Global patient outcomes after elective surgery: prospective cohort study in 27 low-, middle- and high-income countries.

BACKGROUND: As global initiatives increase patient access to surgical treatments, there remains a need to understand the adverse effects of surgery and define appropriate levels of perioperative care. METHODS: We designed a prospective international 7-day cohort study of outcomes following elective adult inpatient surgery in 27 countries. The primary outcome was in-hospital complications. Secondary outcomes were death following a complication (failure to rescue) and death in hospital. Process measures were admission to critical care immediately after surgery or to treat a complication and duration of hospital stay. A single definition of critical care was used for all countries. RESULTS: A total of 474 hospitals in 19 high-, 7 middle- and 1 low-income country were included in the primary analysis. Data included 44 814 patients with a median hospital stay of 4 (range 2-7) days. A total of 7508 patients (16.8%) developed one or more postoperative complication and 207 died (0.5%). The overall mortality among patients who developed complications was 2.8%. Mortality following complications ranged from 2.4% for pulmonary embolism to 43.9% for cardiac arrest. A total of 4360 (9.7%) patients were admitted to a critical care unit as routine immediately after surgery, of whom 2198 (50.4%) developed a complication, with 105 (2.4%) deaths. A total of 1233 patients (16.4%) were admitted to a critical care unit to treat complications, with 119 (9.7%) deaths. Despite lower baseline risk, outcomes were similar in low- and middle-income compared with high-income countries. CONCLUSIONS: Poor patient outcomes are common after inpatient surgery. Global initiatives to increase access to surgical treatments should also address the need for safe perioperative care. STUDY REGISTRATION: ISRCTN5181700

Dexamethasone therapy in preterm infants with developing bronchopulmonary dysplasia: Effect on pulmonary surfactant disaturated phosphatidylcholine kinetics

The role of corticosteroid in severe bronchopulmonary dyplasia (BPD) is still debated. Scanty data are available on the corticosteroids effect on surfactant metabolism. Our objective was to compare surfactant kinetics in preterm infants with developing BPD, before and after dexamethasone (DEXA) treatment. Twenty-eight studies were performed in 14 preterm infants (birth weight 786 +/- 192 g, gestational age 26 +/- 1 wk) on high ventilatory setting, before (age 22 +/- 11 d) and after (age 33 +/- 11 d) DEXA. C-labeled dipalmitoyl-phosphatidylcholine (DPPC) was administered endotrachelly to trace pulmonary surfactant. Surfactant disaturated-phosphatidylcholine (DSPC) kinetics and pools were calculated from DSPC C-enrichment curves of serial tracheal aspirates and bi-compartmental analysis. Total protein and myeloperoxidase (MPO) activity in tracheal aspirates were also measured and expressed per ml of Epithelial Lining Fluid (ELF). After DEXA, DSPC alveolar pool increased significantly from 8.2 +/- 7.6 to 10.6 +/- 11.3 mg/kg (p = 0.039), total proteins and MPO were reduced from 8.8 +/- 8.6 to 3.1 +/- 2.1 mg/ml ELF (p = 0.046) and from 1822 +/- 1224 to 1261 +/- 987 mU/mlELF (p = 0.028) respectively. In conclusion, DEXA treatment in mechanically ventilated preterm infants with severe respiratory failure and at high risk of developing BPD, significantly reduced inflammatory markers and increased alveolar surfactant DSPC pool

ENaC, renal sodium excretion and extracellular ATP

Sodium balance determines the extracellular fluid volume and sets arterial blood pressure (BP). Chronically raised BP (hypertension) represents a major health risk in Western societies. The relationship between BP and renal sodium excretion (the pressure/natriuresis relationship) represents the key element in defining the BP homeostatic set point. The renin–angiotensin–aldosterone system (RAAS) makes major adjustments to the rates of renal sodium secretion, but this system works slowly over a period of hours to days. More rapid adjustments can be made by the sympathetic nervous system, although the kidney can function well without sympathetic nerves. Attention has now focussed on regulatory mechanisms within the kidney, including extracellular nucleotides and the P2 receptor system. Here, we discuss how extracellular ATP can control renal sodium excretion by altering the activity of epithelial sodium channels (ENaC) present in the apical membrane of principal cells. There remains considerable controversy over the molecular targets for released ATP, although the P2Y2 receptor has received much attention. We review the available data and reflect on our own findings in which ATP-activated P2Y and P2X receptors make adjustments to ENaC activity and therefore sodium excretion

Kuluttajabarometri maakunnittain 2000, 2. neljännes

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