Diagnosis and treatment of post-traumatic hypothermia in hospitals - a pilot study.

BACKGROUND: An unintentional drop in core body temperature of trauma victims is associated with increased mortality. Thermoregulation is impaired in these patients, especially when treated with opioids or anesthetics. Careful thermal insulation and active warming are necessary to maintain normothermia. The aim of the study was to assess the equipment and procedures for diagnosing and managing post-traumatic hypothermia in Polish hospitals. METHODS: Survey forms regarding equipment and procedures on monitoring of core temperature (Tc) and active warming were distributed to every hospital that admits trauma victims in the Holy Cross Province. Questionnaires were addressed to surgery departments, intensive care units (ICUs), and operating rooms (ORs). RESULTS: 92% of surgery departments did not have equipment to measure core body temperature and 85% did not have equipment to rewarm patients. Every ICU had equipment to measure Tc and 83% had active warming devices. In 50% of ICUs, there were no rewarming protocols based on Tc and the initiation of rewarming was left to the physician's discretion. In 58% of ORs, Tc was not monitored and in 33% the patients were not actively warmed. CONCLUSIONS: The majority of surveyed ICUs and ORs are adequately equipped to identify and treat hypothermia, however the criteria for initiating Tc monitoring and rewarming remain unstandardized. Surgery departments are not prepared to manage post-traumatic hypothermia.

Immune characteristics correlating with HSV-1 immune control and effect of squaric acid dibutyl ester on immune characteristics of subjects with frequent herpes labialis episodes.

INTRODUCTION: Differences in immune characteristics, including immune gene expression by peripheral blood mononuclear cells (PBMCs), correlating with herpes labialis and good or poor immune control of herpes simplex virus type 1 (HSV-1), and how these characteristics change after dosing with squaric acid dibutyl ester (SADBE), were investigated. METHODS: PBMCs were collected from persons positive for IgG against HSV-1 and having frequent, infrequent, or no herpes labialis outbreaks. The PBMCs were tested for proliferation against HSV-1 and a fungal antigen (Candida) and immune gene expression in the presence of HSV-1 and Candida. On day 1 after blood collection the subjects with frequent outbreaks were dosed topically on the arm once with SADBE, and their PBMCs were collected and tested 8 weeks later. RESULTS: Those with good immune control of their HSV-1 infection (fewer outbreaks) differ from those with poorer immune control in these ways: (1) Greater PBMC proliferation in vitro to HSV-1, HSV-1-infected cell extracts, and Candida considered together (P < 0.01). (2) Higher expression of IFNG and five other immune-related genes (P < 0.05 for each) and lower expression of IL5 and two other immune-related genes (P < 0.05 for each) in PBMCs in vitro stimulated with HSV-1 virus. The subjects with frequent outbreaks were treated once with SADBE, and 56 days later the PBMCs of these subjects differed from PBMCs from the same subjects taken on day 1 before treatment in exactly the same ways listed above as differences between those with good and poor immune control of HSV-1, and at the same levels of significance. CONCLUSIONS: Higher IFNG and lower IL5 expression by PBMCs in the presence of HSV-1 correlate with fewer herpes labialis outbreaks, and a single topical dose of SADBE to the arm of subjects with frequent herpes labialis episodes improves immune response to HSV-1.

Is left ventricular hypertrophy a friend or foe of patients with aortic stenosis?

Left ventricular hypertrophy (LVH) is traditionally considered a physiological compensatory response to LV pressure overload, such as hypertension and aortic stenosis (AS), in an effort to maintain LV systolic function in the face of an increased afterload. According to the Laplace law, LV wall thickening lowers LV wall stress, which in turn would be helpful to preserve LV systolic performance. However, numerous studies have challenged the notion of LVH as a putative beneficial adaptive mechanism. In fact, the magnitude of LVH is associated with higher cardiovascular morbidity and mortality, especially when LVH is disproportionate to LV afterload. We have briefly reviewed: first, the importance of non-valvular factors, beyond AS severity, for total LV afterload and symptomatic status in AS patients; second, associations of excessive LVH with LV dysfunction and adverse outcome in AS; third, prognostic relevance of the presence or absence of pre-operative LVH in patients referred for aortic valve surgery; fourth, time course, determinants and prognostic implications of LVH regression and LV function recovery after surgical valve replacement and transcatheter aortic valve implantation (TAVI) with a focus on TAVI-specific effects; fifth, the potential of medical therapy to modulate LVH before and after surgical or interventional treatment for severe AS, a condition perceived as a relative contraindication to renin-angiotensin system blockade.