Laringitis

01Pathophysiology

Laryngitis refers to inflammation of the laryngeal mucosa, predominantly involving the vocal folds (true vocal cords). The vocal folds are paired structures lined by stratified squamous epithelium that vibrate during phonation to produce voice. Any process that causes edema, erythema, or structural disruption of the vocal fold mucosa impairs their ability to vibrate symmetrically, resulting in the hallmark symptom: hoarseness (dysphonia).

In acute laryngitis, the most common mechanism is direct viral invasion of the laryngeal epithelium, triggering a local inflammatory cascade. Parainfluenza virus, rhinovirus, influenza, and adenovirus are the most frequent pathogens. The resulting mucosal edema and increased mucus production alter vocal fold mass and stiffness, causing the voice to become raspy, breathy, or absent altogether. This is why patients often report hoarseness that develops during or shortly after a typical upper respiratory infection (URI). The inflammation is self-limited, generally resolving within 2 weeks.

In chronic laryngitis (defined as symptoms persisting beyond 3 weeks), the pathophysiology shifts toward ongoing mucosal irritation rather than acute infection. Gastroesophageal reflux disease (GERD), also termed laryngopharyngeal reflux (LPR), is one of the most commonly tested causes. Acid and pepsin from gastric contents reflux onto the posterior larynx, causing chronic chemical irritation of the posterior commissure and arytenoid mucosa. This produces posterior laryngeal erythema, interarytenoid pachydermia, and contact ulcers. Importantly, patients with LPR may not have classic heartburn; instead, they present with throat clearing, globus sensation, chronic cough, and hoarseness, a presentation often described as "silent reflux."

Smoking causes chronic thermal and chemical irritation of the laryngeal mucosa, leading to Reinke edema (polypoid degeneration of the superficial lamina propria) and epithelial metaplasia. This is clinically important because chronic hoarseness in a smoker raises concern for laryngeal squamous cell carcinoma, and laryngoscopy with biopsy becomes mandatory.

Fungal laryngitis (Candida) is a high-yield cause in patients using inhaled corticosteroids for asthma or COPD. The immunosuppressive effect of topical steroids on the oropharyngeal and laryngeal mucosa allows Candida overgrowth. The key preventive measure tested on exams is rinsing the mouth after each inhaled corticosteroid use and using a spacer device.

Voice overuse, or phonotrauma, leads to mechanical stress on the vocal folds. Repetitive collision forces during prolonged or forceful phonation produce localized edema acutely and, over time, can lead to structural changes such as vocal fold nodules or polyps.

02Classification and Clinical Manifestation

03Diagnostic Workup

Acute laryngitis is a clinical diagnosis. When a patient presents with hoarseness in the setting of a recent URI that has lasted fewer than 3 weeks, no imaging or laryngoscopy is required. The diagnosis is made at the bedside. The key teaching point for exams: do not order imaging or endoscopy for acute, self-limited hoarseness in a young, otherwise healthy patient with a clear viral prodrome.

The diagnostic threshold changes entirely when hoarseness persists beyond 3 weeks. At this point, flexible fiberoptic laryngoscopy becomes the best initial diagnostic step. This allows direct visualization of the vocal folds to identify erythema, edema, nodules, polyps, leukoplakia, or a frank mass. This is one of the most commonly tested decision points: the 3-week cutoff is the trigger for laryngoscopy.

If laryngoscopy reveals a suspicious lesion (leukoplakia, erythroplakia, an exophytic mass), the next step is biopsy to rule out laryngeal squamous cell carcinoma. This is particularly critical in patients with a smoking and alcohol history. Any persistent hoarseness in a smoker older than 40 must be evaluated with laryngoscopy; treating it empirically as "chronic laryngitis" without visualization is a classic exam pitfall.

Videostroboscopy is the most accurate method for assessing vocal fold vibratory function and mucosal wave dynamics. It is used primarily by otolaryngologists and voice specialists to detect subtle lesions, early submucosal pathology, and vocal fold paresis that standard laryngoscopy may miss.

For suspected reflux laryngitis, the best initial approach is an empirical trial of twice-daily PPI therapy for 2 to 3 months. If symptoms do not improve, 24-hour dual-probe pH monitoring is the confirmatory test. The proximal probe (placed at the upper esophageal sphincter level) documents acid exposure reaching the larynx.

04Management and Treatment

Acute management is straightforward and almost entirely supportive. The most important intervention is voice rest, which means reducing vocal demands rather than complete silence. Patients should be counseled to avoid whispering, as whispering paradoxically increases tension and collision forces on the vocal folds compared to soft speech. Adequate hydration and inhaled humidified air help maintain mucosal moisture and reduce viscosity of secretions. Analgesics such as acetaminophen or ibuprofen can be used for throat discomfort. Antibiotics are not indicated for routine acute laryngitis because the etiology is overwhelmingly viral.

For reflux-related laryngitis, the standard empirical therapy is a twice-daily PPI (e.g., omeprazole 20 mg before breakfast and before dinner) for a minimum of 2 to 3 months. This duration is longer than typical GERD treatment because the laryngeal mucosa heals more slowly than esophageal mucosa. If there is no response after adequate PPI therapy with confirmed medication compliance, the next step is referral for pH monitoring and consideration of alternative diagnoses.

Candida laryngitis requires systemic antifungal treatment, most commonly fluconazole 100 to 200 mg daily for 1 to 3 weeks. Topical nystatin swish-and-swallow is often insufficient for laryngeal involvement. The underlying cause must also be addressed: if the patient uses an inhaled corticosteroid, ensure they are using a spacer and rinsing the mouth thoroughly after each dose.

For chronic laryngitis secondary to smoking, smoking cessation is the cornerstone. However, the most critical management step in terms of exam questions is not simply telling the patient to quit smoking, but rather ensuring that laryngoscopy with biopsy is performed to exclude squamous cell carcinoma. The "next best step" logic here consistently tests whether the student prioritizes cancer exclusion over empirical treatment.

Voice therapy with a speech-language pathologist is the first-line treatment for vocal fold nodules (which are always bilateral and located at the junction of the anterior one-third and posterior two-thirds of the vocal fold). Surgical excision is generally reserved for vocal fold polyps that fail conservative management or for any lesion where biopsy is needed.

05Differential Diagnosis and Distractors

06Traps and High-Yield Pearls

The most common way students lose points on laryngitis questions involves failing to recognize the 3-week threshold. Exam vignettes will present a patient with hoarseness and a history that subtly places the symptom duration beyond 3 weeks. Students who reflexively choose "voice rest and reassurance" as the answer will miss the correct response, which is laryngoscopy. The test is checking whether the student understands that hoarseness persisting beyond 3 weeks requires direct visualization of the vocal folds to exclude malignancy and other structural pathology.

A second common trap involves the smoker with chronic hoarseness. The vignette may frame this as "chronic laryngitis" and offer treatment options like antibiotics or PPI therapy. The correct answer is laryngoscopy with biopsy, not empirical treatment. Treating a smoker's hoarseness without visualization is a management error that examiners use to separate students who understand cancer screening from those who do not.

Another frequently tested scenario is the asthma patient on inhaled corticosteroids who develops hoarseness and is found to have white plaques on laryngoscopy. Students may choose to stop the inhaled corticosteroid, but the correct answer is to treat the Candida infection with fluconazole and optimize inhaler technique (add spacer, mouth rinsing) rather than discontinuing a necessary medication.

Finally, pay attention to the distractor of epiglottitis versus laryngitis. Both involve the laryngeal region, but epiglottitis is an emergency with drooling, stridor, and toxic appearance. Laryngitis is benign and self-limited. If the vignette describes a patient who appears well with isolated hoarseness and no airway compromise, that is laryngitis. If the patient is sitting forward, drooling, with stridor and fever, that is epiglottitis, and the answer is securing the airway.

The core competency being tested across all laryngitis questions is clinical reasoning around duration thresholds, cancer exclusion in at-risk populations, and distinguishing benign self-limited disease from surgical emergencies.