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Splenic rupture is usually secondary to trauma. Most non-traumatic ruptures are consequent on underlying disease affecting the spleen such as infection (Epstein-Barr virus, hepatitis, salmonella, malaria), neoplasia (lymphoma, leukaemia) and connective-tissue disease.
A previously healthy man of 30 attended the accident and emergency department sixteen hours after eating a seafood meal. From four hours after the meal he had been vomiting two to four times an hour, and one hour before coming to hospital he had developed generalized abdominal pain which radiated into his left shoulder and chest. The pain was worse on movement and on lying flat. On admission he was pale, cold and clammy. His heart rate was 110 and blood pressure was 85/55 mm Hg. There was tenderness and guarding in both upper quadrants; bowel sounds were present. Haemoglobin was 10.2 g/dL, white cell count 16.2 × 109/L. Serum amylase was normal.
Two hours after arrival he fainted on sitting upright. Repeat haemoglobin was 6.3 g/dL. An abdominal ultra-sound scan showed fluid in the peritoneum and around the spleen and at laparotomy he was found to have a ruptured spleen with a large amount of free intraperitoneal blood. No other intra-abdominal abnormalities were detected. A splenectomy was performed and the patient recovered uneventfully. Cultures from blood, sputum, stool and urine were negative, and paired acute-phase and convalescent sera provided no evidence of acute viral infection. Screening for autoantibodies, including antinuclear cytoplasmic antibodies and rheumatoid factors, was negative. The spleen was normal on microscopic and macroscopic examination. On repeated questioning before surgery and after recovery, the patient and his family could recall no history of significant trauma, either recent or in the more distant past.
True spontaneous splenic rupture was first described by Atkins in 1874 and has been a controversial diagnosis ever since. Reviewing all previously published cases, Orloff and Peskin1 found that in only 28 out of 71 was there no alternative explanation. They identified four criteria for the diagnosis of spontaneous splenic rupture—absence of a history of trauma or of unusual effort that could injure the spleen; absence of perisplenic adhesions suggestive of previous trauma; absence of pre-existing splenic disease; and normal microscopic and macroscopic appearances of the spleen. Other workers2 added a fifth criterion—that studies of acute-phase and convalescent sera should show no significant rise in viral antibody titres suggestive of recent infection with types associated with splenic involvement.
In view of the history of vomiting before onset of abdominal pain, we believe that the splenic rupture in our patient was not spontaneous. Rupture of a normal spleen has been reported to occur after trivial effort such as coughing3. To our knowledge only three cases of splenic rupture after vomiting have been published4,5,6, the vomiting being attributed to ingestion of ibuprofen, constipation and a reaction to a metrizamide injection. We suspect the vomiting in our case was related to the seafood meal. A proposed mechanism for splenic rupture secondary to vomiting is that violent contraction of the diaphragm causes tractional force on the spleen via the peritoneal reflections linking the two4.
When there is no history of trauma, splenic rupture tends not to be diagnosed until laparotomy. In Orloff and Peskin's review, only one of the 28 with genuinely spontaneous rupture had been correctly diagnosed pre-operatively. In a case such as ours diagnosis might well be delayed by false attribution of abdominal pain to the prolonged vomiting and dehydration.