Search PubMed⌕ Search

Biomedical subjects

R V Maier

Publications and source records attributed to R V Maier.

At least 19 recordsLinked to original sources

Prevention of immunization to D+ red blood cells with red blood cell exchange and intravenous Rh immune globulin.

BACKGROUND: Although young women who are D- occasionally receive unintentional transfusions with D+ red blood cells (RBCs), there are little data to assist with management of such an event. Two cases of D- girls transfused with D+ RBCs are reported. In an effort to prevent formation of anti-D, RBC exchange followed by administration of intravenous (IV) Rh immune globulin (RhIg) was used. CASE REPORTS: Patient 1, a 56-kg, 16-year-old D- girl, was involved in a motor vehicle crash. She received 4 units of Group O uncrossmatched D+ RBCs. Thirty-six hours after admission, she underwent RBC exchange with 10 units of D- RBCs, followed by a total of 2718 microg of IV RhIg over 32 hours. Six months later, her antibody screen was negative. Patient 2, a 39-kg, 10-year-old D- girl with aplastic anemia, received 1 unit of D+ RBCs. She underwent RBC exchange on the same day with 5 units of D- RBCs, followed by a total of 900 microg of IV RhIg over 8 hours. Six months later her antibody screen was negative. CONCLUSION: RBC exchange followed by a calculated dose of IV RhIg was successful in preventing allo-immunization to D. Several small studies suggest that both trauma and hematology patients may be less capable of becoming immunized with the transfusion of D+ blood components. Until these findings are more clearly defined, there will be times when prevention of immunization of any D- girl is desired. RBC exchange followed by RhIg appears to be one way to achieve this goal.

Adolescent↗

Epithelial cyclooxygenase-2 expression: a model for pathogenesis of colon cancer.

BACKGROUND: Recent studies indicate a close relationship between cyclooxygense-2 (COX-2) expression and the pathogenesis of colorectal cancer, yet little information exists regarding the stimuli and pathways involved in COX-2 expression by the colonic epithelium. We studied the induction of COX-2 in response to such environmental stress as hyperosmolarity and lipopolysaccharide (LPS) in a human colon cell line. We further investigated the transduction cascades mediating COX-2 expression, focusing upon the mitogen-activated protein kinase pathways p38 and extracellular signal-regulated kinase (ERK). MATERIALS AND METHODS: Human colon cancer cells (Caco-2) were stimulated with increasing concentrations of sodium chloride (NaCl) or LPS. Total protein was extracted at different time points and subjected to Western blot analysis with antibodies to human COX-2, COX-1, or phospho-specific antibodies to ERK and p38. RESULTS: LPS failed to induce COX-2 or COX-1 expression. Hyperosmolarity induced COX-2 expression by 2 h, with peak levels occurring at 6-8 h. NaCl at 40 and 100 mM induced a 2-fold and more than 50-fold increase in COX-2 expression, respectively; COX-1 expression was not affected. Hyperosmolarity induced both p38 and ERK activation within 30 min; however, only p38 inhibition attenuated osmotic-induced COX-2 expression; inhibition of ERK activation had no effect. CONCLUSIONS: Increase in osmolarity activates p38 and induces COX-2 expression in the colonic epithelium. The lack of response to LPS is teleologically expected of the colonic epithelium that is in constant contact with the fecal bacteria. This model also predicts that an increase in luminal osmolarity in the colon may induce COX-2 and thereby promote a neoplastic phenotype.

Carcinoma↗

Relationship between trauma center volume and outcomes.

CONTEXT: The premise underlying regionalization of trauma care is that larger volumes of trauma patients cared for in fewer institutions will lead to improved outcomes. However, whether a relationship exists between institutional volume and trauma outcomes remains unknown. OBJECTIVE: To evaluate the association between trauma center volume and outcomes of trauma patients. DESIGN: Retrospective cohort study. SETTING: Thirty-one academic level I or level II trauma centers across the United States participating in the University Healthsystem Consortium Trauma Benchmarking Study. PATIENTS: Consecutive patients with penetrating abdominal injury (PAI; n = 478) discharged between November 1, 1997, and July 31, 1998, or with multisystem blunt trauma (minimum of head injury and lower-extremity long-bone fractures; n = 541) discharged between June 1 and December 31, 1998. MAIN OUTCOME MEASURES: Inpatient mortality and hospital length of stay (LOS), comparing high-volume (>650 trauma admissions/y) and low-volume (</=650 admissions/y) centers. RESULTS: After multivariate adjustment for patient characteristics and injury severity, the relative odds of death was 0.02 (95% confidence interval [CI], 0.002-0.25) for patients with PAI admitted with shock to high-volume centers compared with low-volume centers. No benefit was evident in patients without shock (P =.50). The adjusted odds of death in patients with multisystem blunt trauma who presented with coma to a high-volume center was 0.49 (95% CI, 0.26-0.93) vs low-volume centers. No benefit was observed in patients without coma (P =.05). Additionally, a shorter LOS was observed in patients with PAI and New Injury Severity Scores of 16 or higher (difference in adjusted mean LOS, 1.6 days [95% CI, -1.5 to 4.7 days]) and in all patients with multisystem blunt trauma admitted to higher-volume centers (difference in adjusted mean LOS, 3.3 days [95% CI, 0.91-5.70 days]). CONCLUSIONS: Our results indicate that a strong association exists between trauma center volume and outcomes, with significant improvements in mortality and LOS when volume exceeds 650 cases per year. These benefits are only evident in patients at high risk for adverse outcomes.

Academic Medical Centers↗

Antioxidants in critical illness.

Oxidative stress has been implicated in the manifestations of critical illnesses, including ischemia and reperfusion injury and systemic inflammatory states. This review describes the evidence for increased oxidative stress in critically ill patients and explores the data regarding antioxidant therapy for these conditions. Antioxidant therapies reviewed include N-acetylcysteine, selenium, vitamins E and C, superoxide dismutase, catalase, lazaroids, and allopurinol. We focus on the results of these interventions in animal models and human trials, when available.

Animals↗

Ethanol abuse and the trauma patient.

BACKGROUND: Alcohol intoxication has long been associated with an increased risk of injury from a number of mechanisms and with trauma recidivism. It is less certain whether alcohol abuse is associated with worse outcomes for a given degree of injury. METHODS: Review of the pertinent English-language literature. RESULTS: The vasodilator effects of alcohol may hamper fluid resuscitation, especially in head-injured patients. Acute and chronic alcohol intoxication both have substantial effects on the cellular and molecular responses necessary to fight infection. High alcohol concentrations exert an immunosuppressive effect on production of proinflammatory cytokines such as tumor necrosis factor and interleukin-1. However, the clinical effects of the immunosuppression are variable and difficult to discern in heterogeneous trauma patient populations with variable degrees of intoxication. CONCLUSION: Alcohol has a profound impact on the epidemiology of injury, but the physiology and biochemical effects in an individual patient may be difficult to predict. Identification of intoxicated persons is essential, despite economic disincentives to do so, because even brief targeted intervention programs can decrease substantially the patient's risk of subsequent injury.

Alcohol-Related Disorders↗

Payer status: the unspoken triage criterion.

BACKGROUND: The cost of uncompensated trauma care is a significant barrier to trauma system development. Trauma center designation may burden an institution with an unprofitable mix of underinsured, severely injured patients. Concerns about inadequate reimbursement may motivate interhospital transfers on the basis of insurance status rather than medical necessity, potentially undermining the effectiveness of the system. We set out to explore whether this phenomenon exists in a mature trauma system. METHODS: Trauma patients receiving definitive care at Level III or IV trauma centers were compared with patients transferred from these centers to the only Level I regional center. Insurance status was classified as either commercial or noncommercial. Logistic regression was used to determine the independent predictors of transfer after adjusting for differences in injury severity. RESULTS: Only 12% of 2,008 patients initially evaluated at Level III/IV centers were transferred to the Level I center, an indicator of the effectiveness of prehospital triage protocols in the region. The presence of specific complex injuries, younger age, male gender, and insurance status were all associated with an increased likelihood of transfer. Insurance status was an independent predictor of transfer: patients without commercial insurance were 2.4 (95% confidence interval, 1.6-3.6) times more likely to be transferred to a Level I facility than patients with commercial insurance after adjusting for differences in injury severity. CONCLUSION: Insurance status influences the decision to transfer to higher levels of care. These findings suggest that the financial burden of a trauma system may be inequitably distributed. This inequitable distribution may be necessary for trauma system sustainability and calls for the development of disproportionate reimbursement strategies to support regional referral centers.

Adolescent↗

Stapled versus sutured gastrointestinal anastomoses in the trauma patient: a multicenter trial.

BACKGROUND: Construction of gastrointestinal anastomoses utilizing stapling devices has become a familiar procedure. In elective surgery, studies have shown no significant differences in complications between stapled and sutured anastomoses. Controversy has recently arisen regarding the accurate incidence of complications associated with anastomoses in the trauma patient. The objective of this multi-institutional study was to determine whether the incidence of postoperative complications differs between stapled and sutured anastomoses following the emergent repair of traumatic bowel injuries. METHODS: Using a retrospective cohort design, all trauma registry records from five Level I trauma centers over a period of 4 years were reviewed. RESULTS: A total of 199 patients with 289 anastomoses were identified. A surgical stapling device was used to create 175 separate anastomoses, while a hand-sutured method was employed in 114 anastomoses. A complication was defined as an anastomotic leak verified at reoperation, an intra-abdominal abscess, or an enterocutaneous fistula. The mean abdominal Abbreviated Injury Scale score and Injury Severity Score were similar in the two cohort groups. Stapling and suturing techniques were evenly distributed in both small and large bowel repairs. Seven of the total 175 stapled anastomoses and none of the 114 hand-sewn anastomoses resulted in a clinically significant leak requiring reoperation (RR = undefined, 95% CI 1.08-infinity, p = 0.04). Each anastomotic leak occurred in a separate individual. Nineteen stapled anastomoses and four sutured anastomoses were associated with an intra-abdominal abscess (RR = 2.7, 95% CI 0.96-7.57, p = 0.04). Enterocutaneous fistula formation was not statistically associated with either type of anastomoses (stapled cohort = 3 of 175 and sutured cohort = 2 of 114). Overall, 22 (13%) stapled anastomoses and 6 (5%) sutured anastomoses were associated with an intra-abdominal complication (RR = 2.08, 95% CI 0.89-4.86, p = 0.076). CONCLUSION: Anastomotic leaks and intra-abdominal abscesses appear to be more likely with stapled bowel repairs compared with sutured anastomoses in the injured patient. Caution should be exercised in deciding to staple a bowel anastomosis in the trauma patient.

Adolescent↗

The relationship between trauma center volume and outcome.

In spite of the limited direct evidence available, increasing data support a positive volume-outcome association in trauma care. When coupled with the extensive indirect data suggesting that regions with organized systems of trauma care are associated with lower trauma-related mortality rates than regions where the number of centers and their level of commitment are unlimited and untested, there is little doubt that experience improves outcome and that volume plays a critical role in the accrual of experience. Although regionalization of trauma care has the inevitable consequence of increased prehospital transport times, particularly in rural areas remote from large trauma centers, some states have designed inclusive systems where a large number of smaller centers have been verified and designated as lower level trauma centers (i.e., level 3-5). The process of trauma center verification holds these smaller volume centers to a standard of care such that the quality of care of the trauma patient may exceed that of other, less-regulated aspects of medical or surgical care. Several reports have suggested that trauma outcomes in smaller rural level 3 centers or centers with dedicated trauma programs with appropriate, functional triage protocols are comparable to national norms, thus reflecting the importance of commitment to outcome. These data suggest that quality of care does not only follow volume, particularly when stipulations and requirements are clear regarding the process of care and ongoing quality assurance.

Hospital Mortality↗

The effect of organized systems of trauma care on motor vehicle crash mortality.

CONTEXT: Despite calls for wider national implementation of an integrated approach to trauma care, the effectiveness of this approach at a regional or state level remains unproven. OBJECTIVE: To determine whether implementation of an organized system of trauma care reduces mortality due to motor vehicle crashes. DESIGN: Cross-sectional time-series analysis of crash mortality data collected for 1979 through 1995 from the Fatality Analysis Reporting System. SETTING: All 50 US states and the District of Columbia. SUBJECTS: All front-seat passenger vehicle occupants aged 15 to 74 years. MAIN OUTCOME MEASURES: Rates of death due to motor vehicle crashes compared before and after implementation of an organized trauma care system. Estimates are based on within-state comparisons adjusted for national trends in crash mortality. RESULTS: Ten years following initial trauma system implementation, mortality due to traffic crashes began to decline; about 15 years following trauma system implementation, mortality was reduced by 8% (95% confidence interval [CI], 3%-12%) after adjusting for secular trends in crash mortality, age, and the introduction of traffic safety laws. Implementation of primary enforcement of restraint laws and laws deterring drunk driving resulted in reductions in crash mortality of 13% (95% CI, 11%-16%) and 5% (95% CI, 3%-7%), respectively, while relaxation of state speed limits increased mortality by 7% (95% CI, 3%-10%). CONCLUSIONS: Our data indicate that implementation of an organized system of trauma care reduces crash mortality. The effect does not appear for 10 years, a finding consistent with the maturation and development of trauma triage protocols, interhospital transfer agreements, organization of trauma centers, and ongoing quality assurance.

Accidents, Traffic↗

Hypertonic saline solution induces prostacyclin production by increasing cyclooxygenase-2 expression.

BACKGROUND: Previously, we demonstrated that hypertonic saline solution (HTS) and endotoxin (lipopolysaccharide [LPS]) induce prostacyclin (PGI(2)) production in human endothelial cells. Here, we hypothesized that HTS and LPS may induce PGI(2) production by increasing cyclooxygenase (COX) expression. We further examined the activation of p38 and extracellular signal-regulated kinases (ERK) and questioned whether these transduction cascades might mediate COX expression. METHODS: Human umbilical vein endothelial cells were stimulated with varying concentrations of NaCl or LPS. RESULTS: HTS and LPS induced prompt activation of both p38 and ERKs that peaked at 30 minutes. HTS and LPS also induced a dose-related increase in COX-2 with maximal expression within 4 to 6 hours; there was no change in COX-1. This correlated with an increase in supernatant PGI(2) levels, which became statistically significant for NaCl of more than 40 mmol/L and for all LPS doses. The inhibition of p38 with SB202190 abrogated the osmotic and LPS-induced COX-2 expression and PGI(2) production. Inhibition of ERK activation had no effect on COX-2 expression. CONCLUSIONS: Hyperosmolarity and LPS induce, in chronologic order, p38 and ERK activation, COX-2 expression, and PGI(2) production. Because COX is the rate-limiting enzyme in prostaglandin synthesis, it is likely that the increase in PGI(2) production is due to, at least in part, the increased COX-2 expression. The data also suggest that p38 mitogen-activated protein kinase is involved in the signaling cascade for COX-2 expression.

Cell Survival↗

Pathogenesis of multiple organ dysfunction syndrome--endotoxin, inflammatory cells, and their mediators: cytokines and reactive oxygen species.

Multiple organ dysfunction syndrome (MODS) is caused by an overwhelming, uncontrolled systemic inflammatory response that is activated by a number of hostile stimuli including sepsis, hypovolemic shock, and severe trauma resulting in massive tissue injury. The indiscriminate activation of the inflammatory response due to these insults causes loss of the host's ability to localize the inflammation to the focus of the problem, leading to systemic inflammation and severe host tissue damage and subsequent MODS. While the major players, namely neutrophils, macrophages, endotoxin, cytokines, and oxidants have been known for some time, the disease processes responsible for the pathogenesis of MODS have only recently been elucidated. Our newly found knowledge has resulted in the development of novel therapeutic strategies to prevent or treat MODS, such as scavenging toxic oxygen species and inhibiting endotoxin, or cytokine production, or cytokine activity. Unfortunately, these strategies have not resulted in improved mortality rates among patients with MODS. The complex nature of the host response to severe insults combined with the fact that the host has multiple, redundant parallel systems to deal with various insults has made it difficult for clinical interventions to adequately ameliorate the disease process among patients at risk for MODS. The purpose of this article is to attempt to "dissect out" several individual components of the inflammatory response that play important roles in the development of MODS and to review some potentially beneficial approaches to combat these harmful processes.

Animals↗

Lipid mediators in the pathophysiology of critical illness.

Inflammatory lipid mediators are produced by the metabolism of membrane phospholipids following a number of different stimuli. These mediators lead to a variety of cellular and systemic responses which contribute to the manifestations of the systemic inflammatory response syndrome in the critically ill patient. These mediators include platelet-activating factor and the eicosanoids, including prostaglandins, thromboxanes, leukotrienes, and HETEs. This review seeks to evaluate the current role of these mediators in the pathophysiology of critical illness. We will focus on recent studies concerning the modulation of these pathways as a potential therapeutic strategy for management of these critically ill patients. This includes the gamut from nutritional strategies to alter the cellular membrane lipid composition, thereby effecting the substrate available to produce these lipid byproducts, to intracellular inhibitors to alter production of these mediators, to receptor blockage and enhanced clearance to inhibit their effects.

Cell Membrane↗

Effectiveness of state trauma systems in reducing injury-related mortality: a national evaluation.

BACKGROUND: Regional trauma systems were proposed 2 decades ago to reduce injury mortality rates. Because of the difficulties in evaluating their effectiveness and the methodologic limitations of previously published studies, the relative benefits of establishing an organized system of trauma care remains controversial. METHODS: Data on trauma systems were obtained from a survey of state emergency medical service directors, review of state statutes and a previously published trauma system inventory. Injury mortality rates were obtained from national vital statistics data, whereas motor vehicle crash (MVC) mortality rates were obtained from the Fatality Analysis Reporting System. Mortality rates were compared between states with and without trauma systems. RESULTS: As of 1995, 22 states had regional trauma systems. States with trauma systems had a 9% lower crude injury mortality rate than those without. When MVC-related mortality was evaluated separately, there was a 17% reduction in deaths. After controlling for age, state speed laws, restraint laws, and population distribution, there remained a 9% reduction in MVC-related mortality rate in states with a trauma system. CONCLUSION: These data demonstrate that a state trauma system is associated with a reduction in the risk of death caused by injury. The effect is most evident on analysis of MVC deaths.

Accidents, Traffic↗

Sympathectomy for causalgia: experience with military injuries.

BACKGROUND: Causalgia is a rare disease in civilian practice, and most reports regarding causalgia in the literature are from major extended wars. To increase awareness of this syndrome, our wartime experience with this disease is presented. METHODS: The charts of patients with causalgia referred to two university hospitals for treatment from 1985 to 1989 were retrospectively studied. Characteristics of the cause, clinical manifestations, and the response to therapy were evaluated. RESULTS: Among 1,564 patients with peripheral nerve injuries, there were 54 cases (3.4%) of causalgia. All of the patients, except five, were injured in battle by high-velocity bullets or missiles. Upper extremities were involved in 28 patients (52 %) and lower extremities in 26 patients (48%). The most common presenting symptoms were as follows: burning pain, 100%; wet extremity, 100%; cold extremity, 93%; sensitivity to cold, 89%; paresthesia, 78%; and color changes in the extremities, 55%. In 48 patients (89%), pain was relieved by sympathetic block (3 patients had permanent cure). Six patients had no response to the blocks (11%). Of 45 patients who had temporary relief, all underwent sympathectomy. All of these patients had complete relief of symptoms in the immediate postoperative period and for follow-up from 1 to 6 years. CONCLUSION: Causalgia is essentially a war casualty disease. The condition is associated with burning pain, hyperesthesia, and symptoms of sympathetic overactivity. Sympathectomy is effective and the treatment of choice, particularly for patients who respond temporarily to sympathetic blocks.

Adolescent↗