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Splenectomy renders a patient susceptible to infection by encapsulated bacteria and calls for long-term antibiotic prophylaxis. But splenic function can return.
A man of 54 was admitted with severe lower abdominal pain, of sudden onset and spasmodic in nature, for the past twenty hours. His medical history included a total splenectomy after splenic trauma 20 years before, since when he had been taking penicillin 250 mg twice daily. On examination he was febrile (temperature 37.8 °C) and tachycardic. The abdomen was slightly distended and tender with guarding in the left iliac fossa. Apart from a raised white cell count (14.2×10-9/L) haematological and biochemical indices were normal. A plain supine abdominal radiograph on admission showed normal calibre small and large bowel. The provisional diagnosis was diverticulitis and he was started on intravenous antibiotics. A CT scan suggested a pelvic mass overlying the bladder, but also showed a lobulated spherical mass under the left hemidiaphragm with appearance and size suggestive of spleen. A fibreoptic examination was limited to the rectosigmoid because of inability to negotiate the lumen any further. A water-soluble contrast enema displayed a sigmoid stricture which allowed very little contrast to pass through.
Because of unsettled pain, a laparotomy was undertaken through the previous midline splenectomy scar, and the sigmoid mass was excised with en-bloc resection of involved bladder. Histological examination confirmed complicated diverticular disease. A full-size spleen was obvious under the left hemidiaphragm.
Spleen can regenerate through various mechanisms. Autotransplantation of splenic tissue after traumatic disruption of the splenic capsule is well recognized.1 Splenic tissue can lodge anywhere in the peritoneal cavity following traumatic disruption and regenerates under favourable conditions.2 The incidence of splenic regeneration correlates with the severity of splenic injury:3 patients requiring a splenectomy for trauma tend to be those with greatest splenic damage and dissipation of splenic tissue, which favours autotransplantation. These splenic implants, called splenosis, can be found anywhere in the peritoneal cavity. They are supplied by newly formed arteries that penetrate the capsule.4
Accessory spleens, on the other hand, are common prevalence 10–31% in autopsy series.5 They result from incomplete fusion of separated fetal spleen tissue originating from the dorsal mesogastrium.6 In healthy individuals, accessory spleens usually measure only a few millimetres in diameter5 and may be undetectable on routine imaging. These accessory spleens can enlarge following splenectomy and be the source of recurrent symptoms in those operated on for blood disorders. An accessory spleen derives its blood supply from branches of the splenic artery.4
When a surgeon deals with a bleeding spleen in an emergency, some splenic tissue may remain in situ at the hilum. We suspect that this was the origin of our patient's neoformed spleen, because of its normal anatomical position and blood supply from splenic vessels.7
Overwhelming sepsis from encapsulated bacteria is a major complication of splenectomy.8 The risk of subsequent infection is lowest with traumatic splenectomy,9 possibly because function can return. The notion that regenerated spleens have a functional value is supported by their normal tissue architecture.1 More importantly, the volume of regenerated splenic tissue seems to correlate with protection against postsplenectomy infection.10
The existence of functional splenic tissue is indicated by the absence of Howell–Jolly bodies and presence of normal IgM blood levels.8 These were the findings in our patient, and the prophylactic penicillin was stopped. Some immunologists, to be on the safe side, would also wish to see normal IgG levels to pneumococcal polysaccharides.