Don't take vitals, take a lactate

ArticleinIntensive Care Medicine 33(11):1863-5 · December 2007with71 Reads
DOI: 10.1007/s00134-007-0679-y · Source: PubMed
    • "Conversely, Type B lactic acidosis occurs without evidence of systemic hypoperfusion and may be seen in association with systemic diseases such as hepatic failure, or malignancies or occur as a result of certain classes of drugs such as biguanides [2, 3] . Increased plasma lactate level (hyperlactatemia ) in critically ill patients is associated with high morbidity and mortality [4]. The effective treatment for lactic acidosis (Type A) is correcting the underlying cause and improving tissue oxygenation. "
    [Show abstract] [Hide abstract] ABSTRACT: Lactic acidosis is associated with high morbidity and mortality in hospitalized patients. Treatment of lactic acidosis is targeted on correcting the underlying causes and optimizing adequate oxygen delivery to the tissues. Even though evidence is lacking, continuous renal replacement therapy (CRRT) and dialysis have been advocated as treatments for lactic acidosis. We report a 28-year-old Caucasian male with a history of hemophagocytic lymphohistiocytosis who presented with septic shock, severe lactic acidosis and multiple organ failure. Metabolic acidosis was corrected after bicarbonate therapy and CRRT with a hemofiltration rate of 7 L/h (58 mL/kg/h). Lactate clearance was calculated to be 79 mL/min. Compared with reported rates of lactate overproduction in septic shock, the rate of lactate clearance is quite small. Our case suggests that CRRT with high-volume hemofiltration is not effective for severe lactic acidosis. Lactic acidosis alone should not be considered as a nonrenal indication for CRRT.
    Full-text · Article · Aug 2015
    • "The degree of change due to follow-up study (delta change or dC) that reflects the actual different changes through the follow-up study was significant with P-value 0.011. The results are with study published by Bakker and Jansen, showed that venous lactate predicted 28-day in-hospital mortality [45]. Nguyen and his colleagues observed the evolution of serial lactate levels in patients with severe sepsis during the first 6 h of treatment. "
    Full-text · Article · Jan 2015
    • "Lactic acidosis is the most common cause of anion gap metabolic acidosis in hospitalized patients (Madias, 1986). Increasing or persistently elevated lactate levels are associated with high morbidity and mortality (Bakker and Jansen, 2007). Tissue hypoperfusion in shock, leading to increased anaerobic metabolism, is responsible for type A lactic acidosis. "
    [Show abstract] [Hide abstract] ABSTRACT: Lactic acidosis is the most common cause of anion gap metabolic acidosis and is associated with high morbidity and mortality in hospitalized patients. The association between Hemophagocytic Lymphohistiocytosis (HLH) and lactic acidosis is still unclear. HLH causes cytokine overproduction which in turn induces lactic acidosis. There have been only few reports of type B lactic acidosis in HLH patients. There have been no studies addressing the outcome of cytokine removal for patients with HLH induced lactic acidosis. We reviewed literatures on HLH, focusing on its association with lactic acidosis and treatment options. This review demonstrates thatlactic acidosis in patients with HLH is under-recognized. Physicians should increase awareness of this association. In the setting of cytokine storm with multiorgan failure, cytokine removal with high blood flow, ultrafiltration rate and frequent membrane changes is a potential treatment option. More studies are urgently required to confirm this finding due to high morbidity and mortality of HLH.
    Full-text · Article · Jul 2014
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