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Evaluating the outcome of severe head injury with transcranial Doppler ultrasonography

José A. Moreno, Eduard Mesalles, Juan Gener, Antonio Tomasa, Adolfo Ley, Josep Roca, and Jaime Fernández-Llamazares

The authors conducted a study to determine the value of transcranial Doppler (TCD) ultrasonography in evaluating the outcome of severely head injured patients and to correlate the TCD values with those obtained from intracranial pressure (ICP) and cerebral perfusion pressure (CPP) monitoring.

The authors conducted a prospective study of 125 patients with severe head injury (Glascow Coma Scale scores of less than 9) who underwent TCD ultrasonography according to the standard technique of insonating the middle cerebral artery (MCA) and measuring the mean blood flow velocity and pulsatility index within the first 24 hours of admission. The ICP and CPP values, as well as other clinical, analytical, and neuroimaging data, were also recorded. After 6 months, outcome was evaluated using the Glasgow Outcome Scale. Moderate disability and complete recovery were considered “good” outcome; death, vegetative state, and severe disability were considered “poor.”

In 67 patients (54%) good outcome was demonstrated whereas in 58 (46%) it was poor. The mean blood flow velocity of the MCA in patients with good outcome was 44 cm/second; in those with poor outcomes it was 36 cm/second (p < 0.003). The mean PI in cases of good outcome was 1 whereas in poor outcome was 1.56 (p < 0.0001). The correlations of ICP and CPP to PI were statistically significant (r2 = 0.6; p < 0.0001).

When performed in the first 24 hours of severe head injury, TCD ultrasonography is valid in predicting the patient’s outcome at 6 months and correlates significantly with ICP and CPP values.

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Elevated jugular venous oxygen saturation after severe head injury

Manuela Cormio, Alex B. Valadka, and Claudia S. Robertson

Object

The aim of this study was to investigate the incidence of elevated (≥ 75%) jugular venous oxygen saturation (SjvO2) and its relationship to cerebral hemodynamic and metabolic parameters and to outcome after severe head injury.

Methods

Data from 450 severely head injured patients admitted to the Neurosurgical Intensive Care Unit of Ben Taub General Hospital were analyzed retrospectively. The SjvO2 was measured in blood obtained from indwelling jugular bulb catheters. Patients were classified into the following categories: high (Group I), normal (Group II), or low SjvO2 (Group III) if their mean SjvO2 over the duration of monitoring was 75% or higher, 74 to 56%, or 55% or lower, respectively.

A high SjvO2 occurred in 19.1% of patients. There was no consistent relationship between SjvO2 and simultaneous cerebral blood flow (CBF) or cerebral perfusion pressure measurements. Compared with Groups II and III, the patients in Group I had a significantly higher CBF and lower cerebral metabolic rate of oxygen (CMRO2). In Group I, the out- comes were death or persistent vegetative state in 48.8% of patients and severe disability in 25.6%. These outcomes were significantly worse than for patients in Group II. Within Group I, the patients with a poor neurological outcome were older and more likely to have suffered a focal head injury; they demonstrated a lower CMRO2 and a greater rate of cerebral lactate production than the patients who attained a favorable outcome.

Conclusions

Posttraumatic elevation of SjvO2 is common but cannot be automatically equated with hyperemia. Instead, elevated SjvO2 is a heterogeneous condition that is associated with poor outcome after head injury and may carry important implications for the management of comatose patients.

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Prehospital management of traumatic brain injury

Shirley I. Stiver and Geoffrey T. Manley

.1097/00005373-200008000-00009 124 Rosner MJ , Daughton S : Cerebral perfusion pressure management in head injury . J Trauma 30 : 933 – 940 , 1990 10.1097/00005373-199008000-00001 125 Rosner MJ , Rosner SD , Johnson AH : Cerebral perfusion pressure: management protocol and clinical results . J Neurosurg 83 : 949 – 962 , 1995 10.3171/jns.1995.83.6.0949 126 Rosomoff HL , Holaday DA : Cerebral blood flow and cerebral oxygen consumption during hypothermia . Am J Physiol 179 : 85 – 88 , 1954 10.1152/ajplegacy.1954.179.1.85 127 Roy PD : The value of trauma

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Dynamics of subdural hygroma following decompressive craniectomy: a comparative study

Bizhan Aarabi, David Chesler, Christopher Maulucci, Tiffany Blacklock, and Melvin Alexander

10.2176/nmc.21.397 38 Lang JK , Ludwig HC , Mursch K , Zimmerer B , Markakis E : Elevated cerebral perfusion pressure and low colloid osmotic pressure as a risk factor for subdural space-occupying hygromas? . Surg Neurol 52 : 630 – 637 , 1999 10.1016/S0090-3019(99)00144-5 39 Lee KS , Bae WK , Bae HG , Yun IG : The fate of traumatic subdural hygroma in serial computed tomographic scans . J Korean Med Sci 15 : 560 – 568 , 2000 10.3346/jkms.2000.15.5.560 40 Lee KS , Bae WK , Park YT , Yun IG : The pathogenesis and

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Intracranial Pressure: More Than a Number

Marek Czosnyka, Peter Smielewski, Ivan Timofeev, Andrea Lavinio, Eric Guazzo, Peter Hutchinson, and John D. Pickard

✓Many doctors involved in the critical care of head-injured patients understand intracranial pressure (ICP) as a number, characterizing the state of the brain pressure–volume relationships. However, the dynamics of ICP, its waveform, and secondarily derived indices portray useful information about brain homeostasis. There is circumstantial evidence that this information can be used to modify and optimize patients' treatment. Secondary variables, such as pulse amplitude and the magnitude of slow waves, index of compensatory reserve, and pressure–reactivity index (PRx), look promising in clinical practice. The optimal cerebral perfusion pressure (CPP) derived using the PRx is a new concept that may help to avoid excessive use of vasopressors in CPP-oriented therapy. However, the use of secondary ICP indices remains to be confirmed in clinical trials.

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Increased inspired oxygen concentration as a factor in improved brain tissue oxygenation and tissue lactate levels after severe human head injury

Matthias Menzel, Egon M. R. Doppenberg, Alois Zauner, Jens Soukup, Michael M. Reinert, and Ross Bullock

Object

Early impairment of cerebral blood flow in patients with severe head injury correlates with poor brain tissue O2 delivery and may be an important cause of ischemic brain damage. The purpose of this study was to measure cerebral tissue PO2, lactate, and glucose in patients after severe head injury to determine the effect of increased tissue O2 achieved by increasing the fraction of inspired oxygen (FiO2).

Methods

In addition to standard monitoring of intracranial pressure and cerebral perfusion pressure, the authors continuously measured brain tissue PO2, PCO2, pH, and temperature in 22 patients with severe head injury. Microdialysis was performed to analyze lactate and glucose levels. In one cohort of 12 patients, the PaO2) was increased to 441 ± 88 mm Hg over a period of 6 hours by raising the FiO2 from 35 ± 5% to 100% in two stages. The results were analyzed and compared with the findings in a control cohort of 12 patients who received standard respiratory therapy (mean PaO2 136.4 ± 22.1 mm Hg).

The mean brain PO2 levels increased in the O2-treated patients up to 359 ± 39% of the baseline level during the 6-hour FiO2 enhancement period, whereas the mean dialysate lactate levels decreased by 40% (p < 0.05). During this O2 enhancement period, glucose levels in brain tissue demonstrated a heterogeneous course. None of the monitored parameters in the control cohort showed significant variations during the entire observation period.

Conclusions

Markedly elevated lactate levels in brain tissue are common after severe head injury. Increasing PaO2 to higher levels than necessary to saturate hemoglobin, as performed in the O2-treated cohort, appears to improve the O2 supply in brain tissue. During the early period after severe head injury, increased lactate levels in brain tissue were reduced by increasing FiO2. This may imply a shift to aerobic metabolism.

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Dose response to cerebrospinal fluid drainage on cerebral perfusion in traumatic brain–injured adults

Mary E. Kerr, Barbara B. Weber, Susan M. Sereika, Jack Wilberger, and Donald W. Marion

Object

Intracranial hypertension remains a common complication of traumatic brain injury (TBI). Ventriculostomy drainage is a recommended therapy to decrease intracranial pressure (ICP), but little empirical evidence exists to guide treatment. The authors conducted a study to examine systematically the effect of cerebral spinal fluid (CSF) drainage on ICP and indices of cerebral perfusion.

Methods

Intracranial pressure, cerebral perfusion pressure (CPP), cerebral blood flow velocity (CBFV), and near-infrared spectroscopy–determined regional cerebral oxygenation (rSO2) were measured in 58 patients (with Glasgow Coma Scale scores ≤ 8) before, during, and after ventriculostomy drainage. Three randomly ordered CSF drainage protocols varied in the volume of CSF removed (1 ml, 2 ml, and 3 ml). Physiological variables were time averaged in 1-minute blocks from baseline to 10 minutes after cessation of ventricular drainage.

There was a significant dose–time interaction for ICP with the three-extraction volume protocol, with incremental decreases in ICP (F [20, 1055] = 6.10; p = 0.0001). There was a significant difference in the CPP depending on the amount of CSF removed (F [2, 1787] = 3.22; p = 0.040) and across time (F [10, 9.58] = 11.9; p = 0.0003) without a significant dose–time interaction. A 3-ml withdrawal of CSF resulted in a 10.1% decrease in ICP and a 2.2% increase in CPP, which were sustained for 10 minutes. There was no significant dose, time or dose–time interaction with CBFV or rSO2.

Conclusions

Cerebrospinal fluid drainage (3 ml) significantly reduced ICP and increased CPP for at least 10 minutes. Analysis of these findings supports the use of ventriculostomy drainage as a means of at least temporarily reducing elevated ICP in patients with TBI.

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Cerebral arteriovenous oxygen difference: a predictor of cerebral infarction and outcome in patients with severe head injury

Peter D. Le Roux, David W. Newell, Arthur M. Lam, M. Sean Grady, and H. Richard Winn

Jugular bulb oxygen monitoring can be used to estimate the adequacy of cerebral blood flow to support cerebral metabolism after severe head injury. In the present study, the authors studied the cerebral arteriovenous oxygen difference (AVDO2) before and after treatment in 32 head-injured patients (Glasgow Coma Scale scores ¾ 8) to examine the relationships among AVDO2 and cerebral perfusion pressure (CPP), delayed cerebral infarction, and outcome. Fifteen patients (Group A) underwent craniotomy for hematoma evacuation and 17 (Group B) received mannitol for sustained intracranial hypertension (intracranial pressure > 20 mm Hg, > 10 minutes). Radiographic evidence of delayed cerebral infarction was observed in 14 patients. Overall, 17 patients died or were severely disabled. Cerebral AVDO2 was elevated before craniotomy or mannitol administration; the mean AVDO2 for all patients before treatment was 8.6 ± 1.8 vol%. Following craniotomy or mannitol administration, the AVDO2 decreased in 27 patients and increased in five patients (mean AVDO2 6.2 ± 2.1 vol% in all patients; 6 ± 1.9 vol% in Group A; and 6.4 ± 2.4 vol% in Group B). The mean CPP was 75 ± 9.8 mm Hg and no relationship with AVDO2 was demonstrated. Before treatment, the AVDO2 was not associated with delayed cerebral infarction or outcome. By contrast, a limited improvement in elevated AVDO2 after craniotomy or mannitol administration was significantly associated with delayed cerebral infarction (Group A: p < 0.001; Group B: p < 0.01). Similarly, a limited improvement in elevated AVDO2 after treatment was significantly associated with an unfavorable outcome (Group A: p < 0.01; Group B: p < 0.001). In conclusion, these findings strongly indicate that, despite adequate cerebral perfusion, limited improvement in elevated cerebral AVDO2 after treatment consisting of either craniotomy or mannitol administration may be used to help predict delayed cerebral infarction and poor outcome after traumatic brain injury.

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Cerebral blood flow as a predictor of outcome following traumatic brain injury

Daniel F. Kelly, Neil A. Martin, Rouzbeh Kordestani, George Counelis, David A. Hovda, Marvin Bergsneider, Ehud Shalmon, Duncan Q. McBride, Dena Herman, and Donald P. Becker

As part of a prospective study of the cerebrovascular effects of head injury, 54 moderate and severely injured patients underwent 184 133Xe-cerebral blood flow (CBF) studies to determine the relationship between the period of maximum blood flow and outcome. The lowest blood flows were observed on the day of injury (Day 0) and the highest CBFs were documented on postinjury Days 1 to 5. Patients were divided into three groups based on CBF values obtained during this period of maximum flow: Group 1 (seven patients), CBF less than 33 ml/100 g/minute on all determinations; Group 2 (13 patients), CBF both less than and greater than or equal to 33 ml/100 g/minute; and Group 3 (34 patients), CBF greater than or equal to 33 ml/100 g/minute on all measurements. For Groups 1, 2, and 3, mean CBF during Days 1 to 5 postinjury was 25.7 ± 4, 36.5 ± 4.2, and 49.4 ± 9.3 ml/100 g/minute, respectively, and PaCO2 at the time of the CBF study was 31.4 ± 6, 32.7 ± 2.9, and 33.4 ± 4.7 mm Hg, respectively.

There were significant differences across Groups 1, 2, and 3 regarding mean age, percentage of individuals younger than 35 years of age (42.9%, 23.1%, and 76.5%, respectively), incidence of patients requiring evacuation of intradural hematomas (57.1%, 38.5%, and 17.6%, respectively) and incidence of abnormal pupils (57.1%, 61.5%, and 32.4%, respectively). Favorable neurological outcome at 6 months postinjury in Groups 1, 2, and 3 was 0%, 46.2%, and 58.8%, respectively (p < 0.05). Further analysis of patients in Group 3 revealed that of 14 with poor outcomes, six had one or more episodes of hyperemia-associated intracranial hypertension (simultaneous CBF > 55 ml/100 g/minute and ICP > 20 mm Hg). These six patients were unique in having the highest CBFs for postinjury Days 1 to 5 (mean 59.8 ml/100 g/minute) and the most severe degree of intracranial hypertension and reduced cerebral perfusion pressure (p < 0.0001).

These results indicate that a phasic elevation in CBF acutely after head injury is a necessary condition for achieving functional recovery. It is postulated that for the majority of patients, this rise in blood flow results from an increase in metabolic demands in the setting of intact vasoreactivity. In a minority of individuals, however, the constellation of supranormal CBF, severe intracranial hypertension, and poor outcome indicates a state of grossly impaired vasoreactivity with uncoupling between blood flow and metabolism.

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AANS/CNS Cerebrovascular Section Meeting February 2011

perfusion pressure (CPP), mean arterial pressure (MAP), cerebral temperatures (Temp), and fraction of inspired oxygen (FiO2). Results Among the cohort of patients studied, 67% of those who experienced vasospasm (9), survived the disease. While the correlations between oximetry data (PbO2) and the clinical monitoring data for individual patients varied widely, when pooled for all patients, significant (p less than 0.001) Pearson Regression correlations (R) were observed: 0.370 for CPP, 0.113 for MAP, 0.018 for Temp, -0.305 for FiO2 and -0.404 for ICP. We also