Multiple myeloma presenting as solitary mass in the posterior fossa.

Intracranial plasma cell tumors are extremely rare and can either be solitary lesions or part of systemic multiple myeloma. We report a 42-year-old woman who presented with a posterior fossa mass and successfully underwent surgical resection, leading to the diagnosis of multiple myeloma. To our knowledge, this is the first reported case of multiple myeloma presenting as a posterior fossa mass lesion. This report highlights the importance of maintaining plasma cell tumor in the differential of intracranial mass with bony involvement. Furthermore, once the diagnosis is established, further work up is critical to evaluate for systemic disease.

Pro-inflammatory and pro-apoptotic elements of the neuroinflammatory response are activated in traumatic brain injury.

BACKGROUND: The inflammatory response may contribute to cerebral edema, increased intracranial pressure and cellular loss in traumatic brain injury (TBI). Cytokines are biomarkers of this inflammatory response and new methods allow simultaneous measurement of multiple cytokines. METHODS: We examined the IL-1beta, IL-6, IL-8 and IL-12, TNFalpha, and IL-10 in arterial and jugular blood as well as cerebrospinal fluid in patients with severe traumatic brain injury. FINDINGS: Multiple cytokines, particularly pro-inflammatory cytokines, are up-regulated following TBI. Cerebrospinal fluid and arteriovenous differences of some of the cytokines suggest production within the central nervous system. Antiinflammatory cytokines are not up-regulated. CONCLUSIONS: Cytokine up-regulation may contribute to the neuroinflammatory reaction that follows traumatic brain injury and may contribute to secondary injury.

Adult respiratory distress syndrome: a complication of induced hypertension after severe head injury.

OBJECT: The factors involved in the development of adult respiratory distress syndrome (ARDS) after severe head injury were studied. The presence of ARDS complicates the treatment of patients with severe head injury, both because hypoxia causes additional injury to the brain and because therapies that are used to protect the lungs and improve oxygenation in patients with ARDS can reduce cerebral blood flow (CBF) and increase intracranial pressure (ICP). In a recent randomized trial of two head-injury management strategies (ICP-targeted and CBF-targeted), a fivefold increase in the incidence of ARDS was observed in the CBF-targeted group. METHODS: Injury severity, physiological data, and treatment data in 18 patients in whom ARDS had developed were compared with the remaining 171 patients in the randomized trial in whom it had not developed. Logistic regression analysis was used to study the interaction of the factors that were related to the development of ARDS. In the final exact logistic regression model, several factors were found to be significantly associated with an increased risk of ARDS: administration of epinephrine (5.7-fold increased risk), administration of dopamine in a larger than median dose (10.8-fold increased risk), and a history of drug abuse (3.1-fold increased risk). CONCLUSIONS: Although this clinical trial was not designed to study the association of management strategy and the occurrence of ARDS, the data strongly indicated that induced hypertension in this high-risk group of patients is associated with the development of symptomatic ARDS.

Interstitial brain adenosine and xanthine increase during jugular venous oxygen desaturations in humans after traumatic brain injury.

OBJECTIVE: Adenosine decreases the cerebral metabolic rate for oxygen and increases cerebral blood flow, and it may play an important role in cerebrometabolic and cerebrovascular responses to hypoperfusion after traumatic brain injury. Jugular venous oxygen saturation is monitored after traumatic brain injury to assess brain oxygen extraction, and desaturations may reflect secondary brain insults. We hypothesized that brain interstitial adenosine and related purine metabolites would be increased during jugular venous oxygen saturation desaturations (<50%) and determined associations between the purines, lactate, and glucose to assess the role of adenosine during secondary insults in humans. DESIGN: Study of critically ill adults with severe traumatic brain injury. SETTING: Adult neurointensive care unit. PATIENTS: We prospectively defined periods of normal saturation and desaturation in six patients after severe traumatic brain injury. INTERVENTIONS: During these periods, cerebral microdialysis samples of brain interstitial fluid were collected, and adenosine and purine metabolites were measured by high-pressure liquid chromatography. MEASUREMENTS AND MAIN RESULTS: Adenosine increased 3.1-fold and xanthine increased 2.5-fold during desaturation periods (both p <.05 vs. normal saturation period, signed rank). Adenosine, xanthine, hypoxanthine, and cyclic-adenosine monophosphate correlated with lactate over both study periods (r(2) =.32,.14,.31,.07, and.26, respectively, all p <.05, Pearson product moment correlation). CONCLUSION: The marked increases in interstitial brain adenosine that occur during jugular venous oxygen desaturations suggest that adenosine may play an important role during periods of secondary insults after traumatic brain injury. The correlation of these metabolites with lactate further suggests that adenosine is increased during periods of enhanced glycolytic metabolism.

Midline shift after severe head injury: pathophysiologic implications.

OBJECTIVE: To investigate the mechanism of the adverse effect of midline shift after severe traumatic brain injury. METHODS: This study compared averaged cerebral metabolic parameters of patients with midline shift > 5 mm (S) on initial computerized tomography scan to those of patients with shift < or = 5 mm (NS). The effect of an acute subdural hematoma (SDH) was determined by separating patients into those with and those without SDH and then re-examining the effect of shift in these subgroups. RESULTS: Four hundred fifty-four patients were studied. Cerebral metabolic rate of oxygen (CMRO2, in mL/100 g per min) was always lower with shift: 1.74 for SDH-S versus 2.21 for SDH-NS (p < 0.001), and 1.80 for non-SDH-S versus 2.24 for non-SDH-NS (p < 0.001). No other major effects of shift were seen in SDH patients. Among non-SDH patients, shift was associated with higher intracranial pressure (ICP): 23.1 mm Hg versus 16.3 mm Hg (p < 0.001). Other differences between shift and nonshift patients in the non-SDH group were due at least in part to interventions to treat the elevated ICP. CONCLUSION: Midline shift after severe traumatic brain injury is associated with reduced CMRo2, regardless of whether or not SDH is present. The deleterious effects of subdural blood may be related more to the mass effect of large SDHs than to the biochemical abnormalities caused by small amounts of blood in the subdural space.

Similarities between civilian gunshot wounds to the head and nongunshot head injuries.

BACKGROUND: This investigation compared the cerebral pathophysiologic status of gunshot wounds to the head (GSWH) with that of severe head injury of other causes (non-GSWH). METHODS: Data were collected prospectively from 71 GSWH and 541 non-GSWH patients. The two groups had similar demographic characteristics and injury severities. Cerebral metabolic parameters for each patient were averaged for the entire period of monitoring. These per-patient averages were compared between GSWH and non-GSWH groups. RESULTS: Median intracranial pressure was 21.4 mm Hg in GSWH patients vs. 16.7 mm Hg in non-GSWH patients (p < 0.001). Mean arterial pressures were similar, but the higher intracranial pressure in GSWH patients produced a lower median cerebral perfusion pressure. Cerebral blood flow, cerebrovascular resistance, cerebral metabolic rate of oxygen, average jugular venous oxygen saturation, and number of jugular venous desaturations did not differ significantly between the groups. Three-month outcome was death in 43% of GSWH patients and 32% of non-GSWH patients, persistent vegetative state or severe disability in 33% and 32%, respectively, and moderate disability or good recovery in 24% and 36%, respectively. These outcomes were not significantly different (p = 0.11). CONCLUSION: GSWH patients suffer global cerebral metabolic disturbances that are at least as severe as those seen in non-GSWH patients with injuries of comparable severity. This selected population of GSWH patients may enjoy outcomes comparable to those of non-GSWH patients if they are treated by the same aggressive protocols.

Extracellular glutamate and aspartate in head injured patients.

Eighty-six patients in coma from a severe head injury underwent monitoring of extracellular concentrations of glutamate and aspartate by a microdialysis technique during the first few days after injury. The median value for glutamate was 7.4 microM (interquartile range 3.6-18.8 microM). The median value for aspartate was 2.4 microM (interquartile range 1.1-5.0 microM). Average values for the dialysate concentrations of glutamate and aspartate, were closely related to outcome (p < .001 and p = .002, respectively). Patients who died of their head injury had significantly higher dialysate glutamate and aspartate concentrations compared to patients who recovered to a Glasgow Outcome Score of good recovery or moderate disability. Dialysate glutamate and aspartate levels were also significantly related to type of injury (p = .008 and p = .004, respectively). The highest values were found in patients with gunshot wounds, followed by patients with evacuated and unevacuated mass lesions. Patients with diffuse injuries had the lowest values of glutamate and aspartate. These results suggest that excitatory amino acids may play a role in the evolution of injury to the brain after trauma.

Comparison of jugular venous oxygen saturation and brain tissue Po2 as monitors of cerebral ischemia after head injury.

OBJECTIVE: To compare the characteristics of jugular venous oxygen saturation (Sjvo2) and brain tissue Po2 (Pbto2) as monitors for cerebral ischemia after severe head injury. Sjvo2 has been useful as a monitor for cerebral ischemia, but it is limited by its inability to identify regional cerebral ischemia. Pbto2 may be superior to Sjvo2 for this purpose, because oxygenation in localized areas of the brain can be monitored. DESIGN: Sjvo2 and Pbto2 were successfully monitored in 58 patients with severe head injury. The changes in Sjvo2 and Pbto2 were compared during ischemic episodes. SETTING: Neurosurgical intensive care unit of a level I trauma center. MEASUREMENTS AND MAIN RESULTS: During the monitoring period, which averaged 90 hrs/patient, there were 54 episodes during which Sjvo2 decreased to <50% and/or Pbto2 decreased to <8 torr. Two of these episodes were caused by an infarction in the area of the Po2 probe, leaving 52 episodes of global hypoxia/ischemia that were identified by one of the two monitors. The sensitivities of the two monitors for detecting ischemia, using the thresholds of 50% and 8 torr for Sjvo2 and Pbto2, respectively, were similar. The Sjvo2 catheter detected 69.7% of the episodes and the Pbto2 catheter detected 63.5% of the episodes. In most of the remaining episodes, both probes reflected a decrease in oxygenation, but not to levels below the defined thresholds. The major differences in the two measures of oxygenation included the following: a) Sjvo2 more consistently reflected a reduction in oxygenation during hyperventilation; b) Pbto2 was affected more by changes in arterial Po2; and c) during severe global ischemia, Pbto2 decreased to 0 and remained at 0, whereas Sjvo2 initially decreased but then increased again as cerebral blood flow ceased, and the only blood in the jugular bulb was of extracerebral origin. CONCLUSIONS: The two monitors provide complimentary information, and neither monitor alone identifies all episodes of ischemia. The best strategy for using these monitors is to take advantage of the unique features of each monitor. Sjvo2 should be used as a monitor of global oxygenation; but Pbto2 should be used as a monitor of local oxygenation, ideally with the catheter placed in an area of the brain that is vulnerable to ischemia but that may be salvageable with appropriate treatment.

Prevention of secondary ischemic insults after severe head injury.

OBJECTIVE: The purpose of this study was to compare the effects of two acute-care management strategies on the frequency of jugular venous desaturation and refractory intracranial hypertension and on long-term neurologic outcome in patients with severe head injury. DESIGN: Randomized clinical trial. SETTING: Level I trauma hospital. PATIENTS: One hundred eighty-nine adults admitted in coma because of severe head injury. INTERVENTIONS: Patients were assigned to either cerebral blood flow (CBF)-targeted or intracranial pressure (ICP)-targeted management protocols during randomly assigned time blocks. In the CBF-targeted protocol, cerebral perfusion pressure was kept at >70 mm Hg and PaCO2 was kept at approximately 35 torr (4.67 kPa). In the ICP-targeted protocol, cerebral perfusion pressure was kept at >50 mm Hg and hyperventilation to a PaCO2 of 25-30 torr (3.33-4.00 kPa) was used to treat intracranial hypertension. MEASUREMENTS AND MAIN RESULTS: The CBF-targeted protocol reduced the frequency of jugular desaturation from 50.6% to 30% (p = .006). Even when the frequency of jugular desaturation was adjusted for all confounding factors that were significant, the risk of cerebral ischemia was 2.4-fold greater with the ICP-targeted protocol. Despite the reduction in secondary ischemic insults, there was no difference in neurologic outcome. Failure to alter long-term neurologic outcome was probably attributable to two major factors. A low jugular venous oxygen saturation was treated in both groups, minimizing the injury that occurred in the ICP-targeted group. The beneficial effects of the CBF-targeted protocol may have been offset by a five-fold increase in the frequency of adult respiratory distress syndrome. CONCLUSIONS: Secondary ischemic insults caused by systemic factors after severe head injury can be prevented with a targeted management protocol. However, potential adverse effects of this management strategy may offset these beneficial effects.

Cerebral hemodynamic effects of pentobarbital coma in head-injured patients.

The purpose of this study was to examine the changes in cerebral hemodynamics of head-injured patients undergoing barbiturate treatment of refractory intracranial hypertension. Cerebral blood flow (CBF) and metabolism variables were measured in 67 severely head-injured patients at the following times: before the loading dose of pentobarbital; after the loading dose of pentobarbital (average pentobarbital level 28.1+/-8.3 microg/mL); and 3 days later, when the peak pentobarbital level averaged 42.5+/-17.2 microg/mL. Intracranial pressure (ICP) and mean arterial blood pressure (MAP) were decreased by the loading dose of pentobarbital by an average of 12 and 9 mm Hg, respectively. Cerebral perfusion pressure (CPP) was unchanged when the entire group was analyzed together. CBF, cerebral oxygen consumption (CMR(O)2), and arteriovenous oxygen difference (AVD(O)2) were significantly decreased after the loading dose of pentobarbital, by 20%, 31%, and 11%, respectively. The average cerebrovascular resistance (CVR) was increased by 20%. The change in CMR(O)2 with the loading dose of pentobarbital was closely related to the pretreatment value (n = 67, r2 = 0.65, p < .001). Thirty (45%) of the patients had a "good ICP response," with a reduction in ICP from 34+/-9 to 15+/-5 mm Hg after the initial loading dose of pentobarbital. Twenty-seven (40%) of the patients had a "partial ICP response," with ICP decreasing but still remaining above 20 mm Hg after the loading dose of pentobarbital. In the remaining 10 patients, ICP did not change or even increased after pentobarbital. In the 30 patients with a good ICP response, pretreatment CMR(O)2 and AVD(O)2 were greater before administration of pentobarbital, and CMR(O)2 and AVD(O)2 decreased more with the loading dose of pentobarbital, than in the patients with partial or no ICP response. The outcome was significantly better in the patients with a good or partial ICP response to pentobarbital, with 21% of these patients having a good recovery or moderate disability at 3 months after injury, compared with 100% persistent vegetative state or death in the nonresponders. In summary, barbiturate coma can be a useful treatment modality for acutely reducing ICP in selected patients. Patients with overwhelmingly severe injuries are not likely to benefit, partly because their CMR(O)2 is already markedly reduced by the injury and partly because their outcome is already predetermined by the injury. Patients with systemic hypotension are not likely to have a good response because hypotension limits the amount of barbiturates that can be given.

Extracellular lactate and glucose alterations in the brain after head injury measured by microdialysis.

OBJECTIVE: To study cerebral glucose and lactate metabolism in head-injured patients using microdialysis. DESIGN: Prospective, nonrandomized, clinical study. SETTING: Neurosurgical intensive care unit in a university-affiliated county hospital. PATIENTS: One hundred twenty-six head-injured patients. INTERVENTIONS: Cerebral cortical neurochemical monitoring using microdialysis coupled with systemic hemodynamic and oxygenation monitoring, measurement of cerebral perfusion pressure and intracranial pressure, and measurement of global cerebral oxygenation using jugular venous oxygen saturation in all 126 patients. In selected cases, cerebral blood flow was also measured using cortical thermodilution probes in 33 patients, and regional cerebral oxygenation was measured using PO2 probes in 65 patients. MEASUREMENTS AND MAIN RESULTS: Elevated extracellular lactate, reduced glucose, and an elevated lactate/glucose ratio were observed with cerebral hypoxia and ischemia. Elevated lactate and an increased lactate/glucose ratio strongly correlated with death. Other more subtle alterations of lactate and glucose were seen early after injury that may reflect compensatory alterations in cerebral metabolism. CONCLUSIONS: Clinical neurochemical monitoring of glucose and lactate levels in the extracellular space of the cerebral cortex is technically feasible and provides insight into the bioenergetic status of the brain. Increased lactate and decreased glucose, indicating accelerated glycolysis, commonly occurred with cerebral ischemia or hypoxia, and increased anaerobic glycolysis in this setting is associated with a poor outcome.

Simultaneous measurement of cortical potassium, calcium, and magnesium levels measured in head injured patients using microdialysis with ion chromatography.

Potassium, calcium and magnesium were measured in 3717 microdialysate samples in 43 patients with head injury experiencing refractory increased ICP, episodes of jugular venous oxygen desaturation and brain death. Cation analysis was performed with 'ion chromatography'. Potassium levels remained stable until severe physiological deterioration occurred, whereupon they increased 100-400%, usually associated with release of amino-acids including glutamate, aspartate, and taurine into the extracellular space. The magnesium and calcium levels remained unchanged, regardless of the severity of physiological deterioration.

Relationship of brain tissue PO2 to outcome after severe head injury.

OBJECTIVE: To determine thresholds of brain tissue PO2 (PbtO2) that are critical for survival after severe head injury. DESIGN: Prospective data collection. SETTING: Neurosurgical intensive care unit of Ben Taub General Hospital, a comprehensive academic neurosurgical facility and Level I trauma center. PATIENTS: Forty-three severely head-injured patients who were not obeying commands on presentation or whose condition deteriorated to this level shortly after admission. INTERVENTIONS: Intracerebral placement of Licox (n=39) or Paratrend (n=4) PO2 probes during craniotomy or in the intensive care unit. MEASUREMENTS AND MAIN RESULTS: PbtO2 monitoring continued for an average of 84.6+/-41.8 hrs. The probes were calibrated before insertion according to the manufacturer's specifications. After removal, probes were tested in room air and in blood gas standard calibration solutions. PbtO2 data were analyzed by comparing the average time that PbtO2 was below the values of 20, 15, 10, 8, 6, 4, and 2 torr (2.7, 2.0, 1.3, 1.0, 0.8, 0.5, and 0.3 kPa, respectively) in patients who were living 3 mos after injury vs. those who died. A Tobit regression analysis using maximum likelihood methods was utilized. Both Licox and Paratrend probes functioned well in room air and in the Level I control. However, in the zero-oxygen solution, the Paratrend probes gave an average reading of 7.0+/-1.4 torr (0.9+/-0.2 kPa), compared with 0.3+/-0.3 torr (0.04+/-0.04 kPa) for the Licox probes. CONCLUSIONS: Analysis of the PbtO2 monitoring data suggested that the likelihood of death increased with increasing duration of time at or below a PbtO2 of 15 torr (2.0 kPa) or with the occurrence of any PbtO2 values of < or =6 torr (< or =0.8 kPa).

Comparison of brain tissue oxygen tension to microdialysis-based measures of cerebral ischemia in fatally head-injured humans.

This study investigated the relationship between brain tissue oxygen tension (PbtO2) and cerebral microdialysate concentrations of several compounds in five patients with refractory intracranial hypertension after severe head injury. The following substances were assayed: lactate and glucose; the excitatory amino acids glutamate and aspartate; and the cations potassium, calcium, and magnesium. Glucose concentrations did not correlate with PbtO2, but lactate increased as PbtO2 decreased. The lactate/glucose ratio exhibited a close relationship to PbtO2, increasing sharply only when oxygen tension reached zero. Although glucose and oxygen eventually reached very low levels and zero, respectively, in these fatally head-injured patients, the terminal decrease in PbtO2 slightly preceded that of glucose in four of the five patients. This time lag is the cause of the poor correlation between glucose and PbtO2. Glutamate and aspartate concentrations both demonstrated a close relationship to PbtO2, with sharp increases not occurring until PbtO2 was zero. Concentrations of these amino acids exhibited a similar pattern in response to decreasing glucose concentrations. Potassium concentrations began increasing at a PbtO2 of 35 mm Hg, which is not generally considered indicative of hypoxia. Sharper increases began occurring once PbtO2 dropped below 15 mm Hg, with a slight rise in the minimum potassium concentrations recorded at these low PbtO2 values. Calcium and magnesium concentrations did not vary in response to PbtO2. In summary, the most robust biochemical indicators of cerebral anoxia were elevations in the lactate/glucose ratio and in the concentrations of lactate and of the excitatory amino acids glutamate and aspartate. Furthermore, the fact that glucose concentrations continue to decrease for a short period after oxygen levels reach zero suggests that cells continue to utilize glucose anaerobically for such functions as maintenance of cellular integrity, with collapse of the cell membrane as evidenced by increases of extracellular glutamate and aspartate not occurring until both oxygen and glucose concentrations reach zero.

Metabolic changes in the brain during transient ischemia measured with microdialysis.

Forty-four patients with severe head injury were monitored for episodes of cerebral ischemia using jugular venous oxygen saturation (sjvO2), brain tissue pO2 (ti-pO2), and a microdialysis probe. The concentration of lactate and glucose were measured in the microdialysate. A total of 10 episodes of global ischemia were observed. The characteristic pattern of a simultaneous decrease in sjvO2 and brain ti-pO2 with an increase in the concentration of lactate occurred in all 10 patients. In addition, 3 episodes of regional ischemia were observed. Although brain ti-pO2 decreased to very low values and the concentration of lactate increased in the microdialysate, sjvO2 remained unchanged. Brain ti-pO2 adds another dimension to our cerebral monitoring by allowing the detection of regional cerebral ischemia.

Brain temperature exceeds systemic temperature in head-injured patients.

OBJECTIVE: To identify the temperature differences in readings taken from the brain, jugular bulb, and core body in head-injured patients. DESIGN: Prospective, observational study. SETTING: Neurosurgical intensive care unit of a university-affiliated county hospital. PATIENTS: Thirty patients with severe head injuries had measurements of brain and core body temperatures. Fourteen patients also had measurements of jugular venous blood at the level of the jugular bulb. INTERVENTIONS: None. MEASUREMENTS AND MAIN RESULTS: Brain temperature was increased an average of 2.0 degrees F (1.1 degrees C) over the core body temperature. In individual patients, the average brain temperature increase over the core body temperature ranged from -0.5 degrees to 3.8 degrees F (-0.30 degrees to 2.1 degrees C). Jugular vein and core body temperatures were similar. The difference in the brain and body temperatures increased when cerebral perfusion pressure decreased to between 20 and 50 mm Hg. The difference in the brain and body temperatures decreased in those patients treated with barbiturate coma. CONCLUSIONS: Direct measurement of temperature in head-injured patients is a safe procedure. Temperatures in the brain are typically increased over the core body temperature and the jugular bulb temperatures. Jugular vein temperature measurement is not a good measurement of brain temperature since it reflects body, not brain temperature. These findings support the potential importance of monitoring brain temperature and the importance of controlling fever in severely head-injured patients since brain temperature may be higher than expected.

Cerebral oxygenation during warming after cardiopulmonary bypass.

OBJECTIVES: To evaluate jugular venous oxygen saturation (SjVO2), measured with a fiberoptic oximetry catheter, and brain tissue oxygen saturation, measured by near-infrared spectroscopy (NIRSO2), as monitors of cerebral oxygenation during cardiopulmonary bypass surgery. DESIGN: Prospective, clinical study. SETTING: Operating room of a Veterans Administration Hospital. PATIENTS: Nineteen patients undergoing moderate hypothermic cardiopulmonary bypass surgery. INTERVENTIONS: SjvO2 and NIRSO2 were monitored in the patients during the surgical procedure. MEASUREMENTS AND MAIN RESULTS: Moderate hypothermic cardiopulmonary bypass surgery had two distinct cerebral hemodynamic phases. While the patients were hypothermic, SjvO2 averaged 80 +/- 7% and none of the patients had an increase in cerebral lactate production. During the rewarming period, however, reductions in SjvO2 to < 50% occurred in 16 (84%) patients and increased cerebral anaerobic metabolism developed in 11 (58%) patients. SjvO2 during rewarming was dependent on mean arterial pressure, with 60 mm Hg appearing to be a critical value. Two other factors appeared to also contribute to the jugular desaturation, a low hematocrit and a rapid warming time. The SjvO2 catheter had excellent performance during the surgery. The average difference between paired measurements of SjvO2 by the catheter and in blood samples was -0.4 +/- 4.25%, and the correlation between the two measurements was highly significant (r2 = .93; p < .001). The NIRSO2 trended with the SjvO2 in most patients (r2 = .63; p < .001). CONCLUSIONS: The study confirms other studies showing that jugular venous desaturation can occur during rewarming after cardiopulmonary bypass surgery. Presently, SjvO2 appears to be a better monitor of cerebral oxygenation than NIRSO2. However, NIRSO2 has promise as a noninvasive monitor of cerebral oxygenation if future developments allow more quantitative measurements of oxygen saturation.

Positive end expiratory pressure reduces intracranial compliance in the rabbit.

Acute respiratory distress syndrome is commonly encountered in head-injured patients. Positive and expiratory pressure (PEEP) is useful in improving oxygenation. However, PEEP, by increasing intrathoracic pressure, decreases venous return, mean arterial pressure, and cardiac output and increases jugular vein pressure. There is conflicting evidence in the literature as to the potential effect of PEEP on intracranial pressure (ICP). The present study was undertaken to examine the effect of PEEP on ICP and intracranial compliance. Twelve male rabbits weighing 3.5-4.5 kg were used. The following parameters were monitored: arterial blood pressure, ICP (intraparenchymal Camino device), PaCO2, and PaO2. A space-occupying lesion was produced by inflation of a double lumen pediatric Swan-Ganz catheter placed over the right parietal dura. The amount of fluid required to reach the point of exponential increase of ICP was recorded at PEEP of 0 and 10 cm H2O. The mean volume needed to reach the deflection point of ICP was significantly lower when PEEP was 10 cm H2O compared to the value when PEEP was 0 cm H2O (685 +/- 48 vs. 883.3 +/- 46 microliters, respectively; p < 0.01). The results of the present study indicated that PEEP of 10 cm H2O decreases intracranial compensatory reserves for maintaining ICP at normal levels in the presence of an expanding intracranial mass.

Intraoperative jugular desaturation during surgery for traumatic intracranial hematomas.

Traumatic intracranial hematomas which are present on hospital admission or which develop during the hospital course are associated with a worse neurological outcome than diffuse injuries. The purpose of this study was to monitor jugular venous oxygen saturation (Sjvo2) during surgery for evacuation of traumatic intracranial mass lesions, to determine the incidence and the causes of jugular venous desaturation, and to assess the usefulness of Sjvo2 monitoring in this setting. Twenty-five severely head injured patients were monitored during 27 surgical procedures. At the start of the surgical procedure, the median Sjvo2 was 47% (range 25%-89%). Seventeen (63%) of the patients had a Sjvo2 less than 50%. Five patients had extremely low Sjvo2 values (< or = 30%). Upon evacuation of the intracranial hematoma, there was a significant (P < 0.001) increase in the median Sjvo2 to 65% (range 50%-88%). Intracranial hypertension was the primary cause of the low Sjvo2, as confirmed by the response to surgical evacuation. Hypotension (mean arterial pressure < 80 mm Hg) was a contributing factor in seven of the cases of jugular desaturation. The definitive treatment of a traumatic intracranial hematoma is surgical evacuation. However, during the period prior to evacuation of the hematoma, jugular venous desaturation was common, suggesting that monitoring Sjvo2 might provide useful information about the adequacy of cerebral perfusion.

Lactate and excitatory amino acids measured by microdialysis are decreased by pentobarbital coma in head-injured patients.

Primary traumatic brain injury and secondary ischemic/hypoxic injury are being increasingly characterized at the neurochemical level. Neurochemical monitoring using microdialysis has shown that these forms of tissue damage share many common features. In particular, anaerobic glycolysis with increased lactate production and release of excitatory amino acids into the extracellular space are seen in both conditions. Clinical microdialysis studies have heretofore focused on methodological issues, establishment of basal analyte values, and clinico-neurochemical correlation. Here we report the neurochemical consequences of therapeutic intervention in head injury. Specifically, induction of thiopental coma to manage severe increased intracranial pressure in seven patients was associated with a 37% reduction of lactate, 59% reduction of glutamate, and 66% reduction in aspartate in the extracellular space of the brain.