Upper airway cough syndrome secondary to nasal and nasal real disease is an important cause of chronic cough, with a prevalence of 22.0% – 57.6% of chronic coughs.
I. Shift in the definition of UAcS and PNDS
Postnasal drip syndrome (PNDs) refers to a syndrome in which nasal disease causes secretions to flow backwards into the postnasal and pharyngeal regions or even into the vocal cords or trachea, causing cough as the main manifestation. (2) there are no objective criteria for PNDs and no quantitative indicators for secretions, making it difficult for physicians to make a diagnosis. In 2006, the American College of Chest Physicians (ACCP) guidelines recommended renaming it uAcs and defining it as a syndrome caused by nasal and sinus pathology with or without PNDS and coughing for more than 8 weeks, which is the most common group of diseases causing chronic cough. For the diagnosis of chronic cough, both uAcs and PNDs have limitations, as the underlying otorhinolaryngological diseases causing chronic cough are not only nasal and sinus diseases, but also pharyngeal diseases. In patients with chronic cough of unknown etiology and failed experimental treatment, a comprehensive evaluation of the nose, pharynx, larynx, and even esophagus should be performed.
II. Mechanisms and etiology of cough in UACS
The respiratory tract starts in the nasal cavity and ends in the alveoli. Cough receptors are widely distributed in the submucosa, as well as in the esophagus and even in the external auditory canal and tympanic membrane, among which the cough receptors in the larynx and trachea are the most sensitive. The nerves involved in the cough reflex are mainly the vagus nerve, the glossopharyngeal nerve, the lingual nerve, and the trigeminal nerve, which is widely distributed in the nasal cavity.
1. Pathological mechanisms of uAcs-induced cough.
The pathological mechanism of uAcs-induced cough is not yet clear. The possible mechanism is that nasal diseases lead to extensive inflammatory responses in the respiratory mucosa and stimulation of cough receptors. In normal adults, the nasal cavity secretes more than 1000 ml of fluid every 24 hours, which flows in different forms to the pharynx and is not perceived as a backflow of fluid. When nasal diseases cause a J”-wide inflammatory response of the respiratory mucosa.
(1) mucosal damage leads to exposure of subepithelial cough receptors, and minor stimuli i.e. town provocation receptors cause coughing.
(2) Persistent inflammation, which results in lower than normal subepithelial stimulus sensory excitation thresholds in the airway and a more sensitive than normal cough reflex.
(3) Inflammatory response of cough receptors increases the sensitivity of nerve endings to various physical and chemical stimuli.
(4) Inflammation causes spasm of tracheal smooth muscle and contraction of small airways further stimulates terminal cough receptors, causing cough reflexes.
(5) Sensory nerve endings of the nasal cavity and nasal lining are rich in neuropeptides and neurotransmitters, and the neurogenic inflammatory response leads to hyperreactivity of the upper and lower airway mucosa.
(6) Inflammatory mediators, cytokines and granular proteins produced by eosinophils enter the lower airways via the blood circulation plus the mucosal inflammation of Sensei. The post-secretory flow directly stimulates the submucosal cough receptors in the larynx, epiglottis, and vocal cords to cause coughing; stimulation of the trigeminal nerve and vagus nerve distributed in the nose and sinuses causes coughing through the nasal-pulmonary reflex and the nasal-cardiopulmonary reflex.
2. Common causes of UACS: There is a wide variety of underlying otorhinolaryngological causes of cough. Common nasal diseases include.
(1) Inflammatory diseases of the nose.
Allergic rhinitis, rhinosinusitis, non-allergic rhinitis (common cold, vasomotor, physicochemical irritation, drug, occupational, pregnancy, etc.).
(2) Rhinitis due to abnormal anatomical flashbulbs or obstructive factors.
(1) Adenoid hypertrophy, nasal neoplasia, poor nasal structure, etc.
(3) Nasal polyposis.
This disease is associated with severe airway inflammation and is most common in children and Caucasians. Causes include aspirin intolerance, bronchial asthma, cystic fibrosis, ciliary dyskinesia syndrome, immunodeficiency, and wegener’s granulomatosis. The most common nasal disorders causing uAcs in children are chronic rhinitis, sinusitis, and allergic rhinitis.
Other diseases of the otorhinolaryngology-head and neck that cause slow-onset cough are.
(1) Foreign bodies, cerumen, and shed hairs in the external auditory canal, which can stimulate the vagus nerve auricular branch in the posterior wall of the external auditory canal causing a cough reflex.
(2) Allergic or non-allergic pharyngitis, laryngitis, epiglottitis, new bullous matter in the pharynx.
(3) Foreign bodies in the pharynx and tracheoesophagus.
(4) irritation of the recurrent laryngeal nerve by thyroid disease causing intractable cough.
(5) Cerebrospinal fluid aural-nasal leakage.
(6) Reflux pharyngolaryngology due to gastroesophageal reflux, which, unlike GERD, generally has no symptoms such as retrosternal burning sensation and acid reflux and is easily overlooked by clinicians.
(7) 0sAHs triggers chronic cough town can be associated with the direct inhalation of unfiltered and humidified air from the nasal cavity into the throat and trachea, triggering pharyngitis and bronchitis. Reflux is the main etiology of chronic cough symptoms in patients with OSAHs.
III. Main clinical manifestations and diagnosis of uAcs
The main clinical manifestations of uAcs are chronic cough and sputum, often accompanied by sneezing, nasal itching, increased nasal secretion and nasal congestion, etc. There may be postnasal drip flu, facial pain and olfactory disturbance. It is often accompanied by the following signs: throat clearing action, pharyngeal mucosal congestion, lymphoid follicular hyperplasia (may have a cobblestone-like appearance), and adhesion of mucous secretions to the posterior pharyngeal wall. The above clinical symptoms and signs are not specific, and further examination is needed to confirm the diagnosis of the underlying disease.
1. Allergic rhinitis.
Adequately refers to a disease in which a series of nasal symptoms are triggered by an IgE-mediated inflammatory response after the nasal mucosa is exposed to allergens. Clinical manifestations: episodes of nasal itching, sneezing, watery snot, nasal congestion, itchy eyes and olfactory disturbance. Main signs: pale edema of nasal mucosa, watery mucus. Laboratory asphyxiation: positive ex vivo allergen test (sPlr), increased eosinophilia on nasal secretion smear, and possible increase in blood IgE. Diagnosis: The clinical manifestations and family history of allergic rhinitis help to make the diagnosis.
2. Non-allergic rhinitis.
A wide range of etiologies. Clinical manifestations: mainly nasal congestion, may be accompanied by increased nasal secretions, nasal itching, olfactory disorders, etc. Signs: nasal mucosa congestion, turbinate hypertrophy, viscous and/or mucopurulent secretions. Experimental scuttle tests are mostly nonspecific. The symptoms of vasodilatory rhinitis often change with the temperature and are characterized by transient production of large amounts of thin, watery nasal discharge and marked mucosal congestion. Non-allergic eosinophilic rhinitis is not rare clinically, and is characterized by severe nasal allergic symptoms, highly edematous and pale nasal mucosa, abnormally increased eosinophils in nasal secretion smears and blood, negative allergen gun tests, and low blood IgE. The diagnosis should be made by carefully exploring the medical history.
3. Sinusitis.
Inflammatory disease of the mucosa of the nasal cavity and sinuses. Clinical manifestations: runny nose, nasal congestion, olfactory disturbance, a few patients may have dizziness, pain, nasal – halitosis, memory loss, inattention. Signs: nasal mucosa is filled with JIIL edema, turbinate hypertrophy, and purulent secretions are seen in the nasal passages. The mucous membrane of the pharynx is allowed to bleed, and purulent secretions are seen to flow down the posterior pharyngeal Zhao. Diagnosis: nasal endoscopy or imaging examination is required.
4, abnormal anatomical Gonzo or obstructive factors caused by rhinitis, nasal a sinusitis.
Through the nasal cavity, sinus cT, nasal endoscopy elm to help confirm the diagnosis. Other otorhinolaryngological diseases causing cough: Allergic pharyngitis is mainly characterized by itchy pharynx, paroxysmal irritant cough, pale or edematous pharyngeal mucosa, and is often accompanied by a history of allergic rhinitis or bronchial asthma. Non-allergic pharyngitis is often characterized by sore throat, foreign body sensation in the pharynx, congestion of the pharyngeal mucosa and lymphatic follicular hyperplasia. Inflammation and neoplasia of the larynx are often associated with hoarseness. Esophageal neoplasia is often associated with dysphagia. The above diseases need to be further diagnosed by dynamic laryngoscopy, fiberoptic laryngoscopy, tracheoesophagoscopy, imaging, etc. There is no uniform standard for the diagnosis of LPRD, and dual-probe 24-h esophageal pH monitoring with laryngopharyngeal reflux events (pH <4) more than 3 times can help to confirm the diagnosis.
IV. Treatment of UACS
The idea of uAcs treatment is to stop cough, anti-inflammatory, control clinical symptoms and treat the underlying disease. Since uAcs is the most common cause of chronic cough, chronic cough of more than 8 weeks, after the failure of formal treatment against cough, should be considered firstly for the machinability of uAcs, which can be diagnosed and treated in the order of uAcs, cough variant asthma (CVA) and GERD.
1.Treatment for uACS.
(1) Cough suppressant: central cough suppressants such as dextromethorphan or machinegan can be used. The 1st generation antihistamines are effective in reducing cough, which may be related to their central cough suppressant effect and direct peripheral modulation of histamine levels.
(2) Anti-inflammatory: nasal spray glucocorticoids, sodium cromoglycate and antihistamines can be used. Several doses of leucovorin and antihistamines are often effective in cough due to allergic rhinitis.
(3) Control of clinical symptoms: The use of 1st generation antihistamines (representative drug is chlorpheniramine urethane) and oral decongestants (pseudoephedrine hydrochloride) can rapidly improve symptoms such as nasal congestion, runny nose, and postnasal drip. Most patients produce efficacy within a few days to 2 weeks after initial treatment.
2.Treatment for underlying diseases.
(1) Allergic rhinitis.
Various antihistamines are effective. 2nd generation or new generation antihistamines without sedative effect are recommended. Intermittent allergic rhinitis can be treated with systemic or local antihistamines alone, and the symptoms will disappear completely. In persistent allergic rhinitis, nasal glucocorticoids are the first-line drugs and are recommended to be used for a longer period of time, along with systemic or topical antihistamines (for a longer period of time) and nasal decongestants (for no more than lO d). Patients with unsatisfactory improvement of nasal congestion after anti-inflammatory therapy, with chronic cough and bronchial asthma may be treated with additional antileukodystrophy antagonists (for a period of not less than 3 months). Specific immunotherapy can be effective in town, but it takes a long time to take effect, and anti-inflammatory treatment should not be discontinued until a stable effect is achieved.
(2) Non-allergic rhinitis.
For common cold, the first generation of antihistamine combined with decongestant is preferred (many commonly used cold tablets have this IlIi ingredient). Perennial non-allergic rhinitis focuses on the treatment of the underlying disease and recommends nasal use of nasal glucocorticoids for not less than 3 months, which can be combined with antihistamines. For: vasomotor rhinitis where the aforementioned treatment is not effective, nasal inhalation of ipratropium bromide may be used.
(3) Rhino-sinusitis.
Antibiotic therapy, less than 2 weeks in the acute phase of the small, chronic phase is recommended for 4 – 12 weeks, it is advisable to choose antibiotics with an antibacterial spectrum covering gram-positive, negative and anaerobic bacteria. Some findings suggest that low-dose (1/2 of the most routinely recommended) long-term (no less than 12 weeks) therapy with macrolide antibiotics can reduce inflammation and improve symptoms¨. Nasal glucocorticoids are routinely used for not less than 3 months. A combination of decongestants (no more than l0d), cilia promoters, and saline rinses of the nasal cavity can be used. If medical treatment is not effective, surgical intervention is recommended as appropriate. For the treatment of other underlying diseases, it is advisable to develop a reasonable treatment plan in cooperation with doctors of relevant disciplines.