision; SDH, subdural hematoma; D, dead;DAI, diffuse axonal injury; A, automobile; P, pedestrian; M, motorcycle; IPH, intraparenchymal hematoma.b The predictive mortality rate is based on the APACHE II score.45 The Marshall47 and Rotterdam48 scores are calculated from the admission head computed tomography scan,and the BCS is calculated from the computed tomography obtained immediately before DC. TABLE 4. Model Results for the Prediction of ICP, TIL, and PbtO2 Associated With Decompressive Craniectomya 95% Confidence Parameter Value P Interval Fixed effects: ICP Intercept 17.83 <.0001 (14.88, 20.77) Surgery –7.15 <.0001 (–9.78, –4.52) Hour 0.06 .0224 (0.01, 0.11) Surgery:hour –0.07 .0260 (–0.15, –0.01) Fixed effects: TIL Intercept 10.10 <.0001 (8.23, 11.93) Surgery –3.56 .0008 (–5.48, –1.63) Hour 0.14 <.0001 (–0.09, 0.20) Surgery:hour –0.25 <.0001 (–0.32, –0.18) Fixed effects: PbtO2 FIGURE 1. Line graphs illustrating individual patient therapeutic intensity Intercept 29.94 <.0001 (21.50, 38.38) levels (TIL) before and after decompressive craniectomy (time, 0 hour). The TIL was modified from Maset et al16 (see Table 2). Surgery 9.83 .0029 (3.56, 16.09)a ICP, intracranial pressure; TIL, therapeutic intensity level. nial hypertension, we examined how the procedure influenced the TIL and the CIB as estimated by PbtO2. The results suggestvalue of 53.3. At 30 days after TBI, only 1 patient was dead, result- that DC can reduce TIL and the CIB of the brain. These find-ing in a lower mortality rate than predicted (P = .015). Care was ings imply that DC should be considered early in a patient’s course,withdrawn in the patient who died (case 2). particularly when the TIL is elevated.DISCUSSION Study Limitations In this study of 10 TBI patients who had PbtO2 monitoring Our study has several potential limitations. First, because thebefore and after DC performed for medically intractable intracra- data set included only patients who underwent DC, we do notNEUROSURGERY VOLUME 66 | NUMBER 6 | JUNE 2010 | 1115
  • 6. WEINER ET AL limitations, our findings provide useful physiological data before and after DC for elevated ICP. These data may be used to better time when patients undergo DC and to better identify which patients undergo DC. Decompressive Craniectomy DC is not new, but in recent years, there has been increased interest in using this procedure to control elevated ICP after severe TBI.22-24,26,28,30-32 Previous studies demonstrated an improve- ment in a variety of physiological parameters, including ICP, com- pliance, ICP indexes such as cerebrospinal compensatory reserve and cerebrovascular reactivity, brain oxygen, and metabolic param- eters measured by cerebral microdialysis.34,35,37,64 These physio- logical improvements are often greater in those patients who subsequently have a favorable outcome. Our findings are consis- FIGURE 2. Histograms illustrating the number of minutes each patient had tent with and extend these observations. In particular, we show evidence of mild (PbtO2, 15–20 mm Hg), moderate (PbtO2 10–15 mm Hg), that DC decreases the TIL and that the CIB as estimated by the or severe (PbtO2 ≤ 10 mm Hg) brain hypoxia (or cumulative ischemic bur- cumulative time that PbtO2 is less than threshold. These findings den) before and after decompressive craniectomy (DC). are important because the TIL represents in part a measure of how “sick” the brain is and whether there is any compensatory reserve.have a matched control group for comparison. Second, our sam- Knowing the TIL may allow better patient selection for DC andple size of 10 patients is small. Third, our selection criteria may have more targeted therapy for increased ICP. In addition, our dataintroduced bias toward patients with edema (and elevated ICP) that imply, but do not prove, that early DC may reduce the likelihooddeveloped slowly or who were likely to survive. In addition, because of secondary ischemic or hypoxic injury in the brain.the data were examined retrospectively, we cannot exclude the Despite these various physiological studies, the effect of DCpossibility that a surgical decision was made or influenced by on clinical outcome after TBI is not yet defined and is presentlyPbtO2 even though our institutional policy for DC is based on being studied in 2 randomized trials (RescueICP and DECRA).ICP. We also did not examine patients who had prophylactic DC Data from randomized stroke studies suggest that DC in TBIafter evacuation of mass lesions; thus, we do not know whether patients should improve outcome.65 However, even after the ran-the findings apply to all patients who undergo DC. Fourth, the study domized trials, there are likely to be several unanswered questions.was performed on patients treated at a single institution, so it may In particular, the optimal time to perform a DC for brain edemalack external validity. However, our data reflect a patient popula- and elevated ICP is not precisely known. This is important becausetion managed according to an ICU protocol that is similar to pro- all medical therapies for elevated ICP, decreased CPP, and DCtocols in use at many other institutions. Fifth, the PbtO2 monitor also have side effects, and although ICP may be reduced, outcomewe used measures local PbtO2 and may not always reflect global may not always be improved.7,17-22 Our data may help decidebrain oxygenation. However, studies have shown that PbtO2 indi- when to perform DC for cerebral edema after TBI, ie, when thecates global brain oxygen when the monitor is located in the unin- TIL or the duration of compromised PbtO2 is increased. Whetherjured brain,62 as it was in our study. Sixth, direct comparison of these parameters are useful to select patients for DC, whetherpreoperative and postoperative ICP and PbtO2 values may be sub- there is a specific threshold for TIL or PbtO2, and whether trendsject to unavoidable errors because the monitors after DC are never should be used require further the exact same location as before surgery. Seventh, our methodto calculate a CIB reflects collection of data most commonly used Brain Oxygen and DCin ICUs around the world, ie, a manual entry onto an ICU flow Today, the decision to perform a delayed DC after TBI is basedsheet every 15 minutes. It is conceivable that more subtle find- largely on elevated ICP (> 20 mm Hg) that is not controlled byings may have been apparent if area-under-the-curve analysis had medical means. However, ICP is more than a number, and under-been used. However, this method frequently uses interpolation standing the regulatory processes for ICP and indexes that reflectto account for missing data or times between records that exceed compensatory reserve may permit better selection of patients fora certain threshold.63 Finally, because DC was performed at dif- surgery.12 The evolving concept of multimodality monitoring inferent time points after TBI, it is conceivable that further bias was neurointensive care and, in particular, the use of PbtO2 monitorsintroduced because CBF and PbtO2 may change over time. However, to complement ICP data also may help select patients for DC inwe did use mixed-effects models51 that account for the random a timely and targeted manner. This requires further study. Forvariation associated with individual patients and the varying lengths example, is the patient with controlled ICP but decreased PbtO2of time for which they were monitored. For these various reasons, or decreasing PbtO2 a candidate for DC? Use of PbtO2 data toour findings should be regarded as preliminary, but despite these complement ICP may be important because it is well know that1116 | VOLUME 66 | NUMBER 6 | JUNE 2010
  • 7. DECOMPRESSIVE CRANIECTOMY AND BRAIN OXYGENbrain hypoxia, specifically a longer duration of brain hypoxia, is 2. Clifton GL, Miller ER, Choi SC, Levin HS. Fluid thresholds and outcome fromassociated with poor outcome after TBI.41,57,64,66-68 severe brain injury. Crit Care Med. 2002;30(4):739-745. 3. Juul N, Morris GF, Marshall SB, Marshall LF. Intracranial hypertension and cere- There has been less study of how DC affects PbtO2.35,64,69,70 We bral perfusion pressure: influence on neurological deterioration and outcome inpreviously observed in 7 patients that DC immediately improves severe head injury: the Executive Committee of the International Selfotel Trial.Pbt O 2 and that this effect is sustained. 64 In addition, Pbt O 2 J Neurosurg. 2000;92(1):1-6.remained > 25 mm Hg as medical management for elevated ICP 4. Marmarou A, Anderson RL, Ward JD, Choi SC, Young HF, Eisenberg HM. Impact of ICP instability and hypotension on outcome in patients with severe head trauma.was weaned after DC. There also was a tendency for those patients J Neurosurg. 1991;75:S59—S66.with normal PbtO2 before DC to have a better outcome. Recently, 5. Marshall LF, Smith RW, Shapiro HM. The outcome with aggressive treatment inHo et al35 studied 16 TBI patients who had DC and observed a severe head injuries, part I: the significance of intracranial pressure monitoring.significant improvement in Pbt O 2 and an 85% reduction in J Neurosurg. 1979;50(1):20-25. 6. Narayan RK, Kishore PR, Becker DP, et al. Intracranial pressure: to monitor orepisodes of cerebral ischemia among patients who subsequently had not to monitor? A review of our experience with severe head injury. J Neurosurg.a favorable outcome. This effect was not present in those who had 1982;56(5) unfavorable outcome. In addition, abnormal brain neurochem- 7. Saul TG, Ducker TB. Effect of intracranial pressure monitoring and aggressive treatment on mortality in severe head injury. J Neurosurg. 1982;56(4):498-503.istry, including glutamate, glycerol, and lactate measured with 8. Brain Trauma Foundation; American Association of Neurological Surgeons; Congressmicrodialysis, also improved when a favorable outcome occurred. of Neurological Surgeons; Joint Section on Neurotrauma and Critical Care,Together, these data suggest that multimodality monitoring may AANS/CNS. Guidelines for the management of severe traumatic brain guide treatment and DC selection or, at the very least, indi- J Neurotrauma. 2007;24(suppl 1):S65-S70. 9. Maas AI, Dearden M, Teasdale GM, et al. EBIC-guidelines for management ofcate when management, even after DC, is futile. Whether DC severe head injury in adults: European Brain Injury Consortium. Acta Neurochir (Wien).should be regarded as only a “second-tier” therapy for elevated 1997;139(4):286-294.ICP is not answered by this study, but rather than base manage- 10. Robertson C. Youmans Neurological Surgery. 5th ed. Philadelphia, PA: Saunders;ment on only 1 parameter, we suggest that any monitored param- 2004. 11. Czosnyka M, Guazza E, Whitehouse M, et al. Significance of intracranial pressureeter be interpreted with reference to others that are monitored at waveform analysis after head injury. Acta Neurochir (Wien). 1996;138(5):531-542.the same time. Knowledge about the duration of compromised 12. Czosnyka M, Smielewski P, Timofeev I, et al. Intracranial pressure: more than aPbtO2 may prompt earlier DC for increased ICP. number. Neurosurg Focus. 2007;22(5):E10. 13. Lang EW, Lagopoulos J, Griffith J, et al. Cerebral vasomotor reactivity testing in head injury: the link between pressure and flow. J Neurol Neurosurg Psychiatry.CONCLUSIONS 2003;74(8):1053-1059. 14. Steiner LA, Czosnyka M, Piechnik SK, et al. Continuous monitoring of cerebrovas- The findings of the present study show that in TBI patients cular pressure reactivity allows determination of optimal cerebral perfusion pres- sure in patients with traumatic brain injury. Crit Care Med. 2002;30(4):733-738.DC improves ICP, reduces the TIL for elevated ICP after surgery, 15. Le Roux P, Newell DW, Lam AM, Grady MS, Winn HR. Cerebral arteriovenousimproves average PbtO2, and reduces the CIB estimated by PbtO2. difference of oxygen: a predictor of cerebral infarction and outcome in severe headThese data imply that ICP is “easier” to control after DC, that injury. J Neurosurg. 1997;87(1):1-8.patients therefore are at reduced risk for the potential deleterious 16. Maset AL, Marmarou A, Ward JD, et al. Pressure-volume index in head injury. J Neurosurg. 1987;67(6):832-840.side effects that may occur with various ICP treatments, and that 17. Chestnut RM. Hyperventilation in traumatic brain injury: friend or foe? Crit Carethe likelihood of secondary neuronal injury associated with elevated Med. 1997;25(8):1275-1278.ICP is reduced. Whether DC and subsequent improved ICP are 18. Coles JP, Minhas PS, Fryer TD, et al. Effect of hyperventilation on cerebral bloodassociated with better outcome after TBI is not known and is the flow in traumatic head injury: clinical relevance and monitoring correlates. Crit Care Med. 2002;30(9):1950-1959.subject of current randomized trials. However, our data support 19. Contant CF, Valadka AB, Gopinath SP, Hannay HJ, Robertson CS. Adult respi-a role for DC and, at the very least, provide useful physiological ratory distress syndrome: a complication of induced hypertension after severe headdata that may help decide whom to operate on or when to per- injury. J Neurosurg. 2001;95(4):560-568.form DC. Ideally, a predictive paradigm that not only is based on 20. Eisenberg HM, Frankowski RF, Contant CF, Marshall LF, Walker MD. High-dose barbiturate control of elevated intracranial pressure in patients with severe headICP, PbtO2, the TIL, and CIB but also includes other factors such injury. J Neurosurg. 1988;69(1) age, Glasgow Coma Scale, APACHE II, and the Rotterdam 21. Kaufmann AM, Cardoso ER. Aggravation of vasogenic cerebral edema by multi-scores may best guide who undergoes DC and when it is opti- ple-dose mannitol. J Neurosurg. 1992;77(4):584-589.mally performed. 22. Marshall LF, Smith RW, Rauscher LA, Shapiro HM. Mannitol dose requirements in brain injured patients. J Neurosurg. 1978;48(2):169-172. 23. Aarabi B, Hesdorffer DC, Ahn ES, Aresco C, Scalea TM, Eisenberg HM. OutcomeDisclosures following decompressive craniectomy for malignant swelling due to severe head This work was supported by research grants from Integra Neurosciences (the man- injury. J Neurosurg. 2006;104(4):469-479.ufacturer of the Licox PbtO2 monitor) (P.D.L.R.), the Integra Foundation (P.D.L.R.), 24. Albanèse J, Leone M, Alliez JR, et al. Decompressive craniectomy for severe trau-and the Mary Elisabeth Groff Surgical and Medical Research Trust (P.D.L.R.). matic brain injury: evaluation of the effects at one year. Crit Care Med. 2003;31(10):P.D.L.R. is a member of the Integra Speakers Bureau. 2535-2538. 25. Chibbaro S, Tacconi L. Role of decompressive craniectomy in the management of severe head injury with refractory cerebral edema and intractable intracranial pres-REFERENCES sure: our experience with 48 cases. Surg Neurol. 2007;68(6):632-638. 26. Coplin WM, Cullen NK, Policherla PN, et al. Safety and feasibility of craniec-1. Miller JD, Becker DP, Ward JD, Sullivan HG, Adams WE, Rosner MJ. Significance tomy and duraplasty as the initial surgical intervention for sever traumatic brain injury. of intracranial hypertension in severe head injury. J Neurosurg. 1977;47(4):503-516. J Trauma. 2001;50(6):1050-1059.NEUROSURGERY VOLUME 66 | NUMBER 6 | JUNE 2010 | 1117
  • 8. WEINER ET AL27. Josan VA, Sgouros S. Early decompressive craniectomy may be effective in the 52. Rosenthal G, Hemphill JC 3rd, Sorani M, et al. Brain tissue oxygen tension is treatment of refractory intracranial hypertension after traumatic brain injury. Childs more indicative of oxygen diffusion than oxygen delivery and metabolism in patients Nerv Syst. 2006;22(10):1268-1274. with traumatic brain injury. Crit Care Med. 2008;36(6):1917-1924.28. Münch E, Horn P, Schürer L, Piepgras A, Paul T, Schmiedek P. Management of 53. Scheufler KM, Lehnert A, Rohrborn HJ, Nadstawek J, Thees C. Individual value severe traumatic brain injury by decompressive craniectomy. Neurosurgery. 2000; of brain tissue oxygen pressure, microvascular oxygen saturation, cytochrome redox 47(2):315-323. level and energy metabolites in detecting critically reduced cerebral energy state29. Olivecrona M, Rodling-Wahlströ M, Naredi S, Koskinen LO. Effective ICP reduc- during acute changes in global cerebral perfusion. J Neurosurg Anesthesiol. 2004; tion by decompressive craniectomy in patients with severe traumatic brain injury 16(3):210-219. treated by an ICP-targeted therapy. J Neurotrauma. 2007;24(6):927-935. 54. Scheufler KM, Röhrborn HJ, Zentner J. Does tissue oxygen-tension reliably reflect30. Polin RS, Shaffrey ME, Bogaev CA, et al. Decompressive bifrontal craniectomy cerebral oxygen delivery and consumption? Anesth Analg. 2002;95(5):1042-1048. in the treatment of severe refractory posttraumatic cerebral edema. Neurosurgery. 55. Chang JJ, Youn TS, Benson D, et al. Physiological and functional outcome corre- 1997;41(1):84-94. lates of brain tissue hypoxia in traumatic brain injury. Crit Care Med. 2009;37(1):283-31. Taylor A, Butt W, Rosenfeld J, et al. A randomized trial of very early decompres- 290. sive craniectomy in children with traumatic brain injury and sustained intracra- 56. Hlatky R, Valadka AB, Goodman JC, Contant CF, Robertson CS. Patterns of nial hypertension. Childs Nerv Syst. 2001;17(3):154-162. energy substrates during ischemia measured in the brain by microdialysis. J32. Hutchinson PJ, Corteen E, Czosnyka M, et al. Decompressive craniectomy in trau- Neurotrauma. 2004;21(7):894-906. matic brain injur y: the randomized multicenter RESCUEicp study 57. Maloney-Wilensky E, Gracias V, Itkin A, et al. Brain tissue oxygen and outcome after ( Acta Neurochir Suppl. 2006;96:17-20. severe traumatic brain injury: a systematic review. Crit Care Med. 2009;37(6):2057-33. Rosenfeld JV, Cooper DJ, Murray L. A multicenter prospective randomized trial 2063. of early decompressive craniectomy in patients with severe traumatic brain injury. 58. Nortje J, Gupta AK. The role of tissue oxygen monitoring in patients with acute Neurosurgery. 2006;59:467-468. brain injury. Br J Anaesth. 2006;97(1):95-106.34. Hase U, Reulen HJ, Meinig G, Schürmann K. The influence of the decompres- 59. Pennings FA, Schuurman PR, van den Munckhof P, Bouma GJ. Brain tissue oxy- sive operation on the intracranial pressure and the pressure-volume relation in gen pressure monitoring in awake patients during functional neurosurgery: the patients with severe head injuries. Acta Neurochir (Wien). 1978;45(1-2):1-13. assessment of normal values. J Neurotrauma. 2008;25(10):1173-1177.35. Ho CL, Wang CM, Lee KK, Ng I, Ang BT. Cerebral oxygenation, vascular reac- 60. R Development Core Team. R: a language and environment for statistical com- tivity, and neurochemistry following decompressive craniectomy for severe trau- puting. Vienna, Austria: R Foundation for Statistical Computing; 2008. matic brain injury. J Neurosurg. 2008;108(5):943-949. 61. Hollander M, Wolfe DA. Nonparametric Statistical Methods. 2nd ed. New York,36. Schneider GH, Bardt T, Lanksch WR, Unterberg A. Decompressive craniectomy NY: John Wiley & Sons; 1999. following traumatic brain injury: ICP, CPP and neurological outcome. Acta Neurochir 62. Kiening KL, Unterberg AW, Bardt TF, Schneider GH, Lanksch WR. Monitoring Suppl. 2002;81:77-79. of cerebral oxygenation in patients with severe head injuries: brain tissue PO2 ver-37. Timofeev I, Czosnyka M, Nortje J, et al. Effect of decompressive craniectomy on sus jugular vein oxygen saturation. J Neurosurg. 1996;85(5):751-757. intracranial pressure and cerebrospinal compensation following traumatic brain 63. Vik A, Nag T, Fredriksli OA, et al. Relationship of “dose” of intracranial hyper- injury. J Neurosurg. 2008;108(1):66-73. tension to outcome in severe traumatic brain injury. J Neurosurg. 2008;109(4):678-38. Gopinath SP, Robertson CS, Contant CF, et al. Jugular venous desaturation and out- 684. come after head injury. J Neurol Neurosurg Psychiatry. 1994;57(6):717-723. 64. Stiefel MF, Heuer GG, Smith MJ, et al. Cerebral oxygenation following decompres-39. Menon DK, Coles JP, Gupta AK, et al. Diffusion limited oxygen delivery follow- sive hemicraniectomy for the treatment of refractory intracranial hypertension. J ing head injury. Crit Care Med. 2004;32(6):1384-1390. Neurosurg. 2004;101(2):241-247.40. Vespa PM, O’Phelan K, McArthur D, et al. Pericontusional brain tissue exhibits 65. Vahedi K, Hofmeijer J, Juettler E, et al. Early decompressive surgery in malignant persistent elevation of lactate/pyruvate ratio independent of cerebral perfusion infarction of the middle cerebral artery: a pooled analysis of three randomized con- pressure. Crit Care Med. 2007;35(4):1153-1160. trolled trials. Lancet Neurol. 2007;6(3):215-222.41. van Santbrink H, van den Brink WA, Steyerberg EW, Carmona Suazo JA, Avezaat 66. Dings J, Meixensberger J, Jäger A, Roosen K. Clinical experience with 118 brain CJ, Maas AI. Brain tissue oxygen response in severe traumatic brain injury. Acta tissue oxygen partial pressure catheter probes. Neurosurgery. 1998;43(5):1082- Neurochir (Wien). 2003;145(6):429-438. 1095.42. Stiefel MF, Udoetek J, Spiotta AM, et al. Conventional neurocritical care does not 67. van den Brink WA, van Santbrink H, Steyerberg EW, et al. Brain oxygen tension ensure cerebral oxygenation after traumatic brain injury. J Neurosurg. 2006;105(4):568- in severe head injury. Neurosurgery. 2000;46(4):868-678. 575. 68. Valadka AB, Gopinath SP, Contant CF, Uzura M, Robertson CS. Relationship of43. Bullock MR, Randall R, Ghajar J, et al. Neurosurgery: guidelines for the surgical brain tissue PO2 to outcome after severe head injury. Crit Care Med. 1998;26(9):1576- management of traumatic brain injury. Neurosurgery. 2006;58(suppl):1-62. 1581.44. Teasdale G, Jennett B. Assessment of coma and impaired consciousness: a practi- 69. Jaeger M, Soehle M, Meixensberger J. Improvement of brain tissue oxygen and cal scale. Lancet. 1974;2(7872):81-84. intracranial pressure during and after surgical decompression for diffuse brain45. Knaus WA, Draper EA, Wagner DP, Zimmerman JE. APACHE II: a severity of edema and space occupying infarction. Acta Neurochir Suppl. 2005;95:117-118. disease classification system. Crit Care Med. 1985;13(10):818-829. 70. Reithmeier T, Löhr M, Pakos P, Ketter G, Ernestus RI. Relevance of ICP and ptiO246. McAuley DF. Global RPh. Accessed July 18, for indication and timing of decompressive craniectomy in patients with malig- 2008. nant brain edema. Acta Neurochir (Wien). 2005;147(9):947-952.47. Marshall LF, Marshall SB, Klauber MR. A new classification of head injury based on computerized tomography. J Neurosurg. 1991;75:S14—S20. Acknowledgments48. Maas AI, Hukkelhoven CW, Marshall LF, Steyerberg EW. Prediction of outcome in traumatic brain injury with computed tomographic characteristics: a compari- We acknowledge the hard and passionate work provided by the nurses in the Neuro son between the computed tomographic classification and combinations of com- Intensive Care Unit at the Hospital of the University of Pennsylvania and are puted tomographic predictors. Neurosurgery. 2005;57(6):1173-1182. grateful to the members of the Neurosurgical Clinical Research Division who have49. Hemphill JC 3rd, Knudson MM, Derugin N, Morabito D, Manley GT. Carbon spent endless hours entering data. dioxide reactivity and pressure autoregulation of brain tissue oxygen. Neurosurgery. 2001;48(2):377-384.50. Johnston AJ, Steiner LA, Coles JP, et al. Effect of cerebral perfusion pressure aug- COMMENTS A mentation on regional oxygenation and metabolism after head injury. Crit Care Med. 2005;33(1):189-195; 255-257. lthough several early publications about decompressive craniotomy51. Pinheiro JC, Bates DM. Mixed-Effects Models in S and S-PLUS. New York, NY: did not show a therapeutic advantage, more recently, a growing num- Springer; 2008. ber of reports support the idea. The importance of this article is that it not1118 | VOLUME 66 | NUMBER 6 | JUNE 2010
  • 9. DECOMPRESSIVE CRANIECTOMY AND BRAIN OXYGENonly adds to the idea that decompressive craniotomy is efficacious but Nevertheless, surrogate measures, for better or worse, remain unaccept-also provides information regarding potential indications that could help able in proving clinical benefit. This can be accomplished only throughmake the decision to do the operation. The article is not dissimilar to validated outcome measures in a prospective randomized clinical trial.another recently published paper (their Reference 17). In that article, If indeed the ongoing clinical trials of decompressive craniectomy ref-patients did not fare as well, and only patients with good outcomes showed erenced by the authors prove positive, then the information presentedbrain metabolic improvement. Although we have to wait for the out- in this contribution may be used to refine appropriate candidates forcome of ongoing randomized trials to get the kind of evidence that would decompressive craniectomy. Until then, we continue to use unproven,definitively define the role of decompressive craniotomy, a large num- but enticing, physiological explanations for our clinical interventions.ber of patients who could have been helped may not have a procedurewith relatively low risk, considering the risk of dying and disability in Jack E. Wilbergerpatients with uncontrolled intracranial pressure. Pittsburgh, Pennsylvania Some of the limitations of the article, particularly the small samplesize, are considered in the Discussion. However, in addition, we can neverknow in how many cases the surgeon was influenced by brain O2, which I n this article, the Penn Group has confirmed and extended previous studies demonstrating that decompressive hemicraniectomy reduces intracranial pressure and the Therapeutic Intensity Level in patients within a sense confounds the study. The authors should also tell us how theyformed 3 brain O2 groups. I understand that using brain 02 as a contin- traumatic brain injury. They also show that Pbto2 is improved afteruous function in this study is not really feasible, but I think a statement decompression. As the authors have acknowledged, the low Pbto2 inabout the formation of these groups, even if it is just the authors’ intu- patients before decompressive craniectomy likely represents lower cere-ition and not based on statistics, is important. Lastly, what do the authors bral blood flow (Reference 1). Although this is not exactly “ischemic bur-mean when they say decompressive craniotomy is being done in patients den,” they use this measure as a surrogate. Certainly, it would be informativewithout medical management of intracranial pressure? This is a surprise to also measure other cerebral metabolic indexes such as CMRo2 or OEF,and certainly not the case in our published series. Despite these criti- but this requires resources that are beyond most groups and will mostcisms, I am strongly in favor of the publication. likely not be widely available for routine use. Brain tissue oxygen mon- itoring, on the other hand, is more widely available and is increasingly being Howard M. Eisenberg used to monitor a variety of brain-injured patients. Although its patient Baltimore, Maryland sample size is small, this study demonstrates the added value of moni- toring end points beyond intracranial pressure. To improve the outcomeD ecompressive craniectomy remains a widely used yet controversial and unproven therapy for posttraumatic “refractory” intracranialpressure elevations. Even though not stated as such, it would appear that of brain-injured patients, we need more surrogate measures to target and refine our treatment. Despite the increasing use of decompressive hem- icraniectomy in the treatment of traumatic brain injury, we still do notWeiner et al are attempting to correlate the possibility of improved out- know exactly which patients will benefit from this procedure. The usecomes with surrogate measures such as intracranial pressure, therapeu- of additional neuromonitoring and surrogate measures may help answertic intensity levels and cumulative ischemic burden—based on Pbto2 this important question.monitoring—before and after decompressive craniectomy. It is certainly very important to have physiological evidence, such as that Geoffrey T. Manleyprovided by this study, that a specific intervention works or is likely to work. San Francisco, California SCIENCE TIMESNEUROSURGERY VOLUME 66 | NUMBER 6 | JUNE 2010 | 1119