Tom Van den Hoek, Peter Kayaert, Eva De Caluwé, Philippe Timmermans
BACKGROUND: Pulmonary embolism (PE) is a potentially life-threatening condition and represents the third most common cardiovascular syndrome. Patients with cancer are at markedly increased risk of PE and often present with complex metabolic and haemodynamic alterations. Risk stratification in acute PE relies on clinical parameters, biomarkers, and imaging findings to guide therapeutic decisions. However, elevated lactate levels may have alternative aetiologies in oncologic patients, potentially leading to overtreatment of patients.
CASE SUMMARY: We report the case of a 60-year-old woman presenting with high-risk bilateral pulmonary embolism complicated by obstructive shock. Initial findings included hypotension, tachycardia, right ventricular dysfunction, elevated troponin, and severe hyperlactatemia. Systemic thrombolysis was administered following multidisciplinary discussion within a Pulmonary embolism response team. Despite rapid clinical and haemodynamic improvement, serum lactate levels remained persistently elevated without evidence of metabolic acidosis. Imaging revealed a large soft-tissue mass of the right leg, subsequently diagnosed as high-grade B-cell lymphoma. After exclusion or treatment of other possible explanations, the persistent hyperlactatemia was attributed to tumour-related aerobic glycolysis, consistent with the Warburg effect. Given the favourable clinical evolution, further invasive PE therapies were avoided. The patient was transitioned to anticoagulation and oncologic treatment, with a favourable long-term outcome.
DISCUSSION: This case illustrates how malignancy-associated metabolic alterations, such as the Warburg effect, can interfere with therapy in acute pulmonary embolism. Awareness of alternative causes of hyperlactatemia is essential to avoid unnecessary invasive interventions and to optimize individualized treatment strategies in cancer-associated PE.