|Year : 2008 | Volume
| Issue : 5 | Page : 494
Current Concepts in the Intensive Care Management of Neurosurgical Patients
GS Umamaheswara Rao
Professor of Neuroanaesthesia, National Institute of Mental Health and Neurosciences, (NIMHANS), Bangalore 560 029, India
|Date of Acceptance||02-Aug-2008|
|Date of Web Publication||19-Mar-2010|
G S Umamaheswara Rao
National Institute of Mental Health and Neurosciences (NIMHANS), Bangalore
Source of Support: None, Conflict of Interest: None
There have been some major conceptual changes in the approach to patients with both traumatic and nontraumatic cerebral injury, in recent years. These changes have their basis in a better understanding of the cerebral pathophysiology and availability of some recent monitors of cerebral function. Both traditional and modern therapeutic innovations are being subjected to extensive investigation. Evidence-based guidelines are now available for the management of traumatic brain injury. Increasing emphasis is being laid on monitoring not only intracranial pressure and cerebral perfusion pressure, but also cerebral blood flow, oxygenation and metabolism. Alternative osmotherapeutic choices are being explored. With a large pool of high quality evidence, more focused and precise therapeutic innovations are likely to emerge in near future.
Keywords: Intensive care, Neurosurgery, Head injury, Monitoring, Guidelines, Evidence-based medicine
|How to cite this article:|
Umamaheswara Rao G S. Current Concepts in the Intensive Care Management of Neurosurgical Patients. Indian J Anaesth 2008;52:494
Rapid evolution of concepts in basic and clinical neurosciences combined with intensive care technology has helped to change the outcomes of some of the neurosurgical conditions over the past few decades. The following review is intended to cover some of the areas where recent advances have had some impact on the practices in neurological critical care. It can by no means be considered an exhaustive or comprehensive account of all the advances in this field.
| Management of head injury|| |
Approach to a patient with traumatic brain injury (TBI) has been changing over the past decade based on the evidence emerging from neurological monitoring. The traditional obsession with intracranial pressure (ICP) has given way to approaches based on monitoring cerebral perfusion, oxygenation and metabolism. Evidence-based guidelines have been formulated and updated periodically.
Brain trauma foundation guidelines for the management of traumatic brain injury
The Brain Trauma Foundation (BTF) has published evidence-based guidelines on various aspects of management of head injury for the first time, in 1996 and has been revising them periodically. The latest guidelines published in 2007  are summarized in [Table 1] and [Table 2]. The evidence is classified into three levels based on the strength of the relevant clinical studies. It is to be noted that much of the currently available evidence falls into Class II and III. Class I evidence is available on very few issues.
Management of cerebral perfusion pressure
Two major schools of thought exist currently regarding management of cerebral perfusion pressure (CPP) in patients with TBI: CPP-based management as proposed by Rosner and colleagues  and the intracranial pressure (ICP)-based management as proposed by the Lund group  . While the former advocates high CPP (>70 mmHg), the latter supports aggressive ICP control and modest CPP values (50 mmHg).
The basis of CPP-targeted management
Pathological studies have shown evidence of ischemia in about 90% of patients who died of TBI  implicating ischemia as a major cause of unfavourable outcome. Ultra-early evaluation of cerebral blood flow (CBF) following head injury has documented lowest CBF values during the first six hours following injury  . Cerebral perfusion early after injury has been correlated with the long-term neurological outcome  . Recognizing the role of cerebral ischemia in causing poor neurological outcome, some authors have suggested that CPP should be maintained above 70 mmHg. The advantage claimed for such an approach is that CBF increases passively with CPP when CBF autoregulation is impaired. In addition, an increase in CPP causes cerebral vasoconstriction and reduces cerebral blood volume (CBV) and ICP if the CPP is in the autoregulatory range.
CPP management strategy
In the original strategy of CPP-based management employed by Rosner  , a CPP of 70 mmHg was targeted initially, by draining CSF until the ICP decreased to 15 mmHg. In addition, CSF was continuously drained whenever CPP dropped to below 70 mmHg. If CPP did not increase to 70 mmHg, vasopressors were added. Phenylephrine or norepinephrine with or without dopamine was used to achieve the required mean arterial pressure (MAP). Mannitol in a dose of 0.5 - 1.0 g/kg was used whenever CPP decreased to below 70 mmHg due to ICP elevation. If CPP was maintained at an acceptable level with high but stable ICP, efforts were made to minimize or avoid mannitol. Barbiturates, active hypothermia and decompressive craniectomy were not a part of the protocol. With this strategy, Rosner and colleagues demonstrated better neurological outcome compared to the other contemporary series.
The desirability of high CPP has been questioned and attempts have been made to find out the ideal CPP threshold. Some important evidence suggested that CPP values greater than 70 mmHg do not necessarily achieve the goal of avoiding hypoperfusion and hypoxia. Steiner et al  evaluated the response of CBF in the pericontusional tissue at 70 and 90 mmHg of CPP. Higher CPP caused only a modest increase in CBF that does not justify pharmacological elevation of CPP. A large volume of evidence suggests the critical CPP threshold to be around 60 mmHg. Using cerebral oxygen extraction as an index of adequacy of CBF, Stochetti et al showed that a CPP lower than 60 mmHg was associated with inadequate perfusion  . A significant correlation between CPP and brain tissue oxygen tension (PbtO2) was found below a CPP of 60 mmHg  , but not between 60 and 130 mmHg  .
Interventions used to achieve high CPP may pose special risks to the patients. Robertson et al  compared a CBF-targeted protocol (where the goals were a CPP higher than 70 mmHg and normocapnic ventilation) with an ICP-based protocol (target ICP of less than 20 mmHg and a CPP greater than 50 mmHg). There was a substantial reduction in ischemic episodes in the CBF-targeted group. This was, however, associated with a five-fold increase in the incidence of acute respiratory distress syndrome (ARDS) caused by the use of epinephrine and high dose dopamine to maintain the target CPP. Based on this evidence, the latest BTF recommendations advocate a CPP threshold of 60 mmHg and oppose aggressive attempts to maintain CPP above 70 mm Hg with fluids and pressors should be avoided.
There is growing evidence that CPP therapy guided by cerebral oxygen tension (PbtO2) monitoring may result in better outcomes than therapy with arbitrary ICP or CPP thresholds. Meixensberger et al reported a series of 93 patients of severe TBI who were managed by an ICP target of less than 20 mmHg and a CPP target greater than 70 mmHg. In 53 of these patients, CPP was manipulated to maintain a PbtO 2 greater than 1.3 kPa (10 mmHg). Cerebral hypoxic events were significantly reduced by PbtO 2 monitoring. There was also a positive trend towards better outcome in patients monitored by PbtO2  . In another series with ICP and CPP targets of 20 and 60 mmHg respectively, patients who had concomitant PbtO2 monitoring had a significantly lower mortality (44% vs25%)  .
| Role of hypothermia in cerebral protection|| |
Histopathological evidence of neurological protection has been demonstrated in experimental models of cerebral ischemia, head trauma and cardiac arrest when the body temperature was maintained at 32-35 0 C temperature. Depression of cerebral metabolism alone cannot explain such protection. Alternative explanations offered are: 1. Alterations in ion homeostasis (Ca ++ , K+),2. Increased membrane stability (blood brain barrier), 3. Altered enzyme function (phospholipase, xanthine oxidase, nitric oxide synthase), 4. Alterations in neurotransmitter release or uptake (glutamate and aspartate) and 5. Changes in free radical production or scavenging. Cerebral protection was consistent when mild hypothermia was induced prior to or along with the ischemic event. The role of post-ischemic hypothermia remains controversial. Not withstanding some success in small clinical series, a large multicentre randomised trial of mild hypothermia during the first 48 h after head injury, had to be discontinued as no benefit could be demonstrated . But a more recent Chinese study reports lower mortality and better outcomes at two years after TBI; the hypothermic patients in this study had a higher incidence of pulmonary infection and thrombocytopenia . Two human studies in cardiac arrest reported improved survival and cerebral function with 12 and 24 h of post-arrest hypothermia, . In an observational study of spontaneous intraoperative hypothermia in 50 patients undergoing surgery for ruptured cerebral aneurysms, we found that patients who had no neurological deterioration within 24 h after surgery had a significantly lower intraoperative nasopharyngeal temperatures than patients who had neurological deterioration. Mean temperature for 2 h starting from the time of temporary vascular occlusion was 35.3 ± 1.5 0 C in the deteriorated patients as against 34.2 ± 1.5 0 C in the non-deteriorated patients . A major randomized clinical trial of patients with aneurysmal subarachnoid haemorrhage did not show any improvement in the long term neurological or neuropsychological outcome of the patients subjected to intraoperative moderate hypothermia .
| Monitoring in Neuro-Intensive Care|| |
Accurate monitored information forms the basis of appropriate therapeutic interventions in patients with cerebral injury/insult.
Unequivocal evidence exists at present about the role of secondary injury on the outcome of cerebral insults of varied aetiology. Systemic arterial hypotension and hypoxia are the two major determinants of poor outcome in patients with brain injury  . In a patient with cerebral injury, optimisation of cardiovascular and respiratory function requires monitoring systemic parameters such as arterial blood pressure, central venous pressure, arterial oxygen saturation, blood gases, biochemical parameters, haemogram and urine output. Specific neurological monitoring optimizes the therapeutic interventions.
Monitoring cerebral blood flow, oxygenation and metabolism using transcranial Doppler flowmetry, jugular venous oximetry, direct brain tissue oxygen tension monitoring, electroencepahlography, and microdialysis, have provided insights into practical management of patients with both traumatic and nontraumatic cerebral injury.
Transcranial Doppler (TCD) ultrasonography provides indirect information on blood flow in the branches of circle of Willis. A 2 MHz pulsed ultrasound signal transmitted through the skull (usually through the temporal window) provides a measure of red cell flow velocity (FV) using the Doppler shift principle. Insonation of one of the arteries (most commonly the middle cerebral artery (MCA) produces an arterial flow velocity waveform. Changes in FV correlate closely with changes in CBF provided the angle of insonation and the diameter of the insonated vessel remain constant. In the absence of vessel stenosis, vasospasm, change in arterial blood pressure or blood rheology, FV changes parallel changes in CBF. The pulsatility index (PI) (calculated as PI = (FVsys - FVdias)/ FVmean, where FVsys is the systolic velocity, FVdias diastolic velocity, and FVmean is the mean velocity) reflects the downstream cerebrovascular resistance.
TCD finds its major application in the diagnosis of high velocity states such as cerebral vasospasm or hyperaemia. The differentiation between the two conditions is important in order to target appropriate therapy. MCA flow velocities > 120 cm/s are considered significantly high. If the ratio of MCA flow velocity to extracranial internal carotid flow velocity (Lindegaard Ratio) is > 3, vasospasm is the likely diagnosis.
The major limitation of TCD lies in the fact that what is measured is velocity and not flow. Secondly, the values are highly operator-dependent. Continuous monitoring is possible only by using a specialized head frame with which the probe can be fixed in a given position.
Jugular venous oximetry
Continuous monitoring of jugular venous oxygen saturation (SjVO 2 ) is an indirect method of assessing cerebral oxygen utilisation. When cerebral oxygen demand exceeds the supply, the brain extracts greater amount of oxygen from the CBF, resulting in a decreased jugular bulb oxygen saturation. If CBF decreases to a point at which brain cannot compensate for the decreased CBF, cerebral oxygen consumption decreases and anaerobic metabolism ensues. Increased SjVO2 suggests that cerebral oxygen supply exceeds the demand.
The catheter for SjVO2 monitoring is placed into the internal jugular vein on the side of dominant cerebral venous drainage, usually the right , . In the presence of a focal brain injury, it is controversial if the catheter should be placed on the side ipsilateral to injury or on the dominant side, if different. The dominant side of venous drainage may be determined by comparing the ICP increase caused by manual compression of each internal jugular vein separately  ; it may also be determined by computed tomographic assessment of jugular foramen size  , or by ultrasonography.
The normal value for SjVO2 is approximately 55- 75%. SjVO 2 monitoring provides an early diagnosis of ischemia resulting from either intracranial or systemic causes , . SjVO 2 monitoring has been used to guide hyperventilation or barbiturate therapy, fluid management and oxygenation  , and to optimize cerebral perfusion pressure , . Used along with transcranial Doppler monitor, SjVO2 helps to distinguish cerebral hyperemia from vasospasm.
The major limitation of SjVO2 is that it is a measure of global cerebral oxygenation and is not particularly sensitive to small areas of focal ischemia. The results may be affected by contamination of the jugular bulb blood flow with extracerebral blood flow during sampling. However, there are negligible (approximately 3%) chances of extracerebral contamination if the blood is sampled at a site within 2 cm of the jugular bulb and at a rate of < 2 mL/min  .
Brain tissue oxygenation
Continuous monitoring of brain tissue partial oxygen pressure (PbtiO2) is now possible through microsensors placed into brain parenchyma. PbtiO2 had been shown to have a good relation with the outcome in TBI; its ability to predict the outcome is comparable to that of other powerful predictors such as age, GCS score, and pupil reactivity , . PbtiO 2 and SjVO2 were compared in some studies. Kiening et al  showed a good correlation between different CPP values and both the neuromonitoring parameters (PbtiO 2 and SjVO 2 ). Gopinath et al  monitored SjVO 2 and PbtiO 2 in 58 head-injured patients. The reduction in CBF on decreasing PaCO 2 from 36 to 26 torr, was better detected by SjVO 2 . PbtiO 2 also decreased, but not in all patients, and it even increased in some. In another study, when the inspired oxygen concentration was changed from 40 to 100%, PbtiO 2 reflected the modification better than SjVO2  . The prognostic value of PbtiO 2 in TBI was demonstrated by Valadka et al  ; the length of time the PbtiO 2 remained low (less than 15 mm Hg) correlated with the outcome.
Electroencephalography (EEG) is an important tool for monitoring seizures (especially the non-convulsive status epilepticus) and detecting ischemic cerebral events, arising from intracranial hypertension  . Certain EEG features may also be useful in predicting the survival and outcome. Metabolic suppression using intravenous anaesthetic agents for cerebral protection may be monitored using EEG, where burst suppression or isoelectricity is a useful target.
Several automated EEG processing systems have been developed recently to facilitate continuous EEG monitoring. Power spectral analysis by fast Fourier transformation of EEG provides a graphical representation of the relative power content in the various frequency bands. These spectral diagrams can be helpful in diagnosing changing EEG patterns as the cerebral pathology evolves over time. The same spectral monitoring can also provide some numeric descriptors (e.g.. mean frequency, spectral edge frequency etc.) that can be tracked over time to follow the progress of the disease.
Bispectral index (BIS), normally used for measuring the depth of sedation during anaesthesia, has also been used in neurological intensive care patients. BIS scores obtained prior to sedation in patients of trauma, have been found to be predictive of TBI and neurological outcome at discharge  . The probability of recovery from unconsciousness based on BIS monitoring has also been investigated in unconscious neurosurgical patients  . In a study involving patients with mild and moderate TBI, we showed a statistically good correlation between BIS and GCS. Mean BIS values, in this study were significantly different between moderate and mild head injuries [65.7±16.1 vs 85.76.1, p = 0.006]. However, the scatter of BIS values for any GCS score was high limiting the practical utility of BIS as a measure of depth of coma  .
Clinical studies have shown correlations between adverse clinical events (such as high ICP, low blood pressure, and hypoxia), and brain lactate, glucose, antioxidant, and excitatory amino acid levels. Correlations have been demonstrated between jugular bulb oxygen desaturation and lactate, glutamate adenosine, and xanthenes , . Microdialysis helps to monitor the extracellular fluid concentration of various brain metabolites.
Various studies examined the effects of therapeutic interventions on the levels of extracellular metabolites after cerebral injury. Thiopental coma was associated with a reduction in lactate, glutamate, and aspartate  . Hypothermia significantly reduced glutamate and aspartate levels  . Hyperoxia led to a reduction in lactate  . One study has shown a reduction in lactate, glutamate, lactate/pyruvate ratio, and glycerol after a controlled reduction in the cerebral perfusion pressure in TBI according to the Lund protocol  . Being a monitor that provides information only from a focal area, location of the probe has a very important bearing on its usefulness.
The concept of multimodal monitoring involves continuous monitoring of more than one parameter using two or more of the techniques described above. Multimodal monitoring helps to overcome the limitations of each individual method of monitoring. For example, a change in the ICP associated with an increase in CBF or ischemia can be accurately interpreted when TCD flow velocity information is combined with ICP data. Multimodal monitoring is expensive, and requires highly trained staff. The data generated needs to be acquired in a format that allows quick and easy analysis.
| Hypertonic saline for control of intracranial hypertension|| |
Hypertonic saline has emerged as an alternative to mannitol for hyperosmolar therapy in patients with intracranial hypertension. An intact blood brain barrier (BBB) is less permeable to saline than to mannitol. Hypertonic saline is therefore a more effective and more durable osmotic agent. In clinical and experimental studies, hypertonic saline effectively lowered ICP that was refractory to mannitol,.
In TBI, hypertonic saline has been used for initial resuscitation, as an infusion for prophylaxis against intracranial hypertension and as a bolus substitute for mannitol. Prospective randomized trials have failed to show any overall benefit from resuscitation with hyper tonic saline in TBI ,. However, hypertonic saline doubled the survival rate of a subgroup of patients with both hemorrhagic shock and TBI . Numerous case reports and small cohort studies have reported the efficacy of hypertonic saline bolus dosing to reduce TBIinduced intracranial hypertension that was refractory to mannitol,, . The concentration of NaCl boluses used in these reports varied from 7.5% to 23%. Qureshi et al examined continuous maintenance infusions of 3% NaCl-acetate in a retrospective series of 27 patients with cerebral edema from various causes, 8 of whom had TBI. HS infusions were started although all patients had initial ICPs ranging from 8 to 18 mmHg. A significant trend in ICP reduction and an improvement in midline shift were noted in the hypertonic saline cohort. In a comparative study, 20 patients with TBI were randomized to receive either 20% mannitol or 7.5% HS boluses for ICP elevations of greater than 25 mm Hg for more than 5 minutes . Patients in the mannitol group experienced more frequent ICP episodes requiring interventions; there were significantly fewer refractory ICP episodes in the hypertonic saline group. No difference in clinical outcome was demonstrated between the two groups.
The role of hypertonic saline in hemispheric stroke remains controversial. In a prospective comparison of 20% mannitol versus 7.5% hypertonic saline boluses to control ICP episodes in nine patients with large hemispheric strokes  , hypertonic saline was more reliable in reducing ICP. Bhardwaj et al  examined the effect of continuous hypertonic saline infusion on infarct size in a rat model of middle cerebral artery occlusion. They noted that a continuous infusion of 7.5% NaCl was necessary to increase serum sodium content to 145 to 155 mmol/L. While comparing normal saline, 20% mannitol, 3% NaCl, and 7.5% NaCl, they found that 7.5% NaCl decreased brain water content in the contralateral hemisphere and increased infarct volumes in the ipsilateral hemisphere. They conjectured that hypertonic saline has a deleterious effect on stroke penumbra.
Complications of hypertonic saline therapy
The central pontine myelinolysis resulting from acute increase in serum sodium concentration remains only a theoretical concern. Metabolic changes that may accompany prolonged hypertonic saline therapy include hypo- or hypernatremia, hypokalemia, and hypocalcemia. Volume overload associated with this therapy may have implications in patients with cardiac disease. Acute renal failure may occur if serum osmolality exceeds 320 mOsm/kg. Rebound oedema has been noted with hypertonic saline too. Some authors recommend limiting the infusion to 48-72 h and slow withdrawal to avoid the rebound effect.
| Ventilatory management|| |
Optimal ventilation remains a major goal in managing patients with cerebral injury. The role of hyperventilation is now clearly defined and the beneficial role of hyperoxic ventilation is under investigation.
Hyperventilation is normally used for acute treatment of raised intracranial pressure. But cerebral vaso-constriction caused by hyperventilation has the potential to decrease CBF. In a study of TBI, patients who received severe hyperventilation had high cerebral arterio-venous oxygen difference and CBF values, in the ischemic range  . Hyperventilation was the second common cause for decrease in SjVO2 in patients with TBI  . In a study comparing clinical outcomes of hyperventilated and normoventilated patients, better outcomes were observed at 3 months in normoventilated patients  . A xenon CT study in paediatric TBI showed 28.9% frequency of cerebral ischemia when PaCO 2 was > 35 mmHg as against 73.1% when the PaCO 2 was decreased to 25 mmHg  . Recent Brain Trauma Foundation guidelines advocate against hyperventilation particularly during the first 24 h after injury. Brief periods of hyperventilation may be justified when there is acute neurological deterioration. Prolonged hyperventilation may be used only if the intracranial hypertension is refractory to sedation, paralysis, CSF drainage and osmotic diuretics  . In contradiction with the above evidence, a positron emission tomographic study showed that hyperventilation decreased CBF, but did not cause energy failure. The authors concluded that CBF reduction associated with hyperventilation is unlikely to cause brain injury  .A recent Cochrane review indicates that the data available at present is inadequate to assess any potential benefit or harm caused by hyperventilation  .
Hyperoxia and brain injury
Recent evidence suggests that hyperoxic ventilation may mitigate, to some extent, the adverse effects of hypoperfusion in patients with cerebral pathology. CBF reduction ranging from 9% to 27% and a decrease in cerebral (A-V)DO 2 have been reported in response to hyperoxia ,, .
Hyperbaric oxygen therapy
The amount of oxygen dissolved in the plasma increases linearly with an increase in PaO2. For every atmosphere of pressure increase, 1.8 mL of oxygen/100 mL of blood is dissolved in plasma. Hyperbaric oxygenation thus induces a dramatic increase in blood oxygen-carrying capacity and tissue oxygen diffusion. Despite this theoretical advantage, in a randomized trial where the patients received either standard care or standard care plus hyperbaric oxygen therapy at 1.5 atm, the overall mortality in the treatment and control groups was not significantly different  . Though the mortality was low in a subgroup of patients, this treatment was not associated with an increase in favorable outcomes among survivors. A recent review of the literature also does not support routine use of hyperbaric oxygen therapy for TBI  .
Normobaric oxygen therapy
Normobaric hyperoxia is easily and quickly performed in an ICU setting by increasing the fraction of inspired oxygen (FiO 2 ) on the mechanical ventilator. Menzel et al  tested hyperoxia over a period of 6 hours by raising the FiO2 from 35% to 60% and then to 100% during the first 24 hours after injury. Hyperoxia did not have any effect on ICP and CPP. PbtiO 2 increased in all the oxygen-treated patients. Patients subjected to hyperoxia showed a 40% decrease in lactate by the end of oxygen treatment. The levels of glucose did not show a clear trend during the oxygen enhancement period. Magnoni et al  tested the hypothesis that hyperoxia could improve oxidative metabolism after TBI, by evaluating the lactate/pyruvate ratio. But the data suggested that, in a condition of sufficient oxygen supply, hyperoxygenation does not change oxidative metabolism.
In summary, there have been significant changes in the concepts related to the management of cerebral blood flow, and metabolism and intracranial pressure dynamics. A major proportion of this development has its basis in the developments in technology that enabled a closer observation of the cerebral physiology in disease. Refinement of our concepts with routine use of these newer techniques should pave way for better treatment protocols in the near future.
| References|| |
|1.||Guidelines for the Management of Severe Traumatic Brain Injury 3rd Edition. Accessed from JON_24_Supp1.pdf. |
|2.||Rosner MJ, Rosner SD, Johnson AH. Cerebral perfusion pressure management protocol and clinical results. J Neurosurg 1995;83:949-962. [PUBMED] [FULLTEXT] |
|3.||Eker C, Asgeirsson B, Grande PO, Schalen W, Nordstrom CH. Improved outcome after severe head injury with a new therapy based on principles for brain volume regulation and preserved microcirculation.Crit Care Med. 1998;26:1881-6. |
|4.||Graham DI, Ford L, Adams JH, e al. Ischaemic brain damage is still common in fatal non-missile head injury. J Neurol Neurosurg Psychiatry 1989; 52:346-350. |
|5.||Bouma GJ, Muizelaar JP, Stringer WA, et al. Ultra-early evaluation of regional cerebral blood flow in severely head-injured patients using xenon-enhanced computerized tomography. J Neurosurg. 1992;77:360-8. [PUBMED] [FULLTEXT] |
|6.||Bouma GJ, Muizelaar JP, Choi SC, et al. Cerebral circulation and metabolism after severe traumatic brain injury: the elusive role of ischemia J Neurosurg 1991;75:685-93. |
|7.||Steiner LA, Coles JP, Johnston AJ, et al. Responses of posttraumatic pericontusional cerebral blood flow and blood volume to an increase in cerebral perfusion pressure. J Cerebral Blood Flow Metab 2003;23:1371-1377. |
|8.||Stochetti N, Barbagallo M, Bellini GC, et al: Arteriojugular difference of oxygen and intracranial pressure in comatose head injured patients. II. Clinical correlations. Minerva Anestesiol 1991;57:327-334. |
|9.||Bruzonne P, Dlongi R Bellinzona G, et al. Effects of cerebral perfusion pressure on brain tissue PO 2 in patients with severe head injury. Acta Neurochir Suppl (Wien) 1998; 71:111-113. |
|10.||Cruz J, Jaggi JL, Hoftstad OJ. Cerebral blood flow, vascular resistance and oxygen metabolism in acute brain trauma. Redefining the role of cerebral perfusion pressure. Crit Care Med 1995; 23: 1412-7. |
|11.||Robertson CS, Valadka AB, Hannay HJ, et al. Prevention of secondary ischemic insults after severe head injury. Crit Care Med 1999;27:2086-2095. [PUBMED] [FULLTEXT] |
|12.||Meixensberger J, Jaeger M, Vath A, et al. Brain tissue oxygen guided treatment supplementing ICP/CPP therapy after traumatic brain injury. J. Neurol Neurosurg Psychiatry 2003: 74:760-764. |
|13.||Stiefel MF, Spiotta A, Gracias VH, et al. Reduced mortality rate in patients with traumatic brain injury treated with brain tissue oxygen monitoring. J. Neurosurg 2005; 103:805-811. |
|14.||Clifton GL, Miller ER, Choi SC et al. Lack of effect of induction of hypothermia after acute brain injury. N Engl J Med 2001;344:556-563. |
|15.||Qiu W-S, Liu W-G, Shen H, et al. Therapeutic effect of mild hypothermia on severe traumatic head injury. Chin J Traumatol 2005;8:27-32. |
|16.||Bernard SA, Gray TW, Buist MD et al. Treatment of comatose survivors of out-of-hospital cardiac arrest with induced hypothermia. New Engl J Med 2002;346:557-563. |
|17.||The Hypothermia after Cardiac Arrest Study Group. Mild therapeutic hypothermia to improve the neurologic outcome after cardiac arrest. New Engl J Med 2002; 346: 549-556 |
|18.||Murthy HS, Chidanandaswamy MN, Umamaheswara Rao GS, Kolluri S. Spontaneous intraoperative hypothermia and cerebral protection in aneurysmal subarachnoid hemorrhage. Middle East J Anesthesiol 2005;18:313-32. |
|19.||Todd MM, Hindman BJ, Clarke WR, et al. Mild intraoperative hypothermia during surgery for intracranial aneurysm. N Engl J Med 2005;352:135-45. [PUBMED] [FULLTEXT] |
|20.||Chesnut RM, Marshall LF, Klauber MR, et al. The role of secondary brain injury in determining outcome from severe head injury. J Trauma 1993;34:216-22. [PUBMED] |
|21.||Robertson CS, Narayan RK, Gokosla ZL, et al. Cerebral arteriovenous oxygen difference as an estimation of cerebral blood flow in comatose patients. J Neurosurg 1989; 70:222-30. |
|22.||Cowan F, Thoresen M. Ultrasound study of the cranial venous system in the human new-born infant and the adult. Acta Physiol 1983; 117:131-7. |
|23.||Dearden NM. Jugular bulb venous oxygen saturation in the management of severe head injury. Curr Opin Anesthesiol 1991; 4:279-86. |
|24.||Stochetti N, Paparella A, Bridelli F, et al. Cerebral venous oxygen saturation studied with bilateral samples in the internal jugular veins. Neurosurgery 1994; 34:38-44. |
|25.||Murr R, Schurer L. Correlation of jugular venous oxygen saturation to spontaneous fluctuations of cerebral perfusion pressure in patients with severe head injury. Neurol Res 1995; 17:329-33. |
|26.||Chan KH, Dearden NM, Miller JD, et al. Multimodality monitoring as a guide to treatment of intracranial hypertension after severe brain injury. Neurosurgery 1993;32:547-53. [PUBMED] [FULLTEXT] |
|27.||Matta BF, Lam AM, Mayberg TS. The influence of arterial oxygenation on cerebral venous oxygen saturation during hyperventilation. Can J Anaesth 1994; 41:1041- 6. [PUBMED] |
|28.||Chan KH, Miller JD, Dearden NM, et al. Multimodality monitoring as a guide to treatment of intracranial hypertension after severe brain injury. Neurosurgery 1993; 32:547-53. [PUBMED] [FULLTEXT] |
|29.||Cruz J. Combined continuous monitoring of systemic and cerebral oxygenation in acute brain injury: preliminary observations. Crit Care Med 1993; 21:1225-32. [PUBMED] |
|30.||Matta BF, Lam AM. The rate of blood withdrawal affects the accuracy of jugular venous bulb oxygen saturation measurements. Anesthesiology 1997; 86:806-8. [PUBMED] [FULLTEXT] |
|31.||van den Brink WA, van Santbrink H, Steyeberg EW, et al. Brain oxygen tension in severe head injury. Neurosurgery 2000, 46:868-878. |
|32.||van Santbrink H, Maas AIR, Avezaat CJJ: Continuous monitoring of partial pressure of brain tissue oxygen in patients with severe head injury. Neurosurgery 1996, 38:21-31. |
|33.||Kiening KL, Unterberg AW, Bardt TF, et al. Monitoring of cerebral oxygenation in patients with severe head injuries: brain tissue PO 2 versus jugular vein oxygen saturation. J Neurosurg 1996, 85:751-757. [PUBMED] [FULLTEXT] |
|34.||Gopinath SP, Valadka AB, Uzura M, et al. Comparison of jugular venous oxygen saturation and brain PO2 as monitors of cerebral ischemia after head injury. Crit Care Med 1999, 27:2337-2345. [PUBMED] [FULLTEXT] |
|35.||Fandino J, Stocker R, Prokop S, et al. Correlation between jugular bulb oxygen saturation and partial pressure of brain tissue oxygen during CO 2 and O 2 reactivity tests in severely head-injured patients. Acta Neurochir (Wien) 1999, 141:825-834. [PUBMED] [FULLTEXT] |
|36.||Valadka AB, Gopinath SP, Contant CF, et al. Relationship of brain tissue PO 2 to outcome after severe head injury. Crit Care Med 1998, 26:1576-1581. [PUBMED] [FULLTEXT] |
|37.||Jordan KG. Continuous EEG monitoring in the neurosciences intensive care unit and emergency department. J Clin Neurophysiol 1999; 16:14-39. [PUBMED] [FULLTEXT] |
|38.||Haug E, Miner J, Dannehy M, et al. Bispectral electroencephalographic analysis of head-injured patients in the emergency department. Acad Emerg Med. 2004;11:349-52. |
|39.||Fabregas N, Gambus PL, Valero R, et al. Can bispectral index monitoring predict recovery of consciousness in patients with severe brain injury? Anesthesiology 2004;101:43-51. |
|40.||Paul DB, Umamaheswara Rao GS. Correlation of Bispectral Index with Glasgow Coma Score in mild and moderate head injuries. J Clin Monit Comput 2006;20:399-404. [PUBMED] [FULLTEXT] |
|41.||Goodman JC, Valadka AB, Gopinath SP, et al. Extracellular lactate and glucose alterations in the brain after head injury measured by microdialysis. Crit Care Med 1999, 27:1965-1973. [PUBMED] [FULLTEXT] |
|42.||Robertson CS, Gopinath SP, Goodman JC, et al. SjvO2 monitoring in head-injured patients. J Neurotrauma 1995, 12:891-896. [PUBMED] |
|43.||Bell MJ, Robertson CS, Kochanek PM, et al. Interstitial brain adenosine and xanthine increase during jugular venous oxygen desaturations in humans after traumatic brain injury. Crit Care Med 2001, 29:399-404. [PUBMED] [FULLTEXT] |
|44.||Goodman JC, Valadka AB, Gopinath SP, et al. Lactate and excitatory amino acids measured by microdialysis are decreased by pentobarbital coma in head-injured patients. J Neurotrauma 1996, 13:549-556. [PUBMED] |
|45.||Yamaguchi S, Nakahara K, Miyagi T, et al. Neurochemical monitoring in the management of severe head-injured patients with hypothermia. Neurol Res 2000, 22:657-664. [PUBMED] |
|46.||Menzel M, Doppenberg EM, Zauner A, et al. Cerebral oxygenation in patients after severe head injury: monitoring and effects of arterial hyperoxia on cerebral blood flow, metabolism and intracranial pressure. J Neurosurg Anesthesiol 1999, 11:240-251. [PUBMED] [FULLTEXT] |
|47.||Stahl N, Ungerstedt U, Nordstrom CH. Brain energy metabolism during controlled reduction of cerebral perfusion pressure in severe head injuries. Intensive Care Med 2001, 27:1215-1223. |
|48.||Schwarz S, Schwab S, Bertram M, et al. Effects of hypertonic saline hydroxyethyl starch solution and mannitol in patients with increased intracranial pressure after stroke. Stroke 1998;29:1550-1555. [PUBMED] [FULLTEXT] |
|49.||Vialet R, Albanese J, Thomachot L, et al. Isovolume hypertonic solutes (sodium chloride or mannitol) in the treatment of refractory posttraumatic intracranial hypertension: 2 mL/kg 7.5% saline is more effective than 2 mL/kg 20% mannitol. Crit Care Med 2003;31:1683-1687. |
|50.||Wade C, Grady J, Kramer G. Efficacy of hypertonic saline dextran (HSD) in patients with traumatic hypotension: Meta-analysis of individual patient data. Acta Anaesthesiol Scand Supp 1997;l 110:77-79. |
|51.||Wade CE, Kramer GC, Grady JJ, et al. Efficacy of hypertonic 7.5% saline and 6% dextran-70 in treating trauma: A meta-analysis of controlled clinical studies. Surgery 1997;122:609-616. [PUBMED] [FULLTEXT] |
|52.||Wade CE, Grady JJ, Kramer GC, et al. Individual patient cohort analysis of the efficacy of hypertonic saline/ dextran in patients with traumatic brain injury and hypotension. J Trauma 1997;42[Suppl 5]:S61-S65. |
|53.||Horn P, Munch E, Vajkoczy P, et al. Hypertonic saline solution for control of elevated intracranial pressure in patients with exhausted response to mannitol and barbiturates. Neurol Res 1999;21:758-764. |
|54.||Suarez JI, Qureshi AI, Bhardwaj A, et al. Treatment of refractory intracranial hypertension with 23.4% saline. Crit Care Med 1998;26:1118-1122. [PUBMED] [FULLTEXT] |
|55.||Worthley LI, Cooper DJ, Jones N. Treatment of resistant intracranial hypertension with hypertonic saline: Report of two cases. J Neurosurg 1988;68:478-481. [PUBMED] [FULLTEXT] |
|56.||Qureshi AI, Suarez JI, Bhardwaj A, et al. Use of hypertonic (3%) saline/acetate infusion in the treatment of cerebral edema: Effect on intracranial pressure and lateral displacement of the brain. Crit Care Med 1998;26:440-446. [PUBMED] [FULLTEXT] |
|57.||Bhardwaj A, Harukuni I, Murphy SJ, et al. Hypertonic saline worsens infarct volume after transient focal ischemia in rats. Stroke 2000;31:1694-1701. [PUBMED] [FULLTEXT] |
|58.||Obrist WD, Langfitt TW, Jaggi JL, et al. Cerebral blood flow and metabolism in comatose patients with acute head injury. J Neurosurg 1984; 61:241-253. [PUBMED] [FULLTEXT] |
|59.||Sheinberg M, Kanter MJ, Robertson CS, et al. Continuous monitoring of jugular venous oxygen saturation in head-injured patients. J Neurosurg 1992; 76:212-217. [PUBMED] [FULLTEXT] |
|60.||Muizelaar JP, Marmarou A, Ward JD, et al. Adverse effects of hyperventilation in patients with severe head injury: A randomised clinical trial. J Neurosurg 1991; 75:731-739. [PUBMED] [FULLTEXT] |
|61.||Skippen P, Seear M, Poskitt K, et al. Effect of hyperventilation on regional cerebral flow in head injured children. Crit Care Med 1997; 25: 1402-1409. [PUBMED] [FULLTEXT] |
|62.||Diringer MN, Videen TO, Yundt K, et al. Regional cerebrovascular and metabolic effects of hyperventilation after severe traumatic brain injury. J Neurosurg 2002; 96:103-108. [PUBMED] [FULLTEXT] |
|63.||Schierhout G, Roberts I. Hyperventilation therapy for acute traumatic brain injury (Cochrane Review). In: The Cochrane Library Issue 2, 2002. Oxford: Update Software. |
|64.||Johnston AJ, Steiner LA, Gupta AK, Menon DK. Cerebral oxygen vasoreactivity and cerebral tissue oxygen reactivity. Br J Anaesth 2003, 90:774-786. [PUBMED] [FULLTEXT] |
|65.||Magnoni S, Ghisoni L, Locatelli M, et al. Lack of improvement in cerebral metabolism after hyperoxia in severe head injury: a microdialysis study. J Neurosurg 2003, 98:952-958. [PUBMED] [FULLTEXT] |
|66.||McLeod AD, Igielman F, Elwell C, et al. Measuring cerebral oxygenation during normobaric hyperoxia: a comparison of tissue microprobes, near-infrared spectroscopy, and jugular venous oximetry in head injury. Anesth Analg 2003, 97:851-856. [PUBMED] [FULLTEXT] |
|67.||Rockswold GL, Ford SE, Anderson DC, et al. Results of a prospective randomized trial for treatment of severely brain-injured patients with hyperbaric oxygen. J Neurosurg 1992, 76:929-934. [PUBMED] [FULLTEXT] |
|68.||Alternative Therapy Evaluation Committee for the Insurance Corporation of British Columbia: A review of the scientific evidence on the treatment of traumatic brain injuries and strokes with hyperbaric oxygen. Brain Inj 2003, 17:225-236. |
|69.||Menzel M, Doppenberg EM, Zauner A, et al. Increased inspired oxygen concentration as a factor in improved brain tissue oxygenation and tissue lactate levels after severe human head injury. J Neurosurg 1999, 91:1-10. [PUBMED] [FULLTEXT] |
[Table 1], [Table 2]