COUGH AND HEMOPTYSIS

Cough

• Cough is an essential protective function for human airways and lungs

➢without an effective cough reflex we are at risk for retained
airway secretions and aspirated material predisposing to
infection, atelectasis and respiratory compromise

• Cough is often a clue to the presence of respiratory disease

Cough Mechanism

• Spontaneous cough is triggered by stimulation of sensory nerve endings

that are thought to be primarily rapidly adapting receptors and C fibers
• Both chemical and mechanical stimuli can stimulate cough reflex
• Afferent nerve endings richly innervate the pharynx, larynx & airways to
the level of the terminal bronchioles & extend into the lung
parenchyma
• Located in the external auditory meatus (auricular branch of the vagus nerve,
or the Arnold nerve) and in the esophagus
Cough Mechanism

• Sensory signals travel via the vagus and superior laryngeal nerves to
a region of the brainstem in the nucleus tractus solitarius, identified
as the “cough center”

• The cough reflex involves a highly orchestrated series of involuntary

muscular actions, with the potential for input from cortical pathways
Cough Mechanism

• Bronchial smooth muscle contraction together with dynamic

compression of airways narrows airway lumens and maximizes the
velocity of exhalation

• The kinetic energy available to dislodge mucus from the inside of

airway walls is directly proportional to the square of the velocity of
expiratory flow
 Impaired Cough

• Weak or ineffective cough compromises the ability to clear lower

respiratory tract infections predisposing to more serious infections
• Peak expiratory flow or maximal expiratory pressure at the mouth
can be used as a surrogate marker for cough strength

• How to improve cough strength:

• Splinting of the abdominal muscles
• Mechanical cough assistive device supplied via face mask or tracheal tube
that applies positive airflow
Duration of cough


➢Acute cough (<3 weeks) most commonly d/t respiratory tract

infection, aspiration, inhalation of noxious chemicals or smoke
➢Subacute cough (3-8wks) common residuum of tracheobronchitis
as in pertussis or “postviral tussive syndrome”
➢Chronic cough (>8wks) d/t cardiopulmonary diseases including
those of inflammatory, infectious, neoplastic and cardiovascular
etiologies
✓Most common causes: cough-variant asthma, GERD,
nasopharyngeal drainage, medications such as ACEI
Assessment of Chronic Cough

• details of the sound, time of occurrence during the day and pattern
of coughing
• Regardless of the cause, cough worsens upon first lying down at
night, with talking, or with the hyperpnea of exercise
• frequently improves with sleep
• Useful questions:
➢Circumstances surrounding the cough
➢What makes the cough better or worse
➢Presence of sputum production
Assessment of Chronic Cough

• Physical examination
➢ Wheezing
➢ Crackles
➢ Auditory canals and tympanic membranes (from irritation
resulting in stimulation of Arnold’s nerve)
➢ Nasal passageways (for rhinitis or polyps)
➢ Clubbing of nails
 Chronic Cough with normal CXR

• Account for 90% of chronic cough:

1. Use of ACEI
▪ ACE metabolizes bradykinin and other tachykinins such as substance P
▪ Sensitization of sensory nerve endings due to accumulation of bradykinin
✓Trial period off the medication
✓Discontinuation for at least a month
Chronic Cough with normal CXR

2. Postnasal drainage
▪ Stimulation of sensory receptors of the cough-reflex pathway in
the hypopharynx or aspiration of draining secretions into the
trachea
▪ Frequent sore throat, clearing, sneezing, rhinorrhea
▪ Cobblestoned appearance of the mucosa along the posterior
pharyngeal wall
 Chronic Cough with normal CXR

3. GERD
▪ Reflux of gastric contents into the lower esophagus
▪ Reflux to the level of pharynx causes chemical bronchitis and possibly
pneumonitis
▪ Retrosternal burning after meals or on recumbency, frequent
eructation, hoarseness, throat pain
✓Antacids: H2 receptor antagonists, PPI
 Chronic Cough with normal CXR

4. Asthma
▪ cough-variant asthma: cough without wheezing, shortness of
breath, chest tightness
✓Inhaled glucocorticoids & intermittent B-agonist bronchodilators

5. Chronic eosinophilic bronchitis

➢Characterized by sputum eosinophilia in excess of 3% without
airflow obstruction or bronchial hyperresponsiveness
✓Treated with inhaled glucocorticoids
Symptom-based Treatment of Cough

Chronic idiopathic cough aka Hypersensitivity syndrome

➢Dry cough, Tickle/ sensitivity in the throat
✓ Narcotic cough suppressants: codeine, hydrocodone which acts on
the cough center of the brainstem
▪ Limitations: drowsiness and constipation
▪ Addictive property
✓ Dextromethorphan: centrally acting cough suppressant w/ fewer side
effects
✓ Benzonatate: inhibit neural activity of sensory nerves
HEMOPTYSIS
 HEMOPTYSIS

• The expectoration of blood from the respiratory tract arising from

any location from the alveoli to the glottis
• Important to distinguish hemoptysis from
▪ Epistaxis: bleeding from the nasopharynx
▪ Hematemesis: bleeding from the UGIE
• Most common etiology: infection of the medium-sized airways,
usually from viral or bacterial bronchitis (in the USA)
• Worldwide the most common cause is Mycobacterium tuberculosis
d/t to its predilection to cavity formation
Etiology

Search for potential sites of bleeding from the alveolus to the mouth

• Diffuse alveolar hemorrhage (DAH): diffuse bleeding into the alveolar

space
➢Causes: inflammatory DAH is d/t small-vessel vasculitis/capillaritis from
granulomatosis w/ polyangiitis
➢Systemic autoimmune diseases e.g SLE can manifest as pulmonary capillaritis
➢DAH is suspected in patients with sudden onset dyspnea and hypoxemia in the
first 100 days after bone marrow transplantation
• Direct inhalation injury
▪ Thermal injury from fires
▪ Inhalation of illicit substances (e.g. cocaine)
▪ Inhalation of toxic chemicals

• Bleeding in hemoptysis usually arise from small to medium airways

• Irritation & injury to the bronchial mucosa can lead to small-volume bleeding
• More significant hemoptysis can result from the proximity of the bronchial artery
& vein to the airway, with these vessels and the bronchus running together
referred to as the bronchovasular bundle
• In the smaller airways, these blood vessels are close to the airspace,
and lesser degrees of inflammation or injury can therefore result in
their rupture into the airways

• Bronchial bleeding generally originates from bronchial arteries which

are under systemic pressure & predisposed to larger-volume
bleeding
• Any infection of the airways can result in hemoptysis although acute
bronchitis is most commonly caused by viral infection
• Chronic bronchitis may have bacterial superinfection w/ organisms
such as Steptococcus pneumonia, Haemophilus influenzae or
Moraxella catarrhalis
• Bronchiectasis are prone to hemoptysis d/t chronic inflammation &
anatomic abnormalities that bring the bronchial arteries closer to
the mucosal surface
• Pneumonias of any sort can cause hemoptysis
• Cystic fibrosis: commonly presents with hemoptysis
• Tuberculous infection: can lead to bronchiectasis or cavitary
pneumonia
• Rasmussen’s aneurysm: dilation of a pulmonary artery in a cavity
formed by previous tuberculous infection remains a source of
massive, life-threatening hemoptysis in the developing world
• Infections w/ Staphylococcus aureus & gram negative rods (e.g.
Klebsiella pneumoniae) are likely to cause necrotizing infections
• Pulmonary paragonimiasis (i.e infection with the lung fluke Paragonimus
westermani)
➢ Fever, cough, hemoptysis
➢ Considered in recent immigrants from endemic areas who have new or recurrent
hemoptysis
➢ Secondary to ingestion of crayfish or small crabs

Bronchogenic Lung Cancer

➢ Hemoptysis in approx. 10%
➢ Cancers in the proximal airways are likely to cause hemoptysis
➢ Both Squamous & small cell carcinomas are more adjacent to the proximal airways
• Metastatic disease to the pulmonary parenchyma can bleed
• Breast, colon, testicular, thyroid cancer, melanoma
• Congestive heart failure w/ transmission of elevated left atrial
pressures can lead to rupture of small alveolar capillaries
• Pulmonary arteriovenous malformations, pulmonary embolism,
pulmonary arterial hypertension are prone to bleeding
 History & PE

• Specific characteristic
➢ Blood-tinged, purulent secretions, pink, frothy or pure blood
• Volume of blood expectorated
➢ Determines the cause and the urgency for further diagnostic & therapeutic
maneuvers
➢ Large volume, referred to as massive hemoptysis >200-600ml in 24H; a medical
emergency
• Cigarette smoking
• Medical history of malignancy, rheumatologic disease, vascular disease
 History & PE

• Assessment of vital signs

• tachycardia, hypotension, decreased oxygen saturation mandate a more
expedited evaluation
• Focus on respiratory & cardiac examination
• Inspection of nares, auscultation of the heart & lungs, edema of lower
extremities, evaluation of jugular venous distention
• clubbing of the digits suggests underlying lung disease such as
bronchogenic carcinoma or bronchiectasis
• Mucocutaneous telaniectasias should raise the specter of pulmonary
arterial-venous malformations
Diagnostic Evaluation

• CXR
• CT scan: better delineation of bronchiectasis, alveolar filling,
cavitary infiltrates, and masses
• CT protocol for pulmonary embolism
• CBC: assess hematocrit, hemoglobin, coagulation studies
• UA: pulmonary-renal syndromes presenting with hemoptysis
• AKI/ RBC / casts: suspicion of small-vessel vasculitis
• Sputum GSCS, AFB
• Bronchoscopy if all the tests mentioned are unreaveling
Treatment

• Treatment varies with etiology

• Large-volume, life threatening hemoptysis generally requires
immediate intervention regardless of the cause
• Establish an airway using an ET intubation & MV
• Identify the site of bleeding either by chest imaging or bronchoscopy
(more commonly a rigid than flexible)
• Goals: isolate the bleeding to one lung & not allow the preserved
airspaces in the other lung to be filled with blood
 Treatment

• Patients should be positioned with the bleeding lung in a dependent

position (i.e. bleeding-side down) and if possible, dual-lumen
endotracheal tubes or an airway blocker should be placed in the
proximal airway of the bleeding lung
• Require assistance of anesthesiologists, interventional pulmonologists or
thoracic surgeons
• Angiographic embolization
• In life-threatening cases
• Risk of unintentional spinal-artery embolization & consequent paraplegia
• Cauterization & laser therapy
• Surgical resection of the affected lung
• Treatement of infection
Thank you !