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Biomedical subjects

F C Wagner

Publications and source records attributed to F C Wagner.

At least 19 recordsLinked to original sources
PubMed1999

Intrathecal morphine delivered via subcutaneous pump for intractable pain in pancreatic cancer.

BACKGROUND: Pain secondary to unresectable pancreatic cancer is frequently severe and extremely difficult to control with traditional methods of analgesia. This retrospective study reports the analgesic effects of intrathecal morphine sulfate by implanted infusion pumps in nine patients with unresectable adenocarcinoma of the pancreas. METHODS: Nine patients were implanted over a 2-year period. Preoperative morphine i.v. equivalents were a mean of 81.51 mg/day, with a range of 20-140 mg/day. Patients were hospitalized for a trial dose of 1-2 mg of intrathecal Duramorph, 1 mg/ml, via lumbar puncture to assess whether adequate pain relief could be achieved and whether there would be drug-related side effects. RESULTS: All patients who received a trial dose experienced excellent pain relief, and subsequently underwent implantation of a lumbar subarachnoid catheter and infusion pump during the same hospitalization. The mean number of days from diagnosis to pump implant was 119, with a range of 3-587 days. The mean maximum daily dose was 21.28 mg, with a range of 3-73.10 mg. No patient experienced respiratory depression or excess sedation which prevented achievement of pain control. Minor supplemental narcotic use was documented in three of the nine patients. Assessment of pain control was made by the level of activity and the analog pain scale, with 0 being no pain and 10 being the worst pain imaginable. All of the patients experienced good to excellent relief of pain. The mean duration of intrathecal morphine sulfate use until death was 137.3 days, with a range of 52-354 days. CONCLUSIONS: This series of nine patients indicates that long-term administration of intrathecal morphine via implanted infusion pump in patients with pancreatic cancer is both efficacious and safe. All patients and their families reported an improved quality of life with an increased level of activity.

Adenocarcinoma↗
PubMed1997

Initial small-volume hypertonic resuscitation of shock and brain injury: short- and long-term effects.

BACKGROUND: Initial small-volume hypertonic saline resuscitation of a combined hemorrhagic shock and head injury model was studied. METHODS: Twenty-three sheep underwent hemorrhage (20 mL/kg) and parietal freeze injury followed by initial bolus resuscitation with lactated Ringer's solution (40 mL/kg) or 7.5% hypertonic saline (HS) (4 mL/kg). Cardiac index was maintained with lactated Ringer's solution for either 2 or 24 hours. Parietal lobe water content, blood volume, and blood flow were determined. Intracranial pressure (millimeters of mercury) was followed. RESULTS: Overall fluid requirements (milliliters per kilogram) were less at 2 and 24 hours with HS resuscitation. Early intracranial pressure was less with HS resuscitation. Brain water contents were similar between groups. Blood flow in injured and blood volume in uninjured parietal lobe were less for HS at 2 hours, although not different at 24 hours. CONCLUSIONS: Less fluid was needed in the short- and long-term with HS resuscitation. Early intracranial pressure was higher with lactated Ringer's solution resuscitation, possibly in part owing to increased blood volume.

Animals↗
PubMed1994

Respiratory complications after cervical spinal cord injury.

STUDY DESIGN: Sixty-five consecutive cases of acute cervical spinal cord injuries were reviewed retrospectively for respiratory complications. OBJECTIVES: The objectives were to identify factors that may contribute to respiratory dysfunction and to evaluate therapeutic measures designed to reduce respiratory complications. SUMMARY OF BACKGROUND DATA: Respiratory complications continue to be a major cause of morbidity and mortality after cervical spinal cord injury with a reported incidence from 36 to 83%. METHODS: Multiple factors were evaluated which could potentially influence the incidence or severity of respiratory complications. These included age, pre-existing cardiac or pulmonary disease, accompanying major injuries, and the severity of the spinal cord injury. The effects of various therapeutic measures were also assessed including the benefit of rotating beds, early fracture stabilization and patient mobilization. RESULTS: Respiratory complications occurred in 62% of these patients and were transient in nature, variable in severity and duration, strongly associated with the severity of spinal cord injury, and only marginally affected by therapeutic interventions. CONCLUSIONS: The characteristics of respiratory dysfunction following cervical spinal cord injury correspond to those of spinal shock.

Acute Disease↗
PubMed1993

Stabilization of subaxial cervical spinal injuries.

With subaxial cervical spine fractures, it has not been established which injuries can be adequately stabilized by external orthoses and which will require surgical stabilization. After review of 64 consecutive patients with C3-C7 spinal injuries, fracture characteristics on admission roentgenograms were identified that accurately predict the success or failure of nonoperative management. These include evidence of severe ligamentous injury (SLI) and severe vertebral body injury (SVBI). The presence of SLI, SVBI, or both SLI and SVBI correlated strongly with nonoperative stabilization failure (p < 0.001, p = 0.002, and p = 0.004, respectively). Injuries without SLI or SVBI were all successfully stabilized by cervical orthoses. Additionally, characterizing injuries by evidence of SLI and SVBI directs the approach for surgical stabilization.

Adolescent↗
PubMed1993

The effect of nimodipine on high-energy phosphates and intracellular pH during cerebral ischemia.

Experimental and clinical studies suggest that the calcium channel blocker nimodipine may reduce cerebral ischemic injury. Using rapid acquisition phosphorus-31 nuclear magnetic resonance (31P NMR) spectroscopy, we examined the effect of nimodipine on cerebral energy metabolism during severe ischemia in gerbils. High-energy phosphates and intracellular pH were characterized at baseline and at 2-min intervals following bilateral common carotid artery (CCA) ligation. Serial forebrain spectroscopy was continued until phosphocreatine (PCr) and adenosine triphosphate (ATP) resonances disappeared. Controls (n = 10) were compared to gerbils receiving intraperitoneal nimodipine 30 min prior to carotid ligation, at the following doses: 0.5 mg/kg (n = 8), 1.0 mg/kg (n = 10), 2.0 mg/kg (n = 8), or 4.0 mg/kg (n = 4). In the control group, PCr and ATP peaks were undetectable after a mean of 5.4 +/- 0.47 min following CCA ligation. Compared with controls, the mean time for depletion of high-energy phosphates following carotid ligation was prolonged at nimodipine doses of 0.5 mg/kg and 1.0 mg/kg, but the differences did not reach statistical significance. In the 2.0 mg/kg group, however, ATP was preserved until 9.8 +/- 1.0 min following the onset of ischemia, significantly longer than the control group (p = 0.005, Mann-Whitney test). Nimodipine had no effect on the time course or severity of intracellular acidosis. In this model of severe ischemia, relatively high doses of nimodipine slowed the depletion of high-energy phosphates without altering intracellular acidosis. This suggests that nimodipine may provide cerebral protection by directly altering ischemic cellular metabolism.

Acidosis↗
PubMed1992

Impairment of helper T-cell function following severe head injury.

Major infections, such as sepsis and pneumonia, occur in 50-75% of patients following isolated severe head injury. Previous studies have demonstrated that this high incidence of infection following severe head injury may be related to a decrease in helper T-cell activation and function. The present study was designed to investigate the effect of severe head injury on specific subgroups of helper T cells known to enhance or suppress cellular immune function. Specifically, peripheral blood lymphocytes (PBLs) from 10 head-injured patients and 10 matched controls were evaluated following in vitro stimulation with the T-cell mitogen, phytohemagglutinin (PHA). Subsets of helper T cells evaluated included activated helper (CD4+/CD25+) T cells; helper/inducer (CD4+/CDw29+) T cells, which enhance cellular immune activity; and suppressor/inducer (CD4+/CD45R+) T-cells, which induce suppressor (CD8+) T-cells. In addition, the effect of intraventricular fluid (IVF) on PHA-stimulated in vitro CD4 and CD25 expression was investigated to determine whether severe head injury results in the production of mediators within the central nervous system capable of affecting T-cell activation. The results of this study indicate that isolated severe head injury selectively reduces the ability of PHA-stimulated PBLs to express the helper/inducer (CD4+/CDw29+) T-cell (p = 0.023) and activated helper (CD4+/CD25+) T-cell (P = 0.041) phenotypes. There was no significant change in PHA-stimulated CD4 or CD25 expression following incubation of PBLs with intraventricular fluid (IVF) from head-injured patients. The relationship between these changes in specific helper T-cell subpopulations and the infectious complications of severe head injury are discussed.

Adolescent↗
PubMed1992

Cell-mediated immunity in severely head-injured patients: the role of suppressor lymphocytes and serum factors.

Severe head injury results in suppression of cellular immunity associated with defective in vitro functioning of effector lymphocytes, such as helper T cells and cytotoxic T cells. It is not known whether this suppression in effector lymphocyte function is due to intrinsic lymphocyte dysfunction, to suppressor peripheral blood mononuclear cells (PBMC's) such as suppressor lymphocytes or suppressor monocytes, or to serum factors capable of inhibiting effector lymphocyte function. The purpose of this study was to determine whether a subpopulation of PBMC's and/or serum factor(s) are responsible for this observed suppression in cell-mediated immunity. Cell-mediated immune activity was determined measuring in vitro lymphokine-activated killer (LAK) cytotoxicity following incubation of PBMC's from 15 head-injured patients with those from 15 heterologous normal subjects. The PBMC's were separated into lymphocyte-enriched and monocyte-enriched subpopulations by plastic adherence techniques, and the effect of each population on LAK cytotoxicity was determined. Additionally, the effect on cytotoxicity of serum from the head-injured patients was determined in a dose-response fashion. There was significant depression in LAK cytotoxicity when: 1) PBMC's from normal subjects were incubated with PBMC's from head-injured patients (p < 0.001); 2) lymphocytes (PBMC's depleted of monocytes) from head-injured patients were incubated with PBMC's from normal subjects (p < 0.001); and 3) PBMC's from normal subjects were incubated with serum from head-injured patients (p < 0.001). No suppression in cellular immunity was noted when lymphocytes from normal subjects were incubated with monocytes from head-injured patients. The results indicate that lymphocytes rather than monocytes actively inhibit cellular immunity following severe head injury. The detection of immunosuppressive serum factors suggests a mechanism by which lymphocytes might be modulated by severe head injury.

Adolescent↗
PubMed1992

Management of thoracolumbar fractures with accompanying neurological injury.

The optimal surgical approach for spinal canal reconstruction of thoracolumbar fractures is controversial, and the relationship between spinal canal reconstruction and neurological recovery remains unclear. To address these issues, 22 consecutive cases of thoracolumbar fracture with accompanying neurological deficit were reviewed. Neurological status was graded at the time of admission, postoperatively, and at a mean of 15 months postinjury. By using preoperative and postoperative radiographs and computed tomographic scans, the degree of spinal canal compromise was quantified in the sagittal, coronal, and axial planes. All fractures were stabilized by posterior instrumentation and fusion, and in 10 injuries, retropulsed vertebral body fragments were further reduced by posterolateral decompression. Spinal canal dimensions, neurological function, and operative approach were compared by using nonparametric statistical analysis. The greater the initial spinal canal compromise, the more severe the neurological deficit (P = 0.04). With injuries involving L1 and above, this relationship increased (P = 0.003). The extent of spinal canal reconstruction failed to correlate with neurological recovery. Compared with spinal instrumentation alone, transpedicular decompression showed no benefit in terms of postoperative canal dimensions or neurological outcome. On the basis of this experience, transpedicular decompression offers no advantage over spinal instrumentation alone. The relationship between initial spinal canal encroachment and neurological deficit demonstrates that the degrees of bony and neurological injury directly reflect the kinetic energy transferred at the time of impact. The lack of correlation between the extent of spinal canal reconstruction and neurological recovery suggests that ongoing neural compression/distortion contributes little to the overall neurological injury.

Adolescent↗
PubMed1991

Quantification of midline shift as a predictor of poor outcome following head injury.

A retrospective study of patient outcome, based on admission computed tomography, was carried out in 75 consecutive patients with head injury. Computed tomography data collected included the type and extent of intracranial hemorrhage, the extent of midline shift, and the ratio of midline shift compared with the extent of intracranial hemorrhage. Midline shift was considered to be out of proportion to intracranial hemorrhage when the midline shift of the septum pellucidum exceeded the extent of the hemorrhage as measured radially from the inner table of the skull. When computed tomography data were analyzed by logistic regression, significant predictive factors for poor outcome were intracranial hemorrhage (34%), intracranial hemorrhage with midline shift (61%), and midline shift out of proportion to the extent of intracranial hemorrhage (88%). When patient outcome and mortality rates are considered, our study indicates that midline shift out of proportion to the extent of intracranial hemorrhage is a highly useful predictor of poor patient outcome following head injury.

Adult↗
PubMed1991

Severe head injury: effect upon cellular immune function.

Infection is a major cause of morbidity following severe head injury. Although investigations have demonstrated central nervous system modulation of immune function, the effects of severe head injury on immune activity have not been well documented. This study prospectively investigated cellular immune function in 20 patients with isolated severe head injury. In vivo cellular immune status was determined by responses to delayed-type hypersensitivity (DTH) skin tests. In vitro studies included the effect of the lymphocyte mitogen, phytohaemagglutinin (PHA), on peripheral blood lymphocyte (PBL) phenotype expression and PBL blastogenesis. DTH skin testing demonstrated anergy to all antigens used during the first two weeks following head injury. Analysis of PBLs incubated with PHA demonstrated a decrease in the percent of PBL blastogenesis (p = 0.002), the percentage of cells marking as T-cells (p = 0.018), helper T-cells (p less than 0.001) and those expressing interleukin-2 receptors (p less than 0.001). There was a significant increase in the percentage of cells that marked as monocytes (p = 0.030), whereas there was no significant change in the percentage of B-cells, suppressor/cytotoxic T-cells, natural killer cells or in cells expressing the HLA-DR antigen. The infection rate was 55% with most occurring within 5 days of injury. The results of this study suggest that isolated severe head injury causes suppression of cellular immunity. The decrease in PHA stimulated PBL blastogenesis, helper T-cell phenotypic and interleukin-2 receptor expression, suggests suppression in early helper T-cell activation may be responsible for the high incidence of infection following severe head injury. The possible significance of increased monocyte phenotypic expression is discussed.

Adolescent↗
PubMed1991

Humoral and cellular immunity following severe head injury: review and current investigations.

Infection is a common and serious complication of severe head injury. Immunocompetence in 25 severely head injured patients was investigated by measuring: (1) delayed-type hypersensitivity (DTH) skin test responses to common antigens; (2) phytohaemagglutinin (PHA) stimulated peripheral blood lymphocyte (PBL): blastogenesis, phenotype expression, and lymphokine production; (3) lymphokine-activated killer (LAK) cytotoxicity, antibody dependent cellular cytotoxicity (ADCC) and natural killer (NK) cytotoxicity; and (4) immunoglobulin and complement levels. The incidence of anergy to DTH skin testing was 100%. There was a decrease in PHA stimulated: PBL blastogenesis (p = 0.002), T-cell expression (p = 0.018), helper T-cell expression (p less than 0.001), interleukin-2 receptor expression (p less than 0.001), interleukin-2 production (p = 0.035) and gamma-interferon production (p less than 0.001). LAK cytotoxicity was depressed following incubation with IL-2 (p less than 0.001). There was no significant decrease in immunoglobulin levels and all acute phase reactants tested increased. The results of this study indicate that the cellular arm of immune response, including lymphocyte activation and cytokine production, is suppressed following severe head injury. The lack of enhancement in LAK cytotoxicity following incubation of PBLs with interleukin-2 suggests that factors other than decreased interleukin-2 production, such as the inherent lymphocyte dysfunction, other soluble mediators or suppressor cells, may be responsible for the reduction in cellular immunity observed following severe head injury.

Adolescent↗
PubMed1991

Impairment of helper T-cell function and lymphokine-activated killer cytotoxicity following severe head injury.

Infection is a major complication of severe head injury, occurring in 50% to 75% of patients who survive to hospitalization. Previous investigations of immune activity following head injury have demonstrated suppression of helper T-cell activation. In this study, the in vitro production of interferon-gamma (INF-gamma), interleukin-1 (IL-1), and interleukin-2 (IL-2) was determined in 25 head-injured patients following incubation of peripheral blood lymphocytes (PBL's) with the lymphocyte mitogen phytohemagglutin (PHA). In order to elucidate the functional status of cellular cytotoxicity, lymphokine-activated killer (LAK) cell cytotoxicity assays were performed both prior to and following incubation of PBL's with IL-2 in five patients with severe head injury. The production of INF-gamma and IL-2 by PHA-stimulated PBL's was maximally depressed within 24 hours of injury (p less than 0.001 for INF-gamma, p = 0.035 for IL-2) and partially normalized within 21 days of injury. There was no change in the production of IL-1. When comparing the in vitro LAK cell cytotoxicity of PBL's from head-injured patients and normal subjects, there was a significant depression in LAK cell cytotoxicity both prior to (p = 0.010) and following (p less than 0.001) incubation of PBL's with IL-2. The results of this study indicate that IL-2 and INF-gamma production, normally required for inducing cell-mediated immunity, is suppressed following severe head injury. The failure of IL-2 to enhance LAK cell cytotoxicity suggest that factors other than decreased IL-2 production, such as inhibitory soluble mediators or suppressor lymphocytes, may be responsible for the reduction in cellular immune activity following severe head injury. These findings may have significant implications in designing clinical studies aimed at reducing the incidence of infection following severe head injury.

Adolescent↗
PubMed1990

Suppression of cellular immune activity following severe head injury.

Infection is a major cause of morbidity following multiple traumatic and head injury. Although immunosuppression has been demonstrated after multiple traumatic injury, the effects of head injury on immune function have not been thoroughly investigated. In a prospective study of 10 severely head-injured patients, in vitro and in vivo parameters of cellular immune activity were assessed. In vitro measurements of lymphocyte surface antigen expression following mitogen stimulation were made serially over a 3-week period in 10 patients with severe head injury. The control group consisted of 20 healthy subjects. Phenotyping of peripheral blood lymphocytes (PBLs) was performed following incubation with and without mitogens. Phenotypes were determined by flow cytometry using monoclonal antibodies (MABs) to T lymphocyte subsets and the alpha subunit of interleukin 2 (IL-2) receptors. In vivo cellular immune function was determined by measuring patient responses to delayed-type hypersensitivity (DTH) skin testing within 24 h of injury. When head-injured patients were compared to controls, PBLs incubated in the presence of phytohemagglutinin (PHA) demonstrated a decrease in cells marking as T cells (p = 0.005), helper-inducer T cells (p = 0.001), and in the number of IL-2 receptor-bearing cells (p = 0.001). The functional ability of these lymphocyte subpopulations to proliferate in the presence of PHA was significantly suppressed within 24 h of injury and normalized within 3 weeks of injury. DTH skin testing to Candida, mumps, trichophyton, and PPD antigens was performed within 24 h of injury and resulted in anergic responses in all 10 patients when measured at 24, 48, and 72 h following administration. The overall infection rate was 60%, with the majority of infections occurring within the first 4 days following injury. The results of this study indicate that severe head injury results in suppression of cellular immune function with a corresponding high rate of infection. The possible significance of the decrease in the percentage of helper-inducer T cells and in the number of cells bearing IL-2 receptors following mitogen stimulation is discussed.

Adolescent↗
PubMed1990

Traumatic aneurysm of the superior cerebellar artery: case report and review of the literature.

Less than 10% of the 250 reported cases of traumatic intracranial aneurysms have involved the posterior circulation. Traumatic aneurysms of the superior cerebellar artery are extremely rare, with only three cases previously reported. This is the first report of a traumatic superior cerebellar artery aneurysm in which the diagnosis was suggested by computed tomographic scan. The potential for a good outcome suggests the value of early angiography when the history and diagnostic imaging studies suggest the possibility of a traumatic aneurysm.

Adult↗
PubMed1988

Effect of nimodipine-associated hypotension on recovery from acute spinal cord injury in cats.

The effect of nimodipine on acute spinal cord trauma was studied in cats. Spinal evoked responses (SERs) were abolished after weight drop injury of 100 g-cm. All control animals showed spontaneous recovery of spinal cord function as measured by SERs. Treatment with a moderate intravenous dose of nimodipine resulted in a 32% drop in systemic blood pressure and delay in or failure of spinal cord recovery. We concluded that in this model, nimodipine treatment had deleterious effect on the spinal cord recovery due to the significant associated hypotension. It is likely that marked hypotension in the case of traumatic loss of autoregulation overrides the expected nimodipine-related increase in spinal cord blood flow with resultant additional ischemic damage.

Acute Disease↗