Inpatient Evaluation and Management of Pericarditis and Pleuritis in Children

Introduction

Pericarditis and pleuritis are inflammatory conditions affecting the pericardium (heart lining) and pleura (lung lining), respectively. They can occur from infancy through adolescence, although both are less common in children than in adults. These “serositis” syndromes often result from infection, autoimmune diseases, or other triggers, and can sometimes occur together (for example, in systemic lupus erythematosus, both pericardial and pleural inflammation may be present). In hospitalized children, it is vital to quickly recognize and treat pericarditis and pleuritis, as complications such as cardiac tamponade or pleural empyema can be life-threatening. This guide offers a structured approach to inpatient evaluation and management, emphasizing age-appropriate considerations, common causes, diagnostic workup, and treatment options. We incorporate relevant guidelines (e.g., from cardiology and rheumatology societies) in a balanced manner without relying on strict algorithms.

Pericarditis in Children

Causes and Epidemiology

The causes of pediatric pericarditis are diverse. Broadly, etiologies are classified as infectious or non-infectious. In developed countries, most cases of acute pericarditis in children are presumed to be viral (e.g., enteroviruses such as coxsackievirus, echovirus; also influenza, adenovirus, Epstein-Barr virus, etc.), whereas tuberculosis remains a leading cause in regions with high TB prevalence. Bacterial (purulent) pericarditis is relatively rare but severe – historically, Staphylococcus aureus has been the most common organism (often in infants or neonates with staph sepsis or pneumonia), followed by Streptococcus species. In one series of children with bacterial pericarditis, 31% died despite treatment, underscoring its seriousness; early antibiotic therapy and pericardial drainage are crucial in purulent pericarditis. Fungal pericarditis is rare, primarily seen in immunocompromised hosts. Among non-infectious causes, post-cardiac surgery pericardial inflammation (post-cardiotomy syndrome) has become common in pediatrics. Systemic autoimmune diseases can present with pericarditis—systemic lupus erythematosus (SLE) in children has serositis (pericarditis and/or pleuritis) in up to approximately 30% of cases, and systemic juvenile idiopathic arthritis (Still’s disease) often involves pericarditis during active disease phases. Autoinflammatory syndromes (e.g., familial Mediterranean fever, FMF) are another key category: they cause recurrent bouts of serositis, including pericarditis in some instances. Other causes include uremic pericarditis in renal failure, malignancy (metastatic or leukemic infiltration of the pericardium), and post-radiation pericarditis in oncology patients. Notably, a large pediatric hospital study found that among hospitalized children with pericarditis or pericardial effusion, over 50% had recent cardiac surgery, and other comorbidities (cancer 13%, renal disease 13%) were more common than idiopathic or rheumatologic causes (each approximately 5%). Lastly, the impact of COVID-19 has been recognized: children can develop pericarditis from COVID-19 infection or (rarely) as a post-vaccine phenomenon. Though myocarditis has been more common, pericardial inflammation has been reported with SARS-CoV-2, and standard pericarditis treatments (NSAIDs, colchicine, steroids, and IL-1 inhibitors) have been safely used in these cases. Overall, understanding the likely cause based on age, region, and clinical context is the first step in managing pediatric pericarditis.

Clinical Presentation

Children with acute pericarditis typically present with chest pain that is often sharp and worsens when lying down, but improves when sitting up and leaning forward. Younger children may not be able to verbalize pain and instead show irritability, tachycardia, or shallow breathing due to discomfort. A pericardial friction rub is a key exam finding—an itchy, triphasic sound best heard along the left sternal border with the child leaning forward. However, rubs can be transient or difficult to hear in a noisy pediatric ICU. Fever is common if the cause is infectious or inflammatory. Children with large effusions or tamponade may have muffled heart sounds, jugular venous distension (which can be hard to detect in younger children), hepatomegaly, or pulsus paradoxus (a drop in systolic blood pressure greater than 10 mmHg with inspiration). In practice, the diagnosis of acute pericarditis is based on a combination of features. Adult criteria also apply to children: pericarditis is likely when at least two of four findings are present—(1) characteristic chest pain, (2) pericardial rub, (3) diffuse ST-segment ECG changes, and (4) new or worsening pericardial effusion. Children’s ECGs in pericarditis often show diffuse ST elevation and PR depression (except in neonates, where ECG interpretation is more complex). Laboratory markers typically show signs of systemic inflammation, such as elevated C-reactive protein, ESR, and leukocytosis. Troponin may be elevated if there is myopericarditis, indicating myocardial involvement. In hospitalized patients, assessing severity is crucial: high fevers (over 38°C), a subacute course over weeks, large effusions or signs of tamponade, or evidence of myocarditis (elevated troponin or depressed cardiac function) all suggest a more serious condition. These high-risk features, along with immunosuppression, trauma, or lack of improvement with initial treatment, are indications for hospital admission if not already hospitalized. Infants and young toddlers with pericarditis can be particularly high-risk because they often present late—their symptoms are non-specific—and they may rapidly progress to hemodynamic compromise.

Inpatient Diagnostic Workup

When pericarditis is suspected in a hospitalized child, a thorough diagnostic workup is performed alongside initial treatment. Electrocardiography (ECG) is used to look for the diffuse ST elevation pattern typical of pericarditis or low voltages, which may indicate a large effusion. Chest radiography can show an enlarged cardiac silhouette if an effusion is moderate or large, or may reveal an underlying pneumonia or lung lesion in cases of coexisting pleuritis. The primary imaging modality is echocardiography, which should be obtained promptly to assess for pericardial effusion, its size, and signs of tamponade (e.g., diastolic chamber collapse). Even a small effusion supports the diagnosis in a child experiencing chest pain and a rub. Echocardiography also evaluates ventricular function, which is crucial since myocarditis can occur simultaneously. In unclear cases or complex anatomy, such as post-surgical patients, cardiac MRI can be very helpful to confirm pericardial inflammation (e.g., showing pericardial enhancement) and differentiate it from myocardial injury. Laboratory studies should include inflammatory markers (CRP, ESR), a complete blood count, and a metabolic panel. If an infectious cause is suspected, blood cultures should be obtained, especially if there is fever and an ill appearance, as bacteremic seeding can lead to purulent pericarditis. In adolescents, testing for tuberculosis (TB skin test or IGRA) is indicated if TB is part of the differential diagnosis (e.g., subacute fever, immigrant from a high TB region, or lymphocytic effusion). If features suggest a connective tissue disease (e.g., rash, arthritis, nephritis), an autoimmune workup (ANA, dsDNA, etc.) should be performed to evaluate for SLE or other rheumatic diseases. In post-operative cardiac patients, pericardial fluid may be sterile inflammation (postpericardiotomy syndrome), but infection (such as Staph) must be ruled out, so culturing any drained fluid is essential. Pericardiocentesis for diagnostic purposes is generally reserved for cases with moderate-to-large effusion or tamponade, or when a specific diagnosis is needed (e.g., suspected TB or malignancy). Fluid analysis may include Gram stain/culture, acid-fast bacilli stain and culture, cytology, and PCR for viruses. In summary, the inpatient workup balances supportive care with targeted tests to identify the underlying cause, as specific treatments (e.g., antibiotics, immunosuppressive therapy) depend on knowing the etiology.

Acute Management in the Hospital

General measures: All children with acute pericarditis should be placed on appropriate monitoring, such as frequent vital signs and telemetry if myocardial involvement is suspected. Strict bed rest or activity restriction is recommended during the acute phase to lessen cardiac workload. If signs of cardiac tamponade appear—such as tachycardia, hypotension, distended neck veins, pulsus paradoxus, or collapsing chambers on echo—urgent pericardial drainage is necessary, usually by percutaneous pericardiocentesis guided by echocardiography or fluoroscopy. A pericardial drain (pigtail catheter) may be maintained until output is minimal. Surgical drainage through a subxiphoid pericardial window or video-assisted thoracoscopy may be considered if percutaneous drainage fails or if the fluid is purulent, to allow for washout. In cases of effusive-constrictive or recurrent effusions, a surgical pericardiectomy (removal of the pericardium) is a last-resort option, though it is rarely needed immediately.

Anti- inflammatory therapy: For acute pericarditis without contraindications, high- dose NSAIDs are the first- line treatment to reduce inflammation and relieve pain. This core recommendation is supported by adult and pediatric data – the 2015 European Society of Cardiology (ESC) guidelines give NSAIDs a class I recommendation for acute pericarditis (Level A evidence) . Common choices include ibuprofen, indomethacin, or aspirin (aspirin is used in adults; in children, ibuprofen is often preferred to avoid Reye syndrome risk, except in specific cases). Dosing is weight- based; for example, ibuprofen at anti- inflammatory doses (30–50 mg/kg/day divided TID) is used. NSAIDs should be continued until symptoms resolve and markers of inflammation normalize, then tapered over 2-4 weeks to prevent relapse . Colchicine is recommended as adjunct therapy in acute pericarditis to further reduce the risk of recurrence . Adult studies (and limited pediatric experience) show colchicine significantly cuts recurrence rates . Guidelines suggest a 3- month course of colchicine for a first episode (in adults) , and pediatric dosing is typically weight- adjusted (children over 5 years often receive 1–1. 1.2 mg/day in divided doses; 0. 0.5 mg/day if under 5 years) . Colchicine is generally well tolerated in children, with diarrhea as the main side effect to watch for. Notably, corticosteroids are avoided as first- line therapy in idiopathic or viral pericarditis because studies have linked steroid use to a higher rate of recurrent pericarditis . One multicenter pediatric cohort found that children who received steroids during acute pericarditis had more than double the recurrence rate of those managed with NSAIDs alone . Steroids also carry significant side effects in children. Therefore, glucocorticoids are reserved for specific indications – for instance, if the pericarditis is due to an underlying autoimmune disease (e. g., severe lupus pericarditis) or if NSAIDs are contraindicated or ineffective . In such cases, use the lowest effective steroid dose for the shortest duration. An example is prednisone around 1 mg/kg/day, which would then be tapered as soon as clinically feasible. If a child with pericarditis is already on high- dose steroids for another condition (or due to an underlying disorder like systemic JIA), one may continue and then gradually taper under cover of other agents (colchicine or disease- specific therapy) to prevent rebound inflammation.

Targeted therapies: Management must also address the underlying cause. If a bacterial infection is confirmed or strongly suspected, tailor antibiotic therapy accordingly. Purulent (bacterial) pericarditis requires intensive management: broad-spectrum IV antibiotics should be started empirically (covering Staph aureus and Gram-negatives) and then narrowed based on cultures. Drainage of the pericardium is essential in bacterial cases to clear the infection. Tuberculous pericarditis is treated with standard multi-drug TB therapy (usually 6 months of RIPE therapy), often with the addition of corticosteroids in the acute phase to reduce inflammatory complications like constrictive pericarditis. Autoimmune-associated pericarditis (such as in SLE) improves with control of the systemic disease—high-dose corticosteroids are typically used for severe lupus carditis or serositis, alongside immunosuppressants (e.g., cyclophosphamide or mycophenolate if lupus pericarditis is refractory or part of a generalized flare). In uremic pericarditis, intensifying dialysis is the primary treatment (along with NSAIDs if tolerated) rather than steroids. Post-cardiotomy syndrome is generally managed with NSAIDs and colchicine; occasionally, a course of steroids is given if the inflammation is severe or not improving, as these patients may not have the same high recurrence risk profile.

Throughout treatment, providing symptomatic care is essential. Proper pain management (often with NSAIDs; add acetaminophen or mild opioids if necessary) helps the child breathe comfortably. Monitor for fever and give antipyretics as needed. Gastroprotection (such as a proton pump inhibitor) should be considered if high-dose NSAIDs or aspirin are used over a long period. Regular clinical exams and point-of-care ultrasound can monitor effusion size. Most cases of acute pericarditis respond within a few days to anti-inflammatory treatment, with pain and fever declining. By the time of discharge, the child should have a clear plan for tapering medications and follow-up. Close outpatient follow-up is important to watch for any signs of recurrence or complications.

Pleuritis in Children

Causes of Pleuritis (Pleurisy)

Pleuritis refers to inflammation of the pleural membranes around the lungs, usually causing pleuritic chest pain. In children, pleurisy often develops as a complication of an underlying condition. The most common causes are infectious. Bacterial pneumonia is a leading cause of pleural effusion and pleuritic pain in children: organisms like Streptococcus pneumoniae, Staphylococcus aureus, and Streptococcus pyogenes (especially in younger children) can cause parapneumonic effusions and empyema. Widespread pneumococcal vaccination has changed the epidemiology, making staph and streptococcal empyemas more prominent now. Viral infections can also cause pleurisy—viruses such as influenza, adenovirus, and coxsackievirus may lead to pleural inflammation. For example, Bornholm disease from Coxsackie B causes epidemics of pleurodynia, which presents with severe pleuritic pain but usually follows a benign course. Tuberculosis is a significant cause of pleuritic effusion in regions where TB is endemic or in immunocompromised children; TB pleural effusions tend to be subacute, presenting with fever, weight loss, and a unilateral exudative effusion. Fungal infections like coccidioidomycosis or histoplasmosis can occasionally cause pleural effusions in endemic areas.

Non-infectious causes of pediatric pleuritis overlap with those of pericarditis. Autoimmune diseases are major contributors: in childhood-onset SLE, pleuritis (with or without effusion) is common and can be the first sign. Lupus pleuritis often occurs alongside pericarditis and indicates high disease activity; children with lupus serositis tend to have more severe illness and may need aggressive immunosuppressive therapy. Juvenile idiopathic arthritis rarely affects the pleura, except in systemic JIA, where widespread serositis can happen. Other connective tissue diseases like juvenile dermatomyositis and mixed connective tissue disease can rarely cause pleural effusions. Among autoinflammatory syndromes, familial Mediterranean fever (FMF) frequently presents with episodes of pleuritic pain; FMF flares often cause unilateral pleurisy with fever lasting 1-3 days. Usually, FMF-related pleuritis resolves on its own but can recur periodically, potentially leading to adhesions over time. Tumors may also cause pleural effusions—lymphomas or metastatic sarcomas might present with malignant effusions, and some leukemias can involve serous linings. Pulmonary embolism is an uncommon cause of pleuritic chest pain in children (much less common than in adults unless the child has significant risk factors like a central line or thrombophilia). Uremic pleuritis can develop in advanced kidney disease, often alongside uremic pericarditis. Lastly, pleural effusions after surgery or trauma are common in hospitalized children; for example, after cardiac or chest surgery, effusions can develop and cause pleuritic pain, or reactive pleurisy can occur after chest trauma or rib fractures.

Clinical Presentation

The hallmark of pleuritis is pleuritic chest pain—a sharp, stabbing pain that worsens with deep inspiration, coughing, or chest movement. Children may describe it as “it hurts when I breathe” or “when I cough or take a deep breath.” Young kids might simply have rapid, shallow breathing and splinting (to minimize pain). Pleuritic pain can sometimes radiate to the shoulder or upper abdomen (due to diaphragmatic pleural irritation). Unlike pericarditic pain, pleuritic pain does not typically improve with positional changes like sitting forward; instead, the main factor that worsens it is inhalation. If a pleural effusion becomes large, the pain may actually decrease because the inflamed pleural surfaces are no longer rubbing once fluid separates them. Associated symptoms depend on the cause: in parapneumonic effusion, the child often shows signs of preceding pneumonia—fever, cough, difficulty breathing—and the pleuritic pain may become clearer as the effusion enlarges or fibrinous “rubs” develop. On physical exam, a pleural friction rub may be heard early in pleurisy (a coarse grating sound at the end of inspiration), but this can disappear once fluid accumulates. With significant pleural effusion, exam findings typically include decreased breath sounds, dullness to percussion, and reduced tactile fremitus on the affected side. The child might show signs of respiratory distress if the effusion is large—such as increased work of breathing, asymmetrical chest expansion, or even tracheal deviation if the effusion is massive. Empyema (infected pleural fluid) often presents with persistent fever despite antibiotics, and the child may look toxic. In empyema, pleuritic pain may be less prominent due to fluid buildup, but the overall illness can be severe. In autoimmune-related pleuritis (like lupus), pleuritic pain may occur with fever and other systemic signs (rash, arthritis); such a serositis flare might show only a small effusion on imaging, or just a pleural rub and pain with minimal fluid. Because young children may not localize chest pain, pleurisy in toddlers could present as unexplained irritability, rapid breathing, or referred abdominal pain. Any unexplained splinting respirations or reflexive limitation of deep breaths in a child should prompt consideration of pleural irritation as well as cardiac causes.

Inpatient Evaluation

When a child in the hospital is suspected of having pleuritis or a new pleural effusion, a systematic evaluation is necessary to determine the cause and guide therapy. Imaging is the first step: a chest X-ray (preferably upright) will confirm the presence of a pleural effusion, often seen as blunting of the costophrenic angle or a fluid layer. In an ICU patient who is supine, an effusion may appear as a generalized haze over one lung field. A lateral decubitus X-ray can reveal fluid layering and assess whether it is free-flowing or loculated. However, ultrasound of the chest is the gold standard imaging technique for pleural fluid, as it can quantify fluid, detect septations (such as fibrin strands in empyema), and guide safe thoracentesis. Bedside ultrasound is particularly useful in pediatrics for mapping pockets of fluid to facilitate drainage. If the effusion is moderate or large, or if the cause remains unclear, diagnostic thoracentesis should be strongly considered in the inpatient setting. Fluid analysis is essential: labs on pleural fluid should include cell count with differential, protein and LDH levels (to distinguish exudate from transudate), Gram stain and bacterial culture, and if appropriate, cytology (to assess for malignancy) and AFB stain/culture (for TB). In cases of suspected empyema, the fluid is typically pus with very high cell counts; culture helps identify the pathogen, although it may be negative if antibiotics have already been administered. Blood cultures should be obtained in any child with a parapneumonic effusion and fever, as bacteremia can be associated with pneumonia. Laboratory testing also includes inflammatory markers (CRP, ESR), which are usually elevated in empyema or lupus pleuritis. If an autoimmune cause such as lupus is suspected (especially in adolescent girls with serositis but no obvious pneumonia), testing ANA, double-stranded DNA, and complement levels can provide valuable information. Markers of heart failure (BNP) can be considered if a transudative effusion from cardiac disease is part of the differential diagnosis. In practice, many hospitalized children with pleural effusions already have a diagnosis (e.g., pneumonia, post-operative state, known lupus); thus, the evaluation primarily focuses on severity and potential complications. If a child has a small effusion and is being treated for known pneumonia, one may opt to defer diagnostic tap and monitor for improvement. However, an unexplained effusion or any large or loculated effusion seen on imaging warrants a diagnostic drainage procedure. Additionally, consider a CT scan of the chest if complex loculations, lung abscess, or if the extent of the effusion is not fully delineated by ultrasound—though CT involves radiation and often requires sedation in young children, it can reveal lung parenchymal disease and the pattern of pleural involvement.

Management of Pleuritis and Pleural Effusions

Supportive care and monitoring: Managing pleuritis in children starts with observing respiratory status. Make sure the child has enough oxygen because large effusions can lead to V/Q mismatch or atelectasis, so give supplemental oxygen if necessary. Watch for signs of breathing difficulty or fatigue, especially in younger children who have less respiratory reserve. Position the child comfortably, such as lying on the side of the effusion to help reduce pain, which can be effective. Pain control is crucial: NSAIDs like ibuprofen or ketorolac IV are effective for pleuritic pain and also reduce inflammation, assuming there are no contraindications. For severe pain, low doses of opioids may be necessary to help the child breathe and cough properly, as uncontrolled pain can cause poor deep breathing and a risk of atelectasis. Encourage use of incentive spirometry or blowing bubbles to keep the lungs expanded if pain is managed.

Treat the underlying cause: This is the foundation of pleuritis management. For parapneumonic effusions (effusions secondary to bacterial pneumonia), antibiotic therapy appropriate for the pneumonia pathogen is essential. For typical community-acquired pneumonia in children, IV antibiotics covering pneumococcus (and Staph aureus if empyema is suspected) are initiated— for example, IV vancomycin plus a third-generation cephalosporin is a common empiric regimen if MRSA is a concern. Antibiotics typically continue for 2-4 weeks in total (initially IV, then possibly switched to oral when improving) for empyema. In cases of empyema or large complicated effusions, prompt drainage is usually needed alongside antibiotics. Drainage options include chest tube placement guided by ultrasound or surgery, often combined with intrapleural fibrinolytics (e.g., tPA/DNase) to break down loculations, or primary video-assisted thoracoscopic surgery (VATS) for drainage and decortication. Both approaches are used; protocols vary by institution—some favor chest tube with fibrinolytics as first-line, others prefer early VATS. The goal is to remove the pus and facilitate lung re-expansion. A child with empyema typically has a chest tube draining fluid for several days until output decreases and the lung mostly re-expands. Tuberculous pleuritis is managed with anti-TB medications (usually 4-drug therapy). A moderate TB effusion may also be drained via thoracentesis for symptom relief, but they often aren’t loculated and may resolve with therapy; steroids are sometimes added in TB pleural effusion to reduce inflammation and prevent long-term fibrosis. If pleuritis results from a viral infection, treatment is mainly supportive (NSAIDs for pain, rest), as the condition is usually self-limited. Autoimmune pleuritis (e.g., lupus): Here, corticosteroids are the treatment of choice if the pleurisy is moderate or severe. Lupus pleuritis responds to high-dose prednisone, which alleviates inflammation; NSAIDs can be used for mild cases, but often, by the time a lupus patient experiences pleuritic pain and effusion, they benefit from steroids. Recurrent or refractory lupus pleuritis may require escalation of lupus-specific therapy (such as adding immunosuppressants like azathioprine or rituximab, depending on the situation). In FMF or other autoinflammatory syndromes causing episodic pleurisy, acute episodes are treated with NSAIDs or colchicine for symptom relief, but importantly, colchicine prophylaxis is started to prevent future attacks. According to EULAR recommendations, children diagnosed with FMF should begin colchicine immediately and continue lifelong to fully control attacks. Colchicine effectively prevents most FMF flares of serositis; if a patient on maximal colchicine still has frequent flares, they are considered colchicine-resistant, and biologic agents (such as IL-1 inhibitors) are recommended. Pediatric rheumatologists often co-manage these cases, frequently using agents like anakinra or canakinumab to suppress the autoinflammatory process in colchicine non-responders.

Procedure-based management: Inpatient care of pleuritis with significant effusion often involves procedures. We already noted chest tube insertion for drainage; another method is therapeutic thoracentesis to relieve symptoms if an effusion causes respiratory issues. Removing even a few hundred milliliters can significantly improve breathing in a child. In loculated empyema, VATS surgery allows surgeons to break up pockets and peel off restrictive fibrin (decortication), which can speed recovery. The timing of VATS versus chest tube is debated, but both aim to restore normal lung function. If a child has a small, uncomplicated effusion, it may be managed without invasive drainage, as the body can reabsorb the fluid once the infection is treated; however, close monitoring is necessary to ensure it does not worsen.

Monitoring and complications: As pleuritic effusions resolve, observe the child’s respiratory status and fever pattern. Follow-up ultrasounds or X-rays verify that fluid is decreasing. A potential complication of inadequately treated empyema is fibrothorax (scar tissue encasing the lung), which can cause long-term restriction—timely intervention helps prevent this. Another complication is sepsis if an empyema is not controlled, although in modern series, pediatric empyema prognosis is generally good with proper therapy. Large effusions can cause partial lung collapse (atelectasis), which improves after drainage. Unlike pericarditis, recurrent pleuritis in pediatrics is uncommon except in autoinflammatory diseases or uncontrolled rheumatic disease. Therefore, prevention mainly involves treating the root disease (e.g., maintaining FMF on colchicine, keeping lupus in remission with maintenance medications).

Recurrent Pericarditis: Special Considerations

Recurrent pericarditis (RP) is characterized by the recurrence of pericardial inflammation after a symptom-free period of at least 4-6 weeks following an initial episode of acute pericarditis. In children and adolescents, recurrent pericarditis presents a significant clinical challenge because it often results in multiple hospitalizations and substantial morbidity. Reported recurrence rates in pediatrics range from approximately 15% up to 30% in some series, especially when the initial episodes were idiopathic or inadequately treated. The cause of recurrent pericarditis in children is usually idiopathic or post-viral in the majority (around 89% in one multicenter cohort). A smaller portion is due to specific causes such as post-cardiotomy syndrome (about 9%) or periodic fever syndromes (e.g., FMF, less than 1%). Even when no obvious cause is found, research indicates that many idiopathic cases have an immune-mediated basis—essentially a misdirected immune response triggered by the initial pericarditis episode. This is supported by findings of elevated autoantibodies in idiopathic recurrent pericarditis and the fact that RP can occur in known autoimmune diseases and autoinflammatory syndromes. Risk factors for recurrence in children include a high initial inflammatory load (CRP ≥125 mg/L, ESR ≥50 mm/h), corticosteroid use during the acute phase, and a non-viral or non-idiopathic cause of the first episode. Notably, early use of corticosteroids is linked with higher relapse rates, so avoiding steroids initially (unless absolutely necessary) is a strategy to lower recurrence.

Clinical approach: A child with recurrent pericarditis often presents similarly to the initial episode (chest pain, fever, pericardial rub, etc.), although sometimes the pain may be less intense if they have been through this before and are preemptively treated. The evaluation of each recurrence should include an echo (to check for effusion and myocardial function) and labs to assess inflammation. It is also important to reconsider the differential diagnosis upon recurrence – for example, was there an underlying autoinflammatory disease that was missed? Workup for autoimmune markers or periodic fever symptoms is reasonable in recurrent cases. If the child was non-adherent to colchicine or NSAID taper, that may explain a relapse, so compliance should be reviewed.

Management of recurrent pericarditis relies on anti-inflammatory treatment and strategies to prevent further episodes. Based on adult cardiology guidelines adapted for pediatrics, an acute recurrence is managed with NSAIDs (with a prolonged taper) plus colchicine for an extended period. For a first recurrence, a most recommended course of colchicine is at least 6 months (compared to 3 months for an initial episode). Many pediatric specialists also continue colchicine for 6 to 12 months or longer to maintain remission. The NSAID (e.g., ibuprofen or indomethacin) should be administered until symptoms resolve and CRP levels normalize, then gradually tapered over several weeks. During recurrences, exercise restriction is increased—no sports or strenuous activities until fully recovered—to help prevent triggering symptoms.

If a child was not previously on colchicine, it should be started upon recurrence (assuming age > approximately 2 years). Colchicine is highly effective in reducing further recurrences: one pediatric cohort showed that colchicine use significantly decreased the recurrence rate (from 3.7 to 1.4 episodes per year on average). Corticosteroids in recurrent pericarditis can be a double-edged sword. Low-dose steroids may help control a severe flare, especially if NSAIDs fail or are contraindicated, but steroids often lead to dependency (symptoms rebound when tapering). Guidelines recommend reserving corticosteroids for refractory cases that do not respond to NSAID plus colchicine or if there is a specific indication (e.g., RP as part of a rheumatologic disease). If used, the dose should be kept as low as possible (e.g., prednisone ~0.5 mg/kg/day rather than very high doses in idiopathic RP) with a very slow taper over months to prevent flares. Some protocols use intravenous immunoglobulin (IVIG) to facilitate weaning off steroids in steroid-dependent recurrent pericarditis; pediatric case series have reported IVIG achieving remission or steroid-sparing in difficult cases, though evidence remains limited.

Emerging therapies: A significant advancement in managing difficult recurrent pericarditis involves the use of interleukin-1 (IL-1) inhibitors, reflecting the autoinflammatory nature of many cases. Anakinra, a recombinant IL-1 receptor antagonist administered via daily subcutaneous injection, has demonstrated remarkable effectiveness in children with steroid-dependent or refractory RP. Studies and case series in pediatric patients show that anakinra can lead to rapid symptom relief and enable tapering of corticosteroids and other medications. In a multicenter study, adding anakinra reduced the recurrence rate from 4.3 per year to 0.1 per year in a cohort of children with recurrent pericarditis. The typical pediatric dose is 1-2 mg/kg subcutaneously daily. Many children remain on anakinra for 6-12 months or longer; about 40% may experience flare-ups when discontinuing the medication, but often respond again if therapy is resumed. Another IL-1 blocker, canakinumab (administered monthly), has also been used in recurrent pericarditis cases—with reports of success in some patients, particularly those intolerant of daily injections, although a few children experienced recurrences after switching from anakinra to canakinumab. As of 2021, an IL-1 trap (rilonacept) has even been FDA-approved for recurrent pericarditis in adults, underscoring the role of IL-1 in this disease; while pediatric experience with rilonacept is limited, these biologics are likely to become standard options for refractory cases. Other immunosuppressive agents have been tried anecdotally: azathioprine, methotrexate, or mycophenolate can be added as steroid-sparing agents in recurrent pericarditis, especially when an underlying autoimmune disorder is present. These are considered in chronic cases to help maintain remission.

Surgical option: For the rare child with incessant pericarditis that cannot be managed with medical therapy, pericardiectomy (surgical removal of most of the pericardium) is a last resort. Case series suggest that pericardiectomy in refractory pericarditis can cure the condition in about 80–90% of patients, but surgery carries risks (and in children, it’s a major operation often delayed unless absolutely necessary).

Psychosocial support: Recurrent pericarditis can greatly impact a child’s quality of life, causing repeated pain episodes, hospital stays, and missed school. A multidisciplinary approach is helpful: include cardiology, rheumatology, and pain management specialists as needed. Families should be advised that, with modern treatments, most children eventually reach remission, although it may take time and consistent adherence to therapy. Stress the importance of medication compliance, especially with colchicine, which is preventive. For adolescent patients, addressing concerns about long-term NSAID use or steroid side effects is crucial for gaining their cooperation.

Conclusion

The inpatient management of pericarditis and pleuritis in children requires a careful, age-specific approach that addresses immediate risks and underlying causes. Infectious causes (ranging from viral to purulent bacterial etiologies) must be promptly identified and treated—for example, antibiotics and drainage for empyema or purulent pericarditis can be life-saving. Autoimmune and autoinflammatory causes necessitate anti-inflammatory therapies (NSAIDs, colchicine) and often immunomodulation (corticosteroids or biologics) to achieve control. Key inpatient considerations include vigilant monitoring for complications like cardiac tamponade or respiratory compromise, use of appropriate imaging (echocardiography, ultrasound) to guide interventions, and involvement of subspecialists (cardiology, rheumatology, infectious disease, cardiothoracic surgery) in complex cases. Current guidelines and evidence universally support NSAIDs as the first-line treatment for pericardial and pleural inflammation, with colchicine serving as an effective adjunct in pericarditis to prevent recurrences. Pediatric practice often mirrors adult recommendations, though special caution is exercised with therapies like aspirin and attention is paid to developmental differences in presentation. For recurrent pericarditis, a stepwise approach escalating to IL-1 inhibitors has significantly improved outcomes, transforming a once-protracted disease into a manageable condition for most patients. By combining thorough diagnostic workups with guideline-based treatment strategies, pediatricians and pediatric rheumatologists can effectively manage hospitalized children with pericarditis or pleuritis, ensuring symptom relief and minimizing long-term complications.