COUGH

By Dr. Meghana Patil (Intern Batch 2016)

CONTENTS
Introduction
Mechanism
How Is Cough Analysed Bedside?
Symptomatic Cough
Types of Cough
Impaired Cough
Sputum
Association with GERD
Association with Post Nasal Drip
Association with ACE Inhibitors
Association with History of Atopy
Complications of Cough
Investigations
Treatment of Cough
References
INTRODUCTION
It is the reflex act of forceful expiration against a closed glottis that
helps in clearing the airways including foreign body.
Cough performs an essential protective function for human airways
and lungs without which there is risk for retained airway secretions
and aspirated material predisposing to infection, atelectasis, and
respiratory compromise.
MECHANISM
Spontaneous cough is triggered by stimulation of sensory nerve endings that are
primarily Rapidly Adapting receptors and C fibers. Both chemical (e.g.,
capsaicin) and mechanical (e.g., particulates in air pollution) stimuli may
initiate the cough reflex.
A cationic ion channel—the transient receptor potential vanilloid 1 (TRPV1)
—found on rapidly adapting receptors and C fibers is the receptor for capsaicin,
and its expression is increased in patients with chronic cough.
Afferent nerve endings richly innervate the pharynx, larynx, and airways to the
level of the terminal bronchioles and extend into the lung parenchyma. They
may also be located in the external auditory meatus (the auricular branch of the
vagus nerve, or Arnold’s nerve) and in the oesophagus.
Sensory signals travel via the Vagus and Superior Laryngeal nerves to a region
of the brainstem in the Nucleus Tractus Solitarius vaguely identified as the
“Cough Center.”
The cough reflex involves a series of involuntary muscular actions, with the
potential for input from cortical pathways as well.
The vocal cords adduct, leading to transient
upper-airway occlusion.
Inspiratory phase: deep inspiration through
a widely opened glottis. The expiratory
muscles of cough are stretched, activating
the stretch reflex and creating a stronger
elastic recoil of the lung to aid expiration.
Compressive phase: lasts about 200 ms.
The glottis closes while the expiratory
muscles contract and the intra pleural and
intra alveolar pressure rise rapidly between
40 to 400 cm of H2O.
Expulsive phase: when glottis opens. May
be long lasting with a large expiratory tidal
volume or maybe interrupted by glottic
closures into a series of short expiratory
efforts, each having a compressive and an
expulsive phase.
HOW IS COUGH ANALYSED BEDSIDE?
Duration (days/months/years); acute < 3 weeks, chronic > 3 weeks.
Variability (daytime/nocturnal/morning).
Precipitating factors (dust/fumes/pollen/cold air; lying down-^ gastro-
oesophageal reflux dis ease or CCF).
Sputum examination
Types (dry/wet/bovine etc)
Hemoptysis
Associated symptoms (post-nasal drip, gastro-oesophageal reflux
disease or occult asthma —> these are common causes of long-standing,
undiagnosed cough); wheeze? seasonal?
Chest pain (pleuritis) or breathlessness (COPD) — present or not.
H/O drug intake—ACE-inhibitor, P-blocker.


SYMPTOMATIC COUGH
Cough along with other respiratory symptoms together point to a diagnosis; Eg: cough
accompanied by wheezing, shortness of breath, and chest tightness after exposure to a cat
or other sources of allergens suggests asthma.
Based on duration:
Acute cough (<3 weeks)
Subacute cough (3–8 weeks)
Chronic cough (>8 weeks)
Examples:
When initial assessment with chest examination and radiography is normal, cough-
variant asthma, gastroesophageal reflux, nasopharyngeal drainage, and medications
(angiotensin-converting enzyme [ACE] inhibitors) are the most common identifiable
causes of chronic cough.
In a long-time cigarette smoker, an early-morning, productive cough suggests chronic
bronchitis.
A dry, irritative cough that lingers for >2 months following one or more respiratory tract
infections (“post-bronchitic cough”) is a very common cause of chronic cough,
especially in the winter months.
ACUTE SUBACUTE CHRONIC

Upper respiratory tract

infections, Viral Tuberculosis, Bronchial
syndromes, Sinusitis- Post infectious
asthma
viral/ bacterial


Allergies
Post nasal drip, GERD,
Bacterial sinusitis
Smokers cough

Exacerbation of COPD

Left ventricular heart COPD, Left Ventricular
Asthma
failure heart failure
Pneumonia

Foreign body aspiration Lung cancer

 TYPES OF COUGH
1.Dry cough: Pleural disorders, interstitial lung disease, mediastinal
lesions,Acute dry pleurisy, acute tracheobronchitis
2.Productive cough: Suppurative lung disease, chronic bronchitis, pulmonary
TB , Bronchiectasis, lung abscess, resolution stage of lobar pneumonia
3.Short cough: It is seen in upper respiratory tract infections (common cold)
4.Brassy cough: Cough with metallic sound produced by compression of the
trachea by intrathoracic space occupying lesions, carcinoma of larynx.
5.Bovine cough: Cough with loss of its explosive nature, e.g. tumours pressing on
recurrent laryngeal nerve which is commonly due to bronchogenic carcinoma
6.Prolonged and paroxysmal cough: It is present in chronic bronchitis and
whooping cough
7.Barking cough: It is found in epiglottal involvement as well as in hysterical and
nervous individuals.
8.Hacking (pharyngeal cough) — Heavy smokers.
9.Whooping — Found in whooping cough. There is rapid succession of dry
coughs which gather speed gradually and end in a deep inspiration during
which the characteristic ‘whoop’ (noise) is heard.
10. Spluttering cough In tracheo-oesophageal fistula (cough during swallowing).
11. ’Croupy’ cough — Laryngitis, specially in children.
12. Foetid cough In bronchiectasis and lung abscess, there is foul smelling expectoration.
13. Recurrent cough since childhood Cystic fibrosis, childhood asthma, congenital heart
disease, cystic disease of lung, hypogammaglobulinaemia.
14. Cough with postural variation (postural cough)—Bronchiectasis, lung abscess,
gastro-oesophageal reflux disease (GERD), bronchopleural fistula.

Cough syncope (Post-tussive syncope): It is due to raised intrathoracic pressure, which

reduces venous return to the heart, thereby diminishing cardiac output, resulting in
cerebral hypoperfusion and syncope.
Nocturnal cough: It is present in the following conditions:
1. Chronic bronchitis

2. Left sided failure

3. Bronchial asthma
4. Aspiration

5. Tropical eosinophilia
6. Post-nasal drip.
Drug induced cough is present in drug therapy with ACE inhibitors.
 CHRONIC NON PRODUCTIVE
CHRONIC PRODUCTIVE COUGH
COUGH
Sinobronchial syndrome Cough-variant asthma
Atopic cough

Subacute bacterial sinusitis Cough due to ACE inhibitors
Tracheobronchial tuberculosis GERD
Post nasal drip syndrome Eosinophilic bronchitis without asthma
Chronic bronchitis Laryngeal allergy

Interstitial pulmonary fibrosis
Tracheobronchial tumours
Psychogenic/habitual cough
Foreign body in the airway Trachea-bronchial tuberculosis
Trachea-bronchial tumors

Night time cough Congestive cardiac failure, Bronchial asthma, Pharyngitis

Cough in supine position Congestive cardiac failure

Aggravated with posture Bronchiectasis, Lung abscess

Early morning cough Bronchial asthma

Cough during eating Tracheo-oesophageal fistula, Vocal cord paralysis, Laryngitis

 IMPAIRED COUGH
Weak or ineffective cough compromises the ability to clear lower respiratory tract secretions, predisposing to
more serious infections and their sequelae. Weakness or paralysis of the expiratory (abdominal and intercostal)
muscles and pain in the chest wall or abdomen are some reasons.

Causes of Impaired Cough

Decreased respiratory muscle strength
Chest wall or abdominal pain
Chest wall deformity (e.g., severe kyphoscoliosis)
Impaired glottic closure or tracheostomy
Tracheobronchomalacia
Abnormal airway secretions

Assessment of Impaired Cough

Generally assessed qualitatively by peak expiratory flow or maximal expiratory pressure at the mouth.
Other assistive devices and techniques are:
Simple: splinting of the abdominal muscles with a tightly held pillow to reduce postoperative pain while
coughing)
Complex: a mechanical cough-assist device supplied via face mask or tracheal tube that applies a cycle of
positive pressure followed rapidly by negative pressure).
SPUTUM
It is a mixture of tracheobronchial secretion, cellular debris, micro-organisms and
saliva. The character of sputum is determined by its amount, colour, chronology,
consistency and smell.
Saliva contains squamous cells. Sputum contains epithelial cells. If sputum contains
epithelial cells and eosinophils then suspect: 

a. Bronchial asthma

b. Allergic bronchopulmonary aspergillosis (ABPA).
How sputum (expectoration or ‘phlegm’) is analysed clinically ?
1.Amount (profuse or not).
2.Character (serous, mucoid, purulent, mucopurulent).
3.Colour (yellow, green, black, rusty, pinkish or anchovy-sauce like).
4.Odour or taste (offensive or not).
5.Mixed with blood (haemoptysis) or not.
6.Sputum production influenced by change of posture (bronchiectasis, lung
abscess) or not.
Amount
Bronchorrhoea: When the quantity of sputum production is > 100 ml/day, it is termed as
bronchorrhoea.
Copious sputum production is seen in conditions like:
1. Bronchiectasis

2. Lung abscess

3. Empyema rupturing into the bronchus
4. Necrotising pneumonia
5. Alveolar cell carcinoma.
Copious sputum production upon changes in posture is seen in bronchiectasis and lung
abscess. This postural relationship to cough is due to irritation of the healthy bronchial mucosa.
Large amount of colourless sputum is present in alveolar cell carcinoma.
Colour of the Sputum
a. Green or yellow coloured thick sputum indicates bacterial infections. The green colour to
sputum is imparted by the enzyme myeloperoxidase (verdo- peroxidase)
b. Black coloured sputum is present in coal worker’s pneumoconiosis
c. Rusty sputum is present in pneumococcal pneumonia
d. Red currant jelly sputum is seen in Klebsiella pneumonia
e. Pink frothy sputum is present in pulmonary oedema.
f. Blood stained sputum is present in tuberculosis

g. Anchovy sauce sputum is present in ruptured amoebic liver abscess.
Consistency
Serous: It is clear, watery and frothy. It is seen in broncho- alveolar carcinoma. It may be
pink, as occurs in pulmonary oedema.
Mucoid: It is clear, greyish white or black in colour and frothy. It may be seen in
conditions like chronic bronchitis and chronic asthma.
Mucopurulent or purulent: Yellowish or greenish brown in colour, seen in bacterial
infection.
Profuse purulent sputum : Bronchiectasis, Lung abscess, chronic bronchitis, Empyema
thoracis ruptured into bronchus, Tuberculous cavity, Cystic fibrosis, resolving pneumonia,
necrotising pneumonia also produce offensive sputum.
Bronchial asthma: Macroscopically the sputum is ‘worm like’, which are remnants of
casts of bronchus. Microscopically, the sputum consists of:

a. Eosinophils and Desquamated epithelium

b. Curschmann spirals (whorled mucous plugs)

c. Charcot-Leyden crystals (crystalloid debris of eosinophil membrane)

d. Creola bodies (exfoliated cells due to disruption of mucosal integrity).
Odour of Sputum
Offensive and foetid:

a. Lung abscess

b. Bronchiectasis

c. Anaerobic bacterial infection.
 ASSOCIATION WITH GERD
One of the major respiratory tract complications due to GERD is chronic cough
which primarily occurs by two mechanisms.
Reflex mechanism, in which GER stimulates vagal nerve endings in the lower
oesophagus.
Micro aspiration mechanism in which GER causes micro aspiration of gastric
contents into the trachea and bronchi leading to direct stimulation of airway
smooth muscle and irritant receptors causing cough.
Coughing due to GERD is usually chronic, with a mean duration of 13-58 months.
Some patients have symptoms of GERD such as heart burn that precedes cough.

To confirm a diagnosis of GERD- related cough, 24-h oesophageal pH monitoring

is recommended. In general, esophageal pH is less than 4 in GERD.



 ASSOCIATION WITH POST NASAL DRIP
The clinical presentation of patients with postnasal drip (PNDS), commonly
involves complaints of a sensation of something dripping into the throat, a
need to clear the throat, a tickle in the throat, nasal congestion, nasal discharge
or hoarseness. Some of the associated symptoms include
Drainage in posterior pharynx
Throat clearing

Nasal discharge
Cobblestone appearance of the oropharyngeal mucosa
Mucus in the oropharynx
Cough in postnasal drip is productive. Causes of post nasal drip include:
sinusitis, acute rhinitis, allergic rhinitis, vasomotor rhinitis. The mechanism of
cough involves:
Acute and chronic laryngitis and bronchitis due to post nasal drip
Direct chemical and physical stimulation of cough receptors in the larynx
and trachea by post nasal drip.
ASSOCIATION WITH ACE INHIBITORS
The most common cause of drug induced cough is use of ACE inhibitors.
The incidence of cough varies with the type of ACE inhibiters but is not related
to dose.
Incidence of course is about 10 to 30% and tends to be higher in middle age
women.
ACE inhibitors block Kininase, an enzyme involved in Bradykinin and Substance
P degradation. The local increase in Bradykinin and Substance P concentrations
stimulate C fibres and cough receptors. In addition, ACE inhibitors block the
degradation of prostaglandins which may stimulate C fibres and induce cough.
ACE inhibitor related cough is usually a persistent dry cough that begins a few
weeks after starting therapy and it results within one week after discontinuing the
therapy
 ASSOCIATION WITH HISTORY OF ATOPY
Atopic cough is non-productive scratchy cough in the throat. Patients may feel like sputum is
sticking in their throat. Coughing is most frequent at bedtime, followed by late night to early
morning. Cough can be induced by many triggers, including cold air, warm air, conversation,
talking on the phone, passive smoking, exercise and perfumes
Findings suggesting an atopic predisposition:

• Current or past history of an allergic disorder.
• Peripheral blood eosinophilia.

• Increased serum total IgE.

• Positive for specific IgE.

• Positive intradermal allergen test.
Diagnostic criteria for atopic cough
(Must fulfil all criteria 1-4)
I. Dry cough for at least 3 weeks without wheezing or dyspnea.
2. No response to bronchodilator therapy.
3. One or more findings suggesting an atopic predisposition or induced sputum eosinophilia
4. Relief of cough with Histamine Hl antagonist and/or steroids.
 COMPLICATIONS OF COUGH
CARDIOVASCULAR NEUROLOGIC GI GENITOURINARY MUSCULOSKELETAL RESPIRATORY MISCELLANEOUS

• Pulmonary
• Arterial • Cough interstitial • Petechiae
syncope emphysema with and purpura
hypotension
• Loss of • Headache
• Gastro-
potential risk of
pneumatosis
• Disruption
consciousness • Cerebral air
oesophageal intestinalis, of surgical
embolism wounds
Rupture of
• CSF fluid
reflux • From pneumomediasti
num, • Constitution
sub- disorder asymptomati pneumoperitone
rhinorrhoea al symptoms
conjunctival,
• Acute
• Hydrothorax
• Urinary
c elevation of um,
• Lifestyle
nasal and anal in peritoneal serum pneumoretro
cervical incontinence peritoneum, changes
veins dialysis creatinine
• Dislodgement
radicalulopat
• Malfunction • Inversion of
phosphokinas
pneumothorax, • Self
hy bladder subcutaneous consciousne
or of e to rupture emphysema
malfunctionin • Malfunctioni
gastrostomy
through
of rectus • Laryngeal
ss,
ng urethra trauma hoarseness
g of button abdominis
ventriculoatr • Trachea dizziness
intramuscular
ial shunt
• Splenic muscles bronchial trauma • Fear of
catheters
• Seizures
rupture • Rib fractures (bronchitis serious
• Bradyarrhyth
• Stroke due
• Inguinal bronchial
disease
mia hernia rupture)
• Tachyarrhyth
to vertebral • Exacerbation of • Decrease in
artery asthma quality of
mia • Intercostal lung
dissection life
herniation
 INVESTIGATIONS
• Sputum Gram stain: for Staphylococcus, Pneumococcus, Moxarella, Hemophilus
• Special Stains:
• ZN stain and fluorescent stains: Mycobacterium and non mycobacterium TB
• Gimenez stain: Leigionella
• PAS stain and Grocott stain: Fungi
• Giemsa stain, Toluidene blue stain, Grocott stain: Pneumocystis
• Routine Blood Investigation
• DC, TLC increased in bacterial infections
• CRP for monitoring the degree ad course of inflammation and treatment effects
• Procalcitonin : marker of infections
• Imaging studies: Chest X-ray, HRCT Thorax, Sinus Imaging with CT
• Immunofluorescence assays: useful in Legionella, Chlamydophila, Pnemocystis and Mycoplama
• Antigen test kits for: Influenza, Adenovirus, RS virus, Group A streptococcus, Pnuemococcal urinary antigen,
Legionella urinary antigen
• Genetic tests- DNA probes, PCR, Sputum Cytology: M.TB and Non M.TB, Legionella, Chlamydophila, Pnemocystis,
Mycoplama, CMV.
• Bronchoscopy: in Central lung tours, endobronchial TB, foreign bodies
• Pulmonary Function tests, Airway Reversibility tests, Airway Responsiveness tests, Exhaled breath (nitric
oxide) [higher in asthmatic cough]
• 24 hour oesophageal pH monitoring
• Psychological assessment: in absence of physical cause.
TREATMENT OF COUGH



Empiric treatment of chronic idiopathic cough with inhaled

corticosteroids, inhaled anticholinergic bronchodilators, and
macrolide antibiotics.
Most potent are narcotic cough suppressants, such as codeine or
hydrocodone, which are thought to act in the “cough center” in the
brainstem.
Small case series and randomized clinical trials have indicated benefit
from off-label use of gabapentin, pregabalin, or amitriptyline.
Recent studies suggest a role for behavioral modification using
specialized speech therapy techniques, but widespread application of
this modality is currently not practical.
Approaches that are being explored include the development of
neurokinin receptor antagonists, TRPV1 ion channel antagonists,
and novel opioid and opioid-like receptor agonists.
REFERENCES

Harrisons Principles of Internal Medicine, 20th Edition, Pages 276-8

Bedside Respiratory Medicine, Basanta Hazarika, 2nd Edition, Pages 116-27
Manual of Practical Medicine, R Alagappan, 4th Edition, Pages 201-2
Bedside Clinics in Medicine Part 1, Arup Kumar Kundu, 6th Edition, Pages 101-2
Essentials of Medical Pharmacology, KD Tripathi, 8th Edition, Pages 237-8

Thank you !