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PROBLEMS IN ETIOLOGY AND DIAGNOSIS OF COUGH AND CHRONIC COUGH Muhammad Fachri FKK UMJ    RSIJ Sukapura, RSIJ Pondok Kopi
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PROBLEMS IN ETIOLOGY AND

DIAGNOSIS OF COUGH ANDCHRONIC COUGH 

Muhammad Fachri

FKK UMJ –  RSIJ Sukapura, RSIJ Pondok Kopi

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Introduction

The impact of cough on health is substantial.

It can :

(1) be important defens mechanism that helps clearexcessive secretions and foreign material from

airways

(2) be important factor in the spread of infection(3) present as one the common symptoms for which

 patient seek medical attention.

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How Common is Cough

Cough is one of the most common complaints for

which patients seek medical attention

29,5 million US population visit for cough (1998)

 3,6% of all physician visit

Chronic cough being reported by 3 – 40% of the

 population (Europe)

One of most common reasons for new visit to pulmonologist and respirologists 

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Chronic Cough Physiology

Each cough occurs through the stimulation of acomplex reflex arc.

Cough receptors exist :

1. In the epithelium of the upper and lower

respiratory tracts

2. Pericardium

3. Esophagus4. Diaphragm

5. Stomach.

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Chronic Cough Physiology

 Mechanical cough receptors 

Can be stimulated by triggers such as touch or

displacement. Chemical receptors 

Sensitive to noxious gases or fumes.

 Laryngeal and tracheobronchial receptors Respond to both mechanical and chemical

stimuli.

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An effective

cough have been

classified as

inspiratory,

compressive, and

expiratory.

Chronic Cough Physiology

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Cough - History

Some controversy over definitions

Arguably the best

Acute : less than 3 weeks

Sub acute : 3 to 8 weeks

Chronic : more than 8 weeks

ACCP Evidence-Based Clinical Practice Guidelines CHEST 2006

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I. Common Causesa. Chronic Upper airways cough

syndrome

b. Cough and common cold

c. Asthma

d. GERDe. Bronchitis

f. Bronchiectasis

g. Post Infection cough

h. Lung Tumors

I. Cough in the immunocompromised

II. Uncommon causes

III. Unresolved cough (Idiopathiccough)

Etiology of Cough

i. Cough and aspiration

j. ACE inhibitor induced

k. Psychogenic cough

l. ILD

m. Occupational andenviroment causes

n. Tuberculosis and otherinfection

o. Peritoneal dialysis andcough

ACCP Evidence-Based Clinical Practice Guidelines CHEST 2006

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Etiology of chronic cough

Eur Respir J 2004; 24: 481-492

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Etiology of Chronic Cough

The most common etiology ofchronic cough are :

1. Upper airway cough syndrome

(UACS) due to a variety of

rhinosinus conditions

2. Asthma

3. Nonasthmatic eosinophilic

 bronchitis (NAEB)4. Gastroesophageal reflux disease

(GERD)

ACCP Evidence-Based Clinical Practice Guidelines

CHEST 2006; 129:1S  – 23S

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ACCP Evidence-Based Clinical Practice Guidelines CHEST 2006

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 ACCP Evidence-Based Clinical Practice

Guidelines 

“ In patients with chronic cough and a normal chest

roentgenogram finding who are nonsmokers and are not

receiving therapy with an angiotensin-converting enzyme(ACE) inhibitor, the diagnostic approach should focus on the

detection and treatment of UACS (formerly called PNDS ),

asthma, NAEB, or GERD, alone or in combination. This

approach is most likely to result in a high rate of success in

achieving cough resolution. (Level Evidence B) “ 

CHEST 2006; 129:1S – 23S

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 ACCP Evidence-Based Clinical Practice

Guidelines 

“ In all patients with chronic cough, regardless ofclinical signs or symptoms, because UACS

(formerly called PNDS ), asthma, and GERDeach may present only as cough with no otherassociated clinical findings (ie , “silent PNDS,”“cough variant asthma,” and “silent GERD”),each of these diagnoses must be considered.

(Level Evidence : B) “ 

CHEST 2006; 129:1S – 23S

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Evaluation of Chronic Cough

History

Physical Oropharyngeal mucous or cobblestone appearance

suggests postnasal-drip syndrome

“silent” postnasal-drip syndrome

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Evaluation of Chronic Cough

Heartburn and regurgitation suggest

Gastroesophageal reflux disease

“silent”GERD in up to 75% of patients 

 Wheezing suggests asthma

“silent”asthma (cough variant asthma) in up to 57%

of cases

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Evaluation of Chronic Cough

 Where to start

CXR: normal is consistent with PND, GERD,asthma, chronic bronchitis.

Unlikely : bronchogenic carcinoma, sarcoid, TB andbronchiectasis

Since PND syndromes are most common---startthere

Sinusitis or rhinitis of the following varieties: nonallergic,allergic, postinfectious, vasomotor, drug-induced andenvironmental-irritant induced

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DIAGNOSIS OF CHRONIC COUGH

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DIAGNOSIS OF CHRONIC COUGH

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Cough and Post Nasal Drip (UACS)

UACS (Upper Airway Cough Syndrome)

Secondary to a variety of rhinosinus condition

Underlying reasons for postnasal drip include allergic,

 perennial nonallergic, and vasomotor rhinitis; acutenasopharyngitis; and sinusitis

Symptoms of postnasal drip include frequent nasal

discharge, a sensation of liquid dripping into the back of the

throat, and frequent throat clearing Diagnosis of UACS is determined by considering a

combination of symptoms, physical finding, sinus imaging

and respons to therapy

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Cough and asthma

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Cough and (Cough Variant) Asthma

Suggested when the patient is atopic or has a family historyof asthma

Cough may be seasonal, may follow an upper respiratorytract infection, or may worsen upon exposure to triggers

 Airways hyperreactivity can be demonstrated bybronchoprovocation testing. However, in a patient with

 persistent cough, the presence of reversible airflowobstruction or a positive bronchoprovocation test does notnecessarily prove that the cough is secondary to asthma

the best way to confirm asthma as a cause of cough is todemonstrate improvement in the cough with appropriate

therapy for asthma 

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Chronic Cough -- GERD

Etiology

Gross aspiration including pulmonary aspirationsyndromes, abscess, chronic bronchitis,

bronchiectasis, and pulmonary fibrosis Laryngeal inflammation

 Vagally mediated distal esophageal-tracheobronchialreflex

 When GERD is cause of chronic cough, up to 75%of patients have no GI symptoms

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Chronic Cough -- GERD

24-h esophageal pH monitoring is best

Esophageal pH monitoring, ideally

 performed with event markers to allowcorrelation of cough with esophageal pH,

is generally considered the optimal

diagnostic study, with a sensitivityexceeding 90 percent

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Cough and Non Asthmatic

Eosinophilic Bronchitis

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Chronic cough due to ACE

Inhibitors

A nonproductive cough is a complication of treatmentwith angiotensin converting enzyme (ACE)

inhibitors, Oocuring in 3 to 20 percent of patients treated with

these agents

Pathogenesis seems be an accumulation of

inflammatory mediators: bradykinin, substance Pand/or prostaglandins

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Chronic cough due to ACE

Inhibitors

ACE inhibitor-induced cough has the following generalfeatures 

usually begins within one week of instituting therapy, but the onset can be delayed up to six months

It typically resolves within one to four days ofdiscontinuing therapy, but can take up to four weeks

It generally recurs with rechallenge, either with the sameor a different ACE inhibitor

It is generally not accompanied by airflow obstruction

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DON’T FORGET 

 Tuberculosis

Bronchiectasis

Chronic Bronchitis

Lung tumor

Occ and Env exposure

ILD

others

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CONCLUSION

The most common etiology of chronic cough are UACS,

Asthma, GERD and NAEB

In patients with chronic cough and a normal chest

roentgenogram finding who are nonsmokers and are notreceiving therapy with an angiotensin-converting enzyme

(ACE) inhibitor, the diagnostic approach should focus on the

detection and treatment of UACS (formerly called PNDS ),

asthma, NAEB, or GERD, alone or in combination

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 THANK YOU

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Cough and Non Asthmatic

Eosinophilic Bronchitis Patients with this disorder demonstrate atopic tendencies,

 with elevated sputum eosinophils and active airwayinflammation in the absence of airway hyperresponsiveness

bronchial mucosal biopsies are required to definitively

diagnose eosinophilic bronchitis a trial of therapy is usually performed without biopsy, since

most patients respond well to inhaled corticosteroids

One year follow-up of 367 patients with normal lungfunction and eosinophilic inflammation noted that:

 55 percent remained symptomatic with normal lung function,

 32 percent were free of symptoms

 13 percent developed asthma

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