Rare case of spontaneous splenic rupture

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A 26‐year‐old man presented to the emergency department of a rural hospital in Australia with left upper quadrant abdominal pain. His past medical history was unremarkable. He was otherwise well and had no other gastrointestinal symptoms. During the course of the evening, the abdominal pain became increasingly worse. Initial computed tomography (CT) scan showed splenic vein thrombosis and an enlarged spleen with subcapsular haematoma and free fluid in the peritoneal cavity (Figs 1). Later in the night, the patient had a medical emergency team call due to systolic blood pressure falling below 70 mmHg and severe tachycardia. Clinical signs of hypovolaemic shock mandated laparotomy. This revealed 3 L of blood in the abdominal cavity due to an active bleed from a ruptured spleen. Haemostasis was achieved and an emergency splenectomy was performed. Post‐operatively, the patient was transferred to a tertiary centre for observation in the intensive care unit.
Given this unusual presentation, acute splenic vein thrombosis leading to acute venous congestion was investigated as the cause of splenic rupture. The patient was found to have prothrombin gene mutation and methylenetetrahydrofolate reductase gene mutation. His family history is unremarkable for thrombophilia conditions. Nonetheless, a clear link between these findings and spontaneous non‐traumatic splenic rupture has not been documented in the literature.
Histology of the spleen and splenic vessels were unremarkable. Spontaneous rupture of a histologically normal spleen is an extremely rare occurrence with very few, if any, documented cases. The vast majority of non‐traumatic cases are due to a pathological cause that is infection, malignancy, metabolic disorders, haematological disorders, etc.1 In this case, the spontaneous splenic rupture is likely secondary to acute venous congestion due to splenic vein thrombosis.
Comprehensive history and examination are vital to reaching the preliminary diagnosis, particularly in identifying pathological causes which may trigger spontaneous splenic rupture. CT imaging of the abdomen is 97% specific and sensitive in diagnosing splenic rupture.
Management of the patient involves clinical resuscitation if haemodynamically unstable. There is speculation of the best appropriate treatment if the patient is clinically stable; arguments exist for avoiding splenectomy and observing for 7 to 10 days. Other treatment options include angiography for embolization of the proximal splenic artery, thus reducing pressure, congestion and subsequent splenic rupture.5 In a rural setting without access to angiography, formal laparotomy with splenectomy was the appropriate management.
Spontaneous rupture of a histologically normal spleen is an incredibly rare occurrence. This case highlights the importance of serial examinations, high clinical suspicion and appropriate radiological imaging with early surgical referral for a favourable prognostic outcome.
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