Acute Laryngitis

Etiology

The etiology of acute laryngitis can be classified as either infectious or non-infectious. The infectious form is more common and usually follows an upper respiratory tract infection. Viral agents such as rhinovirus, parainfluenza virus, respiratory syncytial virus, coronavirus, adenovirus, and influenza are all potential etiologic agents (listed in roughly descending order of frequency). It is possible for bacterial superinfection to occur in the setting of viral laryngitis. This classically occurs approximately 7 days after symptoms begin.

The most commonly encountered bacterial organisms are Streptococcus pneumoniae, Haemophilus influenzae, and Moraxella catarrhalis, in that order. Exanthematous febrile illnesses such as measles, chickenpox, and whooping cough are also associated with acute laryngitis symptoms, so it is prudent to obtain an accurate immunization history. Laryngitis caused by fungal infection is very rare in immunocompetent individuals and more often presents as chronic laryngitis in the immunocompromised or in patients using inhaled steroid medications. 

Acute infectious laryngitis in adults is most commonly caused by the viral organisms listed above. These same agents are common in pediatric acute laryngitis, though it is important to remember croup (laryngotracheobronchitis) in children, which is due to parainfluenza virus (most commonly parainfluenza-1). This may present with isolated vocal symptoms but classically includes a characteristic "barking" cough and may progress to inspiratory or biphasic stridor.[2]

Acute non-infectious laryngitis can be due to vocal trauma/abuse/misuse, allergy, gastroesophageal reflux disease, asthma, environmental pollution, smoking, inhalational injuries, or functional/conversion disorders.

Vocal misuse or abuse can be acute in onset, as seen after a day or days of shouting/yelling. This is common in coaches, fans, and athletes after an event. This can also be seen in vocal performers, particularly those whose performance intensity or frequency has increased recently and who have not had formal voice or singing coaching.

Gastroesophageal reflux (GERD), specifically extra-esophageal GERD, termed laryngopharyngeal reflux (LPR), is an exceptionally common cause of voice symptoms and laryngitis. These symptoms can be acute or chronic and may be episodic. They may not follow or accompany the classic GERD symptoms, and 1/3 of patients with GERD experience only laryngeal/voice symptoms. Hallmarks include a history of GERD, frequent throat-clearing or coughing, globus pharyngeus sensation, or coarseness to the voice. Singers may note a loss of their higher range.[3]

Asthma may predispose to laryngitis due to chemical irritation from inhaler use, and chronic steroid inhaler use can predispose to fungal laryngitis, particularly if patients are not drinking plain water after their steroid inhaler use as instructed. There is also cough-variant asthma that may cause a repetitive injury to the vocal cords, leading to voice changes that mimic acute laryngitis. Environmental causes, such as seasonal and environmental allergies or seasonal or constant air pollution, can cause irritation to the vocal cords that may trigger acute laryngeal symptoms. Inhalation of noxious substances, whether intentional from smoking or other drug use or unintentional exposure, irritates the larynx and can cause edema of the vocal folds and voice symptoms. Certain patients may be sensitive to perfumes, colognes, detergents, or other commonly used aromatics in daily life. Functional dysphonia is a term for a group of true conversion disorders and encompasses a wide range of voice symptoms and physical examination findings. This is a diagnosis of exclusion, but recent major life stressors such as the loss of a job or loved one are well-known triggers.[4]

Epidemiology

Acute laryngitis can affect patients of any age, though it is more common in the adult population, usually affecting individuals aged 18 to 40, though it may be seen in children as young as 3. Isolated voice symptoms in children younger than 3 should prompt a more thorough workup for additional pathology, including vocal cord paralysis, GERD, and neurodevelopmental conditions. Accurate incidence measurements of acute laryngitis remain difficult to elucidate as this condition remains under-reported, with many patients appropriately not seeking medical care for this often self-limited condition.[2]

Pathophysiology

Acute laryngitis resolves within 2 weeks and is due to local inflammation of the vocal folds and surrounding tissues in response to a trigger, whether that trigger is infectious or non-infectious. If symptoms persist beyond this timeframe, it is either due to superinfection or a transition to chronic laryngitis.

Acute laryngitis is characterized by inflammation and congestion of the larynx in the early stages. This can encompass the supraglottic, glottic, or subglottic larynx (or any combination thereof), depending on the inciting organism. As the healing stage begins, white blood cells arrive at the site of infection to remove the pathogens. This process enhances vocal cord edema and affects vibration adversely, changing the amplitude, magnitude, and frequency of the normal vocal fold dynamic. As the edema progresses, the phonation threshold pressure can increase. The generation of adequate phonation pressure becomes more difficult, and the patient develops phonatory changes both as a result of the changing fluid-wave dynamics of the inflamed and edematous tissue but also as a result of both conscious and unconscious adaptation to attempt to mitigate these altered tissue dynamics. Sometimes edema is so marked that it becomes impossible to generate adequate phonation pressure. In such a situation, the patient may develop frank aphonia. Such maladaptations may result in prolonged vocal symptoms after an episode of acute laryngitis that can persist long after the inciting event has resolved. In such situations, referral to an otolaryngologist and/or speech-language pathologist is warranted.

History and Physical

The evaluation of an acute laryngitis patient must always begin with a thorough history and physical examination. Special attention should be directed at recent URI or other illnesses, sick contacts, or any other signs of systemic illness. The physician should also explore past medical history, including immune status, immunization status, allergy and travel history, and history of other confounding pathologies such as GERD. Special attention should be paid to the onset and duration of the symptoms, as well as if they have ever happened before. If the patient has been treated prior to presentation, the efficacy and nature of such treatment must be explored also.

Initial symptoms of acute laryngitis are usually abrupt in onset and worsen over 2 or 3 days, though they may persist for up to a week without treatment. These can include:

• Change in quality of voice, in later stages, there may be a complete loss of voice (aphonia)
• Discomfort and pain in the throat, particularly after talking
• Dysphagia, odynophagia (if present, exercise caution - may hint at additional pathology)
• Dry cough
• General symptoms of dryness of throat, malaise, and fever
• Frequent throat-clearing
• Early voice fatigue or loss of vocal range

Diagnosis can usually be made based on history. The examination of the larynx can confirm the diagnosis. Indirect examination of the airway with a mirror or with a flexible laryngoscope is warranted. Laryngeal appearance can vary with the severity of the disease. In the early stages, there is erythema and edema of the epiglottis, aryepiglottic folds, arytenoids, and vocal cords. As the disease progresses, the vocal cords can become erythematous and edematous. The subglottic region may be involved, depending upon the inciting agent, though this is rarer. Sticky, ropy secretions may also be seen between vocal cords or in the inter-arytenoid region. In the case of vocal abuse or misuse, several changes can be seen in the vocal folds. Reinkes edema is a common finding in both acute and chronic laryngitis. Submucosal hemorrhage may be seen in acute vocal trauma, or previously undiagnosed nodules or pseudo-nodules may be present. If left untreated, all of these can progress to chronic voice pathology.[1][5][6][7][1]

Evaluation

Diagnosis is usually made via a very thorough history and physical examination. Formal voice analysis and fiberoptic laryngoscopy can confirm the diagnosis in cases refractory to treatment or otherwise convoluted. Stroboscopy may be normal or reveal asymmetry, aperiodicity, and reduced mucosal wave patterns.[8] Further imaging or laboratory studies are not required unless an atypical pathogen or neoplasm is suspected. Rarely, if the patient has exudate in the oropharynx or vocal cords, culture may be indicated.

Treatment / Management

Treatment is often supportive in nature and depends on the severity of laryngitis. Treatment options may include:

• Voice rest: This is the single most important factor. Use of voice during laryngitis results in incomplete or delayed recovery. Complete voice rest is recommended, although it is almost impossible to achieve. If the patient needs to speak, the patient should be instructed to use a "confidential voice," a normal phonatory voice at low volume without whispering or projecting.l
• Steam Inhalation: Inhaling humidified air enhances moisture in the upper airway and helps remove secretions and exudates.
• Avoidance of irritants: Smoking and alcohol should be avoided. Smoking delays the prompt resolution of the disease process.
• Dietary modification: dietary restriction is recommended for patients with gastroesophageal reflux disease. This includes avoiding caffeinated drinks, spicy food, fatty food, chocolate, and peppermint. Another important lifestyle modification is the avoidance of late meals. The patient should have meals at least 3 hours before sleeping. The patient should drink plenty of water. These dietary measures have been shown to be effective in classic GERD, though their efficacy in LPR is disputed, they are often still employed.[9]
• Medications: Antibiotics prescription for an otherwise healthy patient with acute laryngitis is currently unsupported; however, for high-risk patients and patients with severe symptoms, antibiotics may be given. Some authors recommend narrow-spectrum antibiotics only in identifiable gram stains and cultures.

Fungal laryngitis can be treated with oral antifungal agents such as fluconazole. Treatment is usually required for a 3-week period and may be repeated if needed. This should be reserved for patients with confirmed fungal infection via laryngeal examination and/or culture. Mucolytics like guaifenesin may be used for clearing secretions.

In addition to lifestyle and dietary modifications, LPR-related laryngitis is treated with anti-reflux medications. Medications that suppress acid production, such as H2 receptor and proton pump blocking agents, are effective against gastroesophageal reflux, though proton pump inhibitors are found to be most effective for LPR. These may require higher doses or a twice-daily dosing schedule to be effective in this setting.[10] Prevailing data do not support the prescription of antihistaminics or oral corticosteroids for treating acute laryngitis.(A1)

Differential Diagnosis

The differential diagnoses for acute laryngitis include the following:

• Spasmodic dysphonia
• Reflux laryngitis
• Chronic allergic laryngitis
• Epiglottitis
• Neoplasm

Prognosis

As this is often a self-limiting condition, it carries a good prognosis. If the patient completes the recommended therapy, the prognosis for recovery to a premorbid level of phonation is excellent. If vocal maladaptations have occurred, speech therapy can resolve these problems.