Working Diagnosis:
Acute flare of TTP secondary to viral gastroenteritis

Treatment:
The patient was treated with maintenance hydration fluids due to losses secondary to vomiting/diarrhea as well as hemoglobinuria. One dose of 60mg furosemide was administered prior to transfusion for BP control. One transfusion of 1800mL FFP was administered on the day of admission, as was scheduled. The transfusion was performed over 12 hours. The patient was also treated with diphenhydramine, methylprednisolone, and famotidine due to his prior history of anaphylactic reactions to transfusions.
Labwork was redrawn the following morning and showed slight improvement in platelets to 17,000, Cr to 2.6 and LDH to 912, however the POCT urine dipstick still showed large blood and 300 protein. BP had returned to WNL without further interventions. Based on the lab results, the decision was made to administer a second transfusion of FFP and continue monitoring bloodwork. On the third day of hospitalization labs were repeated again and showed significant improvement of LDH down to 446, platelet count at 47,00 and Cr down to 1.4. Due to dramatic improvement in response to transfusions, dialysis was determined not necessary. He was determined to be stable for discharge at this time.

Outcome:
At the time of discharge the student athlete was restricted from participating in any physical activity. A follow up appointment was scheduled with Heme/Onc 2 days after discharge. Repeat labs at that visit showed platelet count increased to 140,000 and he was cleared for non-contact activity at that time, with return to full contact activity after another 4 days. A blood draw 1 week later showed platelet count 360,000 and the student athlete was permitted to return to full participation in football.

Author's Comments:
This is a case of student athlete playing a contact sport with a condition that predisposed him to thrombocytopenia and bleeding. The athlete experienced a flare secondary to a viral illness, but had few clinical symptoms suggestive of a flare. Luckily, the flare was identified before permanent life-threatening or fatal sequelae occurred. TTP can be a life-threatening condition if care is delayed. When dealing with an athlete with a rare and potentially life-threatening condition, it is essential that all members of the staff be educated about the athlete's condition, including exacerbating factors. It is also especially important to maintain a relationship of trust with student-athletes so they feel comfortable to seek treatment early.

Editor's Comments:
This is a very interesting case and while few of us will treat a patient with TTP wishing to play Division I football it is an excellent example of working together with a broad team, including the patient, athletic trainers, coaches, physicians, and specialists to allow an athlete with a medical condition safely participate in a desired sport at a very high level. Good communication of results and good understanding of requirements for full participation where shared and allowed for the quick identification of a potentially life threatening event and timely return to activity once the condition improved.

References:
1. George JN, Nester CM. Syndromes of thrombotic microangiopathy. N Engl J Med 2014; 371:654.
2. Reese JA, Muthurajah DS, Kremer Hovinga JA, et al. Children and adults with thrombotic thrombocytopenic purpura associated with severe, acquired Adamts13 deficiency: comparison of incidence, demographic and clinical features. Pediatr Blood Cancer 2013; 60:1676.
3. Witmer, C. M. How I approach managing student athletes at risk for bleeding. Pediatric blood & cancer (2019). Available at: https://www.ncbi.nlm.nih.gov/pubmed/30362247.
4. Registry, H. T. T. P. Hereditary TTP Registry. Hereditary TTP Registry Available at: https://ttpregistry.net/.
5. Moatti-Cohen M, Garrec C, Wolf M, et al. Unexpected frequency of Upshaw-Schulman syndrome in pregnancy-onset thrombotic thrombocytopenic purpura. Blood 2012; 119:5888.
6. Fujimura Y, Matsumoto M, Isonishi A, et al. Natural history of Upshaw-Schulman syndrome based on ADAMTS13 gene analysis in Japan. J Thromb Haemost 2011; 9 Suppl 1:283.

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