Decrease In Cerebral Perfusion Pressure Research Articles

Clazosentan, an endothelin receptor antagonist, prevents early hypoperfusion during the acute phase of massive experimental subarachnoid hemorrhage: a laser Doppler flowmetry study in rats

Acute cerebral hypoperfusion and early disturbances in cerebral autoregulation after subarachnoid hemorrhage (SAH) have been demonstrated repeatedly and have been shown to contribute significantly to acute and secondary brain injury. Acute vasoconstriction has been identified as a major contributing factor. Although increasing evidence implicates endothelin (ET)-1 in the development of cerebral vasospasm, its role in the acute phase after SAH has not yet been investigated. The purpose of this study was to further determine the role of ET in the first minutes to hours after massive experimental SAH induced by prophylactic treatment with the ET receptor antagonist clazosentan. Subarachnoid hemorrhage was induced in 22 anesthetized rats by injection of 0.5-ml arterial, nonheparinized blood into the cisterna magna over the course of 60 seconds. In addition to monitoring intracranial pressure (ICP) and mean arterial blood pressure, laser Doppler flowmetry (LDF) probes were placed stereotactically over the cranial windows to allow online recording of cerebral blood flow (CBF) starting 30 minutes prior to SAH and continuing for 3 hours after SAH. The control group (Group A, 11 rats) received vehicle saline solution via a femoral catheter before SAH, and a second group (Group B, 11 rats) was treated prophylactically with clazosentan, an ET(A) receptor antagonist. Treatment was started 30 minutes prior to bolus injection (1 mg/kg body weight), immediately followed by a continuous infusion of 1 mg/kg body weight/hr until the end of the experiment. Induction of SAH in the rats caused an immediate increase in ICP, which led to an acute decrease in cerebral perfusion pressure (CPP). Perfusion, as measured with LDF, was found to have decreased relative to baseline by 30 +/-20% in the control group and 20 +/-9% in the clazosentan-treated group. Intracranial pressure and CPP recovered comparably in both groups thereafter within minutes. Control animals demonstrated prolonged hypoperfusion with a loss of autoregulation independent of CPP changes, finally approaching 80% of baseline values toward the end of the experiment. The authors observed that clazosentan did not influence peracute CPP-dependent hypoperfusion, but prevented continuous CBF reduction. Laser Doppler flowmetry perfusion readings remained depressed in control animals at 73 +/-19% of baseline in comparison with 106 +/-25% of baseline in clazosentan-treated animals (p = 0.001). The first hours after a massive experimental SAH can be characterized by a CPP-independent compromise in cerebral perfusion. Prophylactic treatment with the ET receptor antagonist clazosentan prevented hypoperfusion. It is known that in the first days after SAH, a reduction in CBF correlates clinically to high-grade SAH. Although research currently focuses on delayed vasospasm, administration of vasoactive drugs in the acute phase of SAH may reverse perfusion deficits and improve patient recovery.

The impact of a highly visible display of cerebral perfusion pressure on outcome in individuals with cerebral aneurysms

Nurses' ability to rapidly detect decreases in cerebral perfusion pressure (CPP), which may contribute to secondary brain injury, may be limited by poor visibility of CPP displays. To evaluate the impact of a highly visible CPP display on the functional outcome in individuals with cerebral aneurysms. Patients with cerebral aneurysms (n = 100) who underwent continuous CPP monitoring were enrolled and randomized to beds with or without the additional CPP display. Six-month outcome was assessed. Functional outcome was not significantly different between control and intervention groups after controlling for initial neurologic condition (odds ratio .904, 95% confidence interval 0.317 to 2.573). However, greater time below CPP thresholds (55 to 70 mm Hg) was significantly associated with poorer outcome (P = .005 to .010). Although the enhanced CPP display was not associated with significantly better outcome, longer periods of CPP below set levels were associated with poorer outcome.

Intra-Abdominal Hypertension: Pulmonary and Cerebral Complications

Intra-abdominal hypertension causes many physiologic changes, primarily by reducing thoracic compliance and secondarily causing organ failure, which is the body's normal response to trauma or acute inflammatory response. Compartment syndrome as a cause of abdominal hypertension has adverse effects on the circulation, threatening the function and viability of tissues. Intra-abdominal hypertension with the clinical picture of compartment syndrome is a reperfusion injury that is a cyclic event. Elevated intra-abdominal pressure due to whatever mechanism affects all intra-abdominal viscera, including the abdominal wall. Due to edema reducing thoracic compliance, producing severe encephalopathy and leading to severe ischemia with generation of significant quantities of reactive oxygen free radicals as well peroxidation products released from the intestine, liver and spleen. Elevated intracranial pressure causes encephalopathy and the risk of neuronal damage due to the sharp decrease in cerebral perfusion pressure. Elevated intracranial pressure is due to restriction of outflow from the lumbar venous plexus. The etiology of the sudden increase in capillary permeability remains unclear. Decompressive laparotomy leads to a rapid improvement in pulmonary parameters and oxygen delivery. The clinical state after decompression is an example of ischemia–reperfusion injury requiring therapy with inotropes and other agents to improve cardiac, respiratory, renal and cerebral hemodynamics with life saving effects.

Brain Metabolism During a Decrease in Cerebral Perfusion Pressure Caused by an Elevated Intracranial Pressure in the Porcine Neocortex

Cranial hypertension coincides with a reduction in cerebral blood flow as well as in oxygen delivery and influences outcome. In this study, we monitored changes in energy-related metabolites in the porcine cortex during an increase of intracranial pressure (ICP) and to determine the level at which damage occurs. Male domestic pigs (32-40 kg) were anesthetized, mechanically ventilated, and randomly assigned to either the experimental (n = 6) or control groups (n = 5). A microdialysis probe (CMA 70) was inserted into the cortex to measure extracellular dialysate concentrations of lactate, pyruvate, glucose, glutamate, and glycerol. Every hour an increase of 10 mm Hg in ICP was preformed in the experimental group by infusion of artificial cerebrospinal fluid into the ventricular system of the brain until a maximum ICP of 50 mm Hg was reached. We demonstrated a significant increase of lactate and glycerol compared with control at ICP values > or =30 mm Hg and cerebral perfusion pressure (CPP) below 50 mm Hg. The increase of ICP to > or =40 mm Hg in conjunction with a reduction in CPP below 40 mm Hg led to a significant increase in the lactate/pyruvate-ratio and glutamate, as well as a decrease of glucose in relation to control. Our data strongly suggest that, during a defined ICP increase, lower CPP values may be tolerable until severe damage occurs. Borderline ICP and CPP values of 30 and 40 mm Hg, respectively, could be advised.

Temperature gradient between brain tissue and arterial blood mirrors the flow‐metabolism relationship in uninjured brain: an experimental study

The purpose of the present experimental study was to determine the feasibility and usefulness of brain temperature measurement (T(br)) and the calculated difference between brain temperature and arterial blood temperature (DeltaT(br-a)) in uninjured brain during variations of cerebral perfusion pressure (CPP) and concomitant changes of the regional cerebral blood flow (rCBF). Nine anaesthetized pigs were subjected to controlled CPP decrease to assess the lower cerebral autoregulation threshold. A parenchymal intracranial pressure (ICP) sensor combined with a microthermistor for temperature measurement, a miniaturized Clark-type electrode measuring brain tissue oxygenation (p(ti)O(2)), a small flexible intraparenchymal thermodilution probe for measuring rCBF and cerebral microdialysis were inserted carefully in the frontal white matter. Analysing the p(ti)O(2) during controlled CPP decrease, we found significant breakpoints of p(ti)O(2) at a CPP of 40 mmHg and 20 mmHg, related to an rCBF of 20 ml/100 g/min and approximately 10 ml/100 g/min. Similarly, the relationship between DeltaT(br-a), and CPP or rCBF revealed a characteristic increase of DeltaT(br-a) in the negative direction up to more than -0.30 degrees C assuming a strong flow dependency. The temperature difference between brain tissue and arterial blood DeltaT(br-a) mainly reflects the cerebral blood flow-brain tissue oxygenation-metabolism relationship as far as the estimation of the individual lower cerebral autoregulation threshold.

Paramedic intubation of patients with severe head injury: a review of current Australian practice and recommendations for change

Secondary brain injury may occur early after severe traumatic brain injury due to hypoxia and/or hypotension. Prehospital care by ambulance paramedics has the goal of preventing and treating these complications and, thus, improving outcomes. In Australia, most ambulance services recommend paramedics attempt endotracheal intubation in patients with severe head injury. Even though most patients with severe head injury retain airway reflexes, most states do not allow the use of appropriate drugs to facilitate intubation. In contrast, recent evidence from trauma registries suggests that this approach may be associated with significantly worse outcomes compared with no intubation. Two states allow intubation facilitated by sedative (but not relaxant) drugs, but this has a low success rate and could worsen brain injury because of a decrease in cerebral perfusion pressure. For road-based paramedics, the role of rapid sequence intubation is uncertain. Given the risks of this procedure and the lack of proven benefit, this procedure should not be introduced without supportive evidence from randomised, controlled trials. In contrast, for safety reasons, comatose patients transported by helicopter should undergo rapid sequence intubation prior to flight. However, this is not authorised in most states, despite good supportive evidence that this can be safely and effectively undertaken by paramedics. Finally, there is evidence that inadvertent hyperventilation is associated with adverse outcome, yet only two ambulance services use waveform capnography in head injury patients who are intubated. Overall, current paramedic airway practice in most states of Australia is not supported by the evidence and is probably associated with worse patient outcomes after severe head injury. For road-based paramedics, rapid transport to hospital without intubation should be regarded as the current standard of care. Rapid sequence intubation should be limited to use within appropriate clinical trials, or patients transported by helicopter. For patients who are intubated, waveform capnography is essential to confirm tracheal placement and to prevent inadvertent hyperventilation.

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HYPERTONIC SALINE SOLUTION INCREASES CEREBRAL PERFUSION PRESSURE DURING CLINICAL ORTHOTOPIC LIVER TRANSPLANTATION FOR FULMINANT HEPATIC FAILURE: PRELIMINARY RESULTS

During orthotopic liver transplantation for fulminant hepatic failure, some patients may develop sudden deterioration of cerebral perfusion and oxygenation, mainly due to increased intracranial pressure and hypotension, which are likely responsible for postoperative neurological morbidity and mortality. In the present study, we hypothesized that the favorable effects of hypertonic saline solution (NaCl 7.5%, 4 mL/kg) infusion on both systemic and cerebral hemodynamics, demonstrated in laboratory and clinical settings of intracranial hypertension and hemorrhagic shock resuscitation, may attenuate the decrease in cerebral perfusion pressure that often occurs during orthotopic liver transplantation for fulminant hepatic failure. 10 patients with fulminant hepatic failure in grade IV encephalopathy undergoing orthotopic liver transplantation with intracranial pressure monitoring were included in this study. The effect on cerebral and systemic hemodynamics in 3 patients who received hypertonic saline solution during anhepatic phase (HSS group) was examined, comparing their data with historical controls obtained from surgical procedure recordings in 7 patients (Control group). The maximal intracranial pressure and the corresponding mean arterial pressure values were collected in 4 time periods: (T1) the last 10 min of the dissection phase, (T2) the first 10 minutes at the beginning of anhepatic phase, (T3) at the end of the anhepatic phase, and (T4) the first 5 minutes after graft reperfusion. Immediately after hypertonic saline solution infusion, intracranial pressure decreased 50.4%. During the first 5 min of reperfusion, the intracranial pressure remained stable in the HSS group, and all these patients presented an intracranial pressure lower than 20 mm Hg, while in the Control group, the intracranial pressure increased 46.5% (P < 0.001). The HSS group was the most hemodynamically stable; the mean arterial pressure during the first 5 min of reperfusion increased 21.1% in the HSS group and decreased 11.1% in the Control group (P < 0.001). During the first 5 min of reperfusion, cerebral perfusion pressure increased 28.3% in the HSS group while in the Control group the cerebral perfusion pressure decreased 28.5% (P < 0.001). Serum sodium at the end of the anhepatic phase and 3 hours after reperfusion was significantly higher in the HSS group (153.00 +/- 2.66 and 149.00 +/- 1.73 mEq/L) than in the Control group (143.71 +/- 3.30 and 142.43 +/- 1.72 mEq/L), P = 0.003 and P < 0.001 respectively. Hypertonic saline solution can be successfully used as an adjunct in the neuroprotective strategy during orthotopic liver transplantation for fulminant hepatic failure, reducing intracranial pressure while restoring arterial blood pressure, promoting sustained increase in the cerebral perfusion pressure.

Cerebral microdialysis and Ptio2 for neuro‐monitoring before decompressive craniectomy

We report the case of a young patient with post-traumatic, intractable, intracranial hypertension leading to craniectomy. This intracranial hypertension was preceded by focal signs of ischemia diagnosed through P(ti)O2 monitoring and cerebral microdialysis, and occurred a few hours prior to a decrease in cerebral perfusion pressure below 60 mmHg. The neurological outcome was satisfactory with a Glasgow Outcome Scale of 4 at 3 months. We discuss the potential interest of such neuro-monitoring to determine the optimal time for performing a craniectomy.

Preservation of static and dynamic cerebral autoregulation after mild hypothermic cardiopulmonary bypass

Dysfunction of cerebral autoregulation might contribute to neurological morbidity after cardiac surgery. In this study, our aim was to assess the preservation of cerebral autoregulation after cardiac surgery involving cardiopulmonary bypass (CPB). Dynamic and static components of cerebral autoregulation were evaluated in 12 patients undergoing coronary artery bypass graft surgery, anaesthetized with midazolam, fentanyl, and propofol, and using mild hypothermic CPB (31-33 degrees C). Arterial pressure (ABP), central venous pressure (CVP), and blood flow velocity in the middle cerebral artery (CBFV) were recorded. The cerebral perfusion pressure (CPP) was calculated as a difference between mean ABP and CVP. Rapid decrease of CPP was caused by a sudden change of patients' position from Trendelenburg to reverse Trendelenburg. Cerebral vascular resistance (CVR) was calculated by dividing CPP by CBFV. Index of static cerebral autoregulation (CAstat) was calculated as the change of CVR related to change of CPP during the manoeuvre. Dynamic rate of autoregulation (RoRdyn) was determined as the change in CVR per second during the first 4 s immediately after a decrease in CPP, related to the change of CPP. Measurements were obtained after induction of anaesthesia, and 15, 30, and 45 min after termination of CPB. No significant changes were found in CAstat or RoRdyn after CPB. Significant changes in CVR could be explained by concomitant changes in body temperature and haematocrit. Autoregulation of cerebral blood flow remains preserved after mild hypothermic CPB.

Effect of alfentanil on intracranial pressure during propofol–fentanyl anesthesia for craniotomy. A randomized prospective dose–response study

The effect of alfentanil on intracranial pressure (ICP) in patients with supratentorial cerebral tumors has only been sparsely examined and with somewhat contradictory results. Thirty-one patients were anesthetized with propofol and fentanyl. After removal of the bone flap a bolus-dose of alfentanil 10 (group 1), 20 (group 2), or 30 microg kg(-1) (group 3) was administered followed by an infusion of 10, 20, or 30 microg.kg(-1).h(-1) to patients in groups 1, 2, and 3, respectively. A control group received no alfentanil. Subdural ICP, mean arterial blood pressure (MAP), and cerebral perfusion pressure (CPP) were monitored and arterial and jugular bulb blood were sampled before and every minute for 5 min after the bolus administration of alfentanil and again after 5 min of hyperventilation to be able to calculate cerebral arterio-venous oxygen content difference (AVDO2) and carbon dioxide reactivity (CO2-reactivity). No changes in subdural ICP or AVDO2 from alfentanil in the study period were observed within the groups. However, alfentanil decreased MAP and CPP. The maximum CPP decrease (mean value of each group) was 4 mmHg, 8 mmHg, and 18 mmHg in groups 1, 2, and 3, respectively. There was no difference between groups as regards the CO2-reactivity. We conclude that administration of alfentanil to propofol-fentanyl anesthetized patients with supratentorial cerebral tumors decreases MAP and CPP in a dose-related way, but does not influence subdural ICP, AVDO2 or the CO2-reactivity.

How low can you go? Intracranial pressure, cerebral perfusion pressure, and respiratory obstruction in children with complex craniosynostosis

Elevated intracranial pressure (ICP) is a well-recognized complication affecting children suffering from complex forms of craniosynostosis. The effects of ICP, including those on vision, and the underlying mechanisms involved remain uncertain. The aim of this study was to examine the relationships among ICP, cerebral perfusion pressure (CPP), and the episodic alterations in respiratory obstruction that are common in children with craniosynostosis. Eleven children with complex craniosynostosis underwent monitoring overnight, including simultaneous recording of subdural ICP, arterial blood pressure (ABP), and a variety of respiratory parameters. Sleep status was also analyzed. Mean values were calculated for all variables, including ICP, CPP, and ABP, during both quiet and active sleep. Mean ICP during quiet sleep was elevated in five patients, borderline in three, and normal in three children. During active sleep, plateaus of high mean ICP were observed in all patients. Marked decreases in CPP were demonstrated during active sleep with absolute values as low as 14 mm Hg. During quiet sleep, the mean baseline CPP was 53.3 mm Hg (range 34-70 mm Hg). During active sleep, CPP fell to a mean of 32.6 mm Hg (range 23-52 mm Hg). All patients experienced obstructive breathing problems, including 10 with obstructive sleep apnea, the effects of which demonstrated a temporal relationship to the alterations in sleep status, ICP, and CPP. Elevations of ABP appeared modest and remained within the normal limits for age. The findings of this study indicate that ICP, CPP, and respiratory obstruction interact in a vicious cycle, an observation that helps explain the pattern of plateau waves of elevated ICP characteristic among children with complex forms of craniosynostosis. The data gathered in this series revealed levels of CPP considerably lower than those described previously in clinical reports. Such reductions in CPP most likely contribute to the neurological, cognitive, and ophthalmological morbidity from which these children suffer frequently; therefore, the results of this study have important implications for the management of children with complex forms of craniosynostosis as well as for our understanding of the control of cerebral blood flow in general.

Assessment of critical thresholds for cerebral perfusion pressure by performing bedside monitoring of cerebral energy metabolism.

An intractable increase in intracranial pressure (ICP) leading to a progressive decrease in cerebral perfusion pressure (CPP) and cerebral blood flow (CBF) is the dominating cause of death in patients with severe brain trauma. Arterial hypotension may further compromise CPP (and CBF) and significantly contributes to death. In addition, the injured brain is sensitive to raised CPP due to an increased permeability of the blood-brain barrier (BBB) to crystalloids and an impaired pressure autoregulation of the CBF. Given these circumstances, an increase in CPP will cause a net transport of water across the BBB and a further elevation in ICP. Accordingly, the assessment of the lower critical threshold for CPP is important for neurological intensive care. This level varies among different patients and different areas of the brain. In fact, the penumbral zones surrounding focal brain lesions appear to be the most sensitive. In the individual patient, preservation of normal cerebral energy metabolism within areas at risk during a decrease in CPP can be guaranteed by performing intracerebral microdialysis and bedside biochemical analyses.

Effect of mesocaval shunt on survival of small-for-size liver grafts: experimental study in pigs.

Segmental liver grafts with a calculated ideal liver weight (CILW) less than 40% may be associated with portal flow-related injuries and primary dysfunction. This study evaluated the effect of mesocaval shunts on the survival of grafts with a CILW less than 20%. Sixteen pigs underwent orthotopic transplantation of segmental liver grafts with a CILW less than 20%. In eight animals (study group), transplantation was combined with a mesocaval shunt, and eight animals served as controls without a mesocaval shunt. Liver function, systemic hemodynamics, portal vein pressure, intracranial pressure, and cerebral perfusion pressure were assessed postoperatively. The controls showed a rapid impairment of liver function reflected by a significant elevation in aspartate aminotransferase, international normalized ratio, bilirubin, and intracranial pressure and a decrease in cerebral perfusion pressure compared with the study group (P<0.05). Mesocaval shunts showed protective effects on grafts with CILW less than 20% and may have a clinical role in the salvage of small-for-size liver grafts.

A new rat model of chronic cerebral hypoperfusion associated with arteriovenous malformations.

A new experimental model of chronic cerebral hypoperfusion was developed to study the effects of systemic arterial shunting and obstruction of the primary vessel that drains intracranial venous blood on cerebral perfusion pressure (CPP), as well as cerebral pathological changes during restoration of normal perfusion pressure. Twenty-four Sprague-Dawley rats were randomly assigned to either a sham-operated group, an arteriovenous fistula (AVF) group, or a model group (eight rats each). The animal model was readied by creating a fistula through an end-to-side anastomosis between the right distal external jugular vein (EJV) and the ipsilateral common carotid artery (CCA), followed by ligation of the left vein draining the transverse sinus and bilateral external carotid arteries. Systemic mean arterial pressure (MAP), draining vein pressure (DVP), and CPP were monitored and compared among the three groups preoperatively, immediately postoperatively, and again 90 days later. Following occlusion of the fistula after a 90-day interval, blood-brain barrier (BBB) disruption and water content in the right cortical tissues of the middle cerebral artery territory were confirmed and also quantified with transmission electron microscopy. Formation of a fistula resulted in significant decreases in MAP and CPP, and a significant increase in DVP in the AVF and model groups. Ninety days later, there were still significant increases in DVP and decreases in CPP in the model group compared with the other groups (p < 0.05). Damage to the BBB and brain edema were noted in animals in the model group during restoration of normal perfusion pressure by occlusion of the fistula. Electron microscopy studies revealed cerebral vasogenic edema and/or hemorrhage in various amounts, which correlated with absent astrocytic foot processes surrounding some cerebral capillaries. The results demonstrated that an end-to-side anastomosis between the distal EJV and CCA can induce a decrease in CPP, whereas a further chronic state of cerebral hypoperfusion may be caused by venous outflow restriction, which is associated with perfusion pressure breakthrough. This animal model conforms to the basic hemodynamic characteristics of human cerebral arteriovenous malformations.

Malignant Infarction in Cats After Prolonged Middle Cerebral Artery Occlusion

To study the putative role and predictive significance of glutamate elevation in space-occupying ischemic stroke, we investigated the correlation between perfusional disturbances and glutamate alterations in a transient ischemia model in cats that is susceptible to secondary deterioration after reperfusion. In 10 halothane-anesthetized cats, the left middle cerebral artery was occluded for 3 hours, followed by 6 hours of reperfusion. Laser-Doppler flowmetry (LDF) probes, microdialysis/high-performance liquid chromatography, and pressure sensors measured simultaneously regional cerebral blood flow (CBF), extracellular amino acids, mean arterial blood pressure, and intracranial pressure, respectively. Cerebral perfusion pressure (CPP) was calculated. In complementary experiments (n=2), regional CBF was assessed by sequential positron emission tomography. Middle cerebral artery occlusion reduced LDF-measured CBF in all animals to <25% of control. In 5 of 10 cats, glutamate rose approximately 30-fold during ischemia. LDF-measured CBF and glutamate primarily recovered after reperfusion. Glutamate rose again in the late reperfusion phase, when CPP decreased to <60 mm Hg, and symptoms of transtentorial herniation were recognized. Positron emission tomography revealed ischemic thresholds of 15 to 20 mL/100 g per minute for secondary deterioration. In the other 5 cats, ischemic elevation of glutamate was significantly smaller, and signs of secondary deterioration were not recognized. Glutamate determinations during ischemia predict fatal outcome, as do intracranial pressure and CPP measurements during early reperfusion. Secondary amino acid elevation during reperfusion is presumably caused by a drastic decrease of CPP to <50 mm Hg in the final stage of space-occupying, malignant focal ischemia. At this stage, a further progression of injury due to increased glutamate may be irrelevant with respect to fatal outcome.

Lung recruitment maneuver in patients with cerebral injury: effects on intracranial pressure and cerebral metabolism.

To investigate the effects of a lung recruitment maneuver on intracranial pressure (ICP) and cerebral metabolism in patients with acute cerebral injury and respiratory failure. Prospective investigation. Ten-bed intensive care unit of a university hospital. Eleven patients with acute traumatic or non-traumatic cerebral lesions, who were on mechanical ventilation with acute lung injury. Hemodynamics, ICP, cerebral perfusion pressure (CPP), jugular venous oxygen saturation (SJO(2)), and arterial minus jugular venous lactate content difference (AJDL) were measured before, during and after a volume recruitment maneuver (VRM), which included a 30-s progressive increase in peak pressure up to 60 cmH(2)O and a sustained pressure at the same level for the next 30 s. At the end of VRM, ICP was elevated (16+/-5 mmHg vs 13+/-5 mmHg before VRM, P<0.05) and mean arterial pressure was reduced (75+/-10 vs 86+/-9 mmHg, P<0.01), which resulted in a decrease of CPP (60+/-10 vs 72+/-8 mmHg, P<0.01). SJO(2) deteriorated at the end of the procedure (59+/-7 vs 69+/-6%, P<0.05), AJDL was not altered. In the following period all parameters returned to normal values. An improvement in arterial oxygenation was observed at the end, but not in the period after the maneuver. Our VRM reduced cerebral hemodynamics and metabolism. We conclude that our VRM with high peak pressure effects only a marginal improvement in oxygenation but causes deterioration of cerebral hemodynamics. We therefore cannot recommend this technique for the ventilatory management of brain-injured patients.

Craniocerebral trauma--new pathophysiological and therapeutic viewpoints. 1: Management of the acute phase

As there is only few evidence-based knowledge in the treatment of head trauma, the aim of this work was to demonstrate the close relationship between pathophysiology and clinical treatment modalities during the primary phase of head trauma. Review article. Cerebral hypoxia represents the main source of secondary brain injury. Depending on severity and duration, there results an irreversible brain damage. Under clinical conditions, the continuous monitoring of cerebral perfusion pressure (CPP) allows an estimation of the risk for cerebral hypoxia and the beginning of causal therapy. The priority of treatment lies in normalization of arterial O2 and increase in cerebral blood flow (CBF). In case of unchanged autoregulation of CBF, a decrease of CPP is followed by vasodilation with increase of cerebral blood volume (CBV) and a increase of CPP leads to a decrease of CBV by vasoconstriction. The usual shift of autoregulation on the right side after trauma requires CPP-values > 70 mmHg in the initial posttraumatic phase as there exists the most probable risk of hypoxia. The therapy of elevated ICP > 20 mmHg is oriented on CPP. A decrease in ICP under load of CPP has to be avoided. Beyond it, there is a need of origin of ICP-increase. The priority of initial treatment after head trauma lies in the individual optimization of CBF by maintenance of adequate CPP and cerebrovascular resistance. Afterwards, there will be performed a goal-directed treatment being based on the differentiation of the varying subgroups of head trauma and their related pathophysiology, what leads to the required treatment strategy. For this reason, it is necessary to put in the traditional treatment option by means of the multimodal monitoring as soon as possible.

Intracranial effects of endotracheal suctioning in the acute phase of head injury.

In patients with head injury, endotracheal suctioning (ETS) is a potentially dangerous procedure, because it can increase intracranial pressure (ICP). The purpose of this prospective nonrandomized study was to evaluate the impact of ETS on intracranial dynamics in the acute phase of head injury. Seventeen patients with severe head injury (Glasgow Coma Score < or = 8, range 4-8), sedated and mechanically ventilated, were studied during the first week after trauma. Single-pass ETS maneuver (with a 16-French catheter, negative pressure of 100 mm Hg, and duration of less than 30 seconds) was performed 60 seconds after the FiO2 was increased to 100%. After ETS, FiO2 was maintained at 100% for another 30 seconds. Before and after ETS, arterial blood gases and jugular oxygen saturation (S(j)O2), ICP, and mean arterial pressure (MAP) were measured and cerebral perfusion pressure (CPP) was calculated. A total of 131 ETS episodes, which consisted of repeated assessment of each patient, were analyzed. Six patients in 20 cases coughed and/or moved during ETS because of inadequate sedation. After ETS, ICP increased from 20 +/- 12 to 22 +/- 13 mm Hg in well-sedated patients and from 15 +/- 9 to 28 +/- 9 mm Hg in patients who coughed and/or moved (mean change, 2 +/- 6 versus 13 +/- 6 mm Hg, P <.0001). CPP and S(j)O2 increased in well-sedated patients (from 78 +/- 16 to 83 +/- 19 mm Hg, and from 71 +/- 10 to 73 +/- 13%, respectively) and decreased in patients who reacted to ETS (from 79 +/- 14 to 72 +/- 14 mm Hg and from 69 +/- 7 to 66 +/- 9%, respectively), and the differences were significant (mean change, CPP: 5 +/- 14 versus -7 +/- 15 mm Hg, P =.003; (S(j)O2) 2 +/- 5 vs. -3 +/- 5%, P <.0001). In well-sedated patients, endotracheal suctioning caused an increase in ICP, CPP, and S j O 2 without evidence of ischemia. In contrast, in patients who coughed or moved in response to suctioning, there was a slight and significant decrease in CPP and S(j)O2. In the case of patients with head injuries who coughed or moved during endotracheal suctioning, we strongly suggest deepening the level of sedation before completing the procedure to reduce the risk of adverse effects.

Simultaneous measurement of local cortical blood flow and tissue oxygen saturation by Near infra-red Laser Doppler flowmetry and remission spectroscopy in the pig brain.

In the current study we evaluated the combined use of Near-infrared Laser-Doppler flowmetry (NiLDF) and Remission Spectroscopy (RS) for measurement of regional perfusion and oxygen saturation of the cerebral cortex. An epidural probe for combined measurements of NiLDF and RS was placed above the parietal or frontal cortex of nine anesthetized juvenile pigs. Cerebral perfusion pressure (CPP) was stepwise decreased by intracisternal infusion of artificial CSF at clamped arterial blood pressure (baseline, CPP50, CPP40, CPP30 mmHg, ischemia). Subsequent reperfusion was followed for 3 h. Regional cerebral blood flow (rCBF) was measured with colored microspheres (CMS) and compared with corresponding NiLDF values during CMS injection. Cerebral venous oxygen saturation was measured in blood samples withdrawn from the sagittal sinus and compared with simultaneous recordings of tissue oxygenation during blood withdrawal. Linear regression analysis resulted in a significant correlation (p < 0.001) for changes in regional perfusion during CPP decrease and reperfusion, as measured with CMS and NiLDF (r = 0.92, n = 39). A significant correlation was also found for tissue oxygen saturation--as measured with RS--and cerebral venous oxygen saturation (r = 0.85, n = 67). Although the problem of spatial variability remains to be solved, the combined use of NiLDF and RS allows continuous and non-invasive monitoring of changes of key parameters of oxygen metabolism within the cerebral cortex.