Transient hyperlactatemia during intravenous administration of glycerol: a prospective observational study

Abstract Background Intravenous glycerol treatment, usually administered in the form of a 5% fructose solution, can be used to reduce intracranial pressure. The administered fructose theoretically influences blood lactate levels, although little is known regarding whether intravenous glycerol treatment causes transient hyperlactatemia. This study aimed to evaluate blood lactate levels in patients who received intravenous glycerol or mannitol. Methods This single-center prospective observational study was performed at a 14-bed general intensive care unit between August 2016 and January 2018. Patients were excluded if they were  2.0 mmol/L). The included patients received intravenous glycerol or mannitol to reduce intracranial pressure and provided blood samples for lactate testing before and after the drug infusion (before the infusion and after 15 min, 30 min, 45 min, 60 min, 90 min, 120 min, and 150 min). Results Among the 33 included patients, 13 patients received 200 mL of glycerol over 30 min, 13 patients received 200 mL of glycerol over 60 min, and 7 patients received 300 mL of mannitol over 60 min. Both groups of patients who received glycerol had significantly higher lactate levels than the mannitol group (2.8 mmol/L vs. 2.2 mmol/L vs. 1.6 mmol/L, P < 0.0001), with the magnitude of the increase in lactate levels corresponding to the glycerol infusion time. There were no significant inter-group differences in cardiac index, stroke volume, or stroke volume variation. In the group that received the 30-min glycerol infusion, blood lactate levels did not return to the normal range until after 120 min. Conclusions Intravenous administration of glycerol leads to higher blood lactate levels that persist for up to 120 min. Although hyperlactatemia is an essential indicator of sepsis and/or impaired tissue perfusion, physicians should be aware of this phenomenon when assessing the blood lactate levels

Additional file 5 of Association between hypomagnesemia and coagulopathy in sepsis: a retrospective observational study

Additional file 5: Coagulation parameters between different serum magnesium levels (hypomagnesemia, normal magnesium level, and hypermagnesemia) on day 5 in sepsis

Additional file 3 of Association between hypomagnesemia and coagulopathy in sepsis: a retrospective observational study

Additional file 3: Coagulation parameters for each serum magnesium level

Additional file 8 of Association between hypomagnesemia and coagulopathy in sepsis: a retrospective observational study

Additional file 8: Receiver operating characteristic curves of serum magnesium concentration for DIC

Additional file 11 of Association between hypomagnesemia and coagulopathy in sepsis: a retrospective observational study

Additional file 11: Coagulation parameters according to the quartiles of serum ionized calcium

Additional file 2 of Association between hypomagnesemia and coagulopathy in sepsis: a retrospective observational study

Additional file 2: Histogram of serum ionized calcium concentration by DIC status

Additional file 4 of Association between hypomagnesemia and coagulopathy in sepsis: a retrospective observational study

Additional file 4: Coagulation parameters between different serum magnesium levels (hypomagnesemia, normal magnesium level, and hypermagnesemia) on day 3 in sepsis

Additional file 1 of Association between hypomagnesemia and coagulopathy in sepsis: a retrospective observational study

Additional file 1: Patient characteristics and laboratory parameters of the study population by DIC statu

Additional file 7 of Association between hypomagnesemia and coagulopathy in sepsis: a retrospective observational study

Additional file 7:Time course of coagulation parameters in developed hypomagnesemia and non-hypomagnesemia on day 3

Time course of immature platelet count and its relation to thrombocytopenia and mortality in patients with sepsis

<div><p>Introduction</p><p>The pathogenesis of thrombocytopenia in patients with sepsis is not fully understood. The aims of this study were to investigate changes in thrombopoietic activity over time by using absolute immature platelet counts (AIPC) and to examine the impact of platelet production on thrombocytopenia and mortality in patients with sepsis.</p><p>Methods</p><p>This retrospective observational study included adult patients with sepsis admitted to the intensive care unit at a university hospital. Two hundred five consecutive sepsis patients were stratified into four groups according to nadir platelet count: severe (nadir ≤40×10³/μL), moderate (41–80×10³/μL), or mild thrombocytopenia (81–120×10³/μL), or normal-increased platelet count (>120×10³/μL). The development of thrombocytopenia was assessed during the first week; mortality was assessed at day 28.</p><p>Result</p><p>Of the 205 patients included, 61 (29.8%) developed severe thrombocytopenia. On admission, AIPC did not differ among the four groups. In patients with severe thrombocytopenia, AIPC decreased significantly from days 2 to 7, but remained within or above the normal range in the other three groups (overall group comparison, <i>P</i><0.0001). Multivariate analysis including coagulation biomarkers revealed that AIPC was independently associated with the development of severe thrombocytopenia (day 3 AIPC, odds ratio 0.49 [95% confidence interval (CI) 0.35–0.66], <i>P</i><0.0001; day 5 AIPC, 0.59 [95% CI 0.45–0.75], <i>P</i><0.0001). AIPC was a significant predictor of 28-day mortality in Cox hazard models adjusted for Acute Physiology and Chronic Health Evaluation II and Sequential Organ Failure Assessment scores (day 3 AIPC, hazard ratio 0.70 [95% CI 0.52–0.89], <i>P</i> = 0.0029; day 5 AIPC, 0.68 [95% CI 0.49–0.87], <i>P</i> = 0.0012).</p><p>Conclusions</p><p>Thrombopoietic activity was generally maintained in the acute phase of sepsis. However, a decrease in AIPC after admission was independently associated with the development of severe thrombocytopenia and mortality, suggesting the importance of suppressed thrombopoiesis in the pathophysiology of sepsis-induced thrombocytopenia.</p></div