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Michael Reinert, Ahmad Khaldi, Alois Zauner, Egon Doppenberg, Sung Choi and Ross Bullock

Disturbed ionic and neurotransmitter homeostasis are now recognized to be probably the most important mechanisms contributing to the development of secondary brain swelling after traumatic brian injury (TBI). Evidence obtained from animal models indicates that posttraumatic neuronal excitation via excitatory amino acids leads to an increase in extracellular potassium, probably due to ion channel activation. The purpose of this study was therefore to measure dialysate potassium in severely head injured patients and to correlate these results with intracranial pressure (ICP), outcome, and also with the levels of dialysate glutamate, lactate, and cerebral blood flow (CBF) so as to determine the role of ischemia in this posttraumatic ionic dysfunction.

Eighty-five patients with severe TBI (Glasgow Coma Scale score < 8) were treated according to an intensive ICP management-focused protocol. All patients underwent intracerebral microdialyis. Dialysate potassium levels were analyzed by flame photometry, as were dialysate glutamate and dialysate lactate levels, which were measured using high-performance liquid chromatography and an enzyme-linked amperometric method in 72 and 84 patients respectively. Cerebral blood flow studies (stable Xenon–computerized tomography scanning) were performed in 59 patients.

In approximately 20% of the patients, potassium values were increased (dialysate potassium > 1.8 mmol). Mean dialysate potassium (> 2 mmol) was associated with ICP above 30 mm Hg and fatal outcome. Dialysate potassium correlated positively with dialysate glutamate (p < 0.0001) and lactate levels (p < 0.0001). Dialysate potassium was significantly inversely correlated with reduced CBF (p = 0.019).

Dialysate potassium was increased after TBI in 20% of measurements. High levels of dialysate potassium were associated with increased ICP and poor outcome. The simultaneous increase of potassium, together with dialysate glutamate and lactate, supports the hypothesis that glutamate induces ionic flux and consequently increases ICP due to astrocytic swelling. Reduced CBF was also significantly correlated with increased levels of dialysate potassium. This may be due to either cell swelling or altered potassium reactivity in cerebral blood vessels after trauma.

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Tobias Clausen, Oscar Luis Alves, Michael Reinert, Egon Doppenberg, Alois Zauner and Ross Bullock

Object. Glycerol is considered to be a marker of cell membrane degradation and thus cellular lysis. Recently, it has become feasible to measure via microdialysis cerebral extracellular fluid (ECF) glycerol concentrations at the patient's bedside. Therefore the aim of this study was to investigate the ECF concentration and time course of glycerol after severe traumatic brain injury (TBI) and its relationship to patient outcome and other monitoring parameters.

Methods. As soon as possible after injury for up to 4 days, 76 severely head-injured patients were monitored using a microdialysis probe (cerebral glycerol) and a Neurotrend sensor (brain tissue PO2) in uninjured brain tissue confirmed by computerized tomography scanning. The mean brain tissue glycerol concentration in all monitored patients decreased significantly from 206 ± 31 µmol/L on Day 1 to 9 ± 3 µmol/L on Day 4 after injury (p < 0.0001). Note, however, that there was no significant difference in the time course between patients with a favorable outcome (Glasgow Outcome Scale [GOS] Scores 4 and 5) and those with an unfavorable outcome (GOS Scores 1–3). Significantly increased glycerol concentrations were observed when brain tissue PO2 was less than 10 mm Hg or when cerebral perfusion pressure was less than 70 mm Hg.

Conclusions. Based on results in the present study one can infer that microdialysate glycerol is a marker of severe tissue damage, as seen immediately after brain injury or during profound tissue hypoxia. Given that brain tissue glycerol levels do not yet add new clinically significant information, however, routine monitoring of this parameter following traumatic brain injury needs further validation.

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Michael Reinert, Ahmad Khaldi, Alois Zauner, Egon Doppenberg, Sung Choi and Ross Bullock

Object. Disturbed ionic and neurotransmitter homeostasis are now recognized as probably the most important mechanisms contributing to the development of secondary brain swelling after traumatic brain injury (TBI). Evidence obtained in animal models indicates that posttraumatic neuronal excitation by excitatory amino acids leads to an increase in extracellular potassium, probably due to ion channel activation. The purpose of this study was therefore to measure dialysate potassium in severely head injured patients and to correlate these results with measurements of intracranial pressure (ICP), patient outcome, and levels of dialysate glutamate and lactate, and cerebral blood flow (CBF) to determine the role of ischemia in this posttraumatic ion dysfunction.

Methods. Eighty-five patients with severe TBI (Glasgow Coma Scale Score < 8) were treated according to an intensive ICP management-focused protocol. All patients underwent intracerebral microdialyis. Dialysate potassium levels were analyzed using flame photometry, and dialysate glutamate and dialysate lactate levels were measured using high-performance liquid chromatography and an enzyme-linked amperometric method in 72 and 84 patients, respectively. Cerebral blood flow studies (stable xenon computerized tomography scanning) were performed in 59 patients.

In approximately 20% of the patients, dialysate potassium values were increased (dialysate potassium > 1.8 mM) for 3 hours or more. A mean amount of dialysate potassium greater than 2 mM throughout the entire monitoring period was associated with ICP above 30 mm Hg and fatal outcome, as were progressively rising levels of dialysate potassium. The presence of dialysate potassium correlated positively with dialysate glutamate (p < 0.0001) and lactate (p < 0.0001) levels. Dialysate potassium was significantly inversely correlated with reduced CBF (p = 0.019).

Conclusions. Dialysate potassium was increased after TBI in 20% of measurements. High levels of dialysate potassium were associated with increased ICP and poor outcome. The simultaneous increase in dialysate potassium, together with dialysate glutamate and lactate, supports the concept that glutamate induces ionic flux and consequently increases ICP, which the authors speculate may be due to astrocytic swelling. Reduced CBF was also significantly correlated with increased levels of dialysate potassium. This may be due to either cell swelling or altered vasoreactivity in cerebral blood vessels caused by higher levels of potassium after trauma. Additional studies in which potassium-sensitive microelectrodes are used are needed to validate these ionic events more clearly.

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Matthias Menzel, Egon M. R. Doppenberg, Alois Zauner, Jens Soukup, Michael M. Reinert and Ross Bullock

Object. Early impairment of cerebral blood flow in patients with severe head injury correlates with poor brain tissue O2 delivery and may be an important cause of ischemic brain damage. The purpose of this study was to measure cerebral tissue PO2, lactate, and glucose in patients after severe head injury to determine the effect of increased tissue O2 achieved by increasing the fraction of inspired oxygen (FiO2).

Methods. In addition to standard monitoring of intracranial pressure and cerebral perfusion pressure, the authors continuously measured brain tissue PO2, PCO2, pH, and temperature in 22 patients with severe head injury. Microdialysis was performed to analyze lactate and glucose levels. In one cohort of 12 patients, the PaO2 was increased to 441 ± 88 mm Hg over a period of 6 hours by raising the FiO2 from 35 ± 5% to 100% in two stages. The results were analyzed and compared with the findings in a control cohort of 12 patients who received standard respiratory therapy (mean PaO2 136.4 ± 22.1 mm Hg).

The mean brain PO2 levels increased in the O2-treated patients up to 359 ± 39% of the baseline level during the 6-hour FiO2 enhancement period, whereas the mean dialysate lactate levels decreased by 40% (p < 0.05). During this O2 enhancement period, glucose levels in brain tissue demonstrated a heterogeneous course. None of the monitored parameters in the control cohort showed significant variations during the entire observation period.

Conclusions. Markedly elevated lactate levels in brain tissue are common after severe head injury. Increasing PaO2 to higher levels than necessary to saturate hemoglobin, as performed in the O2-treated cohort, appears to improve the O2 supply in brain tissue. During the early period after severe head injury, increased lactate levels in brain tissue were reduced by increasing FiO2. This may imply a shift to aerobic metabolism.

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Matthias Menzel, Egon M. R. Doppenberg, Alois Zauner, Jens Soukup, Michael M. Reinert and Ross Bullock

Object

Early impairment of cerebral blood flow in patients with severe head injury correlates with poor brain tissue O2 delivery and may be an important cause of ischemic brain damage. The purpose of this study was to measure cerebral tissue PO2, lactate, and glucose in patients after severe head injury to determine the effect of increased tissue O2 achieved by increasing the fraction of inspired oxygen (FiO2).

Methods

In addition to standard monitoring of intracranial pressure and cerebral perfusion pressure, the authors continuously measured brain tissue PO2, PCO2, pH, and temperature in 22 patients with severe head injury. Microdialysis was performed to analyze lactate and glucose levels. In one cohort of 12 patients, the PaO2) was increased to 441 ± 88 mm Hg over a period of 6 hours by raising the FiO2 from 35 ± 5% to 100% in two stages. The results were analyzed and compared with the findings in a control cohort of 12 patients who received standard respiratory therapy (mean PaO2 136.4 ± 22.1 mm Hg).

The mean brain PO2 levels increased in the O2-treated patients up to 359 ± 39% of the baseline level during the 6-hour FiO2 enhancement period, whereas the mean dialysate lactate levels decreased by 40% (p < 0.05). During this O2 enhancement period, glucose levels in brain tissue demonstrated a heterogeneous course. None of the monitored parameters in the control cohort showed significant variations during the entire observation period.

Conclusions

Markedly elevated lactate levels in brain tissue are common after severe head injury. Increasing PaO2 to higher levels than necessary to saturate hemoglobin, as performed in the O2-treated cohort, appears to improve the O2 supply in brain tissue. During the early period after severe head injury, increased lactate levels in brain tissue were reduced by increasing FiO2. This may imply a shift to aerobic metabolism.

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Rajshri Mainthia, Gary W. Tye, Jay Shapiro, Egon M. R. Doppenberg and John D. Ward

The pediatric neurosurgical mission trips led by physicians at Virginia Commonwealth University (VCU) Health Systems began in 1996 with the formation of Medical Outreach to Children, founded by 1 of the authors (J.D.W.) after a visit to Guatemala. Since then, 19 surgical trips to 4 different countries in Central and South America have been coordinated from 1996 to 2008.

This humanitarian work serves a number of purposes. First and foremost, it provides children with access to surgical care that they would otherwise not receive, thereby significantly improving their quality of life. Second, the visiting surgical team participates in the education of local physicians, parents, and caregivers to help improve the healthcare provided to the children. Last, the team works to promote sustainable global health solutions in the countries it travels to by generating a forum for clinical and public health research discourse.

Thus far, a total of 414 children have undergone 463 operations, including 154 initial shunt surgeries, 110 myelomeningocele repairs, 39 lipoma resections, 33 tethered cord releases, 18 shunt revisions, 16 encephalocele repairs, 9 lipomyelomeningocele repairs, and 7 diastematomyelia repairs. The complication rate has been 5–8%, and the team has obtained reliable follow-up in ~ 77% of patients. A correlation was found between an increase in the number of trained neurosurgeons in the host countries and a decrease in the average age of patients treated by the visiting surgical team over time. It is also hypothesized that a decrease in the percentage of myelomeningocele repairs performed by the surgical team (as a fraction of total cases between 1996 and 2006) correlates to an increase in the number of local neurosurgeons able to treat common neural tube defects in patients of younger ages. Such analysis can be used by visiting surgical teams to assess the changing healthcare needs in a particular host country.

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Editorial

Neurosurgical humanitarian aid

Benjamin C. Warf

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Egon M. R. Doppenberg, Joe C. Watson, William C. Broaddus, Kathryn L. Holloway, Harold F. Young and Ross Bullock

✓ The effects of proximal occlusion of the parent artery during aneurysm surgery in humans are not fully understood, although this method is widely used. The reduction in substrate that can be tolerated by normal and subarachnoid hemorrhage (SAH)—affected brain is unknown. Therefore, the authors measured brain oxygen tension (brain PO2), carbon dioxide tension (brain PCO2), pH, and hemoglobin oxygen (HbO2) saturation before and after temporary occlusion in 12 patients with aneurysms. The effect of removal of a traumatic intracranial hematoma on cerebral oxygenation was also studied in four severely head injured patients.

A multiparameter sensor was placed in the cortex of interest and locked by means of a specially designed skull bolt. The mean arterial blood pressure, inspired O2 fraction, and end-tidal PCO2 were analyzed. Brain PO2 and HbO2 saturation data were collected every 10 seconds. Descriptive and nonparametric analyses were used to analyze the data.

A wide range in baseline PO2 was seen, although a decrease from baseline in brain PO2 was found in all patients. During temporary occlusion, brain PO2 in patients with unruptured aneurysm (seven patients) dropped significantly, from 60 ± 31 to 27 ± 17 mm Hg (p < 0.05). In the SAH group (five patients), the brain PO2 dropped from 106 ± 74 to 87 ± 73 mm Hg (not significant). Removal of intracranial hematomas in four severely head injured patients resulted in a significant increase in brain PO2, from 13 ± 9 to 34 ± 13 mm Hg (p < 0.05).

The duration of safe temporary occlusion could not be determined from this group of patients, because none developed postoperative deterioration in their neurological status. However, the data indicate that this technique is useful to detect changes in substrate delivery during intraoperative maneuvers. This study also reemphasizes the need for emergency removal of intracranial hematomas to improve substrate delivery in severely head injured patients.

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Vartan Tashjian, Egon M. R. Doppenberg, Eric Lyders, William C. Broaddus, Pierre Pavot, Gary Tye, Amon Y. Liu, Juan Perez and Nitya Ghatak

✓ The authors present the case of a 27-year-old woman with Erdheim-Chester disease (ECD) and extensive intracranial involvement, in whom the initial diagnosis of ECD was established based on computerized tomography (CT)—guided stereotactic biopsy of a caudate lesion. Erdheim—Chester disease is a rare non-Langerhans cell histiocytosis of unknown origin that is clinically characterized by bone pain, diabetes insipidus, and exophthalmos. The radiological hallmarks of the disease include symmetrical sclerosis of the long bones with epiphysial sparing and increased tracer uptake in lesions seen on scintigraphic imaging. Erdheim—Chester disease is characterized histologically by the presence of infiltrating lipid-laden histiocytes that commonly involve the retroperitoneum, orbits, skin, pericardium, lungs, and long bones. Although the occurrence of diabetes insipidus often precedes the diagnosis of ECD by more than a decade in most patients, magnetic resonance imaging— and CT-documented central nervous system involvement is exceedingly rare. In the setting of neurological involvement, neurosurgical biopsy has been reported seven times in the literature, with only one of these biopsies being the basis for the initial diagnosis of the disease. The authors' case represents only the second time the disease has been diagnosed by means of neurosurgical biopsy, highlighting the diagnostic difficulties that patients with EDC present. Skeletal radiographs were confirmatory in this case and this modality should be emphasized as the simplest and most direct route to the diagnosis. The degree of neurological involvement further distinguishes the case presented from prior reports in the literature. The multiple bilateral intraaxial lesions were intensely enhancing on contrast CT scans, distributed infra- and supratentorially, involving both white and gray matter, and associated with diffuse cerebral edema. The case presented is also remarkable by virtue of the symmetrical involvement of the caudate nuclei, representing the first such example documented in the literature. The diagnosis, treatment, and outcome in this patient are discussed, and a review of the literature is presented.

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Tobias Clausen, Ahmad Khaldi, Alois Zauner, Michael Reinert, Egon Doppenberg, Matthias Menzel, Jens Soukup, Oscar Luis Alves and M. Ross Bullock

Object. Brain tissue acidosis is known to mediate neuronal death. Therefore the authors measured the main parameters of cerebral acid—base homeostasis, as well as their interrelations, shortly after severe traumatic brain injury (TBI) in humans.

Methods. Brain tissue pH, PCO2, PO2, and/or lactate were measured in 151 patients with severe head injuries, by using a Neurotrend sensor and/or a microdialysis probe. Monitoring was started as soon as possible after the injury and continued for up to 4 days.

During the 1st day following the trauma, the brain tissue pH was significantly lower, compared with later time points, in patients who died or remained in a persistent vegetative state. Six hours after the injury, brain tissue PCO2 was significantly higher in patients with a poor outcome compared with patients with a good outcome. Furthermore, significant elevations in cerebral concentrations of lactate were found during the 1st day after the injury, compared with later time points. These increases in lactate were typically more pronounced in patients with a poor outcome. Similar biochemical changes were observed during later hypoxic events.

Conclusions. Severe human TBI profoundly disturbs cerebral acid—base homeostasis. The observed pH changes persist for the first 24 hours after the trauma. Brain tissue acidosis is associated with increased tissue PCO2 and lactate concentration; these pathobiochemical changes are more severe in patients who remain in a persistent vegetative state or die. Furthermore, increased brain tissue PCO2 (> 60 mm Hg) appears to be a useful clinical indicator of critical cerebral ischemia, especially when accompanied by increased lactate concentrations.