Melvin R. Pratter

Diagnosis and management of cough executive summary: ACCP evidence-based clinical practice guidelines

Recognition of the importance of cough in clinical medicine was the impetus for the original evidence-based consensus panel report on “Managing Cough as a Defense Mechanism and as a Symptom,” published in 1998,1 and this updated revision. Compared to the original cough consensus statement, this revision (1) more narrowly focuses the guidelines on the diagnosis and treatment of cough, the symptom, in adult and pediatric populations, and minimizes the discussion of cough as a defense mechanism; (2) improves on the rigor of the evidence-based review and describes the methodology in a separate section; (3) updates and expands, when appropriate, all previous sections; and (4) adds new sections with topics that were not previously covered. These new sections include nonasthmatic eosinophilic bronchitis (NAEB); acute bronchitis; nonbronchiectatic suppurative airway diseases; cough due to aspiration secondary to oral/pharyngeal dysphagia; environmental/occupational causes of cough; tuberculosis (TB) and other infections; cough in the dialysis patient; uncommon causes of cough; unexplained cough, previously referred to as idiopathic cough; an empiric integrative approach to the management of cough; assessing cough severity and efficacy of therapy in clinical research; potential future therapies; and future directions for research.

An Algorithmic Approach to Chronic Cough

Chronic cough is an important medical and economic problem. The prevalence of chronic cough in the United States among nonsmoking adults is reported to range from 14% to 23% [1, 2]. Not only is the symptom itself problematic, but it raises concerns about possible serious underlying disease [3]. Chronic cough is the fifth most common symptom seen by outpatient physicians [4] and is estimated to be the primary reason for 30 million physician visits annually [4]. In the United States alone, approximately

Cough and the common cold : ACCP evidence-based clinical practice guidelines

600 million per year are spent on prescription and over-the-counter antitussives [5]. Major advances in the clinical approach to chronic cough have been made during the last 15 years. In a 1977 review [6], Irwin and colleagues proposed an approach to chronic cough based on the anatomic locations of the receptors and afferent pathways involved in the cough reflex. Using such an approach, Irwin and colleagues reported in 1981 [7] and again in 1990 [8] that the cause of chronic cough could be determined 100% of the time and that subsequent cause-specific treatment was almost always successful. The postnasal drip syndrome, mainly from chronic rhinitis, was the most common cause, followed by asthma [7, 8]. These two diagnoses, alone or in combination, accounted for cough in 75% of the patients [7, 8]. Gastroesophageal reflux was the next most common cause [7, 8]. Poe and colleagues [9] also reported that the postnasal drip syndrome or asthma caused chronic cough in most of their patients. We evaluated a sequential, stepped approach to chronic cough, emphasizing initial treatment of all patients with an antihistamine-decongestant for possible postnasal drip syndrome caused by rhinitis. We also determined the value of routine bronchoprovocation challenge for predicting whether asthma was a causative factor in cough. Methods Patient Selection All patients who came to our university-based pulmonary practice with a chief complaint of chronic cough were considered for inclusion in the study. Cough was considered to be chronic if it had been present for 3 weeks or longer [7, 8]. The following were exclusion criteria: 1) immunocompromise, including known lung cancer or other active malignancy, the acquired immunodeficiency syndrome, or current treatment with corticosteroids or other immunosuppressive agents; 2) cigarette use within 12 months; 3) use of an angiotensin-converting-enzyme inhibitor within 4 weeks; and 4) contraindication to the use of an antihistamine-decongestant or to bronchoprovocation challenge, including pregnancy and an FEV1 less than 70% of predicted value. Algorithm The approach involved a standardized initial evaluation, weekly follow-up, a series of sequential diagnostic and therapeutic steps, and a predefined end point. Initial Evaluation The initial evaluation included a history; physical examination; review of previous diagnostic studies; and a questionnaire on the duration, frequency, and severity of cough, postnasal drip symptoms, dyspnea, wheeze, and symptoms of gastroesophageal reflux. Spirometry was done next, followed by a methacholine bronchoprovocation challenge using a modification of the method of Hargreave and colleagues [10]. Bronchial hyper-responsiveness was defined as a 20% decrease in the FEV1 (Pc 20) at a methacholine concentration of 8 mg/mL or more [11]. Because of its low yield in previous studies [7-9], a chest roentgenogram was not included in the initial evaluation unless there was clinical suspicion of infection or neoplasm (such as fever, weight loss, or hemoptysis). Weekly Follow-up Patients were contacted by phone each week and seen in person whenever clinically necessary. We created a standardized scale for the patient to use in rating weekly cough severity and a second scale for rating side effects of therapy. The cough severity scale ranged from 0 (cough gone) to 7 (cough markedly worse). The descriptors for the scale are shown in Figure 1. Side effects were rated as none, mild, moderate, or severe (intolerable). Figure 1. Response to 1 week of antihistamine-decongestant therapy. End Point The end point for treatment was cough resolution, defined as a patient report of complete absence of cough for 2 consecutive weeks or of diminution to the point that the patient considered the cough insignificant. Step 1 An antihistamine-decongestant preparation containing 1 mg of azatadine maleate plus 120 mg of sustained-release pseudoephedrine sulfate (Trinalin, Key Pharmaceuticals Inc.; Kenilworth, New Jersey) was prescribed to be taken twice daily as empiric therapy for possible postnasal drip syndrome caused by rhinitis (postviral, allergic, or vasomotor). If the cough did not improve at the end of 1 week of antihistamine-decongestant therapy, step 2 was begun immediately. If the cough improved after 1 week of therapy, antihistamine-decongestant alone was continued either until it resolved or until no further improvement occurred. At that point, patients with persistent symptoms of the postnasal drip syndrome (sensation of postnasal drip, throat clearing, nasal congestion, or a tickle in the back of the throat) were given nasal corticosteroids in addition to the antihistamine-decongestant. Sinus imaging was obtained before nasal corticosteroids were prescribed if chronic sinusitis was suspected or subsequently if postnasal drip persisted despite the combination of antihistamine-decongestant and nasal corticosteroid therapy. Patients with sinus roentgenograms consistent with sinusitis (sinus opacification, air-fluid levels, or mucosal thickening) were treated with twice daily oxymetazoline hydrochloride nasal spray (Afrin, Schering-Plough HealthCare Products; Memphis, Tennessee) for 3 days, nasal corticosteroids twice daily, antihistamine-decongestant twice daily, and antibiotics for as long as 6 weeks. If cough still persisted, a computed tomographic study of the sinuses was obtained. If substantial abnormalities were present, the patient was referred for an otolaryngologic evaluation and possible sinus surgery. Substitutions for Trinalin could be made at any time if severe side effects developed. For severe drowsiness, astemizole (Hismanal, Janssen Pharmaceutica, Piscataway, New Jersey), 10 mg once daily, plus pseudoephedrine, 60 mg twice daily, were substituted. For severe insomnia, jitteriness, or urinary obstruction, astemizole once daily plus nasal corticosteroids twice daily were substituted. Step 2 Patients who were still coughing after step 1 were next evaluated for asthma. Because the treatment was the same, no attempt was made to distinguish between asthma and postviral bronchial hyper-responsiveness [12]. Patients who had bronchial hyper-responsiveness on bronchoprovocation challenge were treated for 1 week with an inhaled 2-agonist, albuterol, two puffs four times a day via metered-dose inhaler. If cough persisted, prednisone therapy (1 mg/kg body weight per day [maximum, 60 mg/d]) was added to the albuterol for a week. An oral 2-agonist or theophylline was substituted for the inhaled albuterol if a patient reported marked cough in response to inhaled albuterol. Step 3 Patients who continued to have persistent cough next had chest and sinus roentgenograms if they had not already been obtained. Any abnormalities considered to be clinically significant were evaluated and treated. If no significant abnormalities were found or the patient continued to cough despite appropriate therapy, the patient was advanced to step 4. Step 4 Patients were next evaluated for gastroesophageal reflux. Patients with symptoms consistent with gastroesophageal reflux first had a 2-week trial of therapy with ranitidine, 150 mg twice daily, along with antireflux measures (no eating or drinking for at least 2 hours before going to bed or lying down, 20-cm elevation of the head of the bed using blocks, and avoidance of caffeine, alcohol, chocolate, and other foods known to exacerbate gastroesophageal reflux). Lack of a response to the 2-week trial of ranitidine led to a 24-hour esophageal pH-probe study. Patients without symptoms of gastroesophageal reflux had 24-hour esophageal pH-probe monitoring before therapy for gastroesophageal reflux was begun. pH-probe monitoring was performed and interpreted according to the criteria of Demeester and colleagues [13]. All patients whose pH-probe studies showed pathologic gastroesophageal reflux were treated for at least 8 weeks with omeprazole, 20 mg daily, in addition to antireflux measures. An upper gastrointestinal barium swallow or a gastroenterology consultation or both were obtained if the patient had any persistent gastrointestinal complaints. Step 5 Patients who continued to cough next had bronchoscopy. If the bronchoscopy was nondiagnostic, the patient was treated (or retreated) with asthma therapy even if the bronchoprovocation challenge had been negative or if 2-agonist and prednisone therapy was previously ineffective. If cough persisted, uncommon causes were considered (Table 1) [6-9]. Psychogenic cough was considered a diagnosis of exclusion. Table 1. Uncommon Causes of Chronic Cough Three-Month Follow-up All patients were reevaluated using a standardized questionnaire 3 months after cough had resolved to determine whether cough had recurred and whether they were still taking cough-specific medications. Final Diagnostic Criteria No cause of cough was considered definitive until treatment for that cause had been effective (that is, was associated with marked improvement or resolution). When therapy for only one diagnosis resolved the cough, that diagnosis was considered to be the sole cause of cough. When therapy for a diagnosis effected marked improvement short of resolution, that diagnosis was considered to be one of the causes of cough and treatment was continued while additional diagnoses were investigated. Statistical Analysis Recurring data were analyzed by paired t-tests. The extent of association between two variables in a cross-tab

Acute Respiratory Failure in Pregnancy

Objective: To review the literature on cough and the common cold. Methods: MEDLINE was searched through May 2004 for studies published in the English language since 1980 on human subjects using the medical subject heading terms “cough” and “common cold.” Selected case series and prospective descriptive clinical trials were reviewed. Additional references from these studies that were pertinent to the topic were also reviewed. Results: Based on extrapolation from epidemiologic data, the common cold is believed to be the single most common cause of acute cough. The most likely mechanism is the direct irritation of upper airway structures. It is also clear that viral infections of the upper respiratory tract that produce the common cold syndrome frequently produce a rhinosinusitis. In the setting of a cold, the presence of abnormalities seen on sinus roentgenograms or sinus CT scans are frequently due to the viral infection and are not diagnostic of bacterial sinus infection. Conclusion: Cough due to the common cold is probably the most common cause of acute cough. In a significant subset of patients with “postinfectious” cough, the etiology is probably an inflammatory response triggered by a viral upper respiratory infection (ie, the common cold). The resultant subacute or chronic cough can be considered to be due to an upper airway cough syndrome, previously referred to as postnasal drip syndrome. This process can be self-perpetuating unless interrupted with active treatment.

An algorithmic approach to chronic dyspnea

Acute respiratory failure in pregnancy has multiple etiologies, including thromboembolism, amniotic fluid embolism, venous air embolism, aspiration of gastric contents, respiratory infections, asthma, beta-adrenergic tocolytic therapy, and pneumomediastinum and pneu mothorax. Proper management of acute respiratory fail ure in pregnancy requires an understanding of the specific diseases and the normal gestational changes that occur in maternal respiration (decreased functional re sidual capacity, increased minute ventilation, mild respi ratory alkalosis) and hemodynamics (increased cardiac output, increased blood and plasma volume, unchanged central pressures). Knowledge of the determinants of oxygen delivery to fetal tissue (uterine blood flow, pla cental transfer, fetal circulation) and how they are af fected by changes in maternal hemodynamics, position, acid-base status, and medications can help sustain nor mal fetal development, whenever possible, without compromising maternal care. Diagnostic testing such as radiography, hemodynamic monitoring, and fetal moni toring are considered in terms of attendant risk to the mother or the fetus, alterations in normal values related to gestation, and indications for usage. Similarly, the risks and benefits of supportive and specific therapies for the various etiologies of acute respiratory therapy are reviewed.

The Clinical Value of Pharmacologic Bronchoprovocation Challenge

QUESTION The objective of the study was to prospectively evaluate an algorithmic approach to the cause(s) of chronic dyspnea. MATERIALS/PATIENTS/METHODS: Prospective observational study. The study group consisted of 123 patients with a chief complaint of dyspnea of unknown cause present for >8 weeks. Dyspnea severity scores were documented at entry and after therapy. Patients underwent an algorithmic approach to dyspnea. Therapy could be instituted at any time that data supported a treatable diagnosis. Whenever possible, accuracy of diagnosis was confirmed with an improvement in dyspnea after therapy. Tests required, spectrum and frequency of diagnoses, and the values of individual tests were determined. RESULTS Cause(s) was(were) diagnosed in 122/123 patients (99%); 97 patients had one diagnosis and 25 two diagnoses. Fifty-three percent of diagnoses were respiratory and 47% were non-respiratory. Following therapy, dyspnea improved in 63% of patients. CONCLUSIONS The prospective algorithmic approach led to diagnoses in 99% of cases. A third of patients were diagnosed with each tier of the algorithm, thus minimizing the need for invasive testing. Specific diagnoses led to improvement in dyspnea in the majority of cases. Based on the results of this study, the algorithm can be revised to further minimize unnecessary tests without loss of diagnostic accuracy.

Cough and asthma.

Pharmacologic bronchoprovocation challenge (PBC) can be of considerable clinical value in patients in the pediatric age group and adults because bronchial hyperresponsiveness is present in virtually all symptomatic asthmatics and it can be accurately, reliably, and safely demonstrated by PBC. The principal, proven indication for performing PBC is to rule out or help rule in the diagnostic possibility of asthma as the cause of any unexplained chest complaints in patients with normal or near normal spirometric values.

Endobronchial ultrasound with transbronchial needle aspiration in the diagnosis of bilateral hilar and mediastinal lymphadenopathy.

Purpose of review The intention of this article is to discuss and place into perspective recent articles on cough and asthma. Recent findings Asthma continues to be a major diagnosis in most studies of cough. The first prospective study of sub-acute cough demonstrated an asthma incidence lower than that for chronic cough, a logical finding; upper airway cough syndrome often causes cough in the postinfectious state. The first prospective study of cough in infants suggested asthma to be a minor cause of cough in infants, but methodological flaws make the conclusions uncertain. Efforts to separate cough-variant asthma from classic asthma continue. One group has demonstrated that the maximal bronchoconstrictor response in cough-variant asthma is blunted when compared with classic asthma, a possible explanation for the absence of wheeze and dyspnea in cough-variant asthma. Another look at airway resistance showed a less rapid rate of rise in resistance in cough-variant asthma with increasing methacholine dosing than in classic asthma. On the biochemical front, a group has demonstrated differences in vascular endothelial growth factor, which may be the underpinnings of differences between cough-variant asthma and classic asthma. Summary Recent data suggest that cough-variant asthma is part of a continuum in the expression of asthma symptoms and in the asthmatic inflammatory response.

Safety of ultrasound-guided small-bore chest tube insertion in patients on clopidogrel.

Background:Bilateral hilar and/or mediastinal lymphadenopathy (BHL±ML) is an important radiographic finding. Since it was examined 38 years ago by Winterbauer and colleagues, better diagnostic techniques have been developed. The purpose of this study was to reexamine the diagnosis of BHL±ML by Endobronchial Ultrasound-guided Transbronchial Needle Aspiration (EBUS-TBNA). Methods:We carried out a retrospective analysis of data from 78 consecutive patients with BHL±ML who underwent EBUS-TBNA. Patient’s characteristics including age, sex, symptoms, radiographic abnormalities, lymph node size, procedural complications, and the final pathologic diagnosis were recorded. Results:There were 8 diagnostic categories. Sarcoidosis was the most common diagnosis (73%), followed by lymphoma (10%), and reactive lymphadenopathy (10%). Nonlymphoma malignancy was found in 1 case. Seventy-three percent of the patients with sarcoidosis had stage 1 and 27% had stage 2 disease. The diagnosis was made by EBUS-TBNA in 92.3% of the cases. The diagnostic accuracy for EBUS-TBNA was 95% for stage 1 and 93% for stage 2. Fifty one percent of the patients were asymptomatic. Fifty seven percent of sarcoidosis and 36% of the nonsarcoidosis patients were asymptomatic. There were no significant complications from EBUS-TBNA. Conclusions:EBUS-TBNA is a safe and minimally invasive procedure with a high diagnostic yield for BHL±ML. Sarcoidosis is still the most common diagnosis but the incidence seems to have decreased over the years. The increase in nonsarcoidosis patients and the evidence that lymphoma does occur in some asymptomatic patients suggests that biopsy confirmation with EBUS-TBNA is warranted.

Pleuroscopic Pleurodesis Combined With Tunneled Pleural Catheter for Management of Malignant Pleural Effusion: A Prospective Observational Study.

Background:The safety of small-bore chest tubes insertion with ultrasound (US) guidance has been well demonstrated in patients not receiving antiplatelet therapy. Given the current widespread use of these agents, pulmonologists frequently encounter patients on this therapy and requiring drainage of the pleural space. The use of these agents clearly increases the risk of bleeding, but it is not always possible to stop this therapy before the procedure, especially in patients requiring urgent drainage and those with coronary stents. The purpose of this study is to report our experience on the safety of US-guided small-bore chest tube placement in patients receiving clopidogrel. Methods:This was a retrospective review of the charts of adult patients who underwent small-bore chest tube insertion by the pulmonary service while on clopidogrel. Data collected included patient’s and effusion characteristics, indication for clopidogrel and for the procedure, and any significant bleeding complication defined as hemothorax, chest wall hematoma, a reduction in hemoglobin of >2 g/dL, or any bleeding requiring blood transfusion, surgery, or chest tube insertion. US of the chest was performed before insertion but did not include Doppler study of intercostal arteries. Lateral insertion at or anterior to the posterior axillary line was the preferred choice when possible. Results:Forty-three procedures were performed in 30 patients. Seventy percent were male with a mean age of 71 years. The indications for clopidogrel were coronary stents (50%), acute coronary syndrome (27%), prevention of graft occlusion after coronary artery bypass graft (CABG) (13%), femoral stent or endarterectomy (7%), and carotid endarterectomy (3%). The etiology of the effusions was post-CABG (43%), heart failure (17%), end-stage renal disease (13%), pneumothorax (10%), and others (17%). The procedures were therapeutic in 41 cases and diagnostic in 2. The indications for the procedure were respiratory distress (65%), respiratory failure (23%), and pneumothorax (7%). Fifteen procedures (35%) were performed in 10 patients in the ICU and 6 of them were mechanically ventilated. Nine patients were obese based on body mass index. Neither significant bleeding nor other minor complications were seen. Conclusions:The insertion of small-bore chest tube in patients receiving clopidogrel can be safe if performed by experienced operators and by using US guidance along with lateral insertion site, which has the lowest risk of lacerating the intercostal arteries.