A case of type B lactic acidosis as a complication of chronic myelomonocytic leukaemia: a case report and review of the literature
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  • 作者:Andrew John Gardner (13) (15)
    John Griffiths (14)

    13. Faculty of Medicine
    ; Oxford University ; John Radcliffe Hospital ; Oxford ; OX3 9DU ; UK
    15. Keble College
    ; Oxford ; OX1 3PG ; UK
    14. Nuffield Department of Anaesthetics
    ; John Radcliffe Hospital ; Oxford ; OX3 9DU ; UK
  • 关键词:Acidosis ; Chronic myelomonocytic leukaemia ; Haematological malignancy ; Type B lactic acidosis
  • 刊名:Journal of Medical Case Reports
  • 出版年:2015
  • 出版时间:December 2015
  • 年:2015
  • 卷:9
  • 期:1
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  • 刊物主题:Medicine/Public Health, general; General Practice / Family Medicine; Public Health; Primary Care Medicine;
  • 出版者:BioMed Central
  • ISSN:1752-1947
文摘
Introduction Type B lactic acidosis represents a rare and often lethal complication of haematological malignancy. Here, we present a patient who developed a type B lactic acidosis presumably due to a concurrent chronic myelomonocytic leukaemia. Upon swift initiation of cytoreductive chemotherapy (doxorubicin), the lactic acidosis was rapidly brought under control. This case adds to the literature reporting other haematological malignancies that can cause a type B lactic acidosis and its successful treatment. Case presentation We report the case of a 77-year-old Caucasian man brought to our Accident and Emergency department following an unwitnessed collapse; he was found surrounded by coffee-ground vomit. Although haemodynamically stable on admission, he rapidly deteriorated as his lactic acid rose. An initial arterial blood gas revealed a pH of 7.27 and lactate of 18mmol/L (peaking at 21mmol/L). Conclusions A high degree of clinical suspicion for haematological malignancy should be held when presented with a patient with lactic acidosis in clinical practice, even without evidence of poor oxygenation or another cause. Treatment with emergency chemotherapy, in lieu of a definitive diagnosis, was rapidly successful at lowering lactate levels within 8 hours. This may suggest a causal and perhaps direct relationship between lactic acid production and the presence of leukemic cells. Veno-venous haemofiltration had no apparent effect on reducing the lactic acidosis and therefore its benefit is questioned in this setting, especially at the cost of delaying chemotherapy. In the face of a life-threatening lactic acidosis, pragmatic clinical judgement alone may justify the rapid initiation of chemotherapy.

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