A case of heparin-induced thrombocytopenia associated with respiratory failure due to pseudopulmonary embolism

  • Kotoda Atsushi
    Division of Nephrology, Department of Internal Medicine, Jichi Medical University
  • Kato Maki
    Department of Medicine, Haga Red Cross Hospital
  • Akimoto Tetsu
    Department of Medicine, Haga Red Cross Hospital
  • Takahashi Hideaki
    Division of Nephrology, Department of Internal Medicine, Jichi Medical University
  • Ito Chiharu
    Division of Nephrology, Department of Internal Medicine, Jichi Medical University
  • Takeda Shinichi
    Division of Nephrology, Department of Internal Medicine, Jichi Medical University
  • Ando Yasuhiro
    Division of Nephrology, Department of Internal Medicine, Jichi Medical University
  • Muto Shigeaki
    Division of Nephrology, Department of Internal Medicine, Jichi Medical University
  • Yumura Wako
    Division of Nephrology, Department of Internal Medicine, Jichi Medical University
  • Kusano Eiji
    Division of Nephrology, Department of Internal Medicine, Jichi Medical University

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Other Title
  • 偽性肺塞栓症によると思われた呼吸器症状が診断の契機となったヘパリン起因性血小板減少症の1例
  • 症例報告 偽性肺塞栓症によると思われた呼吸器症状が診断の契機となったヘパリン起因性血小板減少症の1例
  • ショウレイ ホウコク ギセイ ハイ ソクセンショウ ニ ヨル ト オモワレタ コキュウキ ショウジョウ ガ シンダン ノ ケイキ ト ナッタ ヘパリン キインセイ ケッショウバン ゲンショウショウ ノ 1レイ

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Abstract

Heparin-induced thrombocytopenia (HIT) is a relatively common complication of heparin treatment among the patients who are newly treated by hemodialysis. We herein describe an 81-year-old woman with polycythemia vera (PV) who developed HIT associated with respiratory failure. She developed uremia due to diabetic nephropathy and hemodialysis was therefore initiated. Ten days after the first hemodialysis session, an arteriovenous fistula was surgically created to provide permanent access to the blood stream. Several minutes after the intravenous infusion of unfractionated heparin during surgery, the patient developed chest pain and became tachypenic. Thereafter, diagnostic computed tomography demonstrated the presence of thrombus, which had formed around the catheter for hemodialysis and also a right kidney infarction. However, there were no signs of any pulmonary embolism, and the presence of platelet-activating antibodies that recognize the complexes of platelet factor 4 and heparin was serologically confirmed. We therefore discontinued heparin and initiated the administration of argatroban followed by the normalization of the depleted platelet count, and the patient's respiratory symptoms finally subsided. We attributed the sustained respiratory symptoms observed in our patient to a pseudopulmonary embolism that might have resulted from a microembolism of pulmonary capillaries. We must therefore always bear in mind that the development of respiratory symptoms may be associated with the onset of HIT in patients treated with heparin. In our patient, the role that PV may have played in the clinical course of HIT remains to be elucidated. However, the identification of PV among patients with end stage renal failure may facilitate the diagnosis of thrombotic disorders including HIT, since the combination of HIT and PV is not so exceptionally rare in clinical settings.

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