[Personal experience with the surgical treatment of thoracic outlet syndrome]. / Nase zkusenosti s chirurgickou lécbou thoracic outlet syndromu.

The authors describe their experience with surgery of suspected TOS (8 cases) and traumatic TOS after clavicular fracture (1 case) in the last 2 years. In the group there were 7 women and 2 men aged 39-59 years with a history from 6 months to 26 years. Seven patients reported complete or almost complete relief of symptoms. In one case we observed progressive deterioration during 6 weeks postoperatively. All patients underwent decompression of the brachial plexus and subclavian artery from a supraclavicular approach. There was one case of reoperation after 15 years after primary surgery.

Brain tissue PO2: correlation with cerebral blood flow.

This investigation analyzed 22 xenon CT cerebral blood flow (CBF) studies from 18 severely head-injured patients (Glasgow motor score < 6) who underwent xenon CT scanning while brain tissue oxygen tension (PbtO2) was being monitored. CBF was determined both in a localized region of interest around the actual or estimated location of the tip of the PbtO2 probe and in the entire corresponding CT slice. Linear regression analysis was used to examine the relationship between these CBF measurements and PbtO2 values recorded immediately prior to the xenon CT CBF study. PbtO2 varied linearly with both regional CBF (rCBF) and global CBF measurements, but the average global CBF value was significantly higher than the average rCBF value. Very low values were significantly less common for global CBF than for rCBF. Further investigation is necessary to determine how probe placement near contused areas vs. in normal tissue affects our understanding of the relationship between rCBF, global CBF, PbtO2, and cerebral oxygen consumption.

Microdialysate nitrate/nitrite levels following severe head injury.

Nitric oxide (NO) has important regulatory functions within the central nervous system. The purpose of this study was to measure the concentration of nitric oxide in the brain after severe traumatic brain injury. NO is oxidized in vivo to nitrate and nitrite. Measurement of these products gives an index of NO production. Laboratory studies have shown a good correlation between NO measured directly with an electrode, and indirectly by microdialysis nitrate/nitrite. Using chemiluminescence method we measured nitrate/nitrite levels in 2024 microdialysate samples obtained from 24 patients during the first five days following severe head injury. We used CMA 70 probe (AB Microdialysis, Sweden) perfused by normal saline at a rate of 2 microliters/min. The median values of nitrate/nitrite for the whole group were highest on day 1 and gradually decreased over the 5 day monitoring period (day 1-19.2 mumol/l, day 5-12.7 mumol/l). Average values were lowest in the patients that died of their injury (14.3 mumol/l), and highest in patients who recovered by 3 months after injury with a moderate or severe disability (25.8 mumol/l or 31.9 mumol/l). In addition, there was a strong interaction between the severity of neurological injury and the change in dialysate nitrate/nitrite over time. The results suggest that nitric oxide may have a role in secondary injury mechanisms, but that this role is complex and varies as the injury evolves over time.

Comparison of microdialysate arginine and glutamate levels in severely head-injured patient.

L-arginine concentrations in the brain are of interest following TBI because L-arginine is the immediate precursor of nitric oxide (NO). In addition, in vitro studies suggest that glutamate, which is a mediator of secondary injury after TBI, may stimulate release of arginine from glial cells. This study examines arginine concentrations in brain tissue using the microdialysis technique after human TBI. From 78 TBI patients, a total of 1739 microdialysate samples were collected using a CMA-70 probe perfused with normal saline at 2 microliters/min and concentrations of amino acids in microdialysate were determined. Amino acid concentrations for each patient were averaged for 8-hour periods during the first 3 days after injury, and daily for postinjury days 4 and 5. Following an initial rapid decrease in arginine, the dialysate arginine concentrations were low on days 1-3 and then increased over the days 4-5 after injury. In contrast, the microdialysate glutamate levels decreased slowly over the first 48 hours after TBI and thereafter remained low. Thirty-five episodes of jugular venous desaturation (SjvO2 < 50%) occurred during monitoring. Arginine and glutamate levels simultaneously doubled during desaturation and decreased as the clinical episode resolved. The low concentrations of arginine during the first 3 days after TBI may indicate that substrate unavailability could contribute to the decreased NO concentrations that have been observed after TBI. The simultaneous increase in glutamate and arginine during ischemic events is consistent with experimental data which has observed that glutamate induces release of arginine.

Management of cerebral perfusion pressure.

The management of cerebral perfusion pressure is among the most controversial treatment issues. Cerebral perfusion pressure (CPP) is normally expressed as the difference between mean arterial blood pressure and intracranial pressure and has two important physiological roles in the patient with severe head injury. First, CPP represents the pressure gradient acting across the cerebrovascular bed and hence is an important factor in the regulation of cerebral blood flow. Second, CPP contributes to the hydrostatic pressure within the intracerebral vessels, and therefore is one of the factors that determines edema formation in the injured brain. The border between adequate and inadequate CPP should be assessed individually and continuously, as it may fluctuate in time. The treatment plan that includes rapid identification of intracranial hemorrhage, rapid evacuation of extra-axial blood, treatment of intracranial hypertension, and promotion of cerebral and systemic perfusion is likely to provide the best outcome for all patients.

Global and regional techniques for monitoring cerebral oxidative metabolism after severe traumatic brain injury.

The disturbance of normal mechanisms of oxygen delivery and metabolism is a hallmark of severe traumatic brain injury (TBI). In the past, investigations into the status of cerebral oxygen metabolism depended on changes in the differences in oxygen content between arterial and jugular venous blood. The development of jugular venous oximetry permitted continuous monitoring of jugular venous oxygen saturation, thereby overcoming earlier limitations caused by intermittent sampling. Neuromonitoring techniques that utilize only jugular vein sampling provide information only about global cerebral metabolism, but direct measurement of brain tissue oxygen tension via intraparenchymal probes makes possible the assessment of regional cerebral oxygen metabolism. Regional and global neuromonitoring techniques are not competitive or mutually exclusive. Rather, they are best regarded as complementary, with each providing valuable information that has a direct bearing on patient outcomes. The authors review the currently available techniques used in the monitoring of cerebral oxidative metabolism in patients who have sustained severe TBI.