Disgusting disruptions: Capturing the everyday experience and burden of managing gastrointestinal infections in the home

Gastrointestinal (GI) infections exert a significant public health burden in the United Kingdom and the numbers of episodes are increasing. Younger children are considered particularly vulnerable to infection, and can experience 2–3 GI infections episodes per year, with consequences being more severe for more disadvantaged children, who are much more likely to be admitted to hospital. Few qualitative studies have explored the lived experience of GI infection in the community in the UK. The aim of the study reported here was to contribute to addressing this evidence gap, by examining the consequences of GI infection for ‘normal’ family life. Eighteen mothers with young children who had recently experienced a gastrointestinal infection were recruited from two socioeconomically contrasting neighbourhoods in North West of England. The findings demonstrated that GI infections were particularly disruptive: experienced as disgusting, laborious and stressful and significantly impacted normal family routines. Women felt burdened by the heavy physical and emotional demands of caring for a GI infection, resulting in feelings of isolation and insufficient support in their caring role from male partners. Tensions also arose from interactions with external community organisations, particularly in complying with their regulations on infection which often undermined caregivers knowledge and expertise of what was best for their children. This study challenges assumptions that managing GI infections in the home is unproblematic and experienced by caregivers as a ‘minor ailment.’ Infection control measures need to incorporate insights gleaned from the day-to-day realities of caring for sick children in the community.     

Exercise for rheumatoid arthritis

The approach to treating rheumatoid arthritis is changing. Greater emphasis on the exercise component of physical therapy can improve patients' muscle strength, endurance, and emotional well-being, and may even result in decreased joint inflammation.     

Cranial burst fracture in infants: acute recognition and management

In the past, the diagnosis of growing skull fracture or diastatic fracture has included a subset of injuries better referred to as cranial burst fracture. Cranial burst fracture, typically associated with severe injury in infants less than 1 year of age, is a closed, widely diastatic skull fracture accompanied by acute cerebral extrusion outside the calvarium. We treated 11 such infants at the LeBonheur Children's Medical Center and 2 at the Children's National Medical Center from January 1986 through December 1994. Infants ranged in age from 1 to 17 months, with an average age of 5.7 months. All presented with marked scalp swelling and a Glasgow Coma Scale score of 10 or less. Twelve had a history consistent with severe injury (motor vehicle accident, 7, abuse 5). The cause of injury in one patient remains unproven. Surgery (reduction of herniated cerebral tissue, repair of large dural laceration, and cranioplasty) was usually performed within 10 days of injury, a time period long enough to assure hemodynamic stability and resolution of acute cerebral swelling, yet sufficiently brief to avoid the chronic changes (scarring, parasitization of scalp vessels by damaged cortex) associated with a growing skull fracture. Prompt repair of cranial burst fracture may prevent ongoing brain injury such as has been neuropathologically demonstrated in patients with growing skull fracture. Magnetic resonance imaging establishes the diagnosis of cranial burst fracture in equivocal cases, rendering unnecessary a waiting period to see if scalp swelling resolves. Our experience, together with information in the neuropathological and neurosurgicla literature, suggests that cranial burst fracture is associated with severe trauma, requires expeditious treatment, and has been underdiagnosed in the past, leading to growing skull fracture, a condition requiring more extensive surgery.     

Carbon dioxide analysers: accuracy,alarm limits and effects of interfering gases

Six mainstream and twelve sidestream infrared carbon dioxide (CO₂) analysers were tested for accuracy of the CO₂ display value, alarm activation and the effects of nitrous oxide (N₂O), oxygen (O₂) and water vapour according to the ISO Draft International Standard (DIS) #9918. Mainstream analysers (M-type): Novametrix Capnogard 1265; Hewlett Packard HP M1166A (CO₂module HP M1016A); Datascope Passport; Marquette Tramscope 12; Nellcor Ultra Cap N-6000; Heilige Vicom-sm SMU 611/612 ETC. Sidestream analysers: Brüel &; Kjaer Type 1304; Datex Capnomac II; Marquette MGA-AS; Datascope Multinex; Ohmeda 4700 OxiCap (all type S1: respiratory cycles not demanded); Biochem BCI 9000; Bruker BCI 9100; Dräger Capnodig and PM 8020; Criticare Poet II; Heilige Vicom-sm SMU 611/612 A-GAS (all type S2: respiratory cycles demanded). The investigations were performed with premixed test gases (2.5, 5, 10 vol%, error ?1% rel.). Humidification (37° C) of gases were generated by a Dräger Aquapor. Respiratory cycles were simulated by manually activated valves. All monitors complied with the tolerated accuracy bias in CO₂ reading (≤ 12% or 4 mmHg of actual test gas value) for wet and dry test gases at all concentrations, except that the Marquette MGA-AS exceeded this accuracy limit with wet gases at 5 and 10 vol% CO₂. Water condensed in the metal airway adapter of the HP M1166A at 37° C gas temperature but not at 3(P C. The Servomex 2500 (nonclinical reference monitor), Passport (M-type), Multinex (S1-type) and Poet II (S2-type) showed the least bias for dry and wet gases. Nitrous oxide and O₂ had practically no effect on the Capnodig and the errors in the others were max. 3.4 mmHg, still within the tolerated bias in the DIS (same as above). The difference between the display reading at alarm activation and the set point was in all monitors (except in the Capnodig: bias 1.75 mmHg at 5 vol% CO₂) below the tolerated limit of the DIS (difference ≤ 0.2 vol%). The authors conclude that the tested monitors are safe for clinical use (except those failing the DIS limits). The accuracy of the CO₂-reading (average of mean absolute bias) is better in the M-type than in the S1- or S2- type analysers although no statistical (nor clinical) significant differences could be detected. Most manufacturers work with stricter limits than those proposed by the DIS.     

The Effects of IB4, a Monoclonal Antibody to the CD18 Leukocyte Integrin on Phorbol Myristate Acetate (PMA)-Induced Polymorphonuclear Leukocyte (PMN) Accumulation and Endothelial Injury in Rabbit Lungs

A model of acute lung injury induced by intravenous phorbol myristate acetate (PMA) is described. The model is characterized by the accumulation of polymorphonuclear leukocytes (PMNs) and a hemorrhagic edema in bronchoalveolar lavage (BAL) fluid when measured 6 h following the administration of PMA (60 g/kg, i.v.). It was also determined that PMA induces acute leukopenia and neutropenia which were maximal at 5 min following the injection of PMA and were sustained for at least 6 h, with circulating leukocyte numbers returning to control values by 24 h. The extents to which the inflammatory and systemic changes induced by PMA were dependent on the surface expression on leukocytes of the 2-integrins was assessed by comparing responses to PMA in control animals and animals pretreated with the anti-CD18 monoclonal antibody IB4. The administration of IB4 (1 mg/kg, i.v.) 15 min before PMA did not alter the time course or extent of PMA-induced leukopenia and neutropenia. In contrast IB4 administration (0.1 to 1 mg/kg) produced a dose dependent inhibition of PMN accumulation and plasma extravasation measured in BAL fluid. IB4 (1 mg/kg) completely inhibited PMA evoked increases in plasma extravasation (94.5 ± 1.7%, N = 4) and hemorrhage (95.2 ± 2.1%, N = 4) whereas PMN accumulation in BAL fluid was inhibited by 77.8 ± 3.8% (mean ± SEM, N = 4). Thus, a small, but reproducible, component of the PMA-induced PMN accumulation was not inhibited using this regimen of IB4 administration. If IB4 administration was delayed for 3 h post injection of PMA and bronchoalveolar lavage performed 3 h later, the extents of PMN accumulation and edema formation were similar to those observed 3 h following PMA challenge in control animals not dosed with IB4. This suggests that administration of IB4 during an ongoing inflammatory response is capable of preventing the further development of inflammatory changes and further supports the therapeutic potential of CD18 blockade in conditions such as adult respiratory distress syndrome.     

Single-channel and whole-cell analysis of ethanol inhibition of NMDA-activated currents in cultured mouse cortical and hippocampal neurons

The effects of 0.1 to 500 mM ethanol on NMDA-activated currents were studied in primary cultures of mouse cortical and hippocampal neurons. In whole-cell recordings the IC₅₀S for inhibition of NMDA-activated currents by ethanol were 129 mM ± 20 mM in hippocampal neurons and 126 ± 18 mM in cortical neurons. In single-channel recordings from excised outside-out patches of cortical neurons, ethanol inhibited total charge per minute with an IC₅₀ of 174 ± 23 mM, which was not significantly different from the IC₅₀S for inhibition of whole-cell current. The reduction in mean open channel lifetime by ethanol was fit by the logistic equation with an apparent IC₅₀ of 340 ± 28 mM. Analysis of single-channel data indicated that ethanol inhibition of NMDA currents did not involve substantial changes in fast closed state kinetics, changes in open channel conductance, or block of the open channel. At the whole-cell IC₅₀, of ethanol, mean open channel lifetime would decrease by 28% and frequency of opening would decline by 31% to account for the reduction in current. Single-channel data were consistent with ethanol being an allosteric modulator of gating which reduces agonist efficacy.