Quantization of severity of critical illness with special reference to blood lactate

Cady, Lee D.; Weil, Max Harry; Afifi, Abdelmonem A.; Michaels, Sybil F.; Liu, Vinnie Y.; Shubin, Herbert

doi:10.1097/00003246-197303000-00003

Cited by 135 publications

(48 citation statements)

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“…2 The blood lactate concentrations in critically ill and injured adult patients can be used to detect tissue hypoxia at an early stage, assess illness severity, and predict outcome. 3,4 Recent papers have drawn our attention to the prognostic value of lactacidaemia in newborns with severe hypoxaemia. 2,5 The relationship between intrapartum asphyxia and neurological abnormalities is controversial.…”

Section: Introductionmentioning

confidence: 99%

Postnatal Lactate as an Early Predictor of Short-Term Outcome after Intrapartum Asphyxia

2003

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OBJECTIVES:To compare the predictive value of pH, base deficit and lactate for the occurrence of moderate-to-severe hypoxic ischaemic encephalopathy (HIE) and systemic complications of asphyxia in term infants with intrapartum asphyxia. STUDY DESIGN:We retrospectively reviewed the records of 61 full-term neonates (Z37 weeks gestation) suspected of having suffered from a significant degree of intrapartum asphyxia from a period of January 1997 to December 2001.The clinical signs of HIE, if any, were categorized using Sarnat and Sarnat classification as mild (stage 1), moderate (stage 2) or severe (stage 3). Base deficit, pH and plasma lactate levels were measured from indwelling arterial catheters within 1 hour after birth and thereafter alongwith every blood gas measurement. The results were correlated with the subsequent presence or absence of moderate-to-severe HIE by computing receiver operating characteristic curves. RESULTS:The initial lactate levels were significantly higher (p ¼ 0.001) in neonates with moderate-to-severe HIE (mean±SD ¼ 11.09±4.6) as compared to those with mild or no HIE (mean±SD ¼ 7.1±4.7). Also, the lactate levels took longer to normalize in these babies. A plasma lactate concentration >7.5±mmol/l was associated with moderate-or-severe HIE with a sensitivity of 94% and specificity of 67%. The sensitivity and negative predictive value of lactate was greater than that of the pH or base deficit. CONCLUSIONS:The highest recorded lactate level in the first hour of life and serial measurements of lactate are important predictors of moderate-to-severe HIE.

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Section: Introductionmentioning

confidence: 99%

Postnatal Lactate as an Early Predictor of Short-Term Outcome after Intrapartum Asphyxia

2003

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“…In the past century, Weil and colleagues demonstrated an exponential increase in the mortality of critically ill patients with increasing blood lactate concentrations. 10,11 The mortality increases linearly above a lactate concentration of approximately 1 mmol/L and this association is independent of organ dysfunction or the presence of shock.…”

Section: Lactic Acidosis In Sepsismentioning

confidence: 99%

Lactic acidosis, hyperlactatemia and sepsis

Montagnani¹,

Nardi²

2016

Ital J Med

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Among hospitalized patients, lactic acidosis represents the most common cause of metabolic acidosis. Lactate is not just a metabolic product of anaerobic glycolysis but is triggered by a variety of metabolites even before the onset of anaerobic metabolism as part of an adaptive response to a hypermetabolic state. On the basis of such considerations, lactic acidosis is divided into two classes: inadequate tissue oxygenation (type A) and absence of tissue hypoxia (type B). Lactic acidosis is characterized by non-specific symptoms but it should be suspected in all critical patients who show hypovolemic, hypoxic, in septic or cardiogenic shock or if in the presence of an unexplained high anion gap metabolic acidosis. Lactic acidosis in sepsis and septic shock has traditionally been explained as a result of tissue hypoxia when whole-body oxygen delivery fails to meet whole body oxygen requirements. In sepsis lactate levels correlate with increased mortality with a poor prognostic threshold of 4 mmol/L. In hemodynamically stable patients with sepsis, hyperlactatemia might be the result of impaired lactate clearance rather than overproduction. In critically ill patients the speed at which hyperlactatemia resolves with appropriate therapy may be considered a useful prognostic indicator. The measure of blood lactate should be performed within 3 h of presentation in acute care setting. The presence of lactic acidosis requires early identification of the primary cause of shock for the best appropriate treatment. Since most cases of lactic acidosis depend on whole-body oxygen delivery failure, the maximization of systemic oxygen delivery remains the primary therapeutic option. When initial resuscitation does not substantially or completely correct lactic acidosis, it is also essential to consider other causes. The treatment of acidosis with buffering agents (specifically bicarbonate) is generally advocated only in the setting of severe acidosis. Ongoing research into lactate clearance and probable noninvasive surrogate measures may add further insight into outcome-based practices.

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“…Although lactate itself lacks precision, in the appropriate clinical setting, an elevated level (Ն4 mmol/L) is indicative of tissue hypoperfusion and an independent predictor of mortality (32,33). In the initial inflammatory phase, there is often an increase in oxygen delivery, which may be associated with a fall in ScvO 2 or SvO 2 as a result of an inadequate cardiovascular response .…”

Section: Diagnostic Challenges In Sepsismentioning

confidence: 99%