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Description
A 62-year-old man with stage IV follicular lymphoma presented with acute left-sided abdominal pain, acute-on-chronic anaemia and thrombocytopenia. An urgent contrast-enhanced CT scan of the abdomen demonstrated the presence of haemoperitoneum. Irregular linear-branching hypodensities distorting the splenic parenchyma present in both arterial (figure 1) and portovenous phases (figure 2), with presence of ill-defined hypoenhancing regions. Splenomegaly was present. Notably, there was absence of trauma. Overall features were compatible with non-traumatic rupture of the spleen.
The patient underwent emergency laparotomy, revealing 3 L of blood clots in the peritoneal cavity. Slow oozing of blood was noted at the region of the splenic hilum. Splenectomy was performed. Histopathological evaluation demonstrated features of diffuse large B-cell lymphoma with subcapsular infarct and haemorrhage. The surgery was uneventful. However, due to concurrent comorbidities and general ill-health, the patient progressively deteriorated and finally succumbed about a month after the surgery.
Non-traumatic splenic rupture is widely regarded as uncommon,1 but limited case reports advocate the early recognition and intervention of this rare disease entity.2 Several authors have also attributed the low index of suspicion as a major reason for the delayed diagnosis of similar cases of spontaneous splenic rupture secondary to non-Hodgkin’s lymphoma.3 A high index of suspicion should hence be raised in selected patient groups such as those with a background of haematological malignancy and splenomegaly who present with acute abdominal pain, to urgently evaluate for this potentially life-threatening disease.
Learning points
Non-traumatic splenic rupture should be considered in patients with splenomegaly, particularly those with pre-existing disease such as haematological malignancy.
Prompt imaging is useful in confirming splenic rupture and can lead to early splenectomy, reducing morbidity and mortality in this potentially life-threatening disease entity.
Footnotes
Patient consent for publication Obtained.
Contributors VSHC contributed to the radiological interpretation, drafting and writing of the manuscript. YHM contributed to the drafting of the manuscript and obtained patient consent. Y-LK was the primary clinician who managed patient care, and supervised the drafting of the manuscript. SHYL assisted in the radiological diagnosis and supervised in the overall writing of the manuscript.
Funding The authors have not declared a specific grant for this research from any funding agency in the public, commercial or not-for-profit sectors.
Competing interests None declared.
Provenance and peer review Not commissioned; externally peer reviewed.