Overcoming the problem of pseudohypoxemia in myeloproliferative disorders: Another trick in the bag
41 year old male, diagnosed with chronic myeloid leukaemia (CML) for five years with multiple admissions for easy fatiguability, abdominal pain, distension, fever and vomiting was treated conservatively with hydroxyurea and multiple blood transfusions. On this admission he was posted for splenectomy due to massive splenomegaly. Bilateral basal crepitations was noted on chest auscultation. Investigations showed haemoglobin- 8.7 g.dL-1, total leucocyte (WBC) count- 5, 09, 600 cells mm-3, platelet count- 1,14,000 cells mm-3, renal function, serum electrolytes and ECG were normal. Echocardiogram revealed minimal pericardial effusion. Chest X-ray showed cardiomegaly with normal lung fields. Patient underwent splenectomy uneventfully. Intraoperatively, he maintained oxygen saturation (SpO2) of 99-100%. Intraoperative arterial blood gas (ABG) analysis done on FiO20.5 showed a pH- 7.303, PaCO2- 47.9 mmHg, PaO2- 47.8 mmHg, standard bicarbonate- 23.2 mmol. L-1. In view of poor oxygenation as per the report, he was shifted to intensive care unit (ICU) for ventilator support suspecting pulmonary atelectasis. ABGs done in ICU also showed poor oxygenation [].\nBased on clinical improvement and pulse oximetry findings of 99-100%, he was weaned of ventilator support, extubated and discharged out of ICU.\nPostoperatively, patient was diagnosed to be in blast crisis in view of increasing platelet and WBC counts. He was started on hydroxyurea and allopurinol tablets to achieve cytoreduction. He was intubated and readmitted to ICU following an episode of generalised tonic-clonic seizure, altered sensorium and desaturation on oxygen therapy of 60% venturi by face mask.\nABGs done after this admission also showed poor oxygenation with acceptable acid base status [].\nChest radiograph did not show any deterioration. Meanwhile patient regained consciousness over a period of one day and tolerated pressure support ventilation and continued to maintain SpO2 of 98-100%. In view of the continued picture of hypoxaemia on serial ABGs, normal SpO2 and presence of blast crisis, a diagnosis of pseudohypoxaemia was made. Since point-of-care ABG analyser was not available, ABG repeated as rapidly as possible (delay of 7 minutes) from the sample immediately stored in ice showed a PaO2 of 71 mm Hg on FiO2 of 0.4 which was better than about 50 mm Hg consistently obtained in all the previous reports. We were prompted to precool the syringe even before obtaining the sample so that cooling the sampled blood could be hastened and the metabolism of cells be reduced more promptly.\nWe did three ABGs, one from sample obtained in a precooled syringe (kept in the freezer for 30 minutes and taken out just before drawing blood from a pre-existing arterial line), second from syringe immediately cooled in ice after sampling and another sample stored similarly but after a time delay of about 7 minutes after withdrawal. The time delay between sampling and analysis in first two samples was about 3 minutes. The ABGs are depicted in .\nThese values not only proved the diagnosis of pseudohypoxaemia but also indicated the usefulness of precooling of the syringe before sampling. We also noticed a minimal increase in PaCO2 values in samples analysed from the syringes without precooling.\nThe patient was extubated, shifted out of ICU and recovered uneventfully in the ward and was discharged on hydroxyurea and allopurinol medications.