Σύνδρομο PFAPA

 

PFAPA: Όταν ο πυρετός επανέρχεται με… ακρίβεια ρολογιού

**Από Μιχάλη Ιασονίδη, παιδίατρο στο κέντρο υγείας παιδιών και εφήβων “Ηλιακτίδα”, αναπληρωτή καθηγητή παιδιατρικής (Πανεπιστήμιο Λευκωσίας).**

Ένας πρακτικός οδηγός για γονείς και επαγγελματίες υγείας

Οι επαναλαμβανόμενοι πυρετοί αποτελούν μία από τις συχνότερες αιτίες ανησυχίας των γονέων και συχνών επισκέψεων στον παιδίατρο. Στις περισσότερες περιπτώσεις οφείλονται σε διαδοχικές ιογενείς λοιμώξεις, ιδιαίτερα στα παιδιά που φοιτούν σε βρεφονηπιακούς σταθμούς ή σχολεία. Υπάρχει όμως μία ιδιαίτερη κατηγορία παιδιών, στα οποία ο πυρετός εμφανίζεται με εντυπωσιακή περιοδικότητα, χωρίς να αποδεικνύεται λοίμωξη και χωρίς ανταπόκριση στα αντιβιοτικά.
Σε αυτές τις περιπτώσεις πρέπει να τίθεται η υποψία του συνδρόμου PFAPA, του συχνότερου αυτοφλεγμονώδους συνδρόμου της παιδικής ηλικίας.

Τι είναι το σύνδρομο PFAPA;

Το PFAPA είναι τα αρχικά των λέξεων:

• Periodic Fever (Περιοδικός πυρετός)
• Aphthous Stomatitis (Άφθες στο στόμα)
• Pharyngitis (Φαρυγγίτιδα)
• Adenitis (Τραχηλική λεμφαδενίτιδα)

Πρόκειται για ένα αυτοφλεγμονώδες σύνδρομο και όχι για λοίμωξη. Αυτό σημαίνει ότι το ανοσοποιητικό σύστημα ενεργοποιείται χωρίς την παρουσία κάποιου μικροβίου ή ιού, προκαλώντας επεισόδια έντονης φλεγμονής και υψηλού πυρετού.
Η ακριβής αιτία δεν είναι πλήρως γνωστή. Σήμερα γνωρίζουμε ότι σχετίζεται με δυσρρύθμιση της φυσικής ανοσίας και υπερπαραγωγή φλεγμονωδών κυτταροκινών, κυρίως της IL-1β, της IL-6 και του TNF-α.

Ποια παιδιά εμφανίζουν PFAPA;

Το σύνδρομο εμφανίζεται κυρίως:

• πριν από την ηλικία των 5 ετών,
• συχνότερα στα αγόρια,
• σε κατά τα άλλα απολύτως υγιή παιδιά με φυσιολογική ανάπτυξη.

Ένα από τα πιο χαρακτηριστικά στοιχεία είναι ότι ανάμεσα στα επεισόδια το παιδί είναι απολύτως καλά, χωρίς κανένα σύμπτωμα, αναπτύσσεται φυσιολογικά και όλες οι καθημερινές του δραστηριότητες είναι φυσιολογικές.

Πώς εκδηλώνεται;

Τα επεισόδια παρουσιάζουν εντυπωσιακή ομοιότητα μεταξύ τους.
Συνήθως παρατηρούνται:

• υψηλός πυρετός (συχνά 39-41°C),
• έντονος πονόλαιμος,
• αμυγδαλίτιδα, πολλές φορές με λευκά εξιδρώματα,
• διογκωμένοι τραχηλικοί λεμφαδένες,
• άφθες στο στόμα (όχι πάντοτε),
• κακουχία,
• πονοκέφαλος,
• κοιλιακό άλγος,
• μυαλγίες ή αρθραλγίες.

Τα επεισόδια διαρκούν συνήθως 3-7 ημέρες και επανέρχονται κάθε 3-6 εβδομάδες, πολλές φορές με τέτοια σταθερότητα ώστε οι γονείς μπορούν να προβλέψουν περίπου πότε θα εμφανιστεί ο επόμενος πυρετός.

Γιατί συχνά καθυστερεί η διάγνωση;

Το μεγαλύτερο πρόβλημα είναι ότι τα περισσότερα παιδιά διαγιγνώσκονται αρχικά ως πάσχοντα από επαναλαμβανόμενες αμυγδαλίτιδες.

Έτσι:

• λαμβάνουν επανειλημμένα αντιβιοτικά,
• αλλάζουν πολλές διαφορετικές αντιβιοτικές αγωγές,
• υποβάλλονται σε πολλαπλές καλλιέργειες,
• επισκέπτονται πολλές φορές νοσοκομεία και Τμήματα Επειγόντων.

Στην πραγματικότητα όμως:

• οι καλλιέργειες είναι συνήθως αρνητικές,
• τα αντιβιοτικά δεν αλλάζουν την πορεία του επεισοδίου,
• ο πυρετός υποχωρεί μόνος του μετά από λίγες ημέρες.

Το άρθρο παρουσιάζει χαρακτηριστικές περιπτώσεις παιδιών που επί χρόνια λάμβαναν αντιβιοτικά κάθε μήνα, μέχρι να τεθεί τελικά η σωστή διάγνωση.

Πώς γίνεται η διάγνωση;

Δεν υπάρχει μία ειδική εξέταση που να επιβεβαιώνει το PFAPA.
Η διάγνωση βασίζεται κυρίως:

• στο χαρακτηριστικό ιστορικό,
• στην περιοδικότητα των επεισοδίων,
• στα κλινικά ευρήματα,
• και στον αποκλεισμό άλλων νοσημάτων.

Κατά τη διάρκεια των επεισοδίων συνήθως παρατηρούνται:

• αυξημένα λευκά αιμοσφαίρια,
• ουδετεροφιλία,
• αυξημένη CRP,
• αυξημένη ΤΚΕ.

Μετά την υποχώρηση του επεισοδίου οι εξετάσεις επανέρχονται στο φυσιολογικό.

Από ποιες παθήσεις πρέπει να διαφοροδιαγνωστεί;

Η σωστή διάγνωση είναι ιδιαίτερα σημαντική, καθώς υπάρχουν και άλλα περιοδικά εμπύρετα σύνδρομα που απαιτούν διαφορετική αντιμετώπιση.
Η διαφοροδιάγνωση περιλαμβάνει κυρίως:

• Οικογενή Μεσογειακό Πυρετό (FMF),
• κυκλική ουδετεροπενία,
• σύνδρομο υπερ-IgD (Mevalonate kinase deficiency),
• TRAPS,
• άλλα σπανιότερα αυτοφλεγμονώδη σύνδρομα.

Στην Κύπρο και γενικότερα στις μεσογειακές χώρες, ιδιαίτερη προσοχή χρειάζεται στον αποκλεισμό του Οικογενούς Μεσογειακού Πυρετού, λόγω της αυξημένης συχνότητάς του. Το άρθρο παραθέτει συγκριτικό πίνακα των κυριότερων χαρακτηριστικών όλων των περιοδικών εμπύρετων συνδρόμων.

Πώς αντιμετωπίζεται;

Η θεραπεία είναι απλή αλλά ιδιαίτερα αποτελεσματική.

Κορτικοστεροειδή
Η χορήγηση μίας δόσης πρεδνιζολόνης (1–2 mg/kg από το στόμα) στην αρχή του επεισοδίου οδηγεί συνήθως σε θεαματική ύφεση μέσα σε λίγες ώρες.
Η γρήγορη ανταπόκριση αποτελεί συχνά και διαγνωστικό στοιχείο.

Αντιβιοτικά
Τα αντιβιοτικά δεν θεραπεύουν το PFAPA, εκτός αν συνυπάρχει πραγματική βακτηριακή λοίμωξη.

Η άσκοπη χρήση τους πρέπει να αποφεύγεται, καθώς:

• δεν μειώνει τη διάρκεια των επεισοδίων,
• αυξάνει την πιθανότητα μικροβιακής αντοχής,
• επιβαρύνει το παιδί με περιττές παρενέργειες.

Αμυγδαλεκτομή
Σε επιλεγμένες περιπτώσεις με πολύ συχνά ή σοβαρά επεισόδια, ιδιαίτερα όταν η ανταπόκριση στη φαρμακευτική αγωγή δεν είναι ικανοποιητική, η αμυγδαλεκτομή (με ή χωρίς αδενοειδεκτομή) μπορεί να οδηγήσει σε σημαντική βελτίωση ή ακόμη και πλήρη ύφεση.

Ποια είναι η πρόγνωση;

Η πρόγνωση είναι εξαιρετική.

Στα περισσότερα παιδιά:

• τα επεισόδια αραιώνουν με την πάροδο των ετών,
• συνήθως υποχωρούν αυτόματα μέσα σε 4–8 χρόνια,
• δεν επηρεάζεται η σωματική ή πνευματική ανάπτυξη,
• δεν προκαλείται μόνιμη βλάβη στα όργανα.

Σε αντίθεση με άλλα αυτοφλεγμονώδη σύνδρομα, το PFAPA δεν σχετίζεται με ανάπτυξη αμυλοείδωσης, μιας σοβαρής επιπλοκής που παρατηρείται σε ορισμένα κληρονομικά περιοδικά εμπύρετα σύνδρομα.

Πότε πρέπει να υποψιαστεί ο παιδίατρος PFAPA;

Η διάγνωση πρέπει να τίθεται σοβαρά υπόψη όταν ένα παιδί παρουσιάζει:

• επαναλαμβανόμενο υψηλό πυρετό με σχεδόν σταθερά χρονικά διαστήματα,
• αμυγδαλίτιδα με αρνητικές καλλιέργειες,
• απουσία ανταπόκρισης στα αντιβιοτικά,
• πλήρη αποκατάσταση της υγείας μεταξύ των επεισοδίων,
• φυσιολογική ανάπτυξη και ευεξία εκτός των κρίσεων.

Η προσεκτική λήψη ιστορικού είναι συχνά το σημαντικότερο διαγνωστικό εργαλείο.

Το μήνυμα προς τους γονείς

Εάν το παιδί σας εμφανίζει υψηλό πυρετό που επανέρχεται σχεδόν με τον ίδιο τρόπο κάθε λίγες εβδομάδες και κάθε φορά λαμβάνει αντιβιοτικά χωρίς ουσιαστικό αποτέλεσμα, αξίζει να συζητήσετε με τον παιδίατρό σας το ενδεχόμενο του συνδρόμου PFAPA.

Η έγκαιρη αναγνώριση της νόσου:

• αποφεύγει τις περιττές αντιβιώσεις και εξετάσεις,
• μειώνει την ταλαιπωρία του παιδιού και της οικογένειας,
• επιτρέπει την άμεση και αποτελεσματική αντιμετώπιση κάθε επεισοδίου,
• καθησυχάζει τους γονείς γνωρίζοντας ότι πρόκειται για μια καλοήθη πάθηση με πολύ καλή μακροχρόνια πρόγνωση.

What is PFAPA syndrome?

PFAPA Syndrome

PFAPA is a childhood syndrome that causes repeated episodes of fever, mouth sores, sore throat, and swollen lymph nodes. PFAPA usually starts in early childhood between ages 2 and 5.

 

What is PFAPA syndrome?

PFAPA (periodic fever, aphthous stomatitis, pharyngitis, adenitis) is a childhood syndrome that affects both boys and girls. It causes repeated episodes of fever, mouth sores, sore throat, and swollen lymph nodes. PFAPA usually starts in early childhood between ages 2 and 5. In very rare cases, the syndrome may start in adulthood.

The immune system works to help keep you healthy. Its job is to find and destroy things in the body that may cause harm. This includes bacteria and viruses. Inflammation is part of the immune system’s response. It causes cells of the immune system to become active. These cells make substances that signal the brain to raise body temperature and cause a fever. The signals also cause redness and swelling.

PFAPA may occur without a known cause. An abnormal activation of the immune system causes episodes of fever and other symptoms. PFAPA is 1 of a group of disorders that cause fevers due to abnormal inflammation. It’s the most common condition in this group.

Causes

What causes PFAPA syndrome?

Researchers aren’t sure what sets off PFAPA. It doesn’t appear to run in families, unlike some other causes of repeated fevers in children. Researchers haven’t identified a gene linked to PFAPA. The immune response is different from with a normal infection. It's is not contagious. You can’t catch it from someone who has the condition.

Symptoms

What are the symptoms of PFAPA syndrome?

Common symptoms of PFAPA include:

• Fevers at regular intervals of 2 to 8 weeks. They may be high [over 102°F (38.9°C)] and last 3 to 6 days.
• Mouth sores (aphthous stomatitis).
• Sore throat with redness (pharyngitis).
• Enlarged lymph nodes of the neck (adenitis).
• White patches on the tonsils.

Less common symptoms include:

• Headache.
• Joint pain.
• Rash.
• Belly (abdominal) pain.
• Nausea and vomiting.
• Diarrhea.

Episodes of PFAPA usually last a few days to a week. These episodes may come back every few weeks. Between these episodes, children are completely well. Children with PFAPA grow and develop normally.

How is PFAPA syndrome diagnosed?

Your child’s health care provider will ask about your child’s health history and symptoms. Your child will also have a physical exam. The provider will need to make sure the symptoms aren’t caused by another illness, such as an infection, autoimmune disease, or another fever syndrome.

There isn’t a test that can diagnose PFAPA. But your child may have tests, such as:

• Blood tests, such as white blood counts. These look for signs of infection.
• Erythrocyte sedimentation rate and C-reactive protein. These blood tests check for general inflammation.
• Strep culture. This checks for strep throat.
• Imaging tests. These may include an abdominal CT scan to rule out other disorders.
• Genetic tests. These are done to check for other syndromes that cause repeated fevers.

Your child’s provider may not be able to diagnose PFAPA right away. At first, they may diagnose your child with a simple viral illness before figuring out that PFAPA is the cause.

A pediatric rheumatologist often diagnoses PFAPA. For the diagnosis, your child must have had at least 3 episodes of fever. Your child must also have shown the key features of PFAPA, such as a sore throat (pharyngitis) and swollen lymph nodes. If your child has symptoms between PFAPA flare-ups, another diagnosis is more likely. A positive response to treatment (with steroids) also helps providers finalize the diagnosis.

Treatment

How is PFAPA syndrome treated?

Providers are still working to figure out the best treatment for PFAPA. Possible treatments include:

• A short course of steroids. This often shortens or ends the episode.
• Medicines, such as cimetidine or colchicine. These may help prevent future episodes in a small number of children.
• Surgery to remove the tonsils. This may prevent future episodes in some children.

The fever often doesn’t respond well to standard fever-reducing medicines, such as acetaminophen or ibuprofen. But these may still be a possible choice.

Talk with your child’s provider about the risks and benefits of treatments. While steroids shorten or end episodes of PFAPA, they may also shorten the length of time between episodes. Repeated use of steroids can also cause side effects, such as trouble sleeping.

PFAPA doesn’t cause severe symptoms or complications. Because of this, some providers may advise against any treatment. Even without treatment, PFAPA usually stops sometime after age 10. In rare cases, a child may still have symptoms into adulthood, though usually less often.

Complications

What are possible complications of PFAPA syndrome?

PFAPA doesn’t cause any known long-term complications.

Using steroids may have long-term complications. Discuss this with your provider.

Living with PFAPA syndrome

Your child may need to miss several days of school a month. Work closely with your child’s school to provide the best support for your child.

When to Call a Healthcare Provider

When should I contact my child's doctor?

Call your child’s health care provider if you think your child is having an episode of PFAPA symptoms.

Key Points

Key points about PFAPA syndrome

• PFAPA syndrome causes repeated episodes of fever, mouth sores, sore throat, and swollen lymph nodes. It happens because of an abnormal immune system response.
• To diagnose PFAPA, your child’s provider will need to rule out other conditions that may cause repeated fevers.
• Steroid medicines often end or shorten an episode. But they also may cause more frequent episodes.
• Surgery to remove the tonsils may end the syndrome in some children.
• PFAPA does not cause severe symptoms or long-term complications.
• PFAPA syndrome usually goes away on its own in the second decade of life.

 

SOURCE: 

Management of community-associated bacterial skin and soft tissue infections in children and prevention of recurrence (Canadian Paediatric Society)

Management of community-associated bacterial skin and soft tissue infections in children and prevention of recurrence

Posted: May 26, 2026

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The Canadian Paediatric Society gives permission to print single copies of this document from our website. For permission to reprint or reproduce multiple copies, please see our copyright policy.

Principal author(s)

Justin Penner MD, Sergio Fanella MD; Canadian Paediatric Society, Infectious Diseases and Immunization Committee

Abstract

Skin and soft tissue infections (SSTIs) are among the most common infectious diseases encountered in children. Severity of SSTIs range from simple infections that resolve spontaneously to severe necrotizing syndromes requiring intravenous antibiotics, surgical intervention, and intensive care. Inadequate skin barrier resulting from common paediatric conditions such as eczema and skin abrasions predisposes to infection. When antibiotics are needed, their choice and duration should be guided by the most probable organisms involved, their likely susceptibility profiles, and geographical epidemiologic differences. Inappropriate treatment with overly broad-spectrum antibiotics and/or for prolonged durations is detrimental to the microbiomes of patients, increases antimicrobial-related side effects, and perpetuates colonization of resistant organisms, precipitating antimicrobial resistance. This statement provides health care providers with a toolkit for optimal management of bacterial SSTIs, including recurrent episodes. It does not comprehensively examine SSTI treatment principles in immunocompromised or burn patients due to the management complexities of both settings.

Keywords: Abscess; Cellulitis; Decolonization; MRSA; Skin infection

Background

The skin protects its host from infection by acting as a physical barrier. Damage to this barrier from a variety of processes, including atopic disease, skin irritants, xerosis, micro abrasions, ectoparasites (e.g., scabies, lice), trauma, surgery, viral skin infections (e.g., herpes-zoster/herpes simplex [HZV/HSV]), or hair/nail infections, increases vulnerability to infection.

Skin and soft tissue infections (SSTIs) are some of the most common infectious diseases encountered in paediatrics. A Canadian multicentre study of 12 remote/isolated communities estimated the prevalence of SSTIs in some sites at 36.8%, with 60.2% of the total population studied having received at least one antibiotic prescription in the preceding 12 months^[1]. Such high antimicrobial use may be linked to higher rates of antibiotic-resistant infections in these communities. Both the frequency of SSTIs in the paediatric population and the potential for high antimicrobial use resulting in infections with resistant organisms make antimicrobial stewardship a public health issue of paramount concern. This statement provides health care providers with a toolkit for optimizing the management of bacterial SSTIs, including recurrent episodes. It replaces previous guidance on methicillin-resistant Staphylococcus aureus (MRSA) skin abscesses from the Canadian Paediatric Society^[2].

SSTIs have been categorized in various ways, without universal consensus. A list of common terms can be found in Table 1. Bacterial infections of the epidermis are typically less severe than deeper infections, but they can facilitate bacterial entry into deeper tissues. Abscesses can manifest in any of the tissue layers and are characterized by discrete collections of pus (Figure 1).

Table 1. Skin and soft tissue infections: Terms and definitions*

Figure 1. Skin and soft tissue infection anatomy



Delays in initiating treatment and inconsistencies in management practices can cause disease progression, pain, deep-tissue abscesses, musculoskeletal infections, and hypo- and hyperpigmentation. Inappropriate antibiotic initiation, duration, and drug or route selection for simple infections are detrimental to the individual’s microbiome, increase antimicrobial-related side effects (e.g., Clostridioides difficile), and have societal impacts through increased antimicrobial resistance.

Microbiology

The most common pathogens associated with community-acquired bacterial SSTIs include methicillin-susceptible or -resistant Staphylococcus aureus (MSSA or MRSA) and Streptococcus pyogenes (Group A Streptococcus [GAS]). Both pathogens can cause a range of SSTIs, from mild infections (e.g., folliculitis, impetigo) to severe necrotizing infections complicated by toxic shock or sepsis. Recent reports have suggested an increase in invasive GAS infections^[3]. Non-pyogenic cellulitis has been reported more with GAS compared with S. aureus, although microbiological confirmation is rare in this context and Canadian data is lacking in paediatric populations^[4].

Although variable by province/territory, an increase in paediatric MRSA has been recognized in Canada^[5][6]. This rise disproportionately impacts certain minoritized groups, such as Indigenous communities in remote/isolated areas, where MRSA proportions can exceed 50%^[7]. Such prevalence indicates that certain social determinants of health, such as crowded housing, are risk factors for SSTIs^[8]. Colonization rates of up to 67% have been reported in households where one member has had a recent MRSA infection^[9]. Certain behaviours, such as nose-picking, have been associated with increasing rates of S. aureus carriage^[10][11]. Some studies have shown that approximately one-third of individuals colonized with MRSA will develop an SSTI^[12][13], and up to 70% with an MRSA SSTI may experience recurrence(s) over the following 6 to 12 months^[14]. SSTI risk in children also increases with MSSA colonization^[15].

Other bacterial pathogens and non-infectious mimics should be considered based on exposure history and examination. Waterborne pathogens include Aeromonas spp (in fresh water), Vibrio spp (in brackish or salt water), and Pseudomonas aeruginosa (causing hot tub folliculitis, or ecthyma). Anaerobic bacteria can cause SSTIs following a deep puncture wound or animal or human bite, and may feature in cases of longstanding ulcerative lesions, immunocompromised hosts, and prolonged or recent antimicrobial use. Consider non-tuberculous mycobacteria, candida, moulds, and cutaneous dermatophytes when the epidemiology or morphology of lesions suggests such etiologies. VZV infections predispose to SSTIs, including invasive infections (e.g., necrotizing fasciitis)^[16]. Eczema can also be superinfected with HSV (eczema herpeticum) or enteroviruses (eczema coxsackium). Non-infectious mimics of SSTIs include, but not limited to: pyoderma gangrenosum, pyogenic granuloma, psoriasis, non-infected atopic dermatitis, hidradenitis suppurativa, venous stasis or thrombosis, vasculitis, urticaria, contact dermatitis, malignancy, and other non-infectious dermatologic or rheumatologic conditions.

History and physical examination

The epidemiological triad comprises the host, pathogen, and environment. A focused history should consider interactions among the three, including preceding skin trauma, bites (animal or human), water exposures, travel, sick contacts, social, occupational, and recreational activities, and hospitalization(s) or frequent health care admissions or attendance. Chronicity (i.e., acute, subacute, or chronic) and associated symptoms (i.e., fever, pain) should form part of an SSTI history. Past medical history should include personal and family experience of previous SSTIs, underlying medical conditions, known history or risk factors for MRSA colonization, and vaccination status. While most children with recurrent SSTIs are immunocompetent, a careful history should ensure there are no “red flags” for inborn errors of immunity, such as recurrent, invasive, multi-site, or unusual infections, early age of onset, deep skin or lymph node abscesses, failure to thrive, and severe or intractable eczema. In cases of recurrent perianal abscesses, inflammatory bowel disease should be considered.

Severity assessments are largely subjective, though scoring systems have been validated to help define mild, moderate, and severe disease. One scoring system for cellulitis is the Melbourne ASSET score. Higher scores suggest increasing severity, with a cut-off of 4 limiting unnecessary intravenous (IV) antibiotics^[17]. In a case-based survey of paediatricians, the most common findings associated with severity and treatment with IV versus oral antimicrobials included tracking lymphangitis, functional impairment of the affected area, fever, oral antibiotics within the previous 24 hours, size, site, and degree of swelling and tenderness^[18]. Further findings suggestive of severe invasive disease include pain out of proportion to clinical findings, rapidly expanding erythema, necrosis, and crepitus.

Diagnostics

Microbiological samples should be sought for open wounds or lesions with visible pus or fluid. Pus collected by needle aspirate, surgical, or manual drainage of abscesses should be cultured and prioritized over swabs based on their higher microbiological yield. Superficial swabs of intact and non-intact skin or ulcers are of limited use due to isolation of colonizing microbiota. If debridement is indicated, tissue samples for culture are of highest yield. Other samples (e.g., skin biopsy) may be considered in settings of chronic infection, failed therapy, an immunocompromised child, or unusual exposure(s). In such cases, an infectious disease (ID) or dermatology consult (or both) should be sought to guide specimen requests. Specialized viral swabs from deroofed vesicles placed in dedicated media are warranted for HSV, VZV, and enterovirus polymerase chain reaction (PCR) testing. Blood cultures are rarely indicated with clinically mild to moderate SSTIs but should be collected with systemic illness, shock, and severe or deep-seated infections. Dermatophyte and ectoparasite skin scrapings should be collected when clinically indicated, following local laboratory protocols.

Management

(Figure 2)

Medical management

Clinicians should first consider whether antimicrobials are warranted. Minor infections can resolve spontaneously with wound care alone. Best practices for wound care management can be found at woundscanada.ca. In addition to wound care, a short-course prescription (3 to 5 days) of topical antimicrobials may be required. Evidence of benefit for over-the-counter topical antimicrobials (e.g., polymyxin B, bacitracin, neomycin) is unclear^[19]. Empiric antimicrobial choices should be individualized based on history (e.g., exposures), examination findings, and previous microbiology results when available. More recent microbiological results should be prioritized. Local paediatric-specific antibiograms are encouraged to help guide empiric antimicrobial choice.

Empiric antibiotics should target the most common pathogens causing SSTIs (Table 2^[20]-[22]) and most infections are amenable to oral treatment. In the majority of cases, including moderate infections, oral cephalexin is appropriate, provided that adequate dosing is administered^[23]. Combination therapy with cephalexin and trimethoprim/sulfamethoxazole or broad-spectrum outpatient IV antibiotics (e.g., ceftriaxone) are discouraged. Empiric therapy targeting MRSA may be warranted in some cases, such as when children are colonized or living in MRSA-prevalent areas (i.e., where >10% to 15% S. aureus isolates are MRSA)^[24]. Oral trimethoprim/sulfamethoxazole is preferred due to high susceptibility rates for MRSA in Canada. Clindamycin resistance is higher, although this antibiotic may still be considered for children with prior susceptible isolates or when antibiograms demonstrate high susceptibility. When a patient is known to be carrying MRSA (e.g., MRSA-positive nares) or later found to be after initiating antimicrobials but has improved with non-MRSA treatment, switching antimicrobials is not necessary. For children colonized with MRSA or living in highly MRSA-endemic areas and presenting with a non-purulent SSTI (e.g., cellulitis) without systemic features, consider initiating a non-MRSA antimicrobial (e.g., cephalexin) with close follow-up^[25][26].

For hospitalized children, antimicrobial choice is guided by the history and severity of disease. For non-toxic children who have not been exposed to atypical pathogens, IV cefazolin or, when MRSA is suspected, vancomycin, is appropriate. For children who are systemically unwell or toxic (e.g., concern for sepsis, fasciitis/myositis, shock), many experts recommend initiating broad-spectrum coverage (ceftriaxone or piperacillin-tazobactam, plus vancomycin) empirically, then discontinuing vancomycin when MRSA is excluded. The addition of an anti-toxin antibiotic (e.g., clindamycin) should be strongly considered in such cases^[27]. ID consultation should be sought and antibiotics targeted to microbiology results. When SSTIs are complicated by a herpesvirus (e.g., HSV/VZV), IV acyclovir or oral acyclovir/valacyclovir may be warranted.

Table 2. Antimicrobials for treating systemic skin and soft tissue infections (SSTIs)

* Dose adjustments may be required based on hepatic/renal function or for infants. Consult with pharmacy as required.
† Low risk: <10%–15% S. aureus isolates are MRSA; High risk: >10%–15% S. aureus isolates are MRSA GAS Group A streptococcus; IV Intravenous; MRSA Methicillin-resistant Staphylococcus aureus; MSSA Methicillin-susceptible Staphylococcus aureus; TMP/SMX Trimethoprim/sulfamethoxazole 

Surgical management

Source control of abscesses through surgical or manual drainage is vital. Warm compresses can facilitate drainage. When drainage of an uncomplicated small collection is achieved in a healthy host, without significant surrounding cellulitis, antimicrobials are rarely warranted^[28]-[30]. If antimicrobials were started previously, they can typically be discontinued when drainage is achieved. Post-drainage wound care is important for healing and consultation with experts in wound care may be considered.

In cases of necrotizing infection, urgent surgical consultation for debridement is essential. Deep samples of pus and tissue should be sent for aerobic and anaerobic cultures. Debridement of chronic ulcers and biopsies of unusual or chronic lesions and those failing therapy ensures that tissue can be sent for bacterial, mycobacterial, and fungal cultures and for histopathology to aid diagnosis and targeted therapy.

Figure 2. Treatment algorithm for skin and soft tissue infections (SSTIs)

* Abscess, carbuncle, furuncle
† Mild infection (small area): Systemically well, localized SSTI, no or minimal erythema or induration, no deep-seated infection. Outpatient treatment. May resolve with appropriate skin care alone
‡ Moderate infection (e.g., limited cellulitis): Systemically well, not rapidly progressive, no deep-seated infection. Outpatient treatment
§ Severe infection (e.g., widespread cellulitis/deep-seated infection): Extensive infection, clinically unstable, rapidly progressive, necrosis, pain out of proportion, crepitus. Inpatient treatment. If systemically unwell, start empiric antibiotics urgently
¶ Re-evaluate diagnosis (repeat history/examination), need for source control
** Consult ID, refer to local antimicrobial guidelines
‡‡ MRSA risk factors: MRSA colonized, previous or recurrent MRSA SSTIs, local prevalence >10% to 15%
ID Infectious diseases; IV Intravenous; IVIG Intravenous immunoglobulin; MRSA Methicillin-resistant Staphylococcus aureus

Preventing recurrence

Preserving an intact skin barrier, including wound management and control of primary dermatologic disorders, is important to prevent SSTIs, including recurrence. Optimize eczema management, including breaking the pruritus→scratch→skin breakdown cycle. Dermatology consultation should be considered for children with difficult-to-control skin conditions that threaten recurrence or serious infection.

In healthy patients, decolonization has achieved mixed results in preventing SSTI recurrence, and treatment regimens and practices vary with no clear consensus^[31]-[36]. Decolonization practices can also be costly and dry the skin if concurrent moisturizers are not used. Recurrence of colonization is common, even with diligent decolonization practices^[37]-[39]. Some experts reserve decolonization for recurrence of moderate to severe SSTIs, household outbreaks, or to prepare for procedures with high infection risk. Challenging cases often benefit from ID consultation, and the advantages and disadvantages of treatments and their variable success rates should be discussed with families. When recommended, a 5-day trial of 2% mupirocin ointment twice daily to nares, combined with daily cleaning with 4% chlorhexidine soap or 2% chlorhexidine wipes (for 5 to 7 days) is suggested^[40]. Dilute bleach baths (DBBs) are an acceptable alternative and can be used as part of both decolonization regimens (daily for 5 to 7 days) or maintenance suppression (or both)^[41]. Concurrent family/household member decolonization may also be considered to increase chances of decolonization success, although evidence for this practice is inconsistent^[42]-[44]. Use of oral antimicrobial agents for decolonization is discouraged unless directed by ID^[31].

DBBs are prepared with 1/4 to 1/2 cup bleach added to a bathtub of water. Children should be encouraged to sit in the bath for 5 to 10 minutes. Swimming in a chlorinated pool has similar effect. Maintenance DBBs for children with a recurrent SSTI may be continued once or twice per week to suppress bacterial microbiota. Make sure that skin moisturizer is being applied after bathing. Concurrent environmental decolonization measures in the household include cleaning surfaces with bleach-containing solution, focusing on “high-touch” surfaces, washing towels, clothing, and bedding in hot water, and replacing or disinfecting personal hygiene items^[45]-[47]. Sharing such items and sharing athletic equipment are discouraged. To help maximize success, clinicians are encouraged to develop written handouts describing these regimens, including images, detailed instructions, with translation into local languages.

Additional measures to decrease recurrence include diligent wound care, covering open wounds, encouraging universal uptake of varicella vaccination, and regular cleaning of communal, sporting, and exercise equipment (ideally after each use). Scabies and lice predispose to SSTIs and should be treated per local guidelines^[48][49]. Chronic antibiotic suppression is rarely indicated but may be considered in consultation with ID for certain inborn errors of innate immunity, chronic or recurrent dermatologic diseases, or conditions of aberrant lymphatic drainage.

Recommendations

1. Managing skin and soft tissue infections (SSTIs) should be based on a focused history and careful assessment of the severity of infection.
2. Empiric antimicrobial prescribing for SSTIs should be based on locally sourced and paediatric-specific antibiograms. Prioritize the most narrow-spectrum antimicrobial.
3. Manage minor SSTIs with drainage and/or skin care alone. In select cases, the addition of topical antimicrobial treatment may be required.
4. Adequate drainage of abscesses negates the need to initiate antimicrobials in most outpatient cases. If antimicrobials are commenced, they can be discontinued when source control is achieved, provided there is no significant surrounding cellulitis.
5. When oral antimicrobials are warranted, cephalexin monotherapy is the antimicrobial of choice. When methicillin-resistant Staphylococcus aureus is suspected, trimethoprim/sulfamethoxazole monotherapy is the antimicrobial of choice for outpatient management. It also has activity against Group A streptococcal infections.
6. Short courses of antimicrobials (5 to 7 days) are often sufficient. Longer treatment durations should be reserved for more severe or complicated infections. Even severe SSTIs rarely require >7 days of antimicrobials. Failure to respond should prompt re-evaluation of the diagnosis and assessment for source control.
7. Reserve intravenous antimicrobials for severe, deep-seated, or necrotizing infections. Narrow-spectrum, short-courses of antimicrobials should be prioritized based on microbiological testing, with a focus on source control.
8. Preventing recurrent SSTIs should focus on maintenance of intact skin barrier, treatment of underlying skin conditions (e.g., eczema), and good wound and abrasion care.
9. In select individuals and households, decolonization protocols can be considered.

Acknowledgement

This position statement was reviewed by the Community Paediatrics and First Nations, Inuit and Métis Health Committees of the Canadian Paediatric Society (CPS). It was also reviewed by the CPS Community Paediatrics, Hospital Paediatrics, and Paediatric Emergency Medicine Section Executives, and by members of the Association of Medical Microbiology and Infectious Disease Canada (AMMI).

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CANADIAN PAEDIATRIC SOCIETY INFECTIOUS DISEASES AND IMMUNIZATION COMMITTEE (2024-2025)

Members: Michelle Barton MD (Chair), Laura Sauvé MD (Past Chair), Eugene Ng MD (Board Representative), Ari Bitnun MD, Jeannette Comeau MD MSc, Sergio Fanella MD, Justin Penner MD, MSc
Liaisons: Dorothy Moore MD (National Advisory Committee on Immunization), Ari Bitnun MD (Canadian Paediatric and Perinatal HIV/AIDS Research Group), Isabelle Viel-Thériault MD (Committee to Advise on Tropical Medicine and Travel), Marina Salvadori MD (Public Health Agency of Canada), Sean O’Leary (American Academy of Pediatrics, Committee on Infectious Diseases), Rupeena Purewal MD (Immunization Monitoring Program, ACTive), Cora Constantinescu MD (Association of Medical Microbiology and Infectious Disease Canada, Pediatric Committee)
Principal authors: Justin Penner MD, Sergio Fanella MD

Funding
There is no funding to declare.

Potential Conflict of Interest
Dr. Fanella reported receiving funding as a local site PI for MCT for COVID19 vaccines in children (ModernaTx). No other disclosures were reported.

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References

1. Jeong D, Nguyen HNT, Tyndall M, Schreiber YS. Antibiotic use among twelve Canadian First Nations communities: A retrospective chart review of skin and soft tissue infections. BMC Infect Dis 2020;20(1):118. doi: 10.1186/s12879-020-4842-1
2. Robinson JL, Salvadori MI; Canadian Paediatric Society, Infectious Diseases and Immunization Committee. Management of community-associated methicillin-resistant Staphylococcus aureus skin abscesses in children. Paediatr Child Health 2011;16(2):115-6. doi: 10.1093/pch/16.2.115
3. Centers for Disease Control and Prevention. Group A Strep Surveillance and Trends. July 8, 2024 (Accessed October 22, 2025).
4. Stevens DL, Bryant AE. Impetigo, Erysipelas and Cellulitis. February 10, 2016. In: Ferretti JJ, Stevens DL, Fischetti VA, eds. Streptococcus pyogenes: Basic Biology to Clinical Manifestations. Oklahoma City, OK: University of Oklahoma Health Sciences Center; 2016.
5. Nichol KA, Adam HJ, Golding GR, et al; Canadian Antimicrobial Resistance Alliance (CARA) and CANWARD. Characterization of MRSA in Canada from 2007 to 2016. J Antimicrob Chemother 2019;74(Suppl 4):iv55-iv63. doi: 10.1093/jac/dkz288
6. Public Health Agency of Canada. Canadian Antimicrobial Resistance Surveillance System (CARSS) Report 2022. January 2023 (Accessed October 22, 2025).
7. Fanella S, Embree J. Pediatric Staphylococcus aureus infections: Impact of methicillin resistance at a Canadian center. South Med J 2015;108(5):254-7. doi: 10.14423/SMJ.0000000000000274
8. Butler-Jones D, Wong T. Infectious disease, social determinants and the need for intersectoral action. Can Commun Dis Rep 2016;42(Suppl 1):S118-S120.
9. Fritz SA, Hogan PG, Hayek G, et al. Staphylococcus aureus colonization in children with community-associated Staphylococcus aureus skin infections and their household contacts. Arch Pediatr Adolesc Med 2012;166(6):551-7. doi: 10.1001/archpediatrics.2011.900
10. Loewen K, Schreiber Y, Kirlew M, Bocking N, Kelly L. Community-associated methicillin-resistant Staphylococcus aureus infection: Literature review and clinical update. Can Fam Physician 2017;63(7):512-20. Erratum in: Can Fam Physician 2017;63(8):596.
11. Wertheim HFL, van Kleef M, Vos MC, Ott A, Verbrugh HA, Fokkens W. Nose picking and nasal carriage of Staphylococcus aureus. Infect Control Hosp Epidemiol 2006;27(8):863-7. doi: 10.1086/506401
12. Ellis MW, Hospenthal DR, Dooley DP, Gray PJ, Murray CK. Natural history of community-acquired methicillin-resistant Staphylococcus aureus colonization and infection in soldiers. Clin Infect Dis 2004;39(7):971-9. doi: 10.1086/423965
13. Yang ES, Tan J, Eells S, Rieg G, Tagudar G, Miller LG. Body site colonization in patients with community-associated methicillin-resistant Staphylococcus aureus and other types of S. aureus skin infections. Clin Microbiol Infect 2010;16(5):425-31. doi: 10.1111/j.1469-0691.2009.02836.x
14. Creech CB, Al-Zubeidi DN, Fritz SA. Prevention of recurrent staphylococcal skin infections. Infect Dis Clin North Am 2015;29(3):429-64. doi: 10.1016/j.idc.2015.05.007
15. Faden H, Lesse AJ, Trask J, et al. Importance of colonization site in the current epidemic of staphylococcal skin abscesses. Pediatrics 2010;125(3):e618-24. doi: 10.1542/peds.2009-1523
16. Davies HD, McGeer A, Schwartz B, et al. Invasive group A streptococcal infections in Ontario, Canada. Ontario Group A Streptococcal Study Group. N Engl J Med 1996;335(8):547-54. doi: 10.1056/NEJM199608223350803
17. Ibrahim LF, Hopper SM, Donath S, Salvin B, Babl FE, Bryant PA. Development and validation of a cellulitis risk score: The Melbourne ASSET Score. Pediatrics 2019;143(2):e20181420. doi: 10.1542/peds.2018-1420
18. Ibrahim LF, Babl FE, Hopper SM, Bryant PA. Cellulitis: Oral versus intravenous and home versus hospital—What makes clinicians decide? Arch Dis Child 2020;105(4):413-15. doi: 10.1136/archdischild-2019-316824
19. Banerjee S, Argáez C. Topical antibiotics for infection prevention: A review of the clinical effectiveness and guidelines. Ottawa, Ont.: Canadian Agency for Drugs and Technologies in Health; March 30, 2017.
20. Kimberlin DW, Banerjee R, Barnett ED, Lynfield R, Sawyer MH. Tetracyclines. In: Red Book: 2024–2027 Report of the Committee on Infectious Diseases (33rd edn.). Itaska, IL: American Academy of Pediatrics; May 2024.
21. Ravindra D, Huang G, Hallett K, Burgner DP, Gwee A, Silva MJ. Antibiotic exposure and dental health: A systematic review. Pediatrics 2023;152(1):2023061350. doi: 10.1542/peds.2023-061350
22. McCreary EK, Johnson MD, Jones TM, et al. Antibiotic myths for the infectious diseases clinician. Clin Infect Dis 2023;77(8):1120-5. doi: 10.1093/cid/ciad357. Erratum in: Clin Infect Dis 2024;78(6):1780.
23. Trottier ED, Farley St-Amand B, Vincent M, et al. Outpatient management of moderate cellulitis in children using high-dose oral cephalexin. Paediatr Child Health 2022;27(4):213-9. doi: 10.1093/pch/pxac031
24. Kaplan SL. Treatment of community-associated methicillin-resistant Staphylococcus aureus infections. Pediatr Infect Dis J 2005;24(5):457-8. doi: 10.1097/01.inf.0000164162.00163.9d
25. Eells SJ, Chira S, David CG, Craft N, Miller LG. Non-suppurative cellulitis: Risk factors and its association with Staphylococcus aureus colonization in an area of endemic community-associated methicillin-resistant S. aureus infections. Epidemiol Infect 2011;139(4):606-12. doi: 10.1017/S0950268810001408
26. Rajan S. Skin and soft-tissue infections: Classifying and treating a spectrum. Cleve Clin J Med 2012;79(1):57-66. doi: 10.3949/ccjm.79a.11044
27. Farrell CA. Diagnosis and management of severe sepsis in the paediatric patient. Paediatr Child Health 2020;25(7):475-6. doi: 10.1093/pch/pxz178
28. Singer AJ, Thode HC. Systemic antibiotics after incision and drainage of simple abscesses: A meta-analysis. Emerg Med J 2014;31(7):576–8. doi: 10.1136/emermed-2013-202571
29. Daum RS, Miller LG, Immergluck L, et al. A placebo-controlled trial of antibiotics for smaller skin abscesses. N Engl J Med 2017;376(26):2545–55. doi: 10.1056/NEJMoa1607033
30. Wang W, Chen W, Liu Y, et al. Antibiotics for uncomplicated skin abscesses: Systematic review and network meta-analysis. BMJ Open 2018;8(2):e020991. doi: 10.1136/bmjopen-2017-020991
31. Helbo T, Boel JB, Bartels MD, Ahlström MG, Holzknecht BJ, Eriksen HB. Carriage of methicillin-resistant Staphylococcus aureus in children <6 years old: A retrospective follow-up study of the natural course and effectiveness of decolonization treatment. J Antimicrob Chemother 2024;79(4):826-34. doi: 10.1093/jac/dkae036
32. Piewngam P, Otto M. Staphylococcus aureus colonisation and strategies for decolonisation. Lancet Microbe 2024;5(6):e606-18. doi: 10.1016/S2666-5247(24)00040-5
33. Klempner MS, Styrt B. Prevention of recurrent staphylococcal skin infections with low-dose oral clindamycin therapy. JAMA 1988;260(18):2682-5.
34. Raz R, Miron D, Colodner R, Staler Z, Samara Z, Keness Y. A 1-year trial of nasal mupirocin in the prevention of recurrent staphylococcal nasal colonization and skin infection. Arch Intern Med 1996;156(10):1109-12.
35. Coates T, Bax R, Coates A. Nasal decolonization of Staphylococcus aureus with mupirocin: Strengths, weaknesses and future prospects. J Antimicrob Chemother 2009;64(1):9-15. doi: 10.1093/jac/dkp159
36. Creech CB, Beekmann SE, Chen Y, Polgreen PM. Variability among pediatric infectious diseases specialists in the treatment and prevention of methicillin-resistant Staphylococcus aureus skin and soft tissue infections. Pediatr Infect Dis J 2008;27(3):270-2. doi: 10.1097/INF.0b013e31815c9068
37. Doebbeling BN, Reagan DR, Pfaller MA, Houston AK, Hollis RJ, Wenzel RP. Long-term efficacy of intranasal mupirocin ointment. A prospective cohort study of Staphylococcus aureus carriage. Arch Intern Med 1994;154(13):1505-8. doi: 10.1001/archinte.1994.00420130101013
38. Fernandez C, Gaspar C, Vindel AT, Saez-Nieto JA, Cruzet F, Aguilar L. A double-blind, randomized, placebo-controlled clinical trial to evaluate the safety and efficacy of mupirocin calcium ointment for eliminating nasal carriage of Staphylococcus aureus among hospital personnel. J Antimicrob Chemother 1995;35(3):399-408. doi: 10.1093/jac/35.3.399
39. Mody L, Kauffman CA, McNeil SA, Galecki AT, Bradley SF. Mupirocin-based decolonization of Staphylococcus aureus carriers in residents of 2 long-term care facilities: A randomized, double-blind, placebo-controlled trial. Clin Infect Dis 2003;37(11):1467-74. doi: 10.1086/379325
40. Whitman TJ, Herlihy RK, Schlett CD, et al. Chlorhexidine-impregnated cloths to prevent skin and soft-tissue infection in Marine recruits: A cluster-randomized, double-blind, controlled effectiveness trial. Infect Control Hosp Epidemiol 2010;31(12):1207-15. doi: 10.1086/657136
41. Fisher RG, Chain RL, Hair PS, Cunnion KM. Hypochlorite killing of community-associated methicillin-resistant Staphylococcus aureus. Pediatr Infect Dis J 2008;27(10):934-5. doi: 10.1097/INF.0b013e318175d871
42. Fritz SA, Hogan PG, Hayek G, et al. Household versus individual approaches to eradication of community-associated Staphylococcus aureus in children: A randomized trial. Clin Infect Dis 2012;54(6):743-51. doi: 10.1093/cid/cir919
43. Wiese-Posselt M, Heuck D, Draeger A, et al. Successful termination of a furunculosis outbreak due to lukS-lukF-positive, methicillin-susceptible Staphylococcus aureus in a German village by stringent decolonization, 2002-2005. Clin Infect Dis 2007;44(11):e88-95. doi: 10.1086/517503
44. Hogan PG, Parrish KL, Mork RL, et al. HOME2 Study: Household versus personalized decolonization in households of children with methicillin-resistant Staphylococcus aureus skin and soft tissue infection—A randomized clinical trial. Clin Infect Dis 2021;73(11):e4568-77. doi: 10.1093/cid/ciaa752
45. Hogan PG, Mork RL, Thompson RM, et al. Environmental methicillin-resistant Staphylococcus aureus contamination, persistent colonization, and subsequent skin and soft tissue infection. JAMA Pediatr 2020;174(6):552-62. doi: 10.1001/jamapediatrics.2020.0132
46. Huang SS, Singh R, McKinnell JA, et al; Project CLEAR Trial. Decolonization to reduce postdischarge infection risk among MRSA carriers. N Engl J Med 2019;380(7):638-50. doi: 10.1056/NEJMoa1716771
47. Mork RL, Hogan PG, Muenks CE, et al. Longitudinal, strain-specific Staphylococcus aureus introduction and transmission events in households of children with community-associated meticillin-resistant S aureus skin and soft tissue infection: A prospective cohort study. Lancet Infect Dis 2020;20(2):188-98. doi: 10.1016/S1473-3099(19)30570-5
48. Banerji A; Canadian Paediatric Society, First Nations, Inuit and Métis Health Committee. Scabies. Paediatr Child Health 2015;20(7):395-402. doi: 10.1093/pch/20.7.395
49. Cummings C, Finlay JC, MacDonald NE. Head lice infestations: A clinical update. Paediatr Child Health 2018;23(1):e18-e24. doi: 10.1093/pch/pxx165

Disclaimer: The recommendations in this position statement do not indicate an exclusive course of treatment or procedure to be followed. Variations, taking into account individual circumstances, may be appropriate. Internet addresses are current at time of publication.

 

How to Recognize Serious Pediatric Pain

Evaluating Pain in a Child

Pain can be difficult for a child to describe. Also, a child isn't always able to recognize a sensation as pain. An older child may be able to describe tingling, cramping, or sharp sensations and may be able to tell where and when the sensation occurs. When a young child is in pain, the signs can be hard to recognize.

Signs that may mean your child is in pain include:

• Changes in usual behavior. Your child may eat less or become fussy or restless.
• Crying, grunting, or breath-holding.
• Crying that can't be comforted.
• Facial expressions, such as a furrowed brow, a wrinkled forehead, closed eyes, or an angry appearance.
• Sleep changes, such as waking often or sleeping more or less than usual. Even children in severe pain may take short naps because they are tired.
• Body movements, such as making fists, guarding a part of the body (especially while walking), kicking, clinging, or not moving.

Some children may deny that they are in pain because they are afraid of medical procedures. For example, admitting that they are in pain might mean blood tests, which may be painful themselves. Some children may try to ignore their pain rather than take medicines, which often have discomforting side effects.

Pain isn't a visible symptom, so you and your child's treatment team will need to rely on your child as the primary source of information on the status of the pain. Only your child knows if pain is present. And experts say that children rarely pretend to have pain. 

 

How to Recognize Serious Pediatric Pain

The Urgences 2026 conference, organized by the French Society of Emergency Medicine, was held in Paris in early June. To avoid overlooking serious problems, speakers at the session “When to Investigate Pain: Red Flags for Pain in Children” highlighted the warning signs to look for based on the location of pediatric pain.

Hip Pain Red Flags

As noted by Guillaume Lopin , an emergency physician and pediatrician at Toulouse University Hospital, Toulouse, France, about half of the hip pain cases in pediatric emergency departments are due to acute transient synovitis (TS). Other causes include osteoarticular infection, slipped capital femoral epiphysis, primary osteochondritis dissecans (OCD), and, less commonly, tumors, leukemia, abuse, or hemophilia.

Key Points

• Hip pain: TS only if age 3-9, WB+, monoarticular, well-appearing, favorable course.
• Hip red flags: fever, total functional loss, insomnia, chronicity, <3 y, >10 y, multi-joint.
• Abdominal pain: fixed nonperiumbilical pain, insomnia, progression, no pain-free intervals → surgical workup.
• Appendicitis: WBC/neutrophils + PAS; US for intermediate risk; avoid CT radiation.
• Chest pain: <5% cardiac; exertional/sudden/constrictive pain, abnormal exam/ECG, ↑troponin if red flags.\
•  
•  
  
  
  

  Hip Pain Red Flags

  As noted by Guillaume Lopin , an emergency physician and pediatrician at Toulouse University Hospital, Toulouse, France, about half of the hip pain cases in pediatric emergency departments are due to acute transient synovitis (TS). Other causes include osteoarticular infection, slipped capital femoral epiphysis, primary osteochondritis dissecans (OCD), and, less commonly, tumors, leukemia, abuse, or hemophilia.

•  TS should be considered only if all criteria are met: age between 3 and 9 years, typical symptoms and physical examination findings, the ability to bear weight on the affected leg, preserved overall condition, monoarticular involvement, and a favorable prognosis.
• The red flags are as follows: 

• High fever may signal a true medical emergency, including septic arthritis, which typically presents with severe pain, marked loss of function, and joint effusion. A moderate fever may point to osteomyelitis, which usually causes less intense pain and less marked functional limitation, with no effusion and a normal initial x-ray.
• In children younger than 3 years, obtaining a reliable history and performing a thorough physical examination can be difficult, and the initial signs are often nonspecific. In this age group, the condition may represent juvenile idiopathic arthritis (JIA), an unreported injury, or abuse; less commonly, it may be congenital dislocation or hemophilia. In children older than 10 years, a stress fracture should be considered and investigated.
• With total functional impairment or hyperalgesia, septic arthritis should be considered, along with unstable effusion, fracture in children younger than 3 years, abuse, or a spontaneous pathologic fracture. In cases of pain severe enough to cause insomnia, consider osteoarthritis, acute leukemia, a bone tumor, or intra-abdominal infection such as psoitis.
• With chronicity, consider OCD, stable slipped capital femoral epiphysis.
• If another joint is affected, consider viral arthritis, reactive arthritis, or JIA, and consult a pediatric rheumatologist.

In all cases, clinicians should avoid defaulting to easy explanation such as somatization or referred pain, including tendinitis, growing pains, functional pain, or an adolescent crisis, Lopin concluded.

Abdominal Pain Red Flags

Romain Guedj , MD, PhD, a pediatrician in the Department of Emergency Pediatrics, Trousseau University Hospital, Assistance Publique - Hôpitaux de Paris, Paris, France, reassured clinicians, saying not to hesitate to administer level 2 or 3 analgesics as this will not interfere with the clinical examination.

He then outlined the potential surgical causes, including intestinal obstruction, appendicitis or peritonitis, testicular or ovarian torsion, and an abdominal mass, possibly a tumor.

“The pain is typically nonperiumbilical, fixed in location, causes insomnia, worsens over time, and is not associated withpain-free intervals. We would then proceed with laboratory testing and, if indicated, ultrasound,” Guedj said.

Although appendicitis is the most common pediatric surgical emergency, it can be difficult to diagnose. The location of pain depends on the position of the cecum, and clinical findings such as fever, localized tenderness, psoitis, or pain when hopping on one foot are not always highly sensitive or specific.

In laboratory tests, white blood cells — and in particular neutrophils — are highly specific. The pediatrician recommends calculating the Pediatric Appendicitis Score and performing an ultrasound in cases of intermediate risk. Avoid CT scans in children because they expose them to radiation.

In most cases, no definitive diagnosis can be made. The pediatrician therefore advises telling parents that there are no alarming signs at the time of the visit, that the cause of the child’s pain is not yet clear, but that this is common in cases of abdominal pain and often resolves on its own. Parents should also be instructed to return for reevaluation if the pain worsens, keeps the child awake at night, persists, or if other symptoms develop.

The underlying cause may also be medical, involving the digestive system, liver, kidneys, urinary tract, or genital organs. It may likewise reflect an infection, such as an ear, nose, and throat or pulmonary infection; rheumatic purpura; or an endocrine disorder, including diabetic ketoacidosis or acute renal failure.

Chest Pain Red Flags

Common causes of chest pain in pediatric emergency departments include asthma attacks, parietal pain, and chest trauma: fewer than 5% of pediatric chest pain cases are of cardiac origin, according to Alexis Louvel , an emergency medicine physician at Rouen University Hospital Center, Rouen, France.

These cases may involve coronary artery anomalies, which can be difficult to diagnose but typically present with exertional pain, aortic dissection, or pneumothorax, which causes sudden, severe pain. Other possibilities include myocarditis, in which patients experience constricting pain, or pulmonary embolism, where a risk factor is identified in 95% of the cases.

The red flags are as follows:

• During the medical history, clinicians should note pain or discomfort with exertion, sudden-onset pain that reaches maximal intensity immediately, constrictive pain, pain severe enough to disrupt sleep, or a viral or postviral context.
• During the physical examination, although specificity is limited, clinicians should look for unexplained tachycardia, hypotension, low oxygen saturation, asymmetric vesicular breath sounds, a pericardial friction rub, a new-onset murmur — in which case, the parents should be questioned and the medical record reviewed — and hepatomegaly.
• On testing, an abnormal ECG.
• In laboratory testing, a positive troponin result should be considered, but only if one of the warning signs listed above is present.

Finally, for headaches in children presenting to the emergency department, the French National Authority for Health guideline on Headaches in Children and Adolescents: Relevance of Imaging remains the preferred reference. Headaches due to a serious underlying medical condition are rare — fewer than 2% are linked to a brain tumor — and are almost always associated with a clinical abnormality.

This story was translated from Medscape’s French edition.