Section 4 of 5
Discussion
Hamza El Hamzaoui, Hamza Najout, A Bahouch, Lalla Hasnae Leghlimi, Bouchra Armel, Manal Arfaoui, Abdelkader Benhlima, Maha Louriz, and Mustapha Alilou · about 3 minutes
This prospective pilot study evaluated the prognostic value of admission blood lactate levels in patients with septic shock admitted to a multidisciplinary intensive care unit. The observed 28-day mortality rate of 56.1% (n = 23/41) is high but remains consistent with rates reported in international cohorts of septic shock patients, particularly in settings managing severe and complex cases [11,12]. This finding highlights the persistent burden and severity of septic shock despite ongoing advances in critical care management.
The principal finding of this study is the limited prognostic value of a single blood lactate measurement obtained at admission. Although admission lactate levels were higher in non-survivors (n = 23; median 3.9 mmol/L) than in survivors (n = 18; median 2.35 mmol/L), this difference did not reach statistical significance, and the discriminatory performance assessed by ROC curve analysis was poor (AUC = 0.610). These results suggest that initial lactate alone has limited ability to reliably predict short-term mortality in septic shock patients [13].
At first glance, this observation may appear to contrast with the central role attributed to lactate in sepsis management. However, our findings are consistent with an increasing body of literature indicating that while lactate is a valuable marker for early risk stratification and clinical alert, its prognostic relevance is substantially enhanced when evaluated dynamically rather than as a single static measurement [5,14].
The pathophysiology of hyperlactatemia in septic shock is complex and multifactorial. Elevated lactate levels do not exclusively reflect tissue hypoxia due to impaired perfusion (type A lactic acidosis) but may also result from increased aerobic glycolysis driven by catecholamine excess, mitochondrial dysfunction, and reduced hepatic clearance secondary to sepsis-induced organ dysfunction [15]. This complexity likely explains why a single lactate value at admission may inadequately capture the patient’s global physiological status and subsequent clinical trajectory.
Consequently, contemporary clinical practice has shifted from focusing on absolute lactate values to emphasizing lactate kinetics, particularly lactate clearance during the early phases of resuscitation. Several studies have demonstrated that a rapid decrease in lactate levels within the first hours of treatment is strongly associated with improved outcomes and reflects the effectiveness of therapeutic interventions such as fluid resuscitation, vasopressor optimization, and timely antimicrobial therapy [9,14]. The present study, which was designed to assess admission lactate only, did not allow for evaluation of lactate clearance, representing a key limitation.
Despite this limitation, our findings have important clinical implications. They reinforce the concept that elevated admission lactate levels should prompt immediate and aggressive management but should not be used in isolation as a definitive prognostic marker at the initial stage of care. Decisions regarding escalation, limitation, or withdrawal of life-sustaining therapies should not rely solely on a single lactate measurement. Instead, serial lactate monitoring integrated with comprehensive clinical, hemodynamic, and organ function assessments remains the most appropriate approach [14,15].
Several limitations of this study must be acknowledged. The small sample size inherent to its pilot design may have limited statistical power and reduced the ability to detect significant associations. In addition, the single-center nature of the study may limit the generalizability of the results. Future larger, multicenter studies incorporating lactate kinetics and dynamic resuscitation parameters, particularly in low- and middle-income settings, are warranted to better define the prognostic role of lactate in septic shock.