Leukocyte Larceny in AML: A Case of Falsely Low Oxygen Levels - Case Report

Updated: Apr 15

VJM Spring Edition 2026

https://doi.org/10.18130/0824-c493

Authors: Gabriela Tactuk BS1, Ted Raddell DO2, Alex Estrella MD3, Jessica Rais MD4, Farah Ashraf4

Author Affiliations:

1 Cooper Medical School of Rowan University, Camden, NJ 08103

2 Department of Internal Medicine, Cooper University Hospital, Camden, NJ 08103

3 Department of Critical Care, Cooper University Hospital, Camden, NJ 08103

4 Department of Hematology-Oncology, Cooper University Hospital, Camden, NJ 08103

Abstract

Hyperleukocytosis in acute myeloid leukemia (AML) can cause life-threatening complications and rarely “leukocyte larceny,” in which markedly elevated blasts consume oxygen in arterial blood gas (ABG) samples, producing spuriously low PaO₂ values. We report an 82-year-old man with newly diagnosed AML and

WBC 310.8 × 109/L who developed hypoxic respiratory failure requiring intubation. Despite low post-intubation PaO2, pulse oximetry remained consistent with adequate oxygenation, suggesting partially spurious hypoxemia in the setting of true respiratory compromise. Cytoreduction was initiated; however, his course was complicated by tumor lysis syndrome, renal failure, shock, and death. This case highlights the diagnostic pitfall of leukocyte larceny that may complicate clinical decision-making and emphasizes the importance of correlating ABG results with pulse oximetry and considering rapid sample processing or cooling to reduce in vitro oxygen consumption.

Introduction

Acute myeloid leukemia (AML) is a form of cancer that is characterized by infiltration of the bone marrow, blood, and other tissues by proliferative, clonal, abnormally differentiated, and occasionally poorly differentiated cells of the hematopoietic system.¹ Patients presenting with AML can have life-threatening initial complications from hyperleukocytosis including disseminated intravascular coagulation (DIC), tumor lysis syndrome (TLS), infection, inflammation, hypercoagulability, and bone marrow failure.2

A rare but critical finding in AML is “leukocyte larceny,” a phenomenon where WBCs continue to consume oxygen after blood is drawn in the arterial blood gas (ABG) samples collected therefore causing a falsely low PaO₂ by the time it is processed in the lab.3,4 This phenomenon presents diagnostic and management

challenges, as clinicians must distinguish true hypoxemia from artifactual findings to avoid inappropriate escalation of respiratory support.

Case Description

An 82-year-old male with a history of prostate cancer, hyperthyroidism, dyslipidemia, hypertension, chronic kidney disease, and atherosclerotic peripheral vascular disease initially presented to an outside hospital

with shortness of breath for two days. He had endorsed one month of fatigue, early satiety, and recent COVID-19 and influenza infections. He was found to have severe leukocytosis, concern for AML, and TLS, and was transferred for escalation of care.

On arrival, the patient was tachypneic, requiring 40 L/min, FiO2 100% high-flow nasal cannula (HFNC) with an SpO2 of 95–100%, which resulted in initial improvement in work of breathing. Initial laboratory findings showed the following: WBC count 310.8 × 109/L, hemoglobin 9.4 g/dL, platelet count 66 × 109/L, creatinine 2.48 mg/dL, uric acid 10.6 mg/dL, potassium 3.4 mmol/L, calcium 8.3 mg/dL, and phosphorus 2.6 mg/dL, concerning for acute leukemia complicated by TLS. Peripheral smear displayed significant blasts (Figure 1). Fluorescence in situ hybridization (FISH) results were without significant rearrangement. Flow cytometry showed a large population of atypical dim CD45+ monocytoid cells, consistent with AML.

Despite 100% FiO2 on HFNC the patient remained tachypneic with increased work of breathing and had to be intubated around 14:00 on day 1. Despite intubation, FiO2 100% blood gas PaO2 was abnormally low despite pulse oximetry readings between 92–100% (Table 1). Adjustments to mechanical ventilation settings and oxygenation were decided to be made based on SpO2.

Cytoreduction with hydroxyurea and cytarabine was initiated. Unfortunately, despite cytoreduction, continuous renal replacement therapy, broad-spectrum antibiotics, and mechanical ventilatory support, the patient progressed to renal failure, shock, and refractory hypotension, resulting in cardiac arrest around 16:00 on day 2.

Figure 1. Peripheral blood smear from patient demonstrating myeloblasts

Table 1. Arterial blood gas correlation with pulse oximetry over time

Discussion

Hyperleukocytosis can present a challenge in distinguishing true hypoxemia from rare leukocyte-related hypoxia during initial management of AML.¹ In this case, the patient had true respiratory failure requiring intubation; however, the degree of hypoxemia suggested by ABG PaO2 was likely exaggerated by leukocytelarceny rather than purely reflective of physiologic oxygenation status. Although this patient was intubated for increased work of breathing and respiratory failure, his pO2 on ABG was inaccurate and did not correlate to

levels of SpO2 based on the oxygen dissociation curve at those levels of O2. This rare phenomenon has been documented in AML as spurious hypoxemia or “leukocyte larceny.”5 The burden of blast cells was so elevated that even after ABG samples were drawn, the hypermetabolic blasts continued to consume oxygen until the sample was processed.6 This represents a mixed picture of true hypoxemia with superimposed artifactual reduction in measured PaO2. Therefore, it was decided to base medical decision-making on pulse oximetry

instead of PaO2 or PaO2/FiO2 ratios.

This has important implications for clinical decision-making, as reliance on ABG values alone may lead to unnecessary escalation of ventilatory support or misclassification of severity of respiratory failure. Strategies to reduce this artifact include rapid analysis, minimizing processing delays, and sample cooling, which have been shown to reduce ongoing cellular oxygen consumption in vitro, although formal guideline recommendations remain limited.6,8

Since the patient was experiencing TLS, the goal was to cytoreduce with hydroxyurea and cytarabine before the initiation of chemotherapy. Management was further complicated by tumor lysis syndrome, renal failure requiring continuous renal replacement therapy, and hemodynamic instability, limiting available therapeutic options. Although leukapheresis was considered, there is growing evidence that cytoreduction has better mortality benefits than leukapheresis, and leukapheresis comes with significant risks including large bore venous access, anticoagulation, and electrolyte and fluid shifts.7 In this critically ill patient with multipressor shock and renal failure, leukapheresis was not pursued due to concern for poor tolerance of fluid shifts.

Conclusion

A case of AML is presented demonstrating leukocyte larceny to highlight this unusual phenomenon and its implications for hypoxia management. Clinicians should maintain suspicion for leukocyte larceny in patients with extreme leukocytosis and discordant ABG and pulse oximetry values, as recognition is essential to guide appropriate management and avoid unnecessary escalation of respiratory support.

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