Introduction

Most cancer patients experience at least one emergency during the course of the disease. An ageing population is resulting in more people being diagnosed with cancer and an increasing number of treatment options means that many patients live significantly longer with their disease. It is anticipated, therefore, that an increasing number of patients will present to primary and secondary care with acute complications of cancer or the treatment thereof. Physicians should be familiar with oncological emergencies as failure to implement immediate and appropriate treatment may result in significant morbidity or death. This chapter focuses on the common and critical complications of cancer (Table 109.1) in older adults.

Table 109.1 Summary of oncological emergencies.

Haematological Emergencies

Initial antibiotic selection should be guided by the patient’s history, allergies, symptoms, signs, recent antibiotic use and culture data and awareness of institutional nosocomial infection pattern. There is no clear optimal choice for empirical antibiotic therapy.2 Combination therapy and monotherapy (cefepime, ceftazidime) have led to similar outcomes. In critically ill patients, an aminoglycoside should be added for better Gram-negative coverage or a fluoroquinolone or aztreonam when renal function is a cause for concern. (Table 109.2).

Table 109.2 Initial antibiotic therapy of neutropenic fever.

aIn certain circumstances (e.g. suspected infection of a central venous line or device, skin infection, severe mucosal damage), a drug active against Gram-positive bacteria is recommended. Vancomycin is also the most commonly used drug for suspected infections with Gram-positive bacteria. Reproduced with permission from Halfdanarson et al.3

In certain circumstances, a drug active against Gram-positive bacteria is recommended. Such circumstances include known colonization with Gram-positive bacteria, suspected infection of a central venous line or device and severe sepsis with or without hypotension. Gram-positive bacteria should also be considered in patients with suspected skin infection or severe mucosal damage and when prophylactic antibiotics against Gram-negative bacteria have been used.3

In the case of persistent fever after 5 days without an identifiable source, the following options are valuable:

• Continuing treatment with the initial antibiotic(s) if the patient is clinically stable and the neutropenia is expected to resolve within the ensuing 5 days.
  
• Changing or adding antibiotic(s) if there is evidence of progressive disease or a new complication (onset of abdominal pain due to enterocolitis, pulmonary infiltrates or drug toxicity).
  
• Adding an antifungal drug, with or without changing the antibiotics, if the neutropenia is expected to persist for more than 5–7 days.

If an infectious source of fever is identified, antibiotics should be continued for at least the standard duration (e.g. 14 days for bacteraemia). With no known source, the timing of the discontinuation of antibiotics is usually dependent on resolution of fever and neutropenia. If the ANC increases to >500 × 109 cells l−1 and the patient becomes afebrile, antibiotics are usually administered for 7 days.

In older patients, primary prophylactic colony-stimulating factor was observed to be effective in reducing the incidence of neutropenia and infection.4

Thrombocytopenia

Thrombocytopenia (platelet count <150 × 109 l−1) is mainly a consequence of myelotoxicity induced by chemotherapy5 or less frequently by radiotherapy, and rarely a sign of disseminated intravascular coagulation. In addition, certain malignant conditions are associated with immune-mediated thrombocytopenia. Multiple causes of thrombocytopenia may coexist in a given patient.

In the case of chemotherapy, neutropenia almost invariably accompanies the low platelet count. If the degree of thrombocytopenia occurs more rapidly or is more severe or more prolonged than anticipated, then a second mechanism should be suspected. The presence of bone marrow metastases should be suspected if anaemia or thrombocytopenia are observed prior to treatment or if chemotherapy induces a sudden or excessive fall in the haemoglobin or platelet count. Immune-mediated destruction of platelets is commonly seen with lymphoid malignancies. As a general rule, patients with autoimmune thrombocytopenia experience less bleeding for a given platelet count compared with patients with chemotherapy-induced thrombocytopenia or other mechanisms of bone marrow failure.

If there is no obvious relationship between platelet count and administration of chemotherapy, a bone marrow aspirate and trephine examination may be indicated. In immune-mediated thrombocytopenia, plentiful megakaryocytes are expected since platelet destruction occurs in the peripheral circulation. If bone marrow metastasis is the primary mechanism of thrombocytopenia, the bone marrow trephine is the most sensitive diagnostic tool.

Patients who have a platelet count of above 10 × 109 l−1 with absence of bleeding may be managed conservatively, provided that they have a full daily clinical examination including fundal examination. In the absence of bleeding and of evidence of sepsis or coagulopathy, then observation is adequate.

Platelet counts below 10 × 109 l−1 or bleeding need random donor platelets. It should be remembered that the key end point is to arrest the bleeding, and this may occur without a significant platelet rise. However, failure to obtain the expected platelet rise after two consecutive transfusions (platelet refractoriness) may be due to conditions that cause increased platelet consumption (e.g. fever, splenomegaly) or may be related to human leukocyte antigen (HLA) alloimmunization from previous transfusions or pregnancies.

Disseminated Intravascular Coagulation

Disseminated intravascular coagulation (DIC) is a clinical syndrome characterized by systemic activation of coagulation leading to intravascular deposition of fibrin and thrombosis of small vessels. Depletion of natural anticoagulants such as protein C and antithrombin and suppression of fibrinolysis also add to the prothrombotic state. In addition, there may be consumption of multiple coagulation factors and platelets leading to bleeding. The delicate balance between factors that promote thrombosis and factors that lead to bleeding will determine the clinical presentation of the patient.

Clinical evidence of DIC is seen in 10–15% of patients with metastatic cancer and laboratory markers are found in 50–70% of patients (increased levels of fibrinogen, fibrin degradation products and coagulation factors V, VIII, IX and XI).

There is no single diagnostic test for DIC. The presence of a prolonged prothrombin time (PT) and activated partial thromboplastin time (APTT) with elevated levels of D-dimers and a low or low-normal fibrinogen in a clinical setting known to be associated with DIC will confirm the diagnosis in a bleeding patient. A blood film may show fragmented red blood cells. Patients with thrombosis may have a shortened PT and APTT, a high or high-normal fibrinogen and elevated D-dimers. All features may not be present in every patient. Serial tests are required to monitor progression of the condition and response to therapy and to direct further treatment.

The essence of action is supportive care.6 Removal of the underlying precipitant is advised. Therefore, the tumour should be treated where possible and concomitant sepsis should be managed aggressively. Random donor platelets should be given until the platelet count is >20 × 109 l−1 or until bleeding has stopped. If bleeding is life-threatening, then the platelet count should be raise to 50 × 109 l−1. Fresh frozen plasma (FFP) containing all coagulation factors including fibrinogen and von Willebrand’s factor is indicated for bleeding with a prolonged PT and APTT.

Hyperviscosity Syndrome

Hyperviscosity is defined as an increased intrinsic resistance of fluid to flow. Marked elevations in paraproteins, marked leukocytosis or erythrocytosis in some cancer patients can result in elevated serum viscosity and the development of significant sludging, decreased perfusion of the microcirculation and vascular stasis with the development of the hyperviscosity syndrome. Common causes of the hyperviscosity syndrome include Waldenstrom macroglobulinaemia, multiple myeloma and leukaemias. Clinical manifestations of the hyperviscosity syndrome, most apparent with a serum viscosity >5 (the relative viscosity of normal serum ranges between 1.4 and 1.8), include a triad of bleeding, visual disturbances and neurological manifestations (Table 109.1). Management of hyperviscosity should aim at urgent reduction of serum viscosity in symptomatic patients by leukopheresis or plasmapheresis. This should be followed by specific chemotherapeutic agents to treat the underlying disease after relief of symptoms. Temporary measures should focus on adequate rehydration and, in patients with coma and established dysproteinaemia, a two-unit phlebotomy with replacement of the patient’s red blood cells with physiological saline should be performed.

Metabolic Emergencies

The symptoms of hypercalcaemia are multiple and non-specific. Classic symptoms include lethargy, confusion, anorexia, nausea, constipation, polyuria and polydipsia (Table 109.1).

Symptoms vary depending on the degree of hypercalcaemia and the rapidity of onset.8 Changes in mental faculties and strength are more easily recognized in younger individuals, whereas in the elderly such events can be easily blamed on many things, including their poor tolerance of analgesics, anxiolytics, hypnotics and antiemetics.

The definition of hypercalcaemia is an elevation of calcium level above 2.64 mmol l−1 (10.6 mg dl−1) and values above 2.74 mmol l−1 (11.0 mg dl−1) should be considered an indication to initiate treatment. This threshold should be considered (according to the range of normal values from a local laboratory) only in the case of a normal albumin level. If there is any doubt about the validity of the total serum calcium level, measurement of ionized calcium or calculation of the adjusted calcium level to albumin concentrations is essential.

Asymptomatic patients with minimally elevated calcium levels (<3 mmol l−1) may be treated as outpatients with encouragement to adopt oral hydration, mobilization and elimination of drugs that contribute to hypercalcaemia (thiazides, lithium). Patients who are symptomatic or have calcium levels >3 mmol l−1 should be considered for inpatient management using volume expansion with saline infusion, corticosteroids and bisphosphonates, as follows:

• Rehydration generally has mild and transient effects on calcium levels. The volume of saline infusion depends on the extent of the hypovolaemia and also the patient’s cardiac and renal function.
  
• Bisphosphonates9 have supplanted all other drugs except calcitonin, still useful in the few cases of severe refractory hypercalcaemia because of its rapid onset of action (2–4 h versus 72 h for bisphosphonates). The recommended dose is 90 mg i.v. over 2–4 h for pamidronate or 4 mg i.v. over 15 min for zoledronate. In patients with pre-existing renal disease, no change in dosage, infusion time or interval is required.
  
• Glucocorticosteroids can be helpful in the management of hypercalcaemia caused by lymphoma, myeloma and sometimes breast cancer and may be of some value in other malignancies, used at doses of 10–100 mg per day equivalent prednisone.

Hyponatraemia

Serum sodium levels below 135 mmol l−1 (135 mequiv l−1), especially with rapid fall, can lead to brain oedema with altered mental status, lethargy, seizures, coma and death. Routine evaluation of serum electrolytes is mandatory in patients with otherwise unexplained alterations of mental status.

Aetiologies are iatrogenic complication10 (vasopressin, chlorpropamide, carbamazepine, clofibrate, vincristine, ifosfamide and narcotics), water redistribution associated with mannitol infusions, pseudo-hyponatraemia due to hyper-para-proteinaemia or hyperlipidaemia and acute water intoxication, renal sodium loss due to diuretic therapy, extra-renal sodium loss during vomiting/diarrhoea, sudden withdrawal of glucocorticoid therapy and syndrome of inappropriate antidiuretic hormone (SIADH).11

SIADH can cause a severe decrease in sodium that may be life-threatening. Diagnostic features include hypo-osmolality of serum, inappropriately high osmolality of urine for the concomitant plasma hypo-osmolality, continued renal excretion of sodium (Table 109.3), associated with clinical normovolaemia, and normal renal, adrenal and thyroid function.

Table 109.3 Diagnostic criteria of syndrome of inappropriate antidiuretic hormone (SIADH).

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