Scott Syndrome (Platelet Disorder) in a Mixed Breed Dog

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A 3-year-old male intact German Shepherd-Malinois mixed breed dog was presented to the Cornell University Hospital for Animals for evaluation of epistaxis following a rhinoscopy. The patient had been evaluated by another veterinary referral center the day prior for a five day history of mild unilateral epistaxis. Magnetic resonance imaging and rhinoscopy were performed and were suggestive of mild bilateral rhinitis with minimal left nasal hemorrhage. No nasal turbinate destruction, gross masses, or lesions were observed on either study. Biopsies were taken and an Aspergillus sp. antibody serology was submitted. Prior to the procedures, a complete blood count, chemistry panel, prothrombin time (PT), activated partial thromboplastin time (aPTT), and chest radiographs were performed. Aside from a mild hypokalemia and hyperchloremia, the results were unremarkable.

On initial presentation to the Emergency Service, the patient was in hypovolemic shock with increased respiratory rate and effort. Physical examination revealed bilateral serosanguinous nasal discharge, stertorous breathing, and soft crackles in the right caudodorsal lung field. His packed cell volume and total solids were moderately low (25%/3.4g/dL) and adequate platelets (12/hpf) were seen on blood smear. He was volume-resuscitated with two isotonic crystalloid fluid boluses. Thoracic radiographs were consistent with hypovolemia, air bronchograms, and pneumomediastinum. Due to concern for continued blood loss and aspiration pneumonia, the patient was hospitalized and administered ampicillin-sulbactam, maropitant, pantoprazole, aminocaproic acid, and fentanyl. Over the next few days in hospital, the patient required multiple packed red blood cell transfusions and a platelet transfusion to address persistent blood loss and clinical anemia. A disseminated intravascular coagulation (DIC) panel (DIC, PT, aPTT, fibrinogen) revealed elevated fibrinogen and mildly prolonged aPTT. A thromboelastogram (TEG) was also performed and showed both hypo- and hypercoagulable characteristics. Due to concern for a breed-related platelet disorder, platelet flow cytometry was performed. The results revealed a failure of stimulated platelet membrane phospholipid expression consistent with Scott syndrome, an inherited defect of platelet procoagulant activity. Ultimately, the patient was referred to the University of Pennsylvania Ryan Veterinary Hospital for arterial embolization to address intractable epistaxis.

This report will discuss the pathophysiology, clinical characteristics, diagnosis, and treatment of Scott syndrome. Emphasis will be placed on point of care evaluation of a bleeding patient, transfusion medicine, and consideration of inherited platelet disorders.

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Scott syndrome, thrombopathia, platelet activation, coagulation


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