In a case of contrast media-induced anaphylactic shock managed with epinephrine, a 57-year-old male patient developed lactic acidosis without cardiogenic shock or global hypoperfusion, highlighting epinephrine’s potential to trigger lactic acidosis. Despite the previous management of similar reactions with antihistamines and corticosteroids, this case required intensive care unit admission and emergency intervention for alarmingly high lactate level. The rapid resolution of acidosis following epinephrine discontinuation underscores the need for careful monitoring and consideration of alternative vasopressor strategies in severe anaphylaxis, illustrating the complex relationship between epinephrine’s metabolic effects and anaphylaxis-induced tissue hypoperfusion.
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Lactate in Anaphylaxis: 100 Years On Elena Borzova, Bernhard F. Gibbs Sports Medicine.2025; 55(9): 2091. CrossRef
Da Seul Kim, Jong Eun Park, Sung Yeon Hwang, Daun Jeong, Gun Tak Lee, Taerim Kim, Se Uk Lee, Hee Yoon, Won Chul Cha, Min Seob Sim, Ik Joon Jo, Tae Gun Shin
Clin Exp Emerg Med 2022;9(3):176-186. Published online September 30, 2022
Objective We evaluated the performance of diastolic shock index (DSI) and lactate in predicting vasopressor requirement among hypotensive patients with suspected infection in an emergency department.
Methods This was a single-center, retrospective observational study for adult patients with suspected infection and hypotension in the emergency department from 2018 to 2019. The study population was split into derivation and validation cohorts (70/30). We derived a simple risk score to predict vasopressor requirement using DSI and lactate cutoff values determined by Youden index. We tested the score by the area under the receiver operating characteristic curve (AUC). We performed a multivariable regression analysis to evaluate the association between the timing of vasopressor treatment and 28-day mortality.
Results A total of 1,917 patients were included. We developed a score, assigning 1 point each for the high DSI (≥2.0) and high lactate (≥2.5 mmol/L) criteria. The AUCs of the score were 0.741 (95% confidence interval [CI], 0.715–0.768) at hypotension and 0.736 (95% CI, 0.708–0.763) after initial fluid challenge in the derivation cohort and 0.676 (95% CI, 0.631–0.719) at hypotension and 0.688 (95% CI, 0.642–0.733) after initial fluid challenge in the validation cohort, respectively. In patients with scores of 2 points, early vasopressor therapy initiation was significantly associated with decreased 28-day mortality (adjusted odds ratio, 0.37; 95% CI, 0.14–0.94).
Conclusion A prediction model with DSI and lactate levels might be useful to identify patients who are more likely to need vasopressor administration among hypotensive patients with suspected infection.
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Objective Reliable biomarkers of delayed neuropsychological sequelae (DNS) after acute carbon monoxide (CO) poisoning are lacking. This study investigated the associations between potential serum markers and the development of DNS after acute CO poisoning.
Methods Retrospective chart reviews were conducted for patients diagnosed with acute CO poisoning during a 28-month period. The patients were divided into two groups according to the presence or absence of having developed DNS. Multivariate analysis was performed to identify predictors of DNS after CO poisoning.
Results Of a total of 102 patients, 10 (9.8%) developed DNS. The levels of serum osmolarity, S100B protein, and serum lactate, as well as serum anion gap, were statistically significant in univariate analysis. Multiple logistic regression analysis showed that anion gap (adjusted odds ratio [AOR], 1.36; 95% confidence interval [CI], 1.11 to 1.88), serum lactate level (AOR, 1.74; 95% CI, 1.26 to 2.75), and serum S100B protein level ([AOR, 7.02×105; 95% CI, 4.56×102 to 9.00×1010] in model 1, [AOR, 3.69×105; 95% CI, 2.49×102 to 2.71×1011] in model 2) were independently associated with DNS development.
Conclusion Based on our preliminary results, serum lactate level, serum anion gap, and serum S100B protein level in the emergency department could be informative predictors of DNS development in patients with acute CO poisoning. These markers might have the potential to improve early recognition of DNS in patients with acute CO poisoning.
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Objective We investigated the association between lactate clearance or serum lactate levels and neurologic outcomes or in-hospital mortality in cardiac arrest survivors who were treated with targeted temperature management (TTM).
Methods A retrospective analysis of data from cardiac arrest survivors treated with TTM between 2012 and 2015 was conducted. Serum lactate levels were measured on admission and at 12, 24, and 48 hours following admission. Lactate clearance at 12, 24, and 48 hours was also calculated. The primary outcome was neurologic outcome at discharge. The secondary outcome was in-hospital mortality.
Results The study included 282 patients; 184 (65.2%) were discharged with a poor neurologic outcome, and 62 (22.0%) died. Higher serum lactate levels at 12 hours (odds ratio [OR], 1.157; 95% confidence interval [CI], 1.006 to 1.331), 24 hours (OR, 1.320; 95% CI, 1.084 to 1.607), and 48 hours (OR, 2.474; 95% CI, 1.459 to 4.195) after admission were associated with a poor neurologic outcome. Furthermore, a higher serum lactate level at 48 hours (OR, 1.459; 95% CI, 1.181 to 1.803) following admission was associated with in-hospital mortality. Lactate clearance was not associated with neurologic outcome or in-hospital mortality at any time point after adjusting for confounders.
Conclusion Increased serum lactate levels after admission are associated with a poor neurologic outcome at discharge and in-hospital mortality in cardiac arrest survivors treated with TTM. Conversely, lactate clearance is not a robust surrogate marker of neurologic outcome or in-hospital mortality.
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Objective To describe the effect of liver disease (LD) on lactate clearance during early sepsis resuscitation.
Methods This is a multicenter randomized clinical trial. An initial lactate >2 mmol/L and subsequent serum lactate measurement within 6 hours were required for inclusion. LD was categorized by two methods: 1) past medical history (PMH) categorized as no LD, mild LD (no Child’s score criteria, but PMH of hepatitis B/C), cirrhosis; and 2) measurable liver dysfunction determined by the liver component of the sequential organ failure assessment (L-SOFA) score as no dysfunction (L-SOFA score 0), mild dysfunction (score 1), moderate-severe dysfunction (score 2 to 4). Primary outcome was the rate of lactate normalization.
Results One hundred eighty-seven patients were included. When categorized by PMH, 169 patients had no LD, 6 mild LD, and 12 cirrhosis. 63/169 (37%) of patients with no LD achieved lactate normalization, compared to 4/6 (67%) with mild LD, and 1/12 (8%) with cirrhosis (P<0.03). Categorized by L-SOFA score, 59/124 (47%) patients with L-SOFA 0 achieved lactate normalization, compared to 6/31 (19%) with L-SOFA 1, and 3/32 (9%) with L-SOFA 2–4 (P<0.01). Relative lactate clearance [(initial lactate–subsequent lactate)/initial lactate] was lower in patients with more advanced LD by PMH (37.7 vs. 40.4 vs. 21.8, P=0.07), and lower with increasing L-SOFA score (42.0 vs. 30.1 vs. 23.4, P=0.01).
Conclusion Liver dysfunction was significantly associated with impaired lactate clearance and normalization during the early resuscitation of sepsis.
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