True oncological emergencies are uncommon. They can be separated into cancer-derived and iatrogenic emergencies. The most frequently cited cancer-derived emergency is hypercalcaemia of malignancy. Others include pancytopenia and ruptured viscus. Iatrogenic emergencies include neutropenic sepsis, haemorrhagic gastroenteritis and treatment-induced anaphylaxis.

Hypercalcaemia of Malignancy

Patients with hypercalcaemia are classically polydipsic and polyuric. Other clinical signs reported include dysuria, weakness, lethargy, altered behaviour and tremors. In one study, half of the hypercalcaemic dogs had no clinical signs aside from those pertaining to the urinary tract. Potential causes of hypercalcaemia of malignancy include lymphoma, anal sac gland carcinoma and parathyroid tumour as the three most common tumour causes in dogs, and oral squamous cell carcinoma as the most common cause in cats. Dogs or cats with any of these complaints should have their serum calcium concentration assessed even without overt evidence of hypercalcaemia, as there can be significant damage to soft tissue structures from persistent calcium aberrations.

The notion that hypercalcaemia is an emergency does misrepresent the majority of oncological hypercalcaemic cases. The clinical status of hypercalcaemic cases correlates poorly with the degree of calcium concentration abnormality. As a general principle, canine lymphoma cases with hypercalcaemia can be systemically very unwell with modest calcium concentration aberrations. By contrast, patients with hypercalcaemia associated with parathyroid or anal sac tumours may appear surprisingly healthy despite remarkable hypercalcaemia. Regardless, treatment should be aimed at alleviating the clinical signs associated with hypercalcaemia and at reducing the risk of neuromuscular deficits arising due to the metabolic derangement. This is particularly pertinent if a patient is a candidate for anaesthesia.

The most important message at presentation of a patient with hypercalcaemia is to avoid the administration of agents which might later cloud diagnosis of the underlying cause. Since lymphoma is a potential differential diagnosis for a cat or a dog with hypercalcaemia, administration of corticosteroids should be avoided at all costs until diagnostic specimens have been obtained.

Hypercalcaemic patients are dehydrated, despite their increased thirst. This is because calcium interferes with reabsorption of water in the renal collecting ducts, so water is lost which results in a drive to drink. Rehydration is critical to normalisation of haemodynamic parameters. Rehydration using 0.9% sodium chloride optimises calciuresis. Take care to ensure that the water load administered can be excreted. Hypercalcaemia may cause, or may reflect, renal failure.

Serial reassessments of blood calcium concentrations permit modifications to therapy. Additional treatments in the form of bisphosphonates or therapy directed at the cause of the hypercalcaemia are appropriate. Intravenous bisphosphonates can induce fatal cardiac arrhythmias if not administered appropriately. They must be given as a slow intravenous infusion. I prefer to use pamidronate: 1–2 mg/ kg over 1–2 hours is advised. Surgical removal of an enlarged anal sac tumour can lead to prompt normalisation of serum calcium concentration; however, hypercalcaemia of malignancy often reflects an increased burden of disease so it is critical that the clinician in charge is aware of the full extent of the patient's neoplastic complaint before entertaining the idea of surgery with the intent of resolving hypercalcaemia. Removal of an anal sac tumour will not improve hypercalcaemia in a patient with widespread pulmonary metastases.

Persistent hypercalcaemia can be managed by oral bisphosphonate therapy. There are multiple agents available. I prefer to use etidronate at a dose of 20 mg/kg once daily. This almost never results in a restoration of normal serum calcium concentrations but if the patient appears relatively well despite hypercalcaemia, they can survive for prolonged periods (6–9 months) with this therapy alone while their tumour progresses. Bisphosphonates do not appear to exert a direct antineoplastic effect in vivo.

Pancytopenia

Acute leukaemia, stage V lymphoma and myelophthisis are all neoplastic proliferations affecting the bone marrow. Simple competition for resources results in a lack of space and nutrients for the normal haemopoietic stem cells and loss of mature red cells, leucocytes and platelets from the peripheral blood. Patients do not always present with pancytopenia; in some cases a bi- or monocytopenia is present. Management is directed towards the marrow aberration present. Neutropenia results in increased risk of sepsis; bactericidal antibiotics are administered. Thrombocytopenia results in a risk of spontaneous haemorrhage; some patients may require a transfusion of blood products and these are managed with great care to minimise trauma. Anaemia can be managed by serial cross-matched blood transfusions. All of these are symptomatic treatments for the emergency patient. There is no future for these patients if the underlying cause cannot be addressed. This requires a diagnosis and a treatment plan. Many cases are nonresponsive to therapy. In one study, 28% of cases of acute lymphoblastic leukaemia lived to 14 days after diagnosis.

Ruptured Viscus

The most common oncological ruptured viscus emergency is splenic rupture due to haemangiosarcoma. These patients typically present with acute-onset lethargy and marked pallor. Emergency splenectomy can save life. Appropriate preoperative preparation includes restoration of circulating volume, ideally with whole blood. The prognosis for cases diagnosed with splenic haemangiosarcoma is poor: median survival times of approximately 2 months are reported for patients undergoing splenectomy alone; this increases to approximately 6 months if splenectomy is followed by a course of adjuvant chemotherapy. Other tumours can induce splenic rupture including metastatic carcinoma and histiocytic sarcoma. Complete physical examination and thoracic radiographs should be considered a mandatory aid to decision making in the management of these cases.

Neutropenic Sepsis

Chemotherapy can induce myelosuppression. Serial haematology analyses are a routine part of chemotherapy protocols to protect against this eventuality. Despite this, septic events still develop. Such cases typically present 7–10 days after chemotherapy administration with a per-acute onset of listlessness and pyrexia (40°C). Owners must be educated to recognise the signs of sepsis, as prompt action is required. If there is doubt about the diagnosis, manual blood smear examination will reveal a stark absence of neutrophils. Some automated haematology analysers will consistently give error messages and can delay diagnosis. Intravenous antibiotics are recommended, followed by oral therapies. Other supportive care can be provided as indicated. Typically these patients will recover as quickly as they deteriorated. Antibiotic choices vary between oncologists but a combination achieving broad-spectrum coverage such as potentiated amoxicillin and a fluoroquinolone would be appropriate. It is important to forewarn owners that there is a risk of antibiotic resistance in patients exposed to chronic antibiotic therapy or in animals belonging to healthcare workers. If sepsis arises due to the presence of antibiotic-resistant bacteria, the patient would be dead before such information came to light.

Haemorrhagic Gastroenteritis

Severe gastrointestinal complications of chemotherapy administration are rare. Typically they arise due to mismanagement of chemotherapy or due to a pre-existing susceptibility such as seen in cases expressing the mutated p-glycoprotein as seen in some Border Collies and Australian Shepherd Dogs. To further complicate matters, gastrointestinal signs induced by chemotherapy are expected in the first 48–72 hours after treatment administration. Severe toxicity will require a number of days for recovery. Those patients with poor drug metabolism are those likely to develop severe adverse events, and they are also more likely to suffer neutropenic sepsis. These patients must therefore also be monitored carefully for evidence of haematological disturbances. Management of severe gastroenteritis is the same as it would be if the trigger was unrelated to chemotherapy. Patients require intravenous fluid support, antiemetic therapy, antidiarrhoeal treatment, antibiotic therapy to modulate intestinal flora and good nursing care.

In cases of iatrogenic emergency, changes must be made to the treatment protocol to ensure that similar events do not affect that patient in the future.