Background: Ectopic splenic tissue results from the autotransplantation and seeding of splenic tissue, often secondary to
splenic trauma or splenectomy. Splenic implantations occur mostly as nodules within the peritoneal cavity and constitute an
incidental finding at necropsy, surgery, or imaging investigations. This report addresses a case of hemoperitoneum associated
with hepatic splenosis in a dog that became ill several years after splenic trauma.
Case: A 9-year-old castrated female Dachshund was presented to the veterinary assistance due to an acute onset of abdominal
pain and distension. After recovering from a severe trauma caused by a car accident about five years previously, the dog
remained apparently normal. Upon admission the dog also showed anorexia, oliguria (dark yellow urine), increased pulse rate,
tachypnea, and hypothermy (37.1ºC). Palpation revealed abdominal distension attributed to large amounts of peritoneal fluid
and a large multinodular mass detected in the left side of the abdomen. While white cell and platelet counts were within the
normal range, hematocrit (26 to 24%) and erythrocyte counts (3.08 to 2.84 x 106/mL), and hemoglobin content (8.1 to 7.8 g/
dL) decreased as indicated within 36 h after admission. Plasmatic levels of alanine transaminase (ALT-12.1U/L) and creatinine
(1.04 mg/dL) were consistent with normal canine patterns. Abdominocentesis revealed a non-clotting and reddish effusion
with density of 1.032 and numerous nucleated cells (neutrophils 61%, lymphocytes 24%, and macrophages 15%).
Erythrophagocytosis, crystals of hematoidine, and activated macrophages were also observed. Necropsy revealed extensive
hemoperitoneum (360 mL), lobular pattern accentuation and a soft dark red 15-cm multinodular mass adhered to the left
hepatic lobe. The insertion of the nodular mass in the hepatic tissue consisted mainly of sanguineous fluid-filled cystic
structures, some of which were disrupted. There were also multiple, firm, dark red nodules (0.3-2.8 cm) scattered through the
liver parenchyma, and some smaller (0.3-0.5 cm) nodules attached to the omental and diaphragmatic surfaces. The abnormally
shaped spleen was divided in two similar halves by a soft red nodule about 2 cm in diameter. Main microscopic hepatic
changes were nodules formed by lymphocyte aggregates surrounded by fibrous connective tissue. Occasionally these nodules
formed follicular structures surrounded arterioles and intermixed with delicate vascular formations, which were filled with
erythrocytes and lymphocytes. Anti-CD3 immunostaining showed positive reactions in lymphocytes within the intrahepatic
ectopic splenic tissue, especially in lymphocyte aggregates that surrounded arterioles.
Discussion: Some of the necropsy and microscopic findings resembled those previously reported in two dogs affected by
hepatic splenosis. It has been suggested that intrahepatic splenosis may trigger death through hepatic insufficiency. However,
in the present case, the dog had neither altered ALT activity nor suggestive changes in the reminiscent hepatic tissue that could
indicate hepatic insufficiency. The association of a decreased hematocrit, depressed concentration of hemoglobin, and large
volume of peritoneal effusion of probable hemorrhagic origin with the clinical signs seen here and the cyst rupture indicates
that the severity of this case may probably be linked to hypovolemic shock.
