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Biomedical subjects

A B Valadka

Publications and source records attributed to A B Valadka.

32 records · Page 2Linked to original sources

Prevention of secondary ischemic insults after severe head injury.

OBJECTIVE: The purpose of this study was to compare the effects of two acute-care management strategies on the frequency of jugular venous desaturation and refractory intracranial hypertension and on long-term neurologic outcome in patients with severe head injury. DESIGN: Randomized clinical trial. SETTING: Level I trauma hospital. PATIENTS: One hundred eighty-nine adults admitted in coma because of severe head injury. INTERVENTIONS: Patients were assigned to either cerebral blood flow (CBF)-targeted or intracranial pressure (ICP)-targeted management protocols during randomly assigned time blocks. In the CBF-targeted protocol, cerebral perfusion pressure was kept at >70 mm Hg and PaCO2 was kept at approximately 35 torr (4.67 kPa). In the ICP-targeted protocol, cerebral perfusion pressure was kept at >50 mm Hg and hyperventilation to a PaCO2 of 25-30 torr (3.33-4.00 kPa) was used to treat intracranial hypertension. MEASUREMENTS AND MAIN RESULTS: The CBF-targeted protocol reduced the frequency of jugular desaturation from 50.6% to 30% (p = .006). Even when the frequency of jugular desaturation was adjusted for all confounding factors that were significant, the risk of cerebral ischemia was 2.4-fold greater with the ICP-targeted protocol. Despite the reduction in secondary ischemic insults, there was no difference in neurologic outcome. Failure to alter long-term neurologic outcome was probably attributable to two major factors. A low jugular venous oxygen saturation was treated in both groups, minimizing the injury that occurred in the ICP-targeted group. The beneficial effects of the CBF-targeted protocol may have been offset by a five-fold increase in the frequency of adult respiratory distress syndrome. CONCLUSIONS: Secondary ischemic insults caused by systemic factors after severe head injury can be prevented with a targeted management protocol. However, potential adverse effects of this management strategy may offset these beneficial effects.

Adolescent↗

Comparison of jugular venous oxygen saturation and brain tissue Po2 as monitors of cerebral ischemia after head injury.

OBJECTIVE: To compare the characteristics of jugular venous oxygen saturation (Sjvo2) and brain tissue Po2 (Pbto2) as monitors for cerebral ischemia after severe head injury. Sjvo2 has been useful as a monitor for cerebral ischemia, but it is limited by its inability to identify regional cerebral ischemia. Pbto2 may be superior to Sjvo2 for this purpose, because oxygenation in localized areas of the brain can be monitored. DESIGN: Sjvo2 and Pbto2 were successfully monitored in 58 patients with severe head injury. The changes in Sjvo2 and Pbto2 were compared during ischemic episodes. SETTING: Neurosurgical intensive care unit of a level I trauma center. MEASUREMENTS AND MAIN RESULTS: During the monitoring period, which averaged 90 hrs/patient, there were 54 episodes during which Sjvo2 decreased to <50% and/or Pbto2 decreased to <8 torr. Two of these episodes were caused by an infarction in the area of the Po2 probe, leaving 52 episodes of global hypoxia/ischemia that were identified by one of the two monitors. The sensitivities of the two monitors for detecting ischemia, using the thresholds of 50% and 8 torr for Sjvo2 and Pbto2, respectively, were similar. The Sjvo2 catheter detected 69.7% of the episodes and the Pbto2 catheter detected 63.5% of the episodes. In most of the remaining episodes, both probes reflected a decrease in oxygenation, but not to levels below the defined thresholds. The major differences in the two measures of oxygenation included the following: a) Sjvo2 more consistently reflected a reduction in oxygenation during hyperventilation; b) Pbto2 was affected more by changes in arterial Po2; and c) during severe global ischemia, Pbto2 decreased to 0 and remained at 0, whereas Sjvo2 initially decreased but then increased again as cerebral blood flow ceased, and the only blood in the jugular bulb was of extracerebral origin. CONCLUSIONS: The two monitors provide complimentary information, and neither monitor alone identifies all episodes of ischemia. The best strategy for using these monitors is to take advantage of the unique features of each monitor. Sjvo2 should be used as a monitor of global oxygenation; but Pbto2 should be used as a monitor of local oxygenation, ideally with the catheter placed in an area of the brain that is vulnerable to ischemia but that may be salvageable with appropriate treatment.

Adult↗

Elevated jugular venous oxygen saturation after severe head injury.

OBJECT: The aim of this study was to investigate the incidence of elevated (> or = 75%) jugular venous oxygen saturation (SjvO2) and its relationship to cerebral hemodynamic and metabolic parameters and to outcome after severe head injury. METHODS: Data from 450 severely head injured patients admitted to the Neurosurgical Intensive Care Unit of Ben Taub General Hospital were analyzed retrospectively. The SjvO2 was measured in blood obtained from indwelling jugular bulb catheters. Patients were classified into the following categories: high (Group I), normal (Group II), or low SjvO2 (Group III) if their mean SjvO2 over the duration of monitoring was 75% or higher, 74 to 56%, or 55% or lower, respectively. A high SjvO2 occurred in 19.1% of patients. There was no consistent relationship between SjvO2 and simultaneous cerebral blood flow (CBF) or cerebral perfusion pressure measurements. Compared with Groups II and III, the patients in Group I had a significantly higher CBF and lower cerebral metabolic rate of oxygen (CMRO2). In Group I, the outcomes were death or persistent vegetative state in 48.8% of patients and severe disability in 25.6%. These outcomes were significantly worse than for patients in Group II. Within Group I, the patients with a poor neurological outcome were older and more likely to have suffered a focal head injury; they demonstrated a lower CMRO2 and a greater rate of cerebral lactate production than the patients who attained a favorable outcome. CONCLUSIONS: Posttraumatic elevation of SjvO2 is common but cannot be automatically equated with hyperemia. Instead, elevated SjvO2 is a heterogeneous condition that is associated with poor outcome after head injury and may carry important implications for the management of comatose patients.

Adult↗

Metabolic changes in the brain during transient ischemia measured with microdialysis.

Forty-four patients with severe head injury were monitored for episodes of cerebral ischemia using jugular venous oxygen saturation (sjvO2), brain tissue pO2 (ti-pO2), and a microdialysis probe. The concentration of lactate and glucose were measured in the microdialysate. A total of 10 episodes of global ischemia were observed. The characteristic pattern of a simultaneous decrease in sjvO2 and brain ti-pO2 with an increase in the concentration of lactate occurred in all 10 patients. In addition, 3 episodes of regional ischemia were observed. Although brain ti-pO2 decreased to very low values and the concentration of lactate increased in the microdialysate, sjvO2 remained unchanged. Brain ti-pO2 adds another dimension to our cerebral monitoring by allowing the detection of regional cerebral ischemia.

Adult↗

Comparison of brain tissue oxygen tension to microdialysis-based measures of cerebral ischemia in fatally head-injured humans.

This study investigated the relationship between brain tissue oxygen tension (PbtO2) and cerebral microdialysate concentrations of several compounds in five patients with refractory intracranial hypertension after severe head injury. The following substances were assayed: lactate and glucose; the excitatory amino acids glutamate and aspartate; and the cations potassium, calcium, and magnesium. Glucose concentrations did not correlate with PbtO2, but lactate increased as PbtO2 decreased. The lactate/glucose ratio exhibited a close relationship to PbtO2, increasing sharply only when oxygen tension reached zero. Although glucose and oxygen eventually reached very low levels and zero, respectively, in these fatally head-injured patients, the terminal decrease in PbtO2 slightly preceded that of glucose in four of the five patients. This time lag is the cause of the poor correlation between glucose and PbtO2. Glutamate and aspartate concentrations both demonstrated a close relationship to PbtO2, with sharp increases not occurring until PbtO2 was zero. Concentrations of these amino acids exhibited a similar pattern in response to decreasing glucose concentrations. Potassium concentrations began increasing at a PbtO2 of 35 mm Hg, which is not generally considered indicative of hypoxia. Sharper increases began occurring once PbtO2 dropped below 15 mm Hg, with a slight rise in the minimum potassium concentrations recorded at these low PbtO2 values. Calcium and magnesium concentrations did not vary in response to PbtO2. In summary, the most robust biochemical indicators of cerebral anoxia were elevations in the lactate/glucose ratio and in the concentrations of lactate and of the excitatory amino acids glutamate and aspartate. Furthermore, the fact that glucose concentrations continue to decrease for a short period after oxygen levels reach zero suggests that cells continue to utilize glucose anaerobically for such functions as maintenance of cellular integrity, with collapse of the cell membrane as evidenced by increases of extracellular glutamate and aspartate not occurring until both oxygen and glucose concentrations reach zero.

Adult↗

Brain temperature exceeds systemic temperature in head-injured patients.

OBJECTIVE: To identify the temperature differences in readings taken from the brain, jugular bulb, and core body in head-injured patients. DESIGN: Prospective, observational study. SETTING: Neurosurgical intensive care unit of a university-affiliated county hospital. PATIENTS: Thirty patients with severe head injuries had measurements of brain and core body temperatures. Fourteen patients also had measurements of jugular venous blood at the level of the jugular bulb. INTERVENTIONS: None. MEASUREMENTS AND MAIN RESULTS: Brain temperature was increased an average of 2.0 degrees F (1.1 degrees C) over the core body temperature. In individual patients, the average brain temperature increase over the core body temperature ranged from -0.5 degrees to 3.8 degrees F (-0.30 degrees to 2.1 degrees C). Jugular vein and core body temperatures were similar. The difference in the brain and body temperatures increased when cerebral perfusion pressure decreased to between 20 and 50 mm Hg. The difference in the brain and body temperatures decreased in those patients treated with barbiturate coma. CONCLUSIONS: Direct measurement of temperature in head-injured patients is a safe procedure. Temperatures in the brain are typically increased over the core body temperature and the jugular bulb temperatures. Jugular vein temperature measurement is not a good measurement of brain temperature since it reflects body, not brain temperature. These findings support the potential importance of monitoring brain temperature and the importance of controlling fever in severely head-injured patients since brain temperature may be higher than expected.

Adult↗

Relationship of brain tissue PO2 to outcome after severe head injury.

OBJECTIVE: To determine thresholds of brain tissue PO2 (PbtO2) that are critical for survival after severe head injury. DESIGN: Prospective data collection. SETTING: Neurosurgical intensive care unit of Ben Taub General Hospital, a comprehensive academic neurosurgical facility and Level I trauma center. PATIENTS: Forty-three severely head-injured patients who were not obeying commands on presentation or whose condition deteriorated to this level shortly after admission. INTERVENTIONS: Intracerebral placement of Licox (n=39) or Paratrend (n=4) PO2 probes during craniotomy or in the intensive care unit. MEASUREMENTS AND MAIN RESULTS: PbtO2 monitoring continued for an average of 84.6+/-41.8 hrs. The probes were calibrated before insertion according to the manufacturer's specifications. After removal, probes were tested in room air and in blood gas standard calibration solutions. PbtO2 data were analyzed by comparing the average time that PbtO2 was below the values of 20, 15, 10, 8, 6, 4, and 2 torr (2.7, 2.0, 1.3, 1.0, 0.8, 0.5, and 0.3 kPa, respectively) in patients who were living 3 mos after injury vs. those who died. A Tobit regression analysis using maximum likelihood methods was utilized. Both Licox and Paratrend probes functioned well in room air and in the Level I control. However, in the zero-oxygen solution, the Paratrend probes gave an average reading of 7.0+/-1.4 torr (0.9+/-0.2 kPa), compared with 0.3+/-0.3 torr (0.04+/-0.04 kPa) for the Licox probes. CONCLUSIONS: Analysis of the PbtO2 monitoring data suggested that the likelihood of death increased with increasing duration of time at or below a PbtO2 of 15 torr (2.0 kPa) or with the occurrence of any PbtO2 values of < or =6 torr (< or =0.8 kPa).

Adolescent↗

Radiation therapy and malignant degeneration of benign supratentorial gangliogliomas.

OBJECTIVE: Gangliogliomas are indolent tumors comprised of neoplastic glial and neuronal cells. Benign lesions tend to be associated with long survival unless the tumor degenerates to a histologically malignant form. This study reviews four cases of histologically proven benign ganglioglioma that later demonstrated malignant features within the glial component of the tumor. Features common to each case are analyzed, and similar cases from the literature are reviewed. METHODS: The records of 42 supratentorial gangliogliomas operated on at our institution since 1985 were reviewed. Special attention was paid to histological characteristics, use of adjuvant radiotherapy, time to tumor recurrence, and histology of the recurrent tumor. RESULTS: Of the 42 cases of gangliogliomas, 29 were initially histologically benign. Of these 29, 14 received postoperative radiation therapy and 14 did not; it was unclear whether one patient received adjuvant radiotherapy, and this patient was excluded from further analysis. Four benign gangliogliomas exhibited malignant degeneration of the glial component. These four all occurred in patients who had undergone postoperative irradiation. The time to identified histological change within recurrent tumors averaged 65 months (range, 22-144 mo). CONCLUSION: All of the benign gangliogliomas undergoing malignant change had postoperative radiation therapy as a common feature. This represents a potential correlation that requires further study.

Adult↗

Lactic acid and amino acid fluctuations measured using microdialysis reflect physiological derangements in head injury.

We examined the extracellular neurochemical milieu in 34 head injured patients using microdialysis while simultaneously monitoring intracranial pressure, cerebral perfusion pressure, and jugular venous oxygen saturation. Derangements of anaerobic metabolism reflected by increased lactate and lactate/pyruvate ratios, and release of amino acids were seen at the same time as physiological deterioration in the majority of instances. Clinical microdialysis may provide insights into the neurochemistry of head injury, and such information may lead to new methods of monitoring and treating head injured patients.

Adult↗

Surgical management of patients with severe head injuries.

Minutes can make the difference between life and death when patients with severe head injuries require surgery. Subdural, epidural, and intracerebral hematomas and cerebral contusions and gunshot wounds are the pathologic entities encountered most frequently during emergency surgery in patients with severe head injuries. Neurosurgical team members frequently use hyperventilation, mannitol and barbiturates, and sophisticated monitoring modalities to manage patients with severe head injuries during and after surgery. Although monitoring a patient's intracranial pressure (ICP) through a ventriculostomy catheter remains the most widely used gauge of cerebral metabolism, neurosurgical teams also are using fiber-optic ICP monitoring catheters, cerebral blood flow measurement probes, microdialysis catheters, jugular venous oxygen saturation catheters, and brain oxygen content measurement electrodes. Coordinated teamwork by perioperative nurses, neurosurgeons, anesthesia care providers, and emergency department staff members helps ensure the best possible outcomes for patients who require surgery for management of severe head injuries.

Cerebral Hemorrhage↗

Lactate and excitatory amino acids measured by microdialysis are decreased by pentobarbital coma in head-injured patients.

Primary traumatic brain injury and secondary ischemic/hypoxic injury are being increasingly characterized at the neurochemical level. Neurochemical monitoring using microdialysis has shown that these forms of tissue damage share many common features. In particular, anaerobic glycolysis with increased lactate production and release of excitatory amino acids into the extracellular space are seen in both conditions. Clinical microdialysis studies have heretofore focused on methodological issues, establishment of basal analyte values, and clinico-neurochemical correlation. Here we report the neurochemical consequences of therapeutic intervention in head injury. Specifically, induction of thiopental coma to manage severe increased intracranial pressure in seven patients was associated with a 37% reduction of lactate, 59% reduction of glutamate, and 66% reduction in aspartate in the extracellular space of the brain.

Adolescent↗

Updated management strategy for patients with cervical osteophytic dysphagia.

Anterior cervical osteophytes impinging upon the pharynx or esophagus constitute a rare cause of dysphagia. In severe cases, surgical removal of these osteophytes can provide symptomatic relief. We describe a patient of this type who failed to improve postoperatively, only to be found subsequently to have a carcinoma of the base of the tongue. To assist other clinicians in evaluating similar patients, and also to emphasize the great utility of modern radiologic techniques in these cases, we propose a diagnostic algorithm that incorporates magnetic resonance or computerized tomographic imaging.

Aged↗

SjvO2 monitoring in head-injured patients.

Jugular venous oxygen saturation (SjvO2) measures the balance between cerebral oxygen delivery and cerebral oxygen consumption. Abnormalities that increase oxygen consumption (e.g., fever or seizures) or that decrease oxygen delivery (e.g., increased ICP, hypotension, hypoxia, hypocapnia, or anemia) can decrease SjvO2. Measuring SjvO2 continuously in the ICU in 177 patients with severe head injury, jugular venous desaturation (SjvO2 < 50%) was identified at least once in 39% of the patients. Approximately half of the episodes of desaturation were due to intracranial hypertension and half were due to systemic causes. The occurrence of one or more episodes of desaturation was strongly associated with a poor outcome, suggesting that the reduction in oxygen delivery identified with the SjvO2 monitoring contributed to the neurological injury. In the operating room, jugular venous desaturation was identified in 6 of 8 patients who were monitored during emergency evacuation of a traumatic intracranial hematoma. The lowest SjvO2 observed was 28%. In all 8 cases, the SjvO2 increased, from 47 +/- 10% to 63 +/- 5% after evacuation of the hematoma. Additional data supporting the hypothesis that these secondary insults identified with the SjvO2 monitoring contribute to the patient's neurological injury come from measurement of the extracellular concentrations of lactate and excitatory amino acids in the brain using microdialysis. Lactate concentration increased from 0.9 +/- 0.3 to 2.4 +/- 0.5 mumol/L and glutamate increased from 11.5 +/- 8.5 to 55.0 +/- 10.4 mumol/L during 8 episodes of jugular venous desaturation in 7 of 22 patients monitored with microdialysis. SjvO2 identifies global reductions in cerebral oxygenation due to a variety of causes, and is useful as a monitor for secondary insults in patients with severe head injury.

Adult↗

The use of antibodies targeted against the neurofilament subunits for the detection of diffuse axonal injury in humans.

Axonal injury is a common feature of human traumatic brain injury. Typically, damaged axons cannot be recognized unless a patient survives the injury by at least 10-12 hours (h). Limitations associated with the use of the traditional silver methods have been linked with this inability to recognize early posttraumatic reactive axonal change. Recently, we reported that antibodies targeting the neurofilament subunits proved useful in recognizing early traumatically induced axonal change in traumatically brain-injured animals. Accordingly, in the present communication, we employed antibodies to detect at the light microscopic level the 68 kD Nf-L and 170-200 kD Nf-H neurofilament subunits in head-injured patients who survived the traumatic event for periods ranging from 6 h to 59 days. Antibodies targeting all of the above-described subunits revealed a progression of reactive axonal change. Antibodies to the 68 kD subunit proved most useful, as they were not complicated by concomitant immunoreactivity in surrounding nuclei and/or dendritic and somatic elements. These immunocytochemical strategies revealed, at 6 h postinjury, focally swollen axons which appeared intact. By 12 h, this focal swelling had progressed to disconnection, with the immunoreactive swelling undergoing further expansion over 1 week postinjury. These findings demonstrate the utility of the previously described immunocytochemical strategies for detecting reactive axonal change in brain-injured humans, particularly in the early posttraumatic course. More importantly, these methods also demonstrate in humans that reactive axonal change is not necessarily caused by traumatically induced tearing.

Accidental Falls↗