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Suppurative thyroiditis in children and adolescents

Suppurative thyroiditis in children and adolescents
Literature review current through: Jan 2024.
This topic last updated: Apr 11, 2023.

INTRODUCTION — Suppurative thyroiditis (ST) is caused by an infection of the thyroid gland (usually bacterial) and is rare but potentially life-threatening [1-3]. The disease is far less common than other inflammatory conditions of the thyroid gland, including subacute granulomatous thyroiditis (which results from a viral infection of the gland) and chronic thyroiditis (which is usually autoimmune in nature). The signs and symptoms of ST may mimic these and other noninfectious inflammatory conditions. Recognition of the clinical and bacteriologic features of ST is essential for prompt management.

The primary treatment for ST is antimicrobial therapy, directed against the likely bacterial pathogens. Although most cases of ST are caused by aerobic bacteria, anaerobic bacteria are increasingly recognized as a cause of ST, and this has led to revision of treatment protocols for this condition. Rarely, mycobacteria, fungi, or other nonbacterial pathogens may cause a subacute form of ST.

The pathogenesis, diagnosis, and treatment of acute ST in children are discussed here; subacute forms of ST are discussed briefly. The diagnosis and treatment of other inflammatory conditions of the thyroid gland, including subacute granulomatous thyroiditis and chronic thyroiditis, are discussed separately. (See "Clinical manifestations and diagnosis of Graves disease in children and adolescents", section on 'Differential diagnosis: Other causes of thyrotoxicosis' and "Overview of thyroiditis", section on 'Subacute thyroiditis' and "Acquired hypothyroidism in childhood and adolescence", section on 'Autoimmune thyroiditis'.)

PATHOGENESIS — The thyroid gland is relatively resistant to infections [4]. The rarity of thyroid infection has been explained by the high concentration of iodine within the gland, ample supply of blood and lymphatics, and the anatomical isolation of the gland from other neck structures. This isolation is due to the capsule around the thyroid gland and the lack of direct communication with neighboring structures. All of these features make the thyroid gland relatively resistant to infection by direct extension from contiguous sites [1,3].

Pyriform sinus fistula — In children, a fistula from the pyriform sinus associated with a third or fourth branchial arch anomaly is a common route through which bacteria infect the thyroid gland (image 1) [5-8]. This type of fistula extends from the pharynx to the thyroid capsule and is almost always left-sided; the anomaly is particularly likely to be found in children with recurrent or left-sided ST. For a child with a pyriform sinus fistula presenting with a first episode of ST, the risk of recurrent thyroiditis has not been established but appears to be high [5,8,9].

Other predisposing conditions — Other routes through which the thyroid may become infected include a thyroglossal duct remnant [10], patent foramen cecum [11], congenital branchial fistula [12], hematogenous spread [13,14], direct spread from an adjacent site [15], or anterior esophageal perforation [16]. Immunosuppression is a rare predisposing condition [17]. In reports of adults with ST, affected patients often have a previously diseased area of the thyroid, such as goiter, adenomas, or malignant tumor [1,13,18]. In a series of adults with ST, approximately one-quarter of the patients were immunocompromised; one-half of these had HIV [19,20]. A case report has described ST as a presenting feature of juvenile systemic lupus erythematosus [21]. Fungal thyroiditis is rare, and almost all reports are in immunocompromised individuals (mostly HIV and leukemia) [22].

MICROBIOLOGY — The aerobic and facultative organisms most often isolated from ST in children are Staphylococcus aureus, Streptococcus pyogenes, Staphylococcus epidermidis, and Streptococcus pneumoniae, in descending order of frequency [1,3,19,23-25]. The prevalence of infection with methicillin-resistant S. aureus (MRSA) is increasing [26]. Other aerobic bacteria are Klebsiella species [27], Haemophilus influenzae, Streptococcus viridans, Arcanobacterium haemolyticum [28], Eikenella corrodens [29], Salmonella species [30], and Enterobacteriaceae [31,32].

When anaerobic bacteria are isolated from the infected thyroid, they tend to be members of the oropharyngeal flora and may spread to the gland in a similar fashion as the aerobic pathogens of similar origin [1,3,10,13-15,19,23,33]. The frequency of infection with anaerobic bacteria in ST is unknown because adequate methodologies for the recovery of anaerobic bacteria were not uniformly employed in all past studies. One report described two children with recurrent episodes of acute ST [33]. Anaerobic gram-negative bacilli and Peptostreptococcus species were recovered from these patients' infected thyroid glands.

Gram-negative anaerobic bacilli (eg, Prevotella, Porphyromonas, and Fusobacterium species) are increasingly recognized as a cause of ST, and a growing number of strains are penicillin-resistant. These resistant organisms are particularly common among patients recently treated with penicillin, due to induction of beta-lactamase [34]. Bacteroides and Actinomyces species have also been reported in several studies [1,33]. Polymicrobial infection (two to five organisms per abscess) was present in approximately 30 percent of the patients [35]. The recovery of anaerobes in ST has also been associated with postabortal sepsis, subphrenic abscess, pilonidal abscess, urinary tract infection, and perforation of the esophagus [1,3,19,23].

Organisms that are rarely recovered from patients with ST, which can cause chronic or insidious infection, especially in patients with HIV disease, include Mycobacterium tuberculosis [24], atypical mycobacteria, Salmonella species [36], Aspergillus species [37], Coccidioides immitis, Cryptococcus neoformans, Histoplasma capsulatum, Candida species, Nocardia species [38], Treponema pallidum, Echinococcus species, and Pneumocystis jirovecii (previously carinii) [1,3,19,23]. P. jirovecii thyroiditis is found almost exclusively in patients with HIV [20] or in those with underlying malignancy. Rarely, the thyroid is involved in disseminated strongyloidiasis, and cysticercosis.

Viruses have been associated with thyroiditis, but these tend to cause a subacute form. Viruses that have been implicated in this disorder include measles, influenza, enterovirus, Epstein-Barr, adenovirus, cytomegalovirus, echovirus, mumps, and St. Louis encephalitis viruses. Other implicated infections include malaria, Q fever, and the cat-scratch disease agent. (See "Overview of thyroiditis", section on 'Subacute thyroiditis'.)

DIAGNOSIS

Clinical presentation — Most cases of acute ST present with a sudden onset of pain and firm, tender, red, warm swelling in the anterior aspect of the neck that moves on swallowing [1]. There may be associated fever, chills, local warmth, erythema, hoarseness, sore throat, dysphagia, and dysphonia. The symptoms develop over days to a few weeks. Many cases arise shortly after an apparent upper respiratory tract infection or pharyngitis [35]. Neck pain often is unilateral and radiates to the mandible, ears, or occiput. Neck flexion reduces the severity of the pain. The pain worsens with neck hyperextension. Other signs that are related to pressure upon the neck muscle include involuntary depression of the chin upon swallowing and limitation of cervical extension.

Symptoms of ST may be present from days to months (mean 18 days) prior to the establishment of diagnosis. Symptoms in those with tuberculous thyroiditis are present for a mean interval of 105 days (range 14 days to 1 year).

On examination, the thyroid gland is swollen and tender. A single lobe, both lobes, or only the isthmus of the thyroid may be involved, so that the swelling and tenderness may be bilateral or unilateral. In one series of ST in children, the infection preferentially involved the left lobe in 90 percent of cases [35]. Rarely, a thyroid abscess can be manifested as a pulsatile mass. Erythema develops over the gland, and regional lymphadenopathy may be present as the disease progresses. Fluctuance may develop later, if an abscess forms. Case reports have described ST presenting with hyperthyroidism and thyrotoxicosis [39-41]. The hyperthyroidism can be explained by the release of presynthesized and stored thyroid hormone into the circulation as a result of inflammation and disruption of the thyroid follicles.

Pain, fever, and tenderness are less often observed in patients with tuberculous or fungal ST compared with those with acute bacterial infection. The diagnosis of fungal and parasitic thyroiditis is generally first made at surgery. P. jirovecii thyroiditis has no specific clinical features except that most individuals suffer from HIV and present with a diffuse, tender goiter [42]. Fungal ST is more common in immunosuppressed individuals [22].

Differential diagnosis — ST should be differentiated from other more common thyroid conditions such as adenoma, goiter, or subacute granulomatous thyroiditis. Making this distinction can be difficult, particularly early in the course of the disease. As compared with acute ST, subacute granulomatous thyroiditis may present with identical local signs, but systemic manifestations are less severe. Subacute thyroiditis usually subsides over time [43], whereas untreated acute ST generally results in increasing toxicity [35,44]. Other conditions that should be differentiated from ST are intracystic hemorrhage and (rarely) painful Hashimoto thyroiditis. Thyroid malignancy can present as ST [45,46]. (See "Overview of thyroiditis", section on 'Subacute thyroiditis' and "Acquired hypothyroidism in childhood and adolescence", section on 'Autoimmune thyroiditis'.)

Symptoms of neck pain resembling ST may occur in children with cervical lymphadenitis, although the tenderness is less likely to be localized to the thyroid. The differential diagnosis and evaluation of the child with prominent lymphadenitis are discussed separately. (See "Cervical lymphadenitis in children: Diagnostic approach and initial management".)

Laboratory testing — The diagnosis of ST can be supported by laboratory investigations. The serum thyroxine (T4), triiodothyronine (T3), and thyroid-stimulating hormone (TSH) are generally normal. In a series of children with thyroiditis, 93 percent had normal thyroid function tests, 4 percent were slightly hyperthyroid, and 2 percent were slightly hypothyroid [35].

Thyroid function depends in part on the etiology and time course of the thyroiditis. In a series of adults with ST, 83 percent of patients with bacterial thyroiditis had normal thyroid function tests [19]. By contrast, patients with fungal thyroiditis were likely to be hypothyroid (62 percent), and those with mycobacterial infections were most likely to be hyperthyroid (50 percent). Other case reports of fungal thyroiditis describe transient hyperthyroidism followed by hypothyroidism [22]. Hypothyroidism also has been reported in several patients with P. jirovecii infection of the thyroid, in association with HIV disease [42,47,48].

Leukocytosis, an elevated erythrocyte sedimentation rate (ESR), and elevated C-reactive protein (CRP) are usually present in acute bacterial thyroiditis [35]. An elevated ESR is also seen in subacute granulomatous thyroiditis.

Imaging

Neck ultrasound and radiography — For patients with suspected ST, initial imaging is with either ultrasound or conventional radiographs of the neck.

Neck ultrasound – In ST, the ultrasound often reveals unilobular swelling and/or abscess formation (image 2). These findings assist in the differentiation of ST from other causes of anterior neck pain and fever. Sonography of acute ST generally reveals a unifocal perithyroidal hypoechoic space and an effacement of the plane between the thyroid and perithyroid tissues. Atrophy and an unclear hypoechoic or low-density area in and around the affected lobe are observed in the late inflammatory stage [49]. Sonography also is helpful in detecting spread to contiguous structures, in defining the anatomy if surgical exploration is planned, and allows radiographically guided drainage of a thyroid abscess if present [50,51]. (See 'Differential diagnosis' above and 'Culture' below.)

Conventional radiographs – Conventional radiographs are useful to evaluate for compression or deviation of the airway due to edema. Plain radiographs also can be useful in detecting free gas in the tissues produced by gas-forming bacteria or the presence of calcifications associated with Echinococcus or Pneumocystis infection [52]. The presence of soft-tissue gas and/or foul-smelling pus suggests the presence of an anaerobic infection [10].

Other modalities — Imaging modalities that are generally not required are:

Computed tomography (CT) and magnetic resonance imaging (MRI) – CT and MRI scans of the neck are generally not needed unless the ultrasound fails to establish the diagnosis or if the clinical course suggests extension of a thyroid abscess to other locations such as the mediastinum. Like ultrasonography, CT may be used to exclude the possibility of cervical abscess outside the thyroid capsule.

Thyroid scintigraphy – A radionuclide thyroid scan is not necessary for the diagnosis of ST except in cases in which the diagnosis is unclear. When performed, it often shows absent or decreased uptake, with a patchy uptake or a cold area in the affected thyroid lobe [33,35].

Evaluation for pyriform sinus fistula — All children with recurrent or left-sided thyroiditis should be carefully evaluated for a pyriform sinus fistula. We also suggest this evaluation for other children with unexplained ST (ie, those presenting with their first episode and without left-sided disease) as up to 70 percent will have a pyriform sinus fistula [35]. (See 'Pyriform sinus fistula' above.)

Pyriform sinus fistula may be identified by a barium swallow study (image 1) or direct laryngoscopy of the hypopharynx; direct laryngoscopy appears to be somewhat more sensitive [6,35,53-55]. In children with a pyriform sinus fistula, thyroid ultrasonography performed after recovery from ST may show a newly developed echogenic tract, which has been called the "emerging echogenic tract sign" [56]. Patients with this finding should be carefully reevaluated for a pyriform sinus fistula using a barium swallow or direct laryngoscopy [57,58].

Culture — If the lesion is fluctuant or if there is sonographic evidence of an abscess, this should be aspirated if possible or surgically drained if indicated [59]. Specimens should be obtained for Gram stain to assist in the diagnosis and choice of proper antimicrobial therapy, as well as for cytology to ensure that a malignancy has not been missed [3,44]. The aspirate should be cultured for aerobic and anaerobic bacteria, fungi, and mycobacteria. Gram and acid-fast stains should be performed, but a negative Gram stain does not exclude bacterial infection [25].

Other tests — The patient should be tested for tuberculosis using an intradermal skin test or an interferon-gamma release assay. Atypical mycobacteria infection also should be considered, particularly in immunocompromised children or those with prominent lymphadenitis. The differential diagnosis and evaluation for children with lymphadenitis is discussed separately. (See "Tuberculosis infection (latent tuberculosis) in children" and "Tuberculosis disease in children: Epidemiology, clinical manifestations, and diagnosis" and "Cervical lymphadenitis in children: Diagnostic approach and initial management".)

MANAGEMENT — Acute ST is rare in children, with fewer than 100 cases reported in the literature. Thus, the following recommendations for diagnosis and management are based on outcomes of several small series of cases and by analogous experience with the management of other suppurative infections of the head and neck [60].

Antimicrobials — ST requires immediate parenteral antibiotic therapy before abscess formation begins. If fluctuation or sonographic evidence of an abscess is present, surgical drainage is generally necessary in addition to antibiotic therapy.

For patients without fluctuance or sonographic evidence of abscess formation, antimicrobial therapy is begun empirically. Because of the wide range of different bacteria that can cause bacterial thyroiditis, antibiotics with a broad antimicrobial spectrum are indicated, at least until culture results are available. Most patients should be treated parenterally, particularly if there is any evidence of toxicity. Antibiotics should be selected to provide adequate coverage for S. aureus (including methicillin-resistant S. aureus [MRSA]) and S. pyogenes, as well as penicillin-resistant, anaerobic, gram-negative bacilli and Peptostreptococcus. (See 'Microbiology' above.)

Each of the following regimens provides appropriate broad-spectrum coverage for the organisms likely to cause acute ST and is appropriate for initial empiric therapy:

Clindamycin

A penicillin with a beta-lactamase inhibitor (eg, amoxicillin with clavulanate, ampicillin with sulbactam, or piperacillin with tazobactam)

A carbapenem (imipenem or meropenem)

Metronidazole with either a macrolide or amoxicillin

For patients with an abscess that can be aspirated, the selection of empiric antibiotic therapy can be guided initially by the results of a Gram stain of the aspirated pus. The antibiotic regimen is then adjusted based on the results of the culture and sensitivity testing.

Coverage against aerobic and facultative aerobic bacilli can be provided with cefepime or ceftazidime. Coverage against anaerobic bacteria can be achieved with clindamycin, the combination of a penicillin plus a beta-lactamase inhibitor (eg, ampicillin-sulbactam), metronidazole plus a penicillin, or metronidazole plus a macrolide. Empiric coverage against MRSA may be indicated if no aspirate culture is obtained. For infections with methicillin-susceptible S. aureus, the preferred drug is a beta-lactamase-resistant penicillin. Clindamycin is an alternative. Treatment of MRSA infections is discussed separately [26]. (See "Anaerobic bacterial infections" and "Skin and soft tissue infections in children >28 days: Evaluation and management", section on 'Management approach'.)

If no clinical improvement occurs after 36 to 48 hours of therapy, a reassessment of therapy is needed.

For very mild disease or after substantial clinical improvement, treatment with oral antibiotics may be possible. Appropriate oral antibiotics include penicillinase-resistant penicillins such as dicloxacillin (or cloxacillin, where available) or cephalexin, the combination of a penicillin and a beta-lactamase inhibitor (eg, amoxicillin with clavulanate), or clindamycin. Treatment should be administered for at least 14 days or at least five days beyond resolution of acute symptoms, whichever is longer.

Antifungal or antituberculous therapy should be administered when these organisms are recovered or suspected [61].

Surgery — Surgery may be needed to drain the infection and to repair any developmental abnormality that led to the development of ST, such as a fistula from a pyriform sinus or thyroglossal duct remnant. Drainage with or without lavage should be carried out if clinical examination or radiographic findings by ultrasound/CT scan suggest an abscess or if there is evidence of gas formation [62]. If extensive necrosis develops, or if the infection persists despite adequate antibiotics (as evidenced by leukocytosis, continued fever, and progressive signs of local inflammation), thyroid lobectomy may be needed [3,35,44,50]. In this case, debridement of necrotic tissue should be performed and the wound allowed to heal by secondary intention. Endoscopic approaches are an acceptable alternative to open surgical procedures, with similar success and a lower rate of complications [63].

Management of the predisposing conditions is of great importance. Because of an apparently high risk for recurrent infections in individuals with a pyriform sinus fistula or thyroglossal duct remnant, most authors recommend obliteration of these structures if present [6,35,53,54,64]. Earlier series describe surgical excision of the fistula. This procedure was generally successful but has some risk for injury to the recurrent laryngeal nerve [5,6,35]. More recently, several small case series report management of the fistula using endoscopic cauterization, with successful obliteration of the fistula in most cases [53,55,64].

Patients should also be evaluated and treated for preexisting thyroid pathology, such as goiter and adenomas.

COMPLICATIONS — The prognosis following appropriate medical and surgical therapy for ST is generally excellent. The recovery is usually complete, and any abnormalities of thyroid function typically resolve after treatment [3,35,44]. L-thyroxine replacement therapy may be needed in those with transient or prolonged hypothyroidism, which is most likely to occur in individuals with severe, diffuse inflammation and necrosis of the gland.

In a subset of patients, ST is caused by an occult pyriform sinus fistula, and these patients are at risk for recurrent ST unless that fistula is identified and surgically closed. The fistula can develop a tract to the cervical neck skin [65]. (See 'Pyriform sinus fistula' above and 'Evaluation for pyriform sinus fistula' above.)

Local complications are rare and include extension of the infection into adjacent sites and organs (anterior mediastinum, trachea, and esophagus), disruption of regional sympathetic nerves and paralysis of the vocal cords, thrombosis of the internal jugular vein (Lemierre syndrome), descending necrotizing mediastinitis [66], and extrinsic compression of the trachea [67]. Rheumatic fever has been described following group A beta-hemolytic streptococcal thyroiditis [68].

Local and systemic complications may be life-threatening, especially if therapy is postponed or is inadequate. Fungal ST has a high overall mortality. Potential causes of death include pneumonia, tracheal obstruction or perforation, metastatic infection, and rupture of a thyroid abscess causing mediastinitis, pericarditis, or sepsis.

SUMMARY AND RECOMMENDATIONS

Pathogenesis – Acute suppurative thyroiditis (ST) is caused by bacterial infection of the thyroid gland. The condition is rare but potentially life-threatening. Most patients have predisposing conditions. Pyriform sinus fistulas are present in up to 70 percent of children with acute ST. (See 'Pathogenesis' above and 'Pyriform sinus fistula' above.)

Microbiology – The aerobic and facultative organisms most often isolated from ST in children are Staphylococcus aureus, Streptococcus pyogenes, Staphylococcus epidermidis, and Streptococcus pneumoniae. Gram-negative anaerobic bacilli (eg, Prevotella, Porphyromonas, and Fusobacterium species) are increasingly recognized as a cause of ST. Subacute forms of ST may be caused by infections with mycobacteria or fungi, particularly in immunocompromised patients. (See 'Microbiology' above.)

Clinical presentation – Children generally present with the acute onset of pain and tender swelling in the anterior aspect of the neck that develops over days to a few weeks, often associated with fever and leukocytosis. The infection preferentially involves the left lobe in 90 percent of cases but may be bilateral. (See 'Clinical presentation' above.)

Evaluation

Laboratory tests – Thyroid function tests are usually normal in acute ST, but hypothyroidism or hyperthyroidism may develop in patients with a subacute course. (See 'Laboratory testing' above.)

Imaging – Patients with suspected ST should be evaluated with ultrasound and plain radiographs of the neck. The ultrasound will assess for abscess formation and for possible extension of the infection into adjacent structures. The radiographs assess for compression of the airway by edema and may also reveal gas in the tissues produced by gas-forming bacteria. (See 'Imaging' above.)

For children with recurrent or left-sided acute ST, evaluate for a possible pyriform sinus fistula using a barium esophagram or direct laryngoscopy (image 1). We also suggest this evaluation for children presenting with their first episode of thyroiditis or bilateral involvement of the thyroid. (See 'Evaluation for pyriform sinus fistula' above.)

Abscess evaluation – If there is clinical or sonographic evidence of abscess formation, we recommend needle aspiration of the mass for culture and cytology. Ultrasound-guided fine-needle aspiration can be helpful. The specimen should be stained and cultured for aerobic and anaerobic bacteria, fungi, and mycobacteria. (See 'Culture' above.)

Management

Antibiotics – All patients with presumed ST should be treated promptly with antibiotics. For initial empiric therapy, we suggest a regimen that provides coverage for aerobic and anaerobic mouth organisms including S. aureus, S. pyogenes, gram-negative anaerobic bacilli, and Peptostreptococcus species (Grade 2C). Appropriate antibiotic regimens include clindamycin alone, the combination of penicillin and a beta-lactamase inhibitor, or the combination of metronidazole and a macrolide. (See 'Antimicrobials' above.)

Abscess drainage – In cases where an abscess forms, surgical drainage may be necessary. For children with a pyriform sinus fistula, we suggest obliteration of the fistulous tract using surgical excision or endoscopic cauterization (Grade 2C). (See 'Surgery' above.)

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Topic 5822 Version 19.0

References

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