eMedicine Specialties > Pulmonology > Pleural Disorders

Pleurodynia

Irina Petrache, MD, Associate Professor of Medicine, Department of Medicine, Division of Pulmonary, Allergy, Critical Care and Occupational Medicine, Indiana University
Ninotchka Liban Sigua, MD, Fellow, Department of Pulmonary and Critical Care, Indiana University

Updated: Apr 17, 2009

Introduction

Background

Pleurodynia is an uncommon complication of coxsackievirus B infection and is defined as the sudden occurrence of lancinating chest pain or abdominal pain attacks, commonly associated with fever, malaise, and headaches. Coxsackievirus B is an RNA Enterovirus, which usually causes an asymptomatic or brief upper respiratory tract or gastroenteric infection. In rare cases, other severe sequelae of coxsackievirus B infection develop, including meningitis and carditis.¹

Also see the eMedicine article Coxsackieviruses.

Pathophysiology

The striated muscle is the actual anatomic structure targeted by the coxsackievirus B and is responsible for the attacks of severe chest pain. Therefore, the term pleurodynia may be a misnomer because only some patients with the condition actually develop pleuritis (ie, inflammation of the pleural surface). In patients with pleurodynia, the striated intercostal muscles necrose, which explains the frequent elevations in serum creatine kinase levels. Some of the more chronic sequelae, such as myocarditis, dermato-polymyositis, chronic fatigue syndrome, and possibly, juvenile-onset diabetes type I, are believed to be immune mediated.

The virus has an incubation time of 1 week in the gastrointestinal tract and then, through hematogenous dissemination, involves the target organs, most commonly the skeletal muscles but also the CNS (ie, meningitis, encephalitis) and myocardium (ie, carditis with or without associated pericarditis). Coxsackievirus B can be recovered in the stool or pharynx for up to 2 weeks after the resolution of the symptoms.

Frequency

United States

Coxsackievirus B was present in 24% of the 18,000 enteroviruses isolated and reported in the United States from 1970-1979.² The estimated number of nonpolio enteroviral symptomatic infections is 5-10 million per year.

In regions of temperate climate, the infection is seasonal, with about 90% of infections occurring in the summer and early fall, and sometimes infections occur in epidemics.

The incidence of coxsackievirus B infection in neonates is 1 in 2000 live births.

International

Antibodies to coxsackievirus B serotypes are present in 75% of the population in developed countries. In the tropical and subtropical climate areas, the prevalence of the enteroviral infections is year-round.

Mortality/Morbidity

The severity of the coxsackievirus B infection is highest in infants and children. In infants who develop coxsackievirus B infection, 10% die, usually within the first 4 weeks of life most commonly from cardiac involvement. Fulminant hepatic failure, sepsis syndrome, and severe CNS involvement with seizures and apnea are also potential complications in this age group.³

Sex

Males are more commonly affected than females.

Age

Coxsackievirus B infection occurs most commonly in children younger than 15 years; half of these patients are younger than 5 years, and 30% are younger than 1 year. The disease is rare in patients older than 60 years. However, pleurodynia most commonly affects adults infected with the virus, with fewer than 10% of cases occurring in patients younger than 20 years. Of the 372 prospectively studied children aged 4-18 years with nonpolio enteroviral infections, only 3% developed pleurodynia. In contrast, 30 of the 78 mostly adult patients with coxsackievirus B-associated cardiac disease had pleurodynia. Therefore, the location of pain is believed to be predominantly thoracic in adults and abdominal in children.

Clinical

History

The onset of chest pain is acute. During attacks, the pain is severe, intense, and excruciating, lasting seconds to a minute. Pain is paroxysmal, occurring in attacks separated by minutes to hours. Severe attacks can result in difficulty breathing. The thoracic pain is usually over the lower ribs and is unilateral, but it can also occur over the front, back, or substernal area. Between attacks, patients usually have a constant, dull, pleuritic chest pain. The attacks usually persist for 3-5 days and rarely last longer than a month and may go through phases of remission and exacerbation.

• Associated symptoms related to the viral infection may include the following:
  • Upper respiratory tract symptoms, including sore throat, rhinitis, and dry cough
  • Constitutional symptoms, including headaches (50%), fever, and malaise
  • GI symptoms, including nausea, vomiting, diarrhea (50%); abdominal pain (usually in the epigastric area) in children
  • Testicular pain (ie, orchitis) in 10% of males

Physical

• Fever (97%) and appropriate heart rate response (ie, tachycardia)
• Respiratory system findings - Pharyngitis (85%), including herpangina, visible splinting of the chest during attacks, localized chest wall tenderness in the same area of pain (25%), and pleural friction rub (25%)
• Other potential signs associated with the coxsackievirus B infection - Otitis (25%) and dermatitis (30%)

Causes

• The classic etiologic agent for pleurodynia is coxsackievirus B, serotypes B1, B2, B3, B4, and B5, which are small, nonenveloped RNA viruses, in which an icosahedral capsid encloses the single-stranded RNA genome.
• Other nonpolio enteroviruses, including echoviruses type 6 and 19 and coxsackievirus A, are also reported to cause syndromes very similar to that of coxsackievirus B infection, including pleurodynia.
• Humans are the only known reservoir of the enteroviruses; transmission occurs via the fecal-oral route. The incubation time is usually  2-5 days. Potential risk factors for the transmission of the enteroviruses are poor sanitation and overcrowding. Intrafamilial spread is common.

Differential Diagnoses

Other Problems to Be Considered

Pleurisy, viral or idiopathic
Sickle cell crisis
Fractured rib
Mediastinal emphysema
Other tumors of the pleural space, soft tissue sarcoma
Bronchiolitis obliterans with organizing pneumonia (BOOP)
Intercostal neuralgia
Hyperventilation syndrome
Myositis⁴
Drug-induced myalgias: Esomeprazole has been involved in a case report of myalgia, cephalgia, and fever.⁵

Workup

Laboratory Studies

Coxsackie B virus infection can be diagnosed by isolation of the virus in cell culture, detection of virus RNA via polymerase chain reaction (PCR) or serologic evaluation of viral antibodies.⁶

• Viral cultures
  • Primary monkey kidney cells or embryonic lung fibroblasts are the standard cells used for isolation and identification of coxsackievirus B. The addition of Buffalo green monkey kidney cells may increase the sensitivity of this method. Viral growth occurs in 1-4 days, causing a cytopathic effect on the host cells, resulting in rounded, refractile cells that eventually lyse. The cultures may be performed from various clinical specimens, dictated by the presence of clinical symptoms.
  • Throat viral cultures are more sensitive than urine viral cultures and confirm 33% of the enteroviral infections studied. Throat culture findings were positive for coxsackievirus B in 45% of the patients presenting with pleurodynia. Blood cultures are useful in children younger than 3 months. Stool cultures have a higher yield than rectal swabs. Having multiple culture specimens may also increase the yield of virus recovery in culture.
  • A positive enteroviral culture result must be interpreted in light of the clinical context and the history of polio immunization. After vaccination with the live attenuated oral polio vaccine, viral culture results from both throat and stool specimens may remain positive for enteroviruses for several months. Similarly, patients with asymptomatic infections may shed the virus for months after they acquire the infection.
  • Cerebrospinal fluid (CSF) viral cultures have limited clinical utility in the management of enteroviral meningitis due to poor sensitivity (65-75%), high cost, and long turnaround time.
• Fluorescent staining and neutralization assays: Using specific antibodies, these tests are used to further confirm and delineate the type of enterovirus isolated from cell culture.
• Molecular diagnosis
  • Reverse transcriptase PCR (RT-PCR) has gained wide acceptance for the detection of viral nucleic acids, especially from specimens with a low viral load that may be associated with false-negative cell culture results.⁷ In the CSF, RT-PCR has better sensitivity than viral culture. In children, RT-PCR for throat specimens was also more sensitive than viral culture. Another advantage is the rapid turnaround time, which has resulted to improved health care costs, especially in the management of enteroviral meningitis.^8,9
  • Commercial diagnostic RT-PCR kits are available for the identification of coxsackievirus B RNA.
  • One disadvantage of RT-PCR is that the virus serotype cannot be identified. Additional restriction fragment length polymorphism (RFLP) assays may provide a simple strategy to identify the virus subtype.¹⁰
• Serologic studies for viral antigen detection: Specific antibodies against enteroviral groups and serotypes are commercially available, but their application has thus far been limited to fluorescent staining and detection of viral antigens in cell cultures, rather than clinical specimens.
  • Enzyme-linked immunosorbent assay (ELISA) is more sensitive than the neutralization test and can be used as a screening tool, followed by the neutralization test for confirmation.
  • ELISA using an enteroviruses group–specific monoclonal antibody may detect early immunoglobulin M (IgM) antibody secreted during coxsackievirus B infection. The test is more sensitive than the neutralization tests and can be used as a screening tool, followed by the neutralization test. The specificity is not extremely high because the antibodies cross-react with other enteroviruses such as hepatitis A virus.^11,12
  • The neutralization assay measures the ability of the serum to antagonize the viral infectivity in cell culture. Although the test is expensive and awkward, a more specific finding of a positive ELISA result followed by a negative neutralization test result usually signifies an enteroviral infection other than that caused by coxsackievirus B.
• Complement fixation test: This test is another laborious method of measuring antiviral antibodies used to diagnose coxsackievirus B infection.
• Other tests and findings
  • Serum creatine kinase is usually elevated because of muscle necrosis.
  • The white cell count ranges from mild leukopenia to mild leukocytosis.
  • Although seldom performed for the diagnosis of pleurodynia per se, tissue diagnosis can be made by direct detection of the viral antigen or by isolation of RNA virus-specific sequences.
  • Depending on the clinical presentation and suspicion for serositis caused by systemic lupus erythematosus, an antinuclear antibody test can be performed.

Imaging Studies

• Chest radiography
  • A chest radiograph is usually obtained to exclude other causes of chest pain. In pleurodynia, the findings on chest radiography can be normal, or the radiograph may show a small amount of ipsilateral pleural effusion or adjacent atelectasis from splinting.
  • The atelectasis can be linear or in the form of bibasilar consolidation.
  • Infrequently, the coxsackievirus B infection causes pneumonia, with a radiographic pattern of fine perihilar opacities.

Histologic Findings

Necrosis of the striated intercostal muscles is visible. Rarely, adjacent pleural inflammation results in a small exudative pleural effusion.

Treatment

Medical Care

No specific treatment exists. Management is supportive and includes nonsteroidal anti-inflammatory drugs (NSAIDs) for pain and pleurisy (if present).

Aspirin should be avoided in children because of the potential to develop Reye syndrome.

Activity

As tolerated

Medication

Nonsteroidal anti-inflammatory drugs and analgesics are used for the symptomatic relief of pleurodynia.

Nonsteroidal anti-inflammatory drugs (NSAIDs)

These agents have analgesic, anti-inflammatory, and antipyretic activities. Their mechanism of action is not known, but it may inhibit cyclooxygenase activity and prostaglandin synthesis. Other mechanisms may exist as well, eg, inhibition of leukotriene synthesis, lysosomal enzyme release, lipoxygenase activity, neutrophil aggregation and various cell membrane functions. They are used for symptomatic relief of pleurodynia.¹³

Ibuprofen (Motrin, Advil)

Exerts anti-inflammatory effect via inhibition of cyclooxygenase, resulting in decreased formation of prostaglandins and thromboxanes from arachidonic acid. Also may inhibit synthesis and/or actions of other local inflammatory mediators and leukocyte migration. Analgesic effect is thought to result from the drug's action on peripheral pain impulse transmission and on pain receptor modulation.

Dosing

Adult

400-800 mg PO q6-8h
If only analgesia is desired: 200-400 mg PO q6-8h

Pediatric

<6 months: Not established
>6 months: 20-40 mg/kg/d PO divided tid/qid
If only analgesia is desired: 5-10 mg/kg/d PO divided tid/qid

Interactions

Coadministration with aspirin increases risk of inducing serious adverse effects; probenecid may increase concentrations and toxicity; may decrease effects of hydralazine, captopril, and beta-blockers; may decrease diuretic effects of furosemide and thiazides; monitor PT closely in patients on warfarin (instruct patients to watch for signs of bleeding); may increase risk of methotrexate toxicity; phenytoin levels may be increased when administered concurrently

Contraindications

Documented hypersensitivity; GI bleeding, severe peptic ulcer disease, severe coagulopathy

Precautions

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus

Precautions

Caution in CHF, hypertension, and decreased renal and hepatic function; caution in anticoagulation abnormalities or during anticoagulant therapy; adverse GI effects include dyspepsia, ulceration, bleeding, nausea, vomiting, and bloating; liver reactions may be severe and monitoring of liver function tests is recommended in prolonged use; may cause fluid retention and precipitate pulmonary edema in patients with severe heart failure; may cause blurred vision and visual field defects; may inhibit platelet aggregation, and may cause neutropenia, anemia, and thrombocytopenia; may interfere with labor, causing dystocia; may cause premature closure of ductus arteriosum

Ketoprofen (Orudis, Oruvail, Actron)

For relief of mild to moderate pain and inflammation. Small dosages are initially indicated in small and elderly patients and in those with renal or liver disease. Doses of more than 75 mg do not increase therapeutic effects. Administer high doses with caution and closely observe patient for response.

Dosing

Adult

25-50 mg PO q6-8h prn; not to exceed 300 mg/d

Pediatric

25-50 mg PO q6-8h prn; not to exceed 300 mg/d

Interactions

Coadministration with aspirin increases risk of inducing serious NSAID-related adverse effects; probenecid may increase concentrations and toxicity of NSAIDs; may decrease effect of hydralazine, captopril, and beta-blockers; may decrease diuretic effects of furosemide and thiazides; may increase PT when taking anticoagulants (instruct patients to watch for signs of bleeding); may increase risk of methotrexate toxicity; phenytoin levels may be increased when administered concurrently

Contraindications

Documented hypersensitivity

Precautions

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus

Precautions

Caution in CHF, hypertension, and decreased renal and hepatic function; caution in anticoagulation abnormalities or during anticoagulant therapy

Naproxen (Naprelan, Naprosyn, Anaprox, Aleve)

For relief of mild to moderate pain; inhibits inflammatory reactions and pain by decreasing activity of cyclooxygenase, which results in a decrease of prostaglandin synthesis.

Dosing

Adult

500 mg PO followed by 250 mg q6-8h; not to exceed 1.25 g/d

Pediatric

<2 years: Not established
>2 years: 2.5 mg/kg/dose PO; not to exceed 10 mg/kg/d

Interactions

Coadministration with aspirin increases risk of inducing serious NSAID-related adverse effects; probenecid may increase concentrations and toxicity of NSAIDs; may decrease effect of hydralazine, captopril, and beta-blockers; may decrease diuretic effects of furosemide and thiazides; may increase PT when taking anticoagulants (instruct patients to watch for signs of bleeding); may increase risk of methotrexate toxicity; phenytoin levels may be increased when administered concurrently

Contraindications

Documented hypersensitivity; peptic ulcer disease; recent GI bleeding or perforation; renal insufficiency

Precautions

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus

Precautions

Acute renal insufficiency, interstitial nephritis, hyperkalemia, hyponatremia, and renal papillary necrosis may occur; patients with preexisting renal disease or compromised renal perfusion risk acute renal failure; leukopenia occurs rarely, is transient, and usually returns to normal during therapy; persistent leukopenia, granulocytopenia, or thrombocytopenia warrant further evaluation and may require discontinuation of drug

Follow-up

Further Outpatient Care

• Patients must receive follow-up care with their primary care providers to ensure that other potential coxsackievirus B–associated complications are diagnosed and managed in a timely manner.

Deterrence/Prevention

• Common hygiene measures aid in the prevention of the oral-fecal transmission of coxsackievirus B. An outbreak of pleurodynia among high school football players was traced to contaminated water; therefore, avoid direct oral contact with common drinking or ice containers in favor of individual water containers and ice packs.¹⁴
• Coxsackievirus B is a small RNA virus that lacks a lipoprotein envelope and, hence, may be resistant to physical and chemical inactivation. Good sterilization techniques that include ethylene oxide have been shown to inactivate the virus on electrophysiologic catheters.¹⁵

Complications

• Direct complications of pleurodynia are rare. Splinting from pain may result in atelectasis and shortness of breath.
• A postviral syndrome, also called fatigue-dysphoria syndrome, is described in children who were seropositive for coxsackievirus B and who complained of fatigue, weakness, sore throats, and dysphoria. This syndrome may also complicate the patient's recovery.
• In rare cases, coxsackievirus B infection may be complicated by carditis, aseptic meningitis, constrictive pericarditis, orchitis, myalgic encephalomyelitis,¹⁶ hemorrhagic conjunctivitis,¹⁷ hepatitis, pancreatitis,¹⁸ and juvenile-onset diabetes mellitus.
• Dilated cardiomyopathy is a complication of viral myocarditis. It may be acute or related to severe muscle necrosis, or it may occur several years later, possibly due to chronic inflammation and fibrosis as a result of an immune-mediated process.¹⁹

Prognosis

• The prognosis is good, with complete recovery in most cases. The return to normal health may be gradual after a period of weakness and fatigue. No deaths are reported as a direct result of pleurodynia.

Patient Education

• Encourage proper hygiene measures in the patient's household to avoid intrafamilial spread of the virus.
• For excellent patient education resources, visit eMedicine's Lung and Airway Center. Also, see eMedicine's patient education article Chest Pain.

Miscellaneous

Medicolegal Pitfalls

• Failure to correctly diagnose life-threatening causes of acute severe onset of chest pain (see Differentials), including pulmonary embolism,²⁰ myocardial infarction, or aortic dissection
• Failure to provide a thorough clinical evaluation followed by a proper investigative plan, which should (in most cases) aid in the appropriate diagnosis of such disorders

Special Concerns

• Coxsackievirus B may be transmitted to the fetus during pregnancy by transplacental route or during delivery. It may be associated with spontaneous abortions before 12 weeks' gestation. It may also be related to increased incidence of congenital heart defects, and early-onset insulin-dependent diabetes mellitus. Placental infection by the virus may lead to perinatal morbidity and death.²¹

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Keywords

pleurodynia, pleuritis, pleuritic pain, lancinating chest pain, costalgia, epidemic pleurodynia, Bornholm disease, Bornholm's disease, Devil grip, Devil's grip, epidemic myalgia, coxsackievirus B, enteroviruses, meningitis, carditis, Sylvest's disease, Sylvest disease, epidemic benign dry pleurisy

Contributor Information and Disclosures

Author

Irina Petrache, MD, Associate Professor of Medicine, Department of Medicine, Division of Pulmonary, Allergy, Critical Care and Occupational Medicine, Indiana University
Irina Petrache, MD is a member of the following medical societies: American Thoracic Society
Disclosure: Nothing to disclose.

Coauthor(s)

Ninotchka Liban Sigua, MD, Fellow, Department of Pulmonary and Critical Care, Indiana University
Ninotchka Liban Sigua, MD is a member of the following medical societies: American College of Chest Physicians, American College of Physicians, American Thoracic Society, and Society of Critical Care Medicine
Disclosure: Nothing to disclose.

Medical Editor

Helen M Hollingsworth, MD, Director, Adult Asthma and Allergy Services, Associate Professor, Department of Internal Medicine, Division of Pulmonary and Critical Care, Boston Medical Center
Helen M Hollingsworth, MD is a member of the following medical societies: American Academy of Allergy Asthma and Immunology, American College of Chest Physicians, American Thoracic Society, and Massachusetts Medical Society
Disclosure: Nothing to disclose.

Pharmacy Editor

Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: Nothing to disclose.

Managing Editor

Gregg T Anders, DO, Medical Director, Great Plains Regional Medical Command , Brook Army Medical Center; Clinical Associate Professor, Department of Internal Medicine, Division of Pulmonary Disease, University of Texas Health Science Center at San Antonio
Gregg T Anders, DO is a member of the following medical societies: American College of Chest Physicians, American College of Physicians, and American Thoracic Society
Disclosure: Nothing to disclose.

CME Editor

Timothy D Rice, MD, Associate Professor, Departments of Internal Medicine and Pediatrics and Adolescent Medicine, Saint Louis University School of Medicine
Timothy D Rice, MD is a member of the following medical societies: American Academy of Pediatrics and American College of Physicians
Disclosure: Nothing to disclose.

Chief Editor

Zab Mosenifar, MD, Director, Division of Pulmonary and Critical Care Medicine, Director, Women's Guild Pulmonary Disease Institute, Executive Vice Chair, Department of Medicine, Cedars Sinai Medical Center; Professor of Medicine, David Geffen School of Medicine at UCLA
Zab Mosenifar, MD is a member of the following medical societies: American College of Chest Physicians, American College of Physicians, American Federation for Medical Research, and American Thoracic Society
Disclosure: Nothing to disclose.

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