Enhanced peri-operative care to improve outcomes for high-risk surgical patients in Brazil: a single-centre before-and-after cohort study

Mortality and morbidity for high-risk surgical patients are often high, especially in low-resource settings. Enhanced peri-operative care has the potential to reduce preventable deaths but must be designed to meet local needs. This before-and-after cohort study aimed to assess the effectiveness of a postoperative 48-hour enhanced care pathway for high-risk surgical patients (‘high-risk surgical bundle’) who did not meet the criteria for elective admission to intensive care. The pathway comprised of six elements: risk identification and communication; adoption of a high-risk post-anaesthesia care unit discharge checklist; prompt nursing admission to ward; intensification of vital signs monitoring; troponin measurement; and prompt access to medical support if required. The primary outcome was in-hospital mortality. Data describing 1189 patients from two groups, before and after implementation of the pathway, were compared. The usual care group comprised a retrospective cohort of high-risk surgical patients between September 2015 and December 2016. The intervention group prospectively included high-risk surgical patients from February 2019 to March 2020. Unadjusted mortality rate was 10.5% (78/746) for the usual care and 6.3% (28/443) for the intervention group. After adjustment, the intervention effect remained significant (RR 0.46 (95%CI 0.30–0.72). The high-risk surgical bundle group received more rapid response team calls (24% vs. 12.6%; RR 0.63 [95%CI 0.49–0.80]) and surgical re-interventions (18.9 vs. 7.5%; RR 0.41 [95%CI 0.30–0.59]). These data suggest that a clinical pathway based on enhanced surveillance for high-risk surgical patients in a resource-constrained setting could reduce in-hospital mortality.     

Poor retention in early care increases risk of mortality in a Brazilian HIV-infected clinical cohort

Retention in early HIV care has been associated with decreased mortality and improved viral suppression, however the consequences of poor retention in early care in Brazil remain unknown. We assessed the effect of poor retention on mortality in a Brazilian HIV-infected clinical cohort. The analysis included ART-naïve, HIV-infected adults linked to care at the Instituto Nacional de Infectologia Evandro Chagas, Fundação Oswaldo Cruz between 2000 and 2010, who did not become pregnant nor participate in a clinical trial during the first two years in care (early care). Poor retention in early care was defined as less than 3 out of 4 six-month intervals with a CD4 or HIV-1 RNA laboratory result during early care. Cox proportional hazards models were used to identify factors associated with mortality, and Kaplan–Meier plots were used to describe the survival probability for participants with poor retention versus good retention. Among 1054 participants with a median (interquartile range) follow-up time of 4.2 years (2.6, 6.3), 20% had poor retention in early care and 8% died. Poor retention in early care [adjusted hazard ratio (aHR) 3.09; 95% CI 1.65–5.79], AIDS defining illness (aHR 1.95; 95% CI 1.20–3.18) and lower education (aHR 2.33; 95% CI 1.45–3.75) were associated with increased mortality risk. Our findings highlight the importance of adopting strategies to improve retention in early HIV care.     

Long-term effects of the Entre-os-Rios tragedy on grief and traumatic stress symptoms

In 2001, in Entre-os-Rios, Portugal, a bridge fell on Douro River; all 59 passengers from 1 bus and 3 cars died and 36 bodies have never been recovered. The objective is to reveal the cumulative risk from multiple losses and unrecovered bodies, 10 years after, compared with grievers from road accidents. There are 2 groups of relatives of victims: from this tragedy (n?=?20), with at least 1 unrecovered body; and from road traffic accidents (n?=?20), with the same time after loss. The prevalence of prolonged grief was 95% and for traumatic stress was 70%. The associated factors of multiple losses and unrecovered bodies increase the long-term risk (relative risk?=?1.6 to 2.8; R²?=?.20 to .28) for prolonged and traumatic grief, providing evidence that the absence of body is an important long-term factor.     

Influence of the microbiological component of Cariogram® for evaluating the risk of caries in children

Objective: To compare the risk for caries in children as determined by Cariogram^® software (CS; Stockholm, Sweden) with and without its microbiological component and by a form based on Cariogram^® (FBC).

Methods: Children (n?=?28) aged 3–9 years were included. Data were collected clinically and from anamnesis. The salivary levels of Streptococcus mutans (SM) were evaluated. A linear regression model was used to determine which variables were predictive for each type of risk analysis. Caries risk was the dependent variable and the independent variables were caries experience, related disease, plaque amount, diet frequency, salivary levels of SM, fluoride sources and clinical judgment. A paired Student t-test was used for the following comparisons: (a) CS with and without SM; (b) CS without SM and FBC; (c) CS with SM and FBC.

Results: The mean dmft/DMFT was 5.56?±?2.51. There was no difference between the methods (p?p?=?.889). Caries experience, plaque amount, diet frequency and fluoride sources were predictors of caries risk in all assessment methods. Clinical judgment was a significant predictor in CS.

Conclusions: Caries experience, plaque amount, diet frequency and fluoride sources are valuable predictors of caries risk; microbiological tests are not necessary for evaluating caries risk in children, which can be assessed similarly by CS without SM and FBC.     

Antispasmodic effects of essential oil of Pterodon polygalaeflorus and its main constituent β‐caryophyllene on rat isolated ileum

This study investigates the effects of essential oil of Pterodon polygalaeflorus (EOPP) and β‐caryophyllene (β‐CAR). EOPP and β‐CAR relaxed the basal tone of ileum smooth muscle in a concentration‐dependent manner (IC₅₀s = 394.35 ± 62.12 and 68.65 ± 9.51 μg/mL respectively), an effect that was unaltered by hexamethonium, L ‐nitroarginine methyl ester or indomethacin. Both EOPP and β‐CAR evoked a concentration‐dependent relaxation of ileum pre‐contracted with KCl with an IC₅₀ value of 107.78 ± 10.47 and 17.35 ± 0.75 μg/mL, respectively. EOPP and β‐CAR inhibited the contractions induced by acetylcholine (ACh) and by KCl. In ileal preparations, the CaCl₂‐induced contractions were reduced by EOPP (300 μg/mL) and β‐CAR (100 μg/mL). Furthermore, CaCl₂‐induced contractions were also reduced by EOPP (300 μg/mL) and β‐CAR (100 μg/mL) in ileal preparations pretreated with ACh under Ca²⁺‐free condition and in the presence of verapamil. EOPP (100 and 300 μg/mL) and β‐CAR (30 and 100 μg/mL) reduced the ACh‐induced contractions of isolated rat ileum under Ca²⁺‐free conditions. In the presence of high KCl and Ca²⁺‐free conditions, EOPP (300 μg/mL) and β‐CAR (100 μg/mL) reduced the contractions induced by barium. A similar effect was also observed with verapamil. It is concluded that (i) β‐CAR is an important constituent involved in the myorelaxant and antispasmodic effects induced by EOPP; (ii) the inhibitory effect on intestinal contractility is myogenic and seems mainly mediated through an intracellular mechanism. However, the ability of EOPP and β‐CAR to decrease Ca²⁺ influx through cytoplasmic membrane could not be discounted.     

Mitochondrial-dependent apoptosis in Huntington's disease human cybrids

We investigated the involvement of mitochondrial-dependent apoptosis in Huntington's disease (HD) vs. control (CTR) cybrids, obtained from the fusion of human platelets with mitochondrial DNA-depleted NT2 cells, and further exposed to 3-nitropropionic acid (3-NP) or staurosporine (STS). Untreated HD cybrids did not exhibit significant modifications in the activity of mitochondrial respiratory chain complexes I–IV or in mtDNA sequence variations suggestive of a primary role in mitochondrial susceptibility in the subpopulation of HD carriers studied. However, a slight decrease in mitochondrial membrane potential and increased formation of intracellular hydroperoxides was observed in HD cybrids under basal conditions. Furthermore, apoptotic nuclei morphology and a moderate increase in caspase-3 activation, as well as increased levels of superoxide ions and hydroperoxides were observed in HD cybrids upon 3-NP or STS treatment. 3-NP-evoked apoptosis in HD cybrids involved cytochrome c and AIF release from mitochondria, which was associated with mitochondrial Bax translocation. CTR cybrids subjected to 3-NP showed increased mitochondrial Bax and Bim levels and the release of AIF, but not cytochrome c, suggesting a different mode of cell death, linked to the loss of membrane integrity. Additionally, increased mitochondrial Bim and Bak levels, and a slight release of cytochrome c in untreated HD cybrids may help to explain their moderate susceptibility to mitochondrial-dependent apoptosis.     

Prenatal retinoid deficiency leads to airway hyperresponsiveness in adult mice

There is increasing evidence that vitamin A deficiency in utero correlates with abnormal airway smooth muscle (SM) function in postnatal life. The bioactive vitamin A metabolite retinoic acid (RA) is essential for formation of the lung primordium; however, little is known about the impact of early fetal RA deficiency on postnatal lung structure and function. Here, we provide evidence that during murine lung development, endogenous RA has a key role in restricting the airway SM differentiation program during airway formation. Using murine models of pharmacological, genetic, and dietary vitamin A/RA deficiency, we found that disruption of RA signaling during embryonic development consistently resulted in an altered airway SM phenotype with markedly increased expression of SM markers. The aberrant phenotype persisted postnatally regardless of the adult vitamin A status and manifested as structural changes in the bronchial SM and hyperresponsiveness of the airway without evidence of inflammation. Our data reveal a role for endogenous RA signaling in restricting SM differentiation and preventing precocious and excessive SM differentiation when airways are forming.