To lead or not to lead? Prospective controlled study of emergency nurses' provision of advanced life support team leadership

Background and objectives: In many emergency departments advanced life support (ALS) trained nurses do not assume a lead role in advanced resuscitation. This study investigated whether emergency nurses with previous ALS training provided good team leadership in a simulated cardiac arrest situation. Methods: A prospective study was conducted at five emergency departments and one nurses'' association meeting. All participants went through the same scenario. Details recorded included baseline blood pressure and pulse rate, time in post, time of ALS training, and subjective stress score (1 = hardly stressed; 10 = extremely stressed). Scoring took into account scenario understanding, rhythm recognition, time to defibrillation, appropriateness of interventions, and theoretical knowledge. Results: Of 57 participants, 20 were ALS trained nurses, 19 were ALS trained emergency senior house officers (SHOs), and 18 were emergency SHOs without formal ALS training. The overall mean score for doctors without ALS training was 69.5%, compared with 72.3% for ALS trained doctors and 73.7% for ALS trained nurses. Nurses found the experience less stressful (subjective stress score 5.78/10) compared with doctors without ALS training (6.5/10). The mean time taken to defibrillate from the appearance of a shockable rhythm on the monitor by the nurses and those SHOs without ALS training was 42 and 40.8 seconds, respectively. Conclusion: ALS trained nurses performed as well as ALS trained and non ALS trained emergency SHOs in a simulated cardiac arrest situation and had greater awareness of the potentially reversible causes of cardiac arrest. Thus if a senior or middle grade doctor is not available to lead the resuscitation team, it may be appropriate for experienced nursing staff with ALS training to act as ALS team leaders rather than SHOs.     

Hypothalamic Syndrome and Central Sleep Apnoea Associated with Toluene Exposure

We describe a young man who developed extensive hypothalamicdysfunction including diabetes insipidus, adipsia, hyperprolactinaemia,and poikiliothermia together with central sleep apnoea followingexposure to toluene.     

Interventions to support recovery after domestic and sexual violence in primary care

Abstract

Experiences of domestic and sexual violence are common in patients attending primary care. Most often they are not identified due to barriers to asking by health practitioners and disclosure by patients. Women are more likely than men to experience such violence and present with mental and physical health symptoms to health practitioners. If identified through screening or case finding as experiencing violence they need to be supported to recover from these traumas. This paper draws on systematic reviews published in 2013–2015 and a further literature search undertaken to identify recent intervention studies relevant to recovery from domestic and sexual violence in primary care. There is limited evidence as to what interventions in primary care assist with recovery from domestic violence; however, they can be categorized into the following areas: first line response and referral, psychological treatments, safety planning and advocacy, including through home visitation and peer support programmes, and parenting and mother–child interventions. Sexual violence interventions usually include trauma informed care and models to support recovery. The most promising results have been from nurse home visiting advocacy programmes, mother–child psychotherapeutic interventions, and specific psychological treatments (Cognitive Behaviour Therapy, Trauma informed Cognitive Behaviour Therapy and, for sexual assault, Exposure and Eye Movement Desensitization and Reprocessing Interventions). Holistic healing models have not been formally tested by randomized controlled trials, but show some promise. Further research into what supports women and their children on their trajectory of recovery from domestic and sexual violence is urgently needed.     

In vitro and in vivo activity of murine lymphokine-activated killer cells after cryopreservation

The in vitro and in vivo effects of cryopreservation on the cytotoxic activity of murine lymphokine-activated killer (LAK) cells were studied. LAK cells were generated by incubation of spleen lymphocytes of BALB/c mice for 3 days with recombinant interleukin-2 (rIL-2) and subsequent cryopreservation. Cytotoxicity was determined in a 51Cr release assay. After thawing, cytotoxic activity was reduced (40.4% 51Cr release at an effector:target cell ratio of 40:1 as compared to 68.5% 51Cr release before freezing) and could be restored to precryopreserved levels by reincubation with rIL-2 for 2 days after thawing (78.8% 51Cr release). These cells were then tested in BALB/c mice injected with RAW 112 cells, a pre-B-cell lymphoma line. The results demonstrate that the survival rate of mice injected with cryopreserved and restimulated LAK cells (50% survival greater than 180 days after injection) did not differ significantly from that of mice injected with fresh unfrozen LAK cells (60% survival greater than 120 days, 50% survival greater than 180 days). Cryopreserved LAK cells have potential use in adoptive immunotherapy.     

Interferon-α suppressed granulocyte colony stimulating factor production is reversed by CL097, a TLR7/8 agonist

Background and Aim: Neutropenia, a major side‐effect of interferon‐α (IFN‐α) therapy can be effectively treated by the recombinant form of granulocyte colony stimulating factor (G‐CSF), an important growth factor for neutrophils. We hypothesized that IFN‐α might suppress G‐CSF production by peripheral blood mononuclear cells (PBMCs), contributing to the development of neutropenia, and that a toll‐like receptor (TLR) agonist might overcome this suppression. Methods: Fifty‐five patients who were receiving IFN‐α/ribavirin combination therapy for chronic hepatitis C virus (HCV) infection were recruited. Absolute neutrophil counts (ANC), monocyte counts and treatment outcome data were recorded. G‐CSF levels in the supernatants of PBMCs isolated from the patients and healthy controls were assessed by enzyme‐linked immunosorbent assay following 18 h of culture in the absence or presence of IFN‐ α or the TLR7/8 agonist, CL097. Results: Therapeutic IFN‐α caused a significant reduction in neutrophil counts in all patients, with 15 patients requiring therapeutic G‐CSF. The reduction in ANC over the course of IFN‐α treatment was paralleled by a decrease in the ability of PBMCs to produce G‐CSF. In vitro G‐CSF production by PBMCs was suppressed in the presence of IFN‐α; however, co‐incubation with a TLR7/8 agonist significantly enhanced G‐CSF secretion by cells obtained both from HCV patients and healthy controls. Conclusions: Suppressed G‐CSF production in the presence of IFN‐α may contribute to IFN‐α‐induced neutropenia. However, a TLR7/8 agonist elicits G‐CSF secretion even in the presence of IFN‐α, suggesting a possible therapeutic role for TLR agonists in treatment of IFN‐α‐induced neutropenia.