Case Report: High-Grade Splenic Stromal Sarcoma (Undifferentiated Sarcoma) in an Australian Shepherd

A 10-year-old spayed female Australian Shepherd was presented with acute collapse and hemoabdomen associated with rupture of a large splenic mass. Following initial stabilization, splenectomy was performed, and histopathologic examination resulted in a diagnosis of a high-grade primary splenic stromal sarcoma, described in the original pathology report as an undifferentiated sarcoma.

Postoperative management included carprofen and adjuvant carboplatin chemotherapy. Huaier-derived glycan TPG-1 was administered concurrently as an adjunctive nutritional intervention. During the short-term follow-up period documented in this report, the dog remained active and in good general condition. 

At presentation, blood pressure was 100/66 mmHg and serum C-reactive protein (CRP) was 4.1 mg/dL. Abdominal radiography and ultrasonography identified a large right cranial abdominal mass measuring approximately 13 × 8.5 × 8 cm, together with hemorrhagic peritoneal fluid. Based on these findings, rupture of a splenic mass with associated hemoabdomen and hemodynamic compromise was suspected.

After overnight stabilization, splenectomy was performed the following day (Day 1). No gross enlargement of intra-abdominal lymph nodes or gross evidence of hepatic metastasis was identified during surgery. These findings should not be interpreted as complete oncologic staging because thoracic imaging, cross-sectional imaging, and cytologic or histologic assessment of potential metastatic sites were not documented in the available record.

Histopathologic examination resulted in a diagnosis of primary high-grade splenic stromal sarcoma (undifferentiated sarcoma). A mitotic count of 36 was reported. The precise microscopic area over which this count was obtained was not specified in the available source material.

Splenic stromal sarcoma is a heterogeneous group of mesenchymal neoplasms, and reported outcomes vary considerably among studies. Contemporary studies indicate that mitotic count is one of the most consistently identified prognostic factors. [1–3]

In a retrospective study of canine non-angiogenic, non-myogenic splenic stromal sarcomas, dogs with a high mitotic count (≥9 mitoses/10 high-power fields) had a median survival time of 67 days, compared with 439 days in dogs with lower mitotic counts. [3]

More recently, a 2026 multi-institutional study of 115 dogs with splenic stromal sarcoma reported an overall median survival time of 8.4 months. A mitotic count ≥9/10 high-power fields and metastatic disease at diagnosis were both associated with increased risk of tumor-related death. [1]

Accordingly, an approximate 2-month median survival time should not be considered representative of all dogs with splenic stromal sarcoma. Rather, markedly shorter survival has been reported in subsets of dogs with highly proliferative tumors. In the present case, direct comparison with published mitotic-count thresholds is not possible unless the microscopic area used to generate the reported mitotic count of 36 can be confirmed.

Splenectomy was performed on Day 1, and the dog was discharged on Day 3. Skin sutures were removed on Day 15.

Carprofen was initiated on Day 15 at 2.5–3.0 mg/kg once daily.

On Day 19, carboplatin was administered at 208 mg/m² as postoperative adjuvant chemotherapy.  The original clinical record denotes the administration method as “CRI”; further details regarding the infusion protocol were not available.

Huaier-derived glycan TPG-1 was initiated on Day 3 while histopathologic results were pending. Administration began at the standard dose and was increased to twice the standard dose following confirmation of the high-grade histologic features on Day 15.

Because surgery, carprofen, chemotherapy, and TPG-1 were administered concurrently, the independent clinical contribution of TPG-1 cannot be determined from this case.

Clinical and Laboratory Course

Note: Laboratory values and treatment chronology are reproduced from the original clinical record. A dash indicates that no value was provided in the source table.

The dog's general condition improved following stabilization and splenectomy.

Serum CRP was 4.1 mg/dL at presentation, increased to >7.0 mg/dL after surgery, and decreased to 0.6 mg/dL by Day 15. Because a laboratory-specific reference interval was not available, the Day 15 value is reported descriptively rather than being characterized as normalization.

At Day 26, 7 days after carboplatin administration, the WBC count was 10,400/μL and the platelet count was 680,000/μL. Mildly loose stool was reported, but the dog remained active and in good general condition.

No hematologic abnormality suggestive of clinically relevant myelosuppression was identified at this assessment. However, this finding should be interpreted cautiously because the Day 26 assessment occurred only 7 days after carboplatin administration and therefore cannot exclude a subsequent hematologic nadir.

This case documents the early postoperative course of a dog with a ruptured, high-grade splenic stromal sarcoma treated with splenectomy followed by multimodal medical management.

Available evidence indicates that canine splenic stromal sarcomas have heterogeneous biologic behavior. Mitotic count has emerged as one of the more consistently reported prognostic factors, although direct comparison between individual cases requires consistent methodology for mitotic counting. [1–3]

In this case, a mitotic count of 36 was reported; however, the microscopic area used for counting was not specified. Therefore, this value should not be directly compared with published thresholds expressed as mitoses per 10 high-power fields until the original pathology methodology can be confirmed.

Adjuvant carboplatin was selected because of the high-grade histologic features and concern for recurrence or metastatic disease. Available retrospective studies have not demonstrated a clear survival advantage from postoperative chemotherapy in canine splenic stromal sarcoma. [1,2] Accordingly, carboplatin in this case should be regarded as an individualized postoperative treatment decision rather than an established standard of care.

Huaier-derived glycan TPG-1 was administered concurrently beginning on Day 3. The dog remained clinically active during the short observation period documented here. However, because multiple therapies were administered concurrently and no untreated comparator or objective measures of immune function were available, no causal relationship can be established between TPG-1 administration and tumor control, maintenance of immune function, prevention of chemotherapy toxicity, or preservation of quality of life.

Longitudinal follow-up, including standardized restaging, survival data, objective assessment of adverse events, and quality-of-life measures, will be required to characterize the subsequent clinical course.

This case describes a dog with a ruptured, histopathologically diagnosed high-grade splenic stromal sarcoma managed with splenectomy followed by carboplatin, carprofen, and adjunctive Huaier-derived glycan TPG-1.

The markedly elevated reported mitotic count is of potential prognostic importance because mitotic activity has repeatedly been associated with metastatic risk and survival in canine splenic stromal sarcoma. However, confirmation of the microscopic area used for mitotic counting is required before direct comparison with published prognostic thresholds.

During the short-term observation period available, the dog remained active and in good general condition. Because multiple therapies were administered concurrently and follow-up remained limited, no independent therapeutic effect can be attributed to TPG-1 or any other component of the multimodal regimen.

Continued follow-up will be particularly important for evaluating metastatic progression, progression-free interval, overall survival, treatment tolerability, and quality of life.

1. Morey J, Yu J, Brockley L. Splenic stromal sarcomas in dogs: post splenectomy outcomes with and without adjuvant chemotherapy. Australian Veterinary Journal. 2026;104:110–117. doi:10.1111/avj.70035.

2. Ferrari R, Marconato L, Boracchi P, et al. Splenic stromal sarcomas in dogs: Outcome and clinicopathological prognostic factors in 32 cases. Veterinary and Comparative Oncology. 2024;22:12–21. doi:10.1111/vco.12941.

3. Wittenberns BM, Thamm DH, Palmer EP, et al. Canine non-angiogenic, non-myogenic splenic stromal sarcoma: a retrospective clinicopathological analysis and investigation of podoplanin as a marker of tumour histogenesis. Journal of Comparative Pathology. 2021;188:1–12. doi:10.1016/j.jcpa.2021.07.006.

4. Moore AS, Frimberger AE, Sullivan N, Moore PF. Histologic and immunohistochemical review of splenic fibrohistiocytic nodules in dogs. Journal of Veterinary Internal Medicine. 2012;26:1164–1168.

5. Spangler WL, Culbertson MR, Kass PH. Primary mesenchymal (nonangiomatous/nonlymphomatous) neoplasms occurring in the canine spleen: anatomic classification, immunohistochemistry, and mitotic activity correlated with patient survival. Veterinary Pathology. 1994;31:37–47.

6. Weinstein MJ, Carpenter JL, Schunk CJ. Nonangiogenic and nonlymphomatous sarcomas of the canine spleen: 57 cases (1975–1987). Journal of the American Veterinary Medical Association. 1989;195:784–788.