Storing methadone in babies' bottles puts young children at risk.
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Biomedical subjects
Publications and source records attributed to C Quinn.
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AIM: This article explores the impact of technology and potential clinical negligence claims on nursing practice. BACKGROUND: Sophisticated procedures and techniques have led to the development of many types of medical device. Many device functions have moved from being one of supporting clinical practice to that of being an integral requirement in treatment delivery. Clinical negligence claims against National Health Service (NHS) Trusts are also likely to spiral significantly over the next 5 years. The Medical Devices Agency cite inadequate training as a main contributing factor to the yearly increase in adverse incident reports they receive. It is these incidents that will potentially provide 'rich pickings' for the ever increasing litigation conscious Great British public, and their lawyers. KEY ISSUES: The challenge for management is how can staff be trained when they are under pressure to maintain a service in the face of staff and skills shortages and increased activity. CONCLUSION: Investment in training schemes that address and minimize the many areas of clinical negligence risk should be explored and introduced as a matter of urgency. The management of infusion systems and a training scheme which is designed to lead staff through a comprehensive competency based generic training in the use of infusion devices is discussed.
OBJECTIVES: To compare four widely used animal models of acute lung injury and to determine the changes in physiologic variables associated with each model. DESIGN: A prospective, controlled animal study. SETTING: An animal laboratory of a university-affiliated children's hospital. SUBJECTS: Four groups of anesthetized, paralyzed, and ventilated young Yorkshire pigs, weighing 35 to 45 kg. INTERVENTIONS: Acute lung injury was generated by four different methods: a) intrapulmonary arterial infusion of endotoxin of Escherichia colt; b) bronchoalveolar instillation of 0.05N of hydrochloric acid; c) repeated bronchoalveolar warm saline lavage; and d) intrapulmonary arterial infusion of oleic acid. After each acute lung injury procedure, the temporal changes in various physiologic variables were measured, starting at 60 mins and at 15-min intervals thereafter for a total of 165 mins. Systemic and mixed venous serum immunoreactive tumor necrosis factor (TNF)-alpha concentrations were also measured at the same time points. Analysis of variance for repeated measures was employed to determine the absolute and relative significance of the changes observed. MEASUREMENTS AND MAIN RESULTS: Systemic and mixed venous immunoreactive TNF-alpha did not change following any of the acute lung injury procedures. The animals' heart rates and systemic vascular resistances also did not change. Hydrochloric acid instillation as well as bronchoalveolar lavage resulted in significant hypoxemia with no other hemodynamic effects. Endotoxin infusion did not result in hypoxemia but caused significant increases in mean pulmonary arterial pressure and pulmonary vascular resistance and decreases in mean arterial pressure and cardiac output. Oleic acid infusion resulted in a marked hypoxemia with a pronounced increase in mean pulmonary arterial pressure and pulmonary vascular resistance. It also markedly reduced the mean arterial pressure, cardiac output, and the mixed venous PO2. CONCLUSIONS: The surfactant depletion and hydrochloric acid instillation models produce acute hypoxemia in an otherwise hemodynamically stable animal. A brief endotoxin infusion provides a model for cardiovascular instability and pulmonary hypertension but fails to produce hypoxemia in the pig. The oleic acid infusion creates a model of marked cardiovascular instability, pulmonary hypertension, and profound hypoxemia. However, none of the acute lung injury models described was associated with the production of tumor necrosis factor.
This study was conducted to compare blood glucose and glucoregulatory hormone responses to the ingestion of solid and liquid carbohydrate (CHO) during prolonged cycling, followed by 30 min of isokinetic cycling. Eight male cyclists randomly completed three cycling trials (LC = liquid CHO, SCE = solid CHO with water equal to LC, SCA = solid CHO + ad libitum water). Each subject cycled for 120 min at 65% of VO2max with CHO ingestion (0.6 g CHO/ kg/hr) at 0, 30, 60, 90, and 120 min. Subjects then completed a 30-min maximal isokinetic ride at 90 rpm. There was no significant (p < .05) difference between the trials for plasma glucose, insulin, glucagon, glycerol, lactate, RER, HR, VO2, RPE, and total work performed during the isokinetic ride. However, serum glucose was significantly lower in the SCE and SCA trials compared to LC at 80 min. The ingestion of a solid food containing CHO, protein, and fat with added water produced similar blood glucose, metabolic, glucoregulatory hormone, and exercise performance responses to those seen with the ingestion of liquid CHO.
Nine consecutive end-stage patients with cystic fibrosis (CF) awaiting lung transplantation were admitted to the pediatric intensive care unit (PICU) in respiratory decompensation. They all received noninvasive bilevel positive airway pressure (BIPAP) support and were evaluated to determine whether or not it improved their oxygenation and provided them with long-term respiratory stability. BIPAP was applied to all patients after a brief period of assessment of their respiratory status. Inspiratory and expiratory positive airway pressures (IPAP, EPAP) were initially set at 8 and 4 cm H2O respectively. IPAP was increased by increments of 2 cm H2O and EPAP was increased by 1 cm H2O increments until respiratory comfort was achieved and substantiated by noninvasive monitoring. Patients were observed in the PICU for 48 to 72 hours and then discharged to home with instructions to apply BIPAP during night sleep and whenever subjectively required. Regular follow-up visits were scheduled through the hospital-based CF clinic. The patients' final IPAP and EPAP settings ranged from 14 to 18 cm H2O and 4 to 8 cm H2O, respectively. All nine patients showed a marked improvement in their respiratory status with nocturnal use of BIPAP at the time of discharge from the PICU. Their oxygen requirement dropped from a mean of 4.6 +/- 1.1 L/min to 2.3 +/- 1.5 L/min (P < 0.05). Their mean respiratory rate decreased from 34 +/- 4 to 28 +/- 5 breaths per minute (P < 0.05). The oxygen saturation of hemoglobin measured by pulse oximetry, significantly increased from a mean of 80% +/- 15% to 91% +/- 5% (P < 0.05). The patients have been followed up for a period of 2 to 43 months and have all tolerated the use of home nocturnal BIPAP without any reported discomfort. Six patients underwent successful lung transplantation after having utilized nocturnal BIPAP for 2, 6, 14, 15, 26, and 43 months, respectively. Three patients have utilized home BIPAP support for 2, 3, and 19 months, respectively, and continue to await lung transplantation. An acute development of refractory respiratory failure resulted in the demise of the remaining three patients after having utilized BIPAP for 3, 6, and 10 months, respectively. The authors conclude that BIPAP therapy improves the respiratory status of decompensating end-stage CF patients. It is well tolerated for long-term home use and provides an extended period of respiratory comfort and stability for CF patients awaiting lung transplantation.
The authors conducted a single-blind study of auricular acupuncture in 36 cocaine-dependent inpatient veterans on a substance abuse treatment unit to determine whether the treatment could help reduce craving, increase treatment retention, and prevent relapse. Acupuncture was given on a predetermined schedule to both treatment and control groups, with status assessed regularly by independent, blinded raters. The study failed to show a significant difference between treatment and control groups. However, the study patients, as a whole, did remain in treatment longer than a retrospectively analyzed group who received no acupuncture.
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Dendritic cells (DC) are potent APCs that enter resting tissues as precursors and, after Ag exposure, differentiate and migrate to draining lymph nodes. The phenotype of RelB knockout mice implicates this member of the NF kappa B/Rel family in DC differentiation. To further elucidate the role of RelB in DC differentiation, mRNA, intracellular protein expression, and DNA binding activity of RelB were examined in immature and differentiated human DC, as well as other PB mononuclear cell populations. RelB protein and mRNA were detected constitutively in lymphocytes and in activated monocytes, differentiated DC, and monocyte-derived DC. Immunohistochemical staining demonstrated RelB within the differentiated lymph node interdigitating DC and follicular DC, but not undifferentiated DC in normal skin. Active nuclear RelB was detected by supershift assay only in differentiated DC derived from either PB precursors or monocytes and in activated B cells. These RelB+ APC were potent stimulators of the MLR. The data indicate that RelB expression is regulated both transcriptionally and post-translationally in myeloid cells. Within the nucleus, RelB may specifically transactivate genes that are critical for APC function.
PURPOSE: The purpose of this study was to investigate the effects of various intravenous anesthetics on intracranial pressure (ICP) and cerebral perfusion pressure (CPP) in two models of brain edema in a prospective study in a Pediatric critical care animal laboratory in a university hospital. MATERIALS AND METHODS: Intraparenchymal ICP monitors were inserted in 30 anesthetized adult cats. In 15 cats, an intraparenchymal balloon-tipped catheter was placed and inflated to create a space-occupying lesion (SOL) to mimic vasogenic brain edema (VBE). In the other 15 cats, cytotoxic brain edema (CBE) was created by an acute reduction in blood osmolality. We used continuous hemodiafiltration (CAVH-D) and replaced the ultrafiltrate with hypotonic solution to maintain euvolemia. At predetermined points, each cat in each model received multiple intravenous (i.v.) injections of one of the following medications: methohexital 1.5 mg/kg, propofol 2 mg/kg, or ketamine 2 mg/kg. ICP and mean arterial pressure (MAP) were continuously monitored in all animals. RESULTS: In the SOL model, all three anesthetic agents decreased ICP after each administration (P < .05). Ketamine administration also resulted in an increase in CPP in this model (P < .05). In the CBE model, none of these agents resulted in a significant change in either ICP or CPP. CONCLUSIONS: Our results indicate that i.v. anesthetics decrease ICP caused by SOL but have no significant effect on ICP due to CBE. We postulate that in the SOL model, and similarly in VBE, some brain tissue is viable and remains responsive to anesthetics. In contrast, in the CBE model, diffuse intracellular damage occurs, the cerebral metabolic rate may be severely depressed, autoregulation of the cerebral vasculature may be impaired, and unresponsiveness to i.v. anesthetics may occur.
OBJECTIVES: To determine the value of a new bedside monitor in assessing the interactions between spontaneous respiratory activity and ventilator inflations in preterm infants; and to monitor continuously the degree of patient-ventilator synchrony and the stability of spontaneous respiratory effort during different modes of ventilation and in response to care procedures. DESIGN: A prospective, observational study of physiologic variables recorded by a computerized monitoring system. SETTING: A neonatal intensive care unit in a teaching hospital. PATIENTS: Thirty-one neonates (median gestational age of 28 wks [range 24 to 36]; median birth weight of 942 g [range 624 to 2940]) were monitored during conventional mandatory ventilation at rates ranging from 47 to 108 inflations/min, and 22 infants (median gestational age of 27.5 wks [range 25 to 40]; median birth weight of 1345 g [range 510 to 3490]) were monitored during patient-triggered ventilation. All infants were sedated as part of the routine care policy. INTERVENTIONS: Spontaneous respiration (abdominal pressure capsule) and ventilator inflations (airway pressure) were recorded continuously for periods of up to 3 days in mechanically ventilated preterm infants. MEASUREMENTS AND MAIN RESULTS: The monitoring system uses the Frequency Tracking Locus method to derive the interaction Score, which quantifies the degree of entrainment of the spontaneous respiratory pattern by the ventilator. This analysis was applied to airway pressure and abdominal capsule signals. A perfect 1:1 interaction between spontaneous inspirations and mechanical inflations returns an interaction Score of 1.00, and irregular interactions return a score of > 1.5. During conventional mandatory ventilation, a total of 53,074 16-sec epochs (representing 782,811 spontaneous breaths) were studied in 31 preterm infants: 27.4% of epochs showed a 1:1 interaction, 60.5% a non 1:1 interaction, and 12.1% indicated a passive (i.e., infant apneic) response by the infant, despite excluding periods when paralyzing agents were used. The median interaction Score value during 1:1 interactions was 1.2, whereas for non 1:1 interactions the interaction Score was 2.2. One to one entrainment occurred at conventional mandatory ventilation rates between 50 and 85 inflations/min: for many infants, such entrainment was achievable over a range of conventional mandatory ventilation rates, while in some infants respiration was unstable at all rates of conventional mandatory ventilation. During passive ventilation, the median Interaction Score was 1.0. During patient-triggered mechanical ventilation, approximately 67,150 spontaneous respiratory cycles, represented by 3,592 16-sec epochs, were studied in 22 infants. Overall, 19.5% (702) of epochs showed the criteria for ideal triggering by spontaneous inspiration and 19.6% (703) showed autotriggering. In 60.9% (2187) of epochs, a non 1:1 interaction was noted. During ideal patient-triggered mechanical ventilation, the median interaction Score was 1.14; during passive (autotriggered) ventilation, the median Interaction Score was 1.05; and during non 1:1 ventilation, the median score was 1.74. "Autotriggering" was found frequently in infants of < or = 28 wks gestation. The monitor was able to distinguish between stable and unstable interactions and apnea during conventional mandatory ventilation and patient-triggered mechanical ventilation by reference to the Interaction Score value. CONCLUSIONS: We describe a new kind of bedside monitor for the Interpretation of respiratory data. Unlike other methods, it is able to give the clinician a continuous measure of patient-ventilator interaction which is easy to interpret. It appears to have wide-spread application in neonatal intensive care nurseries where the babies' own breathing efforts can affect the efficiency of respiration and cause unwanted physiologic instability. The monitor can be used to determine the optimal ventilatory settings to
OBJECTIVES: To develop a simple method in an animal model to achieve deliberate hypercapnia, which can be used easily and safely to regulate the pulmonary vascular resistance without changing mean airway pressure and compromising oxygenation. DESIGN: Prospective study, with each animal used as its own control. SUBJECTS: Minipigs, weighing 11 to 14 kg (n = 7). INTERVENTIONS: A quadrilumen thermodilution pulmonary artery catheter was placed in minipigs via the internal jugular vein. Systemic blood pressure was measured with use of a femoral arterial catheter. The animals' lungs were ventilated with an FIO2 of 1.0, and a stable state of eucapnia was achieved and maintained for 30 mins. The artificial deadspace was increased every 30 mins, by connecting 45-mL (3- to 4-mL/kg) corrugated tube segments until a total deadspace volume of 180 mL was added. MEASUREMENTS AND MAIN RESULTS: Hemodynamic performance was evaluated at baseline and after 45 mL (3 to 4 mL/kg), 90 mL (6 to 8 mL/kg), 135 mL (9 to 11 mL/kg), and 180 mL (12 to 15 mL/kg) of added deadspace. Data were indexed to the animal's weight (in kg). Increased artificial deadspace produced a significant (p < .05) increase in PaCO2. These increases in PaCO2 were associated with significant (p < .05) increases of 23%, 32%, 45%, and 46% in the mean pulmonary vascular resistance values, and 6%, 16%, 23%, and 23% in the mean pulmonary arterial pressure, respectively. The systemic pH was decreased from a mean baseline value of 7.45 to 7.39, 7.28, 7.20, and 7.11, respectively. There were no significant changes in PaO2, oxygen consumption, systemic vascular resistance, and cardiac output throughout the experiments. CONCLUSIONS: A gradual increase in artificial deadspace ventilation produces a state of deliberate hypercapnia. In our animal model, a moderate increase in artificial deadspace significantly increased the pulmonary vascular resistance but was not associated with detrimental respiratory acidemia. Larger volumes of added artificial deadspace had no detrimental effect on cardiac output, oxygen content, oxygen consumption, and systemic vascular resistance, but were associated with significant respiratory acidemia and therefore should be avoided.
BACKGROUND: Terson's syndrome (vitreous hemorrhage) and other ocular hemorrhages (retinal hemorrhages) have been reported to occur in up to 40% of patients with ruptured cerebral aneurysms. Because microsurgical vitrectomy can safely restore vision in patients with visual loss secondary to Terson's syndrome, we hypothesized that prospectively screening a selected group of patients with aneurysms would result in a higher rate of vitrectomy in patients with more extensive subarachnoid hemorrhage. METHODS: Ninety-nine patients with ruptured cerebral aneurysms were prospectively screened for Terson's syndrome and other forms of ocular hemorrhage by an ophthalmologist. Follow-up data were obtained for seven of eight cases of Terson's syndrome, and vitrectomy was performed for visual restoration when indicated. RESULTS: Ocular hemorrhages were present in 17% of patients with ruptured cerebral aneurysms, and Terson's syndrome was present in 8% of patients. Screening of patients with histories of transient or prolonged comas sensitively identified patients with ocular hemorrhages in 100% of the patients with Terson's syndrome and 89% of the patients with other ocular hemorrhages. Fifty-five percent of the patients in the overall series had histories of transient or prolonged comas, and 53% (specificity) of those patients had ocular hemorrhages. Two of the eight patients with Terson's syndrome underwent vitrectomy, with dramatic improvement in vision. No other ocular hemorrhages required surgery. CONCLUSIONS: Ophthalmological screening of patients with histories of transient or prolonged comas after ruptured cerebral aneurysms very sensitively identifies patients with ocular hemorrhages, which are relatively common in patients with subarachnoid hemorrhage treated in an academic neurosurgical practice. The present study underestimates the true incidence of Terson's syndrome in that patients who died shortly after their subarachnoid hemorrhage were not included. Vitrectomy for patients who do not exhibit spontaneous improvement in vision results in a dramatic reversal of blindness.
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The term medical necessity is difficult to define, a problem for insurers who need to clearly describe what is and is not covered in their contracts with subscribers. An unclear, vague definition of medical necessity leaves insurers vulnerable to litigation by subscribers denied care deemed medically unnecessary. To avoid lawsuits, insurers must make every effort to educate their subscribers about their medical coverage, going beyond merely providing a lengthy subscriber handbook. In decisions on medical necessity, medical directors at insurance companies play a key role. They can bolster the insurer's position in denial-of-care cases in numerous ways, including keeping meticulous records, eliminating unreasonable financial incentives, maintaining a claims denial database, and consulting with other insurers to achieve a consensus on medical necessity.
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Dendritic cells (DC) are the major APC in human peripheral blood (PB) and rheumatoid synovium. We previously identified in PB a population of CD33dim-CD14dim DC precursors, as well as a smaller population of CD33bright CD14dim mature DC. Neither PB DC population expressed the CD28/CTLA4 ligands, suggesting that additional signals are required for full functional DC differentiation. Because rheumatoid synovium is characterized by an ongoing immune response, the expression and function of CD80, CD86, and other markers of DC differentiation by rheumatoid arthritis synovial APC were examined. The phenotype of a large subset of freshly isolated rheumatoid arthritis synovial fluid (SF) DC resembled that of the mature PB DC. These DC expressed CD45R0, CD11c, CMRF-44, and high levels of CD33. Whereas CD80 expression by rheumatoid SF DC and monocytes was minimal, CD86 was expressed by a subset of SF monocytes and by CMRF-44+SF DC. Furthermore, sorted CD86- SF DC spontaneously up-regulated CD86 in vitro. CD80 was expressed diffusely and at low levels by rheumatoid synovial tissue cells, whereas CD86 was expressed by perivascular HLA-DR+HLA-DQ+CD80+CMRF-44+ DC, and by some CD14+ monocytes. Anti-CD86 mAb and CTLA4 Ig, but not anti-CD80 mAb, inhibited the MLR stimulated by SF DC. Both CMRF-44+ and CMRF-44- SF DC were efficient stimulators of the allogeneic MLR, which was in each case blocked by CTLA4 Ig. The data indicate that rheumatoid synovial DC can undergo full functional differentiation, associated with CD86 expression, in vitro and in situ. Synovial DC expressing high levels of MHC molecules and CD86 are strategically located to present arthritogenic Ag to T cells after transendothelial migration.