Pleurodynia Treatment & Management

Updated: Aug 13, 2015
  • Author: Irina Petrache, MD; Chief Editor: Zab Mosenifar, MD, FACP, FCCP  more...
  • Print

Medical Care

No specific treatment exists. Management is supportive and includes nonsteroidal anti-inflammatory drugs (NSAIDs) for pain and pleurisy (if present) or peripheral nerve block (eg, intercostal nerve) with 1% lidocaine (Xylocaine) infusion.

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

Several experimental antiviral treatments have been tested in animal models, as follows:

  • Arbidol inhibited the coxsackievirus-5 (CVB5) cytopathic effect and decreases CVB5-RNA level in vitro and in vivo in a CVB5 systemic infection BALB/c mouse model. [16]

  • IL-12 delivered orally via genetically engineered Bifidobacterium longum downregulated the severity of virus-induced myocarditis and reduced the virus titers in the heart of a CVB3-induced myocarditis BALB/c mouse model. [17]

  • Human cardiac derived adherent proliferating cells (CAPs) characterized by CD105+, CD73+, CD166+, CD44+, CD90+, CD14+, CD34+, CD45+ are similar to human mesenchymal stromal cells in terms of anti-apoptotic and immunomodulatory properties, but lack the multilineage differential potential. CAPs could not be infected by CVB3; when administered to a C57Bl/6 mouse model, engrafted in the heart, lung, liver, kidney, and spleen, it decreased the CVB3-induced myocarditis severity. [18]

  • Benzophenone C-glucosides and gallotannins from mango tree stem bark exhibit ex vivo inhibitory activity against coxsackievirus 3C protease. [19]

  • Combination of soluble extracellular domain of the coxsackie-adenovirus receptor (sCAR-Fc) and 2 short hairpin RNAs (shRdRp2.4) exerted antiviral and anti-inflammatory activity in a coxsackievirus B3-induced myocarditis murine model. [20]

  • N-benzene sulfonyl matrinic amine/amide and matrinic methyl ether analogues exhibited stronger anti-coxsackievirus B3  activity and better therapeutic properties with improved selectivity index. [21]

Pregnancy considerations

Coxsackievirus B may be transmitted to the fetus during pregnancy by transplacental route or during delivery. During pregnancy, the outcomes of coxsackievirus B infection depend on the timing of infection during the age of gestation. Two independent studies reported higher prevalence of coxsackievirus B infection in women experiencing a miscarriage than in women delivering at term or receiving a voluntary termination before 13 weeks gestation. IgM antibody against coxsackie virus B1-5 or semi-nested RT-PCR positive for coxsackievirus B3 in the placental tissue were significantly higher, by 42% and 57.1%, respectively, than in women in the control group. [22, 23] It may also be related to increased incidence of congenital heart defects, and early-onset insulin-dependent diabetes mellitus. 

Transmission of ECHO virus to neonates has also been reported during delivery, by an orofecal route. Similarly to coxsackievirus B, it may cause severe systemic infection in the neonate, such as aseptic meningitis, hepatitis, gastroenteritis, and viral pneumonitis. [24]



Activity is as tolerated.



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, [25] aseptic meningitis, constrictive pericarditis, orchitis, myalgic encephalomyelitis, severe neonatal encephalitis with seizures, [26] hemorrhagic conjunctivitis, hepatitis, pancreatitis, 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. [25]


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. [28]

Coxsackievirus B is a small RNA virus that lacks a lipoprotein envelope and, hence, may be resistant to physical and chemical inactivation, including 70% alcohol or 1% quaternary ammonium compounds. Sodium hypochlorite at a concentration of 3120 ppm, at a contact time of 5 minutes, was sufficient to completely inactivate different Enterovirus strains. [29]  Good sterilization techniques that include ethylene oxide have been shown to inactivate the virus on electrophysiologic catheters. [30]


Long-Term Monitoring

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.