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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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Roberto C. Heros and Alois Zauner

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Ryszard M. Pluta, Alois Zauner, Jay K. Morgan, Karin M. Muraszko and Edward H. Oldfield

✓ Although proliferative arteriopathy has been postulated to play a role in the etiology of vasospasm after subarachnoid hemorrhage (SAH), histological and morphological studies examining cerebral vasospasm have produced conflicting results. To help settle this controversy, the authors used an in vivo label of cell division, bromodeoxycytidine, to assess cell proliferation in a primate model of SAH.

Fifteen cynomolgus monkeys received a clot of either whole blood (11 animals) or red blood cells (four animals) placed around the right middle cerebral artery (MCA). On the day of surgery continuous intravenous infusion of bromodeoxycytidine was begun and continued until the animal was sacrificed immediately after arteriography on Day 7, 12, or 27 following surgery. Sections from the right and left MCA's were stained with a monoclonal antibody against bromodeoxcytidine, and labeled cells were counted.

Arteriographic evidence of vasospasm occurred in nine monkeys on Day 7. On Day 12 and Day 27 no monkeys had persistent vasospasm. Placement of subarachnoid clot around the right MCA increased proliferative activity across all layers of the arterial wall. Most of the labeled cells were in the adventitia and the endothelium. Although there were more dividing cells in all layers of the right MCA than the left MCA (p < 0.01), the number of stained cells per section was limited (range 0.1 to 21.2, mean 8) and the occurrence of vasospasm was not associated with the number of dividing cells in the right MCA on Day 7, 12, 27, or for all days combined (p > 0.6).

Cerebral vasospasm after SAH was not associated with the extent of proliferation of cells in the vessel wall, nor could the intensity of the limited proliferative changes have been responsible for narrowing of the vessel diameter.

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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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Alois Zauner, Tobias Clausen, Oscar L. Alves, Ann Rice, Joseph Levasseur, Harold F. Young and Ross Bullock

Object. Currently, there are no good clinical tools to identify the onset of secondary brain injury and/or hypoxia after traumatic brain injury (TBI). The aim of this study was to evaluate simultaneously early changes of cerebral metabolism, acid—base homeostasis, and oxygenation, as well as their interrelationship after TBI and arterial hypoxia.

Methods. Cerebral biochemistry and O2 supply were measured simultaneously in a feline model of fluid-percussion injury (FPI) and secondary hypoxic injury. After FPI, brain tissue PO2 decreased from 33 ± 5 mm Hg to 10 ± 4 mm Hg and brain tissue PCO2 increased from 55 ± 2 mm Hg to 81 ± 9 mm Hg, whereas cerebral pH fell from 7.1 ± 0.06 to 6.84 ± 0.14 (p < 0.05 for all three measures). After 40 minutes of hypoxia, brain tissue PO2 and pH decreased further to 0 mm Hg and 6.48 ± 0.28, respectively (p < 0.05), whereas brain tissue PCO2 remained high at 83 ± 13 mm Hg. Secondary hypoxic injury caused a drastic increase in cerebral lactate from 513 ± 69 µM/L to 3219 ± 490 µM/L (p < 0.05). The lactate/glucose ratio increased from 0.7 ± 0.1 to 9.1 ± 2 after hypoxia was introduced. The O2 consumption decreased significantly from 18.5 ± 1.1 µl/mg/hr to 13.2 ± 2.1 µl/mg/hr after hypoxia was induced.

Conclusions. Cerebral metabolism, O2 supply, and acid—base balance were severely compromised ultra-early after TBI, and they declined further if arterial hypoxia was present. The complexity of pathophysiological changes and their interactions after TBI might explain why specific therapeutic attempts that are aimed at the normalization of only one component have failed to improve outcome in severely head injured patients.

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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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Stacey Quintero Wolfe, Nils Mueller-Kronast, Mohammad Ali Aziz-Sultan, Alois Zauner and Sanjiv Bhatia

✓Extracranial carotid artery (CA) aneurysms are rare in the pediatric population and are usually the result of connective tissue disorders, traumatic dissection, or infection. The authors present the case of a large calcified internal carotid artery pseudoaneurysm of obscure origins presenting with embolic stroke in a child. Aneurysm excision and CA reconstruction would have been extremely difficult due to the distal location of the lesion, and CA ligation was contraindicated due to a failed balloon test occlusion. Therefore, after anticoagulation therapy, the patient was treated endovascularly with a covered stent and complete exclusion of the aneurysm from the circulation. The patient recovered all neurological function and has remained in excellent condition. A follow-up angiogram performed at 6 months showed no recurrence or stenosis.