Location
Moultrie, GA
Start Date
17-4-2026 12:00 PM
End Date
17-4-2026 1:00 PM
Description
Introduction: Pancytopenia is a severe reduction in erythrocytes, leukocytes, and platelets, often resulting in anemia and increased susceptibility to infection, and is closely associated with Myelodysplastic syndromes (MDS), a group of bone marrow disorders with ineffective hematopoiesis.
The spleen, an important part of the lymphatic and immune systems, filters circulating blood, removes senescent erythrocytes, and supports immune function. Splenomegaly, pathological enlargement of the spleen, can exacerbate pancytopenia by sequestering and prematurely destroying blood cells.
This study examines the relationship between marrow dysfunction, splenic enlargement, and skeletal remodeling observed during cadaveric dissection to better understand the systemic effects of MDS.
Methods: This study involved a cadaveric dissection performed using standard anatomical techniques with isolation of the thoracic and abdominal cavities. The sternum was transected at the level of the second rib to allow access to the thoracic structures. Abdominal organs were examined in situ. The spleen was identified using anatomical landmarks and measured and weighed using a standard ruler and digital scale.
Osseous structures of the clavicles and sternum were inspected for anatomical variations and documented photographically. Limited medical history of the cadaver, including age and cause of death was reviewed, and a literature search was conducted to evaluate relationships between hematologic disorders, splenomegaly, and bone remodeling.
Results: Cadaveric dissection revealed marked splenomegaly occupying a substantial portion of the left upper quadrant. The spleen measured 15.4 cm in length and weighed 653 g, exceeding the expected anatomical reference ranges (≤ 12 cm; ~ 70 g), capsule intact, no evidence of rupture or lesion. Three distinct areas of abnormal osseous remodeling were observed as irregular cortical bony elevations extending from the bone surface, along the bilateral clavicles and the internal surface of the sternum. No evidence of acute fracture, surgical incision, or traumatic deformity was identified. Medical history indicated pancytopenia and myelodysplastic anemia in a 65-year-old male.
Literature review describes a study of 22 patients with MDS demonstrating decreased osteoblast and osteoclast activity, reduced bone formation rate and mineral apposition, consistent with adynamic bone and supporting a mechanistic link between marrow dysfunction and impaired skeletal remodeling. In MDS, the spleen exacerbates peripheral blood cell destruction, perpetuating a cycle of bone marrow dysfunction and splenic enlargement.
Discussion: Ineffective hematopoiesis in MDS disrupts normal marrow function, potentially triggering compensatory mechanisms such as increased marrow turnover and may stimulate osteoblastic and osteoclastic activity, leading to abnormal bone remodeling, which can manifest as periosteal reactions. Recognizing these interconnected pathological processes enhances understanding of how hematologic disorders manifest systemically rather than in isolation, emphasizing the value of cadaveric studies in correlating disease processes with anatomical changes.
Conclusion: This case describes atypical anatomical findings during cadaver dissection, including marked splenomegaly and abnormal osseous remodeling in the setting of pancytopenia and MDS. Although causation cannot be definitively established in this single case, these observations suggest a potential systemic relationship between bone marrow dysfunction, splenic pathology, and skeletal remodeling. Greater awareness of these associations may aid clinicians in identifying disease progression, anticipating complications, and guiding more comprehensive patient evaluation.
Embargo Period
5-26-2026
Included in
Splenomegaly and Abnormal Bone Remodeling with Pancytopenia and Myelodysplastic Anemia: A Cadaveric Case Study
Moultrie, GA
Introduction: Pancytopenia is a severe reduction in erythrocytes, leukocytes, and platelets, often resulting in anemia and increased susceptibility to infection, and is closely associated with Myelodysplastic syndromes (MDS), a group of bone marrow disorders with ineffective hematopoiesis.
The spleen, an important part of the lymphatic and immune systems, filters circulating blood, removes senescent erythrocytes, and supports immune function. Splenomegaly, pathological enlargement of the spleen, can exacerbate pancytopenia by sequestering and prematurely destroying blood cells.
This study examines the relationship between marrow dysfunction, splenic enlargement, and skeletal remodeling observed during cadaveric dissection to better understand the systemic effects of MDS.
Methods: This study involved a cadaveric dissection performed using standard anatomical techniques with isolation of the thoracic and abdominal cavities. The sternum was transected at the level of the second rib to allow access to the thoracic structures. Abdominal organs were examined in situ. The spleen was identified using anatomical landmarks and measured and weighed using a standard ruler and digital scale.
Osseous structures of the clavicles and sternum were inspected for anatomical variations and documented photographically. Limited medical history of the cadaver, including age and cause of death was reviewed, and a literature search was conducted to evaluate relationships between hematologic disorders, splenomegaly, and bone remodeling.
Results: Cadaveric dissection revealed marked splenomegaly occupying a substantial portion of the left upper quadrant. The spleen measured 15.4 cm in length and weighed 653 g, exceeding the expected anatomical reference ranges (≤ 12 cm; ~ 70 g), capsule intact, no evidence of rupture or lesion. Three distinct areas of abnormal osseous remodeling were observed as irregular cortical bony elevations extending from the bone surface, along the bilateral clavicles and the internal surface of the sternum. No evidence of acute fracture, surgical incision, or traumatic deformity was identified. Medical history indicated pancytopenia and myelodysplastic anemia in a 65-year-old male.
Literature review describes a study of 22 patients with MDS demonstrating decreased osteoblast and osteoclast activity, reduced bone formation rate and mineral apposition, consistent with adynamic bone and supporting a mechanistic link between marrow dysfunction and impaired skeletal remodeling. In MDS, the spleen exacerbates peripheral blood cell destruction, perpetuating a cycle of bone marrow dysfunction and splenic enlargement.
Discussion: Ineffective hematopoiesis in MDS disrupts normal marrow function, potentially triggering compensatory mechanisms such as increased marrow turnover and may stimulate osteoblastic and osteoclastic activity, leading to abnormal bone remodeling, which can manifest as periosteal reactions. Recognizing these interconnected pathological processes enhances understanding of how hematologic disorders manifest systemically rather than in isolation, emphasizing the value of cadaveric studies in correlating disease processes with anatomical changes.
Conclusion: This case describes atypical anatomical findings during cadaver dissection, including marked splenomegaly and abnormal osseous remodeling in the setting of pancytopenia and MDS. Although causation cannot be definitively established in this single case, these observations suggest a potential systemic relationship between bone marrow dysfunction, splenic pathology, and skeletal remodeling. Greater awareness of these associations may aid clinicians in identifying disease progression, anticipating complications, and guiding more comprehensive patient evaluation.