Browse the corpus

Cough is the most common symptom prompting outpatient medical visits and represents a significant public health concern. Affecting nearly 10% of adults worldwide and over 12 million individuals in the United States annually, cough can substantially impair quality of life and cause distress for patients, families, and caregivers. Beyond its role in transmitting respiratory pathogens, cough contributes to physical and psychosocial complications, thereby amplifying its impact on individual and population health. Clinicians classify cough by duration as acute, subacute, or chronic, a framework that guides diagnostic evaluation and management. The differential diagnosis is broad, ranging from benign, self-limited conditions to serious cardiopulmonary or systemic diseases, which can complicate assessment. A systematic approach incorporating a thorough history and physical examination is essential for identifying likely etiologies and determining the need for additional testing. Early recognition of warning signs, including hemoptysis, unexplained weight loss, fever, or dyspnea, is critical, as these features may necessitate urgent imaging, laboratory evaluation, or emergency referral. This activity for healthcare professionals is designed to enhance the learner’s competence in evaluating and managing patients presenting with cough. Participants refine diagnostic reasoning, improve recognition of high-risk clinical features, and implement evidence-based management strategies. The activity emphasizes the importance of interprofessional collaboration among clinicians, pulmonologists, radiologists, and primary care teams to optimize patient evaluation, streamline referral pathways, and improve clinical outcomes. Enhanced understanding of cough epidemiology, risk stratification, and coordinated care supports timely interventions and reduces the likelihood of complications or misdiagnosis. Objectives: Differentiate benign causes of cough from high-risk conditions such as malignancy, severe infection, or cardiopulmonary disease that require urgent evaluation. Implement an evidence-based diagnostic approach to cough that incorporates history, physical examination, and appropriate use of diagnostic studies. Apply current clinical guidelines to guide management strategies for acute and chronic cough across inpatient and outpatient settings.

Differentiate benign causes of cough from high-risk conditions such as malignancy, severe infection, or cardiopulmonary disease that require urgent evaluation. Implement an evidence-based diagnostic approach to cough that incorporates history, physical examination, and appropriate use of diagnostic studies. Apply current clinical guidelines to guide management strategies for acute and chronic cough across inpatient and outpatient settings. Collaborate with interprofessional team members, including nurses, pharmacists, respiratory therapists, and specialists, to optimize evaluation and management of persistent or complex cough. Access free multiple choice questions on this topic.

Cough is one of the most common symptoms encountered in medical practice and a leading cause of outpatient and emergency department visits worldwide. Cough has a broad differential diagnosis, ranging from benign, self-limited conditions to serious and potentially life-threatening diseases. Although cough is a protective reflex that clears secretions, irritants, and foreign material from the airways, a persistent or severe cough may indicate significant underlying pathology. The cough reflex consists of an initial deep inspiration followed by forceful expiratory muscle contraction against a closed glottis, generating high intrathoracic pressures, and a subsequent sudden glottic opening that produces rapid, high-velocity airflow to expel airway contents. Clinicians classify cough by duration as acute (less than 3 weeks), subacute (3 to 8 weeks), or chronic (greater than 8 weeks or greater than 4 weeks in children aged 14 and younger), a framework that helps narrow the etiologic spectrum and guide evaluation.[1][2] Upper and lower respiratory tract infections are the most common causes of acute cough and are typically self-limited; however, serious noninfectious conditions, including asthma or chronic obstructive pulmonary disease exacerbations, pneumonia, pulmonary embolism, or heart failure, may also cause an acute cough.[1][3] Subacute cough commonly follows a respiratory infection and is driven by persistent airway or sinonasal inflammation. Chronic cough is more complex and is frequently associated with upper airway cough syndrome, asthma or cough-variant asthma, gastroesophageal reflux disease, chronic bronchitis, nonasthmatic eosinophilic bronchitis, and medication effects; less common causes include malignancy and interstitial lung disease. Beyond physical complications such as rib fractures and hernias, a chronic cough significantly impairs quality of life, sleep, and productivity and is associated with anxiety, depression, and social isolation.[4][5] In children, early recognition and treatment are critical to prevent disease progression, to conditions such as bronchiectasis, and may allow partial reversibility. Emerging data also link chronic productive cough in young adults to increased cardiovascular risk and premature mortality.[6]

Chronic cough is more complex and is frequently associated with upper airway cough syndrome, asthma or cough-variant asthma, gastroesophageal reflux disease, chronic bronchitis, nonasthmatic eosinophilic bronchitis, and medication effects; less common causes include malignancy and interstitial lung disease. Beyond physical complications such as rib fractures and hernias, a chronic cough significantly impairs quality of life, sleep, and productivity and is associated with anxiety, depression, and social isolation.[4][5] In children, early recognition and treatment are critical to prevent disease progression, to conditions such as bronchiectasis, and may allow partial reversibility. Emerging data also link chronic productive cough in young adults to increased cardiovascular risk and premature mortality.[6] Because cough is a symptom rather than a diagnosis, systematic evaluation is essential. A careful history and physical examination help identify red-flag features, such as hemoptysis, dyspnea, hypoxemia, constitutional symptoms, abnormal vital signs, or cardiopulmonary compromise, and guide appropriate diagnostic testing, referral, and management. A clear understanding of cough epidemiology, common causes, and warning signs supports accurate diagnosis, limits unnecessary testing and inappropriate antibiotic use, reduces pathogen transmission, and promotes timely, evidence-based, patient-centered care.

Upper and lower respiratory tract infections most commonly cause an acute cough. However, clinicians must remain alert to potentially life-threatening conditions that can also present acutely, including asthma or chronic obstructive pulmonary disorder (COPD) exacerbations, pulmonary embolism, and acute heart failure. Common causes of acute cough include viral respiratory infections (eg, influenza and SARS-CoV-2), acute bronchitis, pneumonia, pertussis, and tuberculosis in endemic areas, as well as upper airway inflammatory conditions such as acute rhinosinusitis and allergic rhinitis. Additional etiologies include aspiration syndromes, inhalation of environmental irritants, trauma, pleural irritation, and, less commonly, medication effects or malignancy.[3][7][8][9][10][11][12] Subacute cough most often develops following a respiratory infection and is typically driven by persistent irritation of cough receptors due to ongoing or resolving airway or paranasal sinus inflammation. Many causes of subacute cough overlap with both acute and chronic etiologies, reflecting a transitional phase in the disease process. Chronic cough has a broader and more complex differential diagnosis. Asthma is a significant cause in adults and the leading cause in children, along with other eosinophilic airway disorders such as cough-variant asthma and nonasthmatic eosinophilic bronchitis. Upper airway conditions, including upper airway cough syndrome and chronic rhinosinusitis, and lower airway diseases such as chronic bronchitis, COPD, bronchiectasis, and tracheo-bronchomalacia are also common contributors. Clinicians should also consider gastroesophageal and laryngopharyngeal reflux, chronic infections (eg, tuberculosis, nontuberculous mycobacteria, fungal or parasitic infections), prolonged post-pertussis or SARS-CoV-2 cough, structural airway abnormalities, and medication-related causes. Less common but important causes include obstructive sleep apnea, interstitial lung disease, malignancy, and somatic cough disorder, underscoring the need for a systematic and comprehensive evaluation.[13][14][15][16][17]

Cough is among the most common complaints in primary care, with chronic cough affecting approximately 8% to 10% of the global population; however, reported prevalence ranges from 2% to 18% across regions.[18] Rates are higher in North America, Europe, and Oceania than in Asia and Africa, likely reflecting environmental and lifestyle differences. Chronic cough is more common in women, who account for over two-thirds of cases, possibly due to increased sensitivity of the cough reflex. Prevalence rises with age, with the greatest burden in older adults.[18][19][20] In the United States (US), more than 12 million individuals are affected annually, resulting in substantial healthcare utilization and a significantly greater economic burden than that associated with an acute cough.[21][22] Postinfectious cough occurs in up to 25% of patients after respiratory infection. Estimating the prevalence of chronic cough in children is challenging due to variable definitions and study methods. Community studies suggest that approximately 10% of children aged 5 to 11 experience cough lasting longer than 3 weeks, with some reports noting rates as high as 22%, particularly among preschool-aged children.[23][24] Upper airway cough syndrome, asthma (including cough-variant asthma), gastroesophageal reflux disease (GERD), and nonasthmatic eosinophilic bronchitis are the most common causes of chronic cough in the US. Upper airway cough syndrome is the leading etiology and includes allergic and nonallergic rhinitis, as well as chronic rhinosinusitis.[13][25] GERD accounts for a substantial proportion of cases. However, prevalence estimates vary widely because cough may be the sole manifestation, and patients often present only when symptoms persist despite over-the-counter therapy. Multiple concurrent causes are common, affecting more than half of patients, underscoring the need for a systematic, comprehensive diagnostic approach.

Activation of cough receptors in the upper and lower airways and at extrapulmonary sites, including the pericardium, esophagus, diaphragm, and stomach, triggers a reflex arc that initiates cough. Mechanical receptors respond to touch, airway distortion, and pH changes and transmit afferent signals via vagal A-δ fibers from the nodose ganglion. Chemical receptors sensitive to temperature, irritants, and capsaicin-like compounds activate transient receptor potential vanilloid type 1 (TRPV1), transient receptor potential ankyrin type 1 (TRPA1), and adenosine triphosphate-gated P2X3 receptors.[26][27] Afferent impulses travel through the vagus nerve to the medullary cough center, with cortical modulation; efferent signals then activate the respiratory muscles via the vagus, phrenic, and spinal motor nerves. In chronic cough, heightened cough reflex sensitivity enables minimal stimuli, such as airway inflammation, gastroesophageal reflux, air pollution, or tobacco smoke, to provoke persistent symptoms.[28] Multiple pathophysiologic mechanisms converge on irritation or hypersensitization of cough receptors. Upper airway disorders, including acute and chronic rhinosinusitis, cause cough through increased mucus production and postnasal drip, while GERD contributes via laryngopharyngeal irritation and microaspiration. Medications can also provoke cough: angiotensin-converting enzyme inhibitors increase bradykinin and stimulate airway C fibers; calcium channel blockers relax the lower esophageal sphincter and promote reflux; β-blockers may induce bronchospasm; and sitagliptin likely increases cough by elevating substance P, eotaxin, and neuropeptide Y. Lower airway and parenchymal diseases trigger cough through inflammation, structural abnormalities, and impaired mucus clearance. Chronic bronchitis and bronchiectasis cause excessive mucus production and airway inflammation, thereby mechanically stimulating cough receptors and promoting recurrent infection. Nonasthmatic eosinophilic bronchitis causes cough through eosinophilic airway inflammation without airflow obstruction, whereas asthma additionally involves bronchoconstriction. Interstitial lung diseases provoke cough through fibrosis, reduced lung compliance, and chronic inflammatory signaling.[16]

Lower airway and parenchymal diseases trigger cough through inflammation, structural abnormalities, and impaired mucus clearance. Chronic bronchitis and bronchiectasis cause excessive mucus production and airway inflammation, thereby mechanically stimulating cough receptors and promoting recurrent infection. Nonasthmatic eosinophilic bronchitis causes cough through eosinophilic airway inflammation without airflow obstruction, whereas asthma additionally involves bronchoconstriction. Interstitial lung diseases provoke cough through fibrosis, reduced lung compliance, and chronic inflammatory signaling.[16] Mechanical and vascular mechanisms also contribute. Obstructive sleep apnea induces a reflex cough due to recurrent collapse of the upper airway during sleep.[17] Aspiration syndromes result from impaired airway protection and chemical irritation of the airways. Pulmonary embolism may induce cough through vascular obstruction, inflammation, pulmonary congestion, and ischemic injury, leading to cytokine release.[29] Postinfectious cough arises from persistent airway or sinus inflammation after viral infection and is usually self-limited. Overall, chronic cough most often reflects sustained inflammation, structural airway changes, or cough reflex hypersensitivity rather than ongoing infection.[30]

Cough is a symptom rather than a diagnosis, and a thorough history and physical examination are fundamental steps in the evaluation. The clinical presentation varies based on the underlying etiology. The following discusses the presentations of some of the most common causes of cough, but is not all-inclusive. Acute Cough Acute bronchitis: Dry or productive cough lasting less than 3 weeks, often following an upper respiratory infection; associated with wheezing and rhonchi that typically clear with coughing. Acute decompensated heart failure: Dyspnea, orthopnea, paroxysmal nocturnal dyspnea, bibasilar crackles, peripheral edema, S3 gallop, and possible hypotension or tachyarrhythmias.[31] Acute rhinosinusitis: Nasal congestion or discharge, facial pain or pressure, decreased smell, and postnasal drip. Allergic rhinitis: Rhinorrhea, nasal itching, sneezing, cough, allergic conjunctivitis, and fatigue; exam findings include pale, edematous nasal mucosa, clear rhinorrhea, pharyngeal cobblestoning, and infraorbital darkening or edema.[32] Asthma: Episodic cough, wheezing, or dyspnea triggered by cold air, exercise, infections, or environmental exposures; cough may be the predominant or sole symptom in cough-variant asthma.[11] Intermittent expiratory wheezing is typical, whereas fixed or unilateral wheezing suggests an alternative pathology. Bronchiolitis: Primarily affects children younger than 2; begins with upper respiratory symptoms followed by wheezing, crackles, tachypnea, retractions, and sometimes fever. COPD exacerbation: Worsening cough, wheezing, tachypnea, tachycardia, accessory muscle use, difficulty speaking, altered mental status, or signs of hypercapnia such as asterixis.[33] Foreign body aspiration: Acute cough, stridor, focal wheezing, tachypnea, or decreased air entry; severe cases present with respiratory distress, cyanosis, or altered mental status. Pertussis: Progressive cough that worsens after an initial catarrhal phase, followed by paroxysmal coughing fits with inspiratory “whoop,” posttussive vomiting, and possible cyanosis; gradual resolution during the convalescent phase. Pulmonary embolism: Acute cough with dyspnea, pleuritic chest pain, tachypnea, hemoptysis, wheezing, or signs of deep vein thrombosis. Chronic Cough Bronchiectasis: Chronic productive cough with daily mucopurulent sputum, recurrent infections, dyspnea, fatigue, wheezing, and occasional hemoptysis.

Pertussis: Progressive cough that worsens after an initial catarrhal phase, followed by paroxysmal coughing fits with inspiratory “whoop,” posttussive vomiting, and possible cyanosis; gradual resolution during the convalescent phase. Pulmonary embolism: Acute cough with dyspnea, pleuritic chest pain, tachypnea, hemoptysis, wheezing, or signs of deep vein thrombosis. Chronic Cough Bronchiectasis: Chronic productive cough with daily mucopurulent sputum, recurrent infections, dyspnea, fatigue, wheezing, and occasional hemoptysis. Chronic aspiration: Cough associated with eating or drinking, especially thin liquids; may include focal wheezing, hemoptysis, or foul-smelling sputum. Chronic rhinosinusitis: Nasal congestion or drainage, facial pressure, reduced or absent smell; cough is particularly prominent in children.[34] Cystic fibrosis: Persistent productive cough with multisystem involvement, including failure to thrive, pancreatic insufficiency, sinus disease, hepatobiliary disease, rectal prolapse, and nephrolithiasis. Gastroesophageal reflux disease: Cough associated with dysphonia, heartburn, regurgitation, or sour taste. Interstitial lung disease: Chronic cough and progressive dyspnea with fine inspiratory crackles, often in dependent lung zones. Medication-induced cough: Typically dry; angiotensin-converting enzyme inhibitor–associated cough develops within 1 week to 6 months of initiation, resolves within weeks of discontinuation, and recurs on rechallenge. Nonasthmatic eosinophilic bronchitis: Chronic nonproductive cough in patients with atopic tendencies, elevated sputum eosinophils, airway inflammation, and no airway hyperresponsiveness. Obstructive sleep apnea: Chronic cough accompanied by loud snoring, excessive daytime sleepiness, and morning headaches. Protracted bacterial bronchitis: Chronic wet cough lasting 4 weeks or longer, normal spirometry and chest radiography (aside from possible peribronchial cuffing), and resolution with a 2-week course of appropriate antibiotics. Upper airway cough syndrome: Frequent throat clearing, postnasal drip sensation, nasal discharge; exam findings include pharyngeal cobblestoning and visible secretions. Please see StatPearls' companion topic, "Chronic Cough," for an in-depth discussion of the presentation, evaluation, and management of chronic cough.

History and Physical Examination Evaluating a patient with a cough should follow a structured approach that prioritizes identifying serious underlying disease and clinical warning signs warranting further investigation, such as chest radiography, laboratory testing, or computed tomography. Constitutional symptoms, including fever, night sweats, and unintentional weight loss, raise concern for malignancy, chronic infection (eg, tuberculosis or lung abscess), or rheumatologic disease. Purulent sputum suggests pneumonia or sinus infection, whereas hemoptysis may indicate malignancy, infection, heart failure, foreign body aspiration, or systemic inflammatory disease. Dyspnea increases suspicion for airway obstruction, parenchymal lung disease, acute exacerbations of asthma or COPD, or decompensated heart failure. A history of choking, particularly in children, should prompt consideration of foreign body aspiration. Additional concerning features include abnormal vital signs, hypoxia, cyanosis, altered mental status, vomiting, recurrent pneumonia, immunocompromised status, dysphagia, and decreased appetite.[3] A focused history should then characterize cough duration and quality (dry or productive; wet in children), associated symptoms (eg, rhinorrhea, sneezing, fever, hemoptysis, weight loss, dysphagia, dysphonia), and prior episodes. Clinicians should further assess sputum characteristics, tobacco or vaping exposure, medication use, occupational and environmental exposures, diurnal or seasonal variation, aggravating or relieving factors, and a history of asthma, COPD, or heart failure. In infants and children, symptoms present since the neonatal period suggest congenital disease, immune dysfunction, or conditions predisposing to bronchiectasis. Neurologic or developmental disorders increase the risk of aspiration, while feeding difficulties raise concern for laryngeal or tracheal abnormalities. Physical findings such as digital clubbing suggest bronchiectasis or interstitial lung disease. At the same time, patients with asthma, bronchiectasis, bronchiolitis obliterans, bronchopulmonary dysplasia, heart failure, immunodeficiency, or aspiration may present with wheezing. Dextrocardia, situs inversus, tympanic membrane scarring, or chronic otorrhea suggest primary ciliary dyskinesia.

In infants and children, symptoms present since the neonatal period suggest congenital disease, immune dysfunction, or conditions predisposing to bronchiectasis. Neurologic or developmental disorders increase the risk of aspiration, while feeding difficulties raise concern for laryngeal or tracheal abnormalities. Physical findings such as digital clubbing suggest bronchiectasis or interstitial lung disease. At the same time, patients with asthma, bronchiectasis, bronchiolitis obliterans, bronchopulmonary dysplasia, heart failure, immunodeficiency, or aspiration may present with wheezing. Dextrocardia, situs inversus, tympanic membrane scarring, or chronic otorrhea suggest primary ciliary dyskinesia. Patients with a history of tobacco exposure are at increased risk for COPD and lung cancer. According to the American Academy of Chest Physicians, new or changing cough or new-onset hoarseness in patients who smoke and are older than 45, as well as cough in adults aged 55 to 80 years with a 30 pack-year smoking history who currently smoke or quit within the past 15 years, warrants further evaluation. Patients who are immunosuppressed require careful assessment for infection. Clinicians should review travel and environmental exposures and consider tuberculosis in patients with a cough lasting longer than 3 weeks who have relevant risk factors.[35] Physical examination includes assessment of cough characteristics, work of breathing, accessory muscle use, and chest wall abnormalities, followed by auscultation for abnormal breath sounds. Because cerumen impaction can stimulate the auricular branch of the vagus nerve and provoke cough, patients with a chronic cough should undergo an otoscopic examination. Evaluation Acute cough

Clinicians should review travel and environmental exposures and consider tuberculosis in patients with a cough lasting longer than 3 weeks who have relevant risk factors.[35] Physical examination includes assessment of cough characteristics, work of breathing, accessory muscle use, and chest wall abnormalities, followed by auscultation for abnormal breath sounds. Because cerumen impaction can stimulate the auricular branch of the vagus nerve and provoke cough, patients with a chronic cough should undergo an otoscopic examination. Evaluation Acute cough Patients who require COVID-19 treatment or diagnostic confirmation for isolation or infection control should undergo testing with a rapid antigen test or a nucleic acid amplification test. Influenza testing is appropriate when results will affect management, particularly during influenza season, in patients with acute cough who are immunocompromised or at increased risk of complications, who are experiencing asthma or COPD exacerbations, or who are hospitalized with acute respiratory symptoms. When pulmonary embolism is suspected, clinicians should assess pretest probability, then perform D-dimer testing, followed by computed tomography pulmonary angiography when indicated, in patients with acute dyspnea, pleuritic chest pain, tachycardia, or risk factors for venous thromboembolism. Evaluation for pneumonia typically includes chest radiography and complete blood count, with C-reactive protein measured selectively; levels greater than 30 mg/L in the appropriate clinical context increase the likelihood of pneumonia. Testing for Legionella should be reserved for patients with known exposure.[36] Acute bronchitis, most viral upper respiratory infections, acute rhinosinusitis, and allergic rhinitis are clinical diagnoses and do not require initial imaging or laboratory testing unless there are warning signs of complications. Subacute and chronic cough

Evaluation for pneumonia typically includes chest radiography and complete blood count, with C-reactive protein measured selectively; levels greater than 30 mg/L in the appropriate clinical context increase the likelihood of pneumonia. Testing for Legionella should be reserved for patients with known exposure.[36] Acute bronchitis, most viral upper respiratory infections, acute rhinosinusitis, and allergic rhinitis are clinical diagnoses and do not require initial imaging or laboratory testing unless there are warning signs of complications. Subacute and chronic cough Patients with cough lasting 3 weeks or longer and features suggestive of postnasal drip, asthma, or GERD should undergo an empiric trial of targeted therapy for approximately 4 weeks. Please see the StatPearls companion topics, "Gastroesophageal Reflux Disease," "Asthma," and "Pediatric Asthma," for an in-depth discussion of the evaluation and management of these conditions. Patients with purulent sputum, tobacco exposure, exposure to angiotensin-converting enzyme (ACE) inhibitors, or immunocompromising conditions require targeted management, including antibiotics when indicated, smoking cessation, ACE inhibitor discontinuation, and medication adjustment as appropriate. Patients without an identifiable cause, those with suspected parenchymal lung disease, or those who fail initial therapy should undergo chest radiography. All patients aged 15 and older with a cough lasting more than 8 weeks should undergo chest radiography, with further evaluation guided by abnormal findings. Patients with persistent cough despite appropriate treatment and a normal or unrelated chest radiograph should undergo stepwise evaluation for upper airway cough syndrome, asthma, nonasthmatic eosinophilic bronchitis, and GERD, with diagnostic testing tailored to clinical suspicion.[3] If the cough remains refractory, further evaluation may include sputum studies, high-resolution chest computed tomography, bronchoscopy, esophageal evaluation, or cardiac testing. Somatic cough syndrome is a diagnosis of exclusion after adequate evaluation and treatment of all other potential medical causes.[37]

All patients aged 15 and older with a cough lasting more than 8 weeks should undergo chest radiography, with further evaluation guided by abnormal findings. Patients with persistent cough despite appropriate treatment and a normal or unrelated chest radiograph should undergo stepwise evaluation for upper airway cough syndrome, asthma, nonasthmatic eosinophilic bronchitis, and GERD, with diagnostic testing tailored to clinical suspicion.[3] If the cough remains refractory, further evaluation may include sputum studies, high-resolution chest computed tomography, bronchoscopy, esophageal evaluation, or cardiac testing. Somatic cough syndrome is a diagnosis of exclusion after adequate evaluation and treatment of all other potential medical causes.[37] In children aged 14 years and younger without warning signs, evaluation begins with spirometry and, when feasible, fractional exhaled nitric oxide (FeNO) measurement; a reversible obstructive pattern or FeNO of 25 ppb or higher supports a diagnosis of asthma and warrants a 2-week therapeutic trial. Remaining patients should undergo chest radiography. If imaging is normal, consider a habit cough, pertussis, tracheomalacia, or protracted bacterial bronchitis based on clinical features. Patients with a suspected foreign-body aspiration or structural airway abnormalities undergo a flexible bronchoscopy. Sinus imaging or empiric antibiotics may be considered for suspected bacterial sinusitis, recognizing the limited correlation between imaging and clinical disease. Additional testing may include swallow studies, advanced pulmonary function testing, gastrointestinal evaluation, or echocardiography.

In children aged 14 years and younger without warning signs, evaluation begins with spirometry and, when feasible, fractional exhaled nitric oxide (FeNO) measurement; a reversible obstructive pattern or FeNO of 25 ppb or higher supports a diagnosis of asthma and warrants a 2-week therapeutic trial. Remaining patients should undergo chest radiography. If imaging is normal, consider a habit cough, pertussis, tracheomalacia, or protracted bacterial bronchitis based on clinical features. Patients with a suspected foreign-body aspiration or structural airway abnormalities undergo a flexible bronchoscopy. Sinus imaging or empiric antibiotics may be considered for suspected bacterial sinusitis, recognizing the limited correlation between imaging and clinical disease. Additional testing may include swallow studies, advanced pulmonary function testing, gastrointestinal evaluation, or echocardiography. In patients undergoing palliative care, evaluation depends on the patient's overall goals, and clinicians must consider what underlying concerns the cough may elicit for the patient, family, and caregivers. Decisions regarding diagnostic testing must account for the probability of undergoing treatment based on the test results. However, testing should not be dismissed in patients with goals limited to comfort care if testing will help guide symptom-oriented treatment and does not cause undue stress for the patient. With the addition of chemotherapy-induced pulmonary toxicity, ineffective swallowing, and a higher rate of malignancy, the differential diagnoses for patients undergoing palliative care are similar to those of the general population, and clinicians should search for potentially treatable causes. A bedside swallowing evaluation may be necessary if the clinician suspects ineffective swallowing.

Acute Cough Acute upper respiratory tract infection Management of acute cough due to an upper respiratory tract infection is primarily supportive. Short-term use of acetaminophen or nonsteroidal anti-inflammatory drugs effectively relieves fever, headache, myalgias, arthralgias, ear pain, and malaise, with similar efficacy and good tolerability.[38] In adults and children older than 12, combination antihistamine–decongestant products may provide greater symptom relief than either agent alone. In contrast, antihistamines alone offer minimal benefit and commonly cause adverse effects. Over-the-counter cough and cold medications do not effectively treat children younger than 12 and have caused fatal overdoses in children under 2; therefore, clinicians do not recommend decongestants or antihistamines in those younger than 12. Clinicians should strongly encourage avoidance of tobacco smoke. When started early, intranasal or inhaled cromolyn sodium may reduce symptom severity and is generally well tolerated. Intranasal ipratropium bromide improves rhinorrhea and sneezing but does not relieve congestion and may cause nasal dryness or epistaxis. Although these therapies provide symptomatic relief, none shorten illness duration or improve outcomes.[39] Therapies with limited or uncertain benefit include dextromethorphan (inconsistent, modest effects), pseudoephedrine (mild congestion relief), phenylephrine (no better than placebo), saline nasal irrigation (modest benefit), and guaifenesin (weak evidence). Honey reduces cough frequency and severity, particularly in children, and may benefit adults; therefore, it is a potential option for patients aged 1 and older. Evidence for herbal products and zinc supplements is inconsistent, and patients should avoid intranasal zinc due to the risk of permanent anosmia. Antibiotics, antihistamines used alone, and antiviral therapies do not improve outcomes and may cause harm. Acute rhinosinusitis

Therapies with limited or uncertain benefit include dextromethorphan (inconsistent, modest effects), pseudoephedrine (mild congestion relief), phenylephrine (no better than placebo), saline nasal irrigation (modest benefit), and guaifenesin (weak evidence). Honey reduces cough frequency and severity, particularly in children, and may benefit adults; therefore, it is a potential option for patients aged 1 and older. Evidence for herbal products and zinc supplements is inconsistent, and patients should avoid intranasal zinc due to the risk of permanent anosmia. Antibiotics, antihistamines used alone, and antiviral therapies do not improve outcomes and may cause harm. Acute rhinosinusitis Only 0.5% to 2% of cases of acute rhinosinusitis (ARS) are bacterial.[40] In addition to the measures discussed above, some experts recommend saline nasal irrigation with buffered, physiologic, or hypertonic saline using sterile or bottled water. The actual benefit of saline irrigation is unclear.[41] However, irrigation has minimal adverse effects, and anecdotal reports indicate that it may improve nasal symptoms in some patients. Likewise, clinicians can also offer topical nasal steroids for patients with both ARS and acute bacterial rhinosinusitis (ABRS).[42][43][44] The American Academy of Otolaryngology–Head and Neck Surgery recommends watchful waiting for 3 to 5 days in patients with ABRS who have symptoms lasting no more than 14 days and lack severe features. If symptoms fail to improve or worsen, amoxicillin or amoxicillin–clavulanate is first-line therapy for 5 to 7 days. In contrast, the 2012 Infectious Disease Society of America guidelines recommend immediate antibiotics for symptoms lasting 10 or more days, for patients with a biphasic or “double-worsening” course, or for severe symptoms lasting 3 to 4 days (fever of 102.2 °F [39 °C] or higher, purulent discharge, or severe facial pain).[45] Patients at risk for penicillin-resistant Streptococcus pneumoniae should receive high-dose amoxicillin–clavulanate. Doxycycline or a third-generation cephalosporin with or without clindamycin is appropriate for penicillin-allergic patients. Influenza Influenza is typically self-limited. However, infection is associated with increased morbidity and mortality in select populations. The following patients warrant treatment with antivirals: All hospitalized patients with influenza

The American Academy of Otolaryngology–Head and Neck Surgery recommends watchful waiting for 3 to 5 days in patients with ABRS who have symptoms lasting no more than 14 days and lack severe features. If symptoms fail to improve or worsen, amoxicillin or amoxicillin–clavulanate is first-line therapy for 5 to 7 days. In contrast, the 2012 Infectious Disease Society of America guidelines recommend immediate antibiotics for symptoms lasting 10 or more days, for patients with a biphasic or “double-worsening” course, or for severe symptoms lasting 3 to 4 days (fever of 102.2 °F [39 °C] or higher, purulent discharge, or severe facial pain).[45] Patients at risk for penicillin-resistant Streptococcus pneumoniae should receive high-dose amoxicillin–clavulanate. Doxycycline or a third-generation cephalosporin with or without clindamycin is appropriate for penicillin-allergic patients. Influenza Influenza is typically self-limited. However, infection is associated with increased morbidity and mortality in select populations. The following patients warrant treatment with antivirals: All hospitalized patients with influenza Patients at increased risk for complications, such as those 65 and older, non-Hispanic Black persons, Hispanic or Latino persons, and American Indian or Alaska Native persons, and those with asthma Patients with progressive illness who do not require hospitalization Pregnant patients or those who are up to 2 weeks postpartum Patients with asthma, chronic kidney and liver disease, heart disease, chronic lung disease, diabetes, and sickle cell disease Patients with known or expected influenza who may transmit the illness to a high-risk individual [46] Oseltamivir is the antiviral medication of choice for influenza. Additional alternatives are baloxavir, zanamivir, and peramivir. Please see StatPearls' companion topic, "Influenza," for an in-depth discussion on influenza management. Pertussis The following patients should receive antimicrobial treatment for pertussis: All individuals older than 1 year with a clinical or lab-confirmed diagnosis who present within 3 weeks of the onset of cough All individuals younger than 1 year, pregnant individuals, patients with asthma, COPD, or an immunocompromising condition, and those aged 65 and older who present within 6 weeks of cough onset.

The following patients should receive antimicrobial treatment for pertussis: All individuals older than 1 year with a clinical or lab-confirmed diagnosis who present within 3 weeks of the onset of cough All individuals younger than 1 year, pregnant individuals, patients with asthma, COPD, or an immunocompromising condition, and those aged 65 and older who present within 6 weeks of cough onset. Preferred treatment is azithromycin or clarithromycin; trimethoprim-sulfamethoxazole is an alternative, except in infants younger than 2 months due to the risk of kernicterus. Early treatment (within 7 days) may shorten symptom duration. Patients are most contagious during the first 3 weeks of illness or the first 5 days of treatment. Infants younger than 4 months and patients with severe disease require hospitalization. All close contacts exposed within 21 days should receive postexposure prophylaxis regardless of immunization status, and all patients and contacts should receive the pertussis vaccine per guidelines. Acute lower respiratory tract infections Like most upper respiratory tract infections, acute bronchitis is most commonly viral in etiology, and management is supportive. Antivirals and antibiotics have not shown benefit in the treatment of acute bronchitis.[7] Bronchiolitis Management of mild bronchiolitis consists of nasal suctioning and adequate hydration. Medications are unnecessary unless caregivers elect to treat fever when present. Moderate to severe symptoms will likely need evaluation in an emergency department. Treatment consists of supplemental oxygen when necessary and nasal suctioning. Clinicians do not routinely use bronchodilators to manage bronchiolitis; however, they may trial nebulized epinephrine or albuterol in infants and children who present with wheezing and respiratory distress. If the patient demonstrates clinical improvement, clinicians may administer additional doses as needed. If no response occurs, clinicians should discontinue bronchodilator therapy. Similarly, clinicians should reserve glucocorticoids for infants and children with evidence of an underlying reactive airway disease or asthma component. Pneumonia

Management of mild bronchiolitis consists of nasal suctioning and adequate hydration. Medications are unnecessary unless caregivers elect to treat fever when present. Moderate to severe symptoms will likely need evaluation in an emergency department. Treatment consists of supplemental oxygen when necessary and nasal suctioning. Clinicians do not routinely use bronchodilators to manage bronchiolitis; however, they may trial nebulized epinephrine or albuterol in infants and children who present with wheezing and respiratory distress. If the patient demonstrates clinical improvement, clinicians may administer additional doses as needed. If no response occurs, clinicians should discontinue bronchodilator therapy. Similarly, clinicians should reserve glucocorticoids for infants and children with evidence of an underlying reactive airway disease or asthma component. Pneumonia The choice of antibiotic therapy for community-acquired pneumonia depends on the expected pathogen, patient age, risk factors, comorbidities, and local resistance patterns.[47] According to the 2019 American Thoracic Society/Infectious Diseases Society of America guidelines, the preferred empiric antibiotic regimen for community-acquired pneumonia in healthy outpatients 64 and younger is high-dose amoxicillin. Monotherapy with doxycycline or a macrolide, such as azithromycin or clarithromycin (if the local S pneumoniae macrolide resistance rate is below 25%), is an acceptable alternative. Macrolide resistance rates among S pneumoniae are often greater than 30% in the United States and exceed 25% in nearly the rest of the world. Patients 65 and older or with chronic lung, liver, or kidney disease, asplenia, a history of cancer, alcohol use disorder, patients who smoke, or those treated with antibiotics within the last 3 months, should receive amoxicillin-clavulanic acid and a macrolide or doxycycline. Patients who are unable to tolerate amoxicillin-clavulanate should receive a third-generation cephalosporin such as cefpodoxime in combination with a macrolide or doxycycline. Clinicians prescribe a respiratory fluoroquinolone for patients who cannot tolerate a third-generation cephalosporin.

Patients 65 and older or with chronic lung, liver, or kidney disease, asplenia, a history of cancer, alcohol use disorder, patients who smoke, or those treated with antibiotics within the last 3 months, should receive amoxicillin-clavulanic acid and a macrolide or doxycycline. Patients who are unable to tolerate amoxicillin-clavulanate should receive a third-generation cephalosporin such as cefpodoxime in combination with a macrolide or doxycycline. Clinicians prescribe a respiratory fluoroquinolone for patients who cannot tolerate a third-generation cephalosporin. Hospitalized individuals with pneumonia are treated with a respiratory fluoroquinolone or β-lactam antibiotics, along with doxycycline or a macrolide.[36] Lafamulin is a potential alternative to fluoroquinolones. However, clinical use is still limited, and healthcare professionals should avoid its use in patients with moderate to severe hepatic dysfunction, known long QT syndrome, or in patients taking QT-prolonging agents, pregnant and breastfeeding patients, and patients who could become pregnant not using contraception. Additionally, lefamulin does not provide coverage against Enterobacteriaceae. Since macrolides, lefamulin, and fluoroquinolones can all cause a prolonged QT interval, doxycycline is the preferred agent in patients with or who are at risk of a prolonged QT interval. Omadacycline is an additional agent that clinicians may choose in place of fluoroquinolones. Asthma exacerbation Clinicians manage an acute asthma exacerbation with short-acting inhaled bronchodilators and steroids. Patients with severe symptoms (respiratory rate greater than 30 breaths per minute, pulse greater than 120 beats per minute, use of accessory muscles, drowsiness, diminished breath sounds, and hypoxia should receive treatment in the emergency department.[48] COVID-19 Patients at high risk of developing severe disease from SARS-CoV-2 should receive therapy with nirmatrelvir-ritonavir within 5 days of symptom onset to reduce the risk of mortality and hospitalization. Remdesivir is an alternative if nirmatrelvir-ritonavir is not available, but it requires 3 intravenous infusions over 3 days. Though its efficacy is unclear, molnupiravir is an additional option reserved for patients at the highest risk of developing severe disease when both nirmatrelvir-ritonavir and remdesivir are unavailable. Heart failure

Patients at high risk of developing severe disease from SARS-CoV-2 should receive therapy with nirmatrelvir-ritonavir within 5 days of symptom onset to reduce the risk of mortality and hospitalization. Remdesivir is an alternative if nirmatrelvir-ritonavir is not available, but it requires 3 intravenous infusions over 3 days. Though its efficacy is unclear, molnupiravir is an additional option reserved for patients at the highest risk of developing severe disease when both nirmatrelvir-ritonavir and remdesivir are unavailable. Heart failure Supplemental oxygen, noninvasive ventilation when indicated, loop diuretics, and sodium restriction for volume overload are the cornerstones of the treatment of acute decompensated heart failure. Vasodilators such as nitroprusside lower systemic vascular resistance and left ventricular afterload in patients with severe hypertension, acute mitral regurgitation, or acute aortic regurgitation. Nitroglycerine lowers venous tone to relieve respiratory distress when the diuretic response is inadequate. Intravenous inotropes such as dobutamine or milrinone may be necessary in patients with severe systolic dysfunction and end-organ hypoperfusion; however, the use of inotropes in the setting of acute decompensated heart failure with preserved ejection fraction is not appropriate. Additionally, inotropes can worsen left ventricular outflow tract obstruction (LVOT) in patients with hypotension. Appropriate treatment for hypotension in patients with LVOT includes β-blockers and careful fluid resuscitation in patients without significant pulmonary congestion. Patients with severe hypotension and LVOT may need vasopressor therapy with phenylephrine.[49] Pulmonary embolism Hemodynamic status and bleeding risk guide treatment of a pulmonary embolism. High-risk patients with low bleeding risk receive systemic thrombolysis followed by anticoagulation. High-risk individuals with a high bleeding risk undergo catheter-directed therapy or surgical embolectomy. Most low- to intermediate-risk patients receive anticoagulation alone, though select deteriorating patients may benefit from catheter-based reperfusion. Subacute and Chronic Cough

Hemodynamic status and bleeding risk guide treatment of a pulmonary embolism. High-risk patients with low bleeding risk receive systemic thrombolysis followed by anticoagulation. High-risk individuals with a high bleeding risk undergo catheter-directed therapy or surgical embolectomy. Most low- to intermediate-risk patients receive anticoagulation alone, though select deteriorating patients may benefit from catheter-based reperfusion. Subacute and Chronic Cough Management of subacute and chronic cough targets the underlying cause. In children, watchful waiting for 2 to 4 weeks is appropriate, as most cases are postviral and self-limited.[50] Inhaled steroids, bronchodilators, and oral medications do not benefit postinfectious cough.[30] A short trial of bronchodilators or inhaled corticosteroids may be considered for suspected cough-variant asthma, while a 4-week trial of acid suppression is appropriate when GERD features such as recurrent regurgitation, dystonic neck posturing in infants, or heartburn in older children or adults are present. Tuberculosis requires standard multidrug therapy.[51] Clinicians should discontinue ACEIs and other cough-inducing medications when possible and strongly encourage smoking cessation. Asthma and COPD therapy should be optimized if present. Intranasal glucocorticoids are the mainstay of therapy for upper airway cough syndrome with antihistamines, ipratropium, or azelastine as adjuncts. Lack of improvement after 2 to 3 weeks makes this diagnosis unlikely. However, in the presence of nasal symptoms, a computed tomography scan of the paranasal sinuses is recommended to evaluate for structural abnormalities. Patients with chronic rhinosinusitis should combine saline irrigation with intranasal glucocorticoids and expect slow improvement over a few months. According to the International Consensus on Allergy and Rhinology-Rhinosinusitis, patients without polyposis who do not achieve adequate relief may undergo a trial of antibiotics or systemic steroids. However, studies supporting these recommendations are sparse. Those with polyposis should only receive antibiotics in the presence of an overlying acute infection. Patients who do not improve may require sinus surgery. Please see StatPearls' companion topic, "Chronic Sinusitis," for a detailed discussion of the management of chronic rhinosinusitis.

According to the International Consensus on Allergy and Rhinology-Rhinosinusitis, patients without polyposis who do not achieve adequate relief may undergo a trial of antibiotics or systemic steroids. However, studies supporting these recommendations are sparse. Those with polyposis should only receive antibiotics in the presence of an overlying acute infection. Patients who do not improve may require sinus surgery. Please see StatPearls' companion topic, "Chronic Sinusitis," for a detailed discussion of the management of chronic rhinosinusitis. Clinicians manage GERD with proton pump inhibitors and lifestyle modifications and should pursue further diagnostic testing when symptoms remain refractory.[52] Clinicians treat nonasthmatic eosinophilic bronchitis with inhaled corticosteroids. Depending on associated features, clinicians may treat chronic neurogenic cough with neuromodulators such as tramadol, amitriptyline, gabapentin, pregabalin, or baclofen.[14][15][53][54][55] Other Interventions The American College of Chest Physicians recommends a trial of gabapentin for refractory chronic cough, with a weak (grade 2C) recommendation, starting at 300 mg/d and titrating to 1800 mg/d as tolerated, with careful discussion of side effects.[56] Guidance supporting these recommendations is based on limited randomized trial data showing improvements in cough-related quality of life and reductions in cough severity and frequency. Common adverse effects are dizziness and fatigue. European Respiratory Society guidelines recommend a trial of low-dose morphine, 5 to 10 mg twice daily, in adult patients with chronic refractory cough.[57] Alternatively, the American College of Chest Physicians does not recommend morphine for unexplained chronic cough due to limited consensus and concerns about adverse effects and misuse. However, it acknowledges a role for low-dose morphine in interstitial lung disease–associated cough, where the impact on quality of life is severe, and treatment is palliative. Multimodal speech pathology therapy is beneficial for refractory cough associated with unexplained and interstitial lung disease, improving cough frequency and quality of life; combining speech therapy with pregabalin may provide additional benefit.

European Respiratory Society guidelines recommend a trial of low-dose morphine, 5 to 10 mg twice daily, in adult patients with chronic refractory cough.[57] Alternatively, the American College of Chest Physicians does not recommend morphine for unexplained chronic cough due to limited consensus and concerns about adverse effects and misuse. However, it acknowledges a role for low-dose morphine in interstitial lung disease–associated cough, where the impact on quality of life is severe, and treatment is palliative. Multimodal speech pathology therapy is beneficial for refractory cough associated with unexplained and interstitial lung disease, improving cough frequency and quality of life; combining speech therapy with pregabalin may provide additional benefit. Recent meta-analyses suggest gabapentin has the highest probability of improving cough-related quality of life, followed by pregabalin and morphine, though morphine may reduce cough severity more strongly. Amitriptyline is an additional option. Safety considerations are important, particularly the increased risk of severe COPD exacerbations with gabapentinoids. Emerging P2X3 receptor antagonists, such as gefapixant, show promise but are not yet Food and Drug Administration-approved and have notable adverse effects, such as dysgeusia.[58] Overall, treatment remains symptomatic, involves shared decision-making, and requires regular reassessment. Superior laryngeal nerve block may also be beneficial; however, additional randomized controlled trials are necessary to determine its efficacy. Palliative Management of Cough As in the general population, clinicians should address disease-directed causes of cough in the palliative care setting, such as GERD, COPD exacerbations, acute infections, and angiotensin-converting enzyme inhibitor–induced cough, when appropriate and consistent with the patient’s goals of care. Targeting these underlying etiologies can reduce symptom burden and improve quality of life. For mild cough, clinicians may consider nonpharmacologic measures, including honey, breathing techniques, and cough-suppression exercises.

As in the general population, clinicians should address disease-directed causes of cough in the palliative care setting, such as GERD, COPD exacerbations, acute infections, and angiotensin-converting enzyme inhibitor–induced cough, when appropriate and consistent with the patient’s goals of care. Targeting these underlying etiologies can reduce symptom burden and improve quality of life. For mild cough, clinicians may consider nonpharmacologic measures, including honey, breathing techniques, and cough-suppression exercises. Pharmacologic therapy may begin with benzonatate at a dose of 100 to 200 mg 3 times daily. In patients with moderate to severe cough or inadequate response to initial therapy, morphine 5 mg every 4 hours is an effective alternative. For patients already receiving opioids for other indications, clinicians may increase the baseline opioid dose by approximately 25% to manage cough. Gabapentin or pregabalin are potential alternative or adjunctive therapies with appropriate caution.[47] For patients with thick respiratory secretions, guaifenesin, nebulized saline, or acetylcysteine may be beneficial. Glycopyrrolate is an effective option for managing excessive secretions.

Acute The following are common differential diagnoses for patients presenting with an acute cough: Acute bronchitis Acute exacerbations of COPD or asthma ARS Acute viral upper respiratory infection Allergic rhinitis Aspiration syndromes Bronchiolitis Cerebrospinal fluid leak Chemical or inhalation injury Congestive heart failure Croup Pertussis Pneumothorax Pneumonia Pulmonary embolism Subacute The following are common differential diagnoses for patients presenting with a subacute cough: Bronchiectasis Chlamydophila pneumoniae Mycoplasma pneumoniae Pertussis Post-infectious cough Tuberculosis Chronic The following are common differential diagnoses for patients presenting with a chronic cough: Asthma Chronic aspiration Chronic bronchitis Chronic rhinosinusitis COPD GERD Interstitial lung diseases Malignancy Medication effects Neurogenic cough Nonasthmatic eosinophilic bronchitis Obstructive sleep apnea Somatic cough syndrome Upper airway cough syndrome The following are additional but less common potential causes of cough: Amyloidosis Cerumen impaction causes stimulation of the auricular branch of the vagus nerve or Arnold nerve Esophageal achalasia Tracheoesophageal fistula Esophageal-tracheobronchial reflex Holmes-Adie syndrome (anisocoria, abnormal deep tendon reflexes, and patchy areas of hyperhidrosis or anhidrosis, along with chronic cough) Inflammatory bowel disease Ortner syndrome or compression of the left recurrent laryngeal nerve caused by enlarged vascular structures, such as an enlarged left atrium due to mitral stenosis Paradoxical vocal fold motion Pediatric autoimmune neuropsychiatric disorder associated with group A streptococci, causing motor tics Peritoneal dialysis due to GERD, pulmonary edema, or pleuroperitoneal communication Pneumonitis Premature ventricular contractions Relapsing polychondritis Sarcoidosis Syngamus laryngeus infection Tracheobronchial collapse Sensory neuropathy due to B12 deficiency Zenker or distal esophageal diverticulum

Complications related to cough depend on the underlying etiology and severity. Common potential complications include the following: Arterial hypotension Bladder prolapse Bradyarrhythmias and tachyarrhythmias Cerebral air embolism Cerebrospinal fluid rhinorrhea Cervical radiculopathy Death Decreased work productivity Excessive sweating Headache Hernia Impaired sleep quality and daytime sleepiness Laryngeal and tracheobronchial trauma Respiratory failure Rupture of subconjunctival, nasal, and anal veins Seizure Severe anxiety or depression Splenic rupture Stroke due to vertebral artery dissection Syncope Rib fracture Urinary incontinence Vomiting Increased frequency of emergency department visits and hospitalizations [5][9][10]

Cough is a common protective reflex that helps clear the airways of irritants, secretions, and foreign material. However, when persistent, it can significantly impair quality of life and necessitate testing and treatment. Healthcare professionals play a key role in helping patients understand that most acute coughs are self-limited and benign and do not require antibiotics. Clear counseling on the expected duration of cough, often lasting several weeks after the initial illness resolves, can reduce anxiety, inappropriate antibiotic use, and repeat healthcare visits. Clinicians should educate patients on red-flag symptoms, such as hemoptysis, unexplained weight loss, persistent fever, dyspnea, chest pain, or cough lasting longer than 8 weeks, that warrant prompt medical evaluation. Education should emphasize avoidance of known cough triggers, including tobacco smoke, vaping, environmental irritants, and unnecessary exposure to allergens. Medication-related cough, particularly with ACEIs, should be discussed to help patients understand the importance of reporting new or persistent symptoms rather than self-medicating. For chronic cough, patients benefit from understanding that evaluation is typically stepwise and diagnosis-driven, focusing first on common causes such as upper airway cough syndrome, asthma, GERD, and medication effects before pursuing extensive imaging or invasive testing. Reinforcing adherence to prescribed therapies, lifestyle modifications, and follow-up plans helps prevent symptom persistence and frustration. Shared decision-making, including discussion of risks, benefits, and realistic expectations for treatment, supports appropriate care utilization and empowers patients to actively participate in managing their cough.

Cough is a common, often protective respiratory reflex that helps clear the airways of mucus, irritants, and foreign material. However, it can also be a manifestation of a wide range of underlying conditions, from self-limited viral infections to serious cardiopulmonary or systemic diseases. Categorizing cough by duration as acute, subacute, or chronic helps guide diagnostic evaluation and management. While most acute coughs are benign and resolve without intervention, a persistent or progressive cough can significantly impair quality of life. Cough may signal conditions such as asthma, upper airway cough syndrome, GERD, infection, medication-related adverse effects, or malignancy. Effective management, therefore, requires careful history-taking, identification of red-flag symptoms, and a stepwise, evidence-based approach to avoid unnecessary testing and inappropriate antibiotic use. Coordinated, interprofessional collaboration that emphasizes patient-centered strategies, safety, and efficiency enhances and optimizes care for patients with cough. Physicians and advanced practitioners play a central role in diagnostic assessment, risk stratification, and formulation of management plans. Nurses contribute through symptom monitoring, patient education, reinforcement of treatment adherence, and recognition of red-flag symptoms. Pharmacists improve outcomes by identifying medication-related causes of cough, optimizing pharmacotherapy, counseling on proper medication use, and preventing drug interactions or adverse effects. Other healthcare professionals, including respiratory therapists, speech-language pathologists, and specialists, provide specialized interventions, such as inhaler technique training, cough-suppression therapy, and evaluation of refractory or complex cases. Clear communication among team members and with patients ensures consistent messaging, timely escalation of care when needed, and alignment of treatment goals, ultimately improving patient satisfaction, reducing unnecessary interventions, and enhancing overall team performance in the management of cough.