Case Presentation: A 31-year old African American man with no prior medical history presented to the emergency department with epigastric abdominal pain and vomiting. The abdominal pain began while he was on a plane home from a weekend of binge drinking in Miami. The pain was described as sharp with occasional radiation to the back. The patient had tried taking acetaminophen 500 mg twice for the pain with little relief. He denied constipation, diarrhea, or blood in the stool. On presentation, the patient had a normal heart rate (63 bpm), respiratory rate (20 breaths/min), was normotensive (124/79) and afebrile (38.3C). On physical exam, the patient was in minor distress and scleral icterus was noted. There was tenderness to palpation of the upper abdomen, but his abdomen was soft and there was no rebound or guarding. His bowel sounds were normal. Initial laboratory studies were significant for hyperbilirubinemia (7.3 mg/dL), leukocytosis (12.8 x109/L), normal ALT (27 U/L), increased AST (147 U/L), thrombocytopenia (38x 103 platelets/microliter), decreased haptoglobin (0.259 g/L), and increased LDH (658 U/L). Abdominal CT showed multiple areas of low density in his spleen, which were interpreted as splenic infarcts. A second series of tests to further workup the splenic infarcts and thrombocytopenia included ADAMTS13, APTT, D-Dimer, fibrinogen and fibrin split products as thrombotic thrombocytopenic purpura and disseminated intravascular coagulation were part of the differential. Blood cultures, urine drug screen, a viral hepatitis panel and a TB test were also ordered. All of these additional tests came back negative and within normal limits.As the cause of the splenic infarcts remained uncertain, Hemoglobin electrophoresis was ordered and the patient was diagnosed with sickle cell trait (SCT).

Discussion: Physicians are often taught that SCT is a benign carrier condition, which is usually the case. However, SCT is associated with several potential complications including splenic syndrome. Patients with splenic syndrome often present with fever, abdominal pain, and vomiting in addition to the splenic infarcts, as evident in this patient. Labs often show increased lactate dehydrogenase, leukocytosis, thrombocytopenia, and anemia. These splenic infarcts most often develop after exposure to high altitude and other physiologic stress such as dehydration. This patient had been exposed to multiple stressors, such as excessive alcohol intake and traveling at a high altitude in a plane. Treatment is generally supportive with oxygen, analgesia, and hydration. Splenectomy is reserved for unstable patients or in the rare instance of splenic rupture.

Conclusions: It is critical for clinicians to recognize splenic syndrome and its association with SCT to ensure appropriate treatment. Additionally, patients with SCT should be counseled on the risk of this syndrome and to avoid its common triggers of dehydration and hypoxemia.