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Oncologic Emergencies: Pathophysiology, Presentation, Diagnosis, and Treatment

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Oncologic Emergencies: Pathophysiology, Presentation, Diagnosis, and Treatment CA CANCER J CLIN 2011;61:287–314 Oncologic Emergencies: Pathophysiology, Presentation, Diagnosis, and Treatment Mark A. Lewis, MD1; Andrea Wahner Hendrickson, MD, PhD2; Timothy J. Moynihan, MD3 Abstract Oncologic emergencies can occur at any time during the course of a malignancy, from the presenting symptom to end-stage disease. Although some of these conditions are related to cancer therapy, they are by no means confined to the period of initial diagnosis and active treatment. In the setting of recurrent malignancy, these events can occur years after the surveillance of a cancer patient has been appropriately transferred from a medical oncologist to a primary care provider. As such, awareness of a patient’s cancer history and its possible complications forms an im- portant part of any clinician’s knowledge base. Prompt identification of and intervention in these emergencies can prolong survival and improve quality of life, even in the setting of terminal illness. This article reviews hypercalcemia, hyponatremia, hypoglycemia, tumor lysis syndrome, cardiac tamponade, superior vena cava syndrome, neutropenic fever, spinal cord compression, increased intracranial pressure, seizures, hyperviscosity syndrome, leukostasis, and airway obstruction in patients with malignancies. Chemotherapeutic emergencies are also addressed. CA Cancer J Clin 2011;61:287-314. VC 2011 American Cancer Society. Introduction In this review, we discuss the pathophysiology, presentation, diagnosis, and treatment of commonly encountered emergencies in hematology and oncology. We have chosen to categorize emergencies as metabolic, cardiovascu- lar, infectious, neurologic, hematologic, or respiratory to highlight their lack of disease specificity and to facilitate their recognition during system-by-system assessment of the patient. These conditions require prompt recogni- tion and treatment. For providers administering chemotherapy, we also address the problems of extravasation and anaphylactic reactions. Metabolic Emergencies Hypercalcemia Pathophysiology Hypercalcemia will be experienced by up to one-third of cancer patients at some point in their disease course.1 Among patients hospitalized for hypercalcemia, malignancy is the most common cause, although primary hyper- parathyroidism is much more prevalent in the general population.2 Breast, lung, and renal cell carcinomas; multi- ple myeloma; and adult T-cell leukemia/lymphoma are the prevailing causes of hypercalcemia.1,3 A variety of mechanisms can explain elevated calcium in cancer patients: systemic release of parathyroid hormone-related peptide (PTHrP) by the tumor, which does not require the presence of bone metastases; local paracrine stimula- tion of osteoclasts by metastases to bone, leading to osteolytic effects; and systemic secretion of vitamin D ana- logues by the tumor, which also does not require the presence of bone metastases.4 1Senior Hematology and Oncology Fellow, Division of Hematology, Department of Oncology, Mayo Clinic College of Medicine, Rochester, MN; 2Senior Medical Oncology Fellow, Division of Hematology, Department of Oncology, Mayo Clinic College of Medicine, Rochester, MN; 3Associate Professor, Medical Oncology, Department of Oncology, Mayo Clinic College of Medicine, Rochester, MN. Corresponding author: Timothy J. Moynihan, MD, Department of Oncology, Mayo Clinic, 200 First St SW, Rochester, MN 55905; [email protected] DISCLOSURES: The authors report no conflicts of interest. VC 2011 American Cancer Society, Inc. doi:10.3322/caac.20124. Available online at http://cacancerjournal.com VOLUME 61 _ NUMBER 5 _ SEPTEMBER/OCTOBER 2011 287 Oncologic Emergencies Up to 80% of malignant hypercalcemia is caused Even in the setting of profound hypercalciuria, not by PTHrP released by the tumor into the systemic all patients will form kidney stones, which may be circulation.4 Given its homology to parathyroid hor- due to differences in the urine mineral concentration mone (PTH), PTHrP can mimic the action of PTH needed to precipitate calculi.10 Abdominal pain can on the bones and kidneys but, unlike PTH, PTHrP arise from dysregulated intestinal motility, pancreati- does not influence intestinal absorption of calcium.5 tis, or severe constipation. Changes in sensorium can The effects of PTHrP represent a true paraneoplastic occur along a spectrum from lethargy to coma. In syndrome (ie, systemic signs and symptoms caused addition, hypercalcemia shortens the QT interval by a tumor, but not confined to the area in direct and can produce arrhythmias. proximity to the tumor), with circulating PTHrP causing bone resorption and renal retention of cal- Diagnosis cium. Squamous cell carcinomas from the aerodiges- Ionized calcium is the most reliable laboratory test tive and genitourinary tracts commonly cause this with which to detect hypercalcemia and is consid- type of ‘‘humoral’’ hypercalcemia but this can also be ered to be elevated when above 1.29 mmol/L.11 If seen in breast, kidney, cervical, endometrial, and measuring total calcium, it is important to correct ovarian cancer. for hypoalbuminemia, using the following formula: Bone metastases may cause a local paracrine effect corrected calcium in mg/dL ¼ measured total cal- by producing several factors that stimulate osteo- cium in mg/dL þ 0.8(4 À measured albumin in g/ clasts, leading to bone resorption with resultant dL).12 There is no absolute level of calcium at which hypercalcemia and bone destruction.6 This is most patients will become symptomatic, and the rate of commonly seen in metastatic breast cancer and mul- increase is likely more significant than the magni- tiple myeloma. Prostate cancer, despite the frequency tude of elevation; relatively high levels may be well with which it metastasizes to bone, only rarely causes tolerated if the rate of increase has been gradual.13 hypercalcemia, underscoring that it is not just osse- Measuring PTHrP has not been proven to affect ous involvement but the specific tumor-bone inter- outcome and should not guide initial management. action that determines calcium liberation from bone. PTHrP-driven hypercalcemia should be suspected New agents, such as those that alter the receptor on the basis of the underlying tumor type, especially activator of nuclear factor jB ligand (RANKL) when bony metastases are not evident. However, (denosumab) or inhibit osteoclastogenesis (osteopro- patients presenting with PTHrP levels above 12 tegerin), can be used to modify the tumor microen- pmol/L may be less responsive to bisphosphonates vironment to control hypercalcemia and bone and more prone to develop recurrent hypercalce- resorption. mia.14 Serum chloride is a more readily available Very rarely, a tumor will manufacture PTH test, and hypochloremia less than 100 mEq/L sup- itself.7 ports a diagnosis of humoral hypercalcemia.15 PTH Tumor production of vitamin D analogues is a levels can be checked to investigate the possibility of less common etiology of malignant hypercalcemia, primary hyperparathyroidism; however, PTH levels with non-Hodgkin lymphoma and Hodgkin lym- are often low in patients with humoral hypercalce- phoma each capable of producing elevated calcitriol mia due to suppression of endogenous PTH release levels.8 by PTHrP-mediated negative feedback. Presentation Treatment The symptoms of hypercalcemia are nonspecific, and The 30-day mortality rate of cancer patients hospi- delayed recognition of this metabolic derangement talized with hypercalcemia has been shown to can worsen morbidity and mortality.9 The mne- approach 50%.16 Even in patients with advanced monic ‘‘bones, stones, moans, and groans’’ is used to malignancies in whom efforts to lower calcium do emphasize skeletal pain, nephrolithiasis, abdominal not demonstrably prolong life, there can be a pallia- discomfort, and altered mentation as presenting tive benefit to improving the symptoms of hypercal- symptoms. Bone pain is usually related to discrete cemia.16 Urgent intervention is needed to normalize metastases rather than diffuse liberation of calcium. symptomatic hypercalcemia (Table 1). 288 CA: A Cancer Journal for Clinicians CA CANCER J CLIN 2011;61:287–314 TABLE 1. Treatment of Hypercalcemia MEDICATION USUAL DOSE POINTS TO REMEMBER Normal saline Rapid infusion 300-500 cc/h until euvolemic Use caution in patients with heart failure Furosemide 20-40 mg iv every 12-24 h Only after adequate hydration Pamidronate 60-90 mg iv Adjust infusion time to creatinine clearance Zoledronic acid 4 mg iv Consider alternative treatment in patients with renal failure Calcitonin 4-8 IU/kg sq or iv every 12 h Tachyphylaxis occurs quickly Steroids Hydrocortisone, 100 mg iv every 6 h Role usually limited to lymphomas; anticipate hyperglycemia or prednisone, 60 mg orally daily Mithramycin and gallium Of historical interest only Denosumab Under investigation Currently approved only for the prevention of skeletal-related events from bone metastases iv indicates intravenous; sq, subcutaneous. Hydration is the cornerstone of initial manage- zoledronic acid is relatively contraindicated in ment because almost all patients with clinically patients with severe renal insufficiency (glomerular meaningful hypercalcemia have intravascular volume filtration rate < 30 mL/minute or serum depletion. Correction of volume depletion will help creatinine > 3.0 mg/dL) due to the risk of acute to restore a brisk urine output. If the patient has tubular necrosis. Pamidronate can be more safely intact left ventricular systolic function, normal saline administered as
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