Diagnosis And Treatment Of Cough

B. pertussis should be considered as a possible cause of postinfectious cough, especially if B. pertussis infections have been recently reported in the community, the patient has a history of contact with a known case, the cough has followed a biphasic course (mild and nonproductive at first, then violently spasmodic), or the patient presents with the characteristic "whoop" or with a cough-vomit syndrome. Classically, B. pertussis infection has a 1- to 3-week incubation period; a catarrhal phase of conjunctivitis, rhinorrhea, fever, malaise, and cough; and then a paroxysmal phase, during which the cough worsens. Cough from pertussis usually lasts 4 to 6 weeks. The laboratory confirmation of B. pertussis in a clinical setting can be difficult to establish because there is usually a delay between the onset of cough and the suspicion of the disease and because there is no readily available, reliable serologic test for B. pertussis. Cultures of nasopharyngeal secretions are usually negative beyond 2 weeks of infection, and confirmatory serologic testing requires paired acute and convalescent sera samples. Polymerase chain reaction tests for B. pertussis have not yet been standardized. With postinfectious subacute cough from presumed or confirmed pertussis, antibiotic treatment may be helpful if prescribed within the first few weeks.

Cough is a well-known side effect of ACE inhibitors. The pathogenesis may be related to bradykinin sensitization of afferent sensory nerves in the airways. Stimulation of cough appears to be a class effect of these drugs and is not dose related. In patients who experience a cough with one ACE inhibitor, cough usually develops when another ACE inhibitor is substituted. Although the reported frequency of cough associated with ACE inhibitors has varied widely, from 0.2% to 33%, prospective studies have shown that ACE inhibitors account for 2% of chronic cough. Cough has been reported to appear within a few hours of taking a first dose in many patients, but it may not become apparent for weeks, months, or even longer. In a prospective study of lisinopril rechallenge in patients who had previously experienced an ACE inhibitorâ??induced cough, the median time for cough to redevelop was 19 days, and the median time to resolution during placebo washout was 26 days. ACE inhibitor induced cough is diagnosed by stopping the drug and observing resolution of the cough.

UACS is defined as cough caused by mechanical stimulation of the cough reflex by secretions emanating from the nose or sinuses and, possibly, by increased sensitivity of the cough reflex because of physical and mechanical irritation by secretions. Why cough develops in only a minority of patients with rhinosinus disease is not known. Typically, patients with UACS describe the sensation of fluid dripping down into their throats, nasal discharge, or the need to frequently clear their throatsâ??other persons in the patient's vicinity may also notice frequent throat clearing by the patientâ??and physical examination of the nasopharynx and oropharynx reveals mucoid or mucopurulent secretions or a cobblestoned appearance of the mucosa. Unfortunately, none of these criteria, by themselves, is very sensitive or specific. Moreover, in some patients, chronic cough may be the only symptom of UACS (so-called silent UACS). Therefore, the diagnosis of UACS is often made on the basis of response to empirical therapeutic trials. Indeed, because postnasal drip and throat clearing are common complaints in the general population and in patients with chronic cough from other conditions, cough can be definitively ascribed to UACS only when it responds to specific therapy for UACS. Because it is the most common cause of chronic cough in adults in the United States, UACS should be the first diagnosis considered when the patient is a nonsmoker, is not taking an ACE inhibitor, and has a normal or near normal chest radiograph. Empirical therapy for UACS should begin with a trial of a first-generation antihistamine-decongestant unless contraindicated (e.g., because of benign prostatic hypertrophy, hypertension, or glaucoma). Intranasal ipratropium bromide may also be effective; the nonsedating antihistamines are not effective, however, unless the patient has allergic rhinitis or some other histamine-mediated disease process. If the patient experiences resolution or partial resolution of cough in response to treatment, then UACS is considered to have been the cause, or a contributing cause, of cough and the antihistamine-decongestant is continued. Noticeable improvement should occur within a few days. If the response to empirical therapy is only partial and the patient continues to have nasal symptoms suggestive of rhinosinus disease, then the addition of a topical nasal steroid, nasal anticholinergic, or nasal antihistamine should be considered. Persistent UACS symptoms despite topical therapy are an indication for sinus imaging, to look for evidence of occult sinusitis.

GERD should be suspected as the cause of chronic cough whenever a patient complains of frequent episodes of typical gastrointestinal symptoms such as daily heartburn and regurgitation, especially when the chest radiograph or clinical picture suggests an aspiration syndrome. Chronic cough may be the only symptom of GERD; in prospective studies, such so-called silent GERD has accounted for 43% to 75% of cases. In the absence of gastrointestinal symptoms, chronic cough can be confidently attributed to GERD if the patient is a nonsmoker, is not taking an ACE inhibitor, has a normal or near-normal chest radiograph, and asthma, UACS, and nonasthmatic eosinophilic bronchitis have been ruled out; 92% of patients with silent GERD fit this clinical profile. Failure to obtain a history of nocturnal coughing does not exclude GERD as a cause of cough. When the chest radiograph is normal, cough from GERD most commonly occurs while the patient is awake and upright, and it usually does not occur or is not noted at all during sleep. Confirmation of GERD as the cause of cough requires that the cough disappear when the patient starts antireflux therapy. Nevertheless, if treatment with proton pump inhibitors fails to eliminate cough in a patient who fits the clinical profile for GERD-induced chronic cough, GERD may nevertheless be causing the cough, albeit through a nonacid mechanism. The precise mechanism by which GERD causes cough is not known. Although GERD can stimulate cough by irritating the upper respiratory tract without aspiration (e.g., larynx/hypopharynx) or by irritating the lower respiratory tract with aspiration, GERD appears to most commonly cause chronic cough by stimulating an esophageal-bronchial reflex in the mucosa of the distal esophagus.