Oncology nursing case report: canine anal sac adenocarcinoma

Transcription

1 Vet Times The website for the veterinary profession Oncology nursing case report: canine anal sac adenocarcinoma Author : Linda Roberts Categories : RVNs Date : October 1, 2011 Linda Roberts VTS(Oncology), DipAVN(Medical), RVN, discusses the case of Teasel, a nine-yearold female entire cocker spaniel TEASEL was presented to her primary care veterinary surgeon with a two-week history of polydipsia and polyuria, marked weight loss and faecal tenesmus. Eating was normal and no vomiting was reported. Serial blood and urine samples were taken, which revealed the dog to be persistently hypercalcaemic and hyposthenuric (USG [normal to 1.080]). The patient was vaccinated annually and had not travelled outside the UK. Teasel was referred to the oncology service. On physical examination, she was bright, alert and responsive, but nervous and difficult to handle. The patient was in poor physical condition, with a body condition score of 2/5 and a bodyweight of 11.35kg. Vital parameters were within normal limits and hydration status was adequate. On rectal examination, a mass of approximately 5cm 5cm was palpated in the region of the left anal sac (Figure 1). The rest of the physical examination was unremarkable. The patient s problem list included polydipsia, weight loss, hypercalcaemia and a pararectal mass. Differential diagnoses Polydipsia with polyuria causes 1 / 7

2 Diabetes mellitus; diabetes insipidus; acute or chronic renal failure; hepatic disease; hyperadrenocorticism; hypoadrenocorticism; sepsis; hypercalcaemia; neoplasia; drug therapy; or psychogenic polydipsia. Weight loss causes Increased calorie use (such as physical activity, cold environment, pregnancy/lactation, catabolism or cancer); maldigestion or malabsorption; dysphagia; prolonged vomiting and/or diarrhoea; anorexia; poor-quality diet; metabolic derangements (such as organ failure and cancer cachexia); nutrient loss (such as protein-losing enteropathy or nephropathy). Hypercalcaemia causes Hypercalcaemia of malignancy (such as lymphoma and anal sac adenocarcinoma); hyperadrenocorticism; chronic renal failure; hypervitaminosis D; or primary hyperparathyroidism. Rectal mass causes Perianal adenoma; abscess/infection; anal sacculitis; any neoplasia, including perianal adenocarcinoma, anal sac adenocarcinoma, other carcinoma, rectal lymphoma, any soft-tissue sarcoma, melanoma or mast-cell tumour. Diagnostics and results Bloods were taken for a complete blood count (CBC) and biochemistry the only abnormalities noted were a total calcium of 3.74mmol/L (normal range 2.3mmol/L to 3mmol/L) and ionised calcium (ica) of 1.71mmol/L (normal range 1.15mmol/L to 1.5mmol/L). Renal parameters were normal. Urinalysis was performed dipstick examination was unremarkable, USG was and there was scant sediment on microscopy. Water intake over 24 hours was 5ml/kg/hour (normal: approximately 2ml/kg/hour). Thoracic radiographs were taken: no abnormalities. Abdominal ultrasound was performed and medial iliac lymph nodes were seen to be large and misshapen ( Figure 2 ). They surrounded the external iliac artery and compressed the caudal vena cava. The spleen was enlarged, but with no apparent lesions. The kidneys were grossly normal. No other abnormalities were detected. 2 / 7

3 Needle biopsies were taken from the rectal mass and transabdominally from the spleen and sublumbar lymph nodes. On cytological examination, no pathological changes were detected in the spleen. The lymph nodes and rectal mass shared the same pathology a uniform epithelial population of neoplastic cells, likely to be a well-differentiated carcinoma. Diagnosis and prognosis Anal sac adenocarcinoma Given the bulk of unresected diseased lymph nodes and persistent hypercalcaemia, this patient was given a guarded prognosis of six to nine months. It was thought that renal failure resulting from the hypercalcaemia could become a significant clinical problem for the dog before metastatic disease. Anal sac adenocarcinoma (ASAC) has traditionally been given a guarded or poor prognosis, with short predicted survival times, but it has been suggested that, if aggressively treated, the prognosis is fair potentially up to 18 months when treated with surgery and/or radiotherapy and/or chemotherapy. Negative prognostic indicators for ASAC include large tumour size, the presence of metastases and humoral hypercalcaemia of malignancy (HHM) at the time of diagnosis. Treatment Immediate management of the hypercalcaemia: intravenous fluids at 0.9 per cent isotonic saline at 6ml/kg/hour; pamidronate intravenous infusion at 1.5mg/kg (in 500ml 0.9 per cent isotonic saline) over four hours; furosemide at 2mg/kg intravenously every 12 hours; prednisolone at 0.5mg/kg orally, every 12 hours, with food. Surgical extirpation of primary tumour. Four doses of adjuvant carboplatin chemotherapy, given at 300mg/m 2 intravenously every 21 days. Oral clodronate (10mg/kg to 20mg/kg orally, every 12 hours). Case discussion Carcinomas are malignant tumours arising from epithelial cells, in this case the anal sac the paired modified apocrine sebaceous glands at either side of the anus. ASAC is an uncommon tumour in dogs, but is most frequently reported in older female and neutered male dogs. ASAC is highly malignant, affecting one or both anal sacs. It infiltrates the surrounding tissues, metastasising early to regional lymph nodes. Metastases spread via the lymphatics to the abdominal lymph nodes, spleen and liver, and then on to the lungs. The kidneys 3 / 7

4 and lumbar vertebrae may also be affected. ASAC may be an asymptomatic incidental finding. Tumours may be large at the time of diagnosis clinical signs of faecal tenesmus may develop before a mass is noticed. Tenesmus may relate to the primary mass or enlarged sublumbar lymph nodes. Metastases have often developed by the time of presentation. This patient s initial presentation was polydipsia, resulting from paraneoplastic HHM. Polydipsia occurs in hypercalcaemia (serum calcium more than 12mg/dl or ica more than 1.4mmol/L). This dog was drinking in excess of 100ml/kg/day, with a resultant polyuria. Hypercalcaemia is a potentially lifethreatening paraneoplastic syndrome found in up to a quarter of ASAC patients. Hypercalcaemia often leads to a clinical suspicion of tumour, in many cases instigating a tumour hunt, with lymphosarcoma and ASAC the primary differentials. ASAC produces a protein called parathyroid hormone-related protein, which binds parathyroid hormone receptors, causing changes in calcium homeostasis. Clinical signs of polydipsia are associated with renal impairment and inability to concentrate urine hypercalcaemia causes vasoconstriction, decreased glomerular filtration and renal blood flow and, eventually, renal calcification and necrosis. Severe hypercalcaemia is a medical emergency, with effects not only on the kidneys, but also the heart (potentially fatal cardiac arrhythmias) and neuromuscular systems (weakness, tremors or seizures). While this patient was relatively bright, many display lethargy, vomiting and inappetence. ASAC diagnosis is made on cytology or histopathology. Staging uses a tumour, node, metastasis (TNM) protocol ( Table 1 ). It should begin with physical examination and involve full rectal examination of the dorsal pelvic canal and caudal sublumbar lymph nodes, and abdominal palpation for enlarged lymph nodes or organomegaly. Rectal examination of this patient revealed abnormalities that, along with the polydipsia, gave suspicion for neoplasia. Abdominal palpation was unremarkable. This patient was TNM-staged as T4 N3 M0. Other options for staging ASAC patients include abdominal radiographs to assess liver, spleen and sublumbar node size and bone lysis in the lumbar region; or computed tomography to detect lung metastasis and determine the extent of sublumbar lymph node involvement. Treatment of HHM takes priority over other aspects of tumour management. Aggressiveness of treatment depends on the severity of clinical signs. Ionised calcium should be measured as it is the biologically active form and removes the need to correct total serum calcium, which is bound to plasma proteins and may lead to artefactual results. In this case, no single treatment brought the serum calcium to within normal limits. The patient s demeanour improved following aggressive intravenous crystalloid and furosemide administration, but made no real impact on HHM. Total calcium fell from 3.74mmol/L to 3.10mmol/L and ica from 1.71mmol/L to 1.6mmol/L in 24 hours. Physiological saline (0.9 per cent NaCl) is the solution of choice, with potassium supplementation as required to maintain normal serum potassium. Adequate calciuresis was not achieved, so a pamidronate infusion was administered. After 48 hours, the patient s total calcium fell to 3mmol/L and the ica to 1.58mmol/L. Pamidronate is a 4 / 7

5 bisphosphonate bone-resorption inhibitor, causing calcium phosphate crystals to assimilate in bone. Corticosteroids were used to affect calciuresis. This is achieved by ion exchange calcium and potassium are excreted, while sodium and chloride are reabsorbed. Steroids also cause diuresis through mineralocorticoid activity and by decreasing calcium absorption from intestines and bone. The use of steroids in advance of diagnostic sample collection may obscure diagnoses and induce multidrug resistance (particularly suspected lymphoma), so should be reserved for when all samples have been obtained. In many HHM cases, removal of the underlying cause is the definitive treatment in effect, tumour excision/treatment. ASAC is treated with a multimodal approach (surgery, radiation therapy and chemotherapy). Ideally, the mass would have been removed with wide margins, the metastatic lymph nodes excised and the dog referred for follow-up radiotherapy. However, the owners elected for local excision/tumour de-bulking only. They perceived the morbidity of a pelvic split for metastatic lymph node excision too great for the benefit offered to the dog. They were warned of potential surgical complications (wound dehiscence, faecal incontinence, perineal hernia, recurrence of local disease or infection). It was hoped that local excision would reduce the tumour burden sufficiently and normalise serum calcium, with the caveat that overall survival time was likely to be shorter. Postsurgery The patient recovered from surgery without incident. Although aseptic technique was observed, it was considered pertinent to prescribe antibiotics due to the likelihood of faecal wound contamination. A 14-day course of clavulanate-potentiated amoxicillin at 20mg/kg orally, every 12 hours, was given. Postoperative analgesia included an intravenous morphine infusion for the first 24 hours, then buprenorphine every six hours. The patient was kept on intravenous fluids throughout. The wound was checked and cleaned twice daily, with barrier cream applied as required. Stool softeners were added to the patient s food while tissue swelling resolved. An Elizabethan collar was fitted. Vitals were within normal limits during hospitalisation. Bloods were taken daily to assess renal parameters, electrolytes and ica all remained within normal limits except ica, with persistent hyposthenuria. Radiotherapy can begin two weeks after surgery. Palliative radiotherapy may be undertaken to provide symptomatic relief from the tumour (hypercalcaemia and/or tenesmus), with minimal side effects. Although radiation therapy is only likely to be effective in microscopic disease, the owners declined follow-up radiotherapy due to practical and financial constraints. The patient was underweight and cachexic, having lost 10 per cent bodyweight over a short time. A further 1.7kg was lost during hospitalisation. An energy-dense convalescence diet was fed while 5 / 7

6 hospitalised. The patient was sent home on this diet and regained 2kg over the following three months. The patient was discharged six days after surgery with prednisolone and the stool softeners. Clodronate (oral bisphosphonate) tablets were prescribed (20mg/kg orally every 12 hours), aimed at maintenance of eucalcaemia. Clodronate has been associated with oesophagitis therefore, careful instructions were given to the owners about how to avoid this. This is done by giving tablets on an empty stomach and in an upright position, followed by administration of 20ml of water and feeding a full meal 20 minutes later. Although other side effects have been reported, no problems were encountered. At the next hospital visit, ica was just within normal range at 1.5mmol/L. In subsequent months, monitoring of serum calcium helped to assess remission status and treatment efficacy. Due to the high metastatic rate of ASAC, chemotherapy was recommended. When the patient was presented for a surgical wound check, the first chemotherapy treatment was given. The patient was well and gaining weight, and the incision had healed. Carboplatin was given on a 21-day cycle to palliate clinical signs and slow disease progression. It was administered intravenously, alongside a free-flowing saline infusion, to promote diuresis. It is renally excreted and should be used with care in patients with renal insufficiency. Renal function was checked on blood and urine samples before each dose, and it was considered safe to proceed. At each presentation, a recent history was taken from the owners, a full examination performed and blood and urine samples obtained. At subsequent visits, the patient s ica was stable. The polydipsia had abated. There was no local recurrence of the pararectal tumour and no tenesmus. USG showed persistent isosthenuria, with stable renal parameters on blood samples. Quality of life was deemed acceptable by the owners, but the dog lacked energy and had poor muscle tone. At the fourth dose of carboplatin, large abdominal lymph nodes were palpated. The owners declined re-staging and further chemotherapy on financial grounds. They elected to continue bisphosphonates and corticosteroids to maintain eucalcaemia, but were counselled that the dog s quality of life would deteriorate. Teasel was euthanised by her referring vet seven weeks later. The owners considered her treatment a success, given the tumour diagnosis and prognosis, and were pleased with the extra time they had with their pet and the quality of life she maintained. Further reading Withrow S J and MacEwen E G (2001). Small Animal Clinical Oncology (3rd edn), W B Saunders. Dobson J and Lascelles B D (2003). Manual of Canine and Feline Oncology BSAVA, Cheltenham. 6 / 7

7 Powered by TCPDF ( Plumb D C (2008). Plumb s Veterinary Drug Handbook (6th edn), Blackwell Publishing. Bexfield N (2006).The safe use of cytotoxic drugs in companion animal practice, EJCAP 16(1) Ramsey I and McGrotty Y (2002). Investigation of polyuria and polydipsia in the dog, In Practice 24: / 7