Balto and Togo during the cold winter of Alaska (1925): the two canine heroes in the fight against diphtheria.

In recent years, diphtheria has re-emerged in areas with inadequate vaccination coverage, and Europe has not been spared with several cases among migrants. Diphtheria is a potentially fatal infection caused mainly by toxigenic strains of Corynebacterium diphtheriae. Due to the high mortality rate, especially among young children, the fight against diphtheria is considered one of the first conquests of immunization. In the history of medicine, there is a unique case of an unconventional response to a diphtheria outbreak in which sled dogs were used to overcome the supply difficulties of diphtheria antitoxin. The mass media followed the medical response to the outbreak and raised audience awareness of public health issues. The facts of Nome, Alaska, in 1925 can serve as a catalyst to rethink conventional responses to diphtheria outbreaks in low-income countries today and promote mass media awareness of public health importance.

Comparison of Troponin I levels versus myocardial dysfunction on prognosis in sepsis.

In the context of sepsis, we tested the relationship between echocardiographic findings and Troponin, and their impact on prognosis. In this prospective study, we enrolled 325 septic patients (41% with shock), not mechanically ventilated, between October, 2012 and June, 2019 among those admitted to our High-Dependency Unit. By echocardiography within 24 h from the admission, sepsis-induced myocardial dysfunction (SIMD) was defined as left ventricular (LV) systolic dysfunction (speckle-tracking-based global longitudinal peak systolic strain, GLS, > - 14%) and/or right ventricular (RV) systolic dysfunction (Tricuspid Annular Plane Systolic Excursion, TAPSE < 16 mm). Troponin I levels were measured upon admission (T0) and after 24 h (T1); it was considered normal if > 0.1 ng/mL. Mortality was assessed at day-7 and day-28 end-points. One-hundred and forty-two patients had normal Troponin level at T0 and T1 (G1), 69 had abnormal levels at T0 or T1 (G2) and 114 showed abnormal Troponin levels at both T0 and T1 (G3). Compared to G1, patients in G3 had worse LV and RV systolic function (GLS - 11.6 ± 3.4% vs - 14.0 ± 3.5%, p < 0.001; TAPSE 18 ± 0.5 vs 19 ± 0.5 mm, p = 0.047) and greater day-28 (34% vs 20%, p = 0.015) mortality. In a Cox survival analysis including age, Troponin and SOFA score, mortality was predicted by the presence of SIMD (RR 3.24, 95% CI 1.72-6.11, p < 0.001) with no contribution of abnormal Troponin level. While abnormal Troponin levels were associated with SIMD diagnosed by echocardiography, only the presence of SIMD predicted the short- and medium-term mortality rate, without an independent contribution of increased Troponin levels.

Prognostic stratification in septic patients with overt and cryptic shock by speckle tracking echocardiography.

We evaluated the prevalence and prognostic value of left (LV) and right (RV) ventricular systolic dysfunction in the presence of overt and cryptic shock. In this prospective study, between October 2012 and June 2019, we enrolled 354 patients with sepsis, 41% with shock, among those admitted to the Emergency Department High-Dependency Unit. Patients were grouped based on the presence of shock, or by the presence of lactate levels ≥ (LAC +) or < 2 mmol/L (LAC-) evaluated within the first 24 h. By echocardiography performed within 24 h from the admission, LV systolic dysfunction was defined as global longitudinal strain (GLS) > -14%; RV systolic dysfunction as Tricuspid Annular Plane Systolic Excursion (TAPSE) < 16 mm. All-cause mortality was assessed at day-7 and day-28 follow-up. Mean values of LV GLS (-12.3 ± 3.4 vs -12.9 ± 3.8%) and TAPSE (1.8 ± 0.7 vs 1.8 ± 0.5 cm, all p = NS) were similar in patients with and in those without shock. LV GLS was significantly worse in LAC + than LAC- patients (- 11.2 ± 3.1 vs - 12.9 ± 3.7%, p = 0.001). In patients without shock, as well as in those LAC-, LV dysfunction was associated with increased day-28 mortality rate (78% vs 57% in non-survivors and survivors without shock and 74% vs 53% in non-survivors and survivors LAC-, all p < 0.01). LV (RR 2.26, 95% CI 1.37-3.74) and RV systolic dysfunction (RR 1.85, 95% CI 1.22-2.81) were associated with increased 28-day mortality rate in addition and independent to LAC + (RR 1.81, 95% CI 1.15-2.84). In conclusion, LV and RV ventricular dysfunction were independently associated with an increased mortality rate, altogether with the presence of cryptic shock.

Epidemiology of right ventricular systolic dysfunction in patients with sepsis and septic shock in the emergency department.

We evaluated whether in sepsis, right ventricular (RV) systolic dysfunction (RVSD) predicts short-term all-cause mortality, independently to left ventricular (LV) global longitudinal peak systolic strain (GLS). This is a prospective observational study. We enrolled 252 septic patients (40% with shock) between October 2012 and July 2018 among those admitted to High-Dependency Unit. By echocardiography within 24 h from the admission (T1), RVSD was defined as Tricuspid Annular Plane Systolic Excursion (TAPSE) < 16 mm, while left ventricular systolic dysfunction (LVSD) was defined by bi-dimensional speckle-tracking-based global longitudinal peak systolic strain (GLS) > -14%. We assessed all-cause mortality at day-7 and at day-28 from admission. Mortality rate was 14% by day-7 and 26% by day-28 follow-up. RVSD was found in 85 patients (34%), was isolated in 29% (25/85) and coexisted with LVSD in 71% (60/85) patients. LVSD was present in 63% of patients (159/252), and was isolated in 99 patients. Day-7 mortality rate was twofold higher in the presence of RVSD (20% vs 11%), without reaching the statistical significance (p = 0.097). By day-28, mortality rate was as high as 44% with and 23% without RVSD (p = 0.001). In a Cox survival analysis, RVSD predicted higher mortality rate by day-28 follow-up (RR 2.43, 95% CI 1.47-4.00, p = 0.001), independent to shock and in addition to LVSD. In sepsis, RVSD predicted all-cause mortality by day-28 follow-up, independent to LVSD.