Key Clinical Questions
What clinical presentations in cancer patients necessitate immediate action?
Which of these emergencies are consequences of the patient’s underlying malignancy and which are caused, directly or indirectly, by antineoplastic therapy?
Do certain cancers confer a higher risk of developing particular oncologic emergencies than others?
When is it necessary for these conditions to be managed in a multidisciplinary fashion? Who are the consultants whose timely involvement is essential for optimal treatment?
Are there situations in which it is safe to manage these patients in the outpatient setting?
Are there preventive measures one can take to reduce the risk of a patient’s encountering one of these acute complications of malignant disease?
Introduction
A diagnosis of cancer places patients at risk for a number of acute life-threatening complications. Such an event may herald the initial presentation of a malignant condition, represent the underlying progression of a known malignancy, or be a result of a rapid response to treatment; it may be obstructive, metabolic, or infectious in nature. Prompt recognition of these potentially lethal events is essential to timely life-sustaining intervention and preservation of organ function. Several oncologic emergencies will be outlined in this chapter, separated into those entities caused by the cancer itself and those which are related to the treatments delivered.
Emergencies Related to the Underlying Cancer
Carrying an imminent threat of irreversible neurologic disability, malignant spinal cord compression (MSCC) is perhaps the most dramatic of the oncologic emergencies. It is critical that one approach a new symptom of back pain somewhat differently in a patient with a current diagnosis or history of cancer from the way in which one would approach a patient without such a history.
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Back pain is the initial symptom in the vast majority of patients. The pain is usually localized initially, but may later develop a radicular component, which can be unilateral or bilateral. The presence of a Lhermitte sign, parasthesias radiating down the spine on flexion of the neck, may also point to a spinal cord process.
Inquiries must be made as to symptoms of neurologic compromise, though they typically follow the onset of back pain over a period of weeks to months. If present on initial assessment, however, they significantly raise the level of urgency with which a definitive diagnosis must be pursued. These include weakness, spasticity, or loss of sensation in the lower limbs; the patient may complain of difficulty rising from a chair or climbing stairs. Motor and sensory symptoms usually precede autonomic dysfunction, but it is essential to inquire about urinary hesitancy or retention, perhaps accompanied by overflow incontinence.
The targeted physical examination should focus on the evaluation of the nervous system, in particular that of the lower limbs. Most cases of MSCC involve the thoracic region, with the lumbosacral and cervical regions less commonly affected. It is critical to identify any objective weakness or spasticity, sensory deficit, or abnormal deep tendon reflexes. Examination of the perineal region is essential to identify decreased anal sphincter tone or saddle anesthesia. The latter finding, defined as decreased sensation in the region of the buttocks and posterior thighs, is indicative of cauda equina syndrome, resulting from compression of the sacral nerve roots rather than the spinal cord itself.
Any suspicion of neurologic compromise on history or physical examination should result in urgent spinal imaging to confirm or exclude MSCC. The imaging test of choice is magnetic resonance imaging (MRI). MRI offers the best anatomic definition of both the bones and soft tissues, either of which could be the cause of the suspected MSCC, and the superior anatomic detail may be useful for management decisions. It is important to image the entire spine, rather than just the area of clinical suspicion, as up to 25% of patients with MSCC have an additional focus of metastatic disease not initially evident on history or physical examination.
For cancer patients without clinical evidence of neurologic compromise but still concern for MSCC, imaging need not be requested urgently but should nonetheless be investigated within 24 to 72 hours. The differential diagnosis of MSCC in these patients includes, among other conditions, osteoporotic fracture, degenerative disc disease, abscess, tuberculosis, radiation myelopathy, or leptomeningitis (infectious or neoplastic).
Time is of the essence in evaluating and treating a cancer patient with suspected MSCC as the degree of neurologic damage at the time of treatment initiation is the most important determinant of eventual functional outcome. Upon identification of any suggestion of neurologic compromise, several steps should be taken concurrently: corticosteroid therapy should be immediately initiated, imaging should be requested on an urgent basis (preferably an MRI of the total spine, though plain films could be obtained while arrangements are being made for the MRI as they may demonstrate a fracture), and consultants should be notified.
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Corticosteroid therapy typically means dexamethasone, though there is little evidence to suggest superiority of a particular regimen; the specific dose or route of administration is less important than the immediacy of treatment initiation. The first dose is usually given intravenously, though the oral bioavailability of dexamethasone is excellent so it can be given orally if the establishment of intravenous (IV) access is problematic and the patient is able to swallow. A common approach is to give a bolus of 10 to 16 mg intravenously, followed by 4 to 6 mg orally or intravenously every 4 to 6 hours thereafter.
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The consulting service of choice has traditionally been radiation oncology, as radiotherapy has been the most commonly utilized modality. Not surprisingly, results have been better with this modality if the MSCC is caused by a tumor type known to be more radiosensitive (breast cancer or lymphoma) as opposed to less radiosensitive (non-small-cell lung cancer, melanoma, renal cell carcinoma). Interest in neurosurgical consultation has recently increased, however, with the results of a prospective randomized trial demonstrating superior preservation of ambulation in patients who underwent surgical decompression followed by radiation therapy compared with patients who received radiation therapy alone. Thus, patients presenting with MSCC at a single level should generally be evaluated for surgical candidacy as the initial definitive intervention. Neurosurgical consultation should also be considered for a bony collapse and compression of the spinal cord as cause of MSCC. Radiotherapy can then be administered following surgical decompression, or as the definitive modality in its own right for patients not deemed to be suitable for operative management (Table 182-1).
| Factors Favoring Surgery Followed by Radiotherapy | Factors Favoring Radiotherapy |
|---|---|
| Solid tumor | Hematologic malignancy |
| Acceptable surgical candidate | Medical comorbidities prohibit surgery |
| Rapidly evolving neurological symptoms (eg, paraplegia < 48 hours) | Slowly progressive neurological dysfunction (eg, paraplegia > 48 hours) |
| Expected survival > 3 months | Expected survival < 3 months |
| Pathologic fracture compressing the spinal cord | Mass compressing only cauda equina or spinal roots but not cord itself |
| No known cancer diagnosis (unknown histology) | |
| Previous radiotherapy to similar region | |
| Spinal instability |
A second presentation directly related to tumor expansion, superior vena cava syndrome (SVCS), results from compression of the superior vena cava, markedly inhibiting blood return from the head, neck, and upper extremities. Its presentation is usually more insidious than that of MSCC, and generally doesn’t portend the same degree of irreversible functional impairment. Ultimately, obstruction of the superior vena cava tends to lead to collateral blood vessel formation, which is in turn associated with gradual improvement in the presenting symptoms. Almost all cases of SVCS are attributable to malignancy or to thrombosis associated with an indwelling vascular catheter.
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Lung cancer accounts for the vast majority of SVCS presentations, followed by non-Hodgkin lymphoma. The leading conditions responsible for this syndrome in young adults are lymphoma and mediastinal germ cell tumors.
The classic symptoms of SVCS are neck and facial swelling, along with venous distension of the neck and chest wall venous system. Several data series suggest, however, that the most common symptom is dyspnea; patients may also complain of headache, hoarseness, dysphagia, and cough. Urgent evaluation is required when symptoms progress to potential respiratory obstruction, such as stridor, or neurologic compromise, as evidenced by syncope, lethargy, obtundation, or even seizure activity.
The diagnosis of SVCS is made on clinical and radiologic grounds, but the underlying etiology must also be pursued, particularly if the patient does not have a preexisting cancer diagnosis or an indwelling vascular catheter. Abnormalities of vital signs, or of the cardiovascular and respiratory systems on examination, such as cyanosis, indicate the requirement for more urgent workup, usually beginning with a chest X-ray. The most characteristic radiographic finding is widening of the upper mediastinum, occurring more often on the right side than the left. Pleural effusion may also be present. The absence of diagnostic abnormalities on plain film should lead one to proceed to CT scanning, which is more sensitive to mediastinal detail and better able to identify collateral vessels.
If the patient has a history of one of the malignancies mentioned above, tissue acquisition may not be necessary after obtaining a CT scan demonstrating extrinsic superior vena cava compression, but for a patient with no underlying cancer diagnosis or indwelling vascular catheter it is essential to rule out benign causes such as noncancerous tumors or fibrosing mediastinitis related to prior irradiation or infectious causes (eg, histoplasmosis). Depending on the location of the radiographic mass, this can be done using bronchoscopy, percutaneous needle biopsy, mediastinoscopy, or, in some cases, a thoracotomy.
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Most often there is no emergent indication for intervention and therapy, for the SVCS can be directed at treatment of the underlying disease.
If the etiology is a vascular catheter, and the obstruction is detected early, treatment with a fibrinolyic agent and salvage of the catheter may be possible, otherwise catheter removal is necessary in conjunction with anticoagulation.
If it is an underlying cancer responsible for the patient’s symptoms, the first step is to establish whether there is imminent airway compromise; if so, the situation is a true emergency, and the principles of resuscitation should be applied, including preparation for endotracheal intubation and intensive care unit transfer. If abnormalities of the cardiovascular or respiratory vital signs or neurologic signs are present, an intravascular stent should be considered, if appropriate expertise is available, for immediate relief of the obstruction. Subsequent therapy is dependent upon the underlying histology. Glucocorticoids can be initiated right away, and will likely result in rapid effect if the causative cancer is lymphoma, but will be less effective if lung cancer or a germ cell tumor is the culprit. Chemosensitive tumors, such as lymphoma, a germ cell malignancy, or small cell lung cancer, can be treated with rapid initiation of appropriate chemotherapy, given through a vein on the contralateral side of the body from that affected by the obstruction. A less chemosensitive histology such as non–small cell lung cancer is best treated initially with radiation.
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As many as 30% of cancer patients will present with elevated calcium levels over the course of their illness, though the incidence of hypercalcemia of malignancy (HCM) has declined substantially over the past two decades due to the introduction of routine bisphosphonate therapy for the prevention of skeletal events in various advanced malignancies. The underlying mechanisms differ depending on the primary tumor, with the most common being the secretion of humoral-related factors (humoral hypercalcemia of malignancy [HHM]) such as parathyroid hormone–related peptide (PTHrP). Other etiologies include the overproduction of vitamin D and increased osteolytic bone resorption in areas surrounding the malignant cells. Unlike PTHrP, ectopic production of parathyroid hormone (PTH) itself is rare.
The extent of bony metastatic disease is actually less important than the specific tumor histology in accounting for hypercalcemia (Table 182-2
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