Jolivet Franck, Diquélou Armelle, Trumel Catherine, Privat Simon, Dossin Olivier
Department of Clinical Sciences, ENVT, University of Toulouse, 31076, Toulouse, France.
IRSD, INSERM 1220, INSERM, INRA, ENVT, UPS, University of Toulouse, 31024, Toulouse, France.
BMC Vet Res. 2017 Jun 19;13(1):183. doi: 10.1186/s12917-017-1110-8.
Among coagulation disorders, primary fibrinogen deficiency is very rare in dogs. It is divided into hypofibrinogenemia, afibrinogenemia and dysfibrinogenemia. Afibrinogenemia has been described in three dogs. There are, however, no published case reports of primary hypofibrinogenemia in dogs.
A 1.5 year-old male German Pointer dog was evaluated for a locked-jaw syndrome associated with eye protrusion which appeared after a minor head trauma. Three months before the trauma, a persistent increase in coagulation times was detected by the referring veterinarian after a strong suspicion of snake envenomation. Apart for the primary complaint, physical examination was normal. A complete hemostatic profile revealed a moderately increased prothrombin time, activated partial thromboplastin times and a dramatically decreased fibrinogen concentration (0.34 g/L, reference interval [1.3-4.8 g/L]). Platelet count, plasma D-dimers and antithrombin, were all within the reference intervals and not consistent with a disseminated intravascular coagulation. Other possible causes of hypofibrinogenemia such as chronic hemorrhage and liver failure were excluded by laboratory work-up and imaging studies. Finally, antifibrinogen circulating anticoagulants were excluded using a dilution of citrated plasma from the pooled plasma of healthy dogs. These results supported a diagnosis of congenital fibrinogen deficiency and secondary retrobulbar hematoma and/or cellulitis. The dog's condition improved rapidly after symptomatic treatment with corticosteroids and antibiotics. At the 1 year follow-up, the dog was clinically normal but a persistent hypofibrinogenemia (≤ 0.8 g/L) remained.
Various clinical presentations may occur in canine primary hypofibrinogenemia which should be included in the list of coagulation disorders. Diagnosis should include fibrinogen determination by coagulometric and non-coagulometric methods to differentiate from dysfibrinogenemia. There is no specific treatment but care should be taken to prevent bleeding and trauma. Emergency management of bleeding episodes with cryoprecipitate is the treatment of choice.
在凝血障碍中，原发性纤维蛋白原缺乏症在犬类中非常罕见。它分为低纤维蛋白原血症、无纤维蛋白原血症和异常纤维蛋白原血症。已有三只犬被描述为无纤维蛋白原血症。然而，尚无犬原发性低纤维蛋白原血症的公开病例报告。
一只1.5岁的雄性德国短毛指示犬因轻微头部外伤后出现牙关紧闭综合征并伴有眼球突出而接受评估。外伤前三个月，转诊兽医在强烈怀疑蛇咬伤后检测到凝血时间持续延长。除了主要症状外，体格检查正常。完整的止血检查显示凝血酶原时间适度延长、活化部分凝血活酶时间延长，纤维蛋白原浓度显著降低（0.34 g/L，参考区间[1.3 - 4.8 g/L]）。血小板计数、血浆D - 二聚体和抗凝血酶均在参考区间内，与弥散性血管内凝血不符。通过实验室检查和影像学研究排除了其他可能导致低纤维蛋白原血症的原因，如慢性出血和肝功能衰竭。最后，使用健康犬混合血浆的枸橼酸盐血浆稀释液排除了抗纤维蛋白原循环抗凝剂。这些结果支持先天性纤维蛋白原缺乏症及继发性球后血肿和/或蜂窝织炎的诊断。该犬经皮质类固醇和抗生素对症治疗后病情迅速改善。在1年的随访中，该犬临床正常，但仍存在持续性低纤维蛋白原血症（≤0.8 g/L）。
犬原发性低纤维蛋白原血症可能出现多种临床表现，应列入凝血障碍列表中。诊断应包括通过凝固法和非凝固法测定纤维蛋白原，以与异常纤维蛋白原血症相鉴别。目前尚无特异性治疗方法，但应注意预防出血和创伤。出血发作时用冷沉淀进行紧急处理是首选治疗方法。
