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Biomedical subjects

W J Meggs

Publications and source records attributed to W J Meggs.

At least 19 recordsLinked to original sources
PubMed2001

A controlled trial of topical nitroglycerin in a New Zealand white rabbit model of brown recluse spider envenomation.

STUDY OBJECTIVES: Topical nitroglycerin has been reported to prevent skin necrosis from brown recluse spider bites, but this has never been scientifically tested. This study attempts to assess the effects of topical nitroglycerin on experimental Loxosceles reclusa envenomations. METHODS: We performed a randomized, blinded, controlled study in an animal care facility. Twenty-four New Zealand white rabbits were experimentally envenomated by means of subcutaneous injection with 20 microg of brown recluse spider venom. Rabbits were randomized to 1 of 2 experimental groups. The treatment group received 1 in of 2% topical nitroglycerin ointment every 6 hours for 3 days applied directly to the envenomation site. The control group received the vehicle without nitroglycerin. Gross examination of the lesions and measurements of the areas of the lesions were made daily. Creatine phosphokinase (CPK), blood urea nitrogen, creatinine, hemoglobin, and hematocrit levels were measured on days 0, 5, and 10. Lesions were excised after 10 days and examined by a blinded pathologist, who measured the area of necrosis and quantified inflammation and edema using a standard wound-healing score. For all values, mean values plus SD were determined. All comparisons made over multiple time points were assessed for significance by using a repeated-measures analysis of variance followed by Fisher least significant difference and Scheffé post hoc comparisons. A P value of.05 or less was used to determine significance. The Student's t test was used to compare the means of single measures. Significance was determined by using 95% confidence intervals. Comparisons of total area of necrosis were made with the nonparametric Mann-Whitney U test because of the heavy positive skew of the data. RESULTS: Skin necrosis developed in all animals. Mean values of the lesion area were not significantly different over time between the 2 groups of animals. At day 10, the median area of necrosis was 22.3 cm2 for the treatment group and 15.4 cm2 for the control group (P =.12). The inflammation score was 3.33+/-0.78 for the treatment group and 2.79+/-1.29 for the control group (P < .01). The edema score was 1.25+/-1.28 for the treatment group and 0.98+/-1.10 for the control group (not significantly different). CPK levels increased dramatically in both groups, with the greatest increase in the treatment group. In both groups hemoglobin and hematocrit levels decreased significantly, whereas WBC counts and platelet counts increased significantly, without significant differences between the 2 groups. CONCLUSION: At the dose used in this experiment, topical nitroglycerin did not prevent skin necrosis, increased inflammation score, and increased serum CPK levels. The results of this study do not support the use of topical nitroglycerin in the treatment of L reclusa envenomation and suggest that systemic toxicity could be increased.

Administration, Cutaneous↗
PubMed1999

Emergency department hemodialysis in a case of severe ethylene glycol poisoning.

A 36-year-old man with a history of depression presented to the emergency department after ingesting approximately 3,000 mL of ethylene glycol antifreeze in a suicide attempt. The patient's ethylene glycol concentration, 1,889 mg/dL, was higher than any level previously documented in the medical literature. Although his course was complicated by nausea, emesis, lethargy, metabolic acidosis, and kidney failure, the patient survived without persistent kidney failure or other chronic problems. Sustained hemodialysis and ethanol infusion were instituted in the ED, on the basis of the patient's history, before laboratory confirmation of the ingestion was obtained.

Adult↗
PubMed1999

Trends in emergency department utilization, 1988-1997.

OBJECTIVES: To study changes in ED utilization over a ten-year period; and to try to identify factors that affect utilization. METHODS: This study was conducted in a university-affiliated rural tertiary referral center in a stage 1 managed care market, providing primary emergency services to a county of 120,000 and tertiary services to a 29-county area with 1.2 million people. The year of visit, time of visit, level of care required, length of stay (LOS), and admission status were entered into a computer database for each ED visit. RESULTS: Over the period from 1988 to 1997, the population grew by 18.7%. Over the same time period, the number of ED visits grew 27%. By regression analysis, the number of ED visits was directly related to the size of the service population (correlation coefficient 0.97). During the study period, patient acuity increased, with urgent visits increasing from 45% to 52% while nonurgent visits declined from 55% to 48%. Percentage of patients admitted increased from 14% in 1989 to 20% in 1997. Percentage of patients with LOS exceeding six hours also increased, from 8% in 1989 to 16% in 1997. CONCLUSIONS: For the study hospital there was a direct relationship between the ED utilization and population size as well as a historical trend toward increased patient acuity. These trends quantified at one hospital may reflect trends occurring throughout the United States that would affect ED staffing, space, and resource needs.

Emergency Medical Services↗
PubMed1998

Biological homing: hypothesis for a quantum effect that leads to the existence of life.

In biological systems, complex molecules interact with specificity and rapidity. The hypothesis is advanced that there are complementary sites on the surfaces of pairs of biological molecules with an enhanced attraction due to quantum mechanics. I postulate that a biological homing effect arises from the quantum mechanical probability that complementary pairs of molecules will join, and that this phenomenon is the force that drives biology and gives rise to the existence of life. To illustrate the approach, a simplified calculation is given for the interaction cross-section between two molecules, each with N surface charges that have an identical spatial distribution but with paired charges having opposite signs. The resulting cross-section is enhanced by a factor of N2 over the coulomb-scattering cross-section for a single pair of charges. We hypothesize that the existence of life is a direct and inevitable consequence of the principles presented here.

Macromolecular Substances↗
PubMed1998

Fatality resulting from intraventricular vincristine administration.

BACKGROUND: Inadvertent intrathecal administration of vincristine has been reported and is uniformly fatal except in two of three cases treated with spinal fluid exchange. We report a case of inadvertent direct intraventricular vincristine administration. CASE REPORT: A 59-year-old woman developed acute lymphocytic leukemia with meningeal involvement and was being treated with intraventricular cytarabine (beta-cytosine arabinoside, Ara-C) injected via an Ommaya reservoir, intravenous (i.v.) vincristine, prednisone, and i.v. daunorubicin. The vincristine (2 mg in 10 mL diluent) was inadvertently injected into her Ommaya reservoir. Within 10 minutes, the error was realized. Despite optimal care, nausea and vomiting developed the first night, followed sequentially by coarse tremor, disorientation, horizontal nystagmus, and stupor. Her mental status waxed and waned until day 9, at which time she became responsive only to noxious stimuli. By day 11, she was deeply comatose and on day 40 she died without regaining any neurological function. CONCLUSION: Despite aggressive and immediate therapy, intraventricular vincristine infusion produced neurologic toxicity, with progressive loss of mental function, followed by coma and death. Systems need to be developed to prevent inadvertent central nervous system administrations.

Antineoplastic Agents, Phytogenic↗
PubMed1997

Hypothesis for induction and propagation of chemical sensitivity based on biopsy studies.

The reactive airways dysfunction syndrome (RADS), the reactive upper airways dysfunction syndrome (RUDS), the sick building syndrome (SBS), and the multiple chemical sensitivity syndrome (MCS) are overlapping disorders in which there is an intolerance to environmental chemicals. The onset of these illnesses is often associated with an initial acute chemical exposure. To understand the pathophysiology of these conditions, a study of the nasal pathology of individuals experiencing these syndromes was undertaken. Preliminary data indicate that the nasal pathology of these disorders is characterized by defects in tight junctions between cells, desquamation of the respiratory epithelium, glandular hyperplasia, lymphocytic infiltrates, and peripheral nerve fiber proliferation. These findings suggest a model for a relationship between the chronic inflammation seen in these conditions and an individual's sensitivity to chemicals. A positive feedback loop is set up: the inflammatory response to low levels of chemical irritants is enhanced due to the observed changes in the epithelium, and the epithelial changes are propagated by the inflammatory response to the chemicals. This model, combined with the concept of neurogenic switching, has the potential to explain many aspects of RADS, RUDS, SBS, and MCS in a unified way.

Biopsy↗
PubMed1997

Neurogenic inflammation: with additional discussion of central and perceptual integration of nonneurogenic inflammation.

The Working Group on Neurogenic Inflammation proposed 11 testable hypotheses in the three domains of neurogenic inflammation, perceptual and central integration, and nonneurogenic inflammation. The working group selected the term people reporting chemical sensitivity (PRCS) to identify the primary subject group. In the domain of neurogenic inflammation, testable hypotheses included: PRCS have an increased density of c-fiber neurons in symptomatic tissues; PRCS produce greater quantities of neuropeptides and prostanoids than nonsensitive subjects in response to exposure to low-level capsaicin or irritant chemicals; PRCS have an increased and prolonged response to exogenously administered c-fiber activators such as capsaicin; PRCS demonstrate augmentation of central autonomic reflexes following exposure to agents that produce c-fiber stimulation; PRCS have decreased quantities of neutral endopeptidase in their mucosa; exogenous neuropeptide challenge reproduces symptoms of PRCS. In the domain of perceptual and central integration, testable hypotheses included: PRCS have alterations in adaptation, habituation, cortical representation, perception, cognition, and hedonics compared to controls; the qualitative and quantitative interactions between trigeminal and olfactory systems are altered in PRCS; higher integration of sensory inputs is altered in PRCS. In the domain of nonneurogenic inflammation, testable hypotheses included: increased inflammation is present in PRCS in symptomatic tissues and is associated with a heightened neurosensory response; PRCS show an augmented inflammatory response to chemical exposure. The working group recommended that studies be initiated in these areas.

Chemoreceptor Cells↗
PubMed1997

Effects of Prussian blue and N-acetylcysteine on thallium toxicity in mice.

BACKGROUND: Thallium poisoning is now rare but still occurs as a result of homicide attempts. Prussian blue's efficacy in the treatment of experimental thallium poisoning has been demonstrated in animal models, and its use in humans is supported by anecdotal data. Since thallium binds sulfhydryl groups, the use of N-acetylcysteine is also considered as a potential antidote. STUDY OBJECTIVE: To compare the efficacy of Prussian blue and N-acetylcysteine in a murine model of thallium poisoning. METHODS: Female Swiss albino mice with free access to food and water were used. Two study doses of thallium, given as a subcutaneous injection of thallium acetate dissolved in sterile water, were chosen: 70 mg/kg (LD90) and 85 mg/kg (> LD100). A randomized, placebo controlled study was conducted with survival at 120 h chosen as the outcome measure. Four treatment groups were studied: control, Prussian blue, N-acetylcysteine, and the combination of Prussian blue and N-acetylcysteine. Prussian blue was dissolved in water and given by oral gavage at a dose of 50 mg/kg. N-acetylcysteine was diluted in normal saline and given as intraperitoneal injections of 200 mg/kg. Sterile water by gavage and normal saline by peritoneal injection were given as control treatments whenever an active agent was not given. Survival was recorded over a 120 h study period and compared at 120 h by a Fisher's exact test. RESULTS: At 120 h following subcutaneous injection of thallium 70 mg/kg, only 10% of the control animals survived. Treatment with N-acetylcysteine or Prussian blue increased survival to 35% (p = 0.13) and 50% (p = 0.014), respectively. The addition of N-acetylcysteine to Prussian blue offered no benefit over Prussian blue therapy alone. CONCLUSIONS: Prussian blue was found to decrease mortality from thallium poisoning at a dose equal to the LD90 in this model, but not a dose greater than the LD100. No role for N-acetylcysteine in the treatment of thallium poisoning was demonstrated by this study.

Acetylcysteine↗
PubMed1996

Nasal pathology and ultrastructure in patients with chronic airway inflammation (RADS and RUDS) following an irritant exposure.

BACKGROUND: Reactive airways dysfunction syndrome is a chronic asthma-like condition developing after an acute irritant exposure, and chronic inflammation has been seen on endobronchial biopsy. Reactive upper-airways dysfunction syndrome is chronic rhinitis developing in temporal association with a toxic inhalation exposure, but the pathophysiology is unknown. OBJECTIVES: To study biopsies of the nasal mucosa in patients with reactive upper-airways dysfunction syndrome and in some cases reactive airways dysfunction syndrome developing in temporal association with a chlorine dioxide exposure, to see if a histologic basis for the persistent rhinitis and sensitivity to chemical irritants could be determined. METHODS: Specimens were stained with hematoxylin-eosin and immunoperoxidase stains for substance P, vasointestinal peptide, and S-100 (nerve fibers), and fixed in glutaraldehyde for electron microscopy. Biopsies of three nonexposed subjects were performed for comparison. A pathologist blinded to clinical data interpreted the specimens. RESULTS: Inflammation ratings of exposed individuals were higher than for the nonexposed individuals. The number of nerve fibers stained was greater for patients vs controls. Substance P and vasointestinal peptide staining was nonspecific. Electron microscopy showed desquamation of the epithelium and permeability of epithelial cell junctions. CONCLUSION: This study suggests a mechanism by which ongoing low level exposures perpetuate airway inflammation after an inducing toxic inhalation. A possible overlap between reactive airways dysfunction syndrome, reactive upper-airway dysfunction syndrome and the multiple chemical sensitivity syndrome is suggested.

Adult↗
PubMed1995

Neurogenic switching: a hypothesis for a mechanism for shifting the site of inflammation in allergy and chemical sensitivity.

Neurogenic switching is proposed as a hypothesis for a mechanism by which a stimulus at one site can lead to inflammation at a distant site. Neurogenic inflammation occurs when substance P and other neuropeptides released from sensory neurons produce an inflammatory response, whereas immunogenic inflammation results from the binding of antigen to antibody or leukocyte receptors. There is a crossover mechanism between these two forms of inflammation. Neurogenic switching is proposed to result when a sensory impulse from a site of activation is rerouted via the central nervous system to a distant location to produce neurogenic inflammation at the second location. Neurogenic switching is a possible explanation for systemic anaphylaxis, in which inoculation of the skin or gut with antigen produces systemic symptoms involving the respiratory and circulatory systems, and an experimental model of anaphylaxis is consistent with this hypothesis. Food-allergy-iducing asthma, urticaria, arthritis, and fibromyalgia are other possible examples of neurogenic switching. Neurogenic switching provides a mechanism to explain how allergens, infectious agents, irritants, and possibly emotional stress can exacerbate conditions such as migraine, asthma, and arthritis. Because neurogenic inflammation is known to be triggered by chemical exposures, it may play a role in the sick building syndrome and the multiple chemical sensitivity syndrome. Thus neurogenic switching would explain how the respiratory irritants lead to symptoms at other sites in these disorders.

Environmental Exposure↗
PubMed1995

Multiple chemical sensitivities--chemical sensitivity as a symptom of airway inflammation.

The term multiple chemical sensitivity confuses etiology with diagnosis. Chemical sensitivity is a symptom expressed by patients. The symptoms complex is also expressed by the majority of patients with asthma reactive airway dysfunction syndrome or rhinitis following a single acute exposure, called reactive upper airway dysfunction syndrome. The chemically sensitivity patient merits evaluation for upper airway and bronchial reactivity that may cause extra-airway symptomatology.

Humans↗
PubMed1994

The treatment of lead poisoning from gunshot wounds with succimer (DMSA)

Lead poisoning is an unusual complication of gunshot wounds that occurs when retained lead bullet fragments are in contact with body fluids capable of solubilizing lead. The epidemic of violence by gunfire may result in increasing numbers of lead poisoning cases from this exposure. The use of oral chelation for toxicity resulting from this mode of exposure has not been previously discussed. Cases of lead poisoning arising from bullet lead in the synovial cavity of the hip, synovial cavity of the chest, and pleural space are reported. A combination of surgical debridement and chelation therapy with oral succimer produced a satisfactory outcome in all three cases. Oral succimer may be a safe and effective chelation agent for treating lead toxicity in adults with high lead levels secondary to gun shot wounds.

Adult↗
PubMed1994

RADS and RUDS--the toxic induction of asthma and rhinitis.

Inhalation exposures can produce asthma and rhinitis by several mechanisms. Sensitization with the production of IgE specific for a substance can lead to symptoms on reexposure via mast cell degranulation and the release of inflammatory mediators. Some substances, known as environmental adjuvants, enhance the immune response to concomitant exposures with the environmental adjuvant. Respiratory irritants can lead to asthma and rhinitis through interaction with chemical irritant receptors in the airway, leading to release of substance P from sensory nerves and neurogenic inflammation. The reactive airways dysfunction syndrome is a chronic asthma-like syndrome resulting from a single acute exposure to a respiratory irritant, while the reactive upper-airways dysfunction syndrome is chronic rhinitis stemming from an irritant exposure. The dysregulation of neurogenic inflammation by chemical exposures may be an important mechanism in the toxic induction of reactive airways dysfunction syndrome and reactive upper-airways dysfunction syndrome and may play a role in understanding the sick building syndrome and the multiple chemical sensitivity syndrome.

Asthma↗
PubMed1994

Thallium poisoning from maliciously contaminated food.

Four young adults presented two days after one of them had received marzipan balls packaged in a box from an expensive candy manufacturer. Two ate one candy ball, while two others shared a third. The next day, variable gastrointestinal symptoms developed. On the third day, two patients developed painful paresthesiae of the hands and feet, an early but nonspecific clinical marker of thallium poisoning. A tentative diagnosis of thallium poisoning was made based on symptoms, and treatment was initiated. The remaining candies were radiographed. Metallic densities in the candies supported the diagnosis, and atomic absorption spectroscopy was used to quantitate thallium content. Each candy contained a potentially fatal dose. Five to seven days later, hypertension and tachycardia developed in the two patients who had ingested an entire candy. All patients developed alopecia but recovered without overt neurologic or other sequelae. While the diagnosis of thallium poisoning is often delayed until alopecia develops, an early diagnosis favors an effective treatment strategy.

Adult↗
PubMed1993

Neurogenic inflammation and sensitivity to environmental chemicals.

Neurogenic inflammation as a pathway distinct from antigen-driven, immune-mediated inflammation may play a pivotal role in understanding a broad class of environmental health problems resulting from chemical exposures. Recent progress in understanding the mediators, triggers, and regulation of neurogenic inflammation is reviewed. Evidence for and speculations about a role for neurogenic inflammation in established disorders such as asthma, rhinitis, contact dermatitis, migraine headache, and rheumatoid arthritis are presented. The sick building syndrome and multiple chemical sensitivity syndrome have been defined as clinical entities in which exposure to chemical inhalants gives rise to disease. Current data on the existence of chemical irritant receptors in the airway and skin are discussed; neurogenic inflammation arising from stimulation of chemical irritant receptors is a possible model to explain many of the aspects of chemical sensitivities.

Air Pollutants↗