The Fluid Expansion As Supportive Therapy (FEAST) study demonstrated a 45 relative increased risk of mortality with fluid bolus (with albumin or saline) compared with nonbolus controls (95?CI, 1.13 to 1.86; p=0.003) in children with septic shock in settings where there was no access to intensive care facilities Maitland K et al. N Engl J Med 2011; 364:2483–2495. This certainly challenged traditional views on fluid resuscitation in septic shock and international guidelines have been influenced by these findings, suggesting a more conservative approach where intensive care is not available. In a small but detailed, prospective observational study, Obonyo NG et al Pediatric Critical Care Medicine 2022;23:502–513 have described a fluid conservative approach to treating septic shock and examined the physiological effects of a maintenance-only fluid strategy. Case-fatality, haemodynamic and myocardial function endpoints were examined in 30 children (≥60 days to ≤12 years) who presented with severe febrile illness and clinical signs of impaired perfusion. They used IV maintenance fluid (4?mL/kg/hr) unless children had WHO defined shock (≥3 signs) where they received two fluid boluses (20?mL/kg) and transfusion if shock persisted. Clinical, electrocardiographic, echocardiographic, and laboratory data were collected at presentation, during resuscitation and on day 28. Outcome measures were 48-hour mortality, normalisation of hemodynamics, and cardiac biomarkers. Of the thirty children (70 males), six had WHO shock, all of whom died (6/6) vs three of 24 deaths in the non-WHO shock. Median fluid volume received by survivors and nonsurvivors were similar (13 IQR, 9–32 vs 30?mL/kg 28–61?mL/kg, z =1.62, p=0.23). By 24 hours, we observed increases in median (IQR) stroke volume index (39?mL/m2 32–42?mL/m 2 to 47?mL/m2 41–49?mL/m 2 ) and a measure of systolic function: fractional shortening from 30 (27–33) to 34 (31–38) from baseline including children managed with no-bolus. Children with WHO shock had a higher mean level of cardiac troponin ( t= 3.58; 95?CI, 1.24 to 1.43; p=0.02) and alpha-atrial natriuretic peptide ( t =16.5; 95?CI, 2.80 to 67.5; p0.1?μg/mL) and hyperlactatemia (>4?mmol/L) were putative makers predicting outcome. Maintenance-only fluid therapy normalised clinical and myocardial perturbations in shock without compromising cardiac or haemodynamic function whereas fluid-bolus management of WHO shock resulted in high fatality. These authors conclude that their study has demonstrated ‘the normalisation of cardiac and haemodynamic perturbations of shock managed with a no-bolus strategy and evidence of high mortality in children who receiving boluses in accordance with the 2013 WHO paediatric guidelines’. Troponin and lactate biomarkers of cardiac dysfunction could be promising outcome predictors in paediatric septic shock in resource-limited settings. They finally comment that the major challenge in the future is how to support circulatory collapse and myocardial impairment in resource-limited settings which have no access to high dependency care or ventilatory support.
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