Diagnosis and treatment of chronic cough
Cough is one of the most common clinical symptoms. Coughing is a reflexive defensive action that allows the removal of respiratory secretions and foreign bodies from the airways. However, coughing also has a negative side, for example, it can spread infections in the respiratory tract, cause respiratory bleeding due to severe coughing, and even induce spontaneous pneumothorax. Therefore, if frequent coughing interferes with work and rest, it is a pathological condition. According to its course, it is classified as acute cough lasting <3 weeks, subacute cough lasting 3-8 weeks, and chronic cough (8 weeks, no obvious lesions on chest X-ray). The common causes of acute cough are the common cold and acute bronchitis, which are diagnosed relatively easily and treated symptomatically with anti-cough and anti-infection.
Common causes of chronic cough include CVA, UACS [also known as postnasal drip syndrome (PNDS)], EB and GERC, which account for 70% to 95% of the causes of chronic cough in respiratory medicine outpatient clinics. Other etiologies are less common but are widely involved and are associated not only with respiratory diseases but also with diseases of other systems. Most chronic coughs are not associated with infections and do not require treatment with antibacterial drugs. Oral or intravenous glucocorticoids should be used with caution when the cause of cough is unknown or when infection cannot be excluded.
(i) UACS/PNDS
1. Definition: A syndrome in which nasal disease causes secretions to flow backwards behind the nose and throat, directly or indirectly stimulating cough receptors, resulting in a cough as the main manifestation is called PNDS. Since the cause of upper respiratory cough receptors cannot be identified, the 2006 US cough guidelines recommend replacing PNDS with UACS.
UACS is one of the most common causes of chronic cough. In addition to nasal diseases, UACS is often associated with diseases of the pharynx, such as allergic or non-allergic pharyngitis, laryngitis, pharyngeal neoplasia, and chronic tonsillitis.
2. Clinical manifestations: (1) Symptoms: In addition to cough and sputum, it may manifest as nasal congestion, increased nasal secretion, frequent throat clearing, posterior pharyngeal mucus attachment, and postnasal drip influenza. Allergic rhinitis manifests as nasal itching, sneezing, running snot, and itchy eyes. Rhino-sinusitis manifests as mucopurulent or purulent snot, and may be associated with pain (facial pain, toothache, headache) and olfactory disturbance. Allergic pharyngitis is characterized by pharyngeal itching and paroxysmal irritating cough. Non-allergic pharyngitis is often characterized by sore throat, foreign body sensation or burning sensation in the pharynx. Inflammation of the larynx and neoplastic organisms are usually accompanied by hoarseness. (2) Signs: The nasal mucosa of allergic rhinitis mainly shows pallor or edema, and clear or mucous snot can be seen in the nasal passages and the floor of the nasal cavity. In non-allergic rhinitis, the nasal mucosa is mostly characterized by mucosal hypertrophy or congestion-like changes, and in some patients, the mucosa of the oropharynx can be seen to have pebble-like changes or mucopurulent secretions attached to the posterior pharyngeal wall. (3) Auxiliary examination: imaging of chronic rhinosinusitis shows thickening of the sinus mucosa and the presence of fluid planes in the sinuses. When the cough is seasonal or suggests exposure to specific allergens (e.g., pollen, dust mites), allergen testing can be helpful for diagnosis.
3. Diagnosis: UACS/PNDS involves various underlying diseases of the nose, sinuses, pharynx, and larynx, and many of the symptoms and signs vary widely and are not specific, so it is difficult to make a definitive diagnosis by history and physical examination alone.
4. Treatment: Depending on the underlying disease causing UACS/PNDS.
First-generation antihistamines and decongestants are preferred for the following etiologies: (1) non-allergic rhinitis; (2) common cold. Most patients develop efficacy within a few days to two weeks after initial treatment. Nasal inhaled glucocorticoids and oral antihistamines are the preferred treatment for patients with allergic rhinitis. Avoiding or reducing exposure to allergens can help reduce the symptoms of allergic rhinitis. Bacterial sinusitis is mostly a mixed infection and anti-infection is an important therapeutic measure. The antibacterial spectrum should cover gram-positive, negative and anaerobic bacteria for not less than 2 weeks for acute and longer for chronic recommended as appropriate. If internal treatment is not effective, it is recommended to consult a specialist and, if necessary, to undergo nasal endoscopic surgery.
(II) CVA
1. Definition: CVA is a special type of asthma in which cough is the only or main clinical manifestation, without obvious symptoms or signs such as wheezing and shortness of breath, but with airway hyperresponsiveness.
2. Clinical manifestations: The main manifestation is an irritating dry cough, usually violent, with nocturnal cough as its important feature. Cold, cold air, dust and fumes can easily induce or aggravate the cough.
3. Diagnosis: The principles of diagnosis are comprehensive consideration of clinical features, ineffectiveness of conventional anti-cold and anti-infection treatment, positive bronchial excitation test or bronchodilator test, and effective relief of cough symptoms by bronchodilator treatment.
Diagnostic criteria: (1) chronic cough, often accompanied by obvious nocturnal irritant cough; (2) positive bronchial excitation test, or day-to-day variability of peak expiratory flow rate >20%, or positive bronchodilator test; (3) effective bronchodilator treatment. 4.Treatment: The treatment principle of CVA is the same as that of bronchial asthma. Most patients can be treated with low-dose glucocorticoids combined with bronchodilators (β2-agonists or aminophylline, etc.), or with a combination of both, such as budesonide/formoterol, fluticasone/salmeterol, or, if necessary, short-term oral low-dose glucocorticoid therapy. The duration of treatment should be at least 8 weeks. The effectiveness of anti-leukotriene receptor antagonists in the treatment of CVA has been reported, but the number of cases observed is small.
(iii) EB
1. Definition: A non-asthmatic bronchitis characterized by airway eosinophil infiltration and negative airway hyperresponsiveness, mainly manifested by chronic cough, which responds well to glucocorticoid therapy.
2. Clinical manifestations: The main symptom is chronic irritant cough, which is often the only clinical symptom, dry cough or cough with a little white mucus sputum. Some patients are sensitive to fumes, dust, odors or cold air, which are often triggering factors for coughing. Patients do not have symptoms such as shortness of breath or dyspnea. Pulmonary ventilation function and peak expiratory flow rate variability (PEFR) are normal with no evidence of airway hyperresponsiveness.
3. Diagnosis: The clinical manifestations of EB are not characteristic, some of them are similar to CVA, and there are no abnormal findings on physical examination. Specific criteria are as follows: (1) Chronic cough, mostly irritating dry cough or with a small amount of mucous sputum. (2) Normal X-ray chest radiograph. (3) Normal pulmonary ventilation function, negative airway hyperresponsiveness test, and normal day-to-day variability of peak expiratory flow rate. (4) Sputum cytology with eosinophil ratio ≥2.5%. (5) Exclude other eosinophilic diseases. (6) Oral or inhaled glucocorticoids are effective.
4. Treatment: EB responds well to glucocorticosteroid treatment and the cough disappears or is significantly reduced soon after treatment. Usually inhaled glucocorticosteroids are used, such as beclomethasone dipropionate (250-500g per dose) or equivalent doses of other glucocorticosteroids, applied twice daily for more than 4 weeks. Initial treatment can be combined with prednisone orally at 10-20 mg per day for 3-5 days.
(iv) GERC
1. Definition: GERC is a clinical syndrome caused by reflux of gastric acid and other gastric contents into the esophagus, resulting in coughing as a prominent manifestation, and is a special type of gastroesophageal reflux disease and a common cause of chronic cough. The pathogenesis involves trace aspiration, esophageal-bronchial reflex, esophageal motor dysfunction, phytokinesis and neurogenic inflammation of the airway. In addition to gastric acid, a few patients are also associated with bile reflux.
2 Clinical manifestations: Typical reflux symptoms are heartburn (burning sensation behind the sternum), acid reflux, and belching. Some GERD-induced coughs are accompanied by typical reflux symptoms, but many patients have cough as the only manifestation. Most coughs occur in the daytime and in the upright position, with a dry cough or a small amount of white mucous sputum. Eating acidic and oily foods can easily trigger or aggravate the cough.
3. Diagnostic criteria: (1) Chronic cough, mainly daytime cough. (2) 24h esophageal pH monitoring Demeester score ≥12.70, and/or SAP ≥75%. (3) Significant reduction or disappearance of cough after anti-reflux treatment. However, it should be noted that a small number of patients with combined or predominantly non-acid reflux (e.g., bile reflux) may not have abnormal esophageal pH monitoring results, and such patients can be diagnosed by esophageal impedance testing or bile reflux monitoring.
For patients with chronic cough in units without esophageal pH monitoring or with limited financial resources, the following indications may be considered for diagnostic treatment. (1) The patient has a significant feeding-related cough, e.g., postprandial cough, feeding cough, etc. (2) The patient has typical reflux symptoms such as heartburn and acid reflux. (3) Diseases such as CVA, UACS and EB are excluded, or treatment for these diseases is ineffective. Take a standard dose of proton pump inhibitor (e.g. omeprazole 20 mg twice daily) for at least 8 weeks. The cough disappears or is significantly relieved after anti-reflux treatment, and GERC can be clinically diagnosed.
4. Treatment: (1) Lifestyle adjustment: Overweight patients should lose weight, avoid oversaturated bedtime meals, avoid acidic and greasy foods, avoid coffee drinks and smoking. (2) Acid control drugs: Proton pump inhibitors (such as omeprazole, lansoprazole, rabeprazole and esomeprazole, etc.) or H2 receptor antagonists (ranitidine or other similar drugs) are often used, with proton pump inhibitors having the best effect. (3) Gastric stimulants: Domperidone can be used if gastric emptying is impaired. If the effect of acid control alone is not good, the addition of gastrodynamic drugs may be effective. The duration of medical treatment should be more than 3 months, and it usually takes 2-4 weeks to show the effect. If the above treatment is not effective, consider whether the dose and duration of treatment are adequate or whether there is a compound cause. If necessary, consult the relevant specialist to study the treatment plan. In a few patients with severe reflux who have failed medical treatment, anti-reflux surgery may be effective, but the indications for surgery should be strictly controlled due to postoperative complications and recurrence.
The following is a brief description of several common organic diseases.
Bronchial asthma
II. Diagnosis
(a) Diagnostic criteria
1. Recurrent attacks of wheezing, shortness of breath, chest tightness or cough, mostly related to exposure to allergens, cold air, physical and chemical stimuli, as well as viral upper respiratory tract infections and exercise.
2. During the attack, croup may be heard in both lungs, mainly in the expiratory phase, with a prolonged expiratory phase.
3. The above symptoms and signs may be relieved by treatment or may resolve on their own.
4. Except wheezing, shortness of breath, chest tightness and cough caused by other diseases.
5. For atypical clinical manifestations (such as no obvious wheezing or signs), at least one of the following tests should be positive: (1) positive bronchial excitation test or exercise excitation test; (2) positive bronchial diastolic test with FEV1 increase ≥ 12% and absolute FEV1 increase ≥ 200 ml; (3) peak expiratory flow rate (PEF) intra-day (or 2 weeks) variability ≥ 20%.
Asthma can be diagnosed if items 1 to 4 or 4 or 5 are met.
Although asthma is not yet curable, asthma control can usually be achieved through effective asthma management. The goals of successful asthma management are to (1) achieve and maintain symptom control; (2) maintain normal activity, including exercise capacity; (3) maintain lung function levels as close to normal as possible; (4) prevent acute exacerbations of asthma; (5) avoid adverse effects due to asthma medication; and (6) prevent death due to asthma.
Establishing a partnership between the physician and patient is the primary measure to achieve effective asthma management. The goal is to guide patients to self-manage, reach consensus on treatment goals, and develop an individualized written management plan that includes self-monitoring, periodic assessment of treatment regimens and asthma control levels, and timely adjustment of therapy for control levels to achieve and maintain asthma control if symptoms and/or PEF suggest changes in asthma control levels. Among them, asthma education for patients is the most essential part.
1, education content: (1) through long-term standardized treatment can effectively control asthma; (2) avoid trigger, trigger factors methods; (3) the nature of asthma, pathogenesis; (4) long-term asthma treatment methods; (5) drug inhalation device and use; (6) self-monitoring: how to measure, record, and explain the contents of asthma diary: symptom score, application of drugs, PEF, asthma control test ( ACT) changes; (7) asthma aura, asthma attack signs and corresponding self-treatment methods, how and when to seek medical attention; (8) knowledge of asthma control drugs; (9) how to determine the level of control and choose treatment based on self-monitoring results; (10) the role of psychological factors in the development of asthma.
2. Education methods: (1) initial education: the most important basic and initiation education, individualized education at the beginning of the doctor-patient partnership, which should first provide information about the patient’s diagnosis, understand the patient’s expectations and achievable level of asthma treatment, and educate at least the contents of (1) to (6) above, schedule follow-up appointments and provide educational materials; (2) follow-up education and evaluation: a long-term management method. Follow-up visits should be conducted to answer patient questions and assess initial efficacy. Regular evaluation, correction of inhalation techniques and monitoring techniques, evaluation of written management plans, understanding the degree of implementation, and repeated provision of updated educational materials; (3) centralized education: regular asthma schools, study classes, clubs, and fellowships for large classes and centralized question and answer sessions; (4) self-study education: through reading newspapers, magazines, articles, watching TV programs, and listening to the radio; (5) internet education: through the China asthma alliance network (www, chinaasthma, net), global asthma prevention and control creation network GINA (www, ginasthma, org), or interactive multimedia technology to disseminate prevention and control information; (6) Mutual learning: hold patient experience exchange meetings on asthma prevention and control; (7) Targeted education: cooperate with community health units to carry out community, patient and public education in a planned manner (8) mobilize all levels of society to promote and popularize asthma prevention and treatment.
Chronic obstructive pulmonary disease (COPD)
COPD is a preventable and treatable disease characterized by airflow limitation, which is not completely reversible, progressive and associated with an abnormal inflammatory response of the lungs to harmful gases such as cigarette smoke or harmful particles. COPD mainly involves the lungs, but can also cause systemic (or extrapulmonary) adverse effects. Since most COPD in the country is caused by chronic bronchitis, COPD patients are often accompanied by symptoms of chronic bronchitis.
The symptoms are as follows: (1) Chronic cough: usually the first symptom. Initially, the cough is intermittent, heavier in the morning, and later in the morning and evening or throughout the day, but the cough is not significant at night. In a few cases, the cough is not accompanied by sputum. In some cases, the cough is not accompanied by sputum, but there is no coughing symptom although there is obvious airflow limitation. (2) Coughing sputum: after coughing, a small amount of mucus sputum is usually coughed up, more in some patients in the early morning; when combined with infection, the sputum volume increases, often with purulent sputum. (3) Shortness of breath or dyspnea: This is the hallmark symptom of COPD and is the main cause of anxiety in patients, which appears only during exertion in the early stage and gradually worsens to the point that shortness of breath is felt even during daily activities and even at rest. (4) Wheezing and chest tightness: These are not specific symptoms of COPD. Some patients, especially severe patients, have wheezing; tightness in the chest usually occurs after exertion and is associated with respiratory effort and capacitive contraction of intercostal muscles. (5) Systemic symptoms: During the clinical course of the disease, especially in more severe patients, systemic symptoms may occur, such as weight loss, loss of appetite, peripheral muscle atrophy and dysfunction, mental depression and/or anxiety. Coughing up bloody sputum or hemoptysis may occur in the presence of co-infection.
Most patients have the following medical history features: (1) Smoking history: Most have a long history of heavy smoking. (2) History of occupational or environmental exposure to harmful substances: such as a long history of exposure to dust, fumes, harmful particles or harmful gases. (3) Family history: COPD has a tendency to cluster in families. (4) Age of onset and season of prevalence: Most of the disease develops after middle age, and the symptoms occur in the cold season of autumn and winter, often with a history of recurrent respiratory infections and acute exacerbations. As the disease progresses, acute exacerbations become more and more frequent. (5) History of chronic pulmonary heart disease: hypoxemia and/or hypercapnia in late COPD can be complicated by chronic pulmonary heart disease and right heart failure.
Pulmonary function tests: Pulmonary function tests are objective indicators to determine airflow limitation, which are reproducible and have important significance for the diagnosis of COPD, severity evaluation, disease progression, prognosis and treatment response. Chest X-ray examination: X-ray examination is important for determining pulmonary complications and differentiating from other diseases (such as interstitial lung fibrosis, tuberculosis, etc.). CT examination of the chest: CT examination is generally not used as a routine examination. However, CT examinations are beneficial in differential diagnosis. Other laboratory tests, such as blood gas analysis, are of some significance in the diagnosis and response to treatment of COPD.
Severity grading
COPD severity assessment needs to be determined based on the patient’s symptoms, lung function abnormalities, and the presence of comorbidities (respiratory failure, heart failure), among which the decrease in FEV1, which reflects the degree of airflow limitation, has important reference significance. According to the pulmonary function there are 4 levels of COPD severity.
Pulmonary function grading of clinical severity of COPD