INTRODUCTION:Hypoxemia is frequently encountered in the hospital setting and prompt evaluation of this potentially life threatening condition is essential. One under recognized entity in the evaluation of hypoxemia is pseudohypoxemia, or spurious hypoxemia, which occurs when the partial pressure of oxygen (PaO2) from laboratory measurements does not correlate with the bloodstream oxygen tension. This would result in a discrepancy between the oxygen saturation (SaO2) by pulse oximetry and the measured PaO2. Pseudohypoxemia has been reported in patients with extreme leukocytosis and thrombocytosis associated with hematologic malignancies.
CASE PRESENTATION:A 40-year-old African American man presented to the hospital with recurrent bacterial skin infections and leukocytosis with increased blasts. He was consequently diagnosed with acute promyelocytic leukemia (AML) and treatment was initiated with all-trans-retinoic acid (ATRA) and idarubicin. Two days after the initiation of chemotherapy, the patient developed hemoptysis, respiratory distress and increased oxygen requirement. Chest imaging showed diffuse bilateral alveolar infiltrates. The patient progressed to hypoxemic respiratory failure requiring invasive mechanical ventilation. Given the close association with ATRA administration, there was high suspicion for ATRA syndrome. Bronchoscopy confirmed the presences of pulmonary hemorrhage. ATRA was discontinued and treatment with high dose steroids was initiated. Blood gas analysis persistently showed marked hypoxemia, however the SaO2 by oximetry was 95 -100%. This discrepancy and the fact that he had leukocytosis with increased blasts raised the suspicion for pseudohypoxemia. Arterial blood gas with co-oximetry excluded a hemoglobinopathy and showed a PaO2 of 47mmHg. With treatment of AML and improvement in leukocyte count, the discrepancy between PaO2 and pulse oximetry resolved.
DISCUSSIONS:Pulmonary involvement occurs relatively early in the hyperleukocytosis syndrome. Hyperluekocytosis can result in pulmonary leukostasis and may predispose to pseudohypoxemia. The presence of an elevated WBC count can lead to a low measured PaO2. These spuriously low levels of PaO2 are believed to reflect consumption of dissolved oxygen from the arterial blood gas specimen, a phenomenon referred to as “oxygen steal” or “leukocyte larceny”. An inverse correlation has been described between the PaO2 and the leukocyte count. Leukocytes have a comparatively high metabolic rate and thus are an important source of oxygen consumption with immature cells having a higher rate of oxygen consumption. Interference of leukocytes with the O2 electrode by coating the membrane has been proposed as an alternative mechanism to explain the low PaO2.Several techniques have been reported to assess oxygen content in a patient with hyperleukocytosis. These include measurement of oxygen content from plasma, and the use of bedside continuous arterial oxygen content. Leukocyte metabolism can be reduced by immersing the sample immediately in ice or adding metabolic inhibitors. Pulse oximetry utilizes spectrophotometric principles to determine SaO2, whereas the arterial blood gas SaO2 is calculated from the PaO2 value in the sample. The rapid consumption of dissolved oxygen by hypermetabolic cells makes the SaO2 in ABG unreliable. Pulse oximetry remains an invaluable tool in evaluating oxygenation at the bed side and as in our case provides insight into the pathophysiology of the patient’s oxygenation problem.
CONCLUSION:Pseudohypoxemia may be a confounding factor in hypoxemic patients with hematologic disorders. The clinician must maintain a high index of suspicion to diagnose this condition as failure to do so leads to unnecessary escalation of diagnostic work up and therapy.
DISCLOSURE:Jinesh Mehta, No Financial Disclosure Information; No Product/Research Disclosure Information