Spinal cord injury without radiographic abnormality (SCIWORA) in children.

SCIWORA is a syndrome occurring when the spinal cord sustains neural damage during a traumatic event without positive radiographic findings. Anatomic characteristics of the pediatric spine place children at risk for this injury. The injury occurs through extreme flexion, hyperextension, longitudinal distraction or ischemic damage to the spinal cord. Diagnosis is based on MRI findings. Timely diagnosis and stabilization is key to optimizing the child's recovery. Nursing care and evaluation of these children goes beyond the ABCs of resuscitation focusing on astute neurological examination.

A subependymal giant cell astrocytoma in a cat.

A 6-year-old spayed female Domestic Shorthair cat presented with a 1 to 2-month history of blindness and altered behavior. At necropsy, a 1-cm-diameter, firm white mass was found arising from the subependymal region of the right lateral ventricular wall that protruded into and partially filled the lumen. Histologically, there was a well-demarcated, expansile paraventricular neoplasm composed of moderately pleomorphic cells within a richly fibrillar matrix arranged in interlacing streams and perivascular pseudorosette-like patterns. Neoplastic cells varied in morphology from small spindloid cells to larger polygonal cells with eccentric vesicular nuclei to neuronlike cells with vesicular nuclei and prominent nucleoli. The mitotic index was low. Immunohistochemically, neoplastic cells were positive for S-100 protein, glial fibrillary acidic protein, and neuron-specific enolase and negative for neurofilament protein. Ultrastructurally, the cells contained few to abundant bundles of intermediate filaments with variable numbers of mitochondria, endoplasmic reticulum, and ribosomes. These features are characteristic of subependymal giant cell astrocytoma (SEGA) in humans. To our knowledge, this is the first reported case of SEGA in domestic animals.

Case report: a nursing challenge, the unstable pelvic fracture.

A case report is presented that describes the initial care of a severely injured patient who was hemodynamically unstable. The discussion highlights the process used to recognize life-threatening injuries, to differentiate internal sources of hemorrhage, to provide damage-control surgery, and to stop further bleeding with an interventional radiologic examination. The emergency nursing care of a patient with unstable pelvic trauma is included.

Variation among trauma centers' calculation of Glasgow Coma Scale score: results of a national survey.

BACKGROUND: Glasgow Coma Scale (GCS) scoring is enigmatic in intubated patients. To determine if there is consensus among Level I trauma centers, a national telephone survey was conducted. METHODS: Trauma registrars at state-verified or American College of Surgeons-verified Level I trauma centers were questioned about GCS scoring, recording, and reporting in patients who are intubated or intubated and pharmacologically paralyzed. RESULTS: Seventy-three centers were contacted. Seventy-one use initial GCS scores for registry recording. Intubated patients are given 1 point for verbal component plus eye and motor scores at 26% of centers and a total GCS score of 3 at 23%; GCS score is estimated with "T" given for verbal component at 16%, scored as unknown at 10%, always scored as 15 at 10%, and the method of scoring is unknown at 15%. Pharmacologically paralyzed intubated patients are given a total GCS score of 3 at 34%, GCS score is estimated with "T" given for verbal component at 18%, patients are given 1 point for verbal component plus eye and motor scores at 12%, scored as unknown at 11%, always scored as 15 at 8%, and the method of scoring is unknown at 16%. CONCLUSION: Wide variation in GCS scoring among Level I trauma centers was identified. Because GCS scores are used in treatment algorithms, trauma scoring, and outcome prediction (Trauma and Injury Severity Score), uniform scoring is essential and should be pursued. Use of state and national databases and outcome research may be adversely affected by the lack of consistent GCS scoring.

Primitive neuroectodermal tumor in a two-month-old black and white Colobus monkey.

A 2-month-old male black and white Colobus monkey (Colobus guereza kikuyuensis) was euthanatized because of progressive physical deterioration, rear limb paralysis, lymphadenopathy, and the presence of facial and retroperitoneal lumbar masses. At necropsy, soft white masses were present in and around lumbar vertebrae, the subcutis of the face, multiple lymph nodes, and the fourth ventricle of the brain. Histologic and immunohistochemical analysis of these masses revealed a primitive neoplasm with both neuronal and glial differentiation, consistent with a primitive neuroectodermal tumor (PNET) with bipotential differentiation. The extracranial tumors were synaptophysin (SYN)-positive, glial fibrillary acidic protein (GFAP)-negative, and neurofilament protein (NFP)-negative, while the intracranial tumor was SYN-positive, GFAP-positive, and NFP-negative.

Failed rapid sequence intubation in trauma patients: esophageal tracheal combitube is a useful adjunct.

OBJECTIVE: To characterize the use of the esophageal tracheal combitube (ETC) in trauma patients who fail orotracheal rapid sequence intubation (RSI). DESIGN: Prospective protocol design and retrospective chart review. MATERIALS AND METHODS: Flight nurses were trained in the use of the ETC by mannequin simulation, videotape review, and didactic sessions. ETC insertion was attempted after failure of two or more attempts at orotracheal RSI. Over a 12-month period, 12 patients had ETC insertion, and 10 cases qualified for review. Injuries, number of failed orotracheal RSI attempts, definitive airway, initial arterial blood gas results, and outcome were recorded. RESULTS: ETC insertion was successful in all 10 patients in whom it was attempted. Definitive airway control was achieved by conversion to orotracheal intubation in seven patients, emergency department cricothyroidotomy in one patient, and operative room tracheostomy in two patients. No patient died because of failure to control the airway. Seven patients requiring ETC had mandible fractures. CONCLUSION: ETC insertion is an effective method of airway control in trauma patients who fail orotracheal RSI. It may be particularly useful in the patient with maxillofacial trauma and offers a practical alternative to surgical cricothyroidotomy in difficult airway situations.

Esophageal tracheal Combitube in the emergency department.

The Combitube is currently being used in some prehospital cardiac arrest situations and in flight programs for management of airways in trauma patients, as well as in inpatient departments with limited availability to personnel experienced in intubation. The Combitube allows for quick intubation and for continuing airway access while the patient is in the emergency department.

Intubation quality assurance thresholds.

INTRODUCTION: Quality assurance (QA) and continuous quality improvement (CQI) are valued activities within health-care organizations. Quality assurance indicators as guidelines for quality practice usually are established intuitively. The purpose of this study was to determine an appropriate threshold for successful intubation in patients transported by air and to examine factors impacting this success rate. SETTING: Fifteen rotor-wing programs from across the United States participated. METHOD: The study was a prospective descriptive design. A total of 369 flight crew members agreed to participate, and intubations were attempted on 862 patients during the 12-month study. RESULTS: Intubations were attempted on 862 patients and were successful in 788 (91.4%) of the patients. Of the patients not successfully intubated, 14 received supplemental oxygen only, 25 were supported with bag-valve-mask, 26 received a surgical cricothyroidotomy and for nine patients it was unknown what form of airway support was provided. CONCLUSION: Factors impacting successful intubation include cardiac arrest, use of neuromuscular blockade, use of sedatives and facial trauma. Data from the study support a threshold for successful intubation of between 90% and 95%.

Radiation effects of boron neutron capture therapy on brain, skin, and eye of rats.

PURPOSE: The present study was carried out to evaluate the radiation effects of boron neutron capture therapy (BNCT) on the brain, skin, and eyes of nude rats following systemic administration of boronophenylalanine (BPA) and neutron irradiation to the head. METHODS AND MATERIALS: A solution containing 120 mg of 10B-enriched-L-BPA complexed with fructose was administered IP to nude rats. Boron concentrations were approximately 8.4, 9.4, 10.0, and 11.0 micrograms/g in the brain, blood, skin, and eyes, respectively, at 6 h when the animals were irradiated at the Brookhaven Medical Research Reactor (BMRR). As determined in a study carried out in parallel with this one, the BNCT radiation doses were sufficient to cause tumor regression in nude rats carrying intracerebral implants of the human melanoma cell line MRA 27. RESULTS: Mild to moderate increases in loose fibrous tissue were observed in the choroid plexus at estimated physical doses to the brain and blood that ranged from 4.3-7.1 Gy and 4.6-7.7 Gy, respectively, and these appeared to be dose and time dependent. Other changes in the choroid plexus included occasional infiltrates of macrophages and polymorphonuclear leukocytes and vacuolation of epithelial cells. Dose-dependent moist desquamation of the skin was observed in all rats, but this had healed by 28 days following irradiation. Cataracts and keratitis developed in the eyes of most animals, and these were dose dependent. CONCLUSION: The minimal histopathological changes seen in the brain at doses that were sufficient to eradicate intracerebral melanoma indicates that BNCT has the potential to cure a tumor bearing host without producing the normal brain injury usually associated with conventional external beam radiation therapy. Studies in canines, which currently are in progress, should further define the dose-effect relationships of BNCT on critical neuroanatomic structures within the brain.

Growth inhibition of synchronized trigeminal neurinoma cells by nerve growth factor.

Nerve growth factor (NGF) reduces the development of trigeminal neurinomas in vivo. To characterize the action of NGF on these tumors, clonal cells (476-16) isolated from a rat trigeminal neurinoma cell line were synchronized at early S phase by aphidicolin, a reversible inhibitor of DNA polymerase alpha, and effects of NGF on DNA replication were examined in vitro. While NGF did not inhibit DNA replication in the ongoing S phase, it reduced the level of DNA synthesis in the succeeding S phase without altering its timing and duration. The inhibitory action was elicited by a brief exposure to NGF during progression through the preceding S to G1 phases with decreasing effectiveness in the later stage of G1.

Growth inhibition of anaplastic glioma cells by nerve growth factor.

Nerve growth factor (NGF) inhibited cellular DNA synthesis of rat T9 anaplastic glioma cells in a dose-dependent manner in the range of 0.5-5 micrograms/ml. Oxidation of 2 to 3 tryptophan residues of NGF, which had been known to destroy biological and immunological activity, greatly diminished its inhibitory effect on DNA synthesis. The inhibition was also abolished by anti-NGF IgG. Flow cytometric analyses and immunocytochemical assays of DNA synthesis using bromodeoxyuridine incorporation at various times during cell exposure to NGF revealed that the growth inhibition was attributable to gradual accumulation of growth-arrested cells at the G1 phase. Synthesis of nuclear regulatory proteins JUN and p53 was inhibited preferentially and progressively by NGF as inhibition of DNA synthesis increased.

The use of nerve growth factor as a reverse transforming agent for the treatment of neurogenic tumors: in vivo results.

The rationale behind the evaluation of natural differentiating agents, such as nerve growth factor (NGF), for reverse transforming potential is based on the theory that such compounds may represent a nontoxic means of controlling tumor growth. Previous in vitro experiments have shown that NGF is capable of retarding growth and of inducing persistent differentiation of neurogenic tumor cell lines. In vivo, NGF is capable of causing a persistent reduction in the number of ethylnitrosourea-induced neurinomas and of increasing survival time following intracerebral implantation of F98 anaplastic glioma cells. In this study, anaplastic glioma and neurinoma implants were treated with NGF to evaluate the reverse transforming potential of NGF in vivo. Results indicate that NGF is capable of causing a significant decrease in the growth rate of subcutaneous T9 (anaplastic glioma) and clone 16 (anaplastic neurinoma) implants. Significantly, NGF treatment was accompanied by adverse effects that were minimal and transient. Continued tumor growth (although greatly retarded) following NGF treatment is an aspect that requires further investigation. However, the results of this study suggest that NGF may prove useful, alone or in combination with other types of therapy, for the treatment of tumors of neurogenic origin.

ENU-induced in vitro neoplastic transformation of rat mammary epithelial cells.

Normal mammary epithelial cells, originating from female Sprague-Dawley rats, were grown in Dulbecco's Modified Eagles Medium containing 25% horse serum and hormone supplements. Once established as an epithelial cell culture, the cells were treated with N-ethyl-N-nitrosourea (ENU) in various doses (25-500 ug/ml) to study the process of in vitro mammary epithelial cell neoplastic transformation. The ENU-treatment of primary mammary epithelial cell culture resulted in a sequence of phenotypic changes, termed stages I-V. The rat mammary epithelial cells, after a period of approximately 30 days post-ENU exposure, showed a marked proliferation of morphologically altered cells which formed multi-layered colonies. Subsequently, these cells acquired the capacity to form colonies in soft agar and eventually produced a high yield of palpable tumors when inoculated into newborn female isologous hosts or female athymic nude mice. The immediate effect of ENU on these cells was monitored by measurement of cellular DNA content, unscheduled DNA synthesis, cell proliferation and chromosomal aberrations. The ENU effect on cell proliferation and DNA synthesis was dose dependent; doses greater than 100 ug/ml reduced the cell number and DNA synthesis. Cytofluorometric histograms of non-ENU-treated rat mammary epithelial cells showed a near diploid population of cells. The ENU exposed cells subsequently became hyperdiploid (24-72 hours after ENU) and then regained their near diploid pattern at 120 hours after ENU exposure. The ENU-treated cells also showed a second peak of cells with DNA content in the tetraploid and octaploid range at 24-72 hours after ENU exposure. Single chromatid breaks, isochromatid breaks, chromosomal exchanges, multiple chromosomal breaks and double minutes were among the chromosomal aberrations seen in ENU-treated cells. Most of the chromosomal aberrations peaked at 6 hours post-ENU exposure. The ENU-induced model of in vitro meplastic transformation of rat mammary epithelium as described in this communication appears to provide a good model for the systematic study of the early critical cellular events prerequisite to this carcinogenic process.

Chronic toxicity and oncogenicity of inhaled methyl acrylate and n-butyl acrylate in Sprague-Dawley rats.

No exposure-related clinical signs or lesions of systemic toxicity and no oncogenic responses were observed in male and female Sprague-Dawley rats exposed by inhalation to methyl acrylate (MA) or n-butyl acrylate (BA) vapours, at concentrations of 0, 15, 45 and 135 ppm. The rats were whole-body-exposed 6 hr/day, 5 days/wk, for 24 consecutive months. There was a 6-month post-exposure observation period for subgroups of BA-exposed rats. Atrophy of the neurogenic epithelial cells and hyperplasia of reserve cells were observed in the nasal mucosa of all MA- and BA-exposed groups. These changes were dose related and mainly affected the anterior part of the olfactory epithelium. Opacity and neovascularization of the cornea were seen in all MA-exposed groups and in the group exposed to 135 ppm BA. These toxic effects of the olfactory epithelium and cornea were attributed to the known irritancy of MA and BA. In the BA subgroups kept for a 6-month post-exposure observation, reconstructive effects, such as replacement of altered olfactory epithelium with respiratory epithelium, and partial regression of corneal neovascularization were observed.

The reverse transforming effects of nerve growth factor on five human neurogenic tumor cell lines: in vitro results.

The role of nerve growth factor (NGF) in the development, maintenance and regeneration of the mammalian sensory and sympathetic nervous systems has been well characterized, as has the ability of NGF to induce a variety of neoplastic cell lines of neuroecto-dermal (neurogenic) origin to differentiate. The ability to stimulate neoplastic cells of neurogenic origin to differentiate suggests that NGF may prove useful as a reverse transforming agent for the treatment of neurogenic tumors. Five human neurogenic tumor cell lines were evaluated for their response to NGF in vitro to determine whether the NGF is capable of inducing changes consistent with a reverse transforming response. Results indicate that NGF was able to reverse some of the transformed properties of these tumor cell lines, as NGF treatment stimulated neoplastic cells to develop a more differentiated phenotype, diminished or arrested growth, and induced changes that were persistent.

Repeated transplacental transmission of Neospora caninum in dogs.

Four litters of German Shorthaired Pointers from one owner developed a toxoplasmosis-like illness. According to the records, 29 of 39 dogs had hind limb paralysis. Six dogs from 2 litters were necropsied and had generalized encephalomyelitis. Tachyzoites and tissue cysts of Neospora caninum were found in the brain and spinal cord of each dog. Lesions were found in the eyes, extraocular muscles, or both in all of the dogs, and N caninum was detected microscopically in the eyes (retina and choroid in 1 dog), extraocular muscles, or both in 5 of the 6 dogs. Ocular lesions consisted of focal retinitis, choroiditis, mild nonspecific iridocyclitis, and myositis of extraocular muscles. Organisms stained with anti-N caninum serum, but not with anti-Toxoplasma gondii serum in an immunohistochemical test, except in 1 dog. In one dog, aged thick-walled N caninum tissue cysts reacted mildly with anti-T gondii serum.

Characterization of N-nitrosourea-induced tumors of the nervous system; their prospective value for studies of neurocarcinogenesis and brain tumor therapy.

Two decades of research with resorptive neurocarcinogens firmly established the high potency of methyl and ethylnitrosourea (MNU and ENU) as neurocarcinogens, particularly in rats. There are significant differences in susceptibility to these agents among species. There are also differences among age groups. Fetuses are between 50 to 100 times more susceptible than adult rats. One single iv inoculation of 20-50 mg/kg ENU into pregnant rats may produce neurogenic tumors in 100% of the offspring. The tumors produced by these compounds have been well characterized morphologically, biologically, biochemically and histochemically. Tumors produced by both compounds are mostly gliomas and neurinomas (Schwannomas), however, clear differences exist between ENU and MNU produced neoplasms. Transplacental exposure to ENU generally results in a high number of anaplastic neurinomas and mostly differentiated gliomas (astrocytomas, oligodendrogliomas or mixed gliomas). In contrast, multiple exposures of adult rats to MNU result in a moderate number of mostly differentiated neurinomas and a high number of anaplastic gliomas. Tumors usually start out as well differentiated oligodendrogliomas or astrocytomas. As they grow larger, they become more mixed and anaplastic. In contrast to spontaneous gliomas in old rats, MNU and ENU-induced astrocytomas can be readily identified with well established biomarkers such as the S100 protein and particularly GFAP (glial fibrillary acidic protein). Neurinomas are also strongly positive for S100 protein. No reliable markers exist for oligodendrogliomas. Neurogenic tumors induced by MNU or ENU, as well as derived cell lines and clones from such tumors, have been successfully used as models for neurocarcinogenesis and therapeutic screening.(ABSTRACT TRUNCATED AT 250 WORDS)

Immunohistochemical characterization of rat central and peripheral nerve tumors induced by ethylnitrosourea.

Ethylnitrosourea-induced central and peripheral nerve tumors in Sprague-Dawley rats were tested for GFAP (Glial Fibrillary Acidic Protein), S-100 protein, NSE (Neuron Specific Enolase) and Anti-Leu 7 (HNK-1) immunoreactivity utilizing the ABC method (avidin-biotin-complex) for GFAP, S-100 protein and NSE, and the PAP method (peroxidase-antiperoxidase) for Anti-Leu 7. Peripheral nerve neurinomas were consistently positive for S-100 protein and consistently negative for GFAP and Anti-Leu 7. Neurinomas would occasionally exhibit positive staining for NSE (2 of 55 tumors). The staining intensity for S-100 protein varied from strongly positive in differentiated neurinomas to weakly positive in anaplastic tumors. Neoplastic and reactive astrocytes exhibited positive staining for both S-100 protein and GFAP. Variation in the GFAP staining intensity of glial tumors correlated with the degree of differentiation as anaplastic tumors did not stain with the same intensity as their more differentiated counterparts. Oligodendrogliomas exhibited occasional immunoreactivity to S-100 protein (3 of 36 tumors). NSE reactivity in oligodendrogliomas was rarely observed (1 tumor in 36) and immunoreactivity against GFAP or Anti-Leu 7 was consistently absent. Anti-Leu 7 and NSE proved to be of little value in the classification of ENU-induced neural tumors.