COUGH

     Cough is a protective reflex which serves to clear the tracheobronchial tree of irritants.  Cough may be either an acute event or a chronic condition.  Common complications of cough may include exhaustion, self consciousness, insomnia, hoarseness, musculoskeletal pain, sweating and urinary incontinence.  Cough is a common side effect with ACE inhibitors but may also be seen as a symptom of drug related pulmonary disorders in patients taking bleomycin, nitrofurantoin, amiodarone, NSAIDs, sulfonamides, methotrexate, penicillamine, gold salts, and other medications.

     An acute cough of less than three weeks duration usually signals underlying infection.  The majority of patients who have symptoms but do not appear gravely ill will have an underlying tracheobronchitis, the majority of which are viral (rhinovirus, coronavirus, parainfluenza virus, respiratory syncytial virus, adenovirus, and influenza virus in etiology and therefore do not require antibiotics for therapy.  Bordetella pertussis, Chlamydia pneumonia strain TWAR and Mycoplasma pneumonia are possible bacterial pathogens but in the majority of cases they cause a self limited infection.  However, untreated B. pertussis (the 100-day cough) infection may cause a cough that lingers for weeks to months and should be considered in the differential diagnosis of chronic cough.  If a more severe underlying infection (pneumonia) is suspected from the findings on the physical exam, then evaluation with a chest radiograph and white blood cell count with differential will help suggest the diagnosis.  Pulmonary tuberculosis (either reactivation of latent disease or acute infection) should always be considered in patients with a chronic cough and an infiltrate.  Any patient who is immunocompromised but especially patients with chronic obstructive pulmonary disease (COPD) and diabetes mellitus should be considered at risk for acute bacterial bronchitis.  Patients with AIDs should be evaluated thoroughly for bacterial infections, tuberculosis, and Pneumocystis carinii pneumonia (PCP).  Allergic rhinitis should also be considered as an etiology of acute cough especially when it occurs during high pollen counts (spring or late summer/early autumn) or when there are associated symptoms (sneezing, congestion, rhinorrhea, and ocular tearing or itching).

     A cough that persists for more than three weeks is considered chronic and warrants an investigation.  The three most common etiologies for chronic cough in nonsmoking patients include: rhinosinus disease with resultant postnasal drip or upper airway cough syndrome (sinusitis, allergic rhinitis, nonallergic rhinitis), asthma, and gastroesophageal reflux disease.  Other etiologies of chronic cough include: chronic bronchitis (COPD), chronic interstitial pulmonary disease, tuberculosis, pulmonary abscess, post infectious cough, bronchiectasis, congestive heart failure (CHF), drug induced cough, pulmonary malignancies, and psychogenic cough.  Many cases are secondary to multiple underlying etiologies.  In chronic smokers, pulmonary malignancy and COPD are more common compared to non-smoking patients.

     The initial evaluation of chronic cough should include a thorough history and physical exam along with a chest radiograph to exclude possible pulmonary or cardiac causes of cough.  If the radiograph does reveal pathology (cardiomegaly, pulmonary infiltrates or masses), then the cough is most likely a symptom of this underlying illness and the work up should proceed accordingly.  However, if the radiograph is normal, then the next step should include discontinuation of medications which have the potential to induce cough, particularly ACE inhibitors.  If the cough persists one month after discontinuing the medication, then the cough is most likely not drug induced and the medication may be reintroduced if deemed necessary.  Also, if the patient is a smoker, they should be counseled to abstain from tobacco to see if the cough is secondary to their tobacco abuse.  If the patient has signs or symptoms of an underlying etiology for their cough (asthma, GERD, etc) then specific therapy for the suspected etiology should be administered and the response of the patient’s cough should be noted.  Postinfectious cough (lingering cough preceded by an upper respiratory tract illness) may respond to a brief course of an oral corticosteroid.

     Since postnasal drip syndrome/upper airway cough syndrome, which may be symptomatic or asymptomatic, is the most common cause of cough, an empiric trial of therapy should be the next step in patients with a chronic cough with no identifiable etiology.  A first generation antihistamine-decongestant compound such as chlorpheniramine/pseudoephedrine combinations should be used instead of the newer nonsedating second generation antihistamines.  The reason for this is that the PND may not be allergy induced, and in this case, the first gerneration medications will still be effective at alleviating the symptoms of PND whereas the second generation agents will not.  The efficacy of the first generation agents is believed to be secondary to their anticholinergic properties.  If patients cannot tolerate the first generation agents secondary to sedation then a trial with a second generation agent may be initiated; however, if the PND and cough are not allergy induced, they will persist.  If PND is suspected to be secondary to sinus infection, an empiric trial of therapy should be employed.  Coronal sinus CT scanning or referral to an ENT specialist may be necessary to establish the diagnosis in refractory cases.

     If the above therapy proves ineffective, then a trial of empiric therapy for asthma or pre and post bronchodilator pulmonary function testing may reveal the etiology to be asthma induced.  A methacholine or histamine challenge may also be used to establish the diagnosis of asthma if spirometry testing is equivocal or if it is felt to be consistent with a false-negative result.  Therapy for asthma induced cough is the same as general asthma therapy.  If an inciting allergen can be identified, prophylactic therapy with antihistamines, nedrocromil or cromolyn sodium may be effective if used prior to allergen contact.

     The diagnosis of GERD should be considered once PND and asthma have been eliminated with complete confidence, the patient is a nonsmoker, the chest radiograph is normal and ACE inhibitor therapy has been discontinued.  Twenty-four hour ambulatory pH monitoring, esophagogastricduodenoscopy or the Bernstein test may help to establish the diagnosis; however, an empiric trial of anti-reflux therapy (proton pump inhibitor or H₂ receptor antagonist) may be tried initially if there are no associated warning symptoms (weight loss, melena, or anemia).  Empiric therapy can only be used to confirm the diagnosis.  If cough persists despite anti-reflux therapy, further diagnostic studies are required before the diagnosis is eliminated.

     Chronic cough that persists after the above evaluation should be subjected to more definitive studies.  Further testing should include high resolution CT scanning, bronchoscopy, an echocardiogram, and even biopsy.  Persistent chronic cough with no identifiable etiology may be treated with nebulized lidocaine (3mL of 4% topical lidocaine in 1mL of normal saline) one to four times per day for as long as the cough persists.