Imaging Diagnosis—Peritoneal Splenosis in a Dog: Computed Tomographic Findings

ABSTRACT

This report describes a case of peritoneal splenosis in a dog, identified following the discovery of multiple peritoneal nodules on computed tomography (CT) performed for the evaluation of a compressive myelopathy. Histopathologic analysis confirmed the presence of ectopic splenic tissue without evidence of malignancy. In dogs, splenosis results from autotransplantation of splenic tissue within the peritoneal cavity, following splenic injury or surgery. Although most cases are incidental findings, nodule enlargement or rupture may occasionally lead to clinical consequences. This case emphasizes the importance of considering splenosis in the differential diagnosis of peritoneal nodules, particularly when they are not associated with peritoneal effusion and in animals with a history of splenic disease or abdominal trauma.

1. Signalment, History, and Clinical Findings

A 9‐year‐old spayed female Beagle was presented for an acute onset of pain characterized by vocalization, pelvic limb stiffness, and reluctance to sit. Administration of opioids and non‐steroidal anti‐inflammatory drugs (NSAIDs) resulted in partial improvement of the clinical signs.

The dog had a medical history of splenectomy performed 4 years earlier, following a hemoabdomen secondary to spontaneous rupture of a splenic mass. At the time of the surgery, no peritoneal nodules were reported. Histopathologic examination of the excised spleen revealed splenic nodular hyperplasia.

At admission, the dog exhibited a painful posture, low tail carriage, and a cautious gait. Physical examination revealed a Grade 2/6 left apical systolic heart murmur, with no other remarkable abnormalities. Abdominal palpation was non‐painful.

Neurologic and orthopedic examinations were performed. Discomfort was elicited upon lumbar spinal manipulation, but no proprioceptive deficits were identified.

Hematologic and serum biochemical analyses were unremarkable.

Given the clinical suspicion of spinal cord compression, computed tomography (CT) of the spine and abdomen was performed for further evaluation.

2. Imaging, Diagnosis, and Outcome

Abdominal and thoracic CT was performed using a 64‐slice CT scanner (LightSpeed VCT, General Electric Healthcare) with the dog positioned in ventral recumbency under general anesthesia. Images were acquired before and after intravenous hand‐injection of a 2‐mL/kg bolus of iohexol (Omnipaque 300, 300 mg iodine/mL). Acquisition parameters were as follows: helical mode, slice thickness 1.25 mm, rotation time 1 s, table speed 27.5 mm/rotation, tube voltage 120 kV, and tube current 93 mA.

The CT examination identified an accumulation of hyperattenuating, highly mineralized material in the right lateral portion of the vertebral canal at the L5–L6 intervertebral level. The lesion occupied up to 50% of the vertebral canal cross‐sectional area, displacing the dural sac dorsolaterally to the left. These findings were consistent with compressive myelopathy secondary to an extrusive intervertebral disc herniation.

Additionally, the CT scan revealed multiple, well‐demarcated nodules distributed within the peritoneal fat (predominantly ventrally and on the left side) as well as along the hepatic capsule. These nodules were soft‐tissue attenuating, with mean attenuation values of 86 HU (range: 72–98), measured as averages across all nodules, compared with the typical precontrast attenuation of normal splenic parenchyma (approximately 50–60 HU). Postcontrast images showed mostly strong, homogeneous enhancement (mean: 144 HU; range: 128–160 HU), whereas the larger nodules showed moderately heterogeneous enhancement (Figure 1). Their diameter ranged from a few millimeters to 3 cm. No clear vascular connection was identified between these nodules and the remaining splenic vasculature; however, this finding should be interpreted cautiously, as a triple‐phase CT study was not performed. The surrounding fat appeared unaltered, no peritoneal effusion was detected, and abdominal lymph nodes were within normal limits. On the basis of their ventral and parietal distribution and the absence of a visible hilus, a lymph node origin was considered unlikely. The imaging features were suggestive of metastatic disease (peritoneal sarcomatosis in particular, round cell neoplasia), although benign processes, such as granulomas or splenosis were also possible. Carcinomatosis was considered less likely than sarcomatosis given the attenuation characteristics and the lack of peritoneal effusion but could not be definitively ruled out. Primary disseminated neoplasia (e.g., mesothelioma) was also considered in the differential diagnosis.

FIGURE 1.

Sagittal (A) and transverse (B) post‐contrast abdominal CT images in soft‐tissue window. In (A), the patient's right side is oriented to the left. In (B), cranial is oriented to the left. The arrows indicate multiple well‐circumscribed, slightly heterogeneously enhancing peritoneal nodules.

Fine‐needle aspirates were obtained using a 22‐ga needle by the fenestration technique from multiple peritoneal nodules. Cytologic evaluation yielded poor cellularity and was therefore considered non‐diagnostic.

Interestingly, in the hours following the CT examination, the dog exhibited rapid, spontaneous clinical improvement, with full recovery of ambulation and resolution of spinal pain. In light of this favorable evolution, the owner declined surgical decompression of the spinal cord (hemilaminectomy).

Subsequently, after a 1‐month interval and in the absence of any recurrence of neurologic signs, laparoscopic exploration was performed to further investigate the nature of the abdominal nodules. Under general anesthesia (alfaxalone [Alfaxan], diazepam [Valium], methadone [Comfortan], and fentanyl [Fentadon]), a standard three‐port laparoscopic procedure was performed with the dog positioned in dorsal recumbency. As expected, no spleen was identified due to the previous splenectomy. Three dark‐red, highly vascularized, multilobulated nodules were visualized, adherent to the abdominal wall cranial to the urinary bladder (Figure 2), along with one additional 1‐cm nodule located on the omentum. Two of the nodules were excised using a laparoscopic vessel sealing device (LigaSure Atlas, Valleylab, Boulder, CO, USA) and submitted for histopathological examination. The procedure was uneventful, and postoperative management consisted of a short course of an NSAID.

FIGURE 2.

Splenosis nodule adherent to the ventral peritoneum, measuring approximately 1 cm in diameter, was visualized during laparoscopic exploration.

Histopathologic evaluation of the resected nodules revealed a tissue organization typical of the splenic parenchyma, with well‐organized red pulp regions composed of erythrocytes, hematopoietic precursors, macrophages and siderophages, plasma cells, and various other leukocytes, interspersed with white pulp territories characterized by nodular lymphoid aggregates. These splenic tissue collections were circumscribed by a dense peripheral fibrous capsule (Figure 3), occasionally containing Gamna–Gandy bodies. No neoplastic cells were identified in the examined samples. These findings, combined with the patient's medical history and the description of the nodules on CT scan, were consistent with multifocal peritoneal splenosis.

FIGURE 3.

Histologic section of one of the peritoneal nodules, displaying typical splenic parenchyma: peripheral fibrous connective tissue capsule (black arrow), white pulp consisting of lymphoid tissue (white arrow), and red pulp with erythrocytes, hematopoietic precursors, and abundant siderophages (red arrow). Hematoxylin–Eosin–Saffron (HES) staining.

Given the favorable long‐term prognosis and resolution of lumbar pain, no additional treatment was initiated. At the time of writing (1 year postoperatively), the dog remains asymptomatic and in good general health.

3. Discussion

Splenosis results from the autotransplantation of splenic tissue. This rare condition may occur following splenic rupture due to trauma, splenectomy, or other abdominal surgical procedures. In dogs, it accounts for less than 3% of splenic diseases [1]. Disseminated splenic tissue is most commonly located within the peritoneal cavity, although splenosis involving the pleural cavity or pericardial sac has been reported in humans following diaphragmatic injury [2, 3, 4]. Subcutaneous splenosis is occasionally described in humans but has not yet been reported in dogs. The ectopic nodules retain normal splenic function and display histologic features closely resembling native splenic tissue [5, 6].

Splenosis is an acquired condition distinct from congenital accessory spleens, another form of ectopic splenic tissue. Accessory spleens typically consist of a small number of nodules, most often located along the splenic ligaments in the left cranial abdomen. They exhibit a well‐defined hilum and derive their vascular supply exclusively from branches of the splenic artery. In contrast, splenosis results from the implantation or embolization of splenic tissue following splenic rupture or surgery and is characterized by irregularly distributed nodules with nonspecific vascularization. Several mechanisms have been proposed, including implantation of splenic fragments onto serosal surfaces or into adjacent organs, such as the liver or pancreas [6, 7, 8, 9, 10, 11]. According to the recent veterinary series by Stilz et al. [12], accessory spleens are histologically identical to normal spleens, whereas splenosis may lack some key features, such as a well‐developed capsule or organized white pulp, although these differences are often subtle and inconsistently described [12]. Ultimately, the distinction between the two conditions has limited clinical impact, as both are usually incidental and benign findings. In the present case, several features strongly supported a diagnosis of splenosis rather than accessory spleen. The dog had undergone splenectomy 4 years earlier due to hemoabdomen secondary to spontaneous rupture of a benign splenic hyperplastic lesion. At that time, no peritoneal nodules were reported during surgical exploration. On follow‐up imaging and laparoscopic examination, multiple nodules were identified throughout the peritoneal fat and omentum, without any vascular connection to the residual splenic vasculature or to splenic ligaments. These findings, in conjunction with the absence of a hilum and the nodule distribution pattern, were most consistent with splenosis.

In most cases, splenosis was an incidental finding without clinical consequences [7, 11, 13, 14]. However, rare cases of symptomatic splenosis have been reported in dogs and humans, particularly when nodules are large enough to cause compression or rupture [6, 7, 8, 9, 15]. In one reported canine case, hepatic splenosis affected approximately 65% of the hepatic parenchyma, leading to compression atrophy of adjacent liver structures and dilation of bile ducts. Rupture of biliary cysts was suspected as the cause of clinical signs in that case [8]. In humans, rare cases of splenosis, involving the small intestine or thoracic cavity, have also been described, causing digestive obstruction or pulmonary nodules [16, 17, 18, 19, 20]. In the present case, the dog was asymptomatic at the time of diagnosis. In comparison with previously reported cases, this asymptomatic presentation may be attributable to the small size of the nodules and to their location in the omentum or the peritoneum.

Imaging characteristics of splenosis have been described in both human and veterinary medicine [1, 2, 10, 11, 14, 15, 18, 21, 22, 23, 24], but there is considerable overlap with peritoneal sarcomatosis, making differentiation on the basis of imaging alone challenging. Sarcomatosis can present with peritoneal nodules in the absence of effusion or regional lymphadenomegaly, as observed in our case [25]. Moreover, nodules from sarcomatosis typically exhibit higher attenuation and contrast enhancement than those seen with carcinomatosis, a pattern also noted here, although the values in our case were at the upper end of the range reported for peritoneal sarcomatosis in dogs [25]. As mentioned above, carcinomatosis seemed less likely in our case; indeed, dogs with peritoneal carcinomatosis often present with multiple poorly defined nodules and, in most cases, an associated peritoneal effusion [25]. Still, a significant overlap remains between the CT aspect of sarcomatosis and carcinomatosis. Several features, however, supported a benign process: the absence of clinical signs, the lack of regional inflammation (e.g., no fat stranding), the long interval since splenectomy (>4 years), and a histopathologic diagnosis consistent with a benign splenic lesion (nodular hyperplasia). Interestingly, the pre‐contrast attenuation values of splenosis nodules in our case tend to be higher than those reported for normal spleen parenchyma in dogs (around 50–60 HU) [26]. To our knowledge, there is no case report in veterinary medicine comparing attenuation values between splenosis nodules and splenic tissue; in human medicine, splenosis, accessory spleen, and splenic parenchyma often exhibit similar CT characteristics [21, 22].

Consequently, although cross‐sectional imaging may provide suggestive features, neither CT, MRI, nor ultrasound can definitively confirm the splenic origin of these nodules. In human medicine, nuclear scintigraphy using heat‐damaged 99mTechnetium‐labeled erythrocytes is considered the gold standard for noninvasive identification of ectopic splenic tissue [3, 4, 27, 28, 29]. This technique is highly sensitive in detecting functional splenic tissue and has been sporadically reported in dogs, though it is not routinely used in veterinary clinical practice [30]. It may nonetheless be particularly useful in cases with strong clinical suspicion of splenosis, as in the present report.

Splenic nodules may enlarge over time; thus, ultrasonographic monitoring may be advisable when nodules are not surgically removed, initially after a few months and subsequently at longer intervals depending on their stability or growth rate.

As described above, the imaging features of splenosis may mimic neoplasia. It is therefore essential to include splenosis in the differential diagnosis for intra‐abdominal nodules, particularly in animals with a history of splenectomy.

Although cytology may assist in the diagnosis of certain exfoliative tumors, it often remains inconclusive for splenosis, as previously reported in veterinary medicine [31, 32]. Therefore, histopathologic examination remains the gold standard, allowing direct assessment of tissue architecture, including red and white pulp territories. Biopsy samples can be obtained under ultrasound guidance or via laparoscopic or open surgical approaches. One recent canine report described a preoperative histologic diagnosis of hepatic splenosis using needle‐core biopsy14. In addition to providing tissue for diagnosis, laparoscopy or laparotomy also allows evaluation of the nodules for potential hemorrhagic risk, which may justify their removal [16].

4. Conclusion

Splenosis is a rare condition that can mimic disseminated or primary neoplastic disease on imaging studies. However, in most cases, this incidental finding carries no clinical consequences. This case highlights the importance of including peritoneal splenosis in the differential diagnosis of peritoneal nodular lesions, particularly in patients with a history of splenectomy.

Disclosure

The authors have nothing to report.

Conflicts of Interest

The authors declare no conflicts of interest.

Humeau C., Bouhsina N., Lafuma F., Cordier P., Rousseau T., and Hernandez J., “Imaging Diagnosis—Peritoneal Splenosis in a Dog: Computed Tomographic Findings.” Veterinary Radiology & Ultrasound 67, no. 1 (2026): e70136. 10.1111/vru.70136

Data Availability Statement

The data that support the findings of this study are available from the corresponding author upon reasonable request.