Lymphedema occurs when disruption of normal lymphatic drainage leads to accumulation of protein-rich lymph fluid in the interstitial space. Cancer survivors who experience lymphedema report poor physical functioning, impaired ability to engage in normal activities of daily living, and increased psychological distress.[1–5]

Estimates of the prevalence of lymphedema vary widely due to differences in the type of cancer, measurement methods, diagnostic criteria, and timing of evaluations relative to cancer diagnosis and treatment. In a survey conducted in 2006 and 2010, 6,593 cancer survivors were asked to identify ongoing concerns. Approximately 20% of respondents reported concerns related to lymphedema. Of these individuals, 50% to 60% reported receiving care for lymphedema.[6] These results align reasonably well with a survey study of women survivors of ovarian, endometrial, and colorectal cancers, who met criteria for lymphedema based on a validated survey that demonstrated a point prevalence of 37%, 33%, and 31%, respectively.[3] Similarly, a randomized intervention study in women with breast cancer demonstrated, by limb volume measurements or physician diagnosis, that 42% of subjects had lymphedema at 18 months after surgery.[7][Level of evidence: I]

Lymphedema is a common delayed effect of cancer treatment that negatively impacts survivors’ quality of life. This summary reviews the anatomy of the lymphatic system, the pathophysiology of lymphedema secondary to cancer, and epidemiology. The summary also provides clinicians with information related to risk factors, diagnosis, prevention, and treatment. The summary does not deal with congenital lymphedema or lymphedema not related to cancer.

In this summary, unless otherwise stated, evidence and practice issues as they relate to adults are discussed. The evidence and application to practice related to children may differ significantly from information related to adults. When specific information about the care of children is available, it is summarized under its own heading.

Anatomy of the Lymphatic System

The human lymphatic system generally includes superficial or primary lymphatic vessels that form a complex dermal network of capillary-like channels. Primary lymphatic vessels lack muscular walls and do not have valves. They drain into larger, secondary lymphatic vessels located in the subdermal space. Secondary lymphatic vessels run parallel to the superficial veins and drain into deeper lymphatic vessels located in the subcutaneous fat adjacent to the fascia. Unlike the primary vessels, the secondary and deeper lymphatic vessels have muscular walls and numerous valves to accomplish active and unidirectional lymphatic flow.

An intramuscular system of lymphatic vessels that parallels the deep arteries and drains the muscular compartment, joints, and synovium also exists. The superficial and deep lymphatic systems probably function independently, except in abnormal states, although there is evidence that they communicate near lymph nodes.[8] Lymph drains from the lower limbs into the lumbar lymphatic trunk. The lumbar lymphatic trunk joins the intestinal lymphatic trunk and cisterna chyli to form the thoracic duct, which empties into the left subclavian vein. The lymphatic vessels of the left arm drain into the left subclavian lymphatic trunk and then into the left subclavian vein. The lymphatic vessels of the right arm drain into the right subclavian lymphatic trunk and then into the right subclavian vein.

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Pathophysiology of Lymphedema

Body fluids can be discussed in terms of their composition and the specific fluid compartment where they are located. Intracellular fluid includes all fluid enclosed by the plasma membranes of cells. Extracellular fluid (ECF) surrounds all cells in the body. ECF has two primary constituents: intravascular plasma and the interstitial fluid that surrounds all cells not in the plasma. Lymphedema is the abnormal accumulation of protein-rich fluid in the interstitial space that is accompanied by inflammation and, eventually, fibrosis.

The formation of interstitial fluid comes from the movement of intravascular fluid across the capillary membranes due to arteriolar blood pressure. Much of the interstitial fluid returns to the intravascular fluid via the postcapillary venules. The dynamics of fluid production are influenced by arterial and venous hydrostatic pressures, tissue pressure, oncotic pressures of the intravascular and interstitial fluid, and membrane permeability. Normally, the dynamics favor a net gain of interstitial fluid, with the excess removed via lymphatic channels. Because lymphatic vessels often lack a basement membrane, they can resorb molecules too large for venous uptake as well. In short, the lymphatic system controls the pressure, volume, and composition of the interstitial fluid.

Lymphatic obstruction leads to increased interstitial fluid, which often contains large proteins and cellular debris. Through mechanisms not fully understood, the increased interstitial fluid induces inflammation, destruction or sclerosis of the lymphatic vessels, fibrosis, and, ultimately, adipose tissue hypertrophy.

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Epidemiology and Risk Factors

Accurate estimates of the incidence and prevalence of lymphedema are difficult to provide, due in part to differences in the definition of lymphedema (e.g., patient self-reports vs. objective volume measurements) and the timing of assessment for lymphedema relative to cancer treatment. Other factors are differences in surgical techniques related to the type of lymph node dissection or the total dose, fractions, and field of radiation administered.

Common risk factors for developing lymphedema include the following:

Breast Cancer

A systematic review found the prevalence of lymphedema to be 21.4% (14.9%–29.8%) in patients with breast cancer.[1] The incidence increased for up to 2 years after breast cancer diagnosis or surgery, and it was higher in women who underwent axillary lymph node dissection versus sentinel lymph node biopsy (19.9% vs. 5.6%). As a result, omission of axillary dissection in women with an involved sentinel lymph node is now an accepted practice. This practice is a result of a phase III randomized study (ACOSOG-Z0011) that showed no difference in overall survival in women who did not undergo a complete axillary dissection, compared with those who did.[2] Additional risk factors for lymphedema development included greater number of lymph nodes dissected, having a mastectomy, and overweight or obesity.[1,3] In a prospective study of neoadjuvant chemotherapy followed by axillary lymph node dissection (ACOSOG-Z1071), the incidence of lymphedema after a median follow-up of 3 years was 37.8% (95% confidence interval [CI], 33.1%–43.2%). Increasing body mass index (BMI) (hazard ratio [HR], 1.04; 95% CI, 1.01–1.06), duration of neoadjuvant chemotherapy (HR, 1.48; 95% CI, 1.01–2.17), number of lymph nodes removed, and number of involved lymph nodes were associated with lymphedema symptoms.[4]

Several risk factors for breast cancer–related lymphedema (BCRL) were demonstrated in a study using data from a 2-year, prospective observational study of 304 patients with breast cancer who had axillary lymph node dissection and radiation therapy. The cumulative incidence of lymphedema was measured by a more than 10% increase in arm volume, and univariate and multivariable analyses were performed. On multivariable analysis, Black race and Hispanic ethnicity (odds ratio [OR], 3.88; 95% CI, 2.14–7.08, and OR, 3.01; 95% CI, 1.10–7.62, respectively; P < .001 for each), receipt of neoadjuvant chemotherapy (OR, 2.10; 95% CI, 1.16–3.95; P = .01), older age (OR, 1.04; 95% CI, 1.02–1.07 per 1-year increase; P = .001), and a longer follow-up interval (OR, 1.57; 95% CI, 1.30–1.90 per 6-month increase; P < .001) were independently associated with an increased risk.[5][Level of evidence: II]

Another study examined risk factors for BCRL related to treatment, comorbidities, and lifestyle in 918 women enrolled in a Prospective Surveillance and Early Intervention (PSEI) trial. Women were randomly assigned to either bioimpedance spectroscopy (BIS) or tape measurement (TM).[6] In a secondary analysis, risk factors were used to test for factor associations with outcomes (no lymphedema, subclinical lymphedema, progression to chronic lymphedema after intervention, progression to chronic lymphedema without intervention). Factors associated with BCRL risk included axillary lymph node dissection (P < .001), taxane-based chemotherapy (P < .001), regional nodal irradiation (P ≤ .001), BMI greater than 30 (P = .002), and rurality (P = .037).[6]

Gynecological Cancers

A cohort study supports the evidence that a significant proportion of women experience lower-limb lymphedema after treatment of gynecological cancer or colorectal cancer. The highest prevalence (36.5%) among ovarian cancer survivors, followed by endometrial cancer survivors (32.5%) and colorectal cancer survivors (31.4%).[7]

In one study, 802 of 1,774 women diagnosed with a gynecological cancer between 1999 and 2004 responded to a survey about lymphedema.[8] Twenty-five percent of the respondents reported lower-extremity edema; 10% had been diagnosed with lymphedema. Most respondents (75%) had been diagnosed with these conditions within the first year of a cancer diagnosis. Women with vulvar cancer were most likely to have symptoms (36%). Lymph node dissection increased the risk of symptoms in women with cervical cancer but not uterine cancer. The range of symptoms included heavy legs, pain, and skin tightness. Standing all day, long-distance travel, and hot weather were precipitating conditions. The most common treatments were compression garments, massage, and lymphatic exercises. The findings related to high prevalence in patients with vulvar cancer and occurrence of symptoms within the first year have been verified.[9]

Serial limb volume measurements were obtained from a cohort of women who underwent a lymph node dissection for vulvar (n = 42), endometrial (n = 734), or cervical (n = 138) cancer 4 to 6 weeks after surgery and then every 3 months.[10] The incidence of an increase in limb volume of more than 10% was 43% for vulvar cancer, 34% for endometrial cancer, and 33% for cervical cancer. The incidence of severe lymphedema (>40% increase in volume) was less than 2% in all cohorts. The peak incidence was at the 4- to 6-week time point, but new cases were identified at all time points. The risk-factor analysis identified a reduced risk in women older than 65 years and a higher risk in women who had more than eight lymph nodes removed in the endometrial cohort.

Head and Neck Cancer

Patients with head and neck cancer are susceptible to external and internal lymphedema. External lymphedema typically presents with submental edema or lower neck swelling. Internal lymphedema is more widely distributed in the anatomical regions of the oropharynx. In a small cross-sectional study with video-assisted examinations, 59 of 61 patients had some degree of lymphedema.[11][Level of evidence: II] Sixty-one percent of the patients had only internal lymphedema, 35% had internal and external lymphedema, and 4% had only external lymphedema. Postoperative radiation therapy was a risk factor for combined lymphedema. Chemotherapy was a risk factor for patients with internal lymphedema only.

Melanoma

One single-center, cross-sectional study reported on lymphedema after either sentinel lymph node biopsy or lymph node dissection in 435 patients who were treated for melanoma between 1997 and 2015.[12] The authors reported a lymphedema prevalence of 25%. Forty-eight patients (44%) had International Society of Lymphology (ISL) stage I lymphedema (pitting edema), and 61 patients (56%) had ISL stage II or III lymphedema. Multivariate analyses identified as potential predictive factors the primary site of disease on the affected limb, inguinal surgery, and persistent pain at the site of lymph node surgery. Limb cellulitis was a risk factor for ISL stage II and III lymphedema. The same investigators also reported on health-related quality of life in an earlier publication. In another smaller, single-institution, retrospective study of 66 patients who underwent therapeutic nodal dissection, the rate of permanent lymphedema for inguinal node dissection was 38%, compared with 12% for axillary node dissection.[13] Another potentially relevant variable is the type of dissection. A 2017 systematic review did not find an appreciable difference between the rate of lymphedema after therapeutic lymphadenectomy and completion of lymph node sampling after a positive sentinel lymph node biopsy.[14] In both instances, the rate was around 20%.

Prostate Cancer

There are few studies of lymphedema after prostate cancer therapy. A small cross-sectional survey of men who underwent radical prostatectomy reported that 19 of 54 respondents (35.2%) had bilateral lower-extremity lymphedema.[15][Level of evidence: II] Of note, 25 respondents reported that they had received manual lymphatic drainage therapy. Men who did not experience regression experienced more distress related to physical and mental functioning than those who did. An elevated BMI and poor general health were risk factors for lymphedema.

Sarcoma

One study measured patient demographics, surgical outcomes data, functional outcomes, and lymphedema severity with a validated scale for 289 patients who underwent limb preservation surgery of an extremity sarcoma between 2000 and 2007.[16] The mean time from surgery was 35 months (range, 12–60 months). Eighty-three patients had some degree of lymphedema, including 58 with mild but definite swelling, 22 with moderate swelling, and 3 with considerable swelling. No patients had grade 4 or very severe swelling with shiny skin and skin cracking. Univariate analysis demonstrated that radiation therapy, tumor size, and tumor depth correlated with severity. The location of the sarcoma (upper or lower extremity), lymph node dissection (yes or no), and BMI did not correlate with severity. Multivariable analysis demonstrated that tumor size was the only independent predictor.

Signs, Symptoms, and Physical Examination

Lymphedema is typically evident by clinical findings such as unilateral, nonpitting edema, usually with involvement of the digits, in a patient with known risk factors (e.g., a breast cancer patient with previous axillary dissection). Other causes of limb swelling, including deep venous thrombosis, malignancy, and infection, should be considered in the differential diagnosis and excluded with appropriate studies, if indicated.

Lymphedema in patients with head and neck cancer can present slightly differently. External lymphedema does show swelling in the head and neck area, but internal lymphedema does not. Instead, patients with lymphedema related to internal head and neck cancer can present with complaints of voice changes, dysphagia, and possible difficulty breathing.

Diagnostic Testing

Nonsurgical Options

Surgical Options

The surgical options for the treatment of lymphedema include lymphatico-venous anastomoses (LVA), vascularized lymph node transplantation (VLNT), and reduction of excess tissue volume by excision of liposuction. Several informative reviews describe the surgical decision making involved in selecting patients and the type of operation.[14]

There are limited data to guide the choice between liposuction and microsurgical techniques, and some investigators propose a combined approach.[15] The choice of microsurgical techniques may be aided by imaging and clinical grading of lymphedema severity. One proposal suggests that patients are candidates for LVA if they have partial obstruction seen on lymphoscintigraphy and grade 1 or 2 lymphedema with patent lymphatic ducts observed on indocyanine green lymphography . On the other hand, VLNT may be better for patients exhibiting a total obstruction seen on lymphoscintigraphy and grade 3 or 4 lymphedema without patent lymphatic ducts observed on indocyanine green lymphography.[16]

Breast Cancer: Prevention of Lymphedema

Breast Cancer: Treatment of Lymphedema

Cervical Cancer: Prevention of Lymphedema

One study enrolled 120 women with cervical cancer who underwent a laparoscopic radical hysterectomy with pelvic lymphadenectomy. Participants were randomly assigned to an education-alone intervention or a CDT intervention.[11][Level of evidence: I] The CDT consisted of training in manual lymphatic drainage, followed by self-administered manual lymphatic drainage at home, compression hosiery, and an aerobic exercise program. The interventions were initiated 7 to 10 days after surgery. Additional eligibility criteria included more than 20 lymph nodes removed or anticipated radiation therapy (both of which are risk factors for lower-extremity lymphedema after surgery for cervical cancer). The primary outcome was limb volume calculated from multiple circumference measurements. Secondary outcomes included patients’ self-reported symptoms related to lymphedema. After a follow-up of 1 year, 20 of 58 patients (24%) in the control arm and 8 of 59 (14%) in the CDT arm developed lymphedema (P = .008). The excess volume was less in the experimental arm as well. However, there were no differences in patient-reported symptoms or severity grading of the lymphedema. These promising results were supported by a smaller pilot study[12] and a retrospective review of a single-institution experience with women who developed lymphedema after treatment of a variety of gynecological cancers.[13]

Head and Neck Cancer: Treatment of Lymphedema

Sarcoma of the Extremity: Prevention of Lymphedema

One study compared the incidence of lymphedema in a cohort of eight patients with thigh sarcoma, who had lymphatico-venous anastomoses performed in combination with resection of thigh soft-tissue tumors, with a historical cohort of 20 patients.[18] Only one of eight patients experienced lymphedema, compared with nine patients in the historical cohort. Patient self-reported symptoms were uncommon in the eight patients.

Purpose of This Summary

This PDQ cancer information summary for health professionals provides comprehensive, peer-reviewed, evidence-based information about the diagnosis and treatment of lymphedema. It is intended as a resource to inform and assist clinicians in the care of their patients. It does not provide formal guidelines or recommendations for making health care decisions.

Reviewers and Updates

This summary is reviewed regularly and updated as necessary by the PDQ Supportive and Palliative Care Editorial Board, which is editorially independent of the National Cancer Institute (NCI). The summary reflects an independent review of the literature and does not represent a policy statement of NCI or the National Institutes of Health (NIH).

Board members review recently published articles each month to determine whether an article should:

Changes to the summaries are made through a consensus process in which Board members evaluate the strength of the evidence in the published articles and determine how the article should be included in the summary.

The lead reviewers for Lymphedema are:

Any comments or questions about the summary content should be submitted to Cancer.gov through the NCI website’s Email Us. Do not contact the individual Board Members with questions or comments about the summaries. Board members will not respond to individual inquiries.

Levels of Evidence

Some of the reference citations in this summary are accompanied by a level-of-evidence designation. These designations are intended to help readers assess the strength of the evidence supporting the use of specific interventions or approaches. The PDQ Supportive and Palliative Care Editorial Board uses a formal evidence ranking system in developing its level-of-evidence designations.

Permission to Use This Summary

PDQ is a registered trademark. Although the content of PDQ documents can be used freely as text, it cannot be identified as an NCI PDQ cancer information summary unless it is presented in its entirety and is regularly updated. However, an author would be permitted to write a sentence such as “NCI’s PDQ cancer information summary about breast cancer prevention states the risks succinctly: [include excerpt from the summary].”

The preferred citation for this PDQ summary is:

PDQ® Supportive and Palliative Care Editorial Board. PDQ Lymphedema. Bethesda, MD: National Cancer Institute. Updated <MM/DD/YYYY>. Available at: /side-effects/lymphedema/lymphedema-hp-pdq. Accessed <MM/DD/YYYY>. [PMID: 26389244]

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Introduction

Dyspnea is an uncomfortable awareness of breathing. It is a subjective experience involving many factors that affect the quality and intensity of its perception. Patients with comparable degrees of functional lung impairment and disease burden may describe varying intensities of dyspnea, using various words and phrases such as “tightness” and “suffocating.”[1]

Reports on the frequency of dyspnea also vary, depending on the setting and the extent of disease.[2] In one study, 49% of a general cancer population reported breathlessness, and 20% rated their breathlessness as moderate to severe.[3] Patients with advanced cancer experience dyspnea more frequently and more intensely than patients with limited disease. One study found that 75 of 135 patients with advanced cancer reporting to an outpatient palliative care clinic had moderate-to-severe dyspnea.[4] In addition, 60% of 289 patients with lung cancer reported breathlessness at presentation.[5] Results of a large study showed that 70% of patients suffered from dyspnea in the last 6 weeks of life.[6] About one-third of patients who could report the intensity of their dyspnea rated it as moderate to severe. Another study revealed that one-half of patients with advanced cancer scored their dyspnea as moderate to severe.[7]

Pathophysiology and Etiology

The pathophysiological mechanisms of breathlessness are numerous and complex.[8] Peripheral and central mechanisms, as well as mechanical and chemical pathways, are involved with a variety of sensory afferent sources.[9–11]

The qualities of dyspnea can be seen as work/effort, tightness, and air hunger. The experience of excess work/effort is caused by sensory-perceptual mechanisms similar to those involved in muscles exercising. Tightness is caused by stimulation of airway receptors with bronchoconstriction. The intensity of air hunger and unsatisfied inspiration is caused by the following:[12]

Dyspnea in patients with advanced cancer has many possible direct causes, and categorizing them can assist in the etiologic work-up. One approach is to divide direct causes into the following groups:

One study found that in patients experiencing dyspnea from advanced cancer, a median of five different abnormalities could have contributed to their shortness of breath.[7] Spirometry was abnormal in 93% of 100 patients examined, with 5% having obstructive patterns, 41% restrictive patterns, and 47% mixed patterns. Also, 49% of patients had lung cancer, 91% had abnormal chest radiographs, and 65% had parenchymal or pleural involvement. These results show that a subset of patients experience shortness of breath without any apparent lung involvement. The potentially correctable causes of dyspnea included:

No significant association between the type of respiratory impairment and the degree of dyspnea was found. Most of these patients were current or former smokers and had a significant lowering of their maximum inspiratory pressures, suggesting severe respiratory muscle dysfunction.[7] This finding was duplicated in another study.[4] Of patients admitted to hospice care, 34% had histories of cardiac disease, and 24% had histories of respiratory disease.[6] Only 39% of terminally ill patients who reported dyspnea had lung or pleural involvement. The etiology of dyspnea could not be clearly identified in approximately one-quarter of patients. Another study found that 49% of lung cancer patients presented with airflow obstruction.[7,15]

Respiratory muscle dysfunction is an underrecognized factor contributing to dyspnea. Causes of respiratory muscle dysfunction include:[16]

Poor oxygenation, muscle fatigue, abnormal cortisol and catecholamine levels, and circulating cytokines are also implicated.[16]

Although anxiety is commonly thought to be associated with breathlessness, researchers have found that anxiety and shortness of breath do not invariably go together.[7] One study demonstrated that the involvement of the lungs by cancer, anxiety, and poor maximal inspiratory pressures were correlates of the intensity of dyspnea in patients with advanced cancer.[4]

Assessment

The multidimensional nature of dyspnea must be noted in the complicated assessment of this symptom. Patient-reported outcome is the gold standard for assessment of dyspnea. There is no consensus on the best instrument for assessing dyspnea, but some of the tools used include:

These tools are limited, however, because they are unidimensional and do not account for the relative contribution of different factors to a patient’s perception of breathlessness. Assessment should include the impact of dyspnea on the patient’s functional status and recognition of the dynamic component of dyspnea—namely, exertional dyspnea.

Objective signs, such as tachypnea or the use of accessory breathing muscles, frequently do not match a patient’s perception of dyspnea and the degree of functional impairment it causes. Numerous factors, including psychosocial issues, may affect a patient’s experience of dyspnea. Pulmonary function tests, with few exceptions, play a limited role in the assessment of this syndrome.

A comprehensive history and examination are essential to an accurate assessment of dyspnea.[8,17] The temporal onset, qualities of the symptom, associated symptoms, precipitating and relieving events or activities, and responses to medications should be reviewed. Sudden onset may herald a pulmonary embolism or infection, whereas gradual onset may suggest development of a pleural effusion. A history of obstructive airways or cardiac disease can shed some light on possible underlying causes. Investigations such as measuring oxygen saturation can be useful in determining whether a patient is hypoxic. In the setting of advanced, incurable cancer, arterial blood gasses play a limited role.

In the study looking at checkpoint inhibitor immunotherapy–related pneumonitis, one-third of patients were asymptomatic. However, the most common presenting symptoms were dyspnea (53%) and cough (35%).[13]

Melanoma and non-small cell lung cancer were the most common cancers treated in this study. Interestingly, the duration of treatment before the onset of pneumonitis was quite variable, with a median time to onset of 2.8 months (range, 9 days–19 months). In addition, pneumonitis seemed to occur earlier in patients who received combination therapy than in those who received monotherapy (median, 2.7 months vs. 4.6 months).[13]

Diagnostic tests that may help to determine the etiology of dyspnea include the following:[7]

Maximal inspiratory pressure (MIP) measurements may be helpful, particularly if no apparent cause can be found. MIP is a reliable functional test of the strength of the diaphragm and other respiratory muscles. Functional assessments such as the 6-minute walk test and exercise ergometry may also provide valuable information about the severity and impact of dyspnea.[21,22]

Management of Dyspnea

Current Clinical Trials

Use our advanced clinical trial search to find NCI-supported cancer clinical trials that are now enrolling patients. The search can be narrowed by location of the trial, type of treatment, name of the drug, and other criteria. General information about clinical trials is also available.

Significance

Malignant pleural effusions are a common complication of malignancy, and malignancy is a common cause of pleural effusions in general. Malignancy causes roughly 40% of symptomatic pleural effusions, with congestive heart failure and infection being the other leading causes.[1] The cancers that account for approximately 75% of all malignancy-associated effusions include the following:

Significant use of health care resources is attributable to malignant effusions, with approximately 100,000 cases per year diagnosed in the United States and 43 cases detected per 100,000 hospital admissions.[2]

Pathogenesis

The normal pleural fluid space is occupied with approximately 10 mL of fluid with 2 g/dL protein. A pleural effusion is an accumulation of an abnormal amount of fluid between the visceral and parietal pleura of the chest. Normally, pleural fluid is absorbed by pulmonary venous capillaries (80%–90%), with some of it also absorbed by pleural lymphatics. Malignant effusions are usually exudative rather than transudative. Exudative effusions exhibit any one of the following characteristics:[3]

These exudative malignant effusions are generally caused by:

Paramalignant effusions may result from chemotherapy, radiation therapy, atelectasis, or lymph node involvement.

Assessment

Common symptoms associated with malignant pleural effusions include:

About 20% of patients may experience weight loss and malaise. A chest x-ray is most commonly used for radiographic assessment. About 175 mL of pleural fluid will cause a blunted costophrenic angle discernible on chest radiography. A chest computed tomography scan is more sensitive than a simple chest x-ray and is often used for assessment of loculated effusions because, in some instances, up to 500 mL of loculated fluid can be obscured behind the dome of the diaphragm.[1]

Not all pleural effusions detected in cancer patients are malignant effusions. Cancer patients are prone to developing conditions such as:[1]

Each of these conditions may cause a symptomatic effusion for which clinical management would substantially differ from management of a malignant effusion. For this reason, cytological assessment is important. Pleural fluid cytology requires a minimum sample of 250 mL. The morphology of cells obtained from the pleural space can be difficult to assess because of mesothelial and macrophage abnormalities. The diagnostic sensitivity of pleural fluid cytology is approximately 65%, with a specificity of 97%.[1]

Management of Malignant Pleural Effusions

Current Clinical Trials

Use our advanced clinical trial search to find NCI-supported cancer clinical trials that are now enrolling patients. The search can be narrowed by location of the trial, type of treatment, name of the drug, and other criteria. General information about clinical trials is also available.

Incidence and Prevalence

Malignant pericardial effusion occurs in up to 21% of autopsy cases in patients with common malignancies.[4,7] Of patients with lung cancer, 33% have pericardial metastases at autopsy, and one-third of cases of pericardial metastases are caused by lung cancer. Breast cancer causes 25% of pericardial effusions, and about 25% of patients with breast cancer have pericardial effusions. Hematological malignancies (leukemia, Hodgkin disease, non-Hodgkin lymphoma) cause 15% of cases of malignant pericardial effusions.[11]

A retrospective review of 23,592 effusions over a 24-year period revealed 65 malignant effusions (17%) out of 375 pericardial effusions. Lung cancer was the most common cancer found among the malignant pericardial effusions in males, and breast cancer was the most common in females. In 43% of cases, pericardial effusion was the first detected sign of cancer. Of patients diagnosed with malignant pericardial effusions, 86% died within 1 year of diagnosis, with nearly one-third dying within the first month.[8]

In a study of 31 patients with both cancer and pericardial effusions, malignant pericardial effusion accounted for 58% of the effusions, benign idiopathic pericarditis caused 32% of the cases, and radiation pericarditis caused 10% of cases.[11,12]

Pathophysiology

Malignant involvement of the pericardium is the most common reason for development of pericardial effusions, which result from blockage of venous and lymphatic circulation of pericardial fluid. Such blockage may be caused by primary malignancy of the pericardium, such as pericardial mesothelioma, or by tumors arising in the myocardium, including angiosarcoma, rhabdomyosarcoma, and malignant fibrous histiocytosis. Malignancies can also involve the pericardium through direct extension from carcinomas of the lung or esophagus, thymoma, or lymphoma.[9] Lymphatic or hematogenous metastasis to the pericardium occurs most commonly with the following cancers:

Primary tumors of the pleura or pericardium have been termed primary intrathoracic malignant effusions.[13]

Nonmalignant causes of pericardial effusion include:[14–16]

AIDS may also cause pericardial effusion with pericarditis.[17] Radiation therapy or chemotherapy drugs can cause pericarditis without metastatic involvement of the pericardium. Radiation pericarditis is usually associated with radiation doses to the cardiac window exceeding 30 Gy [10] and occurs most frequently in patients who have received mediastinal radiation for Hodgkin lymphoma or breast cancer.[10] Doxorubicin and cyclophosphamide have been associated with the development of acute pericarditis with effusions.[11,12] Other drugs that may cause acute pericarditis include procainamide, hydralazine, isoniazid, methysergide, phenytoin, and anticoagulants.

Pericardial tamponade results from progressive fluid accumulation in the pericardial sac, causing the following:[15]

Hemodynamic compromise occurs when the normal amount of pericardial fluid (approximately 15–50 mL) increases to 200 mL to 1,800 mL.[15,18] When fluid accumulates rapidly, as little as 250 mL of fluid can result in tamponade.[11,19]

Dyspnea occurs in 93% of patients with pericardial effusions.[6] Common symptoms include the following:

Other symptoms of pericardial effusion include:

Signs of effusion include the following:

Pericardial friction rubs and fever are more commonly associated with nonmalignant causes of pericardial effusions than with malignant etiologies.[9]

Signs of pericardial tamponade include:

However, some patients may develop tamponade without this clinical pattern.[4]

Diagnosis

A chest x-ray may show widening of the cardiac silhouette [7] if the amount of pericardial fluid collection exceeds 250 mL.[20] However, a chest x-ray cannot determine the degree of cardiac dysfunction or tamponade. Loculated pericardial effusions may not be apparent on standard posterior/anterior or lateral chest radiographic views.[15]

Transthoracic echocardiography using apical, subxiphoid, and parasternal views can evaluate the presence, quantity, and quality of suspected pericardial effusions, as well as associated pericardial masses and inflammation. Moderate effusions on echocardiography show an echo-free space of 10 mm to 20 mm during diastole in M-mode or 2-dimensional echocardiography, whereas severe effusions have an echo-free space exceeding 20 mm.[21,22] Echocardiography can also determine right and left ventricular function and the possibility of right ventricular or atrial diastolic collapse.[7] Left ventricular collapse caused by large pleural effusions without clinically significant pericardial effusions has been reported.[4,16,23,24] However, transesophageal echocardiography may be useful for loculated effusions resulting from adhesions adjacent to the atria, where the thinness of the atrial wall may not be well visualized on transthoracic echocardiography.[4,16]

Echocardiography in pericardial effusion with tamponade shows right atrial or right ventricular compression, or left atrial compression, decreased left ventricular dimension, and absence of collapse of the inferior vena cava on deep inspiration.[6,25] Echocardiography findings predictive of pericardial tamponade have been reported.[26] Right atrial collapse has a sensitivity of 55% to 60% and a specificity of 50% to 68%. Right ventricular diastolic collapse has a lower sensitivity of 38% to 48% but a higher specificity ranging from 84% to 100%. Because neither finding provides 100% sensitivity and specificity, patients who are clinically symptomatic should have a diagnostic pericardiocentesis, even in the absence of definitive findings on echocardiography.[4,27] One study found right atrial collapse present in only 42% of patients and right ventricular collapse in 62%.[27] Nonetheless, 80% of patients with malignant pericardial effusions had symptomatic relief following pericardiocentesis.

The most definitive test for the diagnosis of cardiac tamponade is equalization of diastolic pressures between all cardiac chambers on right-heart cardiac catheterization.[7] However, this invasive technique is not necessary to diagnose tamponade.

An electrocardiogram (ECG) in patients with pericardial effusions typically shows diminished QRS amplitude in all leads. A classic but uncommonly seen finding in large effusions with pericardial tamponade is variation in the amplitude of the P wave and QRS complex in successive beats on ECG, referred to as electrical alternans. This finding results from movement of the heart within the pericardial sac.[6] Electrocardiography is not sufficiently sensitive to diagnose pericardial effusions.

Pericardial fluid cytology has an accuracy of 80% to 90% in diagnosing malignant pericardial effusion.[6,28] Lymphomas and mesothelioma have higher false-negative detection rates on cytology evaluation.[6,29] Pericardial fluid cytology has a specificity of up to 100%, but sensitivity ranges from 57% to 100% [10][Level of evidence: II] in patients with a known cancer diagnosis and pericardial fluid. Because nonmalignant causes of pericardial effusion can occur in 42% to 62% of patients with cancer and pericardial fluid, a negative cytology examination of pericardial fluid does not help distinguish malignant from nonmalignant causes. The use of more than one cytological preparation (such as concentrating the sample via cytospin, using special markers, or analyzing DNA content) increases the yield over a single preparation. However, multiple samples using the same technique did not significantly increase the diagnostic yield in a retrospective study of 215 patients.[30] In a survey of 80 samples, measurement of DNA index via flow cytometry of pericardial fluid has a sensitivity of 94.8% and a specificity of 100%, compared with routine cytology, which has a sensitivity of 98.5% and a specificity of 92.3%.[31][Level of evidence: II]

Pericardial biopsy may increase the sensitivity of diagnosing pericardial effusions of malignant origin. However, because pericardial effusions usually occur in advanced disease and portend a shorter survival than other sites of metastatic involvement, the relief of symptoms rather than diagnosis should be the overriding factor in determining the extent of the evaluation and the course of treatment. Two studies failed to show a difference in survival in cancer patients with pericardial effusion dependent on the results of fluid cytology.[10,32]

In a study of patients with stage I esophageal cancer who underwent radiation and chemotherapy, risk factors for developing pericardial effusion included advanced age, higher pericardial volume 30 (≥41.6 percentage of cardiac volume receiving more than 30 Gy), high body mass index, and diabetes mellitus.[33]

Treatment

No large controlled, randomized, prospective clinical trials demonstrate the optimal management of malignant pericardial effusions or tamponade. Treatment should therefore be individualized to maximize symptom relief with minimal impact on quality of life. Treatment options include the following:[34][Level of evidence: III]

In choosing a treatment, consider the following:[34][Level of evidence: III]

Large, symptomatic, malignant pericardial effusions are managed by draining the fluid, unless the goals of therapy dictate a less invasive, conservative approach, with concomitant shorter survival balanced against quality-of-life concerns. If treatment is indicated for tamponade, percutaneous subxiphoid pericardiocentesis is the treatment of choice in the acute setting. Echocardiography is recommended for catheter guidance.[6,35] Catheter drainage is recommended for large effusions to prevent rapid reaccumulation of fluid and subsequent tamponade and for the anticipated survival of the patient.

Recurrent pericardial effusion occurs in 21% [36] to 50% [34,35] of patients following pericardiocentesis. Limited case series suggest rates of pericardial fluid reaccumulation at 30 days ranging from 5% to 33% after pericardial drainage followed by intrapericardial treatment with sclerosing agents or phosphorus-colloid, compared with more than 50% for patients treated with pericardial drainage alone.[34,35]

Prolonged catheter drainage can be effective in preventing fluid reaccumulation; however, the mechanism is unclear. One series reported recurrence in 30% of patients at a median time of 39 days. In another series, the reported recurrence rate of the pericardial effusion was 13% by 1 year of follow-up.[37,38]

The prolonged catheter drainage could be left in for several days.[38,39] The catheter should be left in situ until the drainage is minimal (<25–50 mL in a 24-hour period) to none. In one series of 171 patients with malignant pericardial effusion who received echocardiography-guided pericardiocentesis followed by extended catheter drainage, the average time to very little catheter output (<50 mL in 24 hours) was about 3 days.[39] Other treatment options to prevent reaccumulation include intrapericardial sclerosis to obliterate the space within the pericardial sac or pericardiotomy to increase the quantity of fluid drained from the pericardium.

The most effective sclerosing agent for malignant pericardial effusions had been tetracycline, with success rates of up to 80%.[6] However, this agent is no longer available as an intravenous drug in the United States. Alternative sclerosants that have been used include the following:

Most patients may require three or more treatments to achieve adequate sclerosis.[6] Significant pain is reported by 16% of patients undergoing pericardial sclerosis.[6] The side effects of various sclerosing agents (e.g., chest pain and arrhythmias) must be considered. Of patients undergoing pericardial sclerotherapy, 70% to 80% have no fluid reaccumulation within 30 days of the procedure.[35]

A retrospective comparison of pericardiocentesis with sclerotherapy to open surgical drainage in 60 patients showed similar rates of treatment complications, incidence of recurrent effusion, and survival following treatment in both groups.[44] A retrospective review of 59 patients found similar success rates, whether patients were managed with surgical subxiphoid pericardial window or by pericardiocentesis with or without sclerosis.[34] Patients who underwent pericardiocentesis followed by pericardial window had the longest survival, with a median of 6 months. However, selection bias toward patients with better performance status undergoing more aggressive surgical techniques may contribute this reported survival advantage. The surgical procedure group had significantly higher average costs of $4,830 compared with $1,625 for patients managed with pericardiocentesis.[34]

Other studies have reported mortality, recurrence, and survival rates for sclerosis that are similar to or slightly lower than those for subxiphoid window or video-assisted thoracoscopy.[44,45];[46][Level of evidence: II][34][Level of evidence: III] Pericardiocentesis with or without sclerotherapy should be considered instead of more invasive procedures in patients with advanced disease or poor functional status.[47]

Transcutaneous balloon pericardiostomy is another technique that is less invasive than open surgical approaches, which include subxiphoid pericardial windows, thoracotomy with pericardiopleural window formation,[48] and thoracotomy with pericardectomy.

Video pericardioscopy has a diagnostic sensitivity of 97% for detecting malignant effusions.[49] Pericardioscopy also is useful for drainage of loculated effusions.[50][Level of evidence: II] Video-assisted thoracoscopy is preferable to more invasive surgical management and should be considered for patients requiring repeated pericardiocentesis to control symptomatic effusions.[47]

Current Clinical Trials

Use our advanced clinical trial search to find NCI-supported cancer clinical trials that are now enrolling patients. The search can be narrowed by location of the trial, type of treatment, name of the drug, and other criteria. General information about clinical trials is also available.

Overview

Superior vena cava syndrome (SVCS) is an array of symptoms caused by the impairment of blood flow through the superior vena cava (SVC) to the right atrium. Symptoms that suggest this syndrome include the following:[1]

In rare instances, patients may complain of hoarseness, chest pain, dysphagia, and hemoptysis.

Physical signs that may be noted on presentation include the following:

Rarely, cyanosis, Horner syndrome, and a paralyzed vocal cord may also be present.[1]

SVCS is usually a sign of locally advanced bronchogenic carcinoma. Survival depends on the status of the patient’s disease. When small cell bronchogenic carcinoma is treated with chemotherapy, the median survival times with or without SVCS are almost identical (42 weeks or 40 weeks, respectively). The 24-month survival rate is 9% in patients without SVCS and 3% in those with the syndrome. When the malignancy is treated with radiation therapy, 46% of patients who have non-small cell lung cancer experience relief of symptoms, compared with 62% of patients who have small cell bronchogenic carcinoma. The 2-year survival rate of 5% is almost the same for both groups.[2]

Most patients with non-Hodgkin lymphoma and SVCS respond to appropriate chemotherapy or to combined-modality regimens.

Etiology and Physiology

Since William Hunter first described SVCS in 1757, the spectrum of underlying conditions associated with it has shifted from tuberculosis and syphilitic aneurysms of the ascending aorta to malignant disorders. Almost 95% of SVCS cases described in published modern series result from cancer. The most common cause is small cell bronchogenic carcinoma, followed by squamous cell carcinoma of the lung, adenocarcinoma of the lung, non-Hodgkin lymphoma, and large cell carcinoma of the lung.[3] Nonmalignant causes of SVCS in cancer patients include thrombosis that is associated with intracaval catheters or pacemaker wires.[4] A rare cause of SVCS is fibrosing mediastinitis, either idiopathic or associated with histoplasmosis.[5] Additional rare causes of SVCS include metastatic germ cell neoplasms, metastatic breast cancer, colon cancer, Kaposi sarcoma, esophageal carcinoma, fibrous mesothelioma, Behçet syndrome, thymoma, substernal thyroid goiter, Hodgkin lymphoma, and sarcoidosis.[6]

Knowledge of the anatomy of the SVC and its relationship to the surrounding lymph nodes is essential to understand development of the syndrome. The SVC is formed by the junction of the left and right brachiocephalic veins in the mid third of the mediastinum. The SVC extends caudally for 6 to 8 cm, coursing anterior to the right mainstem bronchus and terminating in the superior right atrium, and extends anteriorly to the right mainstem bronchus. The SVC is joined posteriorly by the azygos vein as it loops over the right mainstem bronchus and lies posterior to and to the right of the ascending aorta. The mediastinal parietal pleura is lateral to the SVC, creating a confined space, and the SVC is adjacent to the right paratracheal, azygous, right hilar, and subcarinal lymph node groups. The vessel itself is thin-walled, and the blood flowing in it is under low pressure. Thus, when the nodes or ascending aorta enlarge, the SVC is compressed, blood flow slows, and complete occlusion may occur.

The severity of SVCS depends on the speed of onset and location of the obstruction. The more rapid the onset, the more severe the symptoms because the collateral veins do not have time to distend to accommodate an increased blood flow.[7]

One study suggested that the general recruitment of venous collaterals over time may lead to remission of the syndrome, although the SVC remains obstructed.[8]

Assessment and Diagnosis

Once SVCS is recognized, prompt clinical attention is important. A diagnosis should be established before therapy begins because:[3]

In the absence of tracheal obstruction, SVCS is unlikely to be a life-threatening oncologic emergency, and treatment before definitive diagnosis is not justified.

The initial evaluation of the patient should include a chest x-ray to look for mediastinal masses and associated findings, such as pleural effusion, lobar collapse, or cardiomegaly. Computed tomography (CT) scanning of the thorax yields the most useful diagnostic information and can define the anatomy of the involved mediastinal nodes. Venous patency and the presence of thrombi are assessed using contrast and rapid scanning techniques.[9] Depending on local expertise, contrast or nuclear venography, magnetic resonance imaging, and ultrasonography may be valuable in assessing the site and nature of the obstruction.

If bronchogenic carcinoma is suspected, a sputum specimen should be obtained. If the specimen is negative, a biopsy specimen should be taken from the most accessible site that is clinically involved with disease. The biopsy approach depends on the working diagnosis, location of the tumor, physiological status of the patient, and expertise at the facility. It may include:[10]

The biopsy findings will help the clinician plan appropriate treatment.

Treatment Options for SVCS

The treatment of SVCS depends on the following:

Radiation therapy or chemotherapy should be withheld until the etiology of the obstruction is clear. The treatments discussed here focus on SVC obstruction caused by a malignant tumor. Because the treatment of malignant obstruction may depend on tumor histology, a histological diagnosis should be made before starting treatment. Unless there is airway obstruction or cerebral edema, treatment may be delayed until after an assessment, with no negative effect on outcome.[1,11–15]

Psychosocial Considerations

Patients and family members are often frightened and anxious about the symptoms of SVCS, particularly swelling, dysphagia, coughing, and hoarseness. Patients and family members need information about the cause of the symptoms and short-term measures for palliation, especially during the diagnostic period. When aggressive treatment is declined because of the terminal nature of the underlying disease, symptom management can be offered to patients and family members.

Because most adult patients who develop SVCS have lung cancer, the treatment and psychological support approaches for SVCS should take into account the patient’s prognosis and mental condition, goals of care, and other symptoms caused by the malignancy.[25]

Pediatric Considerations

As described in this summary, SVCS refers to the symptoms associated with the compression or obstruction of the SVC; the compression of the trachea is termed superior mediastinal syndrome (SMS). Because SMS and the resulting respiratory compromise frequently occur in children with SVCS, the two syndromes have become almost synonymous in pediatric practice.[26,27] In adults, the trachea and the right mainstem bronchus are relatively rigid structures compared with the vena cava, but in children, these structures are more susceptible to compression. In addition, the relatively smaller intraluminal diameters of a child’s trachea and bronchus can tolerate little edema before respiratory symptoms occur. Because of this accompanying respiratory component, SVCS in children differs from the adult syndrome and is a serious medical emergency.

The most common symptoms of SVCS in children are similar to those in adults and include the following:[26]

Less common but more serious symptoms include the following:

SVCS is rare in children, appearing at presentation in 12% of pediatric patients with malignant mediastinal tumors.[28,29] The etiology, diagnosis, and treatment of SVCS in children differ from those in adults. The most frequent cause of SVCS in adults is bronchogenic carcinoma;[3] in children, it is non-Hodgkin lymphoma. As in adults, a frequent nonmalignant cause is thrombosis from catheterization for venous access.[26]

A physical examination, chest radiograph, and medical history are usually sufficient to diagnose SVCS. If lymphomas or other malignant diseases are suspected, a tissue sample may aid diagnosis. However, the procedure to obtain the specimen may involve significant risk and may not be clinically feasible. Children with SVCS have a poor tolerance for the necessary general anesthesia because the accompanying cardiovascular and pulmonary changes aggravate the SVCS, often making intubation impossible. Also, extubation may be difficult or impossible, requiring prolonged airway provision (intubation). A CT scan of the chest to determine tracheal size, upright and supine echocardiography, and a flow volume loop may help evaluate anesthetic risk. Because anesthesia use is a serious risk, the diagnosis should be made with the least invasive means possible.[30] Published reports suggest a stepwise approach.[26]

When a malignant mass causes SVCS, the situation may be a medical emergency with no opportunity to establish a tissue diagnosis. In these cases, the most appropriate course may be to initiate empiric therapy before biopsy. The traditional empiric therapy is radiation therapy, with the daily dose governed by the presumed radiosensitivity of the tumor. After radiation therapy, respiratory deterioration from the apparent tracheal swelling may occur. This swelling occurs because narrow lumens in children cannot accommodate edema and because of the greater degree of edema at onset, the result of rapid tumor growth in children. In these situations, a course of prednisone at 10 mg/m2 of body surface area 4 times per day may be necessary.[26]

In addition to radiation, empiric therapy for SVCS has included chemotherapeutic agents incorporating steroids, cyclophosphamide, or both in combination with an anthracycline and vincristine.[26] If the tumor fails to respond, it may be a benign lesion.

If surgery becomes necessary, it should be performed with the patient in the semi-Fowler’s position, allowing the surgeon the ability to rapidly change the patient’s position to lateral or prone. Cardiopulmonary bypass facilities and a rigid bronchoscope should be available in a standby capacity.[30]

Purpose of This Summary

This PDQ cancer information summary for health professionals provides comprehensive, peer-reviewed, evidence-based information about the pathophysiology and treatment of cardiopulmonary syndromes, including dyspnea, malignant pleural effusion, malignant pericardial effusion, and superior vena cava syndrome. It is intended as a resource to inform and assist clinicians in the care of their patients. It does not provide formal guidelines or recommendations for making health care decisions.

Reviewers and Updates

This summary is reviewed regularly and updated as necessary by the PDQ Supportive and Palliative Care Editorial Board, which is editorially independent of the National Cancer Institute (NCI). The summary reflects an independent review of the literature and does not represent a policy statement of NCI or the National Institutes of Health (NIH).

Board members review recently published articles each month to determine whether an article should:

Changes to the summaries are made through a consensus process in which Board members evaluate the strength of the evidence in the published articles and determine how the article should be included in the summary.

Any comments or questions about the summary content should be submitted to Cancer.gov through the NCI website’s Email Us. Do not contact the individual Board Members with questions or comments about the summaries. Board members will not respond to individual inquiries.

Levels of Evidence

Some of the reference citations in this summary are accompanied by a level-of-evidence designation. These designations are intended to help readers assess the strength of the evidence supporting the use of specific interventions or approaches. The PDQ Supportive and Palliative Care Editorial Board uses a formal evidence ranking system in developing its level-of-evidence designations.

Permission to Use This Summary

PDQ is a registered trademark. Although the content of PDQ documents can be used freely as text, it cannot be identified as an NCI PDQ cancer information summary unless it is presented in its entirety and is regularly updated. However, an author would be permitted to write a sentence such as “NCI’s PDQ cancer information summary about breast cancer prevention states the risks succinctly: [include excerpt from the summary].”

The preferred citation for this PDQ summary is:

PDQ® Supportive and Palliative Care Editorial Board. PDQ Cardiopulmonary Syndromes. Bethesda, MD: National Cancer Institute. Updated <MM/DD/YYYY>. Available at: /side-effects/cardiopulmonary-hp-pdq. Accessed <MM/DD/YYYY>. [PMID: 26389275]

Images in this summary are used with permission of the author(s), artist, and/or publisher for use within the PDQ summaries only. Permission to use images outside the context of PDQ information must be obtained from the owner(s) and cannot be granted by the National Cancer Institute. Information about using the illustrations in this summary, along with many other cancer-related images, is available in Visuals Online, a collection of over 2,000 scientific images.

Disclaimer

The information in these summaries should not be used as a basis for insurance reimbursement determinations. More information on insurance coverage is available on Cancer.gov on the Managing Cancer Care page.

Contact Us

More information about contacting us or receiving help with the Cancer.gov website can be found on our Contact Us for Help page. Questions can also be submitted to Cancer.gov through the website’s Email Us.

Many conditions can cause dyspnea.

Dyspnea is the feeling that you can’t catch your breath or you can’t breathe in enough air. It also may be called shortness of breath, breathlessness, or air hunger. In cancer patients, dyspnea can be caused by the following:

A physical exam and health history are important in finding out the cause of dyspnea.

Diagnostic tests and procedures include the following:

There are different ways to treat the causes of dyspnea in cancer patients.

Treatment may include the following:

Treatment of dyspnea will depend on what is causing it.

The treatment of dyspnea depends on its cause, as follows:

Treatment may be to control the signs and symptoms of dyspnea.

Treatment to control the signs and symptoms of dyspnea may include the following:

Chronic coughing may cause much physical distress.

Chronic cough may cause pain, trouble sleeping, dyspnea, or fatigue. The causes of chronic coughing are almost the same as the causes of dyspnea. See Dyspnea section for list of causes.

It may be possible to treat the cause of chronic coughing.

Treatments may include:

Medicines may be used to control chronic coughing.

Medicines may include:

Pleural effusion is extra fluid around the lungs.

The pleural cavity is the space between the pleura (thin layer of tissue) that covers the outer surface of each lung and lines the inner wall of the chest cavity. Pleural tissue usually makes a small amount of fluid that helps the lungs move smoothly in the chest while a person is breathing. A pleural effusion is extra fluid in the pleural cavity. The fluid presses on the lungs and makes it hard to breathe.

Pleural effusion may be caused by cancer, cancer treatment, or other conditions.

A pleural effusion may be malignant (caused by cancer) or nonmalignant (caused by a condition that is not cancer). Malignant pleural effusion is a common problem for patients who have certain cancers. Lung cancer, breast cancer, lymphoma, and leukemia cause most malignant effusions.

Pleural effusion also may be caused by radiation therapy, chemotherapy, a collapsed lung, or cancer that has spread to lymph nodes. Some cancer patients have conditions such as congestive heart failure, pneumonia, blood clot in the lung, or poor nutrition that may lead to a pleural effusion.

Signs and symptoms of pleural effusion include dyspnea (shortness of breath) and cough.

These and other signs and symptoms may be caused by a pleural effusion. Talk to your doctor if you have any of the following problems:

Finding out the cause of pleural effusion will help plan the treatment.

Treatment for a malignant pleural effusion is different from treatment for a nonmalignant effusion, so the right diagnosis is important. Diagnostic tests used to find the cause of the pleural effusion include the following:

The type of cancer, previous treatment for cancer, and your choices also are important in planning treatment.

Treatment may be to control signs and symptoms of pleural effusion and improve quality of life.

A malignant pleural effusion often occurs in cancer that is advanced, cannot be removed by surgery, or continues to grow or spread during treatment. It is also common during the last few weeks of life. The goal of treatment is usually palliative, to relieve signs and symptoms and improve quality of life.

Treatment of the signs and symptoms of malignant pleural effusion includes the following:

Pericardial effusion is extra fluid around the heart.

Pericardial effusion is extra fluid inside the sac that surrounds the heart. The extra fluid causes pressure on the heart, which stops it from pumping blood normally. If fluid builds up, a condition called cardiac tamponade may occur. In cardiac tamponade, the heart cannot pump enough blood to the rest of the body. This is life-threatening and must be treated right away.

Pericardial effusion may be caused by cancer or other conditions.

A pericardial effusion may be malignant (caused by cancer) or nonmalignant (caused by a condition that is not cancer). Malignant pericardial effusion is common in lung cancer, breast cancer, melanoma, lymphoma, and leukemia patients. Pericarditis (swelling of tissues around the heart), a heart attack, hypothyroidism, or systemic lupus erythematosus are examples of nonmalignant causes of pericardial effusion. Radiation therapy or chemotherapy may cause pericarditis, leading to pericardial effusion.

Signs and symptoms of pericardial effusion include dyspnea (shortness of breath) and cough.

At first, a pericardial effusion may not cause any signs or symptoms. These and other signs and symptoms may be caused by a pericardial effusion or cardiac tamponade. Check with your doctor if you have any of the following:

Pericardial effusion usually occurs in advanced cancer.

Pericardial effusion usually occurs in advanced cancer or in the last few weeks of life. During these times, it may be more important to relieve the symptoms than to diagnose the condition. However, in some cases, the following tests and procedures may be used to diagnose pericardial effusion:

Treatment may be to control the symptoms of pericardial effusion and improve quality of life.

The goal of treatment is usually palliative, to relieve symptoms and improve quality of life. If a malignant pericardial effusion is severe, it is usually controlled by draining the fluid.

Treatment options include the following:

Superior vena cava syndrome (SVCS) is a group of signs and symptoms that occur when the superior vena cava is partly blocked.

The superior vena cava is a major vein that leads to the heart. The heart is divided into four parts. The right and left atrium make up the top parts of the heart and the right and left ventricle make up the bottom parts of the heart. The right atrium of the heart receives blood from two major veins:

Different conditions can slow the flow of blood through the superior vena cava. These include a tumor in the chest, nearby lymph nodes that are swollen (from cancer), or a blood clot in the superior vena cava. The vein may become completely blocked. Sometimes, smaller veins in the area become larger and take over for the superior vena cava if it is blocked, but this takes time. Superior vena cava syndrome (SVCS) is the group of signs and symptoms that occur when this vein is partly blocked.

SVCS is usually caused by cancer.

SVCS is usually caused by cancer. In adults, SVCS is most common in the following types of cancer:

Less common causes of SVCS include:

Common signs and symptoms of SVCS include breathing problems and coughing.

The signs and symptoms of SVCS are more severe if the vein becomes blocked quickly. This is because the other veins in the area do not have time to widen and take over the blood flow that cannot pass through the superior vena cava.

The most common signs are:

Less common signs and symptoms include the following:

Tests are done to find and diagnose the blockage.

The following tests may be done to diagnose SVCS and find the blockage:

It is important to find out the cause of SVCS before starting treatment. The type of cancer can affect the type of treatment needed. Unless the airway is blocked or the brain is swelling, waiting to start treatment while a diagnosis is made usually causes no problem in adults. If doctors think lung cancer is causing the problem, a sputum sample may be taken and a biopsy may be done.

Treatment for SVCS caused by cancer depends on the cause, signs and symptoms, and prognosis.

Treatment for SCVS caused by cancer depends on the following:

Treatments for SVCS include watchful waiting, chemotherapy, radiation therapy, thrombolysis, stent placement, and surgery.

Palliative care may be given to relieve signs and symptoms of SVCS.

The signs and symptoms of superior vena cava syndrome can be upsetting. It is important that you and your family ask questions about superior vena cava syndrome and how to treat it. This can help relieve anxiety about signs and symptoms such as swelling, trouble swallowing, coughing, and hoarseness.

If you have advanced cancer you may decide not to have any more treatment. Palliative care can help keep you comfortable by relieving signs and symptoms to improve your quality of life.

Superior vena cava syndrome (SVCS) in a child is a serious medical emergency because the child’s windpipe can become blocked.

Superior vena cava syndrome (SVCS) is rare in children, but when it occurs, it can be life-threatening. In adults, the windpipe is stiff, but in children, it is softer and can more easily be squeezed shut or blocked. A child’s windpipe is narrow, so any amount of swelling can cause breathing problems. Squeezing of the trachea is called superior mediastinal syndrome (SMS). Because SVCS and SMS usually happen together in children, the two syndromes are considered to be the same.

The most common symptoms of SVCS in children are a lot like those in adults.

Common signs and symptoms include the following:

There are other less common but more serious signs and symptoms:

The most common cause of SVCS in children is non-Hodgkin lymphoma.

SVCS in children is rare. The most common cause is non-Hodgkin lymphoma. As in adults, SVCS may also be caused by a blood clot that forms during use of an intravenous catheter (flexible tube used to put fluids into or take blood out of a vein) in the superior vena cava.

SVCS in children may be diagnosed and treated before a diagnosis of cancer is made.

A physical exam, chest x-ray, and medical history are usually all that are needed to diagnose superior vena cava syndrome in children. Even if doctors think cancer is causing SVCS, a biopsy may not be done. This is because the lungs and heart of a child with SVCS may not be able to handle the anesthesia needed. Other imaging tests may be done to help find out if anesthesia can be safely used. In most cases, treatment for SVCS will begin before a diagnosis of cancer is made.

Treatment for SVCS in children may include radiation therapy, drugs, or surgery.

There are several ways to treat SVCS in children.

About PDQ

Physician Data Query (PDQ) is the National Cancer Institute’s (NCI’s) comprehensive cancer information database. The PDQ database contains summaries of the latest published information on cancer prevention, detection, genetics, treatment, supportive care, and complementary and alternative medicine. Most summaries come in two versions. The health professional versions have detailed information written in technical language. The patient versions are written in easy-to-understand, nontechnical language. Both versions have cancer information that is accurate and up to date and most versions are also available in Spanish.

PDQ is a service of the NCI. The NCI is part of the National Institutes of Health (NIH). NIH is the federal government’s center of biomedical research. The PDQ summaries are based on an independent review of the medical literature. They are not policy statements of the NCI or the NIH.

Purpose of This Summary

This PDQ cancer information summary has current information about the pathophysiology and treatment of cardiopulmonary syndromes, including dyspnea, malignant pleural effusion, malignant pericardial effusion, and superior vena cava syndrome. It is meant to inform and help patients, families, and caregivers. It does not give formal guidelines or recommendations for making decisions about health care.

Reviewers and Updates

Editorial Boards write the PDQ cancer information summaries and keep them up to date. These Boards are made up of experts in cancer treatment and other specialties related to cancer. The summaries are reviewed regularly and changes are made when there is new information. The date on each summary (“Updated”) is the date of the most recent change.

The information in this patient summary was taken from the health professional version, which is reviewed regularly and updated as needed, by the PDQ Supportive and Palliative Care Editorial Board.

Clinical Trial Information

A clinical trial is a study to answer a scientific question, such as whether one treatment is better than another. Trials are based on past studies and what has been learned in the laboratory. Each trial answers certain scientific questions in order to find new and better ways to help cancer patients. During treatment clinical trials, information is collected about the effects of a new treatment and how well it works. If a clinical trial shows that a new treatment is better than one currently being used, the new treatment may become “standard.” Patients may want to think about taking part in a clinical trial. Some clinical trials are open only to patients who have not started treatment.

Clinical trials can be found online at NCI’s website. For more information, call the Cancer Information Service (CIS), NCI’s contact center, at 1-800-4-CANCER (1-800-422-6237).

Permission to Use This Summary

PDQ is a registered trademark. The content of PDQ documents can be used freely as text. It cannot be identified as an NCI PDQ cancer information summary unless the whole summary is shown and it is updated regularly. However, a user would be allowed to write a sentence such as “NCI’s PDQ cancer information summary about breast cancer prevention states the risks in the following way: [include excerpt from the summary].”

The best way to cite this PDQ summary is:

PDQ® Supportive and Palliative Care Editorial Board. PDQ Cardiopulmonary Syndromes. Bethesda, MD: National Cancer Institute. Updated <MM/DD/YYYY>. Available at: /side-effects/cardiopulmonary-pdq. Accessed <MM/DD/YYYY>. [PMID: 26389457]

Images in this summary are used with permission of the author(s), artist, and/or publisher for use in the PDQ summaries only. If you want to use an image from a PDQ summary and you are not using the whole summary, you must get permission from the owner. It cannot be given by the National Cancer Institute. Information about using the images in this summary, along with many other images related to cancer can be found in Visuals Online. Visuals Online is a collection of more than 3,000 scientific images.

Disclaimer

The information in these summaries should not be used to make decisions about insurance reimbursement. More information on insurance coverage is available on Cancer.gov on the Managing Cancer Care page.

Contact Us

More information about contacting us or receiving help with the Cancer.gov website can be found on our Contact Us for Help page. Questions can also be submitted to Cancer.gov through the website’s E-mail Us.

Good nutrition is important for people with cancer.

Nutrition is a process in which food is taken in and used by the body for growth, to keep the body healthy, and to replace tissue. Good nutrition is important for good health. A healthy diet includes foods and liquids that have important nutrients (vitamins, minerals, proteins, carbohydrates, fats, and water) the body needs.

Nutrition goals are set for each person with cancer.

Nutrition goals during cancer therapy are based on a person’s cancer type, cancer stage, and other medical conditions. Eating the right amount of protein and calories is important for healing, fighting infection, and having enough energy.

A registered dietitian is an important part of the healthcare team.

A registered dietitian (or nutritionist) is a part of the team of health professionals that help with cancer treatment and recovery. A dietitian will work with you, your family, and the rest of the medical team to manage your diet during and after cancer treatment.

Cancer and cancer treatments may cause side effects that affect nutrition.

Nutrition problems are likely when tumors involve the head, neck, esophagus, stomach, intestines, pancreas, or liver.

For many people, the effects of cancer treatments make it hard to eat well. Cancer treatments that affect nutrition include:

Cancer and cancer treatments may cause malnutrition.

Cancer and cancer treatments may affect taste, smell, appetite, and the ability to eat enough food or absorb the nutrients from food. This can cause malnutrition, which is a condition caused by a lack of key nutrients.

Malnutrition can cause a person to be weak, tired, and unable to fight infection or finish cancer treatment. As a result, malnutrition can decrease the person’s quality of life and become life-threatening. Malnutrition may get worse if the cancer grows or spreads.

Anorexia and cachexia are common causes of malnutrition in people with cancer.

Anorexia is the loss of appetite or desire to eat. It is a common symptom and the most common cause of malnutrition in people with cancer. Anorexia may occur early in the disease or later, if the cancer grows or spreads. Some people already have anorexia when they are diagnosed with cancer. Most people who have advanced cancer will have anorexia.

Cachexia is a condition marked by weakness, weight loss, and fat and muscle loss. It is common in people with tumors that affect eating and digestion. It can occur in people with cancer who are eating well, but are not storing fat and muscle because of tumor growth.

Some tumors change the way the body uses certain nutrients. The body’s use of protein, carbohydrates, and fat may change when tumors are in the stomach, intestines, or head and neck. A person may seem to be eating enough, but the body may not be able to absorb all the nutrients from the food.

People with cancer may have cachexia and anorexia at the same time (CAS), causing weight loss and decreased lean body mass. Treating high-risk patients to prevent this condition, rather than treating those already diagnosed with CAS, may lead to better outcomes. Olanzapine, a drug used to treat certain mental disorders, has side effects including increased appetite and weight gain. It is being studied in the treatment of CAS with mixed success. More clinical trials are needed to develop the best possible therapies for CAS.

Chemotherapy and Hormone Therapy

Radiation Therapy

Surgery

Immunotherapy

Stem Cell Transplant

The healthcare team may ask questions about diet and weight history.

Screening is used to look for health problems that affect the risk of poor nutrition. This can help find out if you are likely to become malnourished, and if nutrition therapy is needed.

The healthcare team may ask questions about the following:

A physical exam is done. Your doctor will check for signs of weight, fat, and muscle loss, and for fluid buildup in your body.

Counseling and diet changes are made to improve the person’s nutrition.

A registered dietitian can counsel you and your family on ways to improve your nutrition. The registered dietitian gives care based on your nutritional and dietary needs during cancer treatment and recovery. Changes to the diet are made to help decrease symptoms from cancer or cancer treatment. These changes may be in the types and amount of food, how often you eat, and how food is eaten (for example, at a certain temperature or taken with a straw).

In addition to the dietitian, the healthcare team may include the following:

The goal of nutrition therapy for people who have advanced cancer depends on the overall plan of care.

The goal of nutrition therapy in people with advanced cancer is to provide the best possible quality of life and control symptoms that cause distress.

People with advanced cancer may be treated with anticancer therapy and palliative care, palliative care alone, or may be in hospice care. Nutrition goals will be different for each person. Some types of treatment may be stopped.

As the focus of care goes from cancer treatment to hospice or end-of-life care, nutrition therapy may become less aggressive to keep the person as comfortable as possible. For more information, see the Nutrition Needs at End of Life section.

Anorexia

The following may help people with cancer who have anorexia (loss of appetite or desire to eat):

If these diet changes do not help with the anorexia, tube feedings may be needed.

Medicines may be given to increase appetite. For more information, see the Medicines to Treat Loss of Appetite and Weight Loss section.

Nausea

The following may help people with cancer control nausea:

Vomiting

The following may help people with cancer control vomiting:

Dry Mouth

The following may help people with cancer who have dry mouth:

Mouth Sores

The following can help people with cancer who have mouth sores:

Taste Changes

The following may help people with cancer who have taste changes:

Sore Throat and Trouble Swallowing

The following may help people with cancer who have a sore throat or trouble swallowing:

Lactose Intolerance

The following may help people with cancer who have symptoms of lactose intolerance:

Weight Gain

The following may help people with cancer prevent weight gain:

Nutrition support helps people who cannot eat or digest food normally.

It is best to take in food by mouth whenever possible. Some people may not be able to take in enough food by mouth because of problems from cancer or cancer treatment.

Nutrition support can be given in different ways.

In addition to counseling by a dietitian and changes to the diet, nutrition therapy includes nutritional supplement drinks and enteral and parenteral nutrition support. Nutritional supplement drinks help people with cancer get the nutrients they need. They provide energy, protein, fat, carbohydrates, fiber, vitamins, and minerals. They are not meant to be the person’s only source of nutrition.

A person who is not able to take in the right amount of calories and nutrients by mouth may be fed using the following:

Nutrition support can improve a person’s quality of life during cancer treatment, but may cause problems that should be considered before making the decision to use it. The patient, family, and healthcare team should discuss the harms and benefits of each type of nutrition support. For more information on the use of nutrition support at the end of life, see the Nutrition Needs at End of Life section.

Enteral Nutrition

Parenteral Nutrition

The catheter may be placed into a vein in the chest or in the arm.

A central venous access catheter is placed beneath the skin and into a large vein in the upper chest. The catheter is put in place by a surgeon. This type of catheter is used for long-term parenteral feeding.

Enlarge

A peripheral venous catheter is placed into a vein in the arm. A peripheral venous catheter is put in place by trained medical staff. This type of catheter is usually used for short-term parenteral feeding for patients who do not have a central venous access catheter.

Enlarge

The patient is checked often for infection or bleeding at the place where the catheter enters the body.

Medicine may be given with nutrition therapy to treat loss of appetite and weight loss.

It is important that cancer symptoms and side effects that affect eating and cause weight loss are treated early. Both nutrition therapy and medicine can help lessen the effects that cancer and its treatment have on weight loss.

Different types of medicine may be used to treat loss of appetite and weight loss.

Medicines that improve appetite and cause weight gain, such as prednisone and megestrol, may be used to treat loss of appetite and weight loss. Studies have shown that the effects of these medicines may not last long, or there may be no effects. Treatment with a combination of medicines may work better than treatment with one medicine but may have more side effects.

Nutrition needs change at end of life.

For people at the end of life, the goals of nutrition therapy are focused on relieving symptoms rather than getting enough nutrients.

Common symptoms that can occur at the end of life include the following:

People who have problems swallowing may find it easier to swallow thick liquids than thin liquids.

People with cancer often do not feel much hunger at all and may want very little food. Sips of water, ice chips, and mouth care can decrease thirst in the last few days of life. Good communication with the healthcare team is important to understand the patient’s changes in nutrition needs.

People with cancer and their families decide how much nutrition and fluids will be given at the end of life.

People with cancer and their caregivers have the right to make informed decisions. The person’s religious and cultural preferences may affect their decisions. The healthcare team may work with the person’s religious and cultural leaders when making decisions. The healthcare team and a registered dietitian can explain the benefits and risks of using nutrition support for people at the end of life. In most cases, there are more harms than benefits if the person is not expected to live longer than a month.

Possible benefits of nutrition support for people expected to live longer than a month include the following:

The risks of nutrition support at the end of life include the following:

Some people with cancer try special diets to improve their prognosis.

People with cancer may try special diets to make their treatment work better, prevent side effects from treatment, or to treat the cancer itself. However, for most of these special diets, there is no evidence that shows they work.

Vegetarian or vegan diet

It is not known if following a vegetarian or vegan diet can help side effects from cancer treatment or the person’s prognosis. If the person already follows a vegetarian or vegan diet, there is no evidence that shows they should switch to a different diet.

A study in patients with non-muscle-invasive bladder cancer showed some benefits from eating a diet rich in ITC, a phytochemical found in raw cruciferous vegetables. Patients who ate large amounts of cruciferous vegetables were less likely to have two or more recurrences of their disease and a lower risk of their disease becoming muscle-invasive cancer. More research on the benefits of phytochemicals is needed.

Macrobiotic diet

A macrobiotic diet is a high-carbohydrate, low-fat, plant-based diet. No studies have shown that this diet will help people with cancer.

Ketogenic diet

A ketogenic diet limits carbohydrates and increases fat intake. The purpose of the diet is to decrease the amount of glucose (sugar) the tumor cells can use to grow and reproduce. It is a hard diet to follow because exact amounts of fats, carbohydrates, and proteins are needed.

Several clinical trials are recruiting people with glioblastoma to study whether a ketogenic diet affects glioblastoma tumor activity. People with glioblastoma who want to start a ketogenic diet should talk to their doctor and work with a registered dietitian. However, it is not yet known how the diet will affect the tumor or its symptoms.

Similarly, a study comparing the ketogenic diet to a high-fiber, low fat diet in women with ovarian cancer or endometrial cancer found that the ketogenic diet was safe and acceptable. There is not enough evidence to know how the ketogenic diet will affect ovarian or endometrial tumors or their symptoms.

Some people with cancer may take dietary supplements.

A dietary supplement is a product that is added to the diet. It is usually taken by mouth, and usually has one or more dietary ingredients. People with cancer may take dietary supplements to improve their symptoms or treat their cancer.

Vitamin C

Vitamin C is a nutrient that the body needs in small amounts to function and stay healthy. It helps fight infection, heal wounds, and keep tissues healthy. Vitamin C is found in fruits and vegetables. It can also be taken as a dietary supplement. For information about the use of intravenous vitamin C as treatment for people with cancer, see Intravenous Vitamin C.

Probiotics

Probiotics are live microorganisms used as dietary supplements to help with digestion and normal bowel function. They may also help keep the gastrointestinal tract healthy.

Studies have shown that taking probiotics during radiation therapy and chemotherapy can help prevent diarrhea caused by those treatments. People with cancer who are receiving radiation therapy to the abdomen or chemotherapy that is known to cause diarrhea may be helped by probiotics. Similarly, studies are looking at potential benefits of taking probiotics for people with cancer who are receiving immunotherapy.

Melatonin

Melatonin is a hormone made by the pineal gland (tiny organ near the center of the brain). Melatonin helps control the body’s sleep cycle. It can also be made in a laboratory and taken as a dietary supplement.

Several small studies have shown that taking a melatonin supplement with chemotherapy and/or radiation therapy for treatment of solid tumors may be helpful. It may help reduce side effects of treatment. Melatonin does not appear to have side effects.

Oral glutamine

Oral glutamine is an amino acid that is being studied for the treatment of diarrhea and mucositis (inflammation of the lining of the digestive system, often seen as mouth sores) caused by chemotherapy or radiation therapy. Oral glutamine may help prevent mucositis or make it less severe.

People with cancer who are receiving radiation therapy to the abdomen may benefit from oral glutamine. Oral glutamine may reduce the severity of diarrhea. This can help people continue with their treatment plan.

National Cancer Institute

For information from the National Cancer Institute (NCI) about nutrition and cancer treatment, see Side Effects.

Organizations

For general nutrition information and other resources, see the following:

Books

About PDQ

Physician Data Query (PDQ) is the National Cancer Institute’s (NCI’s) comprehensive cancer information database. The PDQ database contains summaries of the latest published information on cancer prevention, detection, genetics, treatment, supportive care, and complementary and alternative medicine. Most summaries come in two versions. The health professional versions have detailed information written in technical language. The patient versions are written in easy-to-understand, nontechnical language. Both versions have cancer information that is accurate and up to date and most versions are also available in Spanish.

PDQ is a service of the NCI. The NCI is part of the National Institutes of Health (NIH). NIH is the federal government’s center of biomedical research. The PDQ summaries are based on an independent review of the medical literature. They are not policy statements of the NCI or the NIH.

Purpose of This Summary

This PDQ cancer information summary has current information about nutrition before, during, and after cancer treatment. It is meant to inform and help patients, families, and caregivers. It does not give formal guidelines or recommendations for making decisions about health care.

Reviewers and Updates

Editorial Boards write the PDQ cancer information summaries and keep them up to date. These Boards are made up of experts in cancer treatment and other specialties related to cancer. The summaries are reviewed regularly and changes are made when there is new information. The date on each summary (“Updated”) is the date of the most recent change.

The information in this patient summary was taken from the health professional version, which is reviewed regularly and updated as needed, by the PDQ Supportive and Palliative Care Editorial Board.

Clinical Trial Information

A clinical trial is a study to answer a scientific question, such as whether one treatment is better than another. Trials are based on past studies and what has been learned in the laboratory. Each trial answers certain scientific questions in order to find new and better ways to help cancer patients. During treatment clinical trials, information is collected about the effects of a new treatment and how well it works. If a clinical trial shows that a new treatment is better than one currently being used, the new treatment may become “standard.” Patients may want to think about taking part in a clinical trial. Some clinical trials are open only to patients who have not started treatment.

Clinical trials can be found online at NCI’s website. For more information, call the Cancer Information Service (CIS), NCI’s contact center, at 1-800-4-CANCER (1-800-422-6237).

Permission to Use This Summary

PDQ is a registered trademark. The content of PDQ documents can be used freely as text. It cannot be identified as an NCI PDQ cancer information summary unless the whole summary is shown and it is updated regularly. However, a user would be allowed to write a sentence such as “NCI’s PDQ cancer information summary about breast cancer prevention states the risks in the following way: [include excerpt from the summary].”

The best way to cite this PDQ summary is:

PDQ® Supportive and Palliative Care Editorial Board. PDQ Nutrition in Cancer Care. Bethesda, MD: National Cancer Institute. Updated <MM/DD/YYYY>. Available at: /side-effects/appetite-loss/nutrition-pdq. Accessed <MM/DD/YYYY>. [PMID: 26389440]

Images in this summary are used with permission of the author(s), artist, and/or publisher for use in the PDQ summaries only. If you want to use an image from a PDQ summary and you are not using the whole summary, you must get permission from the owner. It cannot be given by the National Cancer Institute. Information about using the images in this summary, along with many other images related to cancer can be found in Visuals Online. Visuals Online is a collection of more than 3,000 scientific images.

Disclaimer

The information in these summaries should not be used to make decisions about insurance reimbursement. More information on insurance coverage is available on Cancer.gov on the Managing Cancer Care page.

Contact Us

More information about contacting us or receiving help with the Cancer.gov website can be found on our Contact Us for Help page. Questions can also be submitted to Cancer.gov through the website’s E-mail Us.

Hot flashes and night sweats are common in people with cancer and survivors.

A hot flash is a sudden warm feeling over your face, neck, and chest that may cause you to sweat and your face to turn red. Sweating is your body’s way of lowering body temperature by causing heat loss through your skin. Hot flashes combined with sweats that happen while sleeping are often called night sweats or hot flushes. Hot flashes and night sweats are common in people receiving cancer treatment. Some people continue to have hot flashes and night sweats after cancer treatment.

In women and men, hot flashes and night sweats may be caused by surgery, radiation therapy, and taking certain medications.

Hot flashes and night sweats may be controlled with estrogen replacement therapy.

Hot flashes and night sweats during natural or treatment-related menopause can be controlled with estrogen replacement therapy. However, many women are not able to take estrogen replacement (for example, women who have or had breast cancer) and may need to take a drug that does not have estrogen in it. Hormone replacement therapy that combines estrogen with progestin may increase the risk of breast cancer or breast cancer recurrence.

Treatment of hot flashes in men who have been treated for prostate cancer may include estrogens, progestin, antidepressants, and anticonvulsants.

Other drugs may be useful in some people.

Studies of non-estrogen drugs to treat hot flashes in women with a history of breast cancer have reported that many of them do not work as well as estrogen replacement or have side effects. Megestrol and medroxyprogesterone (drugs like progesterone), certain antidepressants, anticonvulsants, and clonidine (a drug used to treat high blood pressure) are non-estrogen drugs used to control hot flashes.

Side effects from drug therapy for hot flashes and night sweats may develop.

Side effects of non-hormonal drug therapy may include:

Side effects from drug therapy may vary from person to person, so treatment and dose will be specific to your needs. If one medicine does not improve your symptoms, switching to another medicine may help.

Treatments that help people cope with stress and anxiety may help manage hot flashes.

Treatments that change how you deal with stress, anxiety, and negative feelings may help you manage hot flashes. These strategies include cognitive behavioral therapy and relaxation techniques. They help you gain a sense of control and develop coping skills to manage your symptoms.

Hypnosis has also been used as a treatment for hot flashes. It is a trance-like state that allows you to be more aware, focused, relaxed, and open to suggestion. Under hypnosis, you can concentrate more clearly on a specific thought or feeling without becoming distracted. A therapist helps you to deeply relax and focus on cooling thoughts. This may lower stress levels, balance body temperature, and calm the heart rate and breathing rate.

Cognitive behavioral therapy, relaxation techniques, or hypnosis may help hot flashes and related problems when used together with drug therapy.

Comfort measures may help relieve hot flashes and night sweats.

Comfort measures may be used to treat hot flashes and night sweats related to cancer treatment. Since body temperature goes up before a hot flash, doing the following may control body temperature and help control symptoms:

Herbs and dietary supplements should be used with caution.

It is important that your health care providers know about all of the dietary supplements, such as soy and herbs, you are taking with your medicines.

Studies of vitamin E for the relief of hot flashes show that it is only slightly better than a placebo (pill or procedure that has no effect). Most studies of soy and black cohosh show they are no better than a placebo in reducing hot flashes. Soy is rich in estrogen-like substances, but how it affects cells in the body is unknown. Studies of ground flaxseed and magnesium oxide to treat hot flashes have shown mixed results.

Claims are made about several other plant-based and natural products as remedies for hot flashes. These include dong quai, milk thistle, red clover, licorice root extract, and chaste tree berry. Since little is known about how these products work or whether they affect the risk of breast cancer, you should talk with your doctor before using them.

Acupuncture has been studied in the treatment of hot flashes.

Pilot studies of acupuncture and randomized clinical trials that compare true acupuncture and sham (placebo) treatment have been done in people with hot flashes and results are mixed. A review of many studies combined showed that acupuncture had slight or no effects in people with breast cancer who had hot flashes. In contrast, a randomized clinical trial that was not included in the review showed that people with breast cancer who were given acupuncture had fewer hot flashes. Another randomized clinical trial showed that breast cancer survivors who were given electroacupuncture had a reduction in hot flash symptoms. To learn more, visit the Vasomotor symptoms section in the health professional version of Acupuncture.

About PDQ

Physician Data Query (PDQ) is the National Cancer Institute’s (NCI’s) comprehensive cancer information database. The PDQ database contains summaries of the latest published information on cancer prevention, detection, genetics, treatment, supportive care, and complementary and alternative medicine. Most summaries come in two versions. The health professional versions have detailed information written in technical language. The patient versions are written in easy-to-understand, nontechnical language. Both versions have cancer information that is accurate and up to date and most versions are also available in Spanish.

PDQ is a service of the NCI. The NCI is part of the National Institutes of Health (NIH). NIH is the federal government’s center of biomedical research. The PDQ summaries are based on an independent review of the medical literature. They are not policy statements of the NCI or the NIH.

Purpose of This Summary

This PDQ cancer information summary has current information about the causes and treatment of hot flashes and night sweats. It is meant to inform and help patients, families, and caregivers. It does not give formal guidelines or recommendations for making decisions about health care.

Reviewers and Updates

Editorial Boards write the PDQ cancer information summaries and keep them up to date. These Boards are made up of experts in cancer treatment and other specialties related to cancer. The summaries are reviewed regularly and changes are made when there is new information. The date on each summary (“Updated”) is the date of the most recent change.

The information in this patient summary was taken from the health professional version, which is reviewed regularly and updated as needed, by the PDQ Supportive and Palliative Care Editorial Board.

Clinical Trial Information

A clinical trial is a study to answer a scientific question, such as whether one treatment is better than another. Trials are based on past studies and what has been learned in the laboratory. Each trial answers certain scientific questions in order to find new and better ways to help cancer patients. During treatment clinical trials, information is collected about the effects of a new treatment and how well it works. If a clinical trial shows that a new treatment is better than one currently being used, the new treatment may become “standard.” Patients may want to think about taking part in a clinical trial. Some clinical trials are open only to patients who have not started treatment.

Clinical trials can be found online at NCI’s website. For more information, call the Cancer Information Service (CIS), NCI’s contact center, at 1-800-4-CANCER (1-800-422-6237).

Permission to Use This Summary

PDQ is a registered trademark. The content of PDQ documents can be used freely as text. It cannot be identified as an NCI PDQ cancer information summary unless the whole summary is shown and it is updated regularly. However, a user would be allowed to write a sentence such as “NCI’s PDQ cancer information summary about breast cancer prevention states the risks in the following way: [include excerpt from the summary].”

The best way to cite this PDQ summary is:

PDQ® Supportive and Palliative Care Editorial Board. PDQ Hot Flashes and Night Sweats. Bethesda, MD: National Cancer Institute. Updated <MM/DD/YYYY>. Available at: /side-effects/hot-flashes-pdq. Accessed <MM/DD/YYYY>. [PMID: 26389162]

Images in this summary are used with permission of the author(s), artist, and/or publisher for use in the PDQ summaries only. If you want to use an image from a PDQ summary and you are not using the whole summary, you must get permission from the owner. It cannot be given by the National Cancer Institute. Information about using the images in this summary, along with many other images related to cancer can be found in Visuals Online. Visuals Online is a collection of more than 3,000 scientific images.

Disclaimer

The information in these summaries should not be used to make decisions about insurance reimbursement. More information on insurance coverage is available on Cancer.gov on the Managing Cancer Care page.

Contact Us

More information about contacting us or receiving help with the Cancer.gov website can be found on our Contact Us for Help page. Questions can also be submitted to Cancer.gov through the website’s E-mail Us.

Hormone Replacement Therapy

Estrogen replacement effectively controls hot flashes associated with biological or treatment-associated postmenopausal states in women. The proposed mechanism of action of estrogen replacement therapy is that it ameliorates hot flashes by raising the core body temperature sweating threshold;[1][Level of evidence: I] however, many women have relative or absolute contraindications to estrogen replacement. Physicians and breast cancer survivors often think there is an increased risk of breast cancer recurrence or de novo breast malignancy with hormone replacement therapies and defer hormonal management of postmenopausal symptoms. Methodologically strong data evaluating the risk of breast cancer associated with hormone replacement therapy in healthy women have been minimal, despite strong basic science considerations suggesting the possibility of such a risk.[2]

In May 2002, the Women’s Health Initiative, a large, randomized, placebo-controlled trial of the risks and benefits of estrogen plus progestin in healthy postmenopausal women, was stopped prematurely at a mean follow-up of 5.2 years (±1.3) because of the detection of a 1.26-fold increased risk of breast cancer (95% confidence interval [CI], 1.00–1.59) in women receiving hormone replacement therapy. Tumors among women in the hormone replacement therapy group were slightly larger and more advanced than tumors among women in the placebo group, with a substantial and statistically significant rise in the percentage of abnormal mammograms at first annual screening; such a rise might hinder breast cancer diagnosis and account for the later stage at diagnosis.[3,4][Level of evidence: I] These results are supported by a population-based case-control study suggesting a 1.7-fold increased risk of breast cancer (95% CI, 1.3–2.2) in women using combined hormone replacement therapy. The risk of invasive lobular carcinoma was increased 2.7-fold (95% CI, 1.7–4.3), the risk of invasive ductal carcinoma was increased 1.5-fold (95% CI, 1.1–2.0), and the risk of estrogen receptor–positive/progesterone receptor–positive breast cancer was increased 2.0-fold (95% CI, 1.5–2.7). The increased risk was highest for invasive lobular tumors and in women who used hormone replacement therapy for longer periods. The risk was not increased with unopposed estrogen therapy.[5]

The very limited data available do not indicate an increased risk of breast cancer recurrence with single-agent estrogen use in patients with a history of breast cancer.[6,7] A series of double-blind, placebo-controlled trials suggested that low-dose megestrol acetate is a promising agent for hot flash management in this population.[8][Level of evidence: I];[9][Level of evidence: II] Limited data suggest that brief cycles of intramuscular depot medroxyprogesterone acetate also play a role in the management of hot flashes.[10][Level of evidence: I] The risk associated with progestin use is unknown.[2]

Examples of hormone-based pharmacological treatments for vasomotor symptoms are summarized in Table 1.

Other Pharmacological Interventions

Numerous nonestrogenic, pharmacological treatment interventions for hot flash management in women with a history of breast cancer and in some men who have undergone androgen deprivation therapy have been evaluated. Options with reported efficacy include the following: [15–17][Level of evidence: I]

Inferior efficacy, lack of large definitive studies, and potential side effects limit the use of many of these agents.

Agents that have been found to be helpful in large, randomized, placebo-controlled clinical trials include the following: [15–17]

Agents that confer a 55% to 60% reduction in hot flashes are venlafaxine extended release, [18] paroxetine controlled release [19,20][Level of evidence: I] or immediate release, [21] gabapentin, [22–25][Level of evidence: I][26][Level of evidence: II] and pregabalin.[27][Level of evidence: I] Other effective agents resulting in a reduction in hot flashes of approximately 50% include citalopram [28][Level of evidence: I] and fluoxetine.[29][Level of evidence: I] Clonidine, transdermal [30] or oral, [31][Level of evidence: I] can reduce hot flashes by approximately 40%.

One study compared the efficacy and patient preference of venlafaxine, 75 mg once daily, to gabapentin, 300 mg 3 times per day, for the reduction of hot flashes. Sixty-six women with histories of breast cancer were randomly assigned in an open-label fashion to receive venlafaxine or gabapentin for 4 weeks; after a 2-week washout period, they received the opposite treatment for an additional 4 weeks. Both treatments reduced hot flash scores (severity multiplied by frequency) by approximately 66%. However, significantly more women preferred venlafaxine to gabapentin (68% vs. 32%, respectively).[22]

A study using citalopram to evaluate hot flashes examined how much of a reduction in hot flashes was needed to have a positive impact on activities of daily living and general health-related quality of life.[32] The authors reported that hot flashes had to be reduced at least 46% for women to report significant improvements in the degree of bother they experienced in daily activities.

In a randomized study of paroxetine versus placebo in postmenopausal survivors of gynecological cancer, paroxetine significantly reduced the severity and frequency of hot flashes and nighttime awakening attributed to vasomotor symptoms, with improvement in sleep duration.[20][Level of evidence: I]

Agents that have been evaluated in phase II trials but have not shown efficacy include bupropion,[33] aprepitant,[34] and desipramine.[35][Level of evidence: II] Interestingly, these agents do not primarily modulate serotonin. In addition, randomized clinical trials with sertraline have not provided convincing evidence of its efficacy in hot flash management.[36–38][Level of evidence: I]

Examples of nonhormonal pharmacological treatments for vasomotor symptoms are summarized in Table 2.

If nighttime hot flashes or night sweats are a particular problem without causing much bother during daytime, strategies to simultaneously improve sleep and hot flashes are in order. Limited data exist related to effective treatments that can target both symptoms. One pilot trial evaluated mirtazapine (a tetracyclic antidepressant that mainly affects serotonin) for hot flashes because it is often prescribed for sleep difficulties. Twenty-two women were titrated up to 30 mg per day of mirtazapine at bedtime over a 3-week period; then they could choose 15 mg or 30 mg at bedtime daily for the fourth week. Hot flashes were reduced by approximately 53% in this nonrandomized trial, and women were statistically significantly satisfied with their hot flash control.[44] However, only 16 of the 22 women stayed on the agent for the entire study period because of excessive grogginess. Although this agent could be further studied in a larger randomized trial, it would be particularly important to evaluate the risk/benefit ratio.

In the short term, side effects for antidepressant agents in the doses used to treat hot flashes are minimal and primarily include:

In the long term, the prevalence of decreased sexual function with the use of SSRIs at doses for treating hot flashes is not known. The anticonvulsants gabapentin and pregabalin can cause sedation, dizziness, and difficulty concentrating, while clonidine can cause dry mouth, sedation, constipation, and insomnia.[25,27,46][Level of evidence: I] Patients respond as individuals to both the efficacy and the toxicity of various medications. Therefore, careful assessment and tailored treatment chosen collaboratively by the provider and patient are needed.

Data indicate that if a medication does not help an individual, switching to another medication—whether a different antidepressant or gabapentin—may be worthwhile. In a randomized phase III trial (NCCTG-N03C5) of gabapentin alone versus gabapentin with an antidepressant in women who had inadequate control of their hot flashes with an antidepressant alone,[47][Level of evidence: I] gabapentin use resulted in an approximately 50% median reduction in hot flash frequency and score, regardless of whether the antidepressant was continued. In other words, for women who were using antidepressants exclusively for the management of hot flashes that were inadequately controlled, initiation of gabapentin with discontinuation of the antidepressant produced results equal to those obtained with combined therapy, resulting in the need for fewer medications. Similarly, in a pilot study of women receiving inadequate benefit from venlafaxine for hot flash reduction, switching to open-label citalopram, 20 mg per day, resulted in a 50% reduction in hot flash frequency and score.[48]

Drug Interactions

Many SSRIs can inhibit the cytochrome P450 enzymes involved in the metabolism of tamoxifen, which is commonly used in the treatment of breast cancer. When SSRIs are being used, drug-drug interactions are noted. Tamoxifen is metabolized by the cytochrome P450 enzyme system, specifically CYP2D6. Wild-type CYP2D6 metabolizes tamoxifen to an active metabolite, 4-hydroxy-N-desmethyl-tamoxifen, also known as endoxifen. A prospective trial evaluating the effects of the coadministration of tamoxifen and paroxetine, a CYP2D6 inhibitor, on tamoxifen metabolism, found that paroxetine coadministration resulted in decreased concentrations of endoxifen. The magnitude of decrease was greater in women with the wild-type CYP2D6 genotype than in those with a variant genotype (P = .03).[49][Level of evidence: II]

In a prospective observational study of 80 women initiating adjuvant tamoxifen therapy for newly diagnosed breast cancer, variant CYP2D6 genotypes and concomitant use of SSRI CYP2D6 inhibitors resulted in reduced endoxifen levels. Variant CYP2D6 genotypes do not produce functional CYP2D6 enzymes.[50][Level of evidence: II] Since this study was published, several researchers have evaluated the clinical implications of this finding.[51];[52–54][Level of evidence: II] One study followed more than 1,300 women for a median of 6.3 years and concluded that women who were poor metabolizers or heterozygous extensive/intermediate metabolizers (hence, less CYP2D6 activity) had higher rates of recurrence, worse event-free survival, and worse disease-free survival than did women who were extensive metabolizers.[53] Similarly, authors of a retrospective cohort study of more than 2,400 women in Ontario, Canada, who were being treated with tamoxifen and had overlapping treatment with an SSRI concluded that women who concomitantly used paroxetine and tamoxifen had an increased risk of death that was proportionate to the amount of time they used these agents together.[54][Level of evidence: II]

The clinical implications of these changes and of other CYP2D6 genotypes [55] have not yet been elucidated, but the pharmacokinetic interaction between tamoxifen and the newer antidepressants used to treat hot flashes merits further study.[56] Likewise, the risk of soy phytoestrogen use on breast cancer recurrence and/or progression has not yet been clarified. Soy phytoestrogens are weak estrogens found in plant foods. In vitro models suggest that these compounds have a biphasic effect on mammary cell proliferation that is dependent on intracellular concentrations of phytoestrogen and estradiol.[57]

Information Specific to Men

Data are scant regarding the pathophysiology and management of hot flashes in men with prostate cancer. The rate of hot flashes in men receiving androgen deprivation therapy is approximately 75%.[58] The limited data suggest that hot flashes in men are related to changes in sex hormone levels that cause instability in the hypothalamic thermoregulatory center. This is analogous to the proposed mechanism of hot flashes that occur in women. As in women with breast cancer, hot flashes impair the quality of life for men with prostate cancer who are receiving androgen deprivation therapy. The vasodilatory neuropeptide, calcitonin gene–related peptide, may be instrumental in the genesis of hot flashes.[58]

In a prespecified secondary analysis of a prostate cancer clinical trial, 93% of men receiving 12 months of androgen deprivation therapy experienced hot flashes. The hot flashes occurred at castrate levels of testosterone, and cessation of hot flashes preceded full recovery of testosterone in most men, with 99% of men reporting resolution of hot flashes.[59][Level of evidence: I]

Cognitive behavioral therapy (CBT) has been studied for the treatment of hot flashes in men undergoing androgen deprivation therapy for prostate cancer.[60][Level of evidence: I] Patients were randomly assigned to a guided self-help CBT regimen that included a booklet and CD with relaxation and breathing exercises, or to treatment as usual. At 6 weeks, those assigned to CBT experienced a statistically significant 40% reduction in hot flash/night sweat symptoms versus a 12% reduction in patients who received treatment as usual. Symptom reduction continued but was not statistically significant at 32 weeks. Adherence to CBT was good, with 88% reading all or more than half of the booklet and 79% using the relaxation CD.

With the exception of clonidine, the agents mentioned previously were effective in treating hot flashes in women have shown similar efficacy rates in men. For more information, see the Other Pharmacological Interventions section.Treatment modalities for men have included the following:[61]

One large, multisite study from France [62] randomly assigned men who were taking leuprorelin for prostate cancer to receive venlafaxine, 75 mg; cyproterone acetate (an antiandrogen), 100 mg; or medroxyprogesterone acetate, 20 mg, when they reported at least 14 hot flashes per week. All three treatments significantly reduced hot flashes, with cyproterone acetate resulting in a 100% median reduction, medroxyprogesterone resulting in a 97% reduction, and venlafaxine resulting in a 57% reduction at 8 weeks. More adverse events were reported with cyproterone acetate, including one serious adverse event (dyspnea) attributable to the drug. Venlafaxine was not associated with any serious adverse events and overall had a 20% adverse event rate. Medroxyprogesterone was the best-tolerated drug, with an adverse event rate of 12%, but with one serious event, urticaria. The most frequent side effects for all agents were gastrointestinal issues: nausea, constipation, diarrhea, and abdominal pain.[62]

On the basis of its efficacy in women, the combination of venlafaxine and soy was studied in hot flash reduction in androgen-deprived men.[63][Level of evidence: I] Patients were randomly assigned to receive venlafaxine with soy protein, venlafaxine with milk protein placebo, soy protein with placebo, or dual placebos during a 12-week period. The number and severity of hot flashes fell for all arms during the study period, but there was no significant difference between arms. The authors concluded that neither agent should be used to treat hot flashes in men, that there is a significant placebo effect in the study of hot flash treatment, and that agents demonstrating success for hot flashes in women may not be successful in men.

A small, multicenter, retrospective review evaluated the use of two doses of intramuscular medroxyprogesterone acetate (400 mg and 150 mg) as a single dose to treat and prevent hot flashes associated with luteinizing hormone-releasing hormone agonist therapy for prostate cancer.[14][Level of evidence: III] Of the 48 men studied, 91% experienced symptomatic improvement in hot flashes, and 46% experienced complete resolution of hot flashes. The trial was not powered to detect a difference between the two doses; however, the authors concluded that they would now use the 400-mg dose.

Pilot studies of the efficacy of the SSRIs paroxetine and fluvoxamine suggest that these drugs decrease the frequency and severity of hot flashes in men with prostate cancer.[64,65] As in women with hormonally sensitive tumors, there are concerns about the effects of hormone use on the outcome of prostate cancer, in addition to other well-described side effects.[58]

Cognitive and Behavioral Methods

Comprehensive nonpharmacological interventions have been developed and evaluated for their ability to reduce hot flashes, night sweats, and the related perception of burden or problems. These interventions have typically included the following:[66–69]

Behavioral interventions as a primary or adjunctive modality may also play a role in hot flash management. Core body temperature has been shown to increase before a hot flash;[70] therefore, interventions that control body temperature could improve hot flash management. Some methods of controlling body temperature include the use of the following:

Since serotonin may be involved as a central hot flash trigger, behavioral interventions such as stress management may modulate serotonin, causing a decrease in hot flashes.

Relaxation training and paced breathing were initially found to decrease hot flash intensity by as much as 40% to 50% in controlled pilot trials;[71,72] however, randomized trials with control arms using a different pace of breathing have not demonstrated significant benefit for paced-breathing interventions.[73,74]

Three large studies [67–69] of similar interventions have been completed using no treatment, usual care, or wait-list control comparison groups. While all of the studies demonstrated significant reductions in problem ratings or bother ratings related to hot flashes and night sweats, none showed actual reductions in hot flash frequency. Only one of the three studies demonstrated some significant improvements in night sweats at some data points.[68] Similar results were seen in a large trial of Internet-based CBT with and without therapist support.[75][Level of evidence: I] Cognitive behavioral interventions may be an important addition to pharmacological treatment to improve a patient’s overall experience with symptoms related to hot flashes. However, data have not supported the sole use of CBT for reducing hot flashes.

Medical hypnosis is a newer intervention for hot flashes that has been shown to be helpful. In medical hypnosis, the provider facilitates a deep relaxation and trance state in the patient and gives suggestions to the subconscious to mitigate the symptom or problem being addressed. For hot flashes, medical hypnosis uses cooling suggestions and stress reduction to prevent rises in core body temperature and to decrease sympathetic activation. On the basis of strong pilot data, a randomized controlled trial of 187 postmenopausal women used an attention-control comparison and demonstrated significantly greater reductions in hot flashes in the hypnosis group than in the control group. The hypnosis intervention was 5 weeks long. At week 6, hot flash frequency was reduced in the hypnosis group by 64%, compared with a 9% reduction in the control group. At week 12, the reduction in the hypnosis group was 75%, compared with a 17% reduction in the control group.[76] Cancer survivors were not included in this study, but previous research has not demonstrated that interventions have a differential effect on hot flashes on the basis of breast cancer history.

Future research on hot flash management may be aided by the development of psychometrically sound assessment tools such as the Hot Flash Related Daily Interference Scale, which evaluates the impact of hot flashes on a wide variety of daily activities.[77]

Integrative Approaches

Current Clinical Trials

Use our advanced clinical trial search to find NCI-supported cancer clinical trials that are now enrolling patients. The search can be narrowed by location of the trial, type of treatment, name of the drug, and other criteria. General information about clinical trials is also available.

Purpose of This Summary

This PDQ cancer information summary for health professionals provides comprehensive, peer-reviewed, evidence-based information about the pathophysiology and treatment of hot flashes and night sweats. It is intended as a resource to inform and assist clinicians in the care of their patients. It does not provide formal guidelines or recommendations for making health care decisions.

Reviewers and Updates

This summary is reviewed regularly and updated as necessary by the PDQ Supportive and Palliative Care Editorial Board, which is editorially independent of the National Cancer Institute (NCI). The summary reflects an independent review of the literature and does not represent a policy statement of NCI or the National Institutes of Health (NIH).

Board members review recently published articles each month to determine whether an article should:

Changes to the summaries are made through a consensus process in which Board members evaluate the strength of the evidence in the published articles and determine how the article should be included in the summary.

The lead reviewers for Hot Flashes and Night Sweats are:

Any comments or questions about the summary content should be submitted to Cancer.gov through the NCI website’s Email Us. Do not contact the individual Board Members with questions or comments about the summaries. Board members will not respond to individual inquiries.

Levels of Evidence

Some of the reference citations in this summary are accompanied by a level-of-evidence designation. These designations are intended to help readers assess the strength of the evidence supporting the use of specific interventions or approaches. The PDQ Supportive and Palliative Care Editorial Board uses a formal evidence ranking system in developing its level-of-evidence designations.

Permission to Use This Summary

PDQ is a registered trademark. Although the content of PDQ documents can be used freely as text, it cannot be identified as an NCI PDQ cancer information summary unless it is presented in its entirety and is regularly updated. However, an author would be permitted to write a sentence such as “NCI’s PDQ cancer information summary about breast cancer prevention states the risks succinctly: [include excerpt from the summary].”

The preferred citation for this PDQ summary is:

PDQ® Supportive and Palliative Care Editorial Board. PDQ Hot Flashes and Night Sweats. Bethesda, MD: National Cancer Institute. Updated <MM/DD/YYYY>. Available at: /side-effects/hot-flashes-hp-pdq. Accessed <MM/DD/YYYY>. [PMID: 26389188]

Images in this summary are used with permission of the author(s), artist, and/or publisher for use within the PDQ summaries only. Permission to use images outside the context of PDQ information must be obtained from the owner(s) and cannot be granted by the National Cancer Institute. Information about using the illustrations in this summary, along with many other cancer-related images, is available in Visuals Online, a collection of over 2,000 scientific images.

Disclaimer

The information in these summaries should not be used as a basis for insurance reimbursement determinations. More information on insurance coverage is available on Cancer.gov on the Managing Cancer Care page.

Contact Us

More information about contacting us or receiving help with the Cancer.gov website can be found on our Contact Us for Help page. Questions can also be submitted to Cancer.gov through the website’s Email Us.

Nonpharmacological Management of Sleep Disturbances

Many people who experience insomnia have poor sleep hygiene (such as smoking and drinking excessive alcohol just before bedtime), which can exacerbate or perpetuate insomnia.[1][Level of evidence: III] A complete assessment of sleep hygiene (i.e., time in bed; napping during the day; intake of caffeine, alcohol, or foods that are heavy, spicy, or sugary; exercise; and sleep environment) and use of behavioral management strategies (i.e., fixed bedtime; restrictions on smoking, diet, and excessive alcohol 4–6 hours before bedtime; and increased exercise) may prove effective in reducing sleep disturbances.

Sleep hygiene in an inpatient setting involves modifying the sleep environment to decrease sleep disruption. Minimizing noise, dimming or turning off lights, adjusting room temperature, and consolidating patient care tasks to reduce the number of interruptions can increase the amount of uninterrupted sleep.[2][Level of evidence: IV]

Cognitive strategies include:[3]

Behavioral strategies include:

Both of these strategies seek to limit the time spent in bed that does not involve sleeping.[3–5] Several large randomized trials and meta-analyses provide the evidence base for the efficacy of cognitive behavioral therapy (CBT) for insomnia (CBT-I).[3,6,7] Most of these trials have been in populations of patients without cancer.

Components of CBT-I include the following:

Relaxation therapy can be used to achieve both behavioral and cognitive outcomes, particularly when it is combined with imagery. Educational objectives around sleep hygiene are also used to treat insomnia and include content on the following:[4]

Practice guidelines from the American Academy of Sleep Medicine clearly state that multicomponent therapy is recommended over single therapies. Because of insufficient evidence about its efficacy, sleep hygiene education is not recommended as a single-modality management approach; other reviews state that sleep hygiene by itself is not effective.[6,8] Information about sleep hygiene should be included in patient education about sleep issues.

Several trials and meta-analyses have shown CBT-I to be at least as effective as conventional pharmacological therapies in treating primary chronic insomnia but without side effects.[6,7,9–11]

A four-arm study (conducted in patients with primary chronic insomnia) that evaluated zolpidem versus CBT versus zolpidem and CBT versus placebo reported a greater effect (P = .05) on sleep-onset latency for both groups involving CBT (change of 44%) versus the group receiving zolpidem alone (change of 29%).[12] Another study, also conducted in patients with primary chronic insomnia, evaluated CBT with temazepam alone versus a combination of CBT and temazepam versus placebo and found that all active treatments were significantly better than placebo and that there was a trend for the most improvement in the combined arm of CBT and temazepam.[13] Both arms with CBT demonstrated greater reductions in time to sleep onset than the pharmacotherapy-alone arm (64% in the combined arm, 55% in the CBT arm, and 47% in the temazepam arm). A meta-analysis examining pharmacological and behavioral studies for persistent insomnia found that pharmacological and behavioral treatments did not differ in magnitude of benefit except for latency to sleep onset, in which greater reductions were found with behavioral therapy.[7]

There are limited data evaluating elements of CBT-I in cancer survivors, and most data are about women with breast cancer. However, there have been at least four randomized controlled trials of CBT-I in cancer survivors.[14–17] The intervention was typically delivered over five to eight weekly, small-group, in-person sessions. One trial included patients with cancer diagnoses other than breast cancer,[16] and results did not differ by cancer diagnosis. All studies showed improvements in numerous sleep parameters over time in the groups receiving CBT-I and demonstrated continued benefits 6 and 12 months later. Two of the four trials did not use active control arms.[14,16]

Most studies using active control arms were in breast cancer survivors. One study compared CBT-I with sleep education and hygiene in 72 women,[15] while the other study used a healthy-eating education control group.[17] In the first study, both groups significantly improved over time, with some significant differences between groups favoring CBT-I for time to fall asleep, time awake after sleep, total sleep time, and overall sleep quality. For example, the group receiving CBT-I improved by 30 minutes in time to fall asleep, compared with 11 minutes in the sleep education and hygiene group.[15]

In the second study, 219 women were randomly assigned to a behavioral therapy group consisting of stimulus control, general sleep hygiene (limiting naps, going to bed and rising at consistent times), and relaxation or to a healthy-eating education control group. The interventions were delivered by trained nurses in person, 2 days before the initiation of chemotherapy, before each chemotherapy treatment, and 30 days after the last chemotherapy treatment. The nurses worked with women assigned to behavioral therapy to individualize and reinforce the behaviors. The Pittsburgh Sleep Quality Index (PSQI) was used to measure subjective sleep quality, complemented by use of a sleep diary and wrist actigraph. Sleep quality significantly improved in the group receiving behavioral therapy, compared with the control group. These differences were also seen in data from the sleep diary and actigraph, with both showing significantly fewer awakenings in the behavioral therapy group.[18] Sleep quality was significantly better at 90 days and at 1 year in the behavioral therapy group, as measured by the PSQI but not the diary or actigraph.[17]

In some places, patients may not have access to in-person, professionally delivered CBT-I. A randomized controlled trial conducted with breast cancer survivors demonstrated that CBT-I delivered via digital media can also produce meaningful clinical improvements, although improvements are not as robust as those produced with professionally delivered CBT-I. This three-armed trial compared video-based CBT-I (VCBT-I) and professionally delivered CBT-I (PCBT-I) with a no-treatment control group in 242 breast cancer survivors. Both the VCBT-I and PCBT-I groups had significantly greater improvements in diary-measured sleep variables, compared with the control group. The patients in the PCBT-I group reported greater improvements in some sleep outcomes and in fatigue and depression levels than did the VCBT-I group.[19]

Pharmacological Management of Sleep-Wake Cycle Disturbances

When cancer survivors experience sleep-wake disturbances, cognitive behavioral intervention counseling should be the first consideration for management. For more information, see the Nonpharmacological Management of Sleep Disturbances section. Resources for education and training in CBT may not be readily available in many cancer centers; therefore, community resources need to be investigated. If CBT is not available or has not been successful, pharmacological management can be considered. In addition, when patients have comorbidities contributing to sleep-wake cycle disturbances (such as hot flashes, uncontrolled pain, anxiety, depression, or other mood disturbances),[26,27] then pharmacological management will probably be necessary. While many pharmacological agents are approved for primary insomnia and many others are used off-label to manage sleep and related symptoms, most of the approved sleep aids have not been studied in cancer populations; therefore, the risk/benefit profiles of these drugs are not delineated in this setting.

Despite the lack of evidence in cancer populations, clinicians widely use pharmacological interventions. Therefore, the following discussion of pharmacological agents and recommendations for use is based on evidence from studies conducted in patients with primary insomnia and clinical experience.[4,28,29]

Several classes of medications are used to treat sleep-wake cycle disturbances, including the following:

Drug characteristics to consider before a drug is chosen to treat an individual patient include the following:

These pharmacokinetic principles are important to match the agent to the type of sleep disturbance (e.g., problems falling asleep versus problems staying asleep). There are also safety issues to be considered, such as potentials for tolerance, abuse, dependence, withdrawal (including risk of rebound insomnia), and drug-drug and drug-disease interactions. Medications for sleep-wake cycle disturbances should be used short term and/or as needed.

Current Clinical Trials

Use our advanced clinical trial search to find NCI-supported cancer clinical trials that are now enrolling patients. The search can be narrowed by location of the trial, type of treatment, name of the drug, and other criteria. General information about clinical trials is also available.

The Patient With Pain

Since enhanced pain control improves sleep, appropriate analgesics or nonpharmacological pain management should be administered before introducing sleep medications. Tricyclic antidepressants can be particularly useful for the treatment of insomnia in patients with neuropathic pain and depression. Patients on high-dose opioids for pain may be at increased risk for the development of delirium and organic mental disorders. Such patients may benefit from the use of low-dose neuroleptics as sleep agents (e.g., haloperidol 0.5–1 mg).

The Older Patient

Older patients frequently have insomnia due to age-related changes in sleep. The sleep cycle in this population is characterized by lighter sleep, more frequent awakenings, and less total sleep time. Anxiety, depression, loss of social support, and a diagnosis of cancer are contributory factors in sleep disturbances in older patients.[1]

Sleep problems in older adults are so common that nearly one-half of all hypnotic prescriptions written are for people older than 65 years. Although normal aging affects sleep, the clinician should evaluate the many factors that cause insomnia, such as:[2]

Nonpharmacological treatment of sleep disorders is the preferred initial management, with the use of medication when indicated and referral to a sleep disorder center when specialized care is necessary.[2]

Providing a regular schedule of meals, discouraging daytime naps, and encouraging physical activity may improve sleep. Hypnotic prescriptions for older patients must be adjusted for variations in metabolism, increased fat stores, and increased sensitivity. Dosages should be reduced by 30% to 50%. Problems associated with drug accumulation (especially flurazepam) must be weighed against the risks of more severe withdrawal or rebound effects associated with short-acting benzodiazepines. An alternate drug for older patients is chloral hydrate.[1]

Sleep Apnea After Mandibulectomy

Anterior mandibulectomy can result in the development of sleep apnea. All patients with head and neck tumors who have had extensive anterior oral cavity resection should be evaluated before decannulation of the tracheostomy tube. Subsequent flap and/or reconstruction of the lower jaw seems to prevent the development of sleep apnea. In contrast, facial sling suspension of the lower lip does not prevent the development of sleep apnea.[3] Assessment for symptoms and preparation for the appearance of symptoms in this population provide indications for interventions related to sleep apnea.

Purpose of This Summary

This PDQ cancer information summary for health professionals provides comprehensive, peer-reviewed, evidence-based information about the pathophysiology and treatment of sleep disorders. It is intended as a resource to inform and assist clinicians in the care of their patients. It does not provide formal guidelines or recommendations for making health care decisions.

Reviewers and Updates

This summary is reviewed regularly and updated as necessary by the PDQ Supportive and Palliative Care Editorial Board, which is editorially independent of the National Cancer Institute (NCI). The summary reflects an independent review of the literature and does not represent a policy statement of NCI or the National Institutes of Health (NIH).

Board members review recently published articles each month to determine whether an article should:

Changes to the summaries are made through a consensus process in which Board members evaluate the strength of the evidence in the published articles and determine how the article should be included in the summary.

The lead reviewers for Sleep Disorders are:

Any comments or questions about the summary content should be submitted to Cancer.gov through the NCI website’s Email Us. Do not contact the individual Board Members with questions or comments about the summaries. Board members will not respond to individual inquiries.

Levels of Evidence

Some of the reference citations in this summary are accompanied by a level-of-evidence designation. These designations are intended to help readers assess the strength of the evidence supporting the use of specific interventions or approaches. The PDQ Supportive and Palliative Care Editorial Board uses a formal evidence ranking system in developing its level-of-evidence designations.

Permission to Use This Summary

PDQ is a registered trademark. Although the content of PDQ documents can be used freely as text, it cannot be identified as an NCI PDQ cancer information summary unless it is presented in its entirety and is regularly updated. However, an author would be permitted to write a sentence such as “NCI’s PDQ cancer information summary about breast cancer prevention states the risks succinctly: [include excerpt from the summary].”

The preferred citation for this PDQ summary is:

PDQ® Supportive and Palliative Care Editorial Board. PDQ Sleep Disorders. Bethesda, MD: National Cancer Institute. Updated <MM/DD/YYYY>. Available at: /side-effects/sleep-disorders-hp-pdq. Accessed <MM/DD/YYYY>. [PMID: 26389467]

Images in this summary are used with permission of the author(s), artist, and/or publisher for use within the PDQ summaries only. Permission to use images outside the context of PDQ information must be obtained from the owner(s) and cannot be granted by the National Cancer Institute. Information about using the illustrations in this summary, along with many other cancer-related images, is available in Visuals Online, a collection of over 2,000 scientific images.

Disclaimer

The information in these summaries should not be used as a basis for insurance reimbursement determinations. More information on insurance coverage is available on Cancer.gov on the Managing Cancer Care page.

Contact Us

More information about contacting us or receiving help with the Cancer.gov website can be found on our Contact Us for Help page. Questions can also be submitted to Cancer.gov through the website’s Email Us.