CASE OF INTEREST

Splenic Pathlogy of Canines

By Lucy Genovese & Trevor Whitbread, Veterinary Pathologists

Recently here at Abbey we began a survey on splenic tumours in dogs. To all those practices that returned questionnaires – thank you very much. Splenic tumours are rather problematic lesions for vets and diagnostic path laboratories. They are often very large which creates problems with fixation and sampling. Haemangiosarcoma is the principle tumour of the spleen in dogs and the disease that practitioners most want to rule in or rule out. But what other conditions do we see in the spleen? It is useful for description purposes to divide splenomegaly into 4 groups.

If the spleen is uniformly enlarged and very congested or bloody in consistency then the main differentials are:
Congestion: torsion, barbiturates, anaesthesia
Acute hyperaemia: inflammation, anthrax, bacterial septicaemia
Acute haemolytic anaemia

If the spleen is uniformly enlarged with a firm or meaty consisitency then consider:
Bacteraemia and low grade septicaemia
Chronic infectious disease
Prolonged haemolytic anaemia
Lymphoid hyperplasia
Neoplasia
Stored or deposits of material
Extramedullary haematopoiesis
Splenic myeloid metaplasia, histiocytosis and hypersplenism

If there are nodules with a bloody consistency consider:
Haematoma
Vascular neoplasia
Incompletely contracted areas of spleen
Acute splenic infarction

If there are nodules with a firm, meaty consistency consider:
Nodular hyperplasia
Neoplasia
Granulomas
Abscesses

So what do we see frequently at Abbey? Below is a pie graph showing the frequency/ distribution of splenic disease in dogs. Hamangiosarcoma is the most prevalent tumour. It is worth remembering that haemangiosarcoma in the spleen can cause a diffuse splenomegaly as well as nodular masses. It may also be quite solid and white (depending on its degree of differentiation). A firm pale mass may still be haemangiosarcoma.

A recently described variant of nodular hyperplasia is the fibrohistiocyitic nodule ^3. These cases show a combined nodular lymphoid and fibrohistiocytic proliferation with some nodules showing a continuum between benign hyperplasia and malignant splenic stromal neoplasia (malignant fibrous histiocytoma). 93/98 dogs had complete 12 months follow up information with 48% alive and 52% dead. Of the 52% that died 44% died from causes linked to their splenic disease, 35% from competing causes and 21% from unknown causes.
A high proportion of lymphoid to fibrohistiocytic cells was associated with increased long term survival, whereas lower lymphoid:fibrohistiocytic proportions and higher mitotic index indicated a probability of higher short-term mortality.

Another recently described condition that is associated with a diffuse splenomegaly is Splenic myeloid metaplasia, histiocytosis and hypersplenism ³. These dogs show severe, diffuse, sustained and progressive splenomegaly. Clinical signs, haematology and serum chemistry were not found to be useful diagnostically. Histologically there was myeloid metaplasia, histiocytosis, erythrophagocytosis, thrombosis and infarction. Only the presence of histiocytic giant cells were prognostically useful and predictive of fatal outcome. In this paper 30% dogs survived 12 months. 53% of dogs with complete post mortem showed multiorgan involvement with histiocytic neoplasia. 47% dogs with complete post mortem only splenic pathology present and a specific cause of death was often not evident. It seems likely that this is a splenic reaction pattern, that may be triggered by more than one clinical condition. Further clinical and pathological correlation will be required.

The next big question is how to sample and how certain can we be that the samples taken are truly representative. The capsule impedes penetration of the fixative and splenic tissue itself fixes poorly possibly because of the blood within the parenchyma. Large portions of splenic tissue in small amounts of formalin fix poorly. If the lesion is very large it is probably best to take large transverse ‘bread slice’ sections through relevant areas. Preferably keeping them less than 2 cm thick. Concentrate on acquiring marginal areas with normal spleen. If multiple nodules are present sample several and not just the large one. If nodules are present in the omentum, sample them too.

With a diagnosis of haematoma can we be certain there was no underlying haemangiosarcoma? The bottom line is that we cannot be certain of this. We cannot sample every area and there are financial constraints on how many sections we can take. This issue was examined in a study conducted at the University of Pennsylvania ⁴. The epidemiologic, clinical, pathologic and prognostic characteristics of splenic haemangiosarcoma and splenic haematoma in 217 canine cases were examined. It was concluded that in most cases splenic haematoma could be differentiated from haemangiosarcoma by histologic examination. The follow up data we received from our recent questionnaire would also suggest that the prognosis for dogs with a diagnosis of haematoma is favourable particularly once beyond the post-operative period.

References

1.Disorders of the Spleen. M. M. Fry and M. D McGavin, (2007) in Pathologic Basis of Veterinary Disease 4th ed. Elsevier. pp809-821.

2.Splenic myeloid metaplasia, histiocytosis and hypersplenism in the dog (65 cases). W.L. Spangler and P.H. Kass. Veterinary Pathology (1999) 36:583-593.

3.Pathologic and prognostic characteristics of splenomegaly in dogs due to fibrohistiocytic nodules: 98 cases W.L. Spangler and P.H. Kass. Veterinary Pathology (1998) 35: 488-498.)

4.Epidemiologic, clinical, pathologic and prognostic characteristics of splenic haemangiosarcoma and splenic haematoma in dogs:217 cases. Prymak C P et al. JAVMA 1988 193(6) pp 706-711.