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Biomedical subjects

A W Unterberg

Publications and source records attributed to A W Unterberg.

At least 19 recordsLinked to original sources
PubMed2001

Secondary insults in severe head injury--do multiply injured patients do worse?

OBJECTIVES: To study the occurrence of secondary insults and the influence of extracranial injuries on cerebral oxygenation and outcome in patients with closed severe head injury (Glasgow Coma Scale score < or =8). DESIGN: Two-year prospective, clinical study. SETTING: Two intensive care units in a level III trauma center. PATIENTS: We studied 119 patients. Eighty patients had severe head injury and were divided into two categories: "isolated" severe head injury patients (n = 36, Injury Severity Score <30), and severe head injury patients with associated extracranial injuries (n = 44, Injury Severity Score >29). Thirty-nine patients with extracranial injuries and no head injury served as the control group. INTERVENTIONS: After patients were admitted to the intensive care unit, we began continuous multimodal cerebral monitoring of intracranial pressure, mean arterial blood pressure, cerebral perfusion pressure, end-tidal Co2, brain tissue Po2 (Licox), jugular bulb oxyhemoglobin saturation in severe head injury patients, and mean arterial blood pressure in the control group. Targets of management included intracranial pressure <20 mm Hg, cerebral perfusion pressure >60 mm Hg, Paco2 > 30 mm Hg, control of cerebral oxygenation, and delayed surgery for non-life-threatening extracranial lesions. MEASUREMENTS AND MAIN RESULTS: Data were analyzed for critical thresholds. The occurrence of secondary insults (intracranial pressure >20 mm Hg, mean arterial blood pressure <70 mm Hg, cerebral perfusion pressure <60 mm Hg, end-tidal Co2 <30 torr, brain tissue Po2 <10 torr, jugular bulb oxyhemoglobin saturation <50%) was comparable in patients with isolated severe head injury and those with severe head injury with associated extracranial lesions (Abbreviated Injury Scale score < or =5). The duration of intracranial hypertension and arterial hypotension significantly correlated with an unfavorable outcome, independent of the Injury Severity Score. In patients with severe head injury, 1-yr outcome was 29% dead or vegetative, 17% severely disabled, and 54% moderate or good outcome. This was similar to patients with severe head injury and extracranial injuries (31% dead or vegetative, 14% severely disabled, and 56% moderate or good outcome) and was independent of the Injury Severity Score. Patients with no head injury had less secondary insults (mean arterial blood pressure <70 mm Hg, p <.01) and a better outcome compared with both severe head injury groups (p <.044). CONCLUSIONS: In patients with severe head injury who have targeted management including intracranial pressure- and cerebral perfusion pressure-guided therapy and delayed surgery for extracranial lesions, the occurrence of secondary insults in the intensive care unit and long-term neurological outcome were comparable and independent of the presence of extracranial lesions (Abbreviated Injury Severity level < or =5). A severe head injury is still a major contributor predicting an unfavorable outcome in multiply injured patients.

Adult↗
PubMed2001

Secondary abscess formation in pituitary adenoma after tooth extraction. Case report.

The presence of an abscess in a pituitary tumor is a very rare finding. The authors report the case of a 69-year-old man with a pituitary adenoma confirmed by neuroimaging results, in whom a high fever, meningismus, and left-sided ophthalmoplegia developed 4 days after tooth extraction. The results of serial cranial magnetic resonance imaging were highly indicative of an abscess formation within the pituitary adenoma. During surgery the tumor was approached transsphenoidally and removed. Histological examination confirmed the presence of an abscess formation within the pituitary adenoma. It is most likely that the tooth extraction caused a bacteremia, which led to an inflammation with abscess formation within the pituitary adenoma. The authors conclude that invasive dental procedures should be avoided before planned resection of a pituitary adenoma.

Adenoma↗
PubMed2001

Role of bedside microdialysis in the diagnosis of cerebral vasospasm following aneurysmal subarachnoid hemorrhage.

OBJECT: Ischemia due to vasospasm is a feared complication in patients following aneurysmal subarachnoid hemorrhage (SAH). Cerebral online microdialysis monitoring may detect the metabolic changes in the extracellular fluid associated with ischemia. The aims of the present study were to correlate clinical course, microdialysis-recorded data, transcranial Doppler (TCD) ultrasonography findings, and angiographic findings in patients with SAH. METHODS: In 60 patients a microdialysis catheter was inserted into the brain parenchyma that is most likely to be affected by vasospasm directly after aneurysm clipping. Hourly analyses of glucose, pyruvate, lactate, and glutamate levels were performed using a bedside device. Blood-flow velocities were obtained using serial TCD measurements. Cerebral angiography was routinely performed on Day 7 after aneurysm clipping or earlier in cases of clinical deterioration (30 patients). In all patients the results of microdialysis monitoring, TCD ultrasonography, and angiography were correlated. The mean duration of monitoring was 7.3+/-2.5 days. In patients with acute ischemic neurological deficits (18 patients) immediate microdialysis-recorded alterations were observed if the probe was placed close to the malperfused region. In 13 of 15 patients with symptomatic vasospasm (delayed ischemic neurological deficit [DIND]), the microdialysis-recorded values revealed secondary deterioration. In terms of confirming DIND, microdialysis had the highest specificity (0.89, 95% confidence interval [CI] 0.78-1) compared with TCD ultrasonography (0.63, 95% CI 0.46-0.8) and angiography (0.53, 95% CI 0.35-0.7). For microdialysis, the positive likelihood ratio was 7.8, whereas this was significantly lower for TCD ultrasonography (1.7) and angiography (2.1). CONCLUSIONS: Although angiography also demonstrates vessel narrowing in asymptomatic patients, online microdialysis reveals characteristic metabolic changes that occur during vasospasm. Thus, online microdialysis may be used to confirm the diagnosis of vasospasm.

Adult↗
PubMed2001

Effects of tacrolimus on hemispheric water content and cerebrospinal fluid levels of glutamate, hypoxanthine, interleukin-6, and tumor necrosis factor-alpha following controlled cortical impact injury in rats.

OBJECT: Disturbance of calcium homeostasis contributes to evolving tissue damage and energetic impairment following traumatic brain injury (TBI). Calcium-mediated activation of calcineurin results in production of tissue-damaging nitric oxide and free oxygen radicals. Inhibition of calcineurin induced by the immunosuppressant tacrolimus (FK506) has been shown to reduce structural and functional damage after ischemia. The aims of the present study were to investigate time- and dose-dependent short-term antiedematous effects of tacrolimus following TBI. METHODS: A left temporoparietal contusion (controlled cortical impact injury [CCII]) was induced in 51 male Sprague-Dawley rats. Tacrolimus (1 or 3 mg/kg body weight) was administered by a single intraperitoneal injection at 5 minutes, 30 minutes, or 4 hours after CCII occurred. Control rats received physiological saline. Water contents of traumatized and nontraumatized hemispheres, as well as cerebrospinal fluid (CSF) levels of mediators reflecting tissue damage (the proinflammatory cytokines interleukin [IL]-6 and tumor necrosis factor [TNF]-alpha, the excitotoxin glutamate, and the adenosine triphosphate-degradation product hypoxanthine), were determined 24 hours after trauma. Although CSF levels of IL-6 and TNFalpha were completely suppressed by tacrolimus at all time points and at both concentrations, CSF levels of glutamate and hypoxanthine, as well as edema formation, were only marginally influenced. Significant reduction of cerebral water content was confined to nontraumatized hemispheres. In addition, the higher dose of tacrolimus failed to exert significant antiedematous effects on traumatized hemispheres. CONCLUSIONS: Under the present study design, the potency of tacrolimus in reducing edema formation following CCII seems limited. However, its immunosuppressive effects could be of value in influencing the posttraumatic inflammatory response known to aggravate tissue damage.

Animals↗
PubMed2000

Increased cerebrospinal fluid glutamate and taurine concentrations are associated with traumatic brain edema formation in rats.

Glutamate-mediated excitotoxicity results in cell swelling and contributes to brain edema formation. Since increased extracellular taurine reflects glutamate-induced cell swelling in vitro, elevated CSF taurine could therefore unmask glutamate-mediated cytotoxic edema formation under in vivo conditions. For this, the temporal profile of brain edema and changes in cisternal CSF glutamate and taurine levels were determined in 28 rats following focal traumatic brain injury. Compared to six non-traumatized rats, CSF glutamate (4. 8+/-0.3 vs. 10+/-0.9 microM) and taurine levels (12+/-1.3 vs. 41+/-3 microM) were significantly increased at 8 h after trauma (P<0.001). Over time, CSF glutamate and taurine were significantly increased by 24 (glutamate: 38+/-4.4 microM) and 48 h (taurine: 51+/-4 microM), respectively. While CSF glutamate closely reflected changes in hemispheric water content, alterations in CSF taurine occurred diametrically to those seen for glutamate. Under the present study design, increased CSF taurine could reflect glutamate-induced cell swelling. In addition, neuronal release of taurine with its inhibitory and antiexcitotoxic functions could explain the observed diametric changes in CSF glutamate, CSF taurine, and hemispheric water content. Therefore, increasing taurine could be a therapeutic approach in attenuating post-traumatic glutamate-mediated cell damage.

Amino Acids↗
PubMed2000

Temporal profile of cerebrospinal fluid glutamate, interleukin-6, and tumor necrosis factor-alpha in relation to brain edema and contusion following controlled cortical impact injury in rats.

Traumatic brain injury is associated with release of the excitotoxin glutamate and production of pro-inflammatory cytokines IL-6 and tumor necrosis factor-alpha (TNF-alpha). Following controlled cortical impact injury, cerebrospinal fluid (CSF) glutamate, IL-6, and TNF-alpha concentrations were measured to investigate their relationship to evolving tissue damage. Compared to non-traumatized rats CSF glutamate, IL-6 and TNF-alpha levels were significantly increased by 8 h after trauma (P<0.005). Parallel to increasing brain swelling and contusion CSF glutamate was significantly elevated over time, reaching highest levels by 48 h (33+/-4 microM) while IL-6 and TNF-alpha showed maximum values at 24 h after trauma (42+/-7 and 4.7+/-1 pg/ml) (P<0.005). The observed different temporal profile of CSF glutamate, IL-6, and TNF-alpha following focal traumatic brain injury could be of therapeutic importance.

Animals↗
PubMed2000

Neuroprotective effect of melatonin on cortical impact injury in the rat.

The pineal hormone melatonin is a highly efficient physiological scavenger of free radicals involved in secondary brain damage. A variety of experimental studies have demonstrated a neuroprotective effect for melatonin, based on its antioxidant activity. The purpose of the present study was to investigate the time-dependency and a possible protective effect of exogenous melatonin in the cortical impact model in rats. The protective effect was quantified determining contusion volume, brain edema and brain water content. 45 anesthetized male Sprague-Dawley rats (250-350 mg) were subjected to cortical impact injury of moderate severity (7 m/s, deformation 2 mm). Melatonin (100 mg/kg bw i.p.), or a vehicle was injected 20 min before trauma, immediately after, and 1 and 2 hours after trauma during daytime and nighttime. Posttraumatic lesion volume using hematoxylin-eosin staining, hemispheric swelling, brain water content, cerebral perfusion pressure and intracranial pressure 24 hours after injury were investigated. Melatonin, given during nighttime, significantly reduced contusion volume corresponding to a mean reduction of contusion volume of 27% (placebo, n = 7: 41.9 +/- 5.2 mm3, melatonin, n = 8: 30.5 +/- 4.2 mm3, p < 0.05). Given during daytime, the reduction in contusion volume was not significant (placebo, n = 8: 42.1 +/- 5.1 mm3, melatonin, n = 8: 35.9 +/- 2.2 mm3, reduction of 15%, p = 0.08, n.s.). Hemispheric swelling was unchanged by melatonin treatment. Mean arterial blood pressure and rectal temperature remained stable before and after the cortical impact injury and injection of melatonin. This study shows that melatonin significantly reduces contusion volume with major effects during night.

Animals↗
PubMed2000

Riluzole reduces brain swelling and contusion volume in rats following controlled cortical impact injury.

Modulation of the glutamatergic and excitotoxic pathway may attenuate secondary damage following traumatic brain injury by reducing presynaptic glutamate release and blocking sodium channels in their inactivated state. The aim of the present study was to investigate the neuroprotective potential of riluzole in traumatic brain-injured rats. A left temporoparietal contusion was induced in 70 male Sprague-Dawley rats (controlled cortical impact injury). Riluzole (8 mg/kg body weight) was given 30 min, and 6, 24, and 30 h after trauma, while control rats received physiological saline. Experiments were performed at two different degrees of trauma severity as defined by penetration depth of the impactor rod (1 vs. 1.5 mm) with the aim of investigating impact of severity of tissue damage on the neuroprotective potential of riluzole. At 48 h after trauma, brains were removed to determine hemispheric swelling and water content and to assess cortical contusion volume. Before brain removal cisternal cerebrospinal fluid (CSF) was collected in all rats to determine the effects of riluzole on substances associated with edema formation. For this, the excitatory transmitter glutamate, the volume-regulatory amino acid taurine, and the ATP-degradation product hypoxanthine were analyzed by high-performance liquid chromatography. Overall, the degree of tissue damage seems to influence the neuroprotective potential of riluzole. In rats with a less severe trauma (1-mm penetration depth), hemispheric swelling, cerebral water content of the traumatized hemisphere and cortical contusion volume were significantly reduced under riluzole compared to controls (p < 0.05). In rats with a more severe trauma (1.5-mm penetration depth), the neuroprotective effect of riluzole failed to reach statistical significance. Following trauma, CSF glutamate, taurine, and hypoxanthine levels were significantly increased compared to nontraumatized rats (p < 0.001). However, these neurochemical parameters as measured in cisternal CSF failed to reflect trauma-dependent increases in severity of tissue damage and did not reveal riluzole-mediated neuroprotection. Under the present study design, riluzole significantly reduced brain edema formation and contusion volume in rats subjected to a mild focal cortical contusion.

Animals↗
PubMed2000

Effects of dopamine on posttraumatic cerebral blood flow, brain edema, and cerebrospinal fluid glutamate and hypoxanthine concentrations.

OBJECTIVES: Dopamine is often used in the treatment of traumatic brain injury to maintain cerebral perfusion pressure. However, it remains unclear whether dopamine contributes to secondary brain injury caused by vasoconstriction and resulting diminished cerebral perfusion. The present study investigated the effects of dopamine in different concentrations on posttraumatic cortical cerebral blood flow (CBF), brain edema formation, and cerebrospinal fluid concentrations of glutamate and hypoxanthine. DESIGN: Randomized, placebo-controlled trial. SETTING: Animal laboratory. SUBJECTS: Eighteen male Sprague-Dawley rats subjected to a focal cortical brain injury. INTERVENTIONS: Four hours after controlled cortical impact, rats were randomized to receive physiologic saline solution (n = 6), 10-12 tig/kg/min dopamine (n = 6), or 40-50 microg/kg/min dopamine (n = 6), for 3 hrs. Cortical CBF was measured over both hemispheres by using laser-Doppler flowmetry before trauma and before, during, and after the infusion period. At 8 hrs after trauma, brains were removed to determine hemispheric swelling and water content. Cisternal cerebrospinal fluid was sampled to measure glutamate and hypoxanthine. MEASUREMENTS AND MAIN RESULTS: After trauma, cortical CBF was significantly decreased by 46% within the vicinity of the cortical contusion in all rats. Infusion of saline and 10-12 ig/kg/min dopamine did not change mean arterial blood pressure (MABP) or cortical CBF. However, infusion of 40-50 microg/kg/min dopamine, which elevated MABP from 89 to 120 mm Hg, significantly increased posttraumatic CBF within and around the contusion by 35%. Over the nontraumatized hemisphere, CBF remained unchanged. Hemispheric swelling, water content, cerebrospinal fluid glutamate, and hypoxanthine levels were not affected by dopamine in the given dosages. CONCLUSIONS: Under the present study design, there was no evidence for a dopamine-mediated vasoconstriction, because posttraumatic cortical CBF was increased by dopamine-induced elevation of MABP. However, the increase in CBF did not significantly affect edema formation or cerebrospinal fluid glutamate and hypoxanthine levels.

Animals↗
PubMed2000

Significant reduction in brain swelling by administration of nonpeptide kinin B2 receptor antagonist LF 16-0687Ms after controlled cortical impact injury in rats.

OBJECT: Identification of new therapeutic agents aimed at attenuating posttraumatic brain edema formation remains an unresolved challenge. Among others, activation of bradykinin B2 receptors is known to mediate the formation of brain edema. The purpose of this study was to investigate the protective effect of the novel nonpeptide B2 receptor antagonist, LF 16-0687Ms, in brain-injured rats. METHODS: Focal contusion was produced by controlled cortical impact injury. Five minutes after trauma, the rats received a single dose of no, low- (3 mg/kg body weight), or high- (30 mg/kg) dose LF 16-0687Ms. After 24 hours, the amount of brain swelling and hemispheric water content were determined. Low and high doses of LF 16-0687Ms significantly reduced brain swelling by 25% and 27%, respectively (p < 0.03). Hemispheric water content tended to be increased in the nontraumatized hemisphere. In a subsequent series of 10 rats, cisternal cerebrospinal fluid (CSF) samples were collected to determine whether changes in substances associated with edema formation could clarify why LF 16-0687Ms increases water content. For this, the volume regulator amino acid taurine, the excitatory transmitter glutamate, and the adenosine triphosphate degradation products hypoxanthine and xanthine were measured. In CSF, the levels of taurine, hypoxanthine, and xanthine were significantly decreased following a single administration of LF 16-0687Ms (p < 0.005); the level of glutamate, however, was double that found in control animals (p < 0.05). CONCLUSIONS: Using the present study design, a single administration of LF 16-0687Ms successfully reduced posttraumatic brain swelling. The decreased levels of taurine, hypoxanthine, and xanthine may reflect reduced posttraumatic brain edema, whereas the increased level of glutamate could account for the elevated water content observed in the nontraumatized hemisphere.

Analysis of Variance↗
PubMed1999

Lubeluzole following traumatic brain injury in the rat.

Lubeluzole, a novel nitric oxide synthase (NOS) pathway modulator, was shown to be neuroprotective in cerebral ischemia as studied in animal models and clinical trials. The present study investigated the effect of lubeluzole on contusion volume and brain edema following traumatic brain injury. Sprague-Dawley rats (n = 36) were subjected to cortical impact injury. Lubeluzole (0.8 mg/kg i.v.; n = 18) or a corresponding volume of vehicle (n = 18) was injected 15 and 75 minutes following trauma. Animals were sacrificed 24 hours following trauma. Contusion volume was measured planimetrically from coronal slices stained with hematoxylin and eosin. In this group, T2-weighted magnetic resonance imaging (MRI) was also performed 90 minutes and 6 and 24 hours after trauma. Hemispheric swelling and water content were determined gravimetrically 24 hours after trauma. In this group, intracranial pressure (ICP), mean arterial blood pressure (MABP), and cerebral perfusion pressure (CPP) were monitored for 30 minutes before sacrifice. Lubeluzole did not reduce contusion volume, hemispheric swelling, or water content. ICP, MABP, and the resulting CPP did not differ between treated and untreated rats 24 hours after injury. T2-weighted MRI revealed a higher volume of edema at 90 minutes after trauma in treated rats. However, at 6 and 24 hours after trauma, no significant difference was discernible. Under these experimental conditions, lubeluzole fails to exert beneficial effects following experimental traumatic brain injury (TBI).

Animals↗
PubMed1999

Effect of cerebral perfusion pressure on contusion volume following impact injury.

OBJECT: Although it is generally acknowledged that a sufficient cerebral perfusion pressure (CPP) is necessary for treatment of severe head injury, the optimum CPP is still a subject of debate. The purpose of this study was to investigate the effect of various levels of blood pressure and, thereby, CPP on posttraumatic contusion volume. METHODS: The left hemispheres of 60 rats were subjected to controlled cortical impact injury (CCII). In one group of animals the mean arterial blood pressure (MABP) was lowered for 30 minutes to 80, 70, 60, 50, or 40 mm Hg 4 hours after contusion by using hypobaric hypotension. In another group of animals the MABP was elevated for 3 hours to 120 or 140 mm Hg 4 hours after contusion by administering dopamine. The MABP was not changed in respective control groups. Intracranial pressure (ICP) was monitored with an ICP microsensor. The rats were killed 28 hours after trauma occurred and contusion volume was assessed using hematoxylin and eosin-stained coronal slices. No significant change in contusion volume was caused by a decrease in MABP from 94 to 80 mm Hg (ICP 12+/-1 mm Hg), but a reduction of MABP to 70 mm Hg (ICP 9+/-1 mm Hg) significantly increased the contusion volume (p < 0.05). A further reduction of MABP led to an even more enlarged contusion volume. Although an elevation of MABP to 120 mm Hg (ICP 16+/-2 mm Hg) did not significantly affect contusion volume, there was a significant increase in the contusion volume at 140 mm Hg MABP (p < 0.05; ICP 18+/-1 mm Hg). CONCLUSION: Under these experimental conditions, CPP should be kept within 70 to 105 mm Hg to minimize posttraumatic contusion volume. A CPP of 60 mm Hg and lower as well as a CPP of 120 mm Hg and higher should be considered detrimental.

Animals↗
PubMed1998

Influence of hyperventilation on brain tissue-PO2, PCO2, and pH in patients with intracranial hypertension.

A harmful effect of prolonged hyperventilation on outcome has been shown in comatose patients after severe head injury. The purpose of this study was to assess the acute effect of moderate hyperventilation for treatment of intracranial hypertension (ICP < 20 mmHg) on invasively measured brain tissue-PO2 (PtiO2), PCO2 (PtiCO2) and pH (tipH) in severely head injured patients. 15 severely head injured patients (GCS < or = 8) were prospectively studied. Intracranial pressure (ICP), mean arterial blood pressure (MABP), cerebral perfusion pressure (CPP), endtidal CO2 (ETCO2), PtiO2, PtiCO2 and tipH (Paratrend or Licox microsensors) were continuously recorded using multimodal monitoring. Following a baseline period of 15 minutes, patients were hyperventilated for 10 minutes. Arterial blood gas analysis was done before, during and after hyperventilation. At least three hyperventilation maneuvers were performed per patient. For statistical analysis the Friedman test was used. Hyperventilation (paCO2: 32.4 +/- 0.6 to 27.7 +/- 0.5 mmHg) significantly reduced ICP from 25.3 +/- 1.5 to 14.2 +/- 1.9 mmHg (p < 0.01). As a consequence, CPP increased by 9.6 +/- 3.4 mmHg to 76.8 +/- 3.2 mmHg. Brain tissue PCO2 decreased from 37.5 +/- 1.3 to 34.6 +/- 1.2 while tipH increased from 7.13 to 7.16. In all patients, hyperventilation led to a reduction of brain tissue PO2 (PtiO2/Licox: 24.6 +/- 1.4 to 21.9 +/- 1.7 mmHg, n.s.; PtiO2/Paratrend: 35.8 +/- 4.3 to 31.9 +/- 4.0 mmHg, n.s.). In one case hyperventilation even had to be stopped after 7 min because the drop in brain tissue PO2 below 10 mmHg signalized imminent hypoxia. As well known, hyperventilation improves CPP due to a reduction in ICP. However, this does not ameliorate cerebral oxygenation as demonstrated by the decrease in PtiO2. This underlines that hyperventilation should only be used with caution in the treatment of intracranial hypertension.

Acid-Base Equilibrium↗
PubMed1998

Neuroprotective properties of aptiganel HCL (Cerestat) following controlled cortical impact injury.

Recent studies revealed a neuroprotective effect of the non-competitive NMDA receptor antagonist Aptiganel HCL (Cerestat CNS 1102) in focal cerebral ischemia. This study investigates the influence of Cerestat on contusion volume, post-traumatic brain edema and intracranial pressure (ICP) following Controlled Cortical Impact Injury (CCII). In rats (n = 54) CCII was applied to the left hemisphere using a pneumatic impactor. Cerestat (2 mg/kg i.v.) or vehicle was injected 15 min after injury animals were sacrificed 24 hours later. Contusion volume was measured planimetrically (n = 18). Hemispheric swelling and water content were determined gravimetrically (n = 20). ICP, mean arterial blood pressure (MABP) and cerebral perfusion pressure (CPP) were monitored for 30 min before sacrifice (n = 16). Cerestat reduced contusion volume from 77.3 +/- 5.8 mm3 to 66.8 +/- 3.9 mm3 (p < 0.05). Hemispheric swelling was also diminished from 11.1 +/- 0.8% to 8.2 +/- 1.4% as soon was water content (Cerestat 82.30 +/- 0.18% vs. control: 82.78 +/- 0.12%, p < 0.05). ICP was decreased by treatment from 31.7 +/- 3.5 mm Hg to 26.3 +/- 2.2 mm Hg and CPP was significantly improved (82.1 +/- 4.4 mm Hg vs 57.7 +/- 4.8 mm Hg; p < 0.05) 24 hours after injury. Cerestat administration was associated with decrease contusion volume, less hemispheric swelling, a lower ICP and increased CPP.

Animals↗
PubMed1998

Monitoring of brain tissue PO2 in traumatic brain injury: effect of cerebral hypoxia on outcome.

This study investigates the effect of hypoxic brain tissue PO2 on outcome, and examines the incidence of possible causes for cerebral hypoxia. We studied 35 patients with severe head injury (GCS < or = 8). Age was 33.2 (+/- 11.3) years. Total time of monitoring of PtiO2, intracranial pressure (ICP), cerebral perfusion pressure (CPP), and endtidal PCO2 (ETCO2) was 119.3 (+/- 65.7) hours. Data were continuously recorded by a computer system. Outcome was assessed at discharge and after 6 months post injury. 56% of the patients with more than 300 minutes of PtiO2 < 10 mm Hg died, 22% had an unfavourable outcome, 22% had a favourable outcome. Cerebral hypoxia was associated with intracranial hypertension (ICP > 20 mm Hg) in 11.5 (+/- 15.1)%. CPP was compromised below 60 mm Hg in 16.8 (+/- 23.4)%. Hypocarbia (ETCO2 < 28 mm Hg) was present in 48.0% of the time of PtiO2 < 10 mm Hg. No obvious cause for cerebral hypoxia was found in 45% of the data. These result underscore the association of cerebral hypoxia with poor neurological outcome and stress the meaning of monitoring of PtiO2 as an independent parameter in patients following TBI.

Adult↗
PubMed1998

Bifrontal measurements of brain tissue-PO2 in comatose patients.

The purpose of this study was to compare brain tissue-PO2 (PtiO2) in lesioned vs. non-lesioned brain tissue. PtiO2 was monitored bifrontally with a "Clark"-type microcatheter in patients following severe head injury (n = 6) and subarachnoid hemorrhage (SAH) (n = 1) from day 2 to day 12 posttrauma/post SAH. Mean arterial blood pressure, intracranial pressure (ICP), cerebral perfusion pressure and end-tidal CO2 were monitored. Data were stored and analyzed by a multimodal cerebral monitoring system. The CT of five patients was classified as "diffuse injury" and of one patients as "evacuated mass lesion". The patient with SAH (Hunt and Hess IV) had a concomitant intracerebral hematoma which was removed. In all cases, one catheter was placed close to the lesion, while the other was situated in an area with no visible pathology. For analysis, bifrontal PtiO2 data were taken from both on-line monitoring and O2 reactivity tests (FiO2 1.0 for 10 min). Two different patterns were identified: periods of concordance (22% of recordings) and periods in which PtiO2 was lower in lesioned cerebral white matter (78%) but always running parallel. In the latter case, O2-reactivity response was markedly reduced on the lesioned side. Our findings demonstrate a decreased PtiO2 and a reduced O2 reactivity in contused or infarcted brain tissue. Future studies have to clarify which PtiO2 is more important to be used as a guide for therapy.

Brain Concussion↗
PubMed1998

Cerebral oxygenation in contusioned vs. nonlesioned brain tissue: monitoring of PtiO2 with Licox and Paratrend.

Brain tissue PO2 in severely head injured patients was monitored in parallel with two different PO2-microsensors (Licox and Paratrend). Three different locations of sensor placement were chosen: (1) both catheters into non lesioned tissue (n = 3), (2) both catheters into contusioned tissue (n = 2), and (3) one catheter (Licox) into pericontusional versus one catheter (Paratrend) into non lesioned brain tissue (n = 2). Mean duration of PtiO2-monitoring with both microsensors in parallel was 68.1 hours. Brain tissue PO2 varied when measured in lesioned and nonlesioned tissue. In non lesioned tissue both catheters closely correlated (delta Licox/Paratrend: mean PtiO2 < 5 mm Hg) after 20 hours post insertion. In pericontusional tissue PtiO2 was reduced relative to non lesioned tissue (delta lesioned/non lesioned: mean PtiO2: 10.3 mm Hg). In contusioned brain tissue PtiO2 was always below the "hypoxic threshold" of 10 mm Hg, independent of the type of microsensor used. During a critical reduction in cerebral perfusion pressure (< 60 mm Hg), PtiO2 decreased measured with both microsensors. Elevation of inspired oxygen fraction, normally followed by a rapid increase in tissue PO2, only increased PtiO2 when measured in pericontusional and nonlesioned brain. To recognize critical episodes of hypoxia or ischemia, PtiO2-monitoring of cerebral oxygenation is recommended in nonlesioned brain tissue.

Adult↗