Acute Laryngitis

Etiology

Acute laryngitis is a clinical syndrome commonly encountered by clinicians. Symptoms typically include a recent onset of hoarseness or a husky voice with reduced projection, often accompanied by a dry cough.[5] Acute laryngitis arises from 2 primary causes: infectious agents and noninfectious factors. Understanding these underlying causes is crucial for effective diagnosis and treatment.

Infectious Agents

Acute viral laryngitis typically occurs following an upper respiratory tract infection. Most major respiratory viruses have been associated with laryngitis. Common viral etiologies include rhinovirus and coronavirus, influenza virus, adenovirus, and respiratory syncytial virus.[6][7][8][9][10] Less common viral etiologies include parainfluenza and human metapneumonvirus.[11][12] Uncommon viral etiologies include herpes simplex virus types 1 and 2, varicella-zoster virus, cytomegalovirus, parvovirus B19, and infections such as measles, chickenpox, and whooping cough.[13][14] 

Bacterial

Bacterial superinfection can occur in patients with viral laryngitis. Reported bacterial pathogens include Streptococcus pneumoniae, Haemophilus influenzae, and Moraxella catarrhalis, as well as methicillin-resistant Staphylococcus aureus and group G β-hemolytic streptococci.[15][16] Additional causes include Bordetella pertussis, Mycoplasma pneumoniae, and Chlamydia pneumoniae. Rare infectious etiologies include rhinoscleroma caused by Klebsiella ozaenae, granulomatous laryngitis caused by Mycobacterium tuberculosis, Paracoccidioides brasiliensis, or Leishmania braziliensis.[17][18]

Fungal 

Fungal laryngitis is more common in patients with immunocompromised conditions or conditions such as uncontrolled diabetes, acquired immunodeficiency syndrome, or chronic corticosteroid use.[19] In immunocompetent individuals, factors that disrupt the mucosal barrier, such as inhaled corticosteroids, laryngopharyngeal reflux, smoking, or prior radiation therapy, may increase risk. Reported fungal pathogens include mucosal candidiasis, Blastomyces species, Anncaliia algerae, Cryptococcus neoformans, and Spirothrix schenckii.[20]

Noninfectious

Noninfectious causes include vocal trauma, allergies and asthma, gastroesophageal reflux disease and laryngopharyngeal reflux disease; environmental pollution and toxins, and inhalational injury.[21][22] Inhalation injury may result from direct irritation, particulate drying effects, or thermal damage. Additional causes include tobacco smoking, irritant exposure, autoimmune and inflammatory diseases (eg, relapsing polychondritis, granulomatosis with polyangiitis, rheumatoid arthritis, systemic lupus erythematosus, and bullous pemphigoid), functional conversion disorders, and idiopathic ulcerative laryngitis. Idiopathic ulcerative laryngitis is a rare disorder characterized by ulceration in the midmembranous portions of the vocal folds; its etiology and optimal management remain poorly understood.[23][24]

Epidemiology

The incidence of acute laryngitis is challenging to predict because many patients experience hoarseness for various reasons and often use conservative measures without seeking medical attention, as their symptoms usually improve spontaneously. Some patients report that hoarseness varies greatly and is short-lived. There is no predilection for age, sex, race, or other factors. Because acute laryngitis is self-limited in most cases, there is no significant morbidity or mortality unless an underlying serious medical condition, such as pneumonia, significant vocal fold injury, or a tumor, is present.

Paradoxically, there was a significant decrease in acute laryngitis cases during the COVID-19 pandemic. Public health restrictions implemented to reduce SARS-CoV-2 transmission also inadvertently reduced the incidence of other respiratory and gastrointestinal tract infections.[25] Notably, laryngeal diseases, such as acute laryngitis, have a substantial economic impact, particularly due to medication costs.[26]

Pathophysiology

The larynx is a gateway to the respiratory airway that is exposed to numerous potential pollutants, allergens, irritants, and pathogens. There is evidence that the larynx plays a distinct role in immune defense.[27] Both animal and human studies have identified larynx-associated lymphoid tissue, a mucosa-associated lymphoid tissue type specific to the larynx, although its exact function remains unclear. Despite recent advances in tissue engineering, there is no effective method to fully replicate laryngeal function in patients undergoing laryngectomy.[28][29] Immune cells, including dendritic cells, T cells, and macrophages, have been detected in histologic sections procured from human fetal laryngeal tissue.[30]

Vocal fold vibration is the source of voice production and may be temporarily disrupted in acute laryngitis. The membranous fold of the vocal cord becomes erythematous and swollen; irregular thickening along its edge results in a lower pitch and a scratchy quality. There is debate over whether the vocal folds stiffen or thicken. Phonation threshold pressure, glottal resistance, glottal efficiency, vibratory amplitude, and vibratory area are used to measure voice quality. Vitamin A is essential for the development and maintenance of the vocal fold epithelium and may help prevent scar formation.[31] 

Animal and in vitro studies suggest that acute laryngitis may be associated with changes in gene expression induced by inflammatory stimuli over time, specifically interleukin-1β, transforming growth factor β1, and their combination, which affect the expression of extracellular matrix proteins and cytokines. Additionally, mechanical vibration downregulates proinflammatory and profibrotic signaling in human vocal fold fibroblasts, and this may be accompanied by a significant decrease in fibrosis-associated proteins, including interleukin-11 and α-smooth muscle actin, following mechanical stimulation.[32]

In laryngopharyngeal reflux disease, symptoms result from direct irritation of the vocal fold mucosa by acidic or pepsin-containing gastric contents. Laryngeal or esophageal afferent sensitization may also contribute, leading to a neural cough reflex. Reactivation of pepsin in the upper aerodigestive tract has also been implicated. Although chronic risk factors for laryngopharyngeal reflux are well established, pregnancy, severe coughing, and specific dietary triggers may acutely increase the frequency of reflux episodes.[33]

Many classification criteria include laryngitis, among conditions such as granulomatosis with polyangiitis, Behçet disease (malignant aphthosis), relapsing polychondritis, eosinophilic granulomatosis with polyangiitis, and Cogan syndrome. Other autoimmune and autoinflammatory diseases may present with widespread inflammation, including sarcoidosis, rheumatoid arthritis, Sjögren disease, systemic lupus erythematosus, and systemic sclerosis. Laryngeal chondritis is a key manifestation of relapsing polychondritis, presenting as pain above the thyroid and dysphonia, and can lead to laryngomalacia or stenosis in severe cases.

Subglottic stenosis, caused by granulomatous inflammation in granulomatosis with polyangiitis, occurs in 2% to 20% of cases, is potentially life-threatening, and often indicates systemic disease involvement. Rheumatoid arthritis is a chronic inflammatory disease that causes symmetrical joint inflammation and may progress to joint damage and bone destruction. Laryngeal manifestations of rheumatoid arthritis primarily involve arthritis of the cricoarytenoid joint and rheumatoid nodules.[34][35][36]

Histopathology

Acute laryngitis is inflammation of the vocal fold mucosa that can extend to the supraglottis, glottis, and subglottis. Most patients develop hoarseness due to swelling of the superficial lamina propria (Reinke space), resulting in Reinke edema. The viscoelastic properties of the mucosal folds are altered due to the expansion of the subepithelial space.[37] Immunohistologically, Reinke edema is characterized by a chaotic distribution of short, scattered connective fibers, a locally thickened, hyperplastic epithelial layer, a thickened basement membrane, and edematous lakes.[38][39] The lamina propria of Reinke edema specimens contains interstitial and inflammatory cells, mainly mast cells and macrophages. Vocal fold fibroblasts, the primary cell type in the lamina propria, have a distinctive expression profile compared to fibroblasts in other tissues and are believed to play a key role in mediating this disease.[40][41][42] 

History and Physical

The assessment of a patient with acute laryngitis should begin with a thorough history and a detailed physical examination. Particular emphasis should be placed on the onset and duration of symptoms, as well as any recurrent episodes. Clinicians should inquire about recent upper respiratory tract infections, other concurrent illnesses, potential exposure to infections, and any signs of systemic or autoimmune disease. 

The hallmark clinical manifestation of acute laryngitis is a noticeable alteration in vocal quality, characterized by huskiness, hoarseness, or, in some cases, complete aphonia. Typical nonspecific symptoms of upper respiratory infections include nasal congestion, postnasal drainage, rhinorrhea, pharyngodynia, fever, and cough. Patients often report dysphonia with associated discomfort or pain (odynophonia) when attempting to speak. Typically, the initial symptoms of acute laryngitis appear suddenly and worsen over 2 to 3 days.

Other manifestations include the following:

• Dysphagia and odynophagia
• Throat burning 
• Otalgia, decreased hearing, and ear popping
• Frequent throat clearing
• Early voice fatigue or loss of vocal range
• General malaise, fatigue, and dry throat sensation
• Dyspnea

A detailed medical history should include the patient's immune and immunization status, allergy symptoms, travel history, exposure to environmental pollutants or toxins, voice misuse, and any comorbid conditions, such as gastroesophageal reflux disease or rheumatologic disease. If the patient has received prior treatment, it is essential to assess the effectiveness of that treatment. A thorough assessment should also address medications, allergies to medications, as well as family and social history, including tobacco and alcohol use, since voice changes may be a sign of laryngeal pathology.

Acute laryngitis is typically a clinical diagnosis, and a detailed laryngeal evaluation may not be performed in all cases. However, the standard of care for physical examination is visual inspection of the hypopharynx and larynx during a thorough head and neck examination. Traditionally, indirect laryngoscopy with a mirror and headlight was used. However, with the advent of newer technology, most otolaryngologists use flexible nasopharyngoscopy (with direct view or video capabilities) or videostroboscopy. The examination should include visualization of the following structures:

• Eustachian tube orifice and lateral pharyngeal recess (Rosenmüller fossa)
• Central lymphoid tissue of the pharyngeal lymphoid ring (Waldeyer ring)
• Posterior nasal septum
• Nasopharyngeal aspect of the soft palate
• Oropharynx
• Hypopharyx
  • Epiglottis
  • Pyriform sinuses
• Larynx
  • Arytenoids
  • Aryepiglottic folds
  • False and true vocal folds
• Subglottis (partial)

Key findings regarding laryngeal appearance vary with the underlying cause and the severity of inflammation. Special focus is given to vocal cord swelling, movement, and the presence of masses, lesions, or obstructions. Videostroboscopy can assess speech by analyzing the vibratory wave created during sound production. Using stroboscopic light to examine the larynx can uncover subtle changes in vocal fold vibration that standard laryngoscopy might miss.[43] Clinicians may look for signs such as erythema and edema of the posterior commissure, as well as cobblestoning, in patients with laryngopharyngeal reflux disease. Often, patients present with pseudosulcus vocalis or infraglottic edema extending from the anterior commissure to the posterior larynx, particularly in those with pH-confirmed laryngopharyngeal reflux.[44]

Evaluation

In most cases, laboratory, radiographic, or other tests are unnecessary because the symptoms usually resolve with conservative treatment. Further evaluation is individualized based on the clinical context and suspicion of underlying conditions.

Treatment / Management

Although the best management of acute laryngitis may involve watchful waiting, time, and conservative measures, patients often desire treatment. The goals of immediate treatment should include moisturizing the upper airway, specifically the vocal folds; reducing inflammation; removing the offending agent; and voice rest. Because the most common cause of acute laryngitis is a viral upper respiratory tract infection, medical therapy is supportive, and medications are aimed at relieving symptoms rather than curing the disease. 

Supportive Measures

• Reduce Physical fatigue: Fatigue may adversely affect voice; encourage rest
• Regular exercise: Exercise increases stamina and muscle tone, which may improve posture and breathing, which are necessary for proper speech
• Voice hygiene
  • Voice rest, if possible
  • Vocal naps, resting the voice for short periods
  • Focus on speaking at a moderate volume, slowing speech, and using brief responses (yes/no answers)
  • Avoid vocal extremes
  • Support the voice with diaphragmatic breathing
  • Minimize vocal strain by avoiding long conversations, singing, yelling, and other loud activities
  • Avoid whispering, which may promote hyperfunction of the larynx and perpetuate inflammation
  • Avoid noisy environments, which may prompt people to speak louder
  • Avoid neck strain by avoiding cradling the phone when talking or using a microphone
  • Humming or lip trills, before heavy vocal use (semioccluded vocal tract exercises) [45]
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 Steam inhalation and hydration

• Increases fluid intake
• Humidifies air
• Removes secretions and exudates
• Reduces vocal fold friction
• Head-of-bed elevation
  • This may be beneficial for patients with gastroesophageal reflux.

Avoidance of triggers

• Avoid irritants, allergens, pollutants, smoking, second-hand smoke, alcohol use, or toxins, as they may act as triggers.
• Avoid mouthwash or gargles that contain alcohol or irritating chemicals.
• Avoid using mouthwash to treat persistent bad breath. Halitosis may result from low-grade infections in the nose, sinuses, tonsils, gums, or lungs, or from gastroesophageal reflux disease.

Diet 

• Avoid spicy foods or acidic beverages.
• Avoid caffeinated drinks, fatty food, chocolate, and peppermint.
• Include plenty of whole grains, fruits, and vegetables. These foods contain vitamins A, E, and C. They also help maintain the mucous membranes that line the throat
• Avoid late meals or overeating.

Medications

• Avoid antihistamines and corticosteroids. These agents may provide temporary false relief, which may encourage detrimental voice use, and their drying effect may be deleterious.
• Osmolyte ectoine mouth and throat spray may be more beneficial than saline lozenges.[46]
• Nonsteroidal anti-inflammatory drugs, such as ibuprofen, can provide short-term symptomatic relief of sore throat and be slightly more effective than acetaminophen for this purpose.[47]
• Antibiotics are not beneficial in the treatment of acute laryngitis. Erythromycin may reduce subjective voice disturbance at 1 week and cough at 2 weeks; however, these effects are unlikely to be clinically relevant.[48]
• Antacid medications such as proton pump inhibitors may be beneficial for patients with gastroesophageal reflux disease and laryngopharyngeal reflux. Proton pump inhibitors are generally more effective than H2 receptor antagonists for laryngopharyngeal reflux and may require twice-daily dosing to achieve symptom control.
• Antifungal medications may be indicated when positive physical findings on laryngoscopy consistent with fungal laryngitis are present.
• Mucolytics such as guaifenesin may reduce throat clearing and vocal irritation.
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Differential Diagnosis

Laryngitis has a very broad differential diagnosis that includes:

• Vocal fold nodules, cysts, or polyps
• Contact granulomas of the vocal folds
• Vocal fold paralysis (iatrogenic, traumatic, or idiopathic)
• Foreign body obstruction
• Presbylaryngis (age-related atrophy)
• Reflux laryngitis (laryngopharyngeal reflux)
• Neurological conditions (Parkinson disease, stroke, multiple sclerosis, myasthenia gravis, amyotrophic lateral sclerosis, and essential tremor)
• Allergic laryngitis
• Epiglottitis
• Croup (laryngotracheobronchitis)
• Pertussis
• Bacterial tracheitis
• Laryngeal stenosis
• Laryngeal cancer
• Peritonsillar or retropharyngeal abscess
• Laryngeal papillomatosis
• Autoimmune or systemic disorders
• Spasmodic dysphonia (laryngeal dysphonia)
• Muscle tension dysphonia
• Medication adverse effects (eg, inhaled corticosteroids)

Prognosis

Acute laryngitis usually resolves with appropriate supportive care and has a good prognosis. However, if hoarseness persists, further evaluation is essential to identify underlying conditions. Otolaryngologists should be alert to the possibility of vocal cord lesions or malignant neoplasms of the upper airway in patients with persistent or worsening symptoms. Speech and voice therapy may also be an option for patients experiencing recurrent symptoms.