# 33 - 41 Hemoptysis

### 41 Hemoptysis

undergo chest CT. Diseases causing cough that may be missed on 
chest x-ray include tumors, early interstitial lung disease, bronchiec­
tasis, and atypical mycobacterial pulmonary infection. On the other 
hand, patients with chronic cough who have normal findings on chest 
examination, lung function testing, oxygenation assessment, and chest 
CT can be reassured as to the absence of serious pulmonary pathology.

■
■GLOBAL CONSIDERATIONS
Regular exposure to air pollution can cause chronic cough and throat 
clearing, as well as lower respiratory tract disease. Smoke from cooking 
and heating fuels in poorly ventilated homes; toxic exposures in work 
settings lacking implementation of occupational safety standards; and 
ambient chemicals and particulates in highly polluted outdoor air are 
all forms of air pollution causing cough. Limited therapeutic options 
are available; treatment focuses on improving environmental air qual­
ity (e.g., use of a stove chimney in the home), removal from the expo­
sure, and use of an appropriate face mask.
PART 2
Cardinal Manifestations and Presentation of Diseases
In areas of the world where tuberculosis is endemic, chronic cough 
conjures the possibility of active pulmonary tuberculosis and mandates 
appropriate evaluation, including chest imaging and sputum analysis.
■
■SYMPTOM-BASED TREATMENT OF COUGH
Empiric treatment of chronic idiopathic cough with inhaled cortico­
steroids, inhaled anticholinergic bronchodilators, and macrolide anti­
biotics has been tried without consistent success. Currently available 
cough suppressants are only modestly effective. Most potent are nar­
cotic cough suppressants, such as codeine, hydrocodone, or morphine, 
which are thought to act in the “cough center” in the brainstem. The 
tendency of narcotic cough suppressants to cause drowsiness and con­
stipation and their potential for addictive dependence limit their appeal 
for long-term use. Dextromethorphan is an over-the-counter, centrally 
acting cough suppressant with fewer side effects and less efficacy than 
the narcotic cough suppressants. Dextromethorphan is thought to have 
a different site of action than narcotic cough suppressants and can be 
used in combination with them if necessary. Benzonatate is thought to 
inhibit neural activity of sensory nerves in the cough-reflex pathway. It 
is generally free of side effects; however, its effectiveness in suppressing 
cough is variable and unpredictable. Inhaled lidocaine, an inhibitor 
of voltage-gated sodium channels, provides transient cough suppres­
sion, but because of associated oropharyngeal anesthesia, it poses an 
increased risk of aspiration.
Attempts to treat cough hypersensitivity syndrome have focused 
on inhibition of neural pathways. 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 behav­
ioral modification using specialized speech therapy techniques, but 
widespread application of this modality is currently not practical. 
Novel cough suppressants without the limitations of currently available 
agents are greatly needed. Approaches that are being explored include 
the development of neurokinin-1 receptor antagonists, transient recep­
tor protein vanilloid-1 (TRPV1) channel antagonists, P2X3 channel 
antagonists, and novel opioid and opioid-like receptor agonists.
Acknowledgment
Christopher H. Fanta contributed to this chapter in the 21st edition and 
some material from that chapter has been retained here.
■
■FURTHER READING
Brightling CE et al: Eosinophilic bronchitis as an important cause of 
chronic cough. Am J Respir Crit Care Med 160:406, 1999.
Carroll TL (ed): Chronic Cough. San Diego, Plural Publishing, Inc., 2019.
Gibson P et al: Treatment of unexplained chronic cough: CHEST 
guideline and expert panel report. Chest 149:27, 2016.
Kahrilas PJ et al: Chronic cough due to gastroesophageal reflux in adults: 
CHEST Guideline and Expert Panel Report. Chest 150:1381, 2016.
Mazzone SB et al: Chronic cough and cough hypersensitivity: From mech­
anistic insights to novel antitussives. Lancet Respir Med 10:1113, 2022.
Morice AH et al: ERS guidelines on the diagnosis and treatment of 
chronic cough in adults and children. Eur Respir J 55:1901136, 2020.
Smith JA, Woodcock A: Chronic cough. N Engl J Med 375:1544, 2016.

Erin M. DeBiasi, Carolyn D’Ambrosio

Hemoptysis
Hemoptysis is the expectoration of blood originating from the lower 
respiratory tract. It can be confused initially with bleeding from the 
gastrointestinal tract (hematemesis) or nasal cavities (epistaxis). The 
amount of blood that is being expectorated (volume and frequency) is 
the most important information to gather as massive or life-threatening 
hemoptysis (variable definitions but commonly expectorating >150 mL 
in 24 h or a bleeding rate of ≥100 mL/h) requires emergent interven­
tion. This chapter focuses on non-life-threatening hemoptysis, which 
is more common.
ANATOMY AND PHYSIOLOGY OF 
HEMOPTYSIS
Hemoptysis originates in the lower respiratory tract, anywhere from 
the glottis to the alveolus. The bleeding most commonly arises from 
the bronchi or medium-sized airways, but a thorough evaluation of the 
entire respiratory tree is important. The blood supply to the lungs is 
from both the pulmonary and bronchial circulations. The pulmonary 
circulation is a low-pressure system that is essential for gas exchange 
at the alveoli; in contrast, the bronchial circulation originates from the 
aorta and, thus, is a higher-pressure system. The bronchial arteries 
supply the airways and can neovascularize tumors, dilated airways in 
bronchiectasis, and cavitary lesions. Most hemoptysis originates from 
the bronchial circulation, the higher-pressure system, which can make 
it difficult to control.
ETIOLOGY
Infection, malignancy, and vascular disease are some of the common 
causes of hemoptysis, but the differential is quite broad. In the 
United States, the most common causes remain viral bronchitis, bron­
chiectasis, or malignancy. In other parts of the world, infections such 
as tuberculosis are the most common causes.
■
■INFECTIONS
Although most small-volume hemoptysis cases are due to viral bron­
chitis, patients with chronic bronchitis are at risk for bacterial super­
infection. Streptococcus pneumoniae, Haemophilus influenzae, and 
Moraxella catarrhalis are the more common bacteria involved, and 
these infections can increase airway inflammation that leads to bleed­
ing. Similarly, patients with bronchiectasis, including those with cystic 
fibrosis, can have hemoptysis during exacerbations. Due to recurrent 
bacterial infection, bronchiectatic airways are dilated, inflamed, and 
highly vascular, supplied by the bronchial circulation. This can cause 
bronchiectasis to also be a significant cause of massive hemoptysis and 
subsequent death.
Tuberculosis used to be the most common cause of hemop­
tysis worldwide, but in industrialized countries, bronchitis and 
bronchiectasis are more common. In patients with tuberculosis, 
development of cavitary disease is frequently the source of bleed­
ing, but rarer complications such as erosion of a pulmonary artery 
aneurysm into a preexisting cavity (i.e., Rasmussen’s aneurysm) can 
also be the source.
Other infectious agents such as endemic fungi, Nocardia, and non­
tuberculous mycobacteria can present as cavitary lung disease com­
plicated by hemoptysis. In addition, Aspergillus species can develop 
into mycetomas within preexisting cavities, with neovascularization to 
these inflamed spaces leading to bleeding. Pulmonary abscesses and 
necrotizing pneumonia can cause bleeding by devitalizing lung paren­
chyma. Common responsible organisms include Staphylococcus aureus, 
Klebsiella pneumoniae, and oral anaerobes.
Paragonimiasis can mimic tuberculosis and is another significant 
cause of hemoptysis seen globally; it is common in Southeast Asia and 
China, although cases have been reported in North America from raw

crayfish ingestion. It should be considered as a cause of hemoptysis in 
recent immigrants from endemic areas.
■
■VASCULAR
Hemoptysis from a vascular cause can be associated with cardiac 
disease, pulmonary embolism, arteriovenous malformation, or dif­
fuse alveolar hemorrhage (DAH). While the classic description of 
the sputum expectorated in pulmonary edema (from elevated left 
end-diastolic pressure) is “pink and frothy,” a spectrum of hemoptysis 
including frank blood can be seen. This observation is particularly true 
now with the more widespread use of anticoagulants and antiplatelet 
medications.
Pulmonary embolism with parenchymal infarction can present with 
hemoptysis, but pulmonary emboli do not commonly cause hemop­
tysis. An ectatic vessel in an airway or a pulmonary arteriovenous 
malformation can be a source of bleeding. A rare vascular cause of 
hemoptysis is the rupture of an aortobronchial fistula; these fistulae 
arise in the setting of aortic pathology such as aneurysm or pseudoa­
neurysm and can cause small bleeding episodes that result in massive 
hemoptysis.
DAH causes significant bleeding into the lung parenchyma but, 
interestingly, is not often associated with hemoptysis. DAH typically 
presents with diffuse ground-glass opacities on chest imaging. A range 
of insults cause DAH, including immune-mediated capillaritis from 
diseases such as systemic lupus erythematosus, toxicity from cocaine 
and other inhalants, and stem cell transplantation. The so-called 

“pulmonary-renal” syndromes, including granulomatosis with polyan­
giitis and anti–glomerular basement membrane (anti-GBM) disease, 
may lead to both hemoptysis and hematuria (though one manifesta­
tion may be present without the other). A recently identified cause of 
hemoptysis and DAH is vaping-induced lung injury.
■
■MALIGNANCY
Bronchogenic carcinoma of any histology is a common cause of hemop­
tysis (both massive and nonmassive). Hemoptysis can indicate airway 
involvement of the tumor and can be a presenting symptom of carcinoid 
tumors, vascular lesions that frequently 
arise in the proximal airways. Small-cell 
and squamous cell carcinomas are fre­
quently central in nature and more likely 
to erode into major pulmonary vessels, 
resulting in massive hemoptysis. Pul­
monary metastases from distant tumors 
(e.g., melanoma, sarcoma, adenocarci­
nomas of the breast and colon) can also 
cause bleeding. Kaposi’s sarcoma, seen 
in advanced acquired immunodeficiency 
syndrome, is very vascular and can 
develop anywhere along the respiratory 
tract, from the bronchi to the oral cavity.
Rule out other sources:
-Oropharynx
-Gastrointestinal tract
Nonmassive
No risk factors
Risk factors
■
■MECHANICAL AND OTHER 
CAUSES
In addition to infection, vascular dis­
ease, and malignancy, other insults 
to the pulmonary system can cause 
hemoptysis. Pulmonary endometrio­
sis causes cyclical bleeding known as 
catamenial hemoptysis. Foreign body 
aspiration can lead to airway irritation 
and bleeding. Diagnostic and thera­
peutic procedures are also potential 
offenders: pulmonary vein stenosis can 
result from left atrial procedures, such 
as pulmonary vein isolation, and pul­
monary artery catheters can lead to 
rupture of the pulmonary artery if the 
distal balloon is kept inflated. Finally, 
in the setting of thrombocytopenia, 
Treat
underlying
disease (usually
infection)
Persistent
bleeding
FIGURE 41-1  Approach to the management of hemoptysis. CBC, complete blood count; CT, computed tomography; CXR, 
chest x-ray; UA, urinalysis.

coagulopathy, anticoagulation, or antiplatelet therapy, even minor 
insults can cause hemoptysis.

EVALUATION AND MANAGEMENT
■
■HISTORY
The initial history should be directed at assessing the pattern, severity, 
and quantity of hemoptysis. An approach to management of hemop­
tysis is outlined in Fig. 41-1. A patient’s description of the sputum 
(e.g., flecks of blood, pink-tinged, frank blood or clot) is helpful if you 
cannot examine it. Quantification is often challenging for patients, 
so using references like cups (one U.S. cup is 236 mL) can be helpful. 
Life-threatening hemoptysis is defined by the presence of significantly 
abnormal gas exchange, hemodynamic compromise, or threat for 
airway obstruction. Patients rarely die of exsanguination but, rather, 
are at risk of death due to asphyxiation from blood filling the airways 
and airspaces. This can occur with blood loss of >400 mL within 24 h 
or >150 mL at one time. Fortunately, life-threatening hemoptysis only 
accounts for 5–15% of cases of hemoptysis.
Hemoptysis
CHAPTER 41
Further history may help define the etiology of hemoptysis. Smok­
ing history and/or unintentional weight loss may point to possible 
malignancy. Preceding fevers, cough, and/or sputum production may 
suggest infection. A history of prior diagnosed chronic lung condi­
tions, especially cystic fibrosis or other chronic bronchiectatic diseases, 
is important to note. Screening for causes of pseudohemoptysis (i.e., 
other upper airway or gastrointestinal) is also helpful.
■
■PHYSICAL EXAMINATION
Patients should initially be assessed for signs of life-threatening hemop­
tysis including hypoxemia, tachycardia, and hemodynamic instability. 
Examination should include possible sites of extrapulmonary bleeding 
such as the nasal and oral cavities. Auscultation of the lungs may sug­
gest a laterality. Other relevant physical findings may suggest other 
etiologies of the hemoptysis and include clubbing, signs of a bleeding 
diathesis (e.g., skin or mucosal ecchymoses and petechiae), telangiec­
tasias, or skin rash.
Patient with hemoptysis
History and physical
examination
Quantify amount of bleeding
Massive
Protect airway
CXR, CBC, UA,
creatinine,
coagulation
studies
Bleeding stops
Bleeding continues
Embolization or
resection
CT scan
Bronchoscopy
Treat underlying
disease
Persistent
bleeding