Short-term lack of cerebral perfusion with good outcome. Advantages of early intracranial pressure monitoring

A 21-year-old man was injured by a tailboard of a truck. He suffered a severe head injury with bilateral depressed skull fractures necessitating surgical decompression. On admission to the hospital the patient showed bending to pain stimuli (Glasgow Coma Score 5). Anisocoria was noticed from the beginning. Initial intracranial pressure (ICP), measured 3 hours after injury, was 30 mm Hg, and the cerebral perfusion pressure (CPP) was 70 mm Hg. During surgical elevation of the skull fracture on the right side an un-explainable rise of ICP to values of 100 mm Hg occurred, which corresponded to the mean arterial blood pressure (MAP). At the same time both pupils were dilated and fixed indicating a lack of cerebral perfusion. Due to immediate trephination of the opposite side, the ICP was lowered to values below 20 mm Hg, and sufficient cerebral perfusion (above 50 mm Hg) was regained. The patient showed a good recovery and was transferred to a rehabilitation center 5 weeks after injury. This case report emphasizes the importance of early and continuous intracranial pressure monitoring for adequate therapy in neurosurgical emergencies.     

Effects of cisatracurium on cerebral and cardiovascular hemodynamics in patients with severe brain injury

BACKGROUND: For neuroanesthesia and neurocritical care the use of drugs that do not increase or preferentially decrease intracranial pressure (ICP) or change cerebral perfusion pressure (CPP) and cerebral blood flow (CBF) are preferred. The current study investigates the effects of a single rapid bolus dose of cisatracurium on cerebral blood flow velocity, ICP, CPP, mean arterial pressure (MAP) and heart rate (HR) in 24 mechanically ventilated patients with intracranial hypertension after severe brain trauma (Glasgow coma scale <6) under continuous sedation with sufentanil and midazolam. METHODS: Patients were randomly assigned to receive either 2xED95 (n=12) or 4xED95 (n=12) of cisatracurium as a rapid i.v. bolus injection. Before and after bolus administration mean cerebral blood flow velocity (BFV, cm/s) was measured in the middle cerebral artery using a 2-MHz transcranial Doppler sonography system, ICP (mm Hg) was measured using an extradural probe, and MAP (mm Hg) and HR (b/min) were measured during a study period of 20 min. Cerebral perfusion pressure (CPP=MAP-ICP) was also calculated. RESULTS: Our data show that a single bolus dose of up to 4xED95 cisatracurium caused no significant (P<0.05) changes in BFV, ICP, CPP, MAP and HR. Possible histamine-related events were not observed during the study. CONCLUSIONS: The results from this study suggest that cisatracurium is a safe neuromuscular blocking agent for use in adult severe brain-injured patients with increased ICP under mild hyperventilation and continuous sedation.     

Assessing baroreflex sensitivity in post-myocardial infarction patients: comparison of spectral and phenylephrine techniques

OBJECTIVE: To comparatively assess outcome of patients undergoing monitoring and management of cerebral extraction of oxygen along with cerebral perfusion pressure vs. outcome of patients undergoing monitoring and management of cerebral perfusion pressure alone in severe acute brain trauma. DESIGN: Prospective, interventional study. SETTING: Intensive care unit of a university hospital. PATIENTS: Adults (n = 353) with severe acute brain trauma. A group of 178 patients underwent continuous monitoring and management of cerebral extraction of oxygen and cerebral perfusion pressure, while a control group of 175 patients underwent monitoring and management of cerebral perfusion pressure only. INTERVENTIONS: Routine neuroemergency procedures. MEASUREMENTS AND MAIN RESULTS: The two groups of patients were matched with regard to age, postresuscitation Glasgow Coma Scale scores, rates of acute surgical intracranial hematomas and brain swelling, pupillary abnormalities, early hypotensive events (before intensive care monitoring), as well as initial levels of intracranial pressure and cerebral perfusion pressure. Outcome at 6 months post injury was significantly better (p < .00005) in the 178 patients undergoing monitoring and management of cerebral extraction of oxygen along with cerebral perfusion pressure, than in the control group of 175 patients undergoing monitoring and management of cerebral perfusion pressure alone. CONCLUSION: In patients with severe acute brain trauma and intracranial hypertension associated with compromised cerebrospinal fluid spaces, monitoring and managing cerebral extraction of oxygen in conjunction with cerebral perfusion pressure result in better outcome than when cerebral perfusion pressure is managed alone.     

Relationship between intracranial pressure and the development of vasospasm after aneurysmal subarachnoid hemorrhage

The relationship between intracranial pressure (ICP) and the development of vasospasm after subarachnoid hemorrhage caused by the rupture of an intracranial aneurysm was investigated. Eleven patients were divided into high (6 cases) and low (5 cases) ICP groups based on ICP data obtained during the perioperative period by continuous ICP monitoring. Transcranial Doppler ultrasonography was performed every 24 hours for 7 days and the severity, distribution, and duration of vasospasm were assessed. The high ICP group tended to have severe, prolonged, and diffuse vasospasm compared with the low ICP group. However, only duration of vasospasm was statistically different. The relationship between cerebral perfusion pressure (CPP) and the development of vasospasm was also examined. CPP had a less significant effect than ICP although similar tendencies for high ICP and low CPP were observed. High ICP worsens vasospasm and treatment for decreasing ICP with perioperative ICP monitoring has potential for avoiding the development of vasospasm.     

Renal artery reconstruction in transplant kidney. Case report

Diaspirin cross-linked haemoglobin (DCLHb) is a new oxygen carrying blood substitute with vasoactive properties. Vasoactive properties may be mediated via high affinity binding of nitric oxide by the haem moiety. Using a rodent model of head injury combined with ischaemia, we studied the effects of DCLHb on cerebral blood flow (CBF) and intracranial pressure (ICP). Twenty anaesthetized rats were allocated randomly to receive treatment with DCLHb 400 mg kg-1 i.v. or placebo (oncotically matched plasma protein substitute 4.5% i.v.). To produce diffusely increased ICP, after a severe weight drop injury, all animals underwent a 30-min period of bilateral carotid ligation combined with a period of induced hypotension. After reperfusion, DCLHb or placebo was infused and the animals instrumented for measurement of intraventricular ICP and CBF in the region of the sensorimotor cortex using the hydrogen clearance technique. Mean arterial pressure (MAP), ICP, cerebral perfusion pressure (CPP) (CPP = MAP - ICP) and CBF were measured 4 h after injury in all animals. DCLHb significantly reduced ICP from mean 13 (SEM 2) to 3 (1) mm Hg (P < 0.001), increased CPP from 52 (8) to 95 (6) mm Hg (P < 0.001) and increased CBF from 21 (2) to 29 (2) ml 100 g-1 min-1 (P = 0.032). We conclude that DCLHb improved CPP without a reduction in CBF in a rodent model of post-traumatic brain swelling.     

Noninvasive prediction of intracranial pressure curves using transcranial Doppler ultrasonography and blood pressure curves

BACKGROUND AND PURPOSE: Until now the assessment of intracranial pressure (ICP) required invasive methods. The objective of this study was to introduce an approach to a noninvasive assessment of continuous ICP curves. METHODS: The intracranial compartment was considered a "black box" system with an input signal, the arterial blood pressure (ABP), and an output signal, the ICP. A so-called weight function described the relationship between ABP and ICP curves. Certain parameters, called transcranial Doppler (TCD) characteristics, were calculated from the cerebral blood flow velocity (FV) and the ABP curves and were used to estimate this weight function. From simultaneously sampled FV, ABP, and (invasively measured) ICP curves of a defined group of patients with severe head injuries, the TCD characteristics and the weight function were computed. Multiple regression analysis revealed a mathematical formula for calculating the weight function from TCD characteristics. This formula was used to generate the ICP simulation. FV, ABP, and ICP recordings from 11 patients (mean age, 46 +/- 14 years) with severe head injury were studied. In each patient, ICP was computed by a simulation procedure, generated from the data of the remaining 10 patients. The simulation period was 100 seconds. RESULTS: Corresponding pressure trends with a mean absolute difference of 4.0 +/- 1.8 mm Hg between computed and measured ICP were observed. Shapes of pulse and respiratory ICP modulations were clearly predicted. CONCLUSIONS: These results demonstrate that this method constitutes a promising step toward a noninvasive ICP prediction that may be clinically applicable under well-defined conditions.     

Temperature of the cerebrovenous blood in a model of increased intracranial pressure

Hypothermia has a considerable protective effect during brain ischemia. On the other hand small increases of brain temperature have a remarkable effect on the exacerbation of neurological damage following an ischemic event. Hyperthermia of the brain tissue after severe head injury is described. The effect of acutely increased intracranial pressure on cerebrovenous blood temperature is not described yet. The aim of this study was to investigate the relationship between temperature in the cerebrovenous compartment (Tcv) and changes of the CPP in an animal model of raised intracranial pressure. METHODS: A thermocouple was inserted in the sagittal sinus in 9 pigs under general anesthesia. By stepwise inflating a supracerebral and infratentorial placed balloon catheter intracranial pressure (ICP) was increased and CPP concomitantly decreased. The central body temperature was measured simultaneously in the abdominal aorta (Ta) with a second thermocouple. RESULTS: In our model th Tcv was lower than Ta at the beginning of the ICP increase. The mean difference between Ta and Tcv, (delta Ta-cv) was 0.86 degree C (+/- 0.44) prior to ICP increase and 1.19 degrees C (0.58) at the maximum ICP increase. Thus, delta Tav increased during CPP reduction. This relation was represented by an adjusted R(square) of r2 = 0.89 (p < 0.001). CONCLUSIONS: The CPP decrease, caused by an increasing ICP, results in changes of the cerebrovenous blood temperature. Interpreting the present results the experimental situation of a relative colder cerebral compartment in comparison to the central body temperature has to be considered. However, the results imply, that simultaneous temperature monitoring of the central body temperature and the cerebrovenous blood temperature is an additional source of information about relative changes of the CBF.     

Significance of intracranial hypertension in severe head injury

Measurements of intracranial pressure (ICP) were begun within hours of injury in 160 patients with severe brain trauma, and continued in the intensive care unit. Some degree of increased ICP (greater than 10 mm Hg) was present on admission in most cases (82%), and in all but two of the 62 patients with intracranial mass lesions requiring surgical decompression; ICP was over 20 mm Hg on admission in 44% of cases, and over 40 mm Hg in 10%. In patients with mass lesions only very high ICP (greater than 40 mm Hg) on admission was significantly associated with a poor neurological picture and outcome from injury, while in patients with diffuse brain injury any increase in ICP above 10 mm Hg was associated with a poorer neurological status and a worse outcome. Despite intensive measures aimed at prevention of intracranial hypertension, ICP rose over 20 mm Hg during the monitoring period in 64 of the 160 patients (40%). Postoperative increases in ICP over 20 mm Hg (mean) were seen in 52% of the patients who had had intracranial masses evacuated, and could not be controlled by therapy in half of these cases. Even in patients without mass lesions, ICP rose above 20 mm Hg in a third of the cases, despite artificial ventilation and steroid therapy. Of the 48 patients who died, severe intracranial hypertension was the primary cause of death in nearly half and even moderately increased ICP (greater than 20 mm Hg) was associated with higher morbidity in patients with mass lesions and those with diffuse brain injury. Measurement of ICP should be included in management of patients with severe head injury.     

Acute vasoconstriction after subarachnoid hemorrhage

OBJECTIVE: Decreased cerebral blood flow (CBF) and cerebral ischemia occurring immediately after subarachnoid hemorrhage (SAH) may be caused by acute microvascular constriction. However, CBF can also be influenced by changes in intracranial pressure (ICP) and cerebral perfusion pressure (CPP). The goal of these experiments was to assess the significance of acute vasoconstriction after SAH and its relationship to changes in CBF, ICP, CPP, and extracellular glutamate concentrations. METHODS: Three experiments were performed using the endovascular filament technique to produce SAH. In the first experiment, CBF, ICP, and CPP were measured for 60 minutes after SAH (n = 21) and were correlated with the 24-hour mortality rate. In the second experiment, rats undergoing SAH (n = 23) or a sham procedure (n = 7) were perfused 60 minutes after SAH for measurement of the circumference and wall thickness of the internal carotid and anterior cerebral arteries and correlation with CBF, ICP, and CPP. In the third experiment (n = 11), extracellular glutamate concentrations determined by hippocampal and cortical microdialysis and high performance liquid chromatography were correlated with physiological changes. RESULTS: CBF reductions to less than 40% of baseline for 60 minutes after SAH predicted 24-hour mortality with 100% accuracy and were used to define "lethal" SAH. In contrast, ICP and CPP 60 minutes after SAH were not correlated with the mortality rate. The vascular circumference was significantly smaller in lethal than in sublethal SAH or sham-operated rats (P < 0.001). Vessel measurements were correlated with both CBF and hemorrhage size (P < 0.01). Extracellular glutamate concentration increased to 600% of baseline after lethal SAH in both hippocampus and cortex and was inversely correlated with CBF (r = 0.9, P < 0.001) but did not increase after sublethal SAH. CONCLUSION: Acute vasoconstriction after SAH occurs independently of changes in ICP and CPP and is associated with decreased CBF, larger hemorrhage size, persistent elevations of extracellular glutamate, and poor outcome. Acute vasoconstriction seems to contribute directly to ischemic brain injury after SAH. Further evaluations of pharmacological agents with the potential to reverse acute vasoconstriction may increase CBF and improve outcome.     

Plasma endothelin 1 concentrations in children with congenital heart defects

A therapy refractory brain edema is causally responsible for the death of approximately 50% of patients following severe craniocerebral trauma. The development of a brain edema which cannot be controlled by conservative means is also the most frequent cause of death with cerebral emergencies not caused by trauma. The cerebral perfusion pressure (CPP), which is the decisive factor for sufficient cerebral oxygenation, can be calculated on condition that the mean arterial pressure (MAP) and the intracranial pressure (ICP) are continually monitored: (CPP = MAP-ICP). On the basis of neurological observations, the computer tomographical results and the jugular vein oxymetry, an incipient cerebral decompensation and consequently the failure of the ongoing conservative treatment becomes apparent at an early stage. At this point at the latest, a bitemporal craniectomy should be considered for treatment. A drop in CPP to below 70 mmHg for adults and 50 mmHg for children is regarded as the intervention limits. Our experience shows that the outcome can be improved if the time of the bitemporal craniectomy lies before that of the cerebral decompensation.     

Intracranial pressure monitoring in patients with severe craniocerebral injury

After severe head injury intracranial pressure (ICP) must be measured continuously for management to assess and maintain the cerebral perfusion. Therefore in our hospital epidural transducers are used. To prove the efficiency of this method in a 12-month period the clinical courses of 23 patients with intracranial pressure transducers were analysed retrospectively. Eighteen patients survived, 5 of them without residuals, 13 with residuals and 2 remained in coma. In 14 patients secondary rises of intracranial pressure were observed between days 3 and 6 post injury. The mean ICP value of the survivors revealed 25 mm Hg. whereas the expired showed 60 mm Hg. In 17 patients the measurements were considered as reliable, 6 measurements were not reliable, which included 1 of the 5 patients who died. One transduce was displaced, another one showed a hemorrhage at the drill hole. There was no infection.     

Dieldrin in fish and shellfish from the Mersey Estuary and Liverpool Bay

OBJECT: The authors studied the reliability of a new method for noninvasive assessment of cerebral perfusion pressure (CPP) in head-injured patients in which mean arterial blood pressure (ABP) and transcranial Doppler middle cerebral artery mean and diastolic flow velocities are measured. METHODS: Cerebral perfusion pressure was estimated (eCPP) over periods of continuous monitoring (20 minutes-2 hours, 421 daily examinations) in 96 head-injured patients (Glasgow Coma Scale score < 13) who were admitted to the intensive care unit. All patients were sedated, paralyzed, and ventilated. The eCPP and the measured CPP (ABP minus intracranial pressure, measured using an intraparenchymal microsensor) were compared. The correlation between eCPP and measured CPP was r=0.73; p < 10(-6). In 71% of the examinations, the estimation error was less than 10 mm Hg and in 84% of the examinations, the error was less than 15 mm Hg. The method had a high positive predictive power (94%) for detecting low CPP (< 60 mm Hg). The eCPP also accurately reflected changes in measured CPP over time (r > 0.8; p < 0.001) in situations such as plateau and B waves of intracranial pressure, arterial hypotension, and refractory intracranial hypertension. A good correlation was found between the average measured CPP and eCPP when day-by-day variability was assessed in a group of 41 patients (r=0.71). CONCLUSIONS: Noninvasive estimation of CPP by using transcranial Doppler ultrasonography may be of value in situations in which monitoring relative changes in CPP is required without invasive measurement of intracranial pressure.     

Intravascular ultrasound in endovascular stent-grafts for peripheral aneurysm: a clinical study

The present series of experiments was performed to investigate the influence of acute intracranial hypertension on the upper limit (UL) of cerebral blood flow (CBF) autoregulation. Three groups of eight rats each--one with normal intracranial pressure (ICP) (2 mmHg), one with ICP = 30 mmHg, and one with ICP = 50 mmHg--were investigated. Intracranial hypertension was maintained by continuous infusion of lactated Ringer's solution into the cisterna magna, where the pressure was used as ICP. Cerebral perfusion pressure (CPP), calculated as mean arterial blood pressure (MABP)-ICP, was increased stepwise by continuous intravenous infusion of norepinephrine. CBF was calculated by the intracarotid 133Xe method. In all three groups the corresponding CBF/CPP curve included a plateau where CBF was independent of changes in CPP, showing intact autoregulation. At normal ICP the UL was found at a CPP of 141 +/-2 mmHg, at ICP = 30 mmHg the UL was 103+/-5 mmHg, and at ICP = 50 mmHg the UL was found at 88+/-7 mmHg. This shift of the UL was more pronounced than the shift of the lower limit (LL) of the CBF autoregulation found previously. We conclude that intracranial hypertension is followed by both a shift toward lower CPP values and a narrowing of the autoregulated interval between the LL and the UL.     

Osmotherapy for increased intracranial pressure: comparison between mannitol and glycerol

Osmotic agents are still the most common treatment for controlling intracranial hypertension (ICH). Mannitol, glycerol, sorbitol, and hypertonic serum saline are the agents currently available. This work was designed to compare mannitol and glycerol in a similar population of brain injured patients, randomly divided into two groups of eight. The following mean day parameters were obtained: number of infusions, hydric balance, mean arterial pressure (MAP), and intracranial pressure (ICP). Cerebral perfusion pressure (CPP) was calculated. Brain computed tomographies (CT) were obtained on arrival, at follow-up whenever justified and at discharge. For comparison of both groups a modified therapeutic intensity level (mTIL) was used. Both agents induced a statistically equally effective decrease on ICP and increase on CPP evaluated at one and two hours post infusion but the mean day mTIL showed a statistically significant difference in favour of glycerol. The possible explanations of this difference are discussed. According to our results mannitol would be most indicated as a bolus to control sudden rises in ICP whereas glycerol would be most indicated as a basal treatment.     

Transient systolic hypotension. A serious problem in the management of head injury

OBJECTIVE: To determine the frequency and clinical impact of transient systolic hypotension (systolic blood pressure < 100 mm Hg) in patients with severe anatomic head injury. DESIGN: Retrospective case-control study. SETTING: Urban level 1 trauma center. PATIENTS: Consecutive trauma patients admitted to the intensive care unit (ICU) with severe anatomic head injury, defined as Head and Neck Abbreviated Injury Scale Score of 4 or higher. One thousand thirteen trauma patients were admitted to the ICU during the study period, 157 of whom met inclusion criteria. MAIN OUTCOME MEASURES: Acute mortality, defined as death during initial ICU admission, and functional status of ICU survivors, assessed as level of function sufficient for discharge to home. RESULTS: One hundred fifty-seven patients with severe head injury had a total of 831 episodes of systolic hypotension. Fifty-five percent of the patients suffered at least one event. Patients were grouped by total number of low systolic blood pressure events and by average number of events per ICU day. The total number of hypotensive events was associated with increased mortality rates and decreased rate of discharge to home. Average daily frequency of events was associated with increased mortality rates. After stratification by admission Glasgow Coma Scale score, the effects were most dramatic in patients with an initial Glasgow Coma Scale score higher than 8. CONCLUSIONS: Transient hypotension is common in the ICU and is associated with increased acute mortality and decreased functional status in patients with head injury. The impact of this secondary insult is greatest in patients with less severe primary injury. Strict avoidance of hypotension through enhanced monitoring and active treatment appears to be important, especially in patients with higher presenting Glasgow Coma Scale scores.     

Central nervous system metabolic and physiologic effects of laparoscopy

We set out to determine whether the increases in intracranial pressure (ICP) associated with CO2 insufflation had any metabolic effect on the central nervous system in a head injury when compared with gasless laparoscopy (GL). To test this hypothesis, we looked at both the ICP and jugular bulb venous saturation (JVS), with and without a coexisting cerebral mass lesion. Twenty-five kilogram male pigs had tracheostomy, epidural balloon, pulmonary arterial catheter, arterial line, and jugular bulb catheter placed. Intravenous Pentobarbital was used for anesthesia. Either CO2 laparoscopy (CL; n=7) or GL (n=7) were performed both with and without an epidural balloon inflated to a baseline ICP of 25. Data were analyzed using the Student's t test with a P value <0.05 being significant. Cerebral perfusion pressure and most hemodynamic values did not differ. Both central venous pressure and peak inspiratory pressure were significantly elevated whenever CO2 insufflation took place, reflecting an increased intrathoracic pressure. When comparing both study groups, the partial pressure of CO2 did not differ. CL increases ICP significantly above the gasless group in our head injury model. This is most likely secondary to increased intrathoracic pressure. The question still remains whether these changes are clinically significant. We could not demonstrate significant metabolic effects secondary to laparoscopy. In patients suffering head injury, GL rather than CL might be safer to avoid ICP elevation. Additional studies looking at central nervous system metabolic and objective histopathologic effects should be undertaken with larger numbers of study animals.     

Shunt patency after creation of a transjugular intrahepatic portosystemic shunt: evaluation with Doppler ultrasound

The presence of lactic acidosis in the cerebral spinal fluid of 50 patients with severe head injury was studied. The GCS scores of these patients were < or = 8. The patients were divided into two groups. We treated 25 patients with a dose of 4 to 5 ml/kg of THAM infused intravenously 2 to 3 times for daily administration. Other 25 patients who were not treated with THAM served as a control group. In each case, a ventricular pressure monitoring device was installed. The ICP was the contineously recorded. In addition, laboratory study, including lactate, pH, HCO-3 and BE in CSF was performed. THAM infusion was associated with improved survival, decreased ICP as compared to that in the control group. We believe that THAM treatment may significantly improve the prognosis of presence of lactic acidosis as a result of severe head injury.     

Effect of hyperventilation on regional cerebral blood flow in head-injured children

OBJECTIVES: To study cerebral blood flow and cerebral oxygen consumption in severe head-injured children and also to assess the effect of hyperventilation on regional cerebral blood flow. DESIGN: Prospective cohort study. SETTING: Pediatric intensive care unit at a tertiary-level university children's hospital. PATIENTS: Twenty-three children with isolated severe brain injury, whose admission Glasgow Coma Scores were <8. INTERVENTIONS: PaCO2 was adjusted by altering minute ventilation. Cerebral metabolic measurements were made at three levels of PaCO2 (>35, 25 to 35, and <25 torr [>4.7, 3.3 to 4.7, and <3.3 kPa]) after allowing 15 mins for equilibrium. MEASUREMENTS AND MAIN RESULTS: Thirty-eight studies (each study consisting of three sets of measurements at different levels of PaCO2) were performed on 23 patients. At each level of PaCO2, the following measurements were made: xenon-enhanced computed tomography scans; cerebral blood flow; intracranial pressure; jugular venous bulb oxygen saturation; mean arterial pressure; and arterial oxygen saturation. Derived variables included: cerebral oxygen consumption; cerebral perfusion pressure; and oxygen extraction ratio. Cerebral blood flow decreased below normal after head injury (mean 49.6 +/- 14.6 mL/min/100 g). Cerebral oxygen consumption decreased out of proportion to the decrease in cerebral blood flow; cerebral oxygen consumption was only a third of the normal range (mean 1.02 +/- 0.59 mL/min/100 g). Neither cerebral blood flow nor cerebral oxygen consumption showed any relationship to time after injury, Glasgow Coma Score at the time of presentation, or intracranial pressure. The frequency of one or more regions of ischemia (defined as cerebral blood flow of <18 mL/min/100 g) was 28.9% during normocapnia. This value increased to 73.1% for PaCO2 at <25 torr. CONCLUSIONS: Severe head injury in children produced a modest decrease in cerebral blood flow but a much larger decrease in cerebral oxygen consumption. Absolute hyperemia was uncommon at any time, but measured cerebral blood flow rates were still above the metabolic requirements of most children. The clear relationship between the frequency of cerebral ischemia and hypocarbia, combined with the rarity of hyperemia, suggests that hyperventilation should be used with caution and monitored carefully in children with severe head injuries.     

Reduction of a model for an Onchidium pacemaker neuron

Local brain tissue oxygenation (p(ti)O2) and global cerebrovenous hemoglobin saturation (SjO2) are increasingly used to continuously monitor patients after severe head injury (SHI). In patients, simultaneous local and global oxygen measurements of these types have shown different results regarding the comparability of the findings during changes in CPP and ICP. This is in contrast to theoretical expectations. The aim of this study was to compare p(ti)O2 measurement with cerebrovenous oxygen partial pressure measurement (p(cv)O2) in an animal intracranial pressure model. To this end, a multisensor probe was placed in the left frontoparietal white matter to measure p(ti)O2, pCO2 (p(ti)CO2), pH (pH[ti]), and temperature (t[ti]) while simultaneously measuring these same parameters (p(cv)O2, p(cv)CO2 pH(cv), t[cv]) in the sagittal sinus of 9 pigs under general anesthesia. By stepwise inflating a balloon catheter, placed in supracerebellar infratentorial compartment, ICP was increased and CPP was decreased. The baseline levels of p(ti)O2, p(ti)CO2, and pH(ti) in the noninjured brain tissue showed more heterogeneity compared to the findings in cerebrovenous blood. Both, p(ti)O2 and p(cv)O2 were significantly correlated to the induced CPP decrease. PCO2 was inversely correlated to the course of CPP in both measurement compartments. Temperature measurement showed a positive correlation with CPP in both compartments. These findings demonstrate that brain tissue oximetry and cerebrovenous PO2 measurement are sensitive to CPP changes. The newly available continuous parameters in multisensor probes could be helpful in interpreting findings of cerebral oxygen measurement in man by analyzing the interrelationship of these parameters.     

The association of leukocytes with secondary brain injury

Shock increases mortality from brain injuries, but the mechanism is poorly understood. We hypothesized that brain injury followed by shock and resuscitation leads to a secondary reperfusion injury mediated in part by polymorphonuclear leukocytes (PMNs). To validate this hypothesis, we studied cerebral perfusion pressure (CPP), intracranial pressure (ICP), cerebral blood flow (CBF), cortical water content (CWC), and hemodynamic variables in a porcine model of focal cryogenic brain injury and hemorrhagic shock. Cerebral PMN accumulation (CPMN) in the injured and uninjured hemispheres was determined histologically from the total PMNs in five high-power fields (400x). Twenty-nine mature swine were randomized to four groups. Group 1, the control group, was instrumented only. Group 2 animals had a brain injury alone and were studied for 24 hours. Group 3 animals had a brain injury and hemorrhagic shock. Group 4 animals had hemorrhagic shock alone. Brain injury followed by shock caused a significantly greater ICP and a significantly lower CBF than brain injury or shock alone. There was no significant difference in CPP between groups after resuscitation. The CWC of the lesioned area was similar in both brain-injured groups but was significantly increased when compared with the controls and the shock-only group. The CWC of the nonlesioned hemisphere was higher in group 3 than in group 2. The CPMN in both hemispheres in group 3 was significantly greater than in either group 2 or group 4. There was a significant positive correlation between CPMN and both ICP and CWC, and a significant negative correlation between CPMN and CBF. These data suggest an association between CPMN accumulation and secondary brain injury.