Case Presentation: A 66 year-old Caucasian male presented to the emergency department with intermittent fevers, chills, fatigue and dyspnea of 1 week duration. He denied any nausea, vomiting, abdominal pain, changes in bowel habit or significant trauma. He lived in a wooded area and had 3 previous Lyme infections but denied any recent tick bite, travels or blood transfusion. On physical examination, he was febrile (temp 39.7oC) with tachycardia (heart rate of 116 beats per minute) and blood pressure of 141/96 mm/Hg . He had no signs of traumatic injury. Abdomen was soft, non-tender with no palpable enlarged organs. Complete blood count showed platelet count 42,000 /µL (130,000 – 400,000 /µL), hemoglobin 9.5 g/dL (12-16 g/dL) and WBC 6, 600 /µL (4, 800 – 10,800 /µL). Liver function test was remarkable for hyperbilirubinemia (total and direct bilirubin 2.5 mg/dL and 0.6mg/dL), AST of 68 IU/L (Normal 13-39IU/L) with normal ALT and alkaline phosphatase. His blood parasite smear was positive for babesia microti with parasitemia of 9%. CT chest was negative for pulmonary embolism with normal visualized portion of spleen and liver. He was started on atovaquone and clindamycin. On day 2, his hemoglobin was 7.2 g/dl with evidence of hemolysis (LDH 1040 IU/L (140-271 IU/L), low haptoglobulin <30 mg/dl). He received 2 units of packed red cells and appeared to be clinically improving with low parasitemia of 0.3% on day 3. However on evening of Day 3 patient developed hemorrhagic shock manifesting with profound hypotension, distended abdomen and sudden loss of consciousness. His hemoglobin was 5.0 g/L. An urgent CT scan of his abdomen revealed hemoperitoneum with evidence of splenic rupture. Patient received massive transfusion of blood products and underwent emergent exploratory laparotomy with splenectomy (splenic rupture confirmed intraoperatively). He had a prolonged postoperative course complicated by fungemia, DIC and multisystem failure. He was subsequently transitioned to comfort care and died on day 21.
Discussion: Atraumatic splenic rupture is a rare and potentially fatal medical emergency. Babesiosis can be asymptomatic or present as a febrile illness with mild anemia, or in severe cases with adult respiratory distress syndrome, disseminated intravascular coagulation, multisystem organ failure and rarely with splenic rupture. Splenic rupture in babesiosis may occur in otherwise healthy patients and despite low parasitemia. Pathogenesis is thought to be related to splenic enlargement from phagocytosis of infected erythrocytes and sequestration of platelets but can also occur without clinical splenomegaly as seen in our patient. Treatment options include conservative management in hemodynamically stable patients, splenic artery embolization and splenectomy.
Conclusions: Physicians need to be aware of spontaneous splenic rupture as a complication of babesiosis especially in patient who rapidly decompensate. Splenic rupture may occur despite apparent clinical improvement and may be fatal.