Background
- Acute infectious (suppurative) thyroiditis is an infection in the thyroid gland resulting in an abscess
- Potentially life-threatening and should be treated as a medical emergency
- Most patients with acute infectious thyroiditis are euthyroid on presentation, but some patients may have hyper- or hypothyroidism depending on the degree of destruction of the thyroid gland
Who is Most Affected
- Most cases occur in children due to its association with pyriform sinus fistula (some cases have also been reported in children receiving chemotherapy treatment for cancer)
- More common in patients with preexisting thyroid disease (Hashimoto thyroiditis/nodular goiter)
Incidence/Prevalence
- Very rare (reported in about 0.1%-0.7% of patients with thyroid disease)
- About 92% of cases are reported to occur in children
- About 8% of cases are reported in adults (primarily with immunocompromised)
Continue Reading
Common Risk Factors
- Preexisting clinical/subclinical thyroid disease
- Congenital abnormalities (piriform sinus fistula or persistent thyroglossal duct)
- Immunocompromised state (such patients are predisposed to unusual bacteria, such as Nocardia and Salmonella, and fungi like Candida, Coccidioides immitis, and Aspergillus)
- Diabetes mellitus
Causes
- Any type of infection involving the thyroid gland (other than viral)
- Mostly caused by bacteria; most common organisms include
- Staphylococcus (predominantly Staphylococcus aureus)
- Streptococcus (predominantly Streptococcus pyogenes, Streptococcus epidermidis, and Streptococcus pneumoniae)
- Escherichia coli
- Clostridium septicum
- Peptostreptococcus
- Some caused by fungal infections (more common in immunocompromised), including
- Coccidioides immitis
- Aspergillus species
- Actinomycosis
- Blastomycosis
- Candida albicans
- Nocardia
- Acinetobacter baumannii
- Cryptococcus
- Pneumocystis jiroveci
- Rarely, may be caused by a parasitic infection (for example, Trypanosoma species)
Pathogenesis
- Normal physiology of the thyroid gland makes it resistant to infection due to
- High vascularity and lymphatic drainage
- High concentration of iodine in thyroid tissue
- Generation of hydrogen peroxide in the thyroid for synthesis of thyroid hormone
- Encapsulation of the thyroid separating it from other structures
- Persistent fistula in the pyriform sinus or fourth branchial arch sinus (particularly in children) can make the left thyroid lobe susceptible to infection and abscess formation
Clinical Presentation
- Most commonly present with acute anterior neck pain (typically more severe in children)
- May be worse when swallowing and patient may be unable to extend the neck without putting pressure on the thyroid gland
- Often unilateral (left side)
- Patients may also present with
- Swollen, tender, hot neck mass (often erythematous)
- Sign of infection (fever, local lymphadenopathy, chills), especially in children (adults may only have mild pain and no fever)
- Compressive symptoms due to focal inflammation (dysphagia/dysphonia)
- Necrotizing mediastinitis and pericarditis if infection spreads to the chest
- Most patients do not present with signs or symptoms of hyper- or hypothyroidism
History
- Ask about trauma to the neck region
- Preexisting clinical or subclinical thyroid disease
- Conditions associated with immunocompromised state
Physical
- Assess for fever (more common in children than adults)
- Evaluate for
- Dysphagia
- Pharyngitis
- Dysphonia
- Perform thyroid examination to assess for
- Swelling (commonly left-sided)
- Tenderness/warmth
- Erythema
- Difficulty extending the neck due to pain
- Assess for cardiac findings associated with
- Thyrotoxicosis – palpitations, tachycardia, widened pulse pressure
- Hypothyroidism – bradycardia, narrowed pulse pressure
Differential Diagnosis
- Subacute thyroiditis
- Rare, self-limited inflammatory disease of the thyroid
- Abnormal TSH levels, and low uptake of iodine-123 on thyroid scanning
- Anterior neck pain – usually less severe than acute thyroiditis
- Hashimoto thyroiditis
- Chronic destructive autoimmune process affecting the thyroid
- Signs/symptoms of hypothyroidism
- Elevated thyroid peroxidase (TPO) antibody
- Occasionally with nontender goiter
- Rarely present with thyrotoxicosis
- Riedel thyroiditis (Riedel struma)
- Rare inflammatory infiltrative fibrosclerotic condition resulting in progressive destruction of thyroid tissue
- Very firm goiter or compressive symptoms (dyspnea, stridor, dysphagia) disproportionate to the size of the thyroid
- May be hypocalcemic due to fibrotic transformation of the parathyroid glands
- Diagnosis is based on thyroid biopsy
- Postpartum thyroiditis (thyroid dysfunction within 1 year of giving birth, miscarriage, or medical abortion) associated with underlying chronic thyroid autoimmune disease
- Amyloid goiter
- Rare condition in which amyloid deposits cause thyroid dysfunction
- Rapidly progressing diffuse goiter that quickly leads to compressive symptoms
- Typically euthyroid
- Diagnosis can be made with fine needle aspiration biopsy
- Immune reconstitution inflammatory syndrome (IRIS)
- Lesions arise at the site of a prior infection (with immune restoration after antimicrobial therapy)
- Symptoms similar to acute infectious thyroiditis
- Lymphadenopathy, organomegaly, and/or fever with negative culture
- Appears after antimicrobial therapy without evidence of new infection
- Retropharyngeal abscess
- Deep neck infection of the retropharyngeal space
- Potential for airway compromise/other life-threatening complications
- Symptoms similar to acute infectious thyroiditis
- Diagnosed/ruled out by CT scan
- Drug-induced thyroiditis – related to
- Amiodarone
- Lithium
- Interferon alfa
- Interleukin-2
- Kinase inhibitors
- Denileukin (Ontak)
- Radiation-induced thyroiditis
- Thyroid pain and transient thyrotoxicosis with history of radiation exposure
- Hemorrhage into thyroid cyst
- Thyroid cancer
Diagnosis
- Rapid diagnosis necessary to avoid potentially life-threatening complications
- Suspect diagnosis in a patient (especially a child) with no history of radiation exposure or thyroid trauma who appears septic with a swollen, painful thyroid, lymphadenopathy, and fever (may not be present in adults), especially if patient:
- Is euthyroid per thyroid function tests (TFTs)
- Is in an immunocompromised state
- Reports recent upper respiratory tract infection
- Blood tests
- TFTs (such as thyroid-stimulating hormone [TSH], thyroxine [T4], triiodothyronine [T3])
- Most patients are euthyroid on presentation; some may present with destructive thyroiditis and thyrotoxicosis
- Complete blood count with differential (elevated leukocytes may be seen in acute or subacute thyroiditis)
- Thyroid autoantibodies (generally absent in acute infectious thyroiditis)
- C-reactive protein and procalcitonin often increased
- TFTs (such as thyroid-stimulating hormone [TSH], thyroxine [T4], triiodothyronine [T3])
- Imaging studies (thyroid ultrasound and CT scan) usually diagnostic
- Findings include hypoechoic lesions in/around affected thyroid lobe, thyroid lobe destruction, and abscess formation
- In early stages, findings may be nonspecific/difficult to distinguish from subacute thyroiditis
- In the acute inflammatory phase, CT may show:
- Swollen thyroid with nonspecific low-density areas
- Displacement of trachea
- Edema of ipsilateral hypopharynx
- Abscess formation
- In the acute inflammatory phase, CT may show:
- Fine-needle aspiration biopsy with gram stain, culture, and cytopathology may be indicated when imaging shows a fluid-filled thyroid mass
- In acute infectious thyroiditis, biopsy will show purulence, and bacteria or fungi will be detected via culturing
- In subacute thyroiditis, biopsy will show lymphocytes, macrophages, some polymorphonuclear leukocytes, and distinctive giant cells
Management
- Immediate management includes securing airway if compromised; perform immediate fine needle aspiration/surgical drainage of fluid to relieve pressure on trachea
- Management involves antibiotics and surgical drainage as guided by clinical judgment
- As the condition can be fatal if not treated urgently, patient should be hospitalized and treated with IV antibiotics
- Start empiric parenteral antibiotics (such as nafcillin plus gentamicin or a third-generation cephalosporin) and adjust based on culture results when available
- Continue antibiotics for 14 days or until after surgery or clinical resolution
- For infection with Candida albicans, treat with amphotericin B and 5 fluconazole 100 mg daily
- If present, treat symptoms of thyrotoxicosis with beta-blockers
- Some abscesses may require open surgical or ultrasound-guided percutaneous drainage in addition to antibiotic treatment
- If abscess persists/progresses following drainage, consider repeat drainage and/or partial or total thyroidectomy (after acute inflammation resolves)
- Patients with underlying pyriform sinus fistula typically require surgical removal of the fistula to avoid recurrent infections (after the period of acute inflammation)
- Start empiric parenteral antibiotics (such as nafcillin plus gentamicin or a third-generation cephalosporin) and adjust based on culture results when available
- Patients with particularly diffuse acute thyroiditis should have a follow-up with routine thyroid function tests to determine whether destruction has led to permanent hypothyroidism
Complications
- Acute complications may include
- Sepsis
- Acute airway obstruction
- Late complications may include
- Transient or permanent hypothyroidism
- Vocal cord paralysis
- Complications of abscess extension or rupture include
- Tracheal or esophageal perforation
- Necrotizing mediastinitis and pericarditis
- Patients who develop hypothyroidism, including subclinical hypothyroidism, may be at increased risk for cardiac complications
Kendra Church MS, PA-C, is a physician assistant at Dana-Farber Cancer Institute/Brigham & Women’s Hospital, and is also a senior clinical editor for DynaMed, an evidence-based, point-of-care database.
Source
World Health Organization. WHO Expert Committee on Leprosy. World Health Organ Tech Rep Ser. 2012;(968):1-61.
White C, Franco-Paredes C. Leprosy in the 21st century. Clin Microbiol Rev. 2015;28(1):80-94. doi:10.1128/CMR.00079-13
Scollard DM, Adams LB, Gillis TP, Krahenbuhl JL, Truman RW, Williams DL. The continuing challenges of leprosy. Clin Microbiol Rev. 2006;19(2):338-81. doi:10.1128/CMR.19.2.338-381.2006
Lastória JC, Abreu MA. Leprosy: a review of laboratory and therapeutic aspects–part 2. An Bras Dermatol. 2014;89(3):389-401. doi:10.1590/abd1806-4841.2014246
Boggild AK, Keystone JS, Kain KC. Leprosy: a primer for Canadian physicians. CMAJ. 2004;170(1):71-78.
Britton WJ, Lockwood DN. Leprosy. Lancet. 2004;363(9416):1209-1219. doi:10.1016/S0140-6736(04)15952-7.