Neurophysiological consequences of three tracheostomy techniques: a randomized study in neurosurgical patients

We describe the effects of different tracheostomy techniques on intracranial pressure (ICP), cerebral perfusion pressure (CPP), and cerebral extraction of oxygen. We attempted to identify the main mechanisms affecting intracranial pressure during tracheostomy. To do so we conducted a prospective, block-randomized, clinical study which took place in a neurosurgical intensive care unit in a teaching hospital. The patients studied consisted of thirty comatose patients admitted to the intensive care unit because of head injury, subarachnoid hemorrhage, or brain tumor. Ten patients per group were submitted to standard surgical tracheostomy, percutaneous dilatational tracheostomy or translaryngeal tracheostomy. In every technique a significant increase of ICP (P < .05) was observed at the time of cannula placement. Intracranial hypertension (ICP > 20 mm Hg) was more frequent in the percutaneous dilatational tracheostomy group (P < .05). Cerebral perfusion pressure dropped below 60 mm Hg in eleven cases, more frequently during surgical tracheostomy. Arterial tension of CO2 significantly increased in all three groups during cannula placement. No other major complications were recorded during the procedures. At follow-up no severe anatomic or functional damage was detected. We conclude that the three tracheostomy techniques, performed in selected patients where the risk of intracranial hypertension was reduced to the minimum, were reasonably tolerated but caused an intracranial pressure rise and cerebral perfusion pressure reduction in some cases.     

Cerebral hemodynamic responses to blood pressure manipulation in severely head-injured patients in the presence or absence of intracranial hypertension

The management of cerebral perfusion pressure (CPP) remains a controversial issue in the critical care of severely head-injured patients. Recently, it has been proposed that the state of cerebrovascular autoregulation should determine individual CPP targets. To find optimal perfusion pressure, we pharmacologically manipulated CPP in a range of 51 mm Hg (median; 25th-75th percentile, 48-53 mm Hg) to 108 mm Hg (102-112 mm Hg) on Days 0, 1, and 2 after severe head injury in 13 patients and studied the effects on intracranial pressure (ICP), autoregulation capacity, and brain tissue partial pressure of oxygen. Autoregulation was expressed as a static rate of regulation for 5-mm Hg CPP intervals based on middle cerebral artery flow velocity. When ICP was normal (26 occasions), there were no major changes in the measured variables when CPP was altered from a baseline level of 78 mm Hg (74-83 mm Hg), indicating that the brain was within autoregulation limits. Conversely, when intracranial hypertension was present (11 occasions), CPP reduction to less than 77 mm Hg (73-82 mm Hg) further increased ICP, decreased the static rate of regulation, and decreased brain tissue partial pressure of oxygen, whereas a CPP increase improved these variables, indicating that the brain was operating at the lower limit of autoregulation. We conclude that daily trial manipulation of arterial blood pressure over a wide range can provide information that may be used to optimize CPP management.     

Relationship of cerebral perfusion pressure and survival in pediatric brain-injured patients

BACKGROUND: Adult brain injury studies recommend maintaining cerebral perfusion pressure (CPP) above 70 mm Hg. We evaluated CPP and outcome in brain-injured children. METHODS: We retrospectively reviewed the hospital courses of children at two Level I trauma centers who required insertion of intracranial pressure (ICP) monitors for management of traumatic brain injury. ICP, CPP, and mean arterial pressure were evaluated hourly, and means were calculated for the first 48 hours after injury. RESULTS: Of 188 brain-injured children, 118 had ICP monitors placed within 24 hours of injury. They suffered severe brain injury, with average admitting Glasgow Coma Scale scores of 6 +/- 3. Overall mortality rate was 28%. No patient with mean CPP less than 40 mm Hg survived. Among patients with mean CPP in deciles of 40 to 49, 50 to 59, 60 to 69, or 70 mm Hg, no significant difference in Glasgow Outcome Scale distribution existed. CONCLUSION: Low mean CPP was lethal. In children with survivable brain injury (mean CPP > 40 mm Hg), CPP did not stratify patients for risk of adverse outcome.     

Reverse Trendelenburg position reduces intracranial pressure during craniotomy.

Cerebral swelling and herniation pose serious surgical obstacles during craniotomy for space-occupying lesions. Positioning patients head-up has been shown previously to reduce intracranial pressure (ICP) in neurotraumatized patients, but has not been investigated during intracranial surgery. The current study examined the effects of 10-deg reverse Trendelenburg position (RTP) on ICP and cerebral perfusion pressure (CPP). Forty adult patients subjected to craniotomy for supratentorial tumors were given standardized propofol-fentanyl-cisatracurium general anesthesia and were moderately hyperventilated. In 26 of 40 patients with expected poor clinical outcome, an additional catheter was placed in the internal jugular bulb to determine internal jugular bulb pressure (JBP). ICP was determined by subdural measurement using a 22-gauge needle advanced through the dura after removal of the bone flap. ICP was referenced to the level of the dural incision. ICP, mean arterial blood pressure, and CPP were compared with repeat measurements 1 minute after RTP. The tension of the dura was graded qualitatively by the surgeon by digital palpation and was compared to post-RTP. ICP decreased from 9.5 mm Hg to 6.0 mm Hg ( P <.001; all values are median) within 1 minute after 10-deg RTP. Mean arterial blood pressure decreased from 82.0 mm Hg to 78.5 mm Hg ( P <.001). CPP was unchanged (70.5 mm Hg versus 71 mm Hg after RTP), whereas JBP decreased from 8 mm Hg to 4 mm Hg ( P <.001). High initial ICP was correlated to the greatest magnitude of decrease in ICP. No significant correlation was found between change in ICP and change in JBP. Intracranial pressure after RTP resulted in decreased tension of the dura. RTP appears to be an effective means of reducing ICP during craniotomy, thereby reducing the risk of cerebral herniation. CPP is not affected. Studies over longer periods of time are warranted, however.     

Head injury and hemorrhagic shock: studies of the blood brain barrier and intracranial pressure after resuscitation with normal saline solution, 3% saline solution, and dextran-40

The effect of fluid resuscitation from hemorrhagic shock on cerebral edema, intracranial pressure (ICP), and blood brain barrier function was investigated in the presence of a simulated head injury. Beagle dogs were anesthetized and ICP was measured via a right subarachnoid bolt while a contralateral epidural balloon was inflated in the left hemicranium to mimic a closed head injury. Forty percent of the dogs' blood was shed and the shock state was maintained for 1 hour. Resuscitation was initiated with shed blood and a volume of either normal saline solution (NS, n = 5), 10% dextran-40 (D-40, n = 6), or hypertonic (3%) saline solution (HS, n = 6) equal to the amount of shed blood. Evans blue solution was infused intravenously, and intravascular volume was then maintained with normal saline solution. Control (n = 5) dogs did not undergo shock, but received equivalent volumes of normal saline solution and Evans blue solution. The dogs were killed after 2 hours of resuscitation, and the brains were removed, weighed, and fixed in formalin. The average intracranial pressure value after epidural balloon inflation was 18.6 +/- 0.80 mm Hg and decreased equally in all groups during the shock period, averaging 10.8 +/- 1.24 mm Hg at the end of the shock period. Fluid resuscitation markedly elevated ICP in the NS and D-40 groups, reaching maximal values of 46.6 +/- 12.11 mm Hg and 45.3 +/- 28.95 mm Hg, respectively. Maximal ICP values in control and HS groups measured 21.8 +/- 1.36 mm Hg and 15.8 +/- 2.04 mm Hg, respectively (p less than 0.25 for HS versus NS control). Wet brain weights were significantly less in the HS group compared with either NS or D-40 groups (p less than 0.05). Coronal sections of fixed HS brains showed deep cortical Evans blue staining on the side of balloon injury. Therefore, in the presence of an intracranial mass lesion, resuscitation with hypertonic (3%) saline solution is accompanied by lower ICP values and less cerebral edema than is isotonic saline or colloid resuscitation. Blood brain barrier function is not restored by hypertonic saline solution resuscitation.     

Effect of decompressive craniectomy on intracranial pressure and cerebrospinal compensation following traumatic brain injury

OBJECTIVE: Decompressive craniectomy is an advanced treatment option for intracranial pressure (ICP) control in patients with traumatic brain injury. The purpose of this study was to evaluate the effect of decompressive craniectomy on ICP and cerebrospinal compensation both within and beyond the first 24 hours of craniectomy. METHODS: This study was a retrospective analysis of the physiological parameters from 27 moderately to severely head-injured patients who underwent decompressive craniectomy for progressive brain edema. Of these, 17 patients had undergone prospective digital recording of ICP with estimation of ICP waveform-derived indices. The pressure-volume compensatory reserve (RAP) index and the cerebrovascular pressure reactivity index (PRx) were used to assess those parameters. The values of parameters prior to and during the 72 hours after decompressive craniectomy were included in the analysis. RESULTS: Decompressive craniectomy led to a sustained reduction in median (interquartile range) ICP values (21.2 mm Hg [18.7; 24.2 mm Hg] preoperatively compared with 15.7 mm Hg [12.3; 19.2 mm Hg] postoperatively; p = 0.01). A similar improvement was observed in RAP. A significantly lower mean arterial pressure (MAP) was needed after decompressive craniectomy to maintain optimum cerebral perfusion pressure (CPP) levels, compared with the preoperative period (99.5 mm Hg [96.2; 102.9 mm Hg] compared with 94.2 mm Hg [87.9; 98.9 mm Hg], respectively; p = 0.017). Following decompressive craniectomy, the PRx had positive values in all patients, suggesting acquired derangement in pressure reactivity. CONCLUSIONS: In this study, decompressive craniectomy led to a sustained reduction in ICP and improvement in cerebral compliance. Lower MAP levels after decompressive craniectomy are likely to indicate a reduced intensity of treatment. Derangement in cerebrovascular pressure reactivity requires further studies to evaluate its significance and influence on outcome.     

The relation between intracranial pressure,mean arterial pressure and cerebral blood flow in patients with severe head injury

In patients with severe head injuries ICP, MAP and CBF were measured continuously. In most patients there was a positive vasopressor response to increasing ICP, but the ICP/MAP ratio varied considerably in individual cases. CBF was diminished either by increasing ICP or by decreasing MAP. This effect was more marked with ICP above 40 mm Hg or MAP below 110 mm Hg. In terminal stages there was often a negative MAP/ICP ratio accompanied by massive cerebral hyperaemia. Key words: Severe head injury--intracranial pressure--mean arterial pressure--cerebral blood flow--cerebral perfusion pressure--critical limit of ICP and CBF. Abbreviations: ICP equals intracranial pressure (mm Hg); CBF, Flow equals cerebral blood flow (ml/min); MAP equals mean arterial pressure (mm Hg); CPP equals cerebral perfusion pressure (mm Hg) (difference between MAP and ICP); BP equals blood pressure.     

Cerebral oxygenation following decompressive hemicraniectomy for the treatment of refractory intracranial hypertension

OBJECT: Medically intractable intracranial hypertension is a major cause of morbidity and mortality after severe brain injury. One potential treatment for intracranial hypertension is decompressive hemicraniectomy (DCH). Whether and when to use DCH, however, remain unclear. The authors therefore studied the effects of DCH on cerebral O2 to develop a better understanding of the effects of this treatment on the recovery from injury and disease. METHODS: The study focused on seven patients (mean age 30.6 +/- 9.7 years) admitted to the hospital after traumatic brain injury (five patients) or subarachnoid hemorrhage (two patients) as part of a prospective observational database at a Level I trauma center. At admission the Glasgow Coma Scale (GCS) score was 6 or less in all patients. Patients received continuous monitoring of intracranial pressure (ICP), cerebral perfusion pressure (CPP), blood pressure, and arterial O2 saturation. Cerebral oxygenation was measured using the commercially available Licox Brain Tissue Oxygen Monitoring System manufactured by Integra NeuroSciences. A DCH was performed when the patient's ICP remained elevated despite maximal medical management. CONCLUSIONS: All patients tolerated DCH without complications. Before the operation, the mean ICP was elevated in all patients (26 +/- 4 mm Hg), despite maximal medical management. After surgery, there was an immediate and sustained decrease in ICP (19 +/- 11 mm Hg) and an increase in CPP (81 +/- 17 mm Hg). Following DCH, cerebral oxygenation improved from a mean of 21.2 +/- 13.8 mm Hg to 45.5 +/- 25.4 mm Hg, a 114.8% increase. The change in brain tissue O2 and the change in ICP after DCH demonstrated only a modest relationship (r2 = 0.3). These results indicate that the use of DCH in the treatment of severe brain injury is associated with a significant improvement in brain O2.     

The influence of some inhalation anaesthetics on the intracranial pressure with special reference to nitrous oxide (author's transl)]

The influence of inhalation anaesthetics on intracranial pressure (ICP), arterial blood pressure and cerebral perfusion pressure (CPP) was investigated on 12 unconscious patients with head injury having an initial ICP of about 20 mm Hg. Halothane, enflurane and nitrous oxide induced a considerable rise of ICP during a 15 to 25 minute period of observation. The moderate fall in blood pressure caused by halothane and enflurane enhanced the reduction of the calculated CPP. Besides, a regular fall in blood pressure of about 16% was observed under the influence of nitrous oxide, subsequently reducing the CPP in some cases under 40 mm Hg. Inhalation anaesthetics, including nitrous oxide, should therefore not be used in patients with decreased intracranial compliance before the increased ICP is treated.     

Physiological consequences of experimental cerebral missile injury and use of data analysis to predict survival.

The authors describe cerebrovascular and cerebral metabolic changes in monkeys, subjected to cerebral missile injury. After injury with BB pellet at 90 m/sec, there is a rapid rise in intracranial pressure (ICP), which reaches a peak 2 to 5 minutes posttrauma, and then falls to about 20 to 30 mm Hg. This, with a fall in mean blood pressure (MBP), results in a 50% reduction in cerebral perfusion pressure (CPP), Cerebral blood flow (CBF) is also reduced, although acutely there is no close relationship with (CPP). Cerebrovascular resistance falls initially and then at 30 minutes rises to very high values. Cerebral metabolic rates (CMR's) for oxygen fall after injury and remain low for the rest of the animal's life; CMR's for lactate rise immediately after injury and persists for 5 hours, then fall. After injury with a faster missile (180 m/sec), the ICP rises higher and faster, and the peak is shorter. The CCP is reduced in this injury to approximately 30 mm Hg, and only one animal survived more than 1 hour. With the conventional forms of data analysis, the length of survival after injury correlates well with MBP, ICP, and CBF, but separately they were completely unsatisfactory for prediction of an individuals prognosis. With the technique of multiple linear regression analysis, the survival of individual animals could be predicted with great accuracy. This is possible also when two postinjury parameters,CBF and MBP, are used.     

The effect of cerebrospinal fluid drainage on cerebral perfusion in traumatic brain injured adults

Cerebrospinal fluid drainage is a first line treatment used to manage severely elevated intracranial pressure (> or = 20 mm Hg) and improve outcomes in patients with acute head injury. There is no consensus regarding the optimal method of cerebrospinal fluid removal. The purpose of this investigation was to determine whether cerebrospinal fluid drainage decreases intracranial pressure and improves cerebral perfusion and to identify factors that impact treatment effectiveness. This study involved 31 severely head injured patients. Intracranial pressure and other indices of cerebral perfusion (cerebral perfusion pressure, cerebral blood flow velocity, and regional cerebral oximetry) were measured before, during, and after cerebrospinal fluid drainage. Arterial and jugular venous oxygen content was measured before and after cerebrospinal fluid drainage. Patients underwent three randomly ordered cerebrospinal fluid drainage protocols that varied in the volume of cerebrospinal fluid removed (1 mL, 2 mL, and 3 mL) for a total of 6 mL of cerebrospinal fluid removed. There was a significant change in the intracranial pressure from a mean at baseline of 26.1 mm Hg (SD = 4.4) to 22.1 mm Hg immediately after drainage. One third of patients experienced a decrease in the intracranial pressure below 20 mm Hg; in two patients the intracranial pressure dropped less than 1 mm Hg. The following factors predicted 61.5% of the variance in the responsiveness of intracranial pressure to drainage: vecuronium hypothermia, baseline cerebral perfusion pressure and acuity of illness. Cerebrospinal fluid drainage provides a transient decrease in intracranial pressure without a measurable improvement in other indices of cerebral perfusion.     

Phenylephrine increases cerebral perfusion pressure without increasing intracranial pressure in rabbits with balloon-elevated intracranial pressure.

Using a rabbit model of intracranial hypertension, we studied the effects of infusion of phenylephrine on intracranial pressure (ICP) and cerebral perfusion pressure (CPP). Seven New Zealand white rabbits were anesthetized with isoflurane and normocapnia was maintained. An extradural balloon was used to raise ICP to 25 +/- 1 mm Hg. Infusion of phenylephrine increased mean arterial blood pressure (MAP) (77 +/- 6 --> 95 +/- 8 mm Hg) and CPP (52 +/- 7 --> 70 +/- 7 mm Hg). ICP was unchanged during infusion of phenylephrine (25 +/- 1 vs. 25 +/- 2 mm Hg). The phenylephrine infusion was stopped after 45 minutes and MAP returned to baseline (76 +/- 8 mm Hg). We conclude that phenylephrine increased CPP because of its effect on MAP, but did not alter ICP. Phenylephrine may be used to increase CPP without raising ICP when autoregulation is intact.     

Adverse impact of a calcium entry-blocker (verapamil) on intracranial pressure in patients with brain tumors

In order to examine the effects of verapamil on intracranial pressure (ICP) in patients with compromised intracranial compliance, five hypertensive patients with supratentorial tumors were given verapamil, 5 mg intravenously, at the time of anesthesia induction. Within 4 minutes, ICP increased 67% from 18 +/- 4 mm Hg (standard error) to 27 +/- 5 mm Hg (p less than 0.05), whereas mean arterial pressure decreased 20% from 111 +/- 7 mm Hg to 89 +/- 4 mm Hg (p less than 0.05), and cerebral perfusion pressure (CPP) decreased 33% from 93 +/- 11 mm Hg to 62 +/- 6 mm Hg (p less than 0.05). The increases in ICP responded promptly to hyperventilation and intravenous lidocaine (1.5 mg/kg). A control group of five hypertensive patients with supratentorial tumors received the same anesthetic agents without verapamil. In this group, ICP and CPP were unchanged. The authors conclude that calcium entry-blockers, such as verapamil, should be avoided in patients with compromised intracranial compliance unless ICP is being monitored and proper therapy for intracranial hypertension can be rapidly instituted.     

Effect of positive end expiratory pressure ventilation on intracranial pressure in man.

THsi study was designed to define the effect of positive end expiratory pressure (PEEP) ventilation on intracranial pressure (ICP). In 25 patients with severe head trauma with and without associated pulmonary injury the following parameters were simultaneously monitored under mechanical ventilation with and without PEEP:ICP, arterial blood pressure, central venous pressure, arterial blood gases, and cardiac rate. In addition, the volume-pressure response (VPR) was evaluted in each patient to assess cerebral elastance. The results indicate a significant increase in ICP with the application of PEEP only in the 12 patients who manifested increased cerebral elastance by VPR. Half of this latter group manifested impairment of cerebral perfusion pressure to levels less than 60 mm Hg. Return to baseline CIP levels was observed with termination of PEEP. No significantly consistent changes in other parameters were noted.     

The use of indomethacin to treat acute rises of intracranial pressure and improve global cerebral perfusion in a child with head trauma

Background: The use of vasoconstrictors (e.g. dihydroergotamine, indomethacin) for the treatment of increased intracranial pressure (ICP) secondary to brain trauma is controversial. In particular, it has been suggested that vasoconstrictors be employed only for intracranial hypertension secondary to hyperemia, when venous jugular bulb saturation (SjO₂) is >75%. Method We administered indomethacin as a bolus i.v. (5–10 mg) on 18 occasions to a multiple-injured 3-year-old child with acute rises of ICP secondary to severe brain trauma (GCS score 7) determining a large hypodensity area in and swelling of the right hemisphere. Results: Before indomethacin administration the average of mean ICP was 68.1 ± 10.8 (SD) mm Hg (range 47–84) and the cerebral perfusion pressure (CCP) was 38.4±10.4 mm Hg (range 30–65). In response to indomethacin, ICP dropped in a few seconds to 22.7±5.6 and CCP increased to 82.4±6.1 mm Hg (P <0.001), while the mean arterial pressure remained unchanged. On 6 occasions SjO₂ was also evaluated immediately before and 5 and 10 min after indomethacin administration. Before indomethacin administration, SjO₂ values were within the normal range on 2 occasions and abnormally low on four. SjO₂ increased from the mean value of 45.6215.7 to 59.828.9 (after 5 min) and 60.6212.4% (after 10 min) (P< 0.01 versus pre-indomethacin). At the same time the cerebral venous pH increased from 7.4320.01 to 7.4550.01 (P=0.01). These findinge suggest that the global cerebral perfusion was improved. Eighteen days after injury the child was awake and was discharged from the ICU. Conclusion: To our knowledge, increase of SjO, in response to indomethacin has not been previously reported. Although great caution is necessary in the use of indomethacin for the treatment of ICE these findings suggest that indomethacin can be useful for the treatment of acute rises of ICP compromising severely the CCP, even if SjO, is normal or abnormally low. Under these circumstances, indomethacin can improve the global cerebral perfusion.     

Effects of mannitol bolus administration on intracranial pressure, cerebral extracellular metabolites, and tissue oxygenation in severely head-injured patients

BACKGROUND: Osmotic agents are widely used to lower elevated intracranial pressure (ICP). However, little data are available regarding cerebral oxygenation and metabolism in the traumatized brains studied under clinical conditions. The present prospective, open-labeled clinical study was designed to investigate whether administration of mannitol, with the aim of reducing moderate intracranial hypertension, improves cerebral metabolism and oxygenation in patients after severe traumatic brain injury (TBI). METHODS: Multimodal cerebral monitoring (MCM), consisting of intraparenchymal ICP, tissue oxygenation (ptiO2), and micro dialysis measurements was initiated in six male TBI patients (mean age 45 years; Glasgow Coma Scale score <9). A total of 14 mannitol boli (20%, 0.5g/kg, 20 minutes infusion time) were administered to treat ICP exceeding 20 mm Hg (2.7 kPa). Temporal alterations determined by MCM after mannitol infusions were recorded for 120 minutes. Microdialysates were assayed immediately for extracellular glucose, lactate, pyruvate, and glutamate concentrations. RESULTS: Elevated ICP was successfully treated in all cases. This effect was maximal 40 minutes after start of infusion (25 +/- 6 mm Hg [3.3 +/- 0.8 kPa] to 17 +/- 3 mm Hg [2.3 +/- 0.4 kPa], p < 0.05) and lasted up to 100 minutes. Cerebral ptiO2 remained unaffected (21 +/- 5 mm Hg [2.8 +/- 0.7 kPa] to 23 +/- 6 mm Hg [3.1 +/- 0.8 kPa], n.s.). Microdialysate concentrations of all analytes rose unspecifically by 10% to 40% from baseline, reaching maximum concentrations 40 to 60 minutes after start of the infusion. CONCLUSIONS: Mannitol efficiently reduces increased ICP. At an ICP of up to 30 mm Hg [4 kPa] it does not affect cerebral oxygenation. Unspecific increases of extracellular fluid metabolites can be explained by transient osmotic dehydration. Additional mechanisms, such as increased cerebral perfusion and blood volume, might explain an accelerated return to baseline.     

Effect of head elevation on intracranial pressure, cerebral perfusion pressure, and cerebral blood flow in head-injured patients.

The traditional practice of elevating the head in order to lower intracranial pressure (ICP) in head-injured patients has been challenged in recent years. Some investigators argue that patients with intracranial hypertension should be placed in a horizontal position, the rationale being that this will increase the cerebral perfusion pressure (CPP) and thereby improve cerebral blood flow (CBF). However, ICP is generally significantly higher when the patient is in the horizontal position. This study was undertaken to clarify the issue of optimal head position in the care of head-injured patients. The effect of 0 degree and 30 degrees head elevation on ICP, CPP, CBF, mean carotid pressure, and other cerebral and systemic physiological parameters was studied in 22 head-injured patients. The mean carotid pressure was significantly lower when the patient's head was elevated at 30 degrees than at 0 degrees (84.3 +/- 14.5 mm Hg vs. 89.5 +/- 14.6 mm Hg), as was the mean ICP (14.1 +/- 6.7 mm Hg vs. 19.7 +/- 8.3 mm Hg). There was no statistically significant change in CPP, CBF, cerebral metabolic rate of oxygen, arteriovenous difference of lactate, or cerebrovascular resistance associated with the change in head position. The data indicate that head elevation to 30 degrees significantly reduced ICP in the majority of the 22 patients without reducing CPP or CBF.     

Cerebral cortical oxygenation: a pilot study

BACKGROUND: Cerebral hypoxia (cerebral cortical oxygenation [Pbro2] < 20 mm Hg) monitored by direct measurement has been shown in animal and small clinical studies to be associated with poor outcome. We present our preliminary results observing Pbro2 in patients with traumatic brain injury (TBI). METHODS: A prospective observational cohort study was performed. Institutional review board approval was obtained. All patients with TBI who required measurement of intracranial pressure (ICP), cerebral perfusion pressure (CPP), and Pbro2 because of a Glasgow Coma Scale score < 8 were enrolled. Data sets (ICP, CPP, Pbro2, positive end-expiratory pressure (PEEP), Pao2, and Paco2) were recorded during routine manipulation. Episodes of cerebral hypoxia were compared with episodes without. Results are displayed as mean +/- SEM; t test, chi2, and Fisher's exact test were used to answer questions of interest. RESULTS: One hundred eighty-one data sets were abstracted from 20 patients. Thirty-five episodes of regional cerebral hypoxia were identified in 14 patients. Compared with episodes of acceptable cerebral oxygenation, episodes of cerebral hypoxia were noted to be associated with a significantly lower mean Pao2 (144 +/- 14 vs. 165 +/- 8; p < 0.01) and higher mean PEEP (8.8 +/- 0.7 vs. 7.1 +/- 0.3; p < 0.01). Mean ICP and CPP measurements were similar between groups. In a univariate analysis, cerebral hypoxic episodes were associated with Pao2 < or = 100 mm Hg (p < 0.01) and PEEP > 5 cm H2O (p < 0.01), but not ICP > 20 mm Hg, CPP < or = 65 mm Hg, or Pac2 < or = 35 mm Hg. CONCLUSION: Cerebral oxymetry is confirmed safe in the patient with multiple injuries with TBI. Occult cerebral hypoxia is present in the traumatic brain injured patient despite normal traditional measurements of cerebral perfusion. Further research is necessary to determine whether management protocols aimed at the prevention of cerebral cortical hypoxia will affect outcome.     

Cerebral autoregulation following head injury.

OBJECT: The goal of this study was to examine the relationship between cerebral autoregulation, intracranial pressure (ICP), arterial blood pressure (ABP), and cerebral perfusion pressure (CPP) after head injury by using transcranial Doppler (TCD) ultrasonography. METHODS: Using ICP monitoring and TCD ultrasonography, the authors previously investigated whether the response of flow velocity (FV) in the middle cerebral artery to spontaneous variations in ABP or CPP provides reliable information about cerebral autoregulatory reserve. In the present study, this method was validated in 187 head-injured patients who were sedated and receiving mechanical ventilation. Waveforms of ICP, ABP, and FV were recorded over intervals lasting 20 to 120 minutes. Time-averaged mean FV and CPP were determined. The correlation coefficient index between FV and CPP (the mean index of autoregulation [Mx]) was calculated over 4-minute epochs and averaged for each investigation. The distribution of averaged mean FV values converged with the shape of the autoregulatory curve, indicating lower (CPP < 55 mm Hg) and upper (CPP > 105 mm Hg) thresholds of autoregulation. The relationship between the Mx and either the CPP or ABP was depicted as a U-shaped curve. Autoregulation was disturbed in the presence of intracranial hypertension (ICP > or = 25 mm Hg) and when mean ABP was too low (ABP < 75 mm Hg) or too high (ABP > 125 mm Hg). Disturbed autoregulation (p < 0.005) and higher ICP (p < 0.005) occurred more often in patients with unfavorable outcomes than in those with favorable outcomes. CONCLUSIONS: Autoregulation not only is impaired when associated with a high ICP or low ABP, but it can also be disturbed by too high a CPP. The Mx can be used to guide intensive care therapy when CPP-oriented protocols are used.