APPROACH TO COUGH
BY
DR SABNA
FIRST YEAR PGT
DEPT OF CHEST MEDICINE
COUGH
• Cough is a protective mechanism to facilitatae
the removal of mucus,noxious substances or
pathogens from the airways& lungs.
• Impairment can be harmful or even fatal
• Usually start as a deep inspiration followed by
expiration against a closed glottis, which then
opens with an expulsive flow of air.
• Can be reflex or voluntary.
MECHANICS OF COUGHING
• INSPIRATORY PHASE: deep inspiration
through widely opened glottis. Large lung
volume provides better mechanical efficiency
for expiratory muscles as they are stretched
&stronger elastic recoil of lung aid expiration
• COMPRESSIVE PHASE: Lasts for 200ms.glottis
closes while expiratory muscles contract &
intrapleural& intra-alveolar pressures rise
rapidly ( 40-400 cm H2O)
• EXPIRATORY PHASE :
• May be long lasting with a large expiratory
tidal volume,or interrupted by glottic closures
into series of short expiratory efforts.
• Effectiveness of cough depends on peak
airflow & therefore be greater with larger
elastic recoil of lung which creates driving
pressure, & a greater stiffness of central
airways, which prevents dynamic collapse.
NEUROBIOLOGY OF COUGH
SENSORY RECEPTORS
• Structures innervated by Vagus nerve.
• Include larynx, tracheobronchial tree, lower
part of oropharynx, tympanic membrane and
external auditory meatus.
• 2 types of cough evoking sensory nerve fibers:
vagal nociceptors & vagal mechanoreceptors
• Vagal nociceptors : respond to
bradykinin ,prostaglandins ,leukotrienes ,
proteases & cytokines, noxious irritants like
capsaicin, acid, nicotine & acrolein
• Vagal mechanoreceptors: stimuli include acid
solution, hypotonic solution including inhaled
fog, mechanical stimulation by catheter,
mucus or dust.
MEMBRANE RECEPTORS OR CHANNELS FOR
COUGH TRANSDUCTION:
• Transient receptor potential channels(TRP)
• Tetradoxin insensitive voltage gated sodium
channel
• G protein coupled receptors
• Mechanically gated membrane ion channel
• Acid sensing ion channel (ASIC)
• Voltage sensitive ion channel like NaV1.7
• P2X2& P2X3 channels
APPROACH TO PATIENT WITH COUGH
• COUGH: acute - <3 weeks
subacute -3-8 weeks
chronic- >8 weeks
• Goal: 1) determine severity
2)assess possible cause
3)plan investigations & treatment
COMMON CAUSES OF COUGH
APPROACH TO ADULT WITH COUGH
COUGH IN CHILDREN
ACUTE COUGH
• Acute may suggest:
Upper RT
• Common cold –Self limiting ,resolves in 2 wks,
• Sinusitis
Lower RT
• Pneumonia
• Bronchitis
• Exacerbation of COPD, asthma
• Inhalation of bronchial irritant (eg, smoke or fumes)
SUBACUTE COUGH
• Commonly due to prior infection
• Exacerbation of underlying disease like COPD,
asthma, upper airway cough syndrome
• pertussis
CHRONIC COUGH
• COPD
• Pulmonary TB
• Asthma
• Gastro-esophageal reflux
• Psychogenic
• Upper airway cough syndrome (UACS)
• postnasal drip (PND)
• Bronchiectasis
• Drugs (eg, ACE inhibitors)
• Lung malignancy
• Cardiac failure / pulmonary edema
• Pulmonary embolism
ASSOCIATED SYMPTOMS
• Fever, recent symptoms, SOB – Pneumonia
• History of smoking with intermittent sputum –COPD
• Daily purulent sputum for long periods , or whooping
cough in childhood , recurrent hemoptysis -
bronchiectasis
• Persistant cough especialy in smokers , any
hemopstysis , pneumonia that fail to clear in 4-6wks,
LOA ,LOW - Lung cancer
• Heartburn or regurgitation of acid after eating,
bending or lying ,nocturnal as well as daytime
cough –oesophageal reflux
• Postnasal drip , sinus congestion , headache –
UACS
• Persistant dry cough with excertional SOB-ILD
• Long history with negative signs and
investigations-idiopathic cough
• Wheezing
episodic, bilateral & polyphonic - asthma
Monophonic –intraluminal obstruction-fb/tumor
• Pleuritic chest pain- Pleural effusion, Pneumonia
• Joint pain, dry eyes, LN enlargement -SLE,
SJOGREN (with interstitial lung dss)
• Worse in morning- COPD
• H/o stroke, neurogenic dysphagia-ASPIRATION
PNEUMONIA
COUGH WITH SPUTUM
• Frequency of sputum (How frequent?)
• Quantity of sputum (How much?)
• Appearance of sputum
• Colour of sputum
• Is there any blood in the sputum
• “”””””
“’;
• ;
COLOUR:
• Clear (mucoid) : COPD or bronchectasis
without current infection.
• Yellow(mucopurulent): acute LRTI or asthma.
• Green(purulent): current infection-acute
disease or exacerbation of chronic disease.
• Red(rusty):pneumococcal pneumonia
• Pink(serous or frothy) : acute pulmonary
edema.
CONSISTENCY:
• An increase in stickiness or viscosity:
exacerbation of bronchiectasis.
• Large volume of frothy secretion over week or
months : uncommon bronchoalveolar cell
carcinoma.
• Firm plug : asthma
• Foul smelling sputum : lung abscess
HEMOPTYSIS :
• If with purulent and long standing sputum
a. CHRONIC BRONCHITIS (small amount of blood)
b. BRONCHIECTASIS (large amount of blood)
• If with fever, recent onset, SOB : PNEUMONIA
• If LOA, LOW, H/O smoking : BRONCHIAL
CARCINOMA
• If sputum is pink in color and frothy : PULMONARY
EDEMA
• If sudden onset
a. PULMONARY EMBOLISM
b. ACUTE RT INFECTIONS
• If had contact with TB patients / HIV status : TB
• If with long history of SOB
a. CHRONIC LUNG DSS
b. MITRAL STENOSIS
• If with hematuria, proteinuria
a. GOODPASTURE SYNDROME,
b. WEGENER'S GRANULOMATOSIS (h/o sinusitis)
• If with other bleeding sites
a. COAGULATION DISORDER
b. USE OF ANTICOAGULANTS
Character of cough
• Lack of the usual explosive beginning may
indicate vocal cord paralysis (the 'bovine'
cough).
• A muffled, wheezy, ineffective cough suggests
obstructive pulmonary disease.
• A very loose productive cough suggests
excessive bronchial secretions due to chronic
bronchitis, pneumonia or bronchiectasis.
• A dry, irritating cough may occur with chest
infection,asthma,carcinoma of bronchus or acid
irritation of lungs in GORD.It is also typical of
cough produced by ACE-I
• A barking or croupy cough may suggest problem
with URT or pertussis infection.
Cough hypersensitivity syndrome
• Abnormal state of chronic coughing accompanied by other
sensations like persistent or intermittent tickling, irritating
sensation, rawness or itch or a chocking sensation in throat
with repeated throat clearing, chest tightness, hoarse voice
and dysphagia.
• Triggers include change in temprature,taking a deep
breath,laughing,talking,smoking,aerosol spray and perfumes.
• It is due to increased sensitivity called peripheral
sensitisation which is related to neuroplasticity in vagal
sensory fibres.
• Can also be accompanied by central sensitisation.
COUGH SUPPRESSION THERAPIES
NON PHARMACOLOGICAL PHARMACOLOGICAL
• Speech pathology • Antitussive therapy
management • Neuromodulators
• Expectorants
• Mucolytics –
• Include breathing exercise, acetylcysteines,bromhexine
vocal & laryngeal hygeine & methylcysteine: reduces
training & viscosity in patients with
psychoeducational chronic bronchitis.
counselling.
ANTI TUSSIVES
Narcotic Non narcotic
• Include morphine , • Dextromethorphan
diamorphine and codeine. • Should be avoided in
• At effective dose they cause children.
sedation, physical • At higher doses causes
dependance, respiratory dizziness,nausea,vomiting
depression and constipation and headache
• Levodropropizine-cause
peripheral inhibition of
sensory cough receptors.
NEUROMODULATORS
• Effective in idiopathic or refractory cough.
• Centrally acting : amitriptyline ,gabapentine
morphine.
• Amitryptiline & gabapentine have central
aminoceptive action & modulate presynaptic
N-methyl-D-aspartate receptors, leading to
reduced transmitter release & postsynaptic
excitability.
POTENTIAL NEUROMODULATORS
• New cough suppressant in development include
blockers of ion channels on vagal afferent endings
and centrally acting agents.
• P2X2/3 antagonist gefapixant –currently in phase 3.
• Centrally acting agonist of the alpha 7 nicotinic
acetyl choline receptor-under development
• Alpha 7 cholinergic receptor agonists acting on
central pathway that mediate cough inhibition-
under development
• Centrally acting neurokinin 1 recptor antagonist-
phase 2 trial
