Continuous monitoring of cerebral hemodynamic reserve in acute brain injury: relationship to changes in brain swelling.

A new concept of cerebral hemodynamic and metabolic physiology, cerebral hemodynamic reserve (CHR), was evaluated in 20 comatose adults with acute traumatic brain swelling who were undergoing continuous monitoring of the arteriojugular difference in oxyhemoglobin saturation, along with cerebral perfusion pressure and expired PCO2. The CHR was measured as the ratio of relative (percent) changes in cerebral oxygen extraction to relative changes in cerebral perfusion pressure during spontaneous increases in intracranial pressure. In patients with initially severe brain swelling, the CHR was more frequently abnormal (compromised) on the first day, and tended to improve on the second day. In patients with initially moderate brain swelling, the CHR was more frequently normal (preserved) on the first day, but tended to become compromised on the second day if the brain swelling exacerbated. It is concluded that cerebral hemodynamic reserve abnormalities very closely associate with signs of increased intracranial "tightness" on computed tomographic scans of the head. Cerebral hemodynamic reserve could therefore become an important guide in the functional evaluation and management of acute brain swelling (focusing on cerebral oxygenation and perfusion pressure) in a variety of predominantly diffuse acute intracranial disorders.     

Continuous monitoring of cerebral oxygenation in acute brain injury: injection of mannitol during hyperventilation

Global cerebral oxygenation, perfusion pressure, and expired pCO2 were continuously monitored in 10 adults with acute severe closed head trauma. Cerebral oxygenation was monitored by fiberoptic catheter oximetry, which allowed simultaneous measurements of arterial and jugular bulb oxyhemoglobin saturation. Intracranial pressure levels over 20 mm Hg were recorded several times in all patients, in spite of sedation, muscle paralysis, and profound hyperventilation. Intracranial hypertension was frequently associated with oligemic cerebral hypoxia, identified as abnormally low jugular oxygen saturation in the presence of normal arterial oxygenation. Intracranial hypertension was then managed with intravenous administration of mannitol boluses, which yielded simultaneous decreases in intracranial pressure and increases in cerebral oxygenation to highly statistically significant levels. Monitoring cerebral oxygenation was clinically useful because it allowed identification of impaired cerebral oxygenation even when cerebral perfusion pressure was normal. It is therefore proposed as a new monitoring technique, to supplement conventional monitoring of cerebral perfusion pressure.     

Continuous monitoring of cerebral oxygenation in acute brain injury: multivariate assessment of severe intracranial "plateau" wave--case report.

A case of acute closed brain trauma is presented in which, for the first time, a full spectrum of multivariate physiologic abnormalities was clearly documented in association with a severe posttraumatic intracranial "plateau" wave and clinical signs of tentorial herniation. Prompt therapeutic measures proved effective, ultimately contributing to a favorable outcome.     

Measuring brain tissue oxygenation compared with jugular venous oxygen saturation for monitoring cerebral oxygenation after traumatic brain injury

Jugular bulb oximetry is the most widely used method of monitoring cerebral oxygenation. More recently, measurement of brain tissue oxygenation has been reported in head-injured patients. We compared the changes in brain tissue oxygen partial pressure (PbO2) with changes in jugular venous oxygen saturation (SjVO2) in response to hyperventilation in areas of brain with and without focal pathology. Thirteen patients with severe head injuries were studied. A multiparameter sensor was inserted into areas of brain with focal pathology in five patients and outside areas of focal pathology in eight patients. A fiberoptic catheter was inserted into the right jugular bulb. Patients were hyperventilated in a stepwise manner from a PaCO2 of approximately 35 mm Hg to a PaCO2 of 22 mm Hg. There was no significant change in cerebral perfusion pressure or arterial partial pressure of oxygen with hyperventilation. In areas without focal pathology, there was a good correlation between changes in SjVO2 and PbO2 (deltaSjVO2 and deltaPbO2; r2 = 0.69, P < 0.0001). In areas with focal pathology, there was no correlation between deltaSjVO, and APbO2 (r2 =0.07, P = 0.23). In this study, we demonstrated that measurement of local tissue oxygenation can highlight focal differences in regional cerebral oxygenation that are disguised when measuring SjVO2. Thus, monitoring of PbO2 is a useful addition to multimodal monitoring of patients with traumatic head injury. IMPLICATIONS: Brain oxygenation is currently monitored by using jugular bulb oximetry, which attracts a number of potential artifacts and may not reflect regional changes in oxygenation. We compared this method with measurement of brain tissue oxygenation using a multiparameter sensor inserted into brain tissue. The brain tissue monitor seemed to reflect regional brain oxygenation better than jugular bulb oximetry.     

Intravenous paracetamol for fever control in acute brain injury patients: cerebral and hemodynamic effects

Background

Fever occurs frequently in acute brain injury patients, and its occurrence is associated with poorer outcomes. Paracetamol, an antipyretic frequently employed in patients with cerebral damage, may cause hypotension. We evaluated the cerebral and hemodynamic effects of intravenous (IV) paracetamol for the control of fever in Neuro-Intensive Care Unit (NICU) patients.

Methods

This is a prospective observational study in which we enrolled 32 NICU patients: Subarachnoid Hemorrhage (SAH, n?=?18), Traumatic Brain Injury (TBI, n?=?10), Intracerebral Hemorrhage (ICH, n?=?2) and Acute Ischemic Stroke (AIS, n?=?2).

Results

The administration of paracetamol resulted in a decrease of core body temperature (Tc) (p?=?0,0001), mean arterial pressure (MAP) (p?=?0,0006), cerebral perfusion pressure (CPP) (p?=?0,0033), and jugular venous oxygen saturation (SjVO2) (p?=?0.0193), and in an increase of arteriojugular venous differences of oxygen (AVDO2) (p?=?0.0012). The proportion of patients who had an infusion of norepinephrine increased from 47 % to 75 % (p?=?0.0039 McNemar Test). When intracranial pressure (ICP) at the start of paracetamol infusion (t-0) was compared with the measurement of ICP after 2 h, a significant correlation was observed (r?=?0.669, p?=?0.0002). This marked and significant correlation can be explained by the fact that for the higher levels of ICP assessed at t-0 (greater than 15 mmHg), we observed a marked reduction of ICP concomitant with the decrease of Tc. No problems related to norepinephrine administration and/or increase in dosage were observed.

Conclusion

Paracetamol administration is effective but exposes patients to hypotensive episodes that must be recognized and treated expeditiously to prevent further damage to the injured brain.     

Invasive monitoring of cerebral oxygenation

Despite medical and technological advances in neurosurgical intensive care, severe traumatic brain injury still carries a poor prognosis. Invasive monitoring of cerebral oxygenation has recently been proposed as a means for the detection and prevention of cerebral ischemia in comatose patients; however, it has not proven to influence the patient’s outcome after severe brain injury. Eight recent reports selected from the literature are reviewed, and the authors’ own clinical experience is presented in order to define the indications, usefulness, limitations, and potential complications of the available methodology for the invasive monitoring of cerebral interstitial oxygen saturation.     

Conventional neurocritical care and cerebral oxygenation after traumatic brain injury

OBJECT: Control of intracranial pressure (ICP) and cerebral perfusion pressure (CPP) is the foundation of traumatic brain injury (TBI) management. In this study, the authors examined whether conventional ICP- and CPP-guided neurocritical care ensures adequate brain tissue O2 in the first 6 hours after resuscitation. METHODS: Resuscitated patients with severe TBI (Glasgow Coma Scale score < or = 8 and Injury Severity Scale score > or = 16) who were admitted to a Level I trauma center and who underwent brain tissue O2 monitoring within 6 hours of injury were evaluated as part of a prospective observational database. Therapy was directed to maintain an ICP of 25 mm Hg or less and a CPP of 60 mm Hg or higher. Data from a group of 25 patients that included 19 men and six women (mean age 39 +/- 20 years) were examined. After resuscitation, ICP was 25 mm Hg or less in 84% and CPP was 60 mm Hg or greater in 88% of the patients. Brain O2 probes were allowed to stabilize; the initial brain tissue O2 level was 25 mm Hg or less in 68% of the patients, 20 mm Hg or less in 56%, and 10 mm Hg or less in 36%. Nearly one third (29%) of patients with ICP readings of 25 mm Hg or less and 27% with CPP levels of 60 mm Hg or greater had severe cerebral hypoxia (brain tissue O2 < or = 10 mm Hg). Nineteen patients had both optimal ICP (< 25 mm Hg) and CPP (> 60 mm Hg); brain tissue O2 was 20 mm Hg or less in 47% and 10 mm Hg or less in 21% of these patients. The mortality rate was higher in patients with reduced brain tissue O2. CONCLUSIONS: Brain resuscitation based on current neurocritical care standards (that is, control of ICP and CPP) does not prevent cerebral hypoxia in some patients. This finding may help explain why secondary neuronal injury occurs in some patients with adequate CPP and suggests that the definition of adequate brain resuscitation after TBI may need to be reconsidered.     

Continuous regional cerebral blood flow monitoring in acute craniocerebral trauma

Regional cortical cerebral blood flow (rCBF) and intracranial pressure (ICP) were monitored continuously with a combined thermal diffusion probe/ICP monitor in 12 patients (8 men and 4 women; mean age, 31 years; range, 7-65 years) with acute head injuries. The mean Glasgow Coma Scale score at admission was 6 (range, 4-12). The rCBF/ICP probes were placed during surgical procedures (n = 11) or in an intensive care unit (n = 1) for subdural hematomas (n = 7), cerebral contusions (n = 4), and an epidural hematoma (n = 1). No probe-related complications occurred. Reduced CBF often occurred and was often inversely proportional to elevations in ICP. Posttraumatic cerebral arterial vasospasm in one patient was detected by rCBF monitoring and confirmed by angiography. In 6 patients who progressed to brain death, rCBF patterns disappeared, which correlated with their clinical and electroencephalographic examinations. Several patients with severe, diffuse brain injuries and high ICP had hyperemic rCBF patterns. In 2 of these patients, increases in rCBF preceded rises in ICP, which implied loss of autoregulation as a mechanism in the development of malignant cerebral edema. This method of CBF monitoring has not yet been established for clinical decision making. The early detection of ischemic or hyperemic responses by continuous CBF monitoring could hasten intervention aimed at restoring adequate tissue perfusion. The technique could also serve as an index of the efficacy of therapeutic interventions and is suitable to gain more insight into the pathophysiology of head injury, especially the relationship of CBF to ICP.     

Role of nociceptin/orphanin FQ in age-dependent cerebral hemodynamic effects of brain injury

This study was designed to compare the role of the newly described endogenous opioid nociceptin/orphanin FQ (NOC/oFQ) in the reductions of cerebral blood flow (CBF) and pial artery diameter observed following fluid percussion brain injury (FPI) in chloralose anesthetized newborn and juvenile pigs as a function of time postinsult. FPI elevated CSF NOC/oFQ concentration from 70 +/- 3 to 444 +/- 51 within 1 h and to 1,931 +/- 112 pg/mL (n = 7) within 8 h, whereas concentrations returned to control value within 168 h in the newborn. In contrast, FPI elevated CSF NOC/oFQ from 77 +/- 4 to 202 +/- 16 pg/mL (n = 7) within 1 h, while values returned to control value within 8 h in the juvenile. Topical NOC/oFQ (10(-8), 10(-6) M) induced vasodilation was reversed to vasoconstriction by FPI in the newborn while such responses were only attenuated in the juvenile at 1 h post insult (control, 9 +/- 1 and 16 +/- 1%; FPI newborn, -8 +/- 1 and -14 +/- 1%; FPI juvenile, 2 +/- 1 and 5 +/- 1%, n = 7). Such altered dilation returned to control value within 168 h in newborns and 8 h in juveniles. Blood flow in the cerebrum was reduced from 57 +/- 4 to 23 +/- 3 mL x min(-1) x 100 g(-1) (n = 7) within 1 h and returned to control value with 168 h post FPI in newborns. In animals pretreated with [F/G] NOC/oFQ (1-13) NH2 (1 mg/kg, i.v.), a NOC/oFQ antagonist, however, CBF only fell to 39 +/- 4 mL x min(-1) x 100 g(-1) (n = 7) at 1 h post insult in newborns. In contrast, CBF was only reduced from 57 +/- 6 to 32 +/- 2 in untreated and to 39 +/- 3 mL/min(-1) x 100 g(-1) (n = 7) in treated juveniles within 1 h post FPI. Similar observations for reductions in pial artery diameter were made in untreated and treated newborns and juveniles. These data suggest that an elevated CSF NOC/oFQ concentration and altered vascular responsiveness to this opioid contribute to reductions in CBF and pial artery diameter observed following FPI. Because such NOC/oFQ changes were greater in newborns versus juveniles, these data further suggest that NOC/oFQ contributes to age-related cerebral hemodynamic differences in the effects of FPI.     

Continuous cerebral compliance monitoring in severe head injury: its relationship with intracranial pressure and cerebral perfusion pressure

Summary Background. Cerebral compliance expresses the capability to buffer an intracranial volume increase while avoiding a rise in intracranial pressure (ICP). The autoregulatory response to Cerebral Perfusion Pressure (CPP) variation influences cerebral blood volume which is an important determinant of compliance. The direction of compliance change in relation to CPP variation is still under debate. The aim of the study was to investigate the relationship between CPP and compliance in traumatic brain injured (TBI) patients by a new method for continuous monitoring of intracranial compliance as used in neuro-intensive care (NICU).Method. Three European NICU’s standardised collection of CPP, compliance and ICP data to a joint database. Data were analyzed using an unpaired student t-test and a multi-level statistical model.Results. For each variable 108,263 minutes of data were recorded from 21 TBI patients (19 patients GCS≤8; 90% male; age 10–77 y). The average value for the following parameters were: ICP 15.1±8.9 mmHg, CPP 74.3±14 mmHg and compliance 0.68±0.3 ml/mmHg. ICP was ≥20 mmHg in 20% and CPP<60 mmHg for 10.7% of the time. Compliance was lower (0.51±0.34 ml/mmHg) at ICP≥20 than at ICP<20 mmHg (0.73±0.37 ml/mmHg) (p<0.0001). Compliance was significantly lower at CPP<60 than at CPP≥60 mmHg: 0.56±0.36 and 0.70±0.37 ml/mmHg respectively (p<0.0001). The CPP – compliance relationship was different when ICP was above 20 mmHg compared with below 20 mmHg. At ICP<20 mmHg compliance rose as CPP rose. At ICP≥20 mmHg, the relation curve was convexly shaped. At low CPP, the compliance was between 0.20 and 0.30 ml/mmHg. As the CPP reach 80 mmHg average compliance was 0.55 ml/mmHg., but compliance fell to 0.40 ml/mmHg when CPP was 100 mmHg.Conclusions. Low CPP levels are confirmed to be detrimental for intracranial compliance. Moreover, when ICP was pathological, indicating unstable intracranial equilibrium, a high CPP level was also associated with a low volume-buffering capacity.     

A comparison of the cerebral and hemodynamic effects of mannitol and hypertonic saline in a rabbit model of acute cryogenic brain injury

There has recently been an increased interest in the use of hypertonic saline solutions in the fluid resuscitation of trauma victims and patients with uncontrollable intracranial hypertension. In this study, the cerebral and hemodynamic effects of 3.2% hypertonic saline solution were compared with those of an equiosmolar (20%) mannitol solution or 0.9% saline in a rabbit model of acute cryogenic brain injury. Forty-five minutes following the creation of a left hemispheric cryogenic brain lesion, equal volumes (10 ml/kg) of hypertonic saline, 0.9% saline, or mannitol were infused over a 5-min period. Monitored variables over the ensuing 120 min included mean arterial pressure, central venous pressure, intracranial pressure (ICP), hematocrit, and serum osmolality. At the conclusion of the 2-h study period, hemispheric water contents were determined by gravimetric analysis and the wet/dry weight method. There were no significant differences in mean arterial pressure between the three groups at any time during the experiment. Plasma osmolality was significantly increased by +/- 10 mOsm/kg following infusions in both the mannitol and hypertonic groups compared to the saline group. The infusion of either mannitol or hypertonic saline produced a transient and significant decrease in ICP during the first 60-90 min but not at 120 min after cryogenic brain lesion, whereas animals in the saline group demonstrated a continual increase in ICP. However, there appeared to be no significant differences in ICP between animals receiving mannitol or hypertonic saline at any time point following infusion of solutions. We conclude that following acute cryogenic brain injury, infusions of equal volumes of equiosmolar solutions of hypertonic saline or mannitol will transiently reduce ICP as compared to equal volumes of normal saline. However, hypertonic saline is not superior to mannitol in its ability to reduce ICP in this model of intracranial hypertension.     

Perfluorocarbon emulsion improves cerebral oxygenation and mitochondrial function after fluid percussion brain injury in rats

OBJECTIVE: Cerebral ischemia is a common secondary sequela of traumatic brain injury (TBI). Experimental models of stroke have demonstrated reductions in ischemia after perfluorocarbon (PFC) administration; however, there are no published reports of PFC efficacy after TBI. The current study analyzed the effect of the PFC emulsion Oxygent (AF0144; Alliance Pharmaceutical Corp., San Diego, CA) on cerebral oxygenation, mitochondrial redox potential, and free radical formation after lateral fluid percussion injury. METHODS: After fluid percussion injury, five 2.25 ml/kg doses of PFC or saline were administered to rats breathing 100% O(2), and oxygen tension was recorded. In a second experiment, a single bolus (11.25 ml/kg) of PFC or saline was given after injury, and redox potential and free radical formation were measured at 1 or 4 hours with Alamar blue dye and dihydrorhodamine 123, respectively. RESULTS: Cerebral oxygen tension was significantly increased in both injured and sham animals treated with 11.25 ml/kg of PFC as compared with saline (P < 0.05). Likewise, PFC significantly increased mitochondrial redox potential as compared with saline at 4 hours after injury (P < 0.01). Mitochondrial peroxynitrite and peroxide production also increased with the administration of PFC (P < 0.05). CONCLUSION: The current study demonstrates that a PFC emulsion can significantly increase cerebral oxygenation after TBI and enhance mitochondrial function at 4 hours after injury as compared with saline. This study demonstrates a new therapeutic potential for PFC to enhance cerebral oxygenation and aerobic metabolism after TBI. However, the increased free radical formation with high-dose PFCs suggests the need for further studies combining PFCs with free radical scavengers.     

脑灌注压对创伤性脑损伤后急性脑缺血的影响

目的 观察不同脑灌注压(CPP)对创伤性脑损伤后急性脑缺血的影响.方法 实验家兔60只,随机分为正常对照组(无损伤组)、高CPP组(90～110)mm Hg、中CPP组(70～80)mm Hg、低CPP组(50～60)mm Hg、极低CPP组(35～45)mm Hg.采用Feeney's自由落体撞击法建立急性局灶性脑挫裂伤模型,伤后80 min静脉给予升压和降压药物调控血压使CPP达到设计要求,同步进行脑血流、CPP测定,并进行图像分析,且观察不同CPP下颅脑损伤后急性脑缺血动物脑含水量及神经组织超微结构改变.结果 对照组局部脑血流量(rCBF)为156.18±6.22;高CPP组实验组rCBF为140.03±17.32,中CPP组rCBF为100.46±21.37,低CPP组rCBF为86.46±10.30,极低CPP组rCBF为60.36±8.32.对照组脑含水量为(78.21±0.26)%;高CPP组实验组脑含水量为(80.15±0.52)%,中CPP组脑含水量为(80.27±0.36)%,低CPP组脑含水量为(81.18±0.62)%,极低CPP组脑含水量为(81.34±0.83)%.实验组脑组织含水量高于对照组(P<0.01);实验组rCBF较对照组明显降低,差异有统计学意义(P<0.01);高CPP组rCBF明显高于低CPP组及极低CPP组,差异有统计学意义(P<0.01);中CPP组rCBF虽低于对照组及高CPP组,而高于低CPP组及极低CPP组,但组间比较筹异无统计学意义(P>0.05).低CPP组及极低CPP组脑含水量、超微结构较对照组差异有统计学意义(P<0.05).结论 在缺血急性期及时有效地改善脑循环、恢复脑供血是阻止脑缺血发展成为脑组织不可逆损伤的重要环节.     

The role of tissue oxygen monitoring in patients with acute brain injury

Cerebral ischaemia is implicated in poor outcome after braininjury, and is a very common post-mortem finding. The inabilityof the brain to store metabolic substrates, in the face of highoxygen and glucose requirements, makes it very susceptible toischaemic damage. The clinical challenge, however, remains thereliable antemortem detection and treatment of ischaemic episodesin the intensive care unit. Outcomes have improved in the traumaticbrain injury setting after the introduction of progressive protocol-driventherapy, based, primarily, on the monitoring and control ofintracranial pressure, and the maintenance of an adequate cerebralperfusion pressure through manipulation of the mean arterialpressure. With the increasing use of multi-modal monitoring,the complex pathophysiology of the injured brain is slowly beingunravelled, emphasizing the heterogeneity of the condition,and the requirement for individualization of therapy to preventsecondary adverse hypoxic cerebral events. Brain tissue oxygenpartial pressure (     

Focal cerebral oxygenation and neurological outcome with or without brain tissue oxygen-guided therapy in patients with traumatic brain injury

Background  

In patients with severe traumatic brain injury (TBI), the depth and duration of cerebral hypoxia are independent predictors of outcome. This study aimed to evaluate the efficacy of brain oxygen-guided therapy in improving cerebral oxygenation and neurological outcome in severe TBI patients.     

Continuous conjunctival oxygen tension (Pcjo2) monitoring for assessment of cerebral oxygenation and metabolism during carotid artery surgery

The clinical value of noninvasive continuous monitoring of conjunctival oxygen tension for assessment of cerebral perfusion during carotid endarterectomy performed under general anaesthesia has been evaluated. The patients (n = 17; mean age 62.5 +/- 1.7 years) were monitored as follows: conjunctival oxygen tension (PcjO2); internal jugular venous oxygen tension at the skull base level (PcijvO2); arterial blood pressure; arterial and internal jugular venous blood gases; acid-base data and lactate, pyruvate levels; end-tidal CO2 concentration. The mean preanaesthetic PcjO2 level of 4.86 +/- 0.40 kPa was significantly lower than PaO2(PcjO2)/PaO2 ratio of 0.48). Following anaesthesia, a larger PcjO2-PaO2 gradient (ratio 0.32) was seen in spite of the hyperoxic situation (FiO2 = 0.40) due to vasoconstriction induced by slight hypocapnia (reduction of PaCO2 from 5.13 +/- 0.08 to 4.64 +/- 0.10 kPa). The carotid artery crossclamping resulted in a rapid and pronounced decrease of PcjO2, while PcijvO2 remained unchanged. No relationship between PcjO2 and stump pressure was found, while a significant correlation (P less than 0.02) between PcjO2 and lactate in effluent venous blood from the brain was demonstrable. It is concluded that PcjO2 monitoring seems a clinically useful trend indicator of cerebral perfusion in the individual patient. Due to large interindividual variations in basal PcjO2 readings and in PcjO2 changes during carotid artery clamping, however, transconjunctival oxygen tension monitoring does not seem to allow early and accurate recognition of impending cerebral ischaemia during carotid endarterectomy, and its routine use therefore seems of limited value.