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Abstract Rationale Hyperlactatemia in sepsis may derive from a prevalent impairment of oxygen supply/demand and/or oxygen use. Discriminating between these two mechanisms may be relevant for the early fluid resuscitation strategy. Objectives To understand the relationship among central venous oxygen saturation (ScvO2), lactate, and base excess to better determine the origin of lactate. Methods This was a post hoc analysis of baseline variables of 1,741 patients with sepsis enrolled in the multicenter trial ALBIOS (Albumin Italian Outcome Sepsis). Variables were analyzed as a function of sextiles of lactate concentration and sextiles of ScvO2. We defined the “alactic base excess,” as the sum of lactate and standard base excess. Measurements and Main Results Organ dysfunction severity scores, physiologic variables of hepatic, metabolic, cardiac, and renal function, and 90-day mortality were measured. ScvO2 was lower than 70% only in 35% of patients. Mortality, organ dysfunction scores, and lactate were highest in the first and sixth sextiles of ScvO2. Although lactate level related strongly to mortality, it was associated with acidemia only when kidney function was impaired (creatinine >2 mg/dl), as rapidly detected by a negative alactic base excess. In contrast, positive values of alactic base excess were associated with a relative reduction of fluid balance. Conclusions Hyperlactatemia is powerfully correlated with severity of sepsis and, in established sepsis, is caused more frequently by impaired tissue oxygen use, rather than by impaired oxygen transport. Concomitant acidemia was only observed in the presence of renal dysfunction, as rapidly detected by alactic base excess. The current strategy of fluid resuscitation could be modified according to the origin of excess lactate.

Lactic acidosis is commonly associated with tissue hypoperfusion and gives rise to concern regarding hypoxia or underlying hypotension. In the cancer patient, especially one undergoing chemotherapy, there is always concern for sepsis; however, in the otherwise clincially stable patient with cancer, type B lactic acidosis can also be related to their underlying malignancy. It is considered a haematological emergency given its high mortality rate. However, despite the urgency to treat type B lactic acidosis in these circumstances, treatment options beyond treatment of the malignancy are limited, and its presence portends a poor prognosis. This case highlights our current understanding of type B lactic acidosis and an approach to lactic acidosis evaluation in the cancer patient.

When lactic acidosis accompanies low-flow states or sepsis, mortality rates increase sharply. This review summarizes our current understanding of the pathophysiological aspects of lactic acidosis, as well as the approaches to its diagnosis and management. Lactic acidosis results from the accumulation of lactate and protons in the body fluids and is often associated with poor clinical outcomes. The effect of lactic acidosis is governed by its severity and the clinical context. Mortality is increased by a factor of nearly three when lactic acidosis accompanies low-flow states or sepsis, 1 and the higher the lactate level, the worse the outcome. 2 Although hyperlactatemia is often attributed to tissue hypoxia, it can result from other mechanisms. Control of the triggering conditions is the only effective means of treatment. However, advances in understanding its pathophysiological features and the factors causing . . .

Prior studies have suggested that transfusion of stored red blood cells (RBCs) with increased levels of cell-free hemoglobin might reduce the bioavailability of recipient nitric oxide (NO) and cause myocardial strain. Ugandan children (ages 6-60 months) with severe anemia and lactic acidosis were randomly assigned to receive RBCs stored 1-10 days versus 25-35 days. B-type natriuretic peptide (BNP), vital signs, renal function test results, and plasma hemoglobin were measured. Most children had either malaria or sickle cell disease and were thus at risk for reduced NO bioavailability. Seventy patients received RBCs stored 1-10 days, and 77 received RBCs stored 25-35 days. The median (interquartile range) cell-free hemoglobin was nearly 3 times higher in longer-storage RBCs (26.4 [15.5-43.4] μmol/L) than in shorter-storage RBCs (10.8 [7.8-18.6] μmol/L), P < .0001. Median (interquartile range) BNP 2 hours posttransfusion was 156 (59-650) pg/mL (shorter storage) versus 158 (59-425) pg/mL (longer storage), P = .76. BNP values 22 hours posttransfusion were 110 (46-337) pg/mL (shorter storage) versus 96 (49-310) pg/mL (longer storage), P = .76. Changes in BNP within individuals from pretransfusion to 2 hours (or 22 hours) posttransfusion were not significantly different between the study groups. BNP change following transfusion did not correlate with the concentration of cell-free hemoglobin in the RBC supernatant. Blood pressure, blood urea nitrogen, creatinine, and change in plasma hemoglobin were not significantly different in the 2 groups. In a randomized trial among children at risk for reduced NO bioavailability, we found that BNP, blood pressure, creatinine, and plasma hemoglobin were not higher in patients receiving RBCs stored for 25-35 versus 1-10 days.

Background Severe malarial anaemia requiring blood transfusion is a life-threatening condition affecting millions of children in sub-Saharan Africa. Up to 40% of children with severe malarial anaemia have associated lactic acidosis. Lactic acidosis in these children is strongly associated with fatal outcomes and is corrected by blood transfusion. However, it is not known whether the storage age of blood for transfusion affects resolution of lactic acidosis. The objective of this pilot study was to evaluate the effect of blood storage age on resolution of lactic acidosis in children with severe malarial anaemia and demonstrate feasibility of conducting a large trial. Methods Children aged six to 59 months admitted to Acute Care Unit of Mulago Hospital (Kampala, Uganda) with severe malarial anaemia (haemoglobin ≤ 5 g/dL) and lactic acidosis (blood lactate ≥5 mmol/L), were randomly assigned to receive either blood of short storage age (one to 10 days) or long storage age (21–35 days) by gravity infusion. Seventy-four patients were enrolled and randomized to two equal-sized study arms. Physiological measurements, including blood lactate, oxygen saturation, haemoglobin, and vital signs, were taken at baseline, during and after transfusion. The primary outcome variable was the proportion of children whose lactic acidosis resolved by four hours after transfusion. Results Thirty-four of 37 (92%) of the children in the short storage treatment arm compared to 30/37 (81%) in the long storage arm achieved a blood lactate <5 mmol/L by four hours post transfusion (p value = 0.308). The mean time to lactic acidosis resolution was 2.65 hours (95% CI; 2.25–3.05) in the short storage arm, compared to 3.35 hours (95% CI; 2.60–4.10) in the long storage arm (p value = 0.264). Conclusion Pilot data suggest that among children with severe malarial anaemia and lactic acidosis transfused with packed red blood cells, the storage age of blood does not affect resolution of lactic acidosis. The results support a larger and well-powered study which is under way. Trial registration clinicaltrials.gov NCT01580111

Metformin associated lactic acidosis (MALA) and severe acute kidney injury (AKI) is a life-threatening condition, often requiring renal replacement therapy. However, the optimal renal replacement therapy regimen in this setting remains unclear. Furthermore, limited data exist on the use of regional citrate anticoagulation, as severe hyperlactatemia is associated with increased risk of citrate accumulation. We retrospectively analyzed the medical records of all patients with MALA and severe AKI requiring renal replacement therapy at our hospital between June 2011 and December 2021. All patients were treated with high dose CVVHDF. Anticoagulation was achieved using either heparin or regional citrate anticoagulation. A total of 27 patients with MALA and AKI requiring renal replacement therapy were identified. In all patients, CVVHDF was started within one hour of the diagnosis. Four deaths were recorded, resulting in an overall mortality rate of 14.8%. In the remaining 23 patients (85.2%), we observed the correction of the metabolic disorder and the recovery of renal function that allowed for the discontinuation of dialysis. Mean lactatemia at diagnosis was 12.9 mmol/l (range 7.0–24.0) and mean pH 6.99 (range 6.50–7.22). CVVHDF mean effluent rate was as high as 52.1 ml/kg/h. In thirteen patients regional citrate anticoagulation was safely employed. In our experience, CVVHDF prescribed at the appropriate dose have yielded favorable results, in terms both of patient survival and metabolic control of the disease. Regional citrate anticoagulation can be safely used in selected cases.

Metformin-associated lactic acidosis (MALA) is a life-threatening complication. Treatment of MALA includes supportive care and dialysis. However, the role of kidney replacement therapy (KRT) in MALA is controversial, this study aimed to compare patient and kidney outcomes between MALA-acute kidney injury (AKI) patients receiving KRT (KRT group) vs. supportive care (supportive care group). A cohort study was conducted on 143 adult patients with MALA-AKI from 1 January 2015 to 31 December 2021. The primary outcome was the patient mortality rate and predictive factors of mortality, while the secondary outcomes were kidney survival. The overall mortality rate in our MALA-AKI cohort was 20.3% (29 of 143 patients). The KRT group had a lower mortality rate compared with the supportive care group (16% vs. 28.6%,  = 0.006). Among patients who received dialysis, hemodialysis (HD) was associated with a lower mortality rate compared with acute peritoneal dialysis (APD) (8.9% vs. 30.8%,  = 0.044). Patients who received late KRT (≥6 h) had a trend toward higher mortality compared with those who received early KRT (<6 h). Independent predictors of mortality were oliguria (HR 8.59,  = 0.002), prolonged prothrombin time (HR 1.20,  = 0.001) and higher Sequential Organ Failure Assessment (SOFA) scores (HR 1.26,  = 0.006). MALA-AKI was associated with high mortality, and KRT reduced mortality rate when compared with supportive care. HD was the most effective treatment in MALA-AKI, early KRT initiation (<6 h) showed a trend toward lower mortality and oliguria, prolonged prothrombin time, and higher SOFA scores were identified as prognostic markers.