Reasons for splenectomy include splenic neoplasia, splenic torsion, infiltrative disease and infarction, traumatic injury, nonneoplastic masses, and immuno-mediated processes. 48% to 59% of splenic masses in dogs are malignant and 51% to 73% of these are haemangiosarcomas (HSA). Other differentials for splenic masses include nonneoplastic lesions such as nodular hyperplasia and haematomas (Fig. 1) or less common splenic malignancies, such as histiocytic sarcoma, leiomyosarcoma, and fibrosarcoma (Wendelburger al. 2014). Mast cell tumors are the most common reason for splenectomy in cats followed by haemangiosarcoma (Fig. 2) and lymphoma (Gordon et al. 2009).
Splenic haemangiosarcoma (Fig. 3) is highly metastatic, it often ruptures resulting in acute haemoabdomen and many dogs have macroscopic metatstatic disease in the liver and other sites upon initial evaluation (Fig. 4).
Staging of the patient with splenic haemangiosarcoma include three stages.
- Stage I: haemangiosarcoma confined to the spleen.
- Stage II: ruptured splenic haemangiosarcoma or haemangiosarcoma with nodal metastases.
- Stage III: splenic haemangiosarcoma with distant metastases.
Tumour grading include low, intermediate and high grade on the basis of a cumulative score determined through the assessement of overall differentiation, nuclear pleomorphism, percentage of necrosis, and mitotic index (Wendelburg et al. 2015).
Metastases are considered to be present if they are detected in the lungs by means of thoracic radiographs, in the right atrium by means of echocardiography or in other organs evaluated histologically following sampling of evident lesions. Staging for dogs with splenic mass should therefore always include 3-view thoracic radiographs and through abdominal ultrasonography/ecocardiography. Infacts, 9% of dogs with signs of a splenic haemangiosarcoma has concurrent right atrial HSA (Wendelburger al. 2015). Because cardiac tamponade and haemopericardium secondary to haemorrhage can develop at any time, echocardiography should be recommended to all owners contemplating surgery for their dog with splenic mass.
50% of dogs with splenic haemangiosarcoma and macroscopic hepatic abnormalities has HSA metastases. Dogs with splenic HSA and grossly normal liver usually do not present metastases detected on liver histopathology. However, the presence of multiple dark-coloured and active bleeding hepatic nodules is highly associated with malignancy (Clendaniel et al. 2014). Whilst obtaining biopsies of macroscopically normal livers during surgery for splenic HSA is unnecessary, sampling of evident hepatic lesions and possibly of the regional lymphnodes for a correct staging of the patient is recommended. Abdominal ultrasonography can be helpful in detecting hepatic lesions deep within the parenchyma in the pre-operatory phase.
Decision making for a dog with a splenic mass can be difficult for owners because the long-term prognosis varies with the histopathologic diagnosis, and because surgery and aftercare can be very expansive. Dogs with ruptured splenic haemangiosarcoma and haemoabdomen develop sudden clinical signs without warning and owners have to made decision whether to elect surgery or not quickly. Good comunication skills and knowledge of the biological behaviour of this kind of splenic tumor is very important for assisting the owner in the decision making process.
The median survival time (MST) for dogs with splenic haemangiosarcoma treated with splenectomy only is 1.6 months. Clinical stage of the tumour is strongly associated with survival time, being this the shortest among dogs with stage III disease. These dogs are typically euthanized soon after splenectomy because of haemorrhage from progressive metastatic disease. Dogs with stage I disease have longer survival times than dogs with stage II disease, and dogs with stage I or II disease have longer survival times than dogs with stage III disease. MST of dogs with stage I disease undergoing splenectomy only is 5.5 months against 0.9 months MST for dogs with stage III disease. Dogs with a solitary splenic HSA have longer survival time than do dogs with multiple masses (Wendelburger al. 2015).
Survival times for dogs receiving doxorubicin-based chemotherapy appear to be longer than survival times reported for patients treated with surgery alone. Epirubicin, developed to reduce cardiotoxicity, also appears to prolong survival time (Kim et al. 2007).
A study on 208 dogs with splenic haemangiosarcoma newly showed that conventional chemotherapy protocols containing doxorubicin combined with metronomic protocols containing cyclophosphamide are likely to be more efficacious in the treatement of splenic HSA than either type of chemotherapy alone. The combined approach slows cancer progression through impairment of angiogenesis (metronomic chemotherapy) and direct cytotoxicity (conventional chemotherapy). The most important side effect of simultaneous administration is higher risk of gastrointestinal and haematologic toxicoses (Wendelburger al. 2015).
Despite several papers have examined prognostic indicators for survival time in dogs following splenectomy, very few studies have looked at survival of cats after splenectomy. Reported MST of cat that underwent splenectomy for mast cell tumor is 360-570 days with a range of 60-1140 days. Death is usually due to euthanasia after return of clinical signs (Gordon et al. 2010). Splenectomy is also the primary method of treatment of splenic haemangiosarcoma in cats. The MST of cats undergoing splenectomy for haemangiosarcoma has been reported to be 140 days, ranging from 42 to 245 days. The only factor identified as significant prognostic indicator for survival after splenectomy in cats is whether the cats are noted to have preoperative weight loss or not. MST in cats with weight loss is 3 days, whilst for cats with no weight loss noted the MST is 293 days (Gordon et al. 2010).
Peri-operative death in dogs undergoing splenectomy for splenic masses is influenced by the systemic effects of general anaesthesia, age, general health of the dog, changes in blood pressure, tissue perfusion, oxygen carrying capacity, and coagulation. It is also important to consider mortality rate in light of the resources for peri-operative support and expertise available in primary care practices and in teaching hospitals. In these last, perioperative mortality is understandably expected to be lower than in first opinion practices (Wendelburger al. 2015).
Marked preoperative thrombocytopaenia and aneamia and development of intraoperative ventricular arrhytmias (Fig. 5) are identified as main risk factors for perioperative death in dogs with splenic masses. The risk of death may be limited by preventing thrombotic (Portal System Thrombosis – PST and Pulmonary Thromboembolism – PTE) and coagulopathic ( Disseminated Intravascular Coagulation – DIC) syndromes and controlling all sources of intra-abdominal haemorrhage (Wandelburg et al. 2014). Haemorrhagic and thrombotic events can occur independently or can be simultaneous. Severe intra-abdominal haemorrhage from ruptured splenic masses or metastatic lesions may consume platelets and coagulation factors. These can also become diluted by fluids administered to restore intravascular volume leading to a haemorrhagic tendency. The presence of a large splenic mass can lead to stasis of the intra-abdominal blood flow promoting thromboembolism of large veins such as portal and pulmonary veins and may predispose the patient to DIC (Ponziani et al. 2010). Dogs with PST may develop signs of hypovolemic shock, acute abdomen, ascites and abdominal distension, vomiting and melena. Portal system thrombosis in dogs is associated with thrombocytopaenia, high hepatic enzymes, and hypoalbuminemia. (Respess et al. 2012) Dogs with PTE develop acute, severe, unexplained respiratory distress without previous respiratory signs. Most of these patients have unremarkable thoracic radiographs and evidence of hypoxemia on blood gas analysis (LaRue et al. 1990).
Uncontrolled haemorrhage from intra-abdominal metastases is a common cause of death in dogs with splenic masses. The most common sites for intra-abdominal metastases of splenic haemangiosarcoma is the liver, omentum, and mesentery (Fig. 6). Sites of intra-abdominal haemorrhage may be masked by anaesthesia-related hypotension, and bleeding may develop during recovery.
Low platelets count and PCV < 30% have been found to be most closely associated with perioperative death. In addition to this, development of intra-operative ventricular arrhythmias is aslo considered a negative prognostic indicator (Wendelburger et al. 2014).
The association of severe anaemia and perioperative death reflects the tendency of poor oxygen delivery in these patients. Anaemia, hypocoagulability and evidence of shock should be the triggers for the decision to perform blood transfusion in dogs undergoing splenectomy for splenic masses. Dogs undergoing blood transfusion, however have greater odds of poor long-term outcome compared to dogs that do not undergo transfusion (Lynch et al. 2015).
In the past it has been hypotesized that dogs with a history of previous splenectomy may have an increased odds of gastric dilatation-volvulus (GDV) and a possible association may also exist between GDV and previous splenectomy. Several theories have been proposed for why splenectomy may increase the risk for GDV. First, the anatomic void created after removal of the spleen, particularly if enlarged, may allow increased gastric motility, resulting in GDV. Second, a splenic mass or torsion of the spleen may stretch the gastrosplenic, hepatoduodenal, or hepatogastric ligaments, resulting in increased gastric motility (Millis at al. 1995). In cases of splenic torsion (Fig.7), dogs may initially be predisposed to developing GDV for reasons unrelated to splenic disease and may develop intermittent gastric dilatation without volvulus first, thus stretching the gastrosplenic ligaments or displacing the spleen, ultimately resulting in splenic torsion. These patients may subsequently develop GDV due to their preexisting propensity (Millis at al. 1995). The occurrence of GDV following splenectomy may be coincidental, considering that both GDV and conditions necessitating splenectomy, such as haemangiosarcoma and splenic torsion, occur most commonly in large-breed dogs (Sartor et al. 2013).
Despite the relationship between splenectomy and GDV has not yet been clearly defined in veterinary patients, authors of several reports have recommended prophylactic gastropexy following splenectomy in dogs (Grange et al. 2012). In a recent study, Grange et al. (2012) did not find splenectomy to be a risk factor for GDV in 219 dogs that underwent splenectomy for reasons other than splenic torsion (splenic neoplasia, benign masses, trauma, infarction). In the contrary, Sartor et al.( 2013) did find an increased odds of GDV in dogs with splenectomy and supported prophylactic gastropexy in particular if other risk factors for GDV such as breed, age, and body condition score were present.
Length of the follow up period of dogs undergoing splenectomy is particularly relevant. Dogs should be followed up until death to know the true incidence of GDV after splenectomy. It is the author’s opinion infact that the nature of the splenic disease necessitating splenectomy may have greater relevance in increasing the risk of GDV than removal itself. This may be supported by the fact that being splenic haemangiosarcoma one of the most frequent diseases needing splenectomy and being the median survival time of these patients 5.5 months, GDV following splenectomy may not be identified simply because the early death of the patients. In addition, as splenic torsion has significantly a better prognosis than splenic haemangiosarcoma and therefore longer life expectations, prophylactic gastropexy may decrease the risk of GDV in this group of patients.
Neverthless, other factors should be always considered in evaluating the potential role of prophylactic gastropexy at the time of splenectomy. These include the anaesthetic condition of the patient, the breed, and the age.
References
- Clendaniel DC et al. Association between macroscopic appearance of liver lesions and liver histology in dogs with splenic hemangiosarcoma: 79 cases (2004-2009). J Am Anim Hosp Assoc 2014; Jul/Aug e6-e10
- Gordon SSN et al. Outcome following splenectomy in cats. J Fel Med Surg 2010; 12: 256-261
- Grange AM et al. Evaluation of splenectomy as a risk factor for gastric dilatation-volvulus. J Am Vet Med Assoc 2012; 241: 461-466
- Kim SE et al. Epirubicin in the adjuvant treatment of splenic hemangiosarcoma in dogs: 59 cases (1997-2004). J Am Vet Med Assoc 2007; 231: 1550-1557
- La Rue MJ et al. Pulmonary thromboembolism in dogs: 47 cases (1986-1987). J Am Vet Med Assoc 1990; 197: 1368-1372
- Lynch AM et al. Transfusion practices for treatment of dogs undergoing splenectomy for splenic masses: 542 cases (2001-2012). J Am Vet Med Assoc 2015; 247: 363-642
- Millis DL et al. Gastric dilatation-volvulus after splenic torsion in two dogs. J Am Vet Med Assoc 1995; 207: 314-315
- Ponzizni FR et al. Portal vein thrombosis: insight into physiopathology, diagnosis, and treatment. World J Gastroenterol 2010; 16:143-155
- Respess M et al. Portal vein thrombosis in 33 dogs: 1988-2011. J Vet Intern Med 2012; 26: 230-237
- Sartor AJ et al. Association between previous splenectomy and gastric dialatatio-volvulus in dogs: 453 cases (2004-2009). J Am Vet Med Assoc 2013; 242: 1381-1384
- Wendelburg KM et al. Risk factors for perioperative death in dogs undergoing splenectomy for splenic masses: 539 cases (2001-2012). J Am Vet Med Assoc 2014; 245: 1382-1390
- Wendelburg KM et al. Survival time of dogs with splenic hemangiosarcoma treated by splenectomy with or without adjuvant chemotherapy: 208 cases (2001-2012). J Am Vet Med Assoc 2015; 247: 393-403