The appropriate management of these emergencies is greatly influenced by the age and condition of the patient, the type, extent, and stage of the tumour, and the wishes of the patient and his or her family.

Superior vena caval (SVC) obstruction occurs in between 3 and 8 per cent of patients with lymphoma or lung cancer (particularly the small cell type). Shortness of breath and swelling of the face, upper limbs, or trunck are the most common presenting signs. Tachypnoea, venous distension, or oedema of the face and arms are common clinical findings. Non-malignant causes of SVC obstruction are rare, although it may be precipitated by central venous catheterization. Untreated SVC compression may lead to thrombosis, central nervous system (CNS) damage, or respiratory impairment. However, if the obstruction develops slowly, collateral venous channels may develop, the patient may be asymptomatic, and the risk of serious sequelae low.

The diagnosis of SVC obstruction is largely clinical, although chest radiology or computed tomographic (CT) scanning generally confirms a mediastinal mass. Venography is rarely indicated and is relatively contraindicated because the raised venous pressure increases the risk of haemorrhage. When SVC obstruction is the presenting condition, a tissue diagnosis should be sought prior to starting treatment for the compression. Ideally, tissue should be obtained using the least invasive procedure as SVC obstruction increases the risk of haemorrhage following surgical manipulations. In occasional cases with rapidly progressing disease, treatment may be justified in the absence of a tissue diagnosis. However, this is likely to compromise the further management of the patient and should be avoided if possible.

Radiation is the most common treatment for SVC obstruction. The response begins within 3 to 4 days and 90 per cent of patients respond subjectively within 7 days. Failure of response may indicate that venous thrombosis has occurred. Resolution of symptoms is more prompt and more complete in lymphoma than in lung cancer, where only a minority have complete resolution of symptoms. Where the tumour is chemosensitive, and where disease is also present outside the chest, chemotherapy should be considered for primary treatment. In such cases, resolution of symptoms occurs as promptly as after radiotherapy. Surgical bypass of SVC obstruction has been successful in some cases, but it is hazardous.

Cardiac tamponade due to a malignant pericardial effusion is a life-threatening but treatable condition. The symptoms of tamponade are non-specific and most patients complain only of breathlessness. The characteristic clinical features comprise a raised jugular venous pressure, tachycardia, hypotension, and marked pulsus paradoxus. Patients with tamponade are at risk of sudden death from a catastrophic drop in cardiac output, cardiac arrhythmia, or cardiac ischaemia. Tamponade may be produced by a rapidly accumulating effusion as small as 200 ml, but over 1 litre may accumulate slowly before symptoms develop. A chest radiograph may show the typical large, globular heart, but this may be normal with a small effusion. Echocardiography will quickly and accurately diagnose pericardial effusion and should be performed when tamponade is suspected or when there is unexplained breathlessness in the cancer patient.

When a significant effusion is detected, immediate pericardiocentesis should be performed. Placement of a pericardiac catheter at the same time will allow complete drainage of the fluid and the instillation of tetracycline to sclerose the pericardiac sac and prevent reaccumulation. Systemic chemotherapy may prevent recurrence in chemosensitive tumours, while radiotherapy may also be beneficial, particularly if the tumour can be treated without irradiating the whole heart. Surgical intervention, usually to form a pleuropericardial window, is indicated when other methods of control fail and when the patient has a reasonable life expectancy. The recently reported technique of percutaneous balloon pericardiotomy appears as effective but safer than an open surgical procedure and may well become the technique of choice in recurrent malignant effusion.

Cardiac tamponade may also be produced by tumour infiltration of the pericardium. The symptoms and signs will be similar but echocardiography will show a thickened pericardium and little fluid. Effective antitumour therapy may relieve the constriction, but surgery is unlikely to be of benefit.

Respiratory impairment is common in cancer patients. Metastatic tumour, lymphangitis carcinomatosa, malignant pleural effusion, infection, haemorrhage, emboli, and the effects of drugs and radiation can all cause life-threatening pulmonary failure. Accurate diagnosis is most critical where the underlying cause is both treatable and rapidly progressive. Extensive, symptomatic lung metastases or pulmonary infiltrations are generally associated with a poor prognosis. When the underlying tumour can be cured with chemotherapy (for example, lymphomas or germ cell tumours) vigorous resuscitation is warranted, including ventilatory support if necessary. This may be needed particularly following the start of chemotherapy, when pulmonary function may deteriorate as a result of tumour lysis. In responsive but non-curable tumours (for example, breast cancer or prostate cancer) dramatic responses to hormone or chemotherapy may also occur and pulmonary support may be indicated.

A tumour arising in, or metastatic to, the main bronchi may cause life-threatening airways obstruction even when the tumour is small. Patients usually present with stridor or wheeze, which may be mistaken for bronchoconstriction. Respiratory function may deteriorate quickly. Radiotherapy produces relief of symptoms in most patients, as will chemotherapy in patients with small cell carcinoma. Where more rapid relief is required, or when the tumour recurs following radiotherapy, endobronchial laser resection can be effective.

Many cytotoxic drugs can cause pulmonary reactions. Pulmonary fibrosis, for instance, has been described, particularly after bleomycin and the alkylating agents. Bleomycin can also produce acute breathlessness, for which high-dose prednisolone is indicated to prevent progression to chronic fibrosis. Great care should also be taken in anaesthetizing patients who have been treated with bleomycin, as exposure to high concentrations of oxygen may precipitate an acute, life-threatening pulmonary reaction.

Renal failure due to tumour progression generally occurs as a terminal event for which no specific therapy is indicated. Where the underlying tumour is chemosensitive, more aggressive intervention is indicated. Bilateral ureteric obstruction may be bypassed by retrograde ureteral stents or by percutaneous nephrostomies, allowing time for cytotoxic chemotherapy to produce tumour shrinkage. Where irreversible renal damage has occurred, but where the tumour is treatable, haemo- or peritoneal dialysis may be indicated, and may be given at the same time as chemotherapy and radiotherapy.

Renal failure may be induced by several commonly used cytotoxic drugs, for example, cisplatin, ifosfamide, or high-dose methotrexate. Appropriate schedules for administering these drugs reduce the risk of significant renal damage but, when this does occur, alternative, non-nephrotoxic drugs may need to be used.

Gastrointestinal haemorrhage is common in cancer patients, but in only 12 to 17 per cent is it due to the malignancy. The management of such cases should therefore be based on standard protocols. Similarly, two-thirds of perforations are not due directly to tumour. Lymphomas are most commonly associated with bleeding and perforation. As many as 33 per cent of gastrointestinal, high-grade lymphomas perforate either at presentation or during treatment. The highest risk of perforation is during the early stages of treatment when highly chemosensitive lymphomas show the maximum rate of tumour regression. The risk of perforation and/or bleeding can be greatly reduced by surgical resection of the lymphoma before starting chemotherapy. This should be undertaken, where possible. Other chemosensitive tumours, such as ovarian cancer, may also perforate due to dramatic tumour lysis following the first cycle of chemotherapy. It should therefore not be assumed that perforation is a sign of treatment failure. It may, conversely, herald rapid tumour regression.

Spinal cord compression occurs most commonly in tumours (such as those of breast, lung, and prostate) that metastasize to bone. Early recognition and prompt treatment are essential to prevent permanent neurological damage, disability, and shortened survival.

Pain is the initial symptom in almost all patients, and any back pain in a cancer patient should be assessed urgently. The pain may be localized to the spine or it may have nerve-root distribution. When thoracic in origin, nerve-root pain may radiate into the chest or abdomen and cause diagnostic confusion. Weakness is also common at presentation. As the compression progresses, paraesthesiae, sensory loss, and bladder and bowel dysfunction may develop. The prognosis is critically dependent on the neurological condition of the patient at diagnosis. Sixty per cent of patients ambulatory at diagnosis remain so after treatment, while only 20 per cent of those paraplegic at diagnosis improve significantly. Additional adverse prognostic features include loss of bladder function, a rapid-onset lesion, or a high-thoracic lesion.

Magnetic resonance imaging is the investigation of choice in suspected spinal cord compression and gives excellent images of the spinal canal. Where this is not available, myelography is indicated to show the extent and number of lesions.

In all cases, high-dose steroids (usually dexamethasone) should be given while the diagnosis is confirmed and definitive treatment planned. The best treatment for spinal cord compression is unknown as no prospective studies have compared the possible therapies—surgery, radiotherapy, and chemotherapy—either alone or in combination. The choice is influenced by the nature of the tumour (whether radiosensitive or chemosensitive), the level of block, the rapidity of onset, and the clinical skills available locally. Surgery gives the quickest relief of spinal compression and may be the best approach when the compression is progressing rapidly. It is unlikely to be able to remove all the tumour and should be followed by radiotherapy to prevent local recurrence. There is no evidence that the quicker relief of compression achieved by surgery makes it a better overall approach than radiotherapy, which is considered by many to be the standard therapy. In highly chemosensitive tumours, particularly when there is systemic disease and the compression is progressing slowly, chemotherapy should be considered, perhaps in conjunction with radiotherapy.

Spinal infection is another, although rarer, cause of spinal cord compression in the cancer patient. Infection in the epidural space may occur in isolation or may be secondary to vertebral osteomyelitis. In either case it is usually due to haematogenous spread from infection elsewhere. The neurological signs are similar to those described above, but they progress rapidly and occur in association with marked pain, local tenderness, and fever. Urgent surgical decompression is indicated in conjunction with appropriate antibiotics.

The patient with cancer commonly has reduced resistance to infection for multiple reasons related to their disease and its treatment. In such patients infection is probably the major cause of morbidity and mortality. Although many infections occur in the terminal stages of disease, when vigorous treatment may not be indicated, they may also threaten the survival of patients whose tumours are potentially curable.

The most common infectious emergency is the onset of fever in a patient who is neutropenic as a result of chemotherapy or radiotherapy. Many such patients have a septicaemia which, if not treated with appropriate antibiotics, may progress rapidly with fatal consequences. Febrile, neutropenic patients should be started on broad-spectrum, intravenous antibiotics at the earliest opportunity and before the results of bacteriological investigations are known. Most septicaemias are due to the patient's endogenous flora, usually mouth or enteric Gram-negative pathogens. The antibiotics chosen should cover such organisms. The synergistic combination of an aminoglycoside and a broad-spectrum penicillin is widely used (for example, piperacillin/gentamicin).

Patients with indwelling, intravenous catheters, particularly central venous catheters, are also at risk of Gram-positive septicaemia. In such patients, or where fever does not respond to first-line antibiotics, vancomycin should be added to cover possible Gram-positive infection.

The management of patients who remain febrile despite standard antibiotics is complex, and firm guidelines are difficult to formulate. Such patients should be carefully re-examined and reassessed. Samples should be sent for repeat bacteriological examination. Fungal infection is a particular concern as it is difficult to diagnose and is a major cause of mortality. Fungal infections are increasingly common the longer the neutropenia persists. For these reasons empirical antifungal therapy should be considered if fever and neutropenia persist. If abnormalities develop on chest radiography, this may suggest infections by unusual organisms such as Aspergillus, Pneumocystis, or Legionella. The presence of CNS signs should also prompt careful assessment of the patient for signs of meningitis or brain abscess.

It is well recognized that many malignancies are associated with an increased risk of venous thrombosis, although the precise mechanism for this is unclear. Some are due to venous compression, but many are due to changes in coagulation. The treatment of such thromboses does not differ from that in non-malignant cases, although they may be refractory to treatment. Recurrent pulmonary embolism refractory to anticoagulation may require the placement of an inferior vena caval filter.

Disseminated intravascular coagulation may well have the same mechanism as malignant thrombosis, and may coexist with it. It is clinically manifest by impaired coagulation, thrombocytopenia, and haemorrhage, but small-vessel thrombosis may also occur, resulting in ischaemia. The best approach to disseminated intravascular coagulation is to treat the underlying malignancy. Direct treatment of the haemostatic disturbances is complex and unsatisfactory. Bleeding episodes can be treated by intravenous infusion of concentrated clotting factors and platelet transfusion. However, this does not reverse the underlying pathological processes, and the transfused factors may simply be consumed. Heparin can interrupt the processes of disseminated intravascular coagulation and thus restore normal haemostasis, but it is not universally effective and may be dangerous in the presence of severe hypofibrinogenaemia or thrombocytopenia.

Thrombocytopenia may follow myelosuppressive, cytotoxic chemotherapy, but does not always require intervention. When the platelet count falls below 10 × 10&sup6;/1, platelet transfusion is recommended, but a lower limit has been suggested by some. The presence of bleeding, infection, or other haemostatic deficits would encourage a higher threshold. Thrombocytopenia may also be due to the haemolytic-uraemic syndrome produced by cytotoxic drugs such as mitomycin-C.

The most common metabolic complication of malignancy is hypercalcaemia, which occurs in about 10 to 20 per cent of all cases. The majority of patients with malignant hypercalcaemia have either lung cancer (notably squamous carcinoma) or breast cancer, but myeloma, lymphoma, and renal cell carcinoma also contribute significant numbers. Extensive bone metastases can induce hypercalcaemia by producing locally acting cytokines that induce bone resorption. Other tumours induce hypercalcaemia, even in the absence of bone metastases, by hormonal mechanisms, such as release of parathyroid hormone related peptide. This has structural homology and similar actions to parathyroid hormone. It promotes renal resorption of calcium and increases bone resorption.

Patients with hypercalcaemia have thirst, polyuria, nausea, and vomiting, leading to dehydration, hypovolaemia, and diminishing renal function. In severe hypercalcaemia, electrocardiographic abnormalities and a diminished level of consciousness may develop, leading to coma, ventricular arrhythmias, and asystole.

The initial treatment of malignant hypercalcaemia comprises intravenous saline to correct hypovolaemia followed by specific calcium-lowering therapy. The treatment of choice is intravenous bisphosphonates (such as pamidronate or clodronate) which are potent inhibitors of osteoclastic bone resorption and produce a fall in serum calcium over 3 to 6 days. Patients who do not respond to bisphosphonates can be treated with calcitonin or the cytotoxic drug plicamycin (mithramycin). Traditionally, glucocorticosteroids have been used but several reports show them to be ineffective in hypercalcaemia due to solid tumours. They may be helpful in myeloma and lymphoma, but by a direct antitumour effect. Where the underlying tumour is responsive to chemotherapy or hormone therapy this should be used to prevent recurrence of hypercalcaemia.

Mild hyponatraemia is common in cancer patients, particularly those with advanced disease. In a few cases hyponatraemia is more marked and is due to the tumour secreting antidiuretic hormone, being most frequent in small cell lung cancer, but having been reported with a wide range of tumours. This syndrome is characterized by a reduced serum osmolarity, suggested by a low serum sodium, in the presence of an inappropriately concentrated urine. In mild cases, patients may be asymptomatic or have only malaise, anorexia, or headaches. When the serum sodium falls below 115 mmol/1, drowsiness, confusion, coma, and occasionally death result.

Restriction of fluid intake to 1000 to 500 ml/day will result in a slow but steady increase in serum sodium. For patients who are unresponsive to fluid restriction or unable to comply, an antidiuretic hormone antagonist such as demeclocycline should be used. This causes a reversible, dose-dependent, diabetes insipidus and reliably raises serum sodium. It can, however, induce uraemia and should not be used in conjunction with fluid restriction. Secretion of antidiuretic hormone due to small cell lung cancer should also be treated with cytotoxic chemotherapy. This will generally produce prompt resolution, even before tumour shrinkage is seen. Where hyponatraemia is causing coma or convulsions, more rapid correction of serum sodium may be needed. Intravenous saline should be given partially to correct the serum sodium to 115 mmol/1 at a rate not exceeding 0.5 to 1.0 mmol/1.h. More rapid correction may induce central pontine myelinosis.

Emergencies arising in the cancer patient may be complex and, like many oncological problems, are best managed by a multidisciplinary approach. In order to prevent undue morbidity or mortality all those managing cancer patients should be aware of the correct treatment for the common emergencies that arise in these patients.

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