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Fever, Sweats, and Hot Flashes

Normal human body temperature displays a circadian rhythm. Body temperature is lowest in the predawn hours, at 36.1°C (97°F) or lower, and rises to 37.4°C (99.3°F) or higher in the afternoon. Normal body temperature is maintained by thermoregulatory mechanisms that balance heat loss with heat production.[1,2,3]

Abnormal elevations of temperature result from either hyperthermia or pyrexia (fever). Hyperthermia results from failure of thermal control mechanisms. In fever, thermoregulatory mechanisms are intact, but the hypothalamic set-point is elevated above normal by exogenous or endogenous pyrogens. There are three phases to fever. In the initiation phase, cutaneous vasoconstriction promotes heat retention and shivering generates additional heat. When the new (elevated) set-point is reached, heat production balances heat loss and shivering stops. With lowering of the set-point to normal, cutaneous vasodilatation promotes heat loss to the environment in the form of sweating. These same mechanisms maintain normal core body temperature in afebrile individuals.[1,2,3,4]

Response to fever varies with age. In older people, inadequate thermoregulatory mechanisms may contribute to hyperthermia and result in arrhythmias, ischemia, mental status changes, or heart failure from increased metabolic demands. In children between the ages of 6 months and 6 years, febrile convulsions may occur.

The major causes of fever in cancer patients include infection, tumor (also known as paraneoplastic fever), drugs (allergic or hypersensitivity reactions), blood product transfusion, and graft-versus-host disease (GVHD).[2,3,4,5,6,7,8] Infection is a particularly important cause in the neutropenic host, given its high frequency (almost two-thirds of patients) and potentially fatal outcome. Whereas gram-negative infections predominated as the cause of neutropenic fever in cancer patients in the 1970s and early 1980s, gram-positive infections, mainly streptococci and coagulase staphylococci, have predominated since. The increased incidence of staphylococcal and streptococcal infections relates to the use of intravascular devices, severe mucositis due to high-dose chemotherapy, and prophylactic antibiotic therapy with fluoroquinolones. Although fluoroquinolone use has not decreased the morbidity or mortality of neutropenic fever, it has resulted in increased incidence of resistant gram-negative bacteremia.[9] Many consider paraneoplastic fever to be more common in primary tumors such as renal cell carcinomas and lymphomas, but available data suggest that it occurs in tumors of diverse primary sites.[2] Hypersensitivity reactions, pyrogen production, primary cytokine production and tumor necrosis with secondary cytokine production are among the postulated causes of tumor fever. Drug causes of fever include a variety of cytotoxic chemotherapy agents, biologic response modifiers, vancomycin, amphotericin, and multiple other medications. Tumor-associated fevers may be cyclic, occur at a specific time of the day, or be intermittent, alternating with afebrile periods lasting days or weeks.[3,4] Fever pattern does not differentiate drug-associated fever from other causes of fever, except when the temporal relationship is unambiguous. For many drugs, a highly variable lag time between the initiation of the offending agent and the onset of fever masks the causative relationship.[4,6,7,10]

Other etiologies of fever in the cancer patient include drug withdrawal (i.e., opioids, benzodiazepines), neuroleptic malignant syndrome (NMS), obstruction of a viscus (i.e., bladder, bowel, kidney), and tumor embolization. Comorbid medical conditions such as thrombosis, connective tissue disorders, and central nervous system bleeds or strokes may also produce fever.[4] The differential diagnosis of fever in the cancer patient is extensive, and differentiating infection from other causes may be difficult. From a palliative perspective, establishing a fever-specific diagnosis is important, as the specific diagnosis impacts management, comfort, and patient prognosis.

Assessment of fever requires careful history taking, medication review, and a physical examination that includes all major body systems. Individuals with suspected infection, especially those with neutropenic fever, should undergo meticulous evaluation of the skin, all body orifices (i.e., mouth, ears, nose, throat, urethra, vagina, rectum), finger stick and venipuncture sites, biopsy sites, and skin folds (i.e., breasts, axilla, groin). Oral assessment includes evaluation of the teeth, gingiva, tongue, floor of the mouth, nasopharynx, and sinuses. The perirectal area is a common source of infection, especially in individuals with leukemia. Vascular access devices (VAD) and other artificial indwelling devices (i.e., percutaneous nephrostomy tubes, biliary drainage tubes, gastrostomy or jejunostomy tubes) are other commonly implicated sources of infection. Urine, sputum, and blood cultures (peripheral and from ports or lumens of VADs) and radiographic imaging with chest radiography as directed by these findings complete the initial evaluation. Individuals undergoing cytotoxic chemotherapy should be instructed to seek immediate medical attention if they develop fever when neutrophil counts are low or declining. Frequent reassessment, including physical examination, is especially important in the neutropenic host, as signs and symptoms of infection may be minimal. Evaluation for recurrent or progressive tumor can be performed at the same time as evaluation for potential infection and other causes of fever.[3]

The presence of fever is associated with the potential metabolic consequences of dehydration and increased metabolic demand. Effects may be especially pronounced in debilitated cancer patients and include uncomfortable constitutional symptoms such as fatigue, myalgias, diaphoresis, and chills. Potential interventions for fever management include primary interventions directed at the underlying cause, hydration with parenteral fluids or by hypodermoclysis, nutritional support, and nonspecific palliative measures. The specific interventions utilized are determined by the patient's location in the disease trajectory and patient-determined goals of care. Some patients near the end of life may decide not to treat the underlying cause. For example, patients with advanced cancer may decline treatment of pneumonia or other infections but still seek nonspecific palliative measures and hydration to optimize quality of life. Alternatively, others may elect antibiotic therapy for the palliation of symptoms such as cough, fever, dyspnea, or abscess pain. (Refer to the Nonspecific Interventions for Palliation of Fever section of this summary for more information.)

Primary Interventions

Infection-associated fever

Effective antibiotic treatment results in palliation of fever-associated constitutional symptoms, as well as palliation of site-specific symptoms such as cough secondary to pneumonia or localized pain due to abscess formation. For febrile neutropenic patients (granulocyte count <500), immediate initiation of broad-spectrum antibiotic treatment is imperative, as the mortality rate is 70% for patients not receiving antibiotics within 48 hours. For the purposes of neutropenia, fever is defined as a single temperature elevation above 38.5°C or three elevations above 38°C in a 24-hour period.[4]

Since the cause of neutropenic fever is not documented in 50% to 70% of patients, antibiotic use is guided by knowledge of the treating institution's antimicrobial spectrum and antibiotic resistance pattern, as well as the suspected cause. There is no consensus on the particular antibiotic or combination of antibiotics to be used, but empiric antibiotic therapy generally falls into one of four protocols:

1. Aminoglycoside plus antipseudomonal beta-lactam.
2. Combination of two beta-lactams.
3. Vancomycin plus aminoglycoside and antipseudomonal beta-lactam.
4. Monotherapy.

When multiple-lumen catheters are present, antibiotic therapy should be rotated through each lumen. Bacteriostatic antibiotics (i.e., tetracycline, erythromycin, chloramphenicol) are not beneficial in the absence of granulocytes, which, when given concomitantly, reduce the efficacy of the bactericidal antibiotics.[4,11]

Treatment regimens are further modified by the duration of fever and individual patient risk factors such as the presence of central lines or other artificial devices, history of steroid use, and history of injection drug use. Various investigators have developed models predicting risk groups of febrile neutropenia, with implications for management strategies. Therapeutic options under evaluation include early hospital discharge, home intravenous antibiotic therapy, and oral antibiotic regimens. A subset of these studies focus on the pediatric population. Because of rapid changes in the field, the reader is directed to specialized sources for specific management recommendations of febrile neutropenia.[12,13,14]

After a specific pathogen is isolated, antibiotic therapy is modified to provide optimal therapeutic response with minimal toxicity. Broad-spectrum coverage must be maintained to prevent secondary bacterial and fungal infections. Antibiotic therapy is usually discontinued after 5 to 7 days provided that the patient's granulocyte count exceeds 500 and the patient remains free of fever and infection. There is no consensus as to appropriate management in cases of persistent granulocytopenia when the patient is afebrile. Some advocate continued therapy, whereas others favor discontinuing antibiotics once the patient stabilizes. Empirical antifungal therapy is often added if a neutropenic patient remains febrile after 1 week of broad-spectrum antibiotics or has recurrent fever, since continued granulocytopenia is usually associated with the development of nonbacterial opportunistic infections, particularly those caused by Candida and Aspergillus. Prolonged therapy (>10–14 days) is indicated in the patient with a residual focus of bacterial or mycotic infection. Amphotericin B is usually the agent of choice. Alternative antifungal agents (5-fluorocytosine, miconazole, fluconazole, or itraconazole) are indicated when organisms develop resistance to amphotericin B.

Acyclovir is the drug of choice in the treatment of herpes simplex or varicella zoster viral infection. Ganciclovir has activity against cytomegalovirus. Both agents can be used prophylactically in the management of patients at high risk for these infections. Foscarnet is useful in the treatment of cytomegalovirus and acyclovir-resistant herpes simplex virus.

Paraneoplastic fever

When available, the best management of tumor-associated fevers is treatment of the underlying neoplasm with definitive antineoplastic therapies. In the absence of effective antineoplastic therapy, nonsteroidal anti-inflammatory drugs (NSAIDs) are a mainstay of treatment. Naproxen may preferentially control paraneoplastic fever relative to other NSAIDs or acetaminophen. Response to naproxen has been considered diagnostic of tumor fever; however, efficacy of naproxen and other NSAIDs for infection-related fever is a common clinical observation. Release of tumor fever may respond to treatment with a structurally different NSAID.

Drug-associated fever

The occurrence of fever is predictable for some drugs, such as biologic response modifiers, amphotericin B, and bleomycin. For many other drugs, drug fever is a diagnosis of exclusion. Drug-associated fever responds to cessation of the offending agent, when possible. Fever and related symptoms with biologic response modifier administration is type-, route-, dose-, and schedule-dependent. These factors may sometimes be altered for fever control without sacrificing efficacy. Fever may also be attenuated by the use of acetaminophen, nonsteroidal anti-inflammatory, and steroid premedication. The same may be true for fever associated with some cytotoxic agents and antimicrobials (i.e., amphotericin).[6,7,10] It is common clinical practice to administer meperidine to attenuate severe chills associated with a febrile reaction, although empirical data confirming its efficacy are not available.

Neuroleptic malignant syndrome

Neuroleptic malignant syndrome (NMS) is a rare but potentially fatal syndrome that may develop during treatment with neuroleptic drugs for conditions such as psychotic disorders, delirium, nausea, and vomiting. It is marked by fever, rigidity, confusion, and autonomic instability, as well as by elevations in white blood cell count, creatinine phosphokinase, and urine myoglobin. NMS should be considered in the differential diagnosis of the delirious patient receiving neuroleptic agents who develops rigidity and whose condition does not improve on neuroleptics (e.g., haloperidol). Treatment of NMS includes discontinuation of neuroleptic agents, supportive measures, and occasionally, administration of bromocriptine or dantrolene. (Refer to the PDQ summary on Delirium for more information.)

Blood product–associated fever

Suspected febrile reactions can be minimized by the use of leukocyte-depleted or irradiated blood products, when clinically appropriate. Common clinical practice includes premedication with acetaminophen and diphenhydramine.[8]

Nonspecific Interventions for Palliation of Fever

Along with treatment of the underlying cause, comfort measures are helpful in alleviating the distress that accompanies fever, chills, and sweats. During febrile episodes, increasing a patient's fluid intake, removing excess clothing and linens, and tepid water bathing/sponging may provide relief. Results of a pediatric randomized placebo-controlled trial of sponging with ice water, isopropyl alcohol, or tepid water, with or without acetaminophen, demonstrated that all combinations enhanced fever control. Comfort was greatest in children receiving a placebo or sponging, followed by those who received acetaminophen combined with tepid-water sponging. Sponging with either ice water or isopropyl alcohol, with or without acetaminophen, resulted in the greatest discomfort.[15] During periods of chills, replacing wet blankets with warm, dry blankets, keeping patients out of drafts, and adjusting ambient room temperature may also improve patient comfort.

Symptomatic relief of persistent or intermittent fevers can be aided by the use of NSAIDs (e.g., naproxen) or acetaminophen.[15] Aspirin may also be effective in reducing fever but should be used with caution in patients with Hodgkin lymphoma and cancer patients at risk for thrombocytopenia. Because of the associated risk of Reye syndrome, aspirin is not recommended in patients with fever.[4]

3. Young LS: Fever and septicemia. In: Rubin RH, Young LS, eds.: Clinical Approach to Infection in the Compromised Host. 2nd ed. New York, NY: Plenum Medical, 1988, pp 75-114.
4. Cleary JF: Fever and sweats: including the immunocompromised hosts. In: Berger A, Portenoy RK, Weissman DE, eds.: Principles and Practice of Supportive Oncology. Philadelphia, Pa: Lippincott-Raven Publishers, 1998, pp 119-131.
5. Knockaert DC, Vanneste LJ, Vanneste SB, et al.: Fever of unknown origin in the 1980s. An update of the diagnostic spectrum. Arch Intern Med 152 (1): 51-5, 1992.
6. Mackowiak PA, LeMaistre CF: Drug fever: a critical appraisal of conventional concepts. An analysis of 51 episodes in two Dallas hospitals and 97 episodes reported in the English literature. Ann Intern Med 106 (5): 728-33, 1987.
7. Mackowiak PA: Drug fever. In: Machowiak PA, ed.: Fever: Basic Mechanisms and Management. New York, NY: Raven Press, 1991, pp 255-265.
8. Huh YO, Lichtiger B: Transfusion reactions in patients with cancer. Am J Clin Pathol 87 (2): 253-7, 1987.
9. Marchetti O, Calandra T: Infections in neutropenic cancer patients. Lancet 359 (9308): 723-5, 2002.
10. Quesada JR, Talpaz M, Rios A, et al.: Clinical toxicity of interferons in cancer patients: a review. J Clin Oncol 4 (2): 234-43, 1986.
11. Pizzo PA: Management of fever in patients with cancer and treatment-induced neutropenia. N Engl J Med 328 (18): 1323-32, 1993.
12. Karthaus M, Carratalà J, Jürgens H, et al.: New strategies in the treatment of infectious complications in haematology and oncology: is there a role for out-patient antibiotic treatment of febrile neutropenia? Chemotherapy 44 (6): 427-35, 1998 Nov-Dec.
13. Klastersky J, Paesmans M, Rubenstein EB, et al.: The Multinational Association for Supportive Care in Cancer risk index: A multinational scoring system for identifying low-risk febrile neutropenic cancer patients. J Clin Oncol 18 (16): 3038-51, 2000.
14. Talcott JA, Siegel RD, Finberg R, et al.: Risk assessment in cancer patients with fever and neutropenia: a prospective, two-center validation of a prediction rule. J Clin Oncol 10 (2): 316-22, 1992.
15. Steele RW, Tanaka PT, Lara RP, et al.: Evaluation of sponging and of oral antipyretic therapy to reduce fever. J Pediatr 77 (5): 824-9, 1970.

Sweats and Hot Flashes

Sweats and hot flashes are common in cancer survivors, from those in the adjuvant setting to those living with advanced disease. Pathophysiologic mechanisms are complex. Treatment options are broad-based, including hormonal agents, nonhormonal pharmacotherapies, and diverse integrative medicine modalities.[1]

Physiologically, sweating mediates core body temperature by producing transdermal evaporative heat loss.[2,3] Sweating occurs in disease states such as fever and in nondisease states such as warm environments, exercise, and menopause. Limited data suggest that sweating occurs in 14% to 16% of advanced cancer patients receiving palliative care, with severity typically rated as moderate to severe.[4,5,6]

Sweating is part of the hot flash complex that characterizes the vasomotor instability of menopause. Hot flashes occur in approximately two-thirds of postmenopausal women with a breast cancer history and are associated with night sweats in 44%.[7,8] For most breast cancer and prostate cancer patients, hot flash intensity is moderate to severe. Distressing hot flashes appear to be less frequent in postmenopausal women with nonbreast cancer.

Sweats in the cancer patient may be associated with the tumor, its treatment, or unrelated (comorbid) conditions. Sweats are characteristic of certain primary tumor types such as Hodgkin lymphoma, pheochromocytoma, and functional neuroendocrine tumors (i.e., secretory carcinoids). Other causes include fever, menopause, castration (male), drugs, hypothalamic disturbances, and primary disorders of sweating. Causes of menopause include natural menopause, surgical menopause, or chemical menopause, which in the cancer patient may be caused by cytotoxic chemotherapy, radiation, or androgen treatment. Causes of "male menopause" include orchiectomy, gonadotropin-releasing hormone use, or estrogen use. Drug-associated causes of sweats include tamoxifen, aromatase inhibitors, opioids, tricyclic antidepressants, and steroids. Women who are extensive metabolizers of tamoxifen related to CYP2D6 may have more severe hot flashes than those who are poor metabolizers.[11] Distinct from menopausal effects, hormonal therapies, biologic response modifiers, and cytotoxic agents associated with fever secondarily cause sweats.

As with interventions for fever, primary interventions directed at the underlying cause of sweats or hot flashes form the basis of management. In the absence of effective therapy or when onset is delayed, nonspecific palliative interventions are key.

Primary Interventions

The primary interventions for fever-associated sweats are those directed at the underlying cause of the fever (refer to the Primary Interventions for fever section for more information). Effective antineoplastic therapies control the sweats associated with tumor recurrence or progression. Somatostatin analogs are a primary treatment for flushes and sweats associated with some neuroendocrine tumors.

Hot flashes

Hormone replacement therapy

Estrogen replacement effectively controls hot flashes associated with biologic or treatment-associated postmenopausal states in women. The proposed mechanism of action of estrogen replacement on hot flash amelioration is by raising the core body temperature sweating threshold;[12][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.[13]

In May 2002, the Women's Health Initiative (WHI), 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 breast cancer risk (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 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.[14,15][Level of evidence: I] These results are supported by a population-based case-control study suggesting a 1.7-fold (95% CI, 1.3–2.2) increased risk of breast cancer 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). Increased risk was highest for invasive lobular tumors and in women who used hormone replacement therapy for longer periods of time. Risk was not increased with unopposed estrogen therapy.[16]

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.[17,18] A series of double-blind placebo-controlled trials suggests that low-dose megestrol acetate (i.e., 20 mg by mouth twice a day) and selective serotonin reuptake inhibitors (SSRIs) are among the more promising agents for hot flash management in this population. Limited data suggest that brief cycles of intramuscular depot medroxyprogesterone acetate also play a role in the management of hot flashes.[19][Level of evidence: I] Risk associated with progestin use is unknown.[13]

Other pharmacologic interventions

Agents that have been found to be helpful in large, randomized, placebo-controlled clinical trials include venlafaxine, paroxetine, citalopram, fluoxetine, gabapentin, pregabalin, and clonidine.[20,21,22] These agents demonstrate a 40% to 60% reduction in hot flash frequency and score (a measure combining severity and frequency).[23] Agents conferring a 55% to 60% reduction in hot flashes are venlafaxine extended release, 75 mg daily;[24] paroxetine, 12.5 mg controlled release [25] or 10 mg daily;[26] gabapentin, 300 mg tid;[27,28][Level of evidence: I][29][Level of evidence: II] and pregabalin, 75 mg bid.[30][Level of evidence: I] Other effective agents resulting in about a 50% reduction in hot flashes include citalopram, 10 to 20 mg per day, which was studied in clinical trial NCCTG-N05C9;[31][Level of evidence: I] and fluoxetine, 20 mg per day.[21] Clonidine, 0.1 mg transdermal [32] or oral daily,[33][Level of evidence: I] can reduce hot flashes by about 40%.

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.[35] 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.

Agents that have been evaluated in phase II trials but have not shown efficacy include bupropion,[36] aprepitant,[37] and desipramine.[38][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.[39,40,41][Level of evidence: I]

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 impacts 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 about 53% in this nonrandomized trial, and women were statistically significantly satisfied with their hot flash control.[42] However, only 16 of the 22 women stayed on the agent for the entire study period because of excessive grogginess. Therefore, although this agent could be further studied in a larger randomized trial, it would be particularly important to evaluate the risk/benefit ratio.

Side effects for antidepressant agents in the doses used to treat hot flashes are minimal in the short term and primarily include nausea, sedation, dry mouth, and appetite suppression or stimulation. In the long term, the prevalence of decreases in sexual function with SSRIs at doses used to treat 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.[27,28,30][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 provider and health care consumer are needed.

Drug interactions

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.[46][Level of evidence: II] Since this study was published, several researchers have been evaluating the clinical implications of this finding.[47];[48,49,50][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.[49] Similarly, a retrospective cohort study of more than 2,400 women in Ontario who were being treated with tamoxifen and had overlapping treatment with an SSRI has been completed. Authors 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.[50][Level of evidence: II] Clinical implications of these changes and of other CYP2D6 genotypes [51] have not yet been elucidated, but the pharmacokinetic interaction between tamoxifen and the newer antidepressants used to treat hot flashes merits further study.[52] 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.[53]

Behavioral methods

Integrative approaches

Herbs/dietary supplements

  • Genistein
  • Daidzein
  • Glycitein

Several pilot trials have evaluated the use of acupuncture to treat hot flashes.[87,88,89,90][Level of evidence: I] Research in acupuncture is difficult, owing to the lack of novel methodology—specifically, the conundrum of what should serve as an adequate control arm. In addition, the philosophy surrounding acupuncture practice is quite individualized, in that two women experiencing hot flashes would not necessarily receive the same treatment. It would be important to study acupuncture utilizing relevant clinical procedures; so far, acceptable research methods to accomplish this are lacking. Therefore, the data with respect to the effect of acupuncture on hot flashes are quite mixed, with many studies suffering from ineffective control arms. Therefore, as concluded in at least one review, there is not a body of evidence to definitively delineate the role or practice of acupuncture for hot flashes.[91] (Refer to the Vasomotor symptoms section in the PDQ summary on Acupuncture for more information.)

Prostate cancer

Data regarding the pathophysiology and management of hot flashes in men with prostate cancer are scant. The limited data that exist suggest that hot flashes are related to changes in sex hormone levels that caused instability in the hypothalamic thermoregulatory center analogous to the proposed mechanism of hot flashes that occur in women. As with 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. With the exception of clonidine, the agents mentioned previously (refer to the Other pharmacologic interventions for hot flashes section of this summary) that have been found effective for hot flashes have shown similar rates of efficacy when studied in men. Treatment modalities include estrogens, progesterone, SSRIs, gabapentin 300 mg 3 times per day as an option for men,[92] and cyproterone acetate, an antiandrogen. The latter is not available in the United States.

Pilot studies of the efficacy of the SSRIs paroxetine and fluvoxamine suggest these drugs decrease the frequency and severity of hot flashes in men with prostate cancer.[94,95] As for 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.[96]

Other Pharmacologic Interventions

Clinical experience suggests that the H2 blocker cimetidine may be useful in the management of cancer-associated sweats. Given the vascular action of 5-hydroxytryptamine, somatostatin analogs may play a role in the nonspecific management of sweats. The use of low-dose thioridazine for the management of sweats in advanced cancer is no longer advocated because of reports of torsade de pointes arrhythmias [97] and sudden death.[98]

4. Ventafridda V, De Conno F, Ripamonti C, et al.: Quality-of-life assessment during a palliative care programme. Ann Oncol 1 (6): 415-20, 1990.
5. Quigley CS, Baines M: Descriptive epidemiology of sweating in a hospice population. J Palliat Care 13 (1): 22-6, 1997 Spring.
14. Writing Group for the Women's Health Initiative Investigators.: Risks and benefits of estrogen plus progestin in healthy postmenopausal women: principal results From the Women's Health Initiative randomized controlled trial. JAMA 288 (3): 321-33, 2002.
57. Elkins G, Marcus J, Stearns V, et al.: Randomized trial of a hypnosis intervention for treatment of hot flashes among breast cancer survivors. J Clin Oncol 26 (31): 5022-6, 2008.
97. Cowap J, Hardy J: Thioridazine in the management of cancer-related sweating. J Pain Symptom Manage 15 (5): 266, 1998.
98. Glassman AH, Bigger JT Jr: Antipsychotic drugs: prolonged QTc interval, torsade de pointes, and sudden death. Am J Psychiatry 158 (11): 1774-82, 2001.

Clinical Decision Making in the Management of Fever and Sweats

Effective management strategies for fever and sweats are limited by the paucity of data about symptom epidemiology and contributing pathophysiologies in the advanced cancer patient. Notwithstanding, careful history taking and physical examination can be used to develop a plan for diagnostic evaluation that is consistent with the patient's location in the disease spectrum and goals of care. For some patients, improved quality of life outweighs potential survival advantages. Fever, sweats, and hot flashes detract from quality of life in a significant number of patients with cancer or a history of cancer. Management strategies require an understanding of the underlying causes and pathophysiologic mechanisms, as well as knowledge of the patient's goals of care. Treatment interventions include pharmacologic, physical, dietary, and behavioral modalities.[1]

1. Zhukovsky DS: Fever and sweats in the patient with advanced cancer. Hematol Oncol Clin North Am 16 (3): 579-88, viii, 2002.

Current Clinical Trials

Changes to This Summary (01 / 09 / 2013)

Editorial changes were made to this summary.

Questions or Comments About This Summary

About This PDQ Summary

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 fever, sweats, and hot flashes. It is intended as a resource to inform and assist clinicians who care for cancer patients. It does not provide formal guidelines or recommendations for making health care decisions.

Reviewers and Updates

  • be discussed at a meeting,
  • be cited with text, or
  • replace or update an existing article that is already cited.

Levels of Evidence

Permission to Use This Summary

The preferred citation for this PDQ summary is:

National Cancer Institute: PDQ® Fever, Sweats, and Hot Flashes. Bethesda, MD: National Cancer Institute. Date last modified <MM/DD/YYYY>. Available at: Accessed <MM/DD/YYYY>.

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Last Revised: 2013-01-09


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Computing technologies are ubiquitous. Not since the invention of the printing press has the world seen such a revolution in the way information can be used and disseminated. The social impact has been astounding. As responsible professionals we want to understand the impact our work has had and will continue to have on culture, work and politics.

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Dr. Jan Plaza, Chair
Office: Ausable Hall, Room 307
Phone: (518) 564-2788
Fax: (518) 564-3010
Email: csc@plattsburgh.edu


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Ongole to Hyderabad road map

Ongole is located around 269 KM away from Hyderabad. If your vehicle continuously travels at the speed of 50 KM per hour; your travel time from Ongole to Hyderabad is 5.38 decimal hours. The following driving direction from Ongole to Hyderabad coming from google website. Please check google website for terms of use etc.
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Driving directions from Ongole to Hyderabad

Ongole road map can be used to get the direction from Ongole and the following cities. maddipadu - nasik - singarayakonda - tanguturu - tenali - vijayawada - addanki - annavaram - bangalore - bapatla - chennai - chilakaluripet - chirala - cuddapah - giddalur - goa - guntur - hyderabad - kandukur - kanigiri - kothapatnam - kurnool - macherla - machilipatnam - markapur - nandyal - nellore - piduguralla - podili - shirdi - srisailam - tirupati - vinukonda -

Travel time from Ongole to Hyderabad

If your car maintains an average speed of 50 KM per hour; your travel time will be 5.38 decimal hours.
Approximate train travel time from Ongole is 3.36 hours ( we assumed that your train consistent travel speed is 80 KM per hour ).

Dear Travellers / Visitors you are welcome to write more details about Ongole and Hyderabad.

Note:All or most of the given information about Ongole to Hyderabad are based on straight line ( crow fly distance). So the travel information may vary from actual one. Please check the terms of use and disclaimer.


The wfmt radio network

Symphony, Part 07 (Russian)

Part VII of a massive series on examining the concept of a symphony, widely considered the most important form of symphonic music. Our exploration of the symphony continues with a look at Russia's contributions, from Rubinstein and Rimski through Glazunov and Gliere.

Program 1

This week's programs focus on Russian symphonies from the 19th century and Russian composers whose music is frequently overlooked.

We begin with Anton Rubinstein who was born in 1829. As a young boy, the family moved to Moscow where his father had opened a successful pencil factory. Rubinstein began to study piano while living in Moscow, and took his first lessons from his mother. Rubinstein wrote his first symphony, Ocean, at the age of 21. Bill nremarks that it doesn't sound distinctly Russian because there were no other Russian symphonies to model it after. Just one year later, he began work on his second symphony.

Anton Rubinstein: Symphony No. 1 in F major, Op. 40, I, II, IV
Slovak State Philharmonic Orchestra (Kosice)/Stankovsky
Naxos 8.555476
:52, 2:43, 9:07

Rubinstein: Symphony No. 2 in C Major, Op. 42, Ocean, I, IV, VI, VII
Slovak Philharmonic Orchestra/Gunzenhauser
Marco Polo 8.220449
11:47, 24:31, 1:38

Rubenstein: Kamennoi-Ostrow Op. 10, No. 22
Josef Lhévinne, p
Masters of the roll Disc. 16: James Stewart Music (Amazon)
1:38 excerpt

Program 2

In 1860s Russia, a spirit of liberalism and patriotism swept the nation spurring an artistic renaissance. This was largely due to the 1855 death of Czar Nicholas I, a despot who had a throttling effect on the progress of the country.

One of these artists was Mily Balakirev, a composer who became known as the leader of The Mighty Handful. Balakirev wrote only two symphonies, one in his early 20s and one towards the end of his life. However, he was a huge contributor to a truly Russian style of composition in the 1860s.

One of Balakirev's pupils was Nikolai Rimsky-Korsakov. His first symphony, heard in this program, was written between the years of 1864-1866.

Also during this period, The Mighty Handful discovered the tone poems of Franz Liszt and Hector Berlioz. The group decided that they would like to write symphonies in the style of tone poems and thus Rimksy-Korsakov writes his second symphony, Antar, to have a definite story.

Nikolai Rimsky-Korsakov: Symphony No. 1, Op. 1 in E Minor, I, III
Philharmonia Orchestra/Butt
ASV 1024
9:15, 5:00

Mily Balakirev: Symphony 1 in C, I (excerpt), II (excerpt), III
Philharmonia Orchestra/Karajan
EMI 63316
1:22, 1:07, 3:47, 6:44, :36

Rimsky-Korsakov: Symphony #2 In F Sharp Minor, Op. 9, Antar, I, IV, II (excerpt at end of program)
Pittsburgh Symphony Orchestra/Maazel
Telarc 80131
12:44, 8:20, 1:48

Program 3

Alexander Borodin, another member of The Mighty Handful, was born of distinguished lineage but out of wedlock. However, his father provided so that he could have the best education available and Borodin was educated as a doctor and became a professor of chemistry. He wrote symphonies in his spare time.

Borodin began his first symphony in 1862 and it took him about five years to complete. He started his second symphony almost immediately after the first one was complete in 1869. It took him about the same length of time to complete it. It premiered in 1877.

In 1876 and 1877, Borodin was working on his third symphony but only completed two movements before his death in 1877. The last two movements were written after Borodin's death by the Russian composer Alexander Glazunov.

Alexander Borodin: Polovtsian Dances from Prince Igor (excerpt)
Chicago Symphony Orchestra/Ozawa
EMI 47617

Borodin: Symphony No. 1, I, IV
Toronto Symphony Orchestra/Davis
Sony 62406
:39, 13:18

Borodin: Symphony #2 in B Minor
Vienna Philharmonic Orchestra/Kubelik
Seraphim 69021
27:10, 1:08

Borodin (completed post. by Glazunov): Symphony No. 3, I
Toronto Symphony Orchestra/Davis
Sony 62406

Program 4

Alexander Glazunov (born 1865) was part of the second generation of Russian composers. He was very talented as a child and wrote his first symphony at the age of 16. It is called Slavyanskaya.

In 1906, he had already written eight symphonies. He had started on a ninth, but never completed it. Here is his Symphony No. 7 (Pastoral) written in 1902.

Reinhold Gliere, born ten years later in 1875, wrote a piece called Ilya Muromets. It is about a legendary Ukranian folk figure. The piece was written in 1904 and is a combination of symphony and tone poem. Most Westerners know Gliere's Russian Sailor's Dance from his ballet The Red Poppy.

The program closes with Symphony No. 2 by Sergei Lyapunov (born 1859). It was written in 1917.

Alexander Glazunov: Symphony No. 1 in E major, Op. 5, Slavyanskaya, I
Royal Scottish National Orchestra/Serebrier
Warner 2564-68904-2

Glazunov: Symphony No. 7 in F Maj, Op. 77, Pastoral, II & III
Royal Scottish National Orchestra/Serebrier
Warner 2564-63236-2

Reinhold Gliere: Russian Sailor’s Dance from The Red Poppy (excerpt)
Philadelphia Orchestra/Ormandy
CBS 45659

Gliere: Symphony No. 3 in B minor, Op. 42, Ilya Muromets, I & III
BBC Philharmonic Orchestra/Downes
Chandos 9041

Sergei Lyapunov: Symphony No. 2 in B-flat minor, Op. 66
USSR Symphony Orchestra/Svetlanov
Melodiya 10 00173

Program 5

Alexander Scriabin, born in 1872, was a kind of mystic and saw music in colors. He was also a follower of Friedrich Nietzche. His first symphony was written in 1901, and his Symphony No. 3 was written between 1902-1904. They are characterized by their long and complex nature.

Riccardo Muti, current conductor of the Chicago Symphony Orchestra, is very devoted to conducting the music of Scriabin, something usually reserved for Russian conductors.

Alexander Scriabin: Symphony No. 2 in C minor, Op. 29, III, IV, V
USSR Symphony Orchestra/Svetlanov
RDCD 11057
2:21, 13:25, 2:49

Scriabin: Symphony No. 3 in C minor, Op. 43, The Divine Poem: I. Introduction & III. Jeu Divin
Philadelphia Orchestra/Muti
EMI 49115

Steffen Demeter
Walther Davies
Michael Sanders
Claudia Wertz
Christine Anderson
Sally Rosenbaum
Jean Quay
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